Oral Exams Last Second Factoids

Table of Content

General Principles ............................................................................................................................................. 5

1. Any History: OPQRST AA ADL ROS ................................................................................................... 5
2. Pain............................................................................................................................................................. 5
3. Pre-operative Consideration ............................................................................................................... 5
4. Whenever you see the patient in follow-up, repeat history and physical examination. ................ 5
5. Neurovascular Examination of the Extremities ............................................................................. 5
6. Mnemonic for any surgery: DINA CC PP AAA PPP .......................................................................... 6
7. Perioperative Management.................................................................................................................. 6
8. Always R/O infection if there is any problem postoperatively. .......................................................... 7
9. ABCD of rheumatoid arthritis ............................................................................................................. 7
10. Perioperative Steroids ...................................................................................................................... 8
11. Malignant Hyperthermia ................................................................................................................... 8
12. Principles of Chronic Osteomyelitis Management ................................................................... 8
13. Compartment Syndrome .................................................................................................................. 8
14. Anaphylaxis Shock ............................................................................................................................ 9
15. Postoperative Confusion ................................................................................................................. 9
16. How to Deal with Jehovah‟s Witness Patient booked for elective surgery (e.g. THA) .. 10
17. DVT and PE ........................................................................................................................................ 10
18. Tetanus ............................................................................................................................................... 11
19. Gas Gangrene ................................................................................................................................... 12
20. TB ......................................................................................................................................................... 13
21. Some numbers to remember ........................................................................................................ 13
22. Abdominal Reflexes ........................................................................................................................ 13
23. Conscious Sedation ........................................................................................................................ 13
Trauma ................................................................................................................................................................ 13
24. Open Fracture Spiel......................................................................................................................... 13
25. Intubation ........................................................................................................................................... 14
26. ATLS Spiel ......................................................................................................................................... 15
27. ATLS in Pediatrics.............................................................................................................................. 18
28. ATLS in Pregnancy ............................................................................................................................ 18
29. Hemiarthroplasty after proximal humeral fracture: ................................................................ 18
30. Pelvic Trauma ................................................................................................................................... 18
31. Extended Iliofemoral Approach ................................................................................................... 18
32. Knee dislocation (from summary sheet) ................................................................................... 19
33. Post-traumatic Segmental Bone Loss ........................................................................................ 19
34. Timing of Fracture Repair in presence of Vascular Injury .................................................... 20
35. Approach To Fracture Dislocations of the Elbow ................................................................... 20
36. Tibia Fractures .................................................................................................................................. 23
37. Ankle Fracture................................................................................................................................... 23
38. Talus Fracture ................................................................................................................................... 23
39. Calcaneal Malunion ......................................................................................................................... 24
40. Lisfranc Fracture .............................................................................................................................. 24
41. Sporadic Trauma Pearls ................................................................................................................. 25
42. INVASIVE ATLS PROCEDURES ................................................................................................... 25
43. Vascular Approaches: .................................................................................................................... 27
Pediatrics ........................................................................................................................................................... 29
44. Normal Motor Milestones ............................................................................................................... 29
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45. Summary of Chromosomal and Teratologic Conditions ...................................................... 29
46. Clinical Summaries of Important Skeletal Dysplasias.......................................................................... 30
47. Proximal humerus ............................................................................................................................... 33
48. Pediatric Radial Neck Fractures .................................................................................................. 34
49. Pediatric Monteggia #‟s .................................................................................................................. 34
50. Medial epicondyle # ........................................................................................................................... 34
51. Lateral condyle Fracture ................................................................................................................ 35
52. Distal humeral physeal separations ........................................................................................... 35
53. PEDIATRIC FEMUR FRACTURES ................................................................................................... 35
54. Tibial Spine Fracture ....................................................................................................................... 36
55. Neonatal Pseudoparalysis of the Arm ........................................................................................ 37
56. Congenital Radioulnar Synostosis ............................................................................................. 37
57. Radial Club Hand ............................................................................................................................. 39
58. Congenital Radial Head Dislocations ......................................................................................... 44
59. OCD Capitellum ................................................................................................................................ 47
60. Torticollis ........................................................................................................................................... 47
61. Sprengel‟s Deformity ...................................................................................................................... 50
62. Klippel-Feil Syndrome .................................................................................................................... 55
63. Congenital Scoliosis ....................................................................................................................... 57
64. Infantile Idiopathic Scoliosis (better called Early-Onset)...................................................... 60
65. Juvenile Idiopathic Scoliosis ........................................................................................................ 61
66. Adolescent Idiopathic Scoliosis .................................................................................................. 62
67. ? Fusion levels in scoliosis ........................................................................................................... 62
68. Neuromuscular Scoliosis............................................................................................................... 62
69. Congenital Kyphosis ....................................................................................................................... 62
70. Scheurman‟s Kyphosis .................................................................................................................. 64
71. Scenario of Complication in Scoliosis Surgery ....................................................................... 64
72. Slipped Verebtral Apophysis ........................................................................................................ 64
73. Idiopathic Juvenile osteoporosis ................................................................................................ 65
74. Child with painless limp ................................................................................................................. 65
75. Toe Walking ....................................................................................................................................... 67
76. CP ......................................................................................................................................................... 68
77. Differential Diagnosis of Unilateral Hip Pain in Pediatrics ................................................... 73
78. Hemophilia........................................................................................................................................... 74
79. KID PRESENTS WITH AN IRRITABLE (PAINFUL) HIP: .......................................................... 74
80. DDH ...................................................................................................................................................... 74
81. Acetabular osteotomies ................................................................................................................. 83
82. Perthes ................................................................................................................................................ 84
83. Coxa Vara ........................................................................................................................................... 90
84. Marfan‘s (PREOP CARDIAC) ......................................................................................................... 96
85. Friedrich‟s Ataxia -- PREOP CARDIAC ..................................................................................... 96
86. CMT ...................................................................................................................................................... 97
87. Normal Knee Alignment in Pediatrics ........................................................................................ 97
88. D/D of Genu Varum:......................................................................................................................... 97
89. Blount‟s Disease .............................................................................................................................. 97
90. D/D Genu Valgum ............................................................................................................................. 99
91. Epiphysiodesis ............................................................................................................................... 100
92. Hemiepiphysiodesis ...................................................................................................................... 101
93. Tibial Bowing................................................................................................................................... 101
Posteromedial Bowing: ............................................................................................................................ 101
Anteromedial Bowing: .............................................................................................................................. 102
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 Anterolateral Bowing: ............................................................................................................................... 102
94. Clubfeet............................................................................................................................................. 107
95. Approach to Congenital Vertical Talus (Congenital Convex Pes Valgus) ...................... 114
96. Causes of Cavus Foot................................................................................................................... 116
97. Myelomeningocele .............................................................................................................................. 117
98. Spinal Muscular Atrophy ............................................................................................................. 119
99. Osteogenesis Imperfecta ............................................................................................................. 123
100. Approach to Adolescent Hallux Valgus ................................................................................... 123
101. Congenital Hallux Varus.................................................................................................................. 124
102. Disorders associated with scoliosis ......................................................................................... 126
103. Disorders of Cardiomyopathy .................................................................................................... 126
Spine.................................................................................................................................................................. 127
104. Important history aspects ............................................................................................................ 127
105. Spiel for neurological examination (SPINE) ........................................................................... 127
106. Dural Leak Spiel ............................................................................................................................. 128
107. Complications after neck surgery ............................................................................................. 128
108. Indications for surgery in spinal metastases ......................................................................... 128
109. Gun Shot Wounds Spine.............................................................................................................. 129
110. Spinal Infection (discitis/OM)...................................................................................................... 129
111. RA C-spine ........................................................................................................................................ 130
112. Harvest of Posterior iliac crest bone graft ...................................................................................... 131
113. Failed Back Surgery ...................................................................................................................... 132
114. Paraplegia care: pre and postoperative care ......................................................................... 132
Upper Extremity.............................................................................................................................................. 132
115. Spiel for Shoulder Arthroscopy ...................................................................................................... 132
116. Subscapularis Lengthening ............................................................................................................ 132
117. Cuff Tear Arthropathy ...................................................................................................................... 133
118. Approach to Brachial Plexus Injury .......................................................................................... 133
119. Posterior shoulder dislocation ................................................................................................... 134
120. Detailed Treatment of Posterior Shoulder Dislocation ........................................................ 134
121. Approach To Posterior Recurrent Instability of the Shoulder ........................................... 136
122. Distal Biceps Two Incision Technique ..................................................................................... 138
123. Stiff Elbow ........................................................................................................................................ 139
124. Elbow instability (terrible triad – coronoid/rad head #/elbow dislocation) .................... 142
125. DRUJ pathology ............................................................................................................................. 143
126. TFCC Tears....................................................................................................................................... 148
127. Hook of Hamate Fractures.............................................................................................................. 148
128. Complex MCP Dislocation .............................................................................................................. 149
129. Scaphoid Fracture ......................................................................................................................... 149
130. Perilunate injuries .......................................................................................................................... 150
131. Carpal Metacarpal OA ........................................................................................................................ 152
132. SLAC .................................................................................................................................................. 154
133. Wrist Fusion ........................................................................................................................................ 156
134. Radius Malunion ................................................................................................................................. 157
135. Scaphoid #......................................................................................................................................... 158
136. Keinbock‟s ....................................................................................................................................... 158
137. Carpal Tunnel Release.................................................................................................................... 159
138. PIP Joint Fusion ............................................................................................................................. 160
139. Rheumatoid Wrist .......................................................................................................................... 161
140. Rheumatoid Wrist (Vaughan Jackson)..................................................................................... 163
141. Tendon Transfer Details for Radial Nerve Palsy ................................................................... 165
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Sports ................................................................................................................................................................ 168
142. Spiel for Knee Arthroscopy ......................................................................................................... 168
143. Spiel for ACL (Hamstring) Reconstruction ............................................................................. 168
144. Lack of full extension 8 wks following ACL ............................................................................ 168
145. Meniscal Repair Spiel (INSIDE-OUT TECHNIQUE) ................................................................ 169
Arthroplasty ..................................................................................................................................................... 170
146. Hip Pain History in the young (AVN, FAI, Dysplasia, Labral Tear, Infection, Tumor) .. 170
147. Gait in relation to arthroplasty: Trendelenberg for hips, Lateral or medial thrust for knees
171
148. Steps to deal with intraoperative instability of THA ............................................................. 171
149. THA after DDH – Issues ................................................................................................................ 171
150. THA after DHS ................................................................................................................................. 172
151. Spiel for TKA ................................................................................................................................... 173
152. Unable to Evert the Patella During TKA (SOLUTIONS) ........................................................ 174
153. Patellar Mal-tracking During TKA (REASONS)....................................................................... 174
154. Treatment Options for Unicompartment Arthritis of the Knee .......................................... 174
155. UKA .................................................................................................................................................... 175
156. TKA after HTO (issues) ................................................................................................................. 175
157. TKA post UKA (issues) ................................................................................................................. 176
158. Patellar Fractures in TKA ............................................................................................................. 176
159. Revision TKA................................................................................................................................... 176
Foot and Ankle ................................................................................................................................................ 177
160. Tib Post Deficiency........................................................................................................................ 177
161. Hallux Rigidus ................................................................................................................................. 178
162. Rheumatoid Foot ............................................................................................................................ 178
163. Cavovarus Foot (peds and adult) .............................................................................................. 180
164. Charcot Foot.................................................................................................................................... 182
165. Plantar Fasciitis .............................................................................................................................. 182
166. Chronic achilles tendon rupture.(OKU F&A) .......................................................................... 183
167. Hallux Valgus .................................................................................................................................. 184
168. Hallux Varus .................................................................................................................................... 184
Oncology .......................................................................................................................................................... 185
169. Principles of Biopsy Spiel ........................................................................................................... 185
170. SEVEN QUESTIONS of tumor X-ray description ................................................................... 186
171. Principles in Osteosarcoma and Ewing‟s Sarcoma: ............................................................ 186
172. Local and Systemic Staging for Bone Tumor .............................................................................. 186
173. Metastatic Lesions in the Bone ...................................................................................................... 186
174. Soft Tissue Lesions.......................................................................................................................... 188
175. Hypercalcemia .................................................................................................................................. 189
176. Small round blue cells (LIME E) ................................................................................................ 190
177. Myeloma and Lymphoma: treat with chemotherapy and radiotherapy.................................... 190
178. Five things that can look like anything: ................................................................................... 190
179. Causes of pathology on both sides of the joint..................................................................... 190
180. Fibrous Dysplasia .......................................................................................................................... 190
191. Common Syndromes in Orthopaedic Oncology .......................................................................... 194

There is a separate document for summarized anatomical approaches, and another for vascular
exposures.
Walsh and Petemod summaries are great as well as Brad’s modification of Brian Kwon’s “Approach
to ..”

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General Principles
1. Any History: OPQRST AA ADL ROS

2. Pain
1. Onset
2. Point of maximum pain
3. Quality
4. Radiation
5. Severity
6. Temporal
7. Aggravating & Alleviating, Treatment so far
8. ADL affected?
9. ROS: associated symptoms: locking, catching, instability, numbness, weakness
10. Night pain
11. Rest pain
12. Differential Questions:
1. Congenital or early childhood problems in that area
2. Trauma
3. Constitutional symptoms: fever, chills, night sweats, loss of weight, loss of appetite
4. Other joints involvement

3. Pre-operative Consideration
1. When you take the history and find something significant (e.g., Allergic to penicillin, say ”I
would take note of that and will give him an alternative antibiotic if he needs to go to the OR”
just in case you forgot later on).
2. Ask (MSM, ASA, FOLE): medical, surgical, medications, allergies, smoking, alcohol, family hx,
occupation, leisure, expectations
1. PMH (bleeding diathesis),
1. Hemophilia: correct factor 8 or 9
2. Von Willebrand: DDAVP
3. DM: risk of infection, wound healing complications
2. PSH (any complications with General Anesthetics),
3. Meds:
1. Steroids: need stress doses perioperatively
2. NSAIDs: complications (GI and cardiac), fracture non-union
3. Birth pills: consider blood clots
4. Allergies
5. Smoking: counsel quitting, union complications, skin complications
6. Alcohol: DT prphylaxis (Ativan 2g IV/PO q 2-4 hours, Thiamin 100mg PO/IV OD x3,
multivitamin T PO OD)
7. FH (MH, bleeding diathesis),
8. Occupation,
9. Leisure,
10. Expectations
3. Always postoperatively: consider splint, weight bearing, antibiotics, anti-coagulants,
physiotherapy, follow-up

4. Whenever you see the patient in follow-up, repeat history and physical examination.

5. Neurovascular Examination of the Extremities

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Upper Extremity:
1. For radial nerve, I would check sensation on the dorsum of the 1st web space. I would check
motor with extension of the wrist and elbow.
2. For PIN, I would check motor with extension of the thumb (in the plane of the table)
3. Form median nerve, I would check sensation on the radial aspect of the tip of index finger. I
would check motor with thumb opposition or abduction (perpendicular to the table)
4. For AIN, I would check motor with flexion of the DIP of the index finger.
5. For ulnar nerve, I would check sensation on the distal ulnar aspect of the little finger. I would
check motor with fingers abduction.
6. For axillary nerve, I would check sensation over the regimental patch area. I would check
motor with abduction of the arm.
7. For musculocutaneous, I would check sensation over the lateral aspect of the forearm. I would
check motor with flexion of the elbow.

Lower Extremity:
1. For femoral nerve, I would check sensation in saphenous nerve distribution (medial aspect of
the foot). I would check motor with extension of the knee.
2. For obturator nerve, I would check sensation over the medial aspect of the thigh. I would check
motor with hip adduction.
3. For sciatic nerve, I would check motor with knee flexion.
4. For tibial nerve, I would check sensation over the plantar aspect of the foot (medial and
lateral). I would check motor with ankle plantar flexion.
5. For deep peroneal nerve, I would check sensation in the first web space. I would check motor
with ankle dorsiflexion.
6. For superficial peroneal nerve, I would check sensation over the dorsum of the foot (excluding
the first web space). I would check motor with eversion of the foot.
7. For sural nerve, I would check sensation over the lateral border of the foot.
8. For saphenous nerve, I would check sensation over the medial aspect of the foot.

6. Mnemonic for any surgery: DINA CC PP AAA PPP

1. Diagnosis
2. Investigation
3. N/A: non-operative
4. Consult
5. Consent
6. Pre-op
7. Procedure principles
8. Antibiotic
9. Adjuncts: table, flouro, instruments, tourniquet
10. Approach
11. Pause: surgical pause
12. Postop check
13. Physio

7. Perioperative Management
― My pre-operative plan includes obtaining informed consent for the surgical procedure as well
as blood transfusion and bone graft where deemed necessary. I would obtain standard pre-
operative bloodwork including a CBC, group and screen and coagulation studies. I would
ensure that the patient had all of the up to date imaging studies necessary for pre-operative
planning. I would request and have available old operative reports, medical charts and

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 imaging studies. In the case of advanced age or significant co-morbidities, additional tests
including a CXR and EKG as well as anesthetic and/or medical consultation would be
obtained.‖

―In planning my operative technique I would ensure that the appropriate templates, instruments
and implants were available. I would ensure the availability of bone graft or substitute where
necessary. I would appropriately position the patient in the ____ position using a _______
table. I would/not use a tourniquet. [**Closed reduction with fluoro where necessary] After
appropriate sterile prep and drape of the patient I would utilize a standard _______ approach,
obtain hemostasis and carefully identify and protect relevant neurovascular structures.‖

Pre-Op – Summary
 I would discuss the risks and benefits of the procedure and obtain informed consent for the
procedure, bone grafting and blood products.
 In particular for this case, the patient needs to understand the risk of …
 I would obtain routine pre-operative investigations (and consult…) and notify the OR of
equipment needed for the planned procedure

Intra-Op
 Mark limb in pre-op
 EUA
 Tourniquet, position
 Prep & drape
 Check stability intra-op (for arthroplasty cases)
 Inspect any exposed or at risk nerves
 Check the level for spine cases

Post-Op Care
 Check NVI in PAR
 Post-op x-rays
 Antibiotics
 DVT prophylaxis
 Mobility
 Follow-up

8. Always R/O infection if there is any problem postoperatively.

9. ABCD of rheumatoid arthritis

o A: airway, anesthesia, arytenoids?
o B: bone quality (osteoporosis…may need more levels or longer plate etc..)
o C:
o Cervical spine Flex-Ex (basilar invagination, C1-C2 instability, subaxial disease,
lateral subluxation of C1-C1)
o Consult Rheumatology, Medicine and Anesthesia
o D: drugs:
o Predisone: give stress dose of solucortef 100mg IV.
o Must stop the new biologics (TNF blockers) at least 2 weeks pre-op and until wound
healed
o stop methotrexate a month before surgery (lots of articles say ok for methotrexate)

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10. Perioperative Steroids
o For Major Procedure: need to cover her perioperatively:
- 100 mg hydrocortisone preoperatively
- 100 mg intraoperatively
- then 100 mg IV q8h for 24 hours, 50 mg q8h the next day, and a single dose of 100 mg IV
on the third day.

o For minor surgical procedures

- can give them a single preoperative dose of 100 mg hydrocortisone

11. Malignant Hyperthermia

 Anticipate in :
1. Autosomal dominant form: most common
2. OI
3. Arthrogryposis
4. Duchene Muscular Dystrophy
5. Turner syndrome (45XOfemles,short,web neck,cubitus valgus,kidney,cardiac,short
4/5 MC)
6. Noonan syndrome (short stature,web neck,cubitus valgus)
 Common with halothane, sucinylcholine, methoxyflurane
 Clinical and lab presentation: Tachycardia, Arrhythmia, hypotension, Elevated temperature,
Hypertonia masseter spasm during intubation, generalized muscle rigidity, Hyperkalemia,
Elevated creatine kinase, respiratory and metabolic acidosis
 Complications: pulmonary edema, DIC, acute renal failure
 Treatment
1. Stop all inhaled anesthetics
2. Change rubber tubing
3. Administer 100% O2
4. Dantrolene 2.5 mg/kg bolus then dantrolene 10 mg/kg over 24hrs continuously
5. Adjust ventilation according to blood gas
6. Stop surgery as soon as possible
7. Cooling consider ice water through the NG tube
8. IV fluid
9. Force diuresis
10. Post op ICU bed
11. IM consult post op
12. Follow renal function closely

12. Principles of Chronic Osteomyelitis Management

1. intraop cultures
2. boney stability
3. adequate debridement
4. dead space management: antibiotic beads, antibiotic cement spacer
5. soft tissue coverage options
6. ID consult
7. IV abx

13. Compartment Syndrome

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14. Anaphylaxis Shock
 Manifested as hypotension, shock, life-threatening or irreversible bronchospasm, or impending
airway obstruction due to laryngeal edema

General Approach (Adult Doses)

1. Termination of any further exposure to the allergen
2. High flow 100% O2, get ready for intubation, cricothyrotomy, or tracheostomy
3. Start IV access immediately and bolus normal saline
4. Epinephrine:
a. 0.3 to 0.5 mg 1:1000 epinephrine SQ (0.3 to 0.5 cc)
i. can give same dose IV diluted down to 1:10,000 (up to 5 cc)
5. Obtain ABG ASAP: treat acidosis appropriately or administer 50mEq ampule of bicarbonate
prophylactically for severe hypotension every 5minuted (DOUBLE CHECK THIS POINT)
6. Benadryl 50 mg IV/IM and ranitidine 50mg IV/IM
7. Hydrocortisone (Solucortef) 500-1000 mg IV, or methylprenisolone (Solumedrol) 125 mg IV
8. Add aminophylline (0.5 mg/kg/h IV with 6 mg/kg loading dose over 30 minutes) as needed for
bronchospasm
9. Add catecholamine (dopamine or norepinephrine) if slow response in peripheral blood
pressure
10. After termination of reaction: check airway for laryngeal edema before extubation

Pediatric Doses
 0.01 mg/kg 1:1000 epinephrine SQ
 0.5-1.0 mg/kg IV Benadryl

15. Postoperative Confusion

o Differential Diagnosis: CODE PIE
o CNS – dementia, head trauma, post-ictal, stroke, wernicke‘s encephalopathy (needs
thiamine)
o Organ Failure – hypoxemia, hypercapnea, hypotension
o Drugs – over narcotized – needs narcan
 psychotropic meds
o Endocrine – hyperglycemia, hypoglycemia, Addison crisis
o Psychiatric – mania, schizophrenia
o Infection – meningitis, encephalitis
o Electrolyte abnormalities – sodium, calcium, glucose

o In the orthopaedic post-op patient, must consider:

 hypotension/shock with hypoxemia in the really sick
 over narcotized
 Wenicke‘s in the alcoholic patient – needs thiamine and benzos
 electrolyte abnormalities – especially calcium.
 hypoxemia from a pulmonary embolism.

o Management:
 Do a history
 Do a physical exam – starting with the standard ABC‘s.
 Order bloodwork, CXR, V/Q, everything.

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16. How to Deal with Jehovah‟s Witness Patient booked for elective surgery (e.g. THA)

1. Patient Factors:
 Discuss with the patient the risk of bleeding, MI, Stroke, renal failure (RTA), Wound
complication
 Weigh the benefit of the surgery (quality of life) versus the risks
 Internal Medicine Consult: optimize his medical condition, ensure good cardiac function to
withstand possible prolonged anemia
 Iron and vitamin supplement
 Erythropoietin Supplement: either 300 U/kg/day subcutaneously for 10 days before surgery, on
the day of surgery and for four days after surgery; or 600 U/kg given subcutaneously in one
weekly dose (21, 14, and 7 days before surgery) plus a fourth does on the day of surgery. All
patients should receive iron supplements during PROCRIT treatment to account for the body's
increased iron demands required for red cell production.

2. Anesthesia Factors:
 Anesthesia consult
 Hypotensive Anesthesia
 Spinal Anesthesia

3. Surgical Factors:
 Well planned surgery
 All possible implants and sizes available immediately to avoid wasting time
 CAREFUL RAPID surgery
 METICULOUS hemostasis
 Cell Saver Intraoperatively (discuss with the patient)

17. DVT and PE

Pt 24 hr post op, the nurse call you due to chest pain and desating at room air with PaO2 88. Management:
A- On phone:
1. O2 100% By mask
2. Elevate the head of bed 30 degrees
3. Check the vital signs
4. Blood stat for: CBC, Lytes, BUN & Creatinine, INR and APTT, Troponin, ABG
5. Stat ECG
6. Stat portable CXR
7. Nurse to reassure the pt that you coming soon
8. Crash tray to be available in the room with the pt chart
B- Once you are in the room
1. Asses the air way, while the nurse taking the vital signs
2. Chest and heart examination
3. Complete examination from head to toes with concentration on the site of operation and calf
4. Check the ECG, Lab result and CXR
C- To confirm the Diagnosis you need lung ventilation perfusion scan
 If Large defect or mismatch-----PE
 If Small defect-----Do Venography
o If +ve ----PE
o If -ve------You still suspect PE And pt high risk ---Do Pulmonary Angio.
D- Call ICU to have bed
E- Call thrombo team and you expect the thrombo team to do
1. Confirm the ICU bed
2. Check about the contraindication for Heparin e.g Bleeding diathesis, tumor , peptic ulcer
3. Start Heparin IV Bolus 5000 U, then 18 U / Kg /Hour for 23 Hour ( ie 25000U/ 500 ml 5%Dexrtose in water to run
at 20 ml /Hr , So you deliver 1000U per Hr) or Enoxaparin 30 mg sc bid
4. Maintain the PTT in therapeutic range (1.8-2.8 times normal)

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 5. Repeat PTT every 4-6 Hr
6. Platelet count to be check in day 2-3 to detect heparin induce thrombocytopenia (usually occur at day 7) ----
Protamine sulfate to reverse Heparin
7. If you are treating an established PE: Enoxaparin 70 mg sc bid ( full 1 mg/kg)
8. Consider IVC filter if there is contraindication for Heparin
9. Until renal function is normal don‘t use LMWH
10. Duration of therapy:
a. If post ortho surgery‖ : 3months….
b. If 2 nd DVT : then tx with 6 months and get medical consult

Imaging & investigations

 CBC, SMA7, coags, blood sugar, trops
 ABG (arterial hypoxemia with respiratory alkalosis): PaO2 <80mm Hg, PaCO2 < 40mm Hg
 CxR (often normal r/o pneumothorax, ARDS)
 EKG (Right bundle branch block ―S1Q3T3‖, right axis deviation, sinus tachycardia, ST depression or T wave
inversion in lead 3) – r/o MI and pericarditis
 Resus as per ATLS protocol
 Confirm Dx with: V-Q scan, Spiral chest CT, Pulmanary angio

Differential
 PE, Fat embolus, MI, ARDS, Pneumonia, Atelectasis, CHF
 Sequelae of initial trauma: Pneumothorax, Pulmonary or cardiac contusion, tamponade

Treatment of PE
 Stabilize saturation with 100% O2 rebreather mask
 If patient continues to desaturate intubate to protect airway and ventilate
 Consult ICU and run like ATLS scenario if patient is unstable
 When pt stabilizes start IV anticoagulation if clinical suspicion high and no contra-indications (then order VQ,
spiral chest CT, etc to confirm diagnosis)
 IV heparin bolus 5000 IU IV followed by titration of drip rate to PTT b/w 80 – 120 sec with q6h coagulation
monitoring
 If pt is POD #1 or less do not bolus, just start IV drip
 If pt has contra-indication to anti-coagulation tx (ie s/p spine surgery or post-trauma with bleeding insert IVC filter)
 Oral warfarin x 3 months. D/C IV heparin when INR titrated to b/w 2.0 – 3.0

18. Tetanus
 Clostridium tetani – anaerobic, G+ rod found in soil, animal + human feces. Spores for years
 Pathogenesis: toxin binds to peripheral motor neuron terminals  axons  nerve cell body in CNS. Crosses
synapse to enter inhibitory interneurons where it blocks neurotransmitter release  increase motor activity and
increases sympathetic activity.
 Clinical Manifestations
  muscle tone and generalized spasm – onset after injury – approx. 7 days
o Can occur repetitively. Mild  severe
o 1 – trimus/lockjaw  other muscles involved – rigid abdomen, stiff proximal limb muscle with sparing of
st

hands and feet.

o Sustained contraction of facial muscles
o Can lead to reduced ventilation, apnea or laryngospasm
o Some develop paroxysmal, violent, painful, generalized muscle spasm  cyanosis.
o DTR increased, dysphagia or ileus may preclude oral feeding
 Sympathetic overactivity
o Labile/sustained HTN, tachycardia, fever, profuse sweating, arrhytmias, increased plasma and urine
catecholamine levels
o Late CV collapse – hypotension and bradycardia – reversible with physical stimulation such as suctioning
 Diagnosis: Clinical, Wound cultures can isolate C. tetani
 Treatment Goals:
1. Admit to ICU
2. Eliminate source of toxin
 Thorough I+D wound
 IV penicillin – 2 million units q6h x 10d + streptomycin 0.5g IM q12h; allergic – clindamycin/erythomycin

11
 3. Neutralize unbound toxin
 TIG 500-1000U IM repeated til total dosage of 6000 units IM
4. Prevent muscle spasm
 Diazepam 120mg/day, barbiturates, chlorpromazine
 Pancuronium + mechanical ventilation for spasms unresponsive to medication and causing respiratory
difficulties
 Sympathetic overdrive – can use beta-blockers/morphine
5. Support – especially respiratory
 Intubation/tracheostomy + mechanical ventilation
 Hydration
 Parenteral/enteral nutrition
 Monitor bowel/bladder and renal function
 Watch for GI bleeding and decubitus ulcers

Tetanus Vaccination
 Tetanus prone wounds:
o Age of wound: >6 hours,
o Depth: > 1 cm deep
o Configuration: stellate, avulsion
o Mechanism: missile, crush, burn, frostbite
o Presence of devitalized tissue
o Presence of contaminants: e.g., barnyard
 Immunization schedule
o Previous Immunization within 10 years
 Old wound >24hrs, Tetanus prone – 0.5cc Td > 1 year
 Not prone – 0.5cc Td > 5years
o Previous Immunization > 10 years
 Not prone – 0.5cc Td
 Old wound > 24hrs, Tetanus prone – 250U TIG + 0.55cc TD, consider giving Pen 2 million U IV.
o Never immunized
 Clean minor wound – 0.5cc Td
 Any other wound – Td + TIG + consider penicillin (separate site and needle)
nd rd
 Start immunization schedule – 2 Td 4/52 later, than 3 Td – 6-12 months later
o NB – can give TIG 500 U if severe wound

19. Gas Gangrene

 Clostridium perfringens – G+ anaerobic bacillus without spores. Obligate anaerobes and can‘t
multiply in normal tissue. Introduced in deep muscle  multiple and produce toxins  surrounding
tissue and devitalize them  multiple further and viscous cycle. Incubation: 12-24 hr post injury
Clinical Findings:
 Initially - Pain + local edema and exudation of a thin, dark fluid
 Get elevated HR but normal temp  quick progression to toxemia and local spread of infection
 Wound then becomes bronze in colour with musty odor and gas production. Muscle
involvement greater than what skin wound indicate
Diagnosis: Clinical, XR: gas in soft tissue, Occasionally jaundice, hemoglobinemia & hemoglobinuria
Treatment:
 SURGICAL DEBRIDEMENT
o I+D, excision of involved muscle, amputation if necessary
 Supportive
o IV abx – Penicillin 3 million U q3h, add aminoglycoside if think polymicrobial.
Clindamycin if pen allergic
o Fluid and electrolyte replacement
o Hyperbaric oxygen treatment – 3 atmosphere obtains arterial oxygen tension from
1200-1700 mm Hg. Place in chamber 60-90 minutes q8-12h

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20. TB
Antibiotics: (RIPE) rifampin, isoniazid, pyradizimine, ethambutol

21. Some numbers to remember

punjabi and white > 5 is instability
MESS > or equal to 6 amputate
Mirels > or equal to 8 - stabilize
intubate GCS <8
22. Abdominal Reflexes
o Upper abdominal reflexes are supplied by nerve roots T9-T11. Lower abdominal reflexes are
supplied by roots T11-T12.
o These reflexes can be tested by lightly stroking the abdominal wall diagonally towards the
umbilicus in each of the four quadrants of the abdomen.
o Reflex contractions of the abdominal wall are absent in upper motor neuron lesions above the
segmental level and also in patients who have had surgical operations interrupting the nerves.
They can also be absent in normal people.
o Often abdominal reflexes are lost early in multiple sclerosis, but late in motor neuron disease

23. Conscious Sedation

1. Get consent pre-sedation for Conscious Sedation and for OR
2. Have another physician give drugs and monitor airway.
3. Do it in controlled setting with ECG monitor, pulse ox and BP cuff, O2, intubation tray, suction and
bag.
4. Have reversal medications drawn and ready:
1. Naloxone (0.01 mg/kg initial dose, 0.1 mg/kg second dose. In adults, 0.4mg initial
dose, up to 2mg)
2. Flumazenile (0.2 mg – up to 2mg adults – note not recommended for paeds)
5. Sedate with titrated doses of Fentanyl and Midazolam.
1. fentanyl (dose 2microgram/kg up to 50 in kids)
2. midazolam (Versed) 1mg
3. following this I would titrate the doses of each to achieve satisfactory sedation.

BACK TO TOP

Trauma
24. Open Fracture Spiel
1. After AMPLE history and physical examination, I would perform a gentle closed reduction after removing
any gross debris and cover the wound with sterile gauze.
2. I would start the patient on appropriate antibiotics (Ancef 2g +/- gentamycin 240 mg +/- penicillin 5 million
units; or vancomycin 1g) and confirm tetanus status [nothing for immunized or booster less than 5 years,
0.5 ml toxoid for those never immunized or greater than 5 years, plus immunoglobulin 250 units IM (500 if >
24 hrs or heavy contamination)] and treat accordingly.
3. I would also confirm NPO status.
4. I would get an informed consent from the patient
5. I would notify the operating room to have two separate set-ups, and Jet Lavage, 10L NS, required
instruments.
6. I would do a trauma scrub
7. After sterile prep and drape, I would start the debridement by extending the wound both proximally and
distally to facilitate exposure, excising the wound edges to clean, viable skin. I would proceed layer by

13
 layer from superficial to deep removing any loose debris or non-viable tissue down to bone. Both fractured
bone ends would be delivered out of the wound and debrided. Any non-structural/articular bone that was
devoid of soft tissue attachments would be discarded.
8. I would then irrigate with 10L of NS with gentle pressure.
9. If definitive fracture management was taking place at this setting, it would be performed after a complete
new set-up. This may include internal and or external fixation.
10. Once the fracture was fixed, dead space would be assessed and managed appropriately, possibly with an
antibiotic bead pouch covered with an Op-Site.
11. Extensile incisions would be closed primarily if possible and the wound would be packed open.
12. I would plan to return to the OR q24-48hrs for serial debridements until the wound was clean
13. I would consult the plastic surgery team as required for definitive soft tissue coverage ideally within 3-5
days.
14. The patient would remain on IV antibiotics until the wound was deemed clean when definitive fixation and
bone grafting would take place.

25. Intubation
6 P‟s of Intubation
1. Preparation: equipments LOST MINDS
2. Pre-Oxygenation
3. Pretreatment
4. Paralysis
5. Pass Tube
6. Post Intubation Checks:
 Distance inserted and secure
 End-tidal Co2
 Bilateral auscultation
 SaO2
 CXR

Equipments for Intubation: LOST MINDS

1. L – Laryngoscope: McIntosh 3
2. O – O2 (BVM), oral airway
3. S – Suction, stylet, syringe
4. T – Tubes (ET): 7.5mm women, 8mm men, 4+ age/4 pediatric
5. M – Monitors: ECG, BP, O2 sat, temperature
6. I – IV‘s
7. N – Nurses (help)
8. D – Drugs: Fentanyl, Midazolam (Versed), Xylocaine Spray, Succinylocholine, Lidocaine,
Diazepan (Valium)
9. S – Scalpel

Rapid Sequence Intubation

 Pre-Oxygenate as much as possible, avoid bagging if possible to prevent gastric distention
 Time zero minus 2 minutes: Fentanyl 3μg/kg
 Time zero:
o Induction
 Fentanyl 3-5μg/kg
 Midazolam (versed) 0.15-0.3mg/kg
 Topical Xylocaine: 8-10 mg/ml, 3-4 sprays, 2x
o Paralyzing: RISKY in TRAUMA for the inexperienced
 Succinylcholine 1.5mg/kg (usually 100mg)
 Rocuronium 0.6mg/kg (if hx of malignant hyperthermia or contraindication to
succinylcholine)
14
  Time zero + 45 secs:
 With C-SPINE precautions
 Clear the mouth and pharynx of secretion
 Intubation with cricoid pressure (BURP - backward, upward and rightward
pressure on the cartilage)
 Laryngoscope to visualize the cords
 Insert tube to 22cm (21cm for females, 23cc for males) mark at the teeth
 Check end-tidal, O2 sat, auscultate bilaterally and CXR
 Ventilator settings: 10-14 resp/min, tidal volume 8-10 ml/kg (600-700 cc)
 Once intubated, keep on maintenance of versed and morphine

Consider
 Predosing with Lidocaine 1.5mg/kg to decrease risk increased ICP, and risk
laryngospasm
 Predosing with pancuronium 0.01mg/kg to prevent convulsions with succinylcholine

Seizures post intubation:

1. Concern regarding head injury
2. Check the glucose
3. Valium (diazepam) – long acting benzo . start with 0.2-0.4 mg/kg (so for a 70 kg male that is
you can start with 10 mg Valium) go 5-30 mg.

Narcan: 0.2-0.4 mg
Flumazenial: 02.mg

Desating post-intubation (DOPE):

1. Dislpacement
2. Obstruction
3. Pneumothorax
4. Equipment failure

26. ATLS Spiel

o Before the pt arrives I would mobilize trauma team which consists of a general surgeon,
anesthetist, 2 RNs and RT and ask them to observe universal precaution. Simultaneously, I
would obtain any available details of trauma/pt. I would start by primary survey, assessing the
airway, breathing, circulation, disability and exposure making sure that the patient has a
cervical collar and on a spine board.
AIRWAY:
o Upon entering the trauma bay, I would assess the pt‘s airway with careful c-spine control, while
simultaneously asking for 2 large bore IVs with warmed 2L NS bolus and obtaining trauma
blood work – O2 100% by non-breather mask– and monitors (ECG, oximetry, BP, temperature
probe) and I would ask to be alerted of the vitals every two minutes and of the results of the
blood work when available.
o If he does not have a c-spine collar on already, I would have someone apply gentle in-line
traction until one could be applied.
o I would then start by determining whether the patient can talk and verbalize appropriately.
―What is your name?‖
o An appropriate response indicates a patent airway and the ability to breath.
o If not, I would assess his airway looking and listening for signs of obstruction, breathing or
major trauma.

15
 o Dysphonia and subcutaneous emphysema: think of blunt laryngotracheal trauma
o Treatment:
o If his airway is non protected I would start with basic airway management (suction
obstructions, oral airway, nasal airway)
o I would proceed to definitive airway management with ETT with inline stabilization and
RSI when appropriate
o Surgical airway: cricothyroidotomy

BREATHING:
o After securing his airway, I would proceed to evaluate his breathing and ventilation.
o I would ensure supplemental O2 and an oximetry is applied.
o LOOK: mental status (anxiety, agitation) color, chest movement, respiratory rate/effort
o LISTEN: for air flow, chest wall crepitus, fail segments, sucking chest wound, subQ
emphysema
o FEEL: tracheal shift, ascultate for symmetric BS
o PERCUSS: resonant versus dull
o Treatment
o monitor: rate, O2 sats
o O2: NP, Venture Mask, bag-value mask
o needle thoracostomy
o chest tube

CIRCULATION:
o Assess circulation by:
o looking at overall colour, JVP distention and hemodynamic profile (HR, BP, pulse
pressure)
o listening to his heart
o feeling peripheral pulses
o I would do quick exam of abdo, pelvis and extremities to look for any major source of bleeding
o I would ensure IV fluid was running and assess his response to fluid
o If no response or transient response I would give 2 U pRBC
o Treatment:
o direct pressure to external bleeding, don‘t remove impaled objects, tourniquet is last
resort
o fluid: replace loss blood at rate of 3:1 to maintain intravascular volume
o blood: indicated if no/transient response to IVF bolus, profound hypotension, ongoing
bleeding
o crossmatch (ideal but takes time, ~ 1hr)
o type-specific (takes ~ 10 mins, prefer to O-neg blood)
o O-neg blood: for children and women of child-bearing age
o O-pos blood: for everyone else if no time to cross and match
o Anticipate complications of massive transfusions: FFP if ongoing hemorrhage on
platelet < 50000
o if inadequate response consider ongoing losses
 abdo: DPL, FAST – tx by laparotomy in OR
 pelvis: belt, ex-fix
 chest: chest tube, thorocotomy ideally in OR
 Vasopressors: indicated if hypotenion despite appropriate volume
 Levophed (norepinephrine): 0.5-30 mcg/kg/min for SBP < 70
 Epinephrine:

16
DISABILITY AND EXPOSURE
o assess level of consciousness by APUV/GCS
o size and reactivity of pupils
o gross motor exam of extremities
o undress pt complete and keep pt warm with blanket and heaters to avoid hypothermia

Primary Adjunct
-trauma bloodwork (CBC, Bun Cr, Lytes, INR, PTT, glucose, amylase, B-HCG, tox screen, cross and
type)
-CXR, Shoot through lateral, AP Pelvis
-NG (no if CSF rhinorrhea or basal skull #)
-foley (no if blood at meatus, high riding prostate, …)

Monitor Resuscitation
-u/o, BP, HR, CVP, base deficit, ABG

Massive Transfusion
-if platelets < 100000 transfuse platelets

Secondary Survery
This does not begin until primary survey has been complete, resuscitative efforts are well established,
and the pt is demonstrating normalization of vital functions

History: AMPLE

Detailed head to Toe Exam

H&N
-LOC
-pupils (size, equality, reactive to light)
-EOM, nystagmus, fundscopy
-lacs, tenderness (facial #s esp ethmoid which contraindicate NG through nares)
-ears: tympanic membranes
-Cspine: tenderness, steps, crepitus, hematoma

Chest: IPPA

Abdo: IPPA

Pelvis
-rectal exam, bimanual exam in females (occult open # pelvis)
-exam stability

MSK
-log-rool pt and exam back then remove board
-palpate, ROM, stability
-N/V exam

Neuro: GCS, detailed neuro (CN, motor, sensation, DTR, tone,

Teritary Survey
24 later after pt stabilized to ensure not injury has been missed

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27. ATLS in Pediatrics
o 20cc/kg fluid bolus X3 for resus
o 10cc/kg for prbc‘s
o breslow tape
o ET tube the size of their nares – usually 4-5 (or age +4 divided by ?)
o Head cut out of the spine board to put in proper sniffing position (big disproportionate head
compared to adults)

28. ATLS in Pregnancy

o Plasma expansion, takes greater losses to make hypotensive
o Put in Left lateral decub to improve venous return
o Hypercoagulable
o Radiation exposure to fetus is 5rads (same as 5 cGy)
o Cxr has 0.002cGy and CT abdo has 2.6cGy
o Avoid pressors, they decr uterine blood flow
o Safe drugs: Ancef, tetanus, clina, flagyl
o Unsafe: Coumadin, cipro, gent
o Remember to give O neg blood and if mother RH neg, need to give 300mcg of rhogam

29. Hemiarthroplasty after proximal humeral fracture:

Key points:
1. Anterior approach,
2. ID biceps tendon,
3. Work in between greater and lesser tuberosity to extract head and access shaft.
4. Trial reduction with 35 degrees retroversion based on flexed forearm and soft-tissue
tensioning for proudness (can also use the AO jig).
5. Marked rotation and proudness.
6. Mersilene tape through shaft to tie down tuberosities in tension band fashion.
7. Cemented in implant.

30. Pelvic Trauma

 most important principle is hemodynamic support – ex fix early if pelvis is unstable and
hemodynamically unstable
 if still unstable after ex-fix then angio (only 10-20% arterial source)
 if still unstable and in extremis - consider open packing with general surgeon as a life saving measure!

Ex fix
 In OR - use fluoro, place three 3.5 mm Shanz pins into crest, starting 2 cm posterior to ASIS - aim
posterior and medial to get into strong supra-acetabular cancellous bone
 Do not enter the hip joint
 Attach pins to clamp then construct frame using 2 vertical bars with 1 or 2 cross bars (if Slattis frame)
 Ensure that enough room is available for abdomen in the sitting position

31. Extended Iliofemoral Approach

Indications for the use of the EIF approach have been reported to be:
1. Transverse plus posterior wall or T-shaped fractures with a transtectal configuration.
2. Transverse fractures with an extended posterior wall fracture.

18
3. T-shaped fractures with wide separations of the vertical stem of the T or those with associated
pubic symphysis dislocations.
4. Both-column fractures with complex posterior column components, displaced fractures entering
the SI joint, or wide separation of the anterior and posterior columns at the rim of the acetabulum.
5. Associated fracture patterns or transverse fractures that are operated on more than twenty-one
days after injury.

32. Knee dislocation (from summary sheet)

Approach To Treatment
 Initial treatment is based on recognizing that the PCL and MCL can heal without surgery and that the
ACL and lateral structures do not
 Most ligament injuries do not need acute surgey
 Goal of treatment is to provide a functionally stable knee with full ROM
 Really need to think about incision placement when there is vascular compromise requiring repair
o The work horse incisions will be posteromedial (vasc repair, PCL avulsion fixation, MCL repair
(rarely need to fix it) and anterolateral (PLC, fasciotomies, intraarticular access)

Combined MCL, ACL, and 2+ PCL laxity or less

 PCL has been found to heal in this group
 Studies also showed that patients with 1+ vs 2+ were no different
 Currently surgery cannot reproducibly restore normal PCL stability so to do surgery to decrease from
2+ to 1+ may not help
 This author recommends non surgical treatment of 2+ or less
 Initially placed in cylinder cast with 20 flexion, preventing valgus stress, allowing healing of MCL, and
preventing stress deprivation of the joint surface
 Cast is changed weekly with gentle valgus stress test
 Once stability of MCL is achieved (usually 2 weeks for proximal, 4-5 weeks for distal) cast is stopped
 PCL is allowed to heal at same time
 Once MCL healing is confirmed clinically, start rehab for full ROM – then reassess
 This approach usually results in no medial laxity, acceptable posterior laxity and ACL deficiency
 Patient activity warrants ACL treatment from there

Combined MCL, ACL, and >2+ PCL laxity

 PCL reconstruction is indicated
 Author does not recommend combined ACL/PCL because of increased stiffness
 PCL delayed until knee has little swelling and good ROM
 Autogenous patellar tendon (or allograft)
 If ACL becomes symptomatic, done at later date
 When high grade MCL laxity is present and fails to heal, can make multiple longitudinal perforations in
the MCL to stimulate healing
 Additional options – recessing the femoral attachment, advancing the distal attachment, and reefing the
MCL
 According to Brinker, most sensitive test for PCL disruption is ‗quads active test‘ (knee at 90 deg and
foot planted, quads activated /and tibia comes forward on femur

33. Post-traumatic Segmental Bone Loss

19
34. Timing of Fracture Repair in presence of Vascular Injury
FRACTURE/VASC COMPROMISE
 > 3 h shunt  fix #  vessel
 < 3 h  fix #  vessel repair

35. Approach To Fracture Dislocations of the Elbow

Principles of the Operative Technique

1. Restore coronoid stability through fracture fixation for type II/III or through anterior capsular repair for
type I
2. Restore radial head stability through ORIF or arthroplasty
3. Restore lateral stability through repair of the LCL complex and associated so-called secondary
constraints such as the common extensor origin (CEO) and/or posterolateral capsule
4. Repair the MCL in patients with residual posterior stability
5. Apply a hinged external fixator when conventional repair does not establish sufficient joint stability to
allow early motion

(The three primary indications for hinged ex fix are: (1) persistent instability
in association with an acute fracture-dislocation
despite attempted ligament repair and fracture fixation
or radial head replacement, or both; (2) gross acute instability
in a patient who is not a candidate for surgery;
and (3) delayed treatment (approximately four weeks or
more after the time of injury) of a dislocated and stiff elbow.
A relative indication is the need to protect the stability
and the fracture reduction during rehabilitation
following surgical treatment of an unstable elbow.)
Since the axis
of elbow motion is within the distal aspect of the humerus,
the frame is attached to the humerus first. A
temporary joint-axis pin is placed, and the frame is built
from this temporary axis pin. Once the fixator is properly

20
attached to the humerus, the ulna may be reduced
and attached to the fixator.

General approach
 Repair damaged structures from deep to superficial as seen from the lateral approach (coronoid to
anterior capsule to radial head to lateral ligament complex to CEO)
 Surgical approach either direct lateral incision (and if necessary, separate medial incision) or a
posterior incision with subcutaneous dissection laterally and if required medially
 Keep the arm pronated, use Kocher interval and remember that you will have to dissect distal to
annular ligament so just remember to repair it
 For lateral incision, supine with arm board
 For posterior incision, lateral with arm over bolster

 Most common lateral soft tissue injury pattern is an avulsion of LCL complex from the humerus
leaving a typical bare spot on the posterolateral aspect
 Care is taken to work through any soft tissue disruption created by the trauma (with proximal and distal
extension as required) preserving intact structures as much as possible
 Detached lateral ligament is tagged for later repair
 60% of patients also have disruption of all or part of CEO – also tagged for later repair

Order Of Repair
 Deepest structure, the coronoid, is addressed first and visualization can be dramatically improved by
resection of radial head if there is an irreparable fracture (seen in 60%)
 Type II/III # - ORIF and place 1 or 2 cannulated 3.0 lag screws from the posterior surface of the ulna to
fix it (can use the ACL guide if you like) – in comminuted fractures, fix the largest fragment (typically the
articular portion) as this restores the anterior buttress function and prevents posterior subluxation; if you
can‘t get screw purchase, can use a modular hand plate
 Type I # – repaired by placing lasso-type sutures around the fragment and the attached anterior
capsule and tying those sutures to the base of the coronoid through drill holes made with an eyed
Kwire

In some instances, the coronoid may not be amenable

to fixation because of the size or comminution of the
fracture or because of a delay between the injury and
the treatment. When the coronoid fracture is associated
with a complex fracture of the radial head, a portion of
the radial head can be shaped and secured with one or
two interfragmentary screws. Alternative sources of osteochondral
bone include tricortical iliac-crest bone
graft, an allograft coronoid, and the proximal tip of the
olecranon. If iliac-crest bone graft is used, the capsule
should be interposed between the graft and the trochlea
to prevent direct contact and cartilage erosion.
 Then radial head # evaluated – primary goal is to ORIF if there are one or two fragments which are
reduced and held with Kwires temporarily
 Definitive fixation then performed with small fragment screws countersunk below the articular surface –
Herbert screws are very useful

21
  If comminuted ( >3 fragments), impacted, cartilage damage, or an associated radial neck #, indicates
that a stable ORIF cannot be achieved, excise and replace
Fragments <25% that are too small or too damaged to be fixed are debrided and residual intact head is left in
situ. The two prerequisites
for fragment excision are evidence that the fragments
to be excised do not articulate with the lesser
sigmoid notch of the ulna and involvement of less than
one-third of the radial head

 If replacement – metal and modular with trials and assessment of ROM then definitive components
 Once articular work done, lateral ligament complex is repaired to the humerus with #2 Fiberwire
through bone tunnels (or with suture anchors)
Most important stitch is the one placed in the center of rotation of the elbow laterally, located at the center of
the capitellar circumference of the lateral condyle (the isometric point The center of rotation from the
medial view is
slightly distal and anterior to the medial epicondyle.
From the lateral view, the center of rotation is in the
center of the capitellum.) – check this with suture at this site and then flex/extend and if suture doesn‘t
move, you‘re in the right spot
 Midsubstance tears are occasionally seen – repaired with #1 or 2 non-absorbable using local tissue
only
 Prior to definitive closure, stability is assessed with goal of concentric reduction with no observed
posterior or posterolateral subluxation or dislocation through an arc of flexion 20-130
 Residual instability if seen is in extension and/or supination
 Valgus instability alone is well tolerated and not an indication for further OR
 Residual posterior/posterolateral instability is NOT acceptable
 So if this exists:
o Recheck coronoid
o Recheck radial head
o Recheck placement of LCL sutures
 If these are OK then:
o Perform repair of medial structures (MCL, and if disrupted CFO) OR
o Apply a hinged external fixator
 Standard subcutaneous and skin closure
 Immobilized in well molded posterior splint in 90 flexion and full pronation
 No drains

Post Op Care
 Splint left for 10 days depending on stability
 If patient awake, alert and isolated injury and good stability, start ROM POD#1 allowing active and
active-assisted motion
 Full forearm rotation is allowed with the elbow at 90 flexion
 Unrestricted shoulder and wrist
 Avoid terminal extension of 30 for 4/52

Remember crista supinatorius (point of insertion of posterior LCL) and sublime tubercle (insertion of medial
UCL on ulna)

Dislocated elbows must be evaluated for functional

stability after reduction of the dislocation. Following reduction,

22
instability is assessed by gently moving the elbow
through a range of motion. If the elbow appears to
subluxate or dislocate, a splint is applied and anteroposterior
and lateral radiographs are made. If no subluxation
is seen on radiographs, the patient is discharged
with the arm in the splint or a sling. The patient should
be reevaluated in five to seven days. If the elbow subluxates
or dislocates in extension or is noncongruent on the
radiographs made at the follow-up visit, the forearm
should be pronated and the stability of the elbow should
be reassessed. If stability is restored, a hinged brace or
cast-brace is applied with the forearm in full pronation.
An extension block of 30 degrees is sometimes necessary.
If the elbow requires an extension block of more
than 30 to 45 degrees, surgical repair should be considered.
Extension blocks should be gradually eased so
that by three weeks the brace allows full motion. At
each follow-up examination, the elbow should be reevaluated
in exactly the same manner.

36. Tibia Fractures

o IM nail:
o do dynamization early if there is obvious distraction of the fracture.
o If not obviously distracted, give it 3 months before dynamizing, and allow some
weightbearing.
o Then, at 5 months, if still not healed, do exchange nailing with reamed IM nail.
o Then, at 7 months, consider either a repeat exchange nailing, posterolateral bone
grafting, or compression plating.

37. Ankle Fracture

Malunion (common exam scenario)
 Obviously R/O infection first
 rare complication – occurs more frequently than is reported or is clinically relevant
 typically, fibula heals either short or externally rotated causing a lateral shift of the talus
 surgical Tx entails restoring mortise exact
o osteotomize fibula, lengthen, and rotate
o will need to release ST contractures around distal fib/syndesmosis/possibly medial side
o may need to open the syndesmosis (incisura fibularis sp??)
o fix fibula anatomic +/- bone graft
 results are generally good

38. Talus Fracture

o AVN talus
o If Hawkins sign at 6 weeks and evidence of some fracture healing then they can begin
PWB in PTB.
o May take up to 36 months for creeping revascularization of talus.
o For persistent AVN you can do :

23
 1. Core decompression – posterolateral approach b/w peroneal tendons and Achilles.
Can use a 2.0 mm drill and perforate AVN site under flouro with 8-10 drill holes.
Otherwise you use a 4.0mm drill and perforate 2-4 times. Post op Cast for 2 weeks
and at 6 weeks PWB in PTB ( ** remember the talus is still dead).
2. Bone graft – vascularized and non vascularized ( you need to take out the avascular
portion and insert some iliac crest structural graft)
3. Next step is tibio/talo/calc fusion for painful AVN (versa nail – 5 deg valg, neutral
PF/DF, symmetric ER (or 10-15deg). Should do Blair if ST jt not affected.
4. Most common talar malunion is varus – for symptomatic malunion will do triple, if
Tib/tal affected, do pantalar.

39. Calcaneal Malunion

o Type-I malunions include a large lateral wall exostosis without subtalar arthrosis or hindfoot
malalignment. This exostosis can extend to the calcaneocuboid joint, locking its motion, and
can also impinge on the undersurface of the fibula as well as trap or displace the peroneal
tendons. Treatment is with lateral wall exostectomy and peroneal tenolysis

o Type-II malunions exhibit both a large lateral wall exostosis as well as subtalar arthrosis.
Hindfoot malalignment is minimal if present at all. Treatment is with lateral wall exostosis,
peroneal tenolysis and sub talar bone block arthrodesis.

o Type-
hindfoot malalignment (typically varus). Treatment is with lateral wall exostosis, peroneal
tenolysis and sub talar bone block arthrodesis, and calcaneus osteotomy

Subtalar distraction bone block arthrodesis

o use standard lateral approach
o lateral wall exostectomy
o identify ST jt and decorticate
o laminar spreader and tricortical iliac crest bone graft (has also been described from the
posterlateral approach, be sure to contour the talus/calc to correct any significant
malalignments, can also contour the graft)
o fixation with 7.3canni screws from tuberosity to talus
o improve both calcaneal length (incr bohler) and lateral impingement
o This procedure elevates the talus away from the calcaneus and reestablishes a normal talar
inclination angle, thus allowing for better dorsiflexion of the ankle

40. Lisfranc Fracture

Missed Lisfranc fracture dislocation.
Author‟s Preferred Treatment and Rationale
 Timing – early if possible, otherwise when swelling permits – up to 21 day delay
 Will attempt ORIF up to 3/12 assuming no significant chondral damage that would require primary
fusion
 Reasonable to treat minimally displaced injuries presenting after 3/12 symptomatically and follow
clinical progress knowing that realignment arthrodesis is an option later (generally >6/12 be thinking
about conservative and fuse jts that become symptomatic)
Operative tips

24
  Dorsal incision b/t 1st and 2nd MT b/t EHL & EDL. N/V bundle (dorsalis pedis and deep peroneal nerve)
directly overlies the lisfranc ligament, must be identified and mobilized.
 Expose the base of 2nd MT and key it into the lateral aspect of medial cuneiform (this is KEY). Reduce
w tenaculem and fix w canulated 3.5-4.0 screw, do not lag. Lisfrac lig is strongest plantarly
 Management of jt degen
o V. similar to orif, need to key in 2nd MT to med cuneiform and recreate the 1st MT-cuneiform
angulation of 0 deg
o 1st-3rd can be fused
o 4th-5th rarely need fusion, likely the medial fusion would unload these jts if they were
symptomatic, can do peroneus tertius interposition arthroplasties if need to do something

41. Sporadic Trauma Pearls

1. Don‘t foget prophylactic fasciotomy if ischemia time > 6 hours after vascular repair.
2. Make sure you check with your vascular surgeon the position for ex fix before they do their
repair (usually 20 degree flexion)
3. Foot drop in a trauma patient discovered postoperatively (say patient was intubated on
arrival). Your differential: injury to the nerve at time of injury, injury during surgery,
compartment syndrome, injury higher up (spine, brain).
4. DCO vs ETC: coagulopathy, oxygenation (difficult to ventilate), volume resuscitation, lactate
>5, temp < 35
5. Ways of reducing a dislocated talus: femoral distractor, pin in calcaneus, joy sticks, laminar
spreader, medial malleolar osteotomy (must pre-drill and pre-tap your two screws first, start
with a saw, but complete the cut with an osteotome)
6. Screws in talus: the strongest Biomechanically posterolateral to anteromedial. DO NOT lag
the screw in the medial side, otherwise will fall into varus)
7. Open fracture of humeral shaft with radial nerve palsy: I&D, tag the nerve ends and call
plastics intraoperative. If the initial wound is big, consider antibiotics beads, antibiotic cement
spacer (esp in tibia), VAC. These are options to buy time.
8. After open fracture initial I&D, consider a second look in 48 hours, if still cannot cover, plan
your soft tissue coverage by plastics within 5-7 days.
9. EMG in nerve injury: sharp waves are not good.
10. In ATLS, exposure ensuring the patient temperature is euthermic. Warm patient, warm room,
warm blanket, bear hugger, if hypothermic consider warm IV saline, ……..
11. Principles for ExFix as a temporary fixation of fractures: 1. pins out of the zone injury, 2.
obtain bony aligment and traction, 3. avoid N/V structures, 4. hand drill and pre-drill the pins,
5. frame out of the way from the vascular surgeons field, 6. ensure that the joint is in a safe
position and not distracted.
12. Indications of primary amputation in trauma: 1. massive soft tissue loss, 2. medical
reasons, 3. nerve loss (loss of plantar sensation, ??? not anymore), 4. 6-8 hours warm
ischemia, 5. insufficient resources. Pearls: take a digital picture, obtain a second surgeon
consultation.
13. Day 4 post trauma in ICU white out chest: CHF, ARDS, fat embolism, pulmonary contusion

42. INVASIVE ATLS PROCEDURES

Needle Cricothyroidotomy with Jet Insufflation

o #12 or #14 guage Jelco needle placed through the cricothyroid membrane
o Aim it down at about 45 degrees. Don‘t go through the posterior wall.
o Cut a side hole in the tubing to allow for intermittent ventilation
o Connect to wall oxygen at 15 L/minute
o Give intermittent insufflation – 1 second on, 4 seconds off

25
 o Can oxygenate for about 30-45 minutes before they become hypercarbic

Surgical Circothyroidotomy
o Stabilize thyroid cartilage with left hand
o 3cm transverse skin incision over the cricothyroid memebrane (closer to cricoid)
o Incise through membrane
o Insert curved hemostat to dilate opening between cricoid and larynx
o Insert a #5 or #6 tracheostomy tube, inflate with 10cc air and secure with tapes
o Auscultate and CXR
o Note: do not do in child under 12 - the cricoid is the circumferential support to upper trachea

Needle Thoracentesis
 Assess the patient‘s chest and respiratory status
 Administer high flow oxygen and ventilate as necessary
 Identify 2nd intercostal space, in the midclavicular line, on the side of the tension pneumothorax
 Surgically prepare the chest with local anesthesia prn
 Insert an over-the-needle catheter into the skin and direct the need just over the rib into the
intercostal space
 Puncture the parietal pleura
 Remove the Luer-Lok from the catheter and listen for a sudden escape of air when the needle
enters the parietal pleura, indicating that the tension has been released
 Remove the needle, leaving the plastic catheter in place and cover with dressing
 Prepare for chest tube insertion (nipple line anterior to midaxillary line)
 Connect chest tube to underwater seal
 Obtain CXR

Chest Tube Insertion

 Determine insertion site: usually nipple level (5th intercostal space) anterior the midaxillary
line
 Surgically prep and drape
 Local anesthetic for skin and periosteum
 2-3 cm transverse incision at the predetermined level and bluntly dissect through
subcutaneous tissues just over the top of the rib
 Puncture the parietal pleura with the tip of the clamp and put a gloved finger into the incision to
avoid injury to other organs and to clear any adhesions, clots, etc
 Clamp proximal end of 28 French tube and advance it into the pleural space
 Look for fogging of tube with expiration or listen for air movement
 Connect tube to underwater-seal apparatus
 Suture tube in place, apply a dressing and tape tube in
 Obtain CXR

Pericardiocentesis
 Monitor patients vitals and ECG before, during and after procedure
 Surgically prep the xiphoid and subxiphoid areas if time allows
 Local anesthetize the puncture site if necessary
 Use 16 gauge 6 inch over the needle catheter and attach a 35cc syringe with three way
stopcock
 Assess patient for any mediastinal shift that may have caused heart to shift significantly
 Puncture skin 1-2 cm inferior to the left xiphochondral junction at 45 degree angle to skin

26
  Carefully advance needle cephalad and aim toward the tip of the left scapula
 If needle is advanced too far (like into ventricular muscle) will result in ―current of injury‖ pattern
seen on ECG (extreme ST-T changes or widened QRS) – so withdraw until baseline trace
reappears
 When needle tip enters the blood-filled pericardial sac, withdraw as much nonclotted
blood as possible
 During aspiration, epicardium reapproaches the inner pericardial surface as does the needle
tip so ECG may change again – so withdraw slightly again, and if it persists, withdraw it
completely
 After aspiration is completed, remove the syringe, attach a three-way stopcock, leaving it
closed and secure catheter in place
 Option – applying the Seldinger technique, pass a flexible guidewire through the needle into
the pericardial sac, remove the needle, and pass a 14 gauge flexible catheter over the
guidewire, remove the guidewire and attach three-way stopcock
 Should the tamponade persist, stopcock may be open and the pericardial sac be aspirated
 Consult Thoracic Surgery

Diagnostic Peritoneal Lavage

 Decompress the bladder with Foley & Decompress the stomach with NG tube
 Surgically prep the abdomen
 Inject local using lidocaine with epinephrine
 Vertically incise skin (1/3 the way b/t umbilicus and sympysis in midline (from prox to distal)
and subcutaneous tissues to the fascia
 Grasp fascial edges with clamps, elevate, and incise the peritoneum
 Insert a peritoneal dialysis catheter
 Advance the catheter into the pelvis
 Connect the dialysis catheter to a syringe and aspirate
 If gross blood is not obtained, instill 10 ml/kg warmed Ringer‘s (up to 1L)
 Gentle agitation of the abdomen to mix the contents
 If patient‘s condition is stable, allow fluid to remain for 5-10 minutes
 After fluid has returned, send to lab for white and red cell counts
 Positive test and need for surgical intervention: 100,000 RBCs/mm3 & 500 WBC/mm3
 Negative lavage does not exclude retroperitoneal injuries – pancreas or duodenum, isolated
hollow viscus, diaphragmatic tears

43. Vascular Approaches:

Ilioinguinal Approach to External iliac a. & v.

 incision 1 cm superior to inguinal ligament, through external oblique aponeurosis, to spermatic
cord medially
 divide internal oblique and transversalis in line with incision,
 ligate inferior epigastric a. & v. medial to spermatic cord deep to transversalis fascia,
 mobilize properitoneal fat superiorly revealing external iliac a. & v.
 external iliac has 2 intrapelvic branches – inferior epigastric & deep iliac circumflex arteries

Medial approach to Popliteal artery:

 patient supine on table with knee flexed to 60 degrees

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  start incision 2 cm proximal to adductor tubercle and curve anteroinferiorly 6 cm below joint
line on anteromedial aspect of tibia
 sacrifice infrapatellar branch of saphenous nerve
 identify sartorius and incise fascia anterior to border of sartorius
 retract sartorius posteriorly
 incise fascia posterior to superficial medial ligament
 exposes semitendinosus and gracilis which should be retracted posteriorly
 separate semimembranosus from medial head of gastrocnemius
 must release semimembranosus and medial head of gastrocnemius to identify the popliteal
artery which lies lateral to medial head of gastrocnemius

Vertebral Artery:
 Course – branches off sublcavian artery and ascends anterior to vertebral bodies from C6
below; from C7 above, artery ascendes within foramina of TP‘s
 exposure (from anterior approach):
o C7 and above → dissect tissues off anterior vertebral body and continue out to tip of TP
(located at mid-level of vertebral body in C-spine); at midpoint between edge of body
and tip of TP, use Kerrison to remove bone anteriorly until formanen opened and artery
visualized.
o if unable to get proximal control at vertebral level → perform sternotomy and clamp
artery at origin from subclavian artery
 if unable to surgically expose, BUT able to control bleeding with packing → pack-off & obtain
angiogram/embolization

Subclavian artery:
 on right emerges from brachiocephalic trunk, on left branches from aorta;
 3 parts to each –
o I – from origin to medial aspect of scalenus anterior,
o II – posterior to scalenus anterior,
o III – from lateral aspect of muscle to outer border of first rib (becomes axillary artery) –
o scaleneus anterior passes from TP‘s of C4-6 to tubercle on first rib, this is also deep to
sternocleidomastoid
 branches include vertebral, thyrocervical trunk with inferior thyroid artery and suprascapular
artery, internal thoracic, costocervical trunk and descending scapular – most of these arise
from 1st part of subclavian artery
 Exposure: incision to expose is from lateral border of sternocleidomastoid laterally along
clavicle, can also dissect out clavicle subperiosteally, resect middle third of clavice and
medially retract (or divide origin of) scalenus anterior

Axillary artery Exposure: deltopectoral approach

 protect cephalic vein (retract superiorly);
 release pec minor insertion from coracoid (± coracoid osteotomy) to expose part II (&
thoracoacromial branch);
 divide pec major insertion near humerus and retract to expose part III (& circumflex,
subscapular, thoracodorsal branches);
 perform clavicular osteotomy to expose part I:
o curve incision proximally medially over middle 1/3 of clavicle
o dissect subperiosteally over clavicle
o osteotomize and remove middle 1/3 of clavicle

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  cut subclavius, which runs under clavicle
 retract trapezius superiorly and pec major and minor inferiorly

Cubital fossa approach to brachial artery

 start 5 cm proximal to flexion crease on medial side of biceps and curve incision in front of
elbow and complete it by incising skin along medial border of brachioradialis muscle
o proximally – BR and brachialis
o distally – BR and PT
 find and protect lateral cutaneous nerve of forearm
 locate interval between biceps tendon and brachialis muscle
 identify bicipital aponeurosis (band of fibrous tissue from biceps tendon which extends
medially) and cut it close to its origin at biceps tendon and reflect it laterally
 identify the radial artery as it passes the biceps tendon and trace it proximally to its origin from
the brachial artery
o neurovascular bundle is medially to biceps tendon
o lat to med: tendon, brachial artery, median nerve

BACK TO TOP

Pediatrics
44. Normal Motor Milestones
Head control 3 months
Sitting 6 months
Crawling 8 months
Standing 8 months
Walking 12 months

45. Summary of Chromosomal and Teratologic Conditions

Down‟s Syndrome (trisomy 21)

 Most common chromosomal disorder
 Assoc w: Lig laxity, hypotonia, MR, heart dz (50%), endocrine disorders (hypothyroid and DM)
and premature aging
 Ortho problems
o Metatarsus primus varus, pes planus, atlantoaxial instability, scoliosis,
spondylolisthesis, hip instability, SCFE, patellar dislocation, symptomatic planovalgus
feet.
o Atlantoaxial instability eval w flex/ext. if instability present >5mm then should avoid
contact sports, gymnastics and diving. Complication rate very high with fusion
 Fusion usually reserved for progressive instability, ADI >10mm and neurologic
symptoms.
 DON‘T FORGET THE PRE OP CARDIAC WORKUP FOR POSSIBLE ABNORMALITIES

Turner‟s syndrome
 45, XO females with short stature, sexual infantilism, web neck, cubitus valgus, hormonal
therapy can exacerbate scoliosis, renal anomalies (usually minor) present in 2/3 of pts and
cardiac in 1/3
 malignant hyperthermia is more common

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Noonan‟s syndrome
 short stature, web neck, cubitus valgus in boys w normal sexual genotypes.
 Incr risk of malignant hyperthermia

Prader-Willi syndrome
 chrom 15 abnormality, hypotonic infant becomes retarded
 obese adult w insatiable appetite and growth retard with hip dyplasia, hypoplastic genitalia
and scoliosis

Menkes syndrome (sex linked recessive)

 disorder of copper transport that affects bone growth and causes „kinky‟ hair
 may be differentiated from occipital horn syndrome (also copper transport problem) by the
bony projections from the occiput of the skull in that disorder.

Rett‟s syndrome
 progressive impairment and stereotaxic abnormal hand movements.
 Girls 6-18 months present with devel delay similar to CP
 Have scoliosis w c shaped curve unresponsive to bracing.
 Anterior/post fusion indicated in curves >40

Teratogens
Fetal alcohol syndrome
 Cns dysfunction, dysmorphic facies, hip dislocation, c-spine vertebral and UE congenital
fusions, congenital scoli and myelodysplasia

Maternal DM
 Can lead to heart defects, sacral agenesis (Sacral agenesis consists of a complete or partial
absence of the sacrum). Rarely is it associated with absence of the most caudal segment of
the lumbar spine. The association with maternal diabetes has been well documented.
Kyphosis may occur with this condition, although it is usually not progressive and does not
require treatment.

46. Clinical Summaries of Important Skeletal Dysplasias

Short limbs
Rhizomelic – proximal aspect of bone
Mesomelic – middle
Acromelic – distal
Achondroplasia (AD)
Genetic Transmission: Autosomal dominant, but most patients have de novo mutation (80%)
Defect in endochondral bone formation – physeal dysplasia in proliferative zone
Gene Defect: Highly uniform mutation in fibroblast growth factor receptor-3
Key Clinical Features: Normal trunk, short limbs (rhizomelic – proximal) tib more ffected more than , frontal
bossing, button noses, small nasal bridges, tredent hands (inability to approzimate extended middle and ring
fingers) Stenosis of spine (esp. lumbar) or foramen magnum (mean opening of adult is that of a non
st
achondroplast at birth!); thoracolumbar kyphosis; genu varum, radial head subluxation, hypotonia (in 1
year of life)
Radiographic abnormalities: narrowed interpedicular distance L1-S1, T12-L1 wedging, generalized
posterior vertebral scalloping, delayed appearance of growth plates, ‗champagne glass pelvic outlet‘
 Radial and tibial bowing (ulna and fibula less affected)
 Coxa valga, genu varum, metaphyseal flaring and inverted V shaped distal femoral physis
Key Treatment Points: Brace thoracolumbar kyphosis if over 2 years old; fuse if >60deg (ant/post),
decompress symptomatic stenosis; C-spine is stable; osteotomies for genu varum if symptomatic

30
Pseudoachondroplasia (AD)
Genetic Transmission: Autosomal dominant
Genetic Defect: Cartilage oligomeric matrix protein (COMP)
Key Clinical Features: similar to achondroplasia except these have normal facies. Also, cervical
instability, scoliosis w incr lumbar lordosis, LE bowing, hip/knee/elbow flexion contractures w
precocious arthritis. Ligamentous laxity, windswept knees; size normal at birth, but falls behind

Spondyloepiphyseal Dysplasia Congenita (AD)

Genetic Transmission: Autosomal dominant
Genetic Defect: Type II Collagen, COL2A1
Key Clinical Features: Severely short stature (short trunked), primary vertebral involvement w beaking,
delayed appearance of epiphyses, flattened facies, platyspondyly (flat vertebra, also vertebra plana),
scoliosis, odontoid hypoplasia, coxa vara, genu valgum (achondroplasia is the reverse), retinal
detachment and myopia C1-2 instability, scoliosis, hip dysplasia, possible equinovarus foot

Spondyloepiphyseal Dysplasia Tarda (AD)

Genetic Transmission: X-linked most common
Genetic Defect: Type II collagen (COL2A1)
Key Clinical Features: Hip, back, or knee pain develop in later childhood/adolescence (8-10); mild scoliosis
(Tx like idiopathic scoli)

Chondrodysplasia Punctata (AD and AR)

Genetic Transmission: Multiple (AD form is called Conradi-Hunermann and AR form is rhizomelic form and
st
fatal in 1 year of life)
Genetic Defect: Rhizomelic form from peroxisomal enzyme deficiency; other forms unknown
Key Clinical Features: Neonatal stippling of epiphyses; early mortality (most rhizomelic patients)
Key Treatment Points: Evaluate and treat atlantoaxial instability, congenital scoliosis, coxa vara

Kneist Dysplasia (AD)

Genetic Transmission: Autosomal dominant
Genetic Defect: Type II collagen, COL2A1, usually exons 12–24. may be related to an abnormality of
cartilage proteoglycan metabolism, physes may have characteristic ‗swiss cheese‘ apprearance histologically.
Key Clinical Features: Large stiff joints; equinovarus; risk retinal detachment and odontoid hypoplasia. Xrays
show osteopenia and platyspondyly or hypoplasia. Resp problems and cleft palate. Otitis media and hearing
loss common

Metaphyseal Chondrodysplasias
Mode of Inheritance: McKusick: autosomal recessive; Schmid, Jansen, and Kozlowski: autosomal dominant.
Heterogeneoius group of disorders characterized by metaphyseal changes of tubular bones with normal
epiphyses. The physis (proliferative and hypertrophic zones) are more affected than the metaphysis.
Key Clinical Features: Metaphyseal irregularities with normal epiphyses; genu varum, mild short stature, fine
sparse hair; immune and GI disorders in McKusick type
Key Treatment Points: Rule out rare atlantoaxial instability; correct genu varum if severe; monitor medical
problems in McKusick type
Three types
Jansen’s (rare) AD
Most severe form
Mentally retarded, markedly short limbs, wide eyes, monkey-like stance, hypercalcemia. Striking bulbous
metaphyseal expansion of long bones
Schmid‟s (AD)
More common, less severe.
Short limbed dwarf with bowing of legs due to coax vara and genu varum. Mainly involves proximal femur,
often confused w rickets but has normal lab values
McKusick‟s (AR)
Cartilage-hair dysplasia (hypoplasia of cartilage and small diameter hair). Seen most frequently in amish and
finland. Atlanoaxial instability. Ankle deformity due to fibular overgrowth. Abnormal immunologic competence
(susceptible to severe rxn to chickenpox)

Hypochondroplasia
Genetic Transmission: Autosomal dominant

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 Genetic Defect: Most in fibroblast growth factor receptor protein-3 (different domain)
Key Clinical Features: Mild short stature; mild spinal stenosis
Key Treatment Implications: May benefit from growth hormone and/or limb lengthening

Metatropic Dysplasia (AD or AR)

Genetic Transmission: Autosomal dominant or recessive
Genetic Defect: Unknown
Key Clinical Features: Infant mortality risk; coccygeal tail, enlarged metaphyses, and contractures;
kyphoscoliosis
Key Treatment Points: Rule out cervical instability; possible role for spine fusion

Chondroectodermal Dysplasia
Genetic Transmission: Autosomal recessive
Genetic Defect: Unknown
Key Clinical Features: Cardiac defects, teeth and nails abnormal, postaxial polydactyly; genu valgus, external
femoral rotation

Diastrophic Dysplasia (AR)

Genetic Transmission: Autosomal recessive
Genetic Defect: Diastrophic dysplasia sulfate transporter abnormal in all cartilage. Severe short limbed
disorder of type II collagen in the physis. Typically ‗twisted‘ dwarf has cleft palate, severe jt contractures (esp
hip/knees) and the rest listed below
Key Clinical Features: "Hitchhiker" thumbs and "cauliflower" ears; joint contractures, cervical
kyphosis; scoliosis; rigid clubfeet, degenerative joint disease, equinovarus feet, spina bifida occulta
and atlantoaxial instability due to odontoid hypoplasia
Key Treatment Points: Monitor cervical kyphosis, fuse if increasing; correct feet; treat scoliosis, DJD

Multiple Epiphyseal Dysplasia (AD)

Genetic Transmission: Autosomal dominant. Most common skeletal dysplasia. Two forms Ribbings
(mild) and Fairbanks (severe)
Genetic Defect: Some forms from cartilage oligomeric matrix protein (COMP), other forms from type IX
collagen

Key Clinical Features: Patients typically present later in childhood, for one of several reasons. They may be
referred for joint pain in the lower extremities, decreased range of motion, gait disturbance, or angular
deformities of the knees(127). There may be flexion contractures of knees or elbows. Symptoms may develop
as late as adulthood. These patients have minimal short stature, ranging from 145 to 170 cm (57 to 67 in)
(124). The face and spine are normal. There is no visceral involvement.Near-normal stature; epiphyseal
deformation of large joints with symptoms in late childhood or adulthood. Involves epiphyses and all have
delayed ossification, can look like bilateral perthes, however, MED is bilat and symmetric while perthes is
usually unilateral and asymmetric.

Radiographs of the knees show that the femoral condyles are flattened, and may be in valgus. There may be
irregular ossification, just as in the hip. The condyles are somewhat squared on lateral view. Osteochondritis
dissecans may be superimposed. Some MED patients also show a double-layered patella on the lateral view
(132). This is a complete or partial double radiodensity, which is rarely seen in other conditions. There may be
a synovial-lined joint between the two layers of the patella.

Key Treatment Points: Observation versus acetabular coverage in childhood; joint replacement in adulthood

Diaphyseal Aclasia (Multiple Osteocartilaginous Exostosis)

Genetic Transmission: Autosomal dominant
Genetic Mutation: Mutations found on chromosomes 8, 11, and 19
Key Clinical Features: Short stature, impingement on tendons and nerves, angular deformities, limb length in
equality, malignant degeneration
Key Treatment Implications: Monitor for growth disturbances, remove symptomatic exostoses, educate about
signs of slight malignant degeneration

Dyschondrosteosis (Leri-Weill Syndrome)

Genetic Mutation: Short stature homeobox gene (SHOX)

32
 Key Treatment Points: Osteotomies may be indicated to correct forearm deformities

Cleidocranial Dysplasia(Dysostosis)(AD)
Genetic Transmission: Autosomal dominant
Genetic Defect: Defect in human CBFA1 gene
Key Clinical Features: Widened cranium, clavicles partially or completely absent, unossified pubic rami; hip
abnormalities (usually coxa vara)
Key Treatment Issues: Hip surgery for dysplasia or varus; care of dental, cranial, and obstetric problems

Larsen Syndrome
Genetic Transmission: Autosomal dominant or recessive
Genetic Defect: Unknown
Key Clinical Features: Widely spaced eyes, depressed nasal bridge, multiple joint dislocations, cervical
kyphosis

Dysplasia Epiphysealis Hemimelica (Trevors dz)

Epiphyseal osteochondroma. Most commony seen at the knee. Partial excision of the prominent overgroth
if symptomatic and later osteotomies if required. Recurrence is common.

Progressive Diaphyseal Dysplasia (Camurati-Engelmann dz) (AD)–

Later walkers with symmetric cortical thickening of long bones. Xrays show widened, fusiform diaphyses
with incr bone formation and sclerosis. Tibia/femur/humerus are most affected in that order.affecting only
the diaphyseal portion of the bone.
Tx includes salicylates, NSAIDS, and steroids for refractory cases

Mucopolysaccharidosis – these forms of dwarfism are dx based on presence of complex sugars in urine and are
proportionate dwarfs caused be accumulation of the mucopoly‘s due to hydrolase enzyme deficiency. 4 main types

Morquio‟s syndrome AR –
most common, presents by 18 months to 2 yrs with waddling gait, knock knees, thoracic kyphosis, cloudy
corneas, and normal intelligence. Bony changes include thickening skull, wide ribs, anterior beaking of vertebrae,
nd
wide/flat pelvis, coax vara with unossified femoral heads and bullet-shaped metacarpals. C1-2 instability 2 to
odontoid hypoplasia presents with myelopathy and tx w decompress/fusion. This syndrome assoc with excretion
of keratin sulfate in the urine
Hurler‟s syndrome (AR)
Most severe form, assoc with urinary excretion of dermatan/heparan sulfate
Hunter‟s syndrome (sex linked recessive)
Assoc w excretion of dermatan/heparan sulfate
Sanfilippo’s syndrome
Assoc w excretion of heparan sulhate. All syndromes but morquio‘s are assoc w metal retardation.

47. Proximal humerus

Ossification centre doesn’t appear until 6mo of age

Vanishing epiphysis sign - seen on AP view with post displaced transphyseal fracture. Epiphysis has vanished
as it goes posterior.

GT appears at 1- 3 yrs of age

LT appears at 4-5 yrs

80% of humeral growth

this physis is extra-capsular making it susceptible to injury

33
can accept <50% translation and 20 deg angulation in child >11 yrs

reduction accomplished with combination of flex, abduction and possibly ext rotation

48. Pediatric Radial Neck Fractures

 Age is important:
o For < 10, author will accept up to 45 degrees of angulation and 33% translation,
before resorting to open reduction
o For >10, 30 degrees of angulation and 3 mm of translation may be accepted
 Manipulation technique for closed reduction consists of traction and varus stress, combined with
digital pressure over the radial head
 If unsuccessful, forearm should be pronated and supinated, as pressure over the radial head or
metaphysis is maintained
 Wrapping the arm firmly in an Esmarch bandage produces compression and elongation forces that
may also reduce the fracture
 Alternatively, a percutaneous pin proximally, or a flexible intramedullary wire introduced distally, can
be used to manipulate and stabilize the proximal fragment
 Open reduction is performed when these methods fail
 Another indication for ORIF is a displaced SH IV involving >1/3 articular surface
 Fixation Kwires placed obliquely across the fracture, avoiding the use of a transhumeral pin,
removed in 3-4/52 to begin elbow ROM
 If the metaphyseal fragment is large, minifragment screw can be used

Complications
 Loss of rotation, radioulnar synostosis, injury to PIN, nonunion, premature physeal arrest, and AVN
of the radial head
 Complications are usually observed, unless they are progressive or disabling
 Radial head excision may be performed in growing children when symptoms warrant this procedure

49. Pediatric Monteggia #‟s

 reduction of anterior rad head (type I), supinate and flex w pressure on head
 type II – posterior, traction in extension and pronate w pressure on head

50. Medial epicondyle #

 The distinction between medial condyle and epicondyle fractures is on physical exam and x-
ray (although x-ray can be confusing)
o medial epicondyle fractures are unstable to valgus stress; medial condyle
fractures are unstable to varus stress
o if trochlear ossification center seen but not medial epicondyle, then medial
epicondyle is # & incarcerated in joint (medial epicondyle ossifies 1st)
Treatment
 Immobilization in long arm cast for those with < 5 mm displacement with the understanding
that if symptoms persisted, the fragment could be excised but encouraging early motion (day
3/4) as stiffness is most common complication
 Robert‘s technique of reduction: Valgus/supination/ext/dorsiflex of wrist to put flexor mass on
stretch. Works 40% of the time if done in 24hrs.
 Indications for open reduction & pinning/screw fixation:
o Incarceration of fragment in joint
o Valgus instability in a throwing athlete
o Ulnar nerve dysfunction (nerve incarcerated?)
o 1 cm displacement (possibly > 5 mm displacement)

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  Late reconstruction of displaced fractures is difficult with only fair results so if in doubt, should
probably fix it

Steps in OR:
1. GA,
2. Attempt closed red‘n – failed:
3. EUA – confirmed openned with valgus stress,
4. Positioned prone with arm in behind the back hammer lock position with tournequet,
5. Medial approach careful of ulna nerve.
6. Reduce epicondyle and hold with screw or stay tack. Use an additional screw/K-wire to prevent
rotation.

Postop complication: snapping ulnar N – treated with transposition.

51. Lateral condyle Fracture

 Reduction maneuver: Supination/ext/varus

52. Distal humeral physeal separations

 Reduction Maneuver: Medial displacement corrected in extension. Then flex and pronate to
reduce the fragment. If unstable, pin.

53. PEDIATRIC FEMUR FRACTURES

femur fracture
acceptable alignment

Age Coronal plane Sagittal plane Shortening (MM)

Birth -2 years 30 30 15
2-5 yrs 15 20 20
6-11 yrs 10 15 15
> 11 yrs 5 10 10

Principles
Pavlik harness for newborn – 6 months( must rule out abuse or metabolic bone abnormality
Spica cast good for age 5 and under . After that start thinking flexi nails.
Always conisider traction first for a couple weeks if alignment not acceptable. (Telescoping test – at
time of reduction and casting you apply gentle axial traction and if you get shortening > 3 cm then
go with traction first)

Remember options of ex- fix and plating

Spica principles
The more proximal the fracture , the more the hip should be flexed
Apply below knee cast with foot well padded first. Then with adequate padding of popliteal fossa apply above
knee portion placing a valgus mold to correct the common varus deformity. Place the child on a spica table and
apply the remainder of the cast including the contralateral leg with the hips abducted 30 degrees.
Check xrays/flouro to confirm reduction.
You can wedge a cast for < 15 deg angulation but you need to remove it and put traction or ex-fix for shortening
greater than 2 cm.

35
Traction
No more than 5 lbs traction with skin traction but if you need more you go to skeletal traction
Prefer femoral to tibial traction pin. If you use tibial pin stay posterior to tubercle to avoid growth arrest here
and recurvatum deformity. Go lateral to medial here

Femoral traction pin - Go medial to lateral. Feel adductor tubercle. Local in skin. Cut , spread. Landmark is
1cm proximal to adductor tubercle. Hold knee in 90 deg flexion for insertion of pin. Place pin parallel to joint
line. Use a smooth pin.

Principles with flexi nailing.

Measure width of canal and divide by 2 and subtract 0,5 -1.0 mm for diameter of nail. IE if canal
measure 8 mm at narrowest point then put 3 -3.5 mm nail.
2 rods bent about 30 deg so apex of curve is at fracture site giving 3 point fixation in femur. Bend
the tip to facilitate insertion and bouncing off the far cortex. Insertion point should be 3 cm proximal
to distal femoral physis. Drive the first rod 3 cm past the fracture and then do the second.
Proximally one rod should go up the neck and the other towards the GT.
Post op
Consider supplementary cast. Put them in a zimmer at least and touch down weight bearing and
progress to full w.b. by 6 weeks.

Sarah does zimmer for 2 weeks NWB. Then progresses WB to WBAT by 6 weeks.

54. Tibial Spine Fracture

Treatment

Type I&II – closed treatment, controversial about whether to cast in extension or sl flexion. Rockwoods
preferred Tx is 10 deg of flexion and monitor closely for two weeks for displacement. Aspiration, reduce with
hyperextension and put in LL cast with 10deg of flexion (brinker)

Type III
 open reduction internal fixation (formal open or arthroscopically assisted). Must examine for anterior
horn of medial meniscus caught in fracture site (can be a block to reduction-MCQ)

Children
 absorbable suture around periphery of the #, usually all cartilage in this group

Adolescents
 non absorbable suture through acl and fragment then tie over bone bridge through prox/anterior tibia.
Fix in 10-20deg of flexion
 mini/small fragment screw can also be used

Aftercare
 cast in neutral or 10-20deg of flexion for 6/52
 remove and wbat plus physio

Complications

36
Loss of knee extension – occurs in 60% and rarely a problem
Anterior laxity – occurs in 75% due to plastic deformation of the ACL at time of injury

55. Neonatal Pseudoparalysis of the Arm

 Differential Diagnosis:
1. Fractured clavicle
2. Fractured proximal humerus
3. Fractured scapula or acromion
4. Osteomyelitis of the proximal humerus or clavicle
5. Septic arthritis of the shoulder
6. Weird tumour
7. Brachial plexus palsy
 Work up:
o Get a history – birth history – late gestation, huge baby, shoulder dystocia
o Check the neurology – is there a discrete or diffuse brachial plexus palsy.
o When you move the arm, is it painful: neonate cries, grimaces, increase HR
o Look for infection! The proximal humerus contributes about 80% of growth – if you miss the
proximal humerus infection that bags the physis, you will severely screw up the arm.
o Aspirate, cultures, U/S of shoulder

56. Congenital Radioulnar Synostosis

 Caused by a failure of the radius and ulna to separate at 7th week of gestation (failure of
segmentation), usually proximally and in pronation
 During the embryonic period of fetal development, the humerus, radius, and ulna are
conjoined and longitudinal segmentation begins distally
 Abnormal genetic or teratogenic factors can disrupt radioulnar joint development, leading to
a bony synostosis representing a type I
 If rudimentary joint (PRUJ) development occurs before developmental arrest, a rudimentary
radial head will develop with a less severe degree of coalition - type II
 During this period of intrauterine development, the forearm is anatomically in a position of
varying degrees of pronation and with rare exceptions the forearm is fixed in pronation
 Usually an isolated event
 Bilateral 70-80%, most common in males
 Also seen in disorders such as:
o Acropolysyndactyly (Carpenter syndrome)
o Acrocephalosyndactyly (Apert‘s syndrome)
o Arthrogryposis,
o Acrofacial dysostoses of Najjar and mandibulofacial dystosis
o Klinefelter syndrome and its variants
o Cardiac anomalies (Tetraology, VSD)
o Thoracic anomalies (1st rib and pectoralis hypoplasia)
o Renal anomalies (screen by U/S)
o MSK anomalies (Poly/syndactyly, Madelung‘s, Dislocated hips, clubfeet)
 Although radioulnar synostosis is usually an isolated event, there may be associated
anomalies of the musculoskeletal, cardiovascular, thoracic, gastrointestinal, renal,
and central nervous systems

Clinical and Radiographic Features

 Present for evaluation when they have a functional deficit - generally, the degree of fixed
forearm pronation determines the disability and the age of presentation

37
  Functional complaints are variable
 On physical examination, the elbow often has loss of its normal carrying angle and has a
flexion deformity, usually minimal
 Almost all patients present in fixed pronation
 Pronation of greater than 60 degrees appears to be the most limiting
 Radiographs show anatomic variations from minor radial head deformities in patients with
limited forearm rotation, to full synostosis and absence of the radial head in patients with no
rotation
 Occasionally, a patient will present with limited forearm rotation and normal radiographs -
MRI of the proximal radius and ulna may reveal a cartilaginous synostosis that has yet to
ossify or a fibrous tether that limits motion

Natural History
 In the absence of functional limitation, children with radioulnar synostosis should be
observed

Treatment
Nonoperative Treatment
Unilateral presentation: cosmetically, no functionally limiting usually
Synostosis <60 pronation compensates well

Operative Care
 AIM IS TO PLACE THE FOREARM INTO MORE FUNCTIONAL POSITION BY
OSTEOTOMY (THE AIM IS NO TO IMPROVE THE FOREARM ROTATION BY EXCISION
OF THE SYNOSTOSIS BECAUSE THIS IS DOOMED TO RECUR)
 Ideal treatment would be to restore normal forearm rotation
 Intraoperatively, synostosis takedown procedures can dramatically improve motion, but
there is a high incidence of loss of motion in the 6 to 12 months after surgery
 At present, the functional gain does not seem to warrant this surgical intervention
 The alternative to synostosis excision is derotation osteotomy with the goal to place the
hyperpronated hand in a more functional position
 The dominant extremity is given priority in bilateral cases
 It is easiest to perform the osteotomy through the synostosis distal to the coronoid
process
 Before the procedure, an intramedullary ulnar Kirschner wire is placed to maintain
control of the osteotomy then after completion of the osteotomy, the forearm can be
rotated into the desired position of correction
 Generally, patients undergoing derotation osteotomy have a fixed preoperative position of
60-100 pronation - final corrected position is often 0-20
 Once this position is achieved a second percutaneous Kirschner wire transfixes the
osteotomy site obliquely, from the proximal ulna to the distal radius, across the
derotated synostosis
 Because there is a high risk of compartment syndrome postoperatively, it is
important to avoid internal fixation that would require a second operation for
removal if neurovascular compromise occurs
 Resection of bone at the synostosis site, or dorsal and volar fasciotomies through the
operative incision, lessen the risk of compartment syndrome postoperatively and should be
performed routinely
 Patients undergoing derotation osteotomies have been noted to have significant
improvement in function and cosmesis
38
Complications
 Most significant complication is postoperative compartment syndrome – up to 1/3
 More common in osteotomies with > 85 degrees of rotational correction
 Prophylactic forearm fasciotomy, or resection of a segment of synostotic bone, reduces the
incidence
 Removal of the oblique transfixing Kirschner wire is performed if removal of dressings and
proper elevation fail to improve the situation, allowing the forearm to rotate to its
preoperative position, lessens the tension on the interosseous vessels, and reduces the
volume of the forearm compartments
 Finally, if these maneuvers do not resolve the problem, emergent skin and fascia
decompression is mandatory
 The longitudinal ulnar Kirschner wire helps maintain control of the osteotomy site and
allows for controlled, repeat derotation 5 to 10 days later

57. Radial Club Hand

Approach To Radial Club Hand
 Classified as a longitudinal failure of formation (pre-axial deficiency of the hand, wrist and
forearm)
 1 in 100,000,
 Underdevelopment, or aplasia, of the radius is universally associated with thumb hypoplasia,
or absence, and hypoplasia or absence of the radial aspect of the carpus
 Classified by Bayne and Klug into four types, ranging from a present but defective distal radial
epiphysis (type I), to complete absence of the radius (type IV)
 Severity of the radial deficiency determines the extent of the associated deficiencies of the
thumb, digits, ulna, and elbow
 Thus, the spectrum of anatomic deficiency can range from mild radial deviation of the wrist and
minimal thumb hypoplasia, to complete absence of the thumb and radius; camptodactyly
 Clinodactyly is a congenital condition where the little finger is curved towards the ring finger. It
can occur in isolation, or be associated with chromosomal abnormalities like Down syndrome.
 Camptodactyly is a congenital condition where the little finger, sometimes the ring finger, is
held in fixed in a flexed position) of the index, long, and ring fingers; foreshortening of the ulna;
and a stiff elbow

Pathogenesis
 ? Injury to the apical ectodermal ridge during upper limb development is the cause
 No known genetic cause except when radial deficiency is associated with other congenital
abnormalities
 Pattern of inheritance is AD or AR, depending on the syndrome
 There are many associated congenital syndromes, including cardiac, craniofacial,
hematopoietic, musculoskeletal, gastrointestinal, and renal organ syndromes
 Associated chromosomal abnormalities, including trisomy 13, 18, and 21
 Occurrence is most often sporadic

Associated Anomalies
 Can occur in isolation but is commonly associated with other congenital malformations
 40% with unilateral and 27% of patients with bilateral radial club hand, have associated
malformations
 These organ system malformations may present in a nonsyndromic pattern

39
  Congenital cardiac, genitourinary, respiratory, skeletal, and neurologic problems occur in
children with radial dysplasia
 Similarly, many syndromes have been described in association:
o VACTERLS - includes the classic VATER of vertebral anomalies, anal atresia,
tracheoesophageal fistula, and renal anomalies, as well as cardiac and lower-limb
malformations, with a single umbilical artery
o Holt-Oram syndrome - an AD disease characterized by upper-limb malformations
and major cardiac malformations (ASD, VSD, TEF, MVP, PDA)
o Fanconi anemia - also AD; in infancy, there are usually characteristic facial features
(microphthalmos, strabismus, hearing deficits); progressive pancytopenia often does
not present until later in childhood; can now be identified by a mitomycin C test
o Thrombocytopenia with absent radius (TAR) is AR - thrombocytopenia is present
at birth, platelet count usually improves with growth, and hand surgery should be
delayed until it is safe

Clinical Features
 Presentation depends on severity
 Type I to type IV – with type IV most common

Type I
 Involves a defective distal radial physis leading to minor foreshortening of the radius and a
prominent distal ulna
 Mild radial deviation of the wrist throughout life, problems with radioulnar incongruity such
as triangular fibrocartilage tears, ulnocarpal impaction syndrome, and distal radioulnar joint
pain or loss of motion, usually do not occur
 Major clinical issue is the associated thumb hypoplasia with opposition weakness
Type II
 Involves limited proximal and distal radial physeal growth
 As a consequence, the wrist is more radially deviated, and the ulna bows
 The thumb hypoplasia is usually more significant, with more deficiency of the radial carpus
Type III
 Absence of the distal two-thirds of the radius
 Wrist is more severely deviated, and the hand has limited mechanical support and the ulna
is thickened and bowed
 The associated thumb and finger abnormalities of hypoplasia and camptodactyly are more
common and severe
Type IV (most common)
 Complete absence of the radius with marked ulna bowing
 Thumb is usually absent and index, long, and even ring fingers are often involved
 Elbow may have limited ROM with marked limitation of hand, wrist, and forearm function

40
Pathoanatomy
 Involves skeletal malformations and soft tissue deficiencies on the preaxial or radial side of
the hand, wrist, and forearm
 Severity of soft tissue loss parallels skeletal deficiency
 Preaxial muscles arise from the lateral epicondyle, and are normally innervated by the
radial nerve thus radial wrist extensors and brachioradialis are absent or deficient
 The pronator–flexor muscle mass is affected when its skeletal insertion sites are absent or
hypoplastic
 These structures can be only fibrous tissue (radial anlage) that maintains or worsens wrist
and hand deformity with growth
 Similarly, the neurovascular structures will be affected
 PIN and sensory branches of the radial nerve will be absent in a severe deformity
 Radial artery is usually absent
 Ulnar nerve and artery are usually present and unaffected
 Blood supply to the hand comes through the ulnar artery, and possibly the interosseous
vessels or a persistent median artery
 Median nerve is usually present and serves as a neural supply to the hand with the ulnar
nerve
 However, the more severe the deformity of the hand and wrist, the more limited the neural
and vascular supply will be to the hand

Natural History
 Generally, have an unaffected CNS
 May need to use adaptive mechanisms - generally include a spherical grip and lateral pinch
to compensate for the absence of opposition
 50-62% of patients with radial dysplasia have unilateral involvement (other sources say
bilateral in 50%)
 Lamb noted no functional impairment in patients with unilateral involvement
 Individuals with bilateral involvement have more difficulty – ADLs are affected
 Adaptive techniques and alteration of clothes are often necessary
 Patients without surgical correction were more limited
 Issue of the cosmetic and psychologic impact is difficult to quantify

Principles of Treatment
 Should address the following problems with radial dysplasia:
o Unstable wrist with lack of support for the hand
o Digital weakness secondary to radially deviated wrist
o Intrinsic digital weakness and deformity
o Thumb hypoplasia or aplasia that results in lack of opposition
o Foreshortened ulna
 All of these deformities affect function

Nonsurgical Intervention
 Options include corrective casting, bracing, and physical therapy
 In infancy, first goal is passive correction of the radial deviation deformity
 In mild cases, merely a home exercise program of wrist ulnar deviation, extension, and
distraction stretching
 In more severe cases, involves corrective casting or splinting to gradually stretch the
contracted soft tissues, then maintain the correction

41
  Splints are used in conjunction with a passive ROM
 If attempts to correct the static radial deviation contracture are not successful by 6-12/52 of
vigorous therapy and skilled bracing/casting, the use of distraction external fixation to
obtain soft tissue and musculoskeletal alignment should be considered
 Once passive motion has been achieved, necessary to maintain the correction
 For mild cases, can be done nonsurgically with nighttime corrective splinting program
during infancy and times of rapid growth
 Adequate for the majority of type I and type II
 In severe cases, lack of a stable wrist out of the splint, impairs hand and limb function
 These children are candidates for operative correction at 6-12/12

Surgical Intervention
 At age 6-12 months
 Two indications for surgery:
o Persistent wrist radial deviation contracture: do centralization, radicalization or wrist
fusion
o Functionally limiting thumb deficiency:
 Surgical options for the wrist contracture and lack of support for the hand have included
bone graft procedures to the ulna, centralization, radialization, and wrist fusion
 Surgical options for thumb aplasia are pollicization and microvascular toe–to–thumb
transfer
 Thumb hypoplasia can be surgically corrected with first web space deepening, MCP joint
stabilization, and opponensplasty tendon transfer
 Less clear indications exist for the surgical treatment of digital camptodactyly, ulnar
foreshortening, and radial hypoplasia in type II deformities

 Potential contraindications for surgery include:

o Lack of elbow flexion, such that the wrist deviation enables the patient to perform
hand-to-mouth and hand-to-neck activities
o Severe index digital deformity and weakness that will result in failed pollicization
o Severe medical problems that pose a risk to the patient's well-being
 Centralization of the carpus over the 3rd metacarpal has been a standard treatment
 Soft tissue release of the radial contracture, contouring of the ulna to match the carpus, and
capsular reefing are performed
 Stabilization is performed with pin fixation until healing
 The problem with centralization is a high incidence of recurrence
 Function is clearly impaired when there is less than 30 degrees of wrist motion
postoperatively
 Buck–Gramcko introduced radialization during the thalidomide crisis
 Centralization procedure is modified by aligning the ulna with the 2nd metacarpal
 Tendon transfers from the radial aspect of the wrist (ECR, FCR if present) to the dorsal,
ulnar wrist are performed to rebalance the wrist and hand
 The quality of the radial muscles clearly affects the success
 With both centralization and radialization, correction is performed at the wrist
 If there is a concomitant ulnar bow of greater than 30 degrees ulnar osteotomy should also
be performed - usually involves a multiple–level open osteotomy and intramedullary fixation
 In those rare situations in which passive correction of the wrist is not possible by splinting,
casting, or therapy, distraction and correction with an external fixator is performed
 As described by Kessler, can be performed in infancy

42
  Often, after 3-6/52 of external fixation an open centralization or radialization procedure is
performed
 Wrist fusion is not performed in young patients as it leads to loss of wrist motion and
potential loss of ulnar physeal growth
 Generally, wrist reconstruction is performed before thumb reconstruction
 Ideally, thumb reconstruction is performed before 18/12 limiting the learning process after
CNS maturation regarding pinch
 In the mild forms of radial dysplasia, the thumb hypoplasia causes functional problems
involving decreased first web space, MCP joint instability, and weak thenar muscles
 First web space can be deepened with Z-plasties or rotation flaps
 Release of adductor and first dorsal interosseous fascia is often necessary
 MCP joint can be stabilized with local fascia or use of extra FDS tendon length for ligament
reconstruction
 On occasion, MCP joint chondrodesis (fusion of the proximal phalanx epiphysis to the
metacarpal head) or arthrodesis is appropriate
 Opponensplasty is performed simultaneously with use of the abductor digiti quinti, ring-
finger FDS, or accessory digital extensors
 All have had reported success in providing opposition strength
 Thumb aplasia is best addressed with pollicization
 Toe-to-thumb microvascular transfers have been reported, but to date the results are less
successful than those of index-finger pollicization
 The quality of the index-finger donor determines the quality of the subsequent thumb
 If there is significant camptodactyly the thumb will be stiff, weak, and poorly used in pinch
activities and compensation will occur by lateral pinch between adjacent digits
 In a well-performed pollicization, the results are functionally and cosmetically pleasing to
the patient, family, and surgeon

Complications
1. Recurrent deformity and premature closure of the distal ulnar physis are the two major
complications
o Occurrence of these problems depends on the procedure performed (centralization
versus radialization) and the quality of the preoperative musculoskeletal and soft tissue
anatomy
o With radialization, goal is to dynamically rebalance the wrist and maintain motion
o If this fails to occur, radial deviation and flexion deformity will recur with growth
o In addition, if there is limited elbow flexion, excessive flexion and radial deviation of the
wrist will be used by the patient to compensate for the limited elbow flexion needed for
activities of daily living, such as oral hygiene and feeding contributing to the recurrence
rate
o Physeal arrest is more common with centralization procedures
o The forearm is already foreshortened, but this is exacerbated by further loss of distal
growth
o Because 70 to 80% of forearm growth comes from the distal physis, postoperative
growth arrest is a major cosmetic and functional problem
2. Finally, in patients with radial dysplasia, pollicization procedures can have poorer results in
terms of opposition strength and active range of motion
o The opposition weakness may be improved by opponensplasty transfer, but there
needs to be a strong donor for this to succeed or the patient will continue to
compensate with lateral digital pinch on the ulnar side of the hand

43
58. Congenital Radial Head Dislocations
 a rare condition, may not be diagnosed until school age.
 It is usually an isolated condition, but it may be present in association with other congenital
malformations and syndromes:
o Arthrogryposis
o Cornelia de Lange
o Larsen
o Nail-patella syndromes
o Radioulnar synostosis
 May be associated with other musculoskeletal anomalies:
o Congenital hip dislocation
o Club feet
o Brachydactyly
o Clinodactyly
o Tibial fibular synostosis
o Congenital below-elbow amputation
o Radial or ulnar club hand
o Madelung deformity or familial osteochondromatosis may be acquired
 May be bilateral or unilateral.
 Most congenital dislocations are posterior or posterolateral.
 It is important to distinguish the congenital dislocation from the posttraumatic dislocation.
Because the condition frequently presents late, this distinction can be confusing. This is
especially true for unilateral anterior dislocations in otherwise healthy children.
 Radiographic criteria have been established to distinguish this lesion from a chronic, traumatic
dislocation. These include:
1. Small, dome-shaped radial head;
2. Hypoplastic capitellum;
3. Ulnar bowing with volar convexity in the anterior dislocation and dorsal convexity in the
posterior dislocation; and
4. Longitudinal axis of the radius that does not bisect the capitellum.
o The presence of these characteristics in the absence of any history of trauma to the
affected elbow has been seen as evidence of a congenital radial head dislocation.
o In addition,
 bilateral involvement,
 the presence of other musculoskeletal or systemic malformations,
 a positive family history make a congenital cause more likely.
 Clinical and Radiographic Features
o often present after infancy.
o The most common reasons for presentation are
(i) limited elbow extension: < 30 degrees, and not of functional significance.
usually not noted early in life.
(ii) posterolateral elbow mass/prominence: noted in infancy
(iii) pain with activities, especially athletics. Radiocapitellar incongruity can be a
cause of pain and disability later in life. Unfortunately, many children present
late with pain resulting from radiocapitellar articular changes. There is often
chronic discomfort with school and sports activities.
(iv) On occasion, these children may present with an acute loss of motion
attributable to a loose osteochondral fragment.
(v) Some individuals remain asymptomatic, and the cosmesis of the deformity is
their major concern.

44
 o On physical examination, the elbow may have
 cubitus valgus.
 A flexion contracture of up to 30 degrees often occurs with a posterior
subluxation/dislocation.
 Hyperextension and/or loss of flexion may occur with an anterior dislocation.
 The radial head is palpable in its dislocated position.
 A congenital dislocation is not reducible by forceful manipulation, and should not
be misinterpreted as a nursemaid's pulled elbow or a Monteggia lesion.
 There is usually limited forearm rotation, with supination being affected more
than pronation.
 Clicking and crepitus may be present when there is intraarticular pathology.
o Radiographs reveal the subluxation/dislocation.
 The longitudinal axis of the radius does not bisect the capitellum, regardless of
the angle of the radiograph.
 The radius and ulna are of different lengths.
 The ulna is bowed, with volar convexity in an anterior dislocation and dorsal
convexity in the more common posterior dislocation.
 The capitellum is hypoplastic.
 The radial head will be dome-shaped, with a long, narrow radial neck.
 Natural History
o The presence of a congenital dislocated radial head is not an indication for operative
intervention.
o Many patients with this disorder have no functional limitation and no pain. Their mild
limitation of motion may not restrict them in any significant way.
o The degree of cubitus valgus is usually mild, and does not seem to put them at risk for
ulnar neuropathy. Therefore, in most cases a definitive diagnosis followed by
observation is most appropriate. If the patient develops pain, functional or progressive
limitation of motion, or restriction of elbow-related activities, then surgery needs to be
considered.
 Treatment
o Operative Care
 Ideally, the care of a congenital dislocated radial head would involve open
reduction and restoration of normal anatomy.
 This has led many surgeons to consider open reduction of a congenital
dislocation if the child presents in infancy. The logic is that if the radial head can
be reduced early in infancy, the deformity of the capitellum and the forearm may
not occur or remodel with growth. This may prevent the long-term complications
of pain, loss of motion, and osteochondral loose bodies.
 However, there have been only a small number of published cases of open
reduction of congenital radial head dislocations.Techniques have included:
 ulnar osteotomy and lengthening,
 radial shortening and osteotomy,
 annular ligamentous reconstruction, and
 the use of limb-lengthening devices to reduce the radial head.
 Sachar and Mih's report of open reduction through an anconeus approach,
followed by annular ligament reconstruction, is the most promising series to date.
They described seven cases of open reduction of a congenitally dislocated radial
head with good success. Their operative findings included an abnormality of the
annular ligament that was surgically correctable. The indications for this

45
 procedure, and the age limit, are still being defined in this relatively rare
condition.
 It is reasonable in specialized centers to consider open reduction of the
congenitally dislocated radial head in the infant younger than 1 to 2 years
of age, provided the family is well informed of the limited nature of the
information regarding this procedure.
 Hopefully, clinical surgical research in this area will define the indications
and techniques for open reduction and annular ligament reconstruction in
congenital radial head dislocations.
 Most children with congenital radial head dislocation present later than infancy.
Therefore, the most common procedures for this problem are excision of loose
bodies and excision of the radial head. The indications for excision of a loose
osteochondral fragment are the presence of pain, clicking or locking, and
loss of motion. Usually, degenerative changes are too advanced for repair of
the osteochondral fragment. There is some controversy regarding the indications
and timing for excision of the radial head. In the skeletally immature patient, the
concern is the potential development of postoperative complications. These
concerns have not been supported in the published literature on excision of the
congenitally dislocated radial head. Most of these children do not present until
adolescence with pain or progressive restriction of motion. In our series, the
youngest patient with excision of a symptomatic congenital radial head without
complication was 8 years of age. However, the presence of an asymptomatic
dislocated radial head alone, without painful, progressive restricted range of
motion, is not an indication for radial head excision. Indications for radial head
excision must include progressive pain, progressive loss of motion, and
progressive restriction of activities, regardless of age.
 Complications
o Throughout the 20th century, standard textbooks and journal articles have denounced
the concept of radial head excision in the skeletally immature individual. Postoperative
complications of:
 progressive cubitus valgus and potential associated ulnar neuropathy,
 proximal migration of the radius with recurrent radiocapitellar impingement,
 radioulnar synostosis, and
 reformation of the radial head have been cited.
o However, most of these problems occurred after radial head excisions to treat trauma.
o The admonishment never to excise a radial head in a skeletally immature individual still
holds true in the posttraumatic situation. These complications are rare after excision for
congenital radial head dislocations.
 Reformation of the radial head is the most common problem with excision of a
congenital dislocation. If it leads to recurrent radiocapitellar impingement,
limitation of motion, and/or pain, then repeat radial head excision should be
performed. Wrist pain does occur in the long term but seems to be mild and
nonrestrictive (107). Fortunately, iatrogenic radial nerve injury is rare.

DDx of Congenital Radial Head Dislocation

Trauma
- Missed Monteggia

Conditions which shorten ulna

46
- Ulnar deficiency
- Osteochondromata
- Olliers

Skeletal Dysplasias MAD KEN

- Nail-Patella Syndrome
- Klinefelters
- Achondroplasia
- Down's
- Ehler's Danlos
- Marfans
- Larsens

59. OCD Capitellum

Remember, ocd in 4-8yr olds of capitellum is panners and after that is considered OCD

60. Torticollis
o Combined head tilt and rotatory deformity.
o Head tilt ALONE usually associated with MORE significant pathology
o 1/3 due to ocular causes (see ophthalmologist)
o Orthopaedic Causes: muscular, neurogenic, osseus
o Muscular: 82%. Congenital Muscular Torticollis
 Head tilt Ipsilateral and rotation contralateral to side of pathology
 More in primiparous, multiple births. Etiology: ? compartment syndrome of SCM
 Age 4-6 weeks, tumor in neck, often go missed for a year, later present as
painless head tilt, rotation +- facial asymmetry
 Treatment: Physio if done < 1yr. Start with stretches in neutral position until
maximal then work in extended position.
 Surgery: best between 1-4 yr. Poorer if established facial asymmetry or >30
degree rotational deformity. Surgical options: release of sternal, clavicular or
mastoid heads, Z-plasty). Risks: anterior and external jugular veins, carotid
sheath, facial nerve. Skin incision 1 fingerbreadth proximal to medial end of
clavicle in Langer‘s lines. Brace for 6-12 weeks
o Neurogenic:
 Investigate if associated with pain, restlessness or unresponsive to physio
 Need eye exam
 DD: Chiari, cerebellar or spinal cord tumor, paroxysmal Torticollis of infancy
 Invx: CT and MRI of cord and brain
o Osseous: atlanto-occipital abnormalities, basilar impression, atlantoaxial rotatory
instability
 Atlanto-occipital abnormalities: hypoplastic C1 or occipital condyles, unilateral
absent C1, familial cervical dysplasia. R/O Klippel-Feil Syndrome
 Posterior congenital fusion of C2–C3 is a clue that occiput–C1 anomalies,
or other more distal cervical fusions, may be present
 Dynamic MRI: define SAC
 Treat with bracing/halo.
 If S&S of C1-2 instability: Gallie fusion
 If neurologic symptoms: excise odontoid, fuse O-C2
 Fuse O-C3 if unilateral absence of C1 or fuse O-C2 if familial cervical
dysplasia

47
  Basilar Impression: Similar to adults symptoms. McGregor‘s line most reliable
(>4.5mm above the line abnormal). If neuro S&S: neurosurgery and ENT.
Treatment: trans-oral excision of the odontoid, then O-C2 fusion
 Atlanto-axial Rotatory Instability:
 Spectrum of severity variable
 X-ray to document subluxation and look for O-C1 abnormalities. Dynamic
CT after plain film. CT classification:
o Type I: rotation, no translation. Most common, most self-resolve
o Type II: <5mm anterior translation
o Type III: >5mm anterior translation
o Type IV: posterior translation
 Treatment:
o <1week: soft collar, follow clinically and radiographically
o If not resolved in 1 week: admit, halter traction, analgesics,
diazepam, home halter traction for up to 3 weeks but STOP if
persists beyond this.
o If anterior displacement, then immobilize in halo cast (reduced) for
6/52
o Indications for posterior C1-C2 fusion (Gallie):
 Fixed deformity with subluxation (despite Halo for 6 wk)
 Neurologic deficits
 Unable to obtain or maintain reduction
 Recurrence of deformity after an adequate trial of at least 6
weeks of immobilization after reduction.
 > 3mo duration of fixed torticollis
o Prior to fusion, apply Halo and apply traction for a few days to get
muscles as supple as possible. Do a Gallie fusion because of the
decreased SAC at C2 (NOT Brooks) and protect in Halo for 6
weeks to achieve fusion.

Summary Approach to Torticollis

1. Should be evaluated by ophthalmologist (1/3 due to ocular reasons)
2. Hx: age, progressive or acute, birth trauma (multi or primi), recent illness/infection/head and
neck surgery, trauma, h/o SCM mass, DDH, PAIN, neurological problems (head, occipital pain,
clumsiness), eye problems/nystagmus, GI refulx/swallowing difficulties, FH of torticollis
3. Exam: chin rotated away and head tilted toward affected side, assess mobility, HEENT for
lymph nodes, Neurological exam (inc gait), Opthalmologic exam, Shoulders for Klippel-Feil,
hips for DDH (8% not 20%), feet for metatarsus adductus
4. Imaging:
a. Xray – done only if fixed deformity and no h/o SCM mass: Cervical AP, Lat for anomaly
b. Dynamic CT – done if rotary deformity seen on plain xray
5. Diff
a. Congenital muscular torticollis – children < 6 months, SCM mass, look for DDH
b. Acute muscular torticollis – unknown etiology, possibly Grisel‘s syndrome
c. Trauma
6. Tx
a. Infant < 6 months
i. H/O SCM mass
1. Congenital Muscular Torticollis = check hips and feet, stretching by
parents, re-assess at 2 yrs, unacceptable cosmetic deformity then SCM
release (release at clavicle, then proximal prn)
48
 ii. No H/O SCM mass
1. Fixed – xray
a. Normal = Congenital Muscular Torticollis
b. Anomaly (ie Klippel-Feil, etc) f/u clinically for progression – renal,
scoliosis, may go on to fusion
2. Flexible – could be ocular muscle palsy or tumor
a. MRI brain and spinal cord
b. Ophthalmology
b. Older child
i. No Pain
1. Fixed – xray
a. Normal = missed congenital, if unacceptable deformity release
SCM
b. Anomaly – f/u clinically for progression
2. Flexible – MRI, ophthalmology
ii. Pain – xray
1. Normal = acute muscular torticollis
a. Flexible = f/u
2. Anomaly = Rigid
a. Dynamic CT to assess deformity
i. Rotation only (traction only if within 1 month)
1. NSAIDS + physio x1 wk, halter traction x1 week, if
resolves then soft collar x2-3 weeks
2. If not, traction x6-8 weeks, if still not reduced then
fusion
ii. Other = treat as needed

Sandifer syndrome is characterized by gastroesophageal reflux and torticollis or tilting of the

head, presumably an attempt on the child to be more comfortable. It may present in infancy or
later childhood, usually in children with cerebral palsy.

Different way of D/D of Torticollis

o congenital vs. acquired
o painful vs. non-painful

Congenital:
o Congenital muscular
o Vertebral anomalies:
 Basilar impression (many causes),
 Primary: most common type, a congenital abnormality often associated
with other vertebral defects (e.g., Klippel-Feil syndrome, odontoid
abnormalities, atlantooccipital fusion, atlas hypoplasia)
 Secondary basilar impression: is a developmental condition attributed to
softening of the osseous structures at the base of the skull and any
disorder of osseous softening can lead to secondary basilar impression:
o Metabolic bone diseases (e.g., Paget disease, renal
osteodystrophy, rickets, osteomalacia)
o Bone dysplasias and mesenchymal syndromes (e.g., osteogenesis
imperfecta, achondroplasia, hypochondroplasia, neurofibromatosis)
o rheumatologic disorders (e.g., rheumatoid arthritis, ankylosing
spondylitis)

49
  Unilateral absence C1
o Failure of segmentation
 Klippel-Feil
 Occipitalization of C1
o Failure of formation
o Congenital hemiatlas
o Combined failure of segmentation/format
o Ocular

Acquired & Painful

o Traumatic: Atlantoaxial rotatory displacement, Os odontoideum, C1 fracture
o lammatory
 Atlantoaxial rotatory displacement (Grisel syndrome – after URI)
 JRA
 discitis/ osteomyelitis
 other neck infection
o Tumours: Eosinophilic Granuloma, Osteoid osteoma / osteoblastoma
o Calcified cervical disk
o Sandifer's syndrome (GE reflux/esophagitis)

Acquired & Nonpainful

o Paroxysmal torticollis of infancy
o Tumour of CNS: post fossa, cervical cord, acoustic neuroma
o
o
o Oculogyric crisis
o Associated w. Ligamentous laxity: Down's syndrome, SED/MPS dysplasias

61. Sprengel‟s Deformity

o Complex anomaly associated with malposition and dysplasia of the scapula with muscle
hypoplasia or atrophy, which causes disfigurement and limitation of shoulder movement
o Most common congenital malformation of the shoulder girdle
o Male-to-female ratio is 3:1
o Condition is sporadic - rarely, it may run in families (autosomal dominant pattern of inheritance)

Embryology
o The scapula is a cervical appendage that normally differentiates opposite the fourth, fifth, and
sixth cervical vertebrae at about 5 weeks' gestation
o It normally descends to the thorax by the end of the third month of intrauterine life
o Any impediment to its descent results in a hypoplastic, elevated scapula (Sprengel deformity)
o Congenital elevation of the scapula is caused by an interruption in the normal caudad
migration
o Produces both cosmetic and functional impairment
o Probably occurs between the 9th and 12th week of gestation
o An arrest in the development of bone, cartilage, and muscle also occurs - trapezius, rhomboid,
or levator scapulae muscles may be absent, hypoplastic, or contain multiple fibrous adhesions.
Serratus anterior muscle may be weak, leading to winging of the scapula. Other muscles, such
as the pectoralis major, latissimus dorsi, or the sternocleidomastoid, may be hypoplastic and
similarly involved
o Associated malformations are almost always present and can include anomalies in the
cervicothoracic vertebrae or the thoracic rib cage. The most common anomalies are:

50
 o Absent or fused ribs
o Chest wall asymmetry
o Klippel-Feil syndrome
o Cervical ribs
o Congenital scoliosis: usually cervicothoracic or upper thoracic
o Cervical spina bifida
o Diastematomyelia
o 1/3 have an omovertebral bone which is a rhomboid- or trapezoid-shaped structure of cartilage
or bone, usually is lying in a strong fascial sheath extending from the superomedial border of
the scapula to the spinous processes, lamina, or transverse processes of the cervical spine,
most commonly the fourth to seventh cervical vertebrae
o A well-developed joint can form between the scapula and the omovertebral bone or it can also
be a solid osseous bridge, best visualized on a lateral or oblique radiograph of the cervical
spine

Pathophysiology
The gross pathology can be described as follows:
 Scapula: The scapula is dysplastic and is located higher than normal in the neck or upper
thoracic
 Omovertebral connection: 1/3 of cases
 Periscapular muscles: fibrotic and contracted, with the trapezius being the most commonly
affected.

Clinical
o The hallmarks of this condition are shoulder asymmetry and restriction of shoulder abduction
o Clinically, the affected scapula is usually elevated 2-10 cm, is adducted, and its inferior pole is
medially rotated
o Due to this rotation, the glenoid faces inferiorly and a prominence in the suprascapular region
is characteristic due to the upwardly rotated superomedial angle of the scapula causing the
ipsilateral side of the neck to appear fuller and its normal contour to be lost
o Passive movement of the glenohumeral joint, including abduction and external and internal
rotation, may be normal; however, scapulothoracic movements may be severely limited
o In 40%, combined abduction is limited to less than 100°
o The omovertebral bone may also limit abduction by affecting scapular mobility and can also
limit neck movement if it is attached high in the cervical spine
o Other causes of limited abduction include abnormal and weakened scapular muscles
o The left side is more commonly affected than the right side
o The condition may sometimes be bilateral, in which case, it is cosmetically much more
acceptable, but functionally, it is more disabling
o Problems that may be associated with this condition include syndromes such as the
following:
 Klippel-Feil syndrome
 Greig syndrome
 Poland syndrome
 VATER association, ie, vertebral defects, imperforate anus, tracheoesophageal
fistula, and radial and renal dysplasia
 Velocardiofacial syndrome
 Floating harbor syndrome
 Goldenhar syndrome
 X-linked dominant hydrocephalus, skeletal anomalies, and mental disturbance
syndrome

51
Relevant Anatomy:
 The dorsal scapular nerve: This nerve courses close to the superomedial border of the
scapula in the plane between the rhomboids and the erector spinae muscles. It remains
anterior to the serratus anterior and the subscapular muscles. A risk exists of injuring the nerve
while dissecting the periscapular muscles at the superomedial angle of the scapula and when
the trapezius and the rhomboids are reflected off as a single unit from the spine in the
Woodward procedure. Therefore, staying subperiosteal while freeing the periscapular muscles
is essential, especially at the superomedial angle of the scapula.
 The spinal accessory nerve: This nerve is located between the trapezius and the rhomboids
and is, therefore, at risk theoretically; however, since it is sandwiched between the two
muscles, it is rarely ever injured while these muscles operate as a unit.
 The suprascapular nerve: This nerve runs in the suprascapular notch of the scapula and may
be injured if the dissection is carried too far laterally when the superior portion of the scapula is
resected. This can be avoided by staying at least 1 cm medial to the notch.

Contraindications: Presence of a mild deformity with minimal restriction of movement is a

contraindication to surgery. While the treatment of this condition is essentially surgical, some factors
exist that could compromise the results of surgery and may be considered to be contraindications.
These include presence of associated syndromes that affect the final functional outcome.

Imaging Studies:
 Radiographs
o Sprengel deformity is best visualized on the anteroposterior (AP) view of the chest and
both shoulders.
o A lateral view of the cervical and thoracic spine must also be obtained to rule out
associated spinal anomalies.
 CT scan
o CT scans with 3-dimensional reconstruction may be performed to visualize the
pathoanatomy and to visualize the omovertebral bar.
o CT scans may also help in planning surgery, eg, if the CT scan shows that the height-
to-width ratio is markedly decreased, then the prominent convexity of the vertebral
border along with the supraspinous portion of the scapula should be resected (Cho,
2000).
 Appropriate imaging studies should also be performed for any associated anomalies: spine X-
rays, MRI, abdominal U/S

Medical therapy:
Nonoperative treatment consists of physical therapy. Exercises are used to maintain range of motion
and to strengthen the weak periscapular muscles.

Surgical therapy:
o Many patients with Sprengel deformity do not require operative intervention.
o For those who do require surgery, the aims of correction of Sprengel deformity are twofold.
o First, the cause of the scapular binding must be released.
o Second, the scapula must be relocated.
o The main objectives in performing surgery are to improve the cosmetic appearance and
contour of the neck and to improve the function when it is severely impaired.
o The optimal age for operative intervention is controversial. 4-8yr.
o Surgical options include subperiosteal resection of part of the scapula, extraperiosteal release,
transplantation of the muscular origins of the scapula, excision of the superomedial portion of

52
 the scapula, and vertical scapular osteotomy. Clavicle resection and excision of the
omovertebral bone have also been described. Many of these procedures leave unsightly
scars; therefore, the cosmetic improvement needs to be carefully considered. The ability to
increase shoulder abduction with surgery is also limited.

Preoperative details:
o Explaining the expected outcome of the surgery to the parents and ensuring that they have
realistic expectations of the surgery are extremely important.
o Parents must be told that while cosmesis may be improved, the improvement in the range of
motion may be limited.
o Prior to surgery, certain factors should be considered, including:
o the cosmetic severity,
o the functional impairment,
o the age of the patient,
o other congenital anomalies, and
o the medical fitness for undergoing the surgery.
o Preoperatively, radiographs of both shoulders, including the cervical and thoracic spine, should
be obtained to determine the presence of congenital scoliosis, Klippel-Feil syndrome, or an
omovertebral bone. Furthermore, a CT scan or MRI may be useful to delineate the
attachments of the omovertebral bone or determine the presence of spina bifida occulta or an
intraspinous lesion.

Intraoperative details:
Though multiple surgical procedures are described in literature, the Green and the Woodward
procedures remain the criterion standards. These 2 surgical procedures are described below.

Modified Green scapuloplasty

o This procedure is usually performed for a moderate or severe deformity.
o The patient is placed in the supine position on a radiolucent table.
o A supraclavicular incision is made 2 cm cephalad to the mid portion of the clavicle, in line with
the skin creases. The deep fascia is incised, and the periosteum of the clavicle is divided
longitudinally. The underlying subclavian vessels and brachial plexus must be carefully
protected. The anterior cortex of the middle third of the clavicle is sectioned with an oscillating
saw. Gentle force is then used to produce a greenstick fracture. The periosteum is then closed.
o The patient is then turned to the prone position. A midline incision is made from C4 to T10.
o A plane is developed between the subcutaneous tissues and the fascia underlying the
trapezius muscle. Dissection then proceeds laterally to expose the spine of the scapula.
o The insertion of the entire trapezius muscle onto the scapular spine is sectioned and tagged.
The trapezius is reflected medially. Care must be taken to avoid injury to the spinal accessory
nerve.
o The supraspinatus muscle is then detached extraperiosteally to the greater scapular notch.
The transverse scapular artery and the suprascapular neurovascular bundle must be
protected.
o The omovertebral bar is then excised. The scapular attachment is sectioned first. The
omovertebral bar is then gently detached from its insertion to the cervical spine.
o The insertions of the levator scapulae and the rhomboid muscles are extraperiosteally
dissected, divided, and tagged.
o Starting medially, the subscapularis muscle is elevated extraperiosteally. The suprascapular
neurovascular bundle is protected, and the supraspinous portion of the scapula, along with its
periosteum, is excised.

53
 o The scapular attachments of the latissimus dorsi muscle are divided extraperiosteally. Blunt
dissection is used to create a large pocket in the superior part of the latissimus dorsi muscle.
Fibrous bands may connect the scapula to the chest wall. These should be divided in order to
mobilize the scapula.
o The scapula is then displaced distally. In order to prevent migration, the inferior pole of the
scapula is fixed to the adjacent ribs. If winging is present, the scapula can be fixed to the rib
cage in a lowered and more laterally rotated position.
o The muscles are then reattached in the following order: supraspinatus to the base of the
scapular spine, subscapularis to the vertebral border of the scapula, serratus anterior to the
vertebral border, levator scapulae to the superior border, rhomboids to the medial border,
trapezius to the scapular spine, and the superior edge of the latissimus dorsi to the
inferolateral edge of the trapezius. The wound is then closed in layers.

Woodward procedure
o The Woodward procedure is also performed for a moderate or severe deformity.
o The patient is placed in the prone position.
o A midline incision is made from C1 to T9.
o The wound is dissected laterally to the medial border of the scapula.
o The lateral border of the trapezius is identified. The lower portion of the trapezius is dissected
from the latissimus dorsi muscle. The origin of the trapezius is detached from the scapular
spine. The edges are tagged.
o The origins of the rhomboids are divided and tagged. The entire muscle sheet is retracted
laterally, exposing the omovertebral bar.
o The omovertebral bar is excised extraperiosteally.
o The levator scapula is sectioned at its attachment to the scapula. Fibrous bands may attach
the scapula to the chest wall. These should be sectioned.
o The serratus anterior muscle must be detached from its insertion in the vertebral border of
the scapula.
o The supraspinatus and the subscapularis muscles are elevated extraperiosteally.
o The supraspinous portion of the scapula is resected with its periosteum. Care is taken to avoid
injury to the suprascapular nerve and vessels.
o The scapula is then lowered to the desired position.
o The subscapularis muscle is reattached to the vertebral border, and the supraspinatus is
sutured to the scapular spine. The serratus anterior is reattached to the vertebral border, and
the latissimus dorsi is reattached to the scapula. The trapezius and the rhomboids are then
resutured to the spinous processes at a more distal level. The wound is then closed in layers.

Postoperative details:
The arm is supported with a sling postoperatively, and gentle range of motion (active and passive)
exercises are started. The sling is used for 3 weeks. Gradually, active range of motion and
strengthening exercises are instituted. Physical therapy is continued for up to 6 months.

Follow-up care:
The patient is seen monthly for the first 3 months, every 3 months subsequently for the first year, and
yearly thereafter.

Postoperative complications include the following:

 Winging of the scapula that may result from incomplete reattachment of the serratus anterior
 Brachial plexus injury
 Keloid formation may complicate wound healing

54
Prognostic factors include the following:
 Severity of the deformity
 Age at surgery: Generally, results of surgery in children older than 6 years are not as good.
 Type of procedure: Relocation surgeries have better functional outcomes.
 Associated anomalies: Anomalies such as Klippel-Feil syndrome compromise the eventual
result

62. Klippel-Feil Syndrome

 Consists of congenital fusions of the cervical vertebrae
 50% have Triad of low posterior hairline, short neck and decreased neck ROM
 Incidence approximately 0.7%
 Congenital fusions result from abnormal embryologic formation of the cervical vertebral
mesenchymal anlages (failure of segmentation during 3rd-8th week gestation)
 Associated abnormalities:
o Scoliosis (both congenital and idiopathic like): in 60% (remember it as 2/3)
o Sprengel deformity: 1/3
o Renal anomalies: 1/3, aplasia common
o Deafness: 1/3
o Synkinesis (mirror movements)
o Pulmonary dysfunction
o Congenital heart disease
o Congenital cervical stenosis
o Brain stem abnormalities
 Investigation:
o Xrays show a wide range of deformity, ranging from simple block vertebrae to
multiple and bizarre anomalies
 Flex-ex lateral xrays are used to assess for instability, and should
always be made before any GA
 **Any segment adjacent to unfused segments may develop hypermobility and
neurologic symptoms** CASE GIVEN BY SARAH – C2-3 fusion above a C4-5
fusion, very dangerous as all of the stress at the 3-4 junction increasing
chance of neuro injury at this level
 Common pattern is fusion of C1-C2 and C3-C4, leading to a high risk of
instability at the unfused C2–C3 level
o If the flex-ex views are difficult to interpret, flex-ex CT or MRI
 CT is especially helpful at the C1–C2 level in assessing the SAC; sagittal MRI
is more helpful at other levels
 All children should be further evaluated by a pediatrician for other organ system
problems
o Renal U/S adequate for the initial evaluation
o MRI should be performed whenever any concern for neurologic involvement exists
on a clinical basis, and before any orthopaedic spinal procedure
 Natural history depends on the presence of renal or cardiac problems with the potential
for organ system failure and death
o Cervical spine instability can develop with neurologic involvement, especially in the
upper segments or in segments with iniencephaly (The diagnosis can be made
immediately after birth because the head is so severely retroflexed (bent back) that the
face looks upward. The skin of the face is connected directly to the skin of the chest and
the scalp is directly connected to the skin of the back. Generally, the neck is absent.

55
 o Degenerative joint and disc disease develops in patients with lower-segment
instabilities
o In adulthood, many patients with Klippel-Feil syndrome will complain of
headaches, upper extremity weakness, or numbness and tingling
o Degenerative disc disease, as seen on MRI scans, occurs in nearly 100%

 Management
o 3 Main Issues
1. Instability
2. Degenerative disease
3. Associated Problems-congenital workup
o Because children with large fusion areas are at high risk for developing
instabilities, strenuous activities should be avoided, especially contact sports
o Other nonsurgical methods of treatment - cervical traction, collars, and analgesics
o Arthrodesis for neurologic symptoms because of instability
o Asymptomatic hypermobile segments pose a dilemma
o The need for decompression at the time of stabilization depends on the exact
anatomic circumstance, as will the need for combined anterior and posterior fusions
versus simple posterior fusion alone

How to Approach a Case of Klippel Feil Syndrome

Hx: Take history to rule out instability, degenerative disease, neurologic problems, pain. And
associated congenital problems. PMH/DEV/Med/ALL

Px: Gait, Inspect (Low hairline, web neck), Palpn (tenderness), Range of motion (Often limited),
Neuro-full neurologic exam esp examine for myelopathy

Tests
1. AP/Lat/Flex Ext views
2. Get shoulder xrays to check for sprengels-1/3 have
3. CT/MRI should get to eval bone and also to look for other neurologic abn.
4. Congenital Workup
o Cardiac and renal ultrasound
o MRI
o Peds evaluation

Surgical Indications
1. Neurologic symptoms: us. caused by instability, Diag with FE views, CT/MRI
2. Degenerative disease around fused levels: Causing pain, Ultimately causes instability
3. Cosmetic deformity: Not a real surgical indication

Surgical Principles:
1. Should be done by experienced spine surgeon
2. Need preop CT to see bony anatomy: May have sig deficiencies
3. SSEPs
4. Halo
5. Prone position
6. Posterior approach stay within <1.5cm lateral from midline
7. Iliac crest bone graft
8. Wire from drill holes in the outer table of the calvarium to C2 crossed over top of the bone graft
9. Decorticate the posterior surface of occiput, C1 and C2

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63. Congenital Scoliosis
 Classification
o Failure of Formation: incomplete/complete
 wedge (has 2 pedicles) – incomplete
 hemivertebrae ( has 1 pedicle) – complete
 segmented ―incarcerated‖ (disc above and below)
 partially segmented (fused either above/below)
 unsegmented (fused both above and below)
 hemimetameric shift – hemivertebrae counterbalanced by contralateral
hemivertibrae in the same region
o Failure of Segmentation: involves bony bars
 bilateral – block vertebrae
 unilateral – produces tether to growth
o Mixed

** difficult to dx at times as spine ~ 30% ossified @ birth

** posterior elements may be normal, abnormal (bifid areas, partially/fully fused laminae)
** may have rib abnormalities (fusion or absence) which can stunt the thoracic volume and tether the
spine

Natural History
o depends on many factors
o type: block (most benign) to unilateral bar with contralateral hemivertebrae (most
severe)
o location: upper thoracic is less severe and TL and CT regions are most severe
o spine growth comes from superior and inferior end plates therefore one can assess disc ht to
infer the growth potential
o disc with normal ht and clear definition suggestion healthy growth plates on either side
o progression happens during periods of rapid growth (1-3 yrs and puberty)

Rate of Progression

Type Progression/yr
Block < 2 o /yr
Wedge < 2 o /yr
Hemi 2-5o /yr
Unilateral Bar 5-6 o /yr
Unilateral Bar + Contralateral Hemi 5-10 o /yr

poor prognosis: thoracic, unilateral bar with contralateral hemi, hemi @ LS level

Associated Anomalies
o as many as 61% of pts with congenital scoli have other abnormalies (esp pts with mixed
patterns)
o VACTERL syndrome (Vertebral, Anal, Cardiac, TracheoEsophageal, Renal, Limb<radial
clubhand, thumb hypoplasia>)
o URO: up to 20% urologic therefore pts require U/S/MRI abdo to assess for unilateral absent
kidney or obstructive neuropathy

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 o CARDIAC: anomalies include ASD,VSD, Tetralog of Fallot etc. therefore requires
echo/cardiologist referral
o MSK: congenital C-spine, clubfoot, DDH, limp hypoplasia
o NEURO AXIS: ~20% of pts have intraspinal anomalies (i.e. tethered cord, (most common)
distenotomyelia, syringomelia, dural bands etc.)
o this is especially important as
o intraspinal path may need to be dealt with before scoli sx,
o scoli correction can cause cord injury if tethered
o curve may be progressive due to spinal path not vertebral anomalies
o THUS CT (to accurately quantify bony abnormalities) and MRI all spines

Clinical
O/E:
o ht/wt
o General: CVS (murmurs), Abdo
o Spine: inspect to cutaneous changes (hemangiomas, dimples, hairy patches), back sensation,
neuro exam, abdo reflexes
o UE: clubhand, thumb hypoplasia
o LE: hip knee foot

Radiology
o X-ray spine: supine as infant and standing when child able to, comment on disc spaces,
anomalies, magnitude of curve
o CT for bony abnormalities
o MRI for intraspinal path
o MRI has become the standard for assessing dysraphism and should be done in
any child with congenital scoliosis who is being considered for surgery
o Other MRI indications:
 Significant back or leg pain
 Neurologic deficit
 Foot deformity
 Radiologically evident diastematomyelia or interpedicular widening
 Combined unsegmented bar and hem

Treatment
Nonoperative
o follow till end of growth
o follow more closely during growth spurts
o bracing doesn‘t‘ effect congenital scoli and may cause chest wall deformities
o can on RARE occasions use a brace to help with flexible compensatory curves

Operative
Indications:
o consider age, progression, amount of deformity, location of deformity
o indicated if progression is documented or anomaly is predicted to have high risk of surgery

Goal of surgery is to obtain a balanced spine while maintaining flexibility and preserving as much normal spine
growth as possible

Options:
1. insitu fusion

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2. convex hemiepiphysiodesis
3. hemivertebral excision
4. correction and fusion with instrumentation
5. reconstruction osteotomies
6. growing rods/expandable rib rods

Insitu Fusion (gold standard)

o best for pts with unilateral failure of seg (unilateral bar/ unilateral bar with contralateral hemi)
o done when progression is documented and before major deformity
o is safe to be performed before 5 yo if needed
o requires posterior procedure with fusion of vertebral 1 up and down from anomalus segment
o tx with cast post-op for 4-6/12
o consider anterior fusion to prevent crankshaft
o Anterior release with diskectomies and bone graft either open or video assisted

Convex Hemiepiphysiodesis
o indicated for unilateral failure of formation (hemi)
o contraindicated with segmentation defect as no potential for concave growth
o involves convex lateral ½ discectomy of adjacent disks to hemi and level above and below,
posterior arthrodesis on convexity with no exposure of spine on concave side, cast for 4-6/12
o correction is gradually and unpredictable with most have < 15 o
o best in pts < 5 yo with short progressive curves due to formation defect (i.e. isolated
hemivertebra with short curve < 40 o in absence of spinal imbalance)

Hemivertebral excision
o indicated for pts with marked trunk imbalance
o technically demanding with increased neuro risks
o indicated for pt where in situ fusion/hemiepiphysiodesis would not result in balance spine
o best done @ 2yo when child can still tolerate cast and anatomy is big enough for
instrumentation (< 5 yo curve > 40 o)
o can be performed as isolated posterior or anterior + posterior which is more common
o important to decompress nerve roots
o esp gd technique for isolated hemivertebrae in lumbosacral junction

Correction and Fusion with Instrumentation

o partial curve correction can be done in children with flexible segments above and below
congenital deformity, CANNOT be done through rigid areas
o performed in older children
o consider ant procedure to avoid crankshaft
o Neuro deficits are more common with congenital curves especially with kyphosis
o Careful with distraction – need spinal cord monitoring +/- wake up test

Reconstuction Osteotomies
o pts with severe rigid spine that cannot be managed with any other means due to obliquity of
pelvis, truncal decompensation, progressive deformity, developing neuro deficits

Growing Rods/Expandable Rib Rods

o helps maximize spinal growth (~ 50% of ht) and minimize curve progression
o controversial
o rods places sub-fascial and attached to short fused segments in claw formation

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To summarize:
o Non-segmented hemi-vertebra no progression: observe
o Incarcerated hemi-vertebra slow curve progression: observe
o Semi-segmented vertebra single angled growth plate/slow progression. Adult deformity does
not exceed 40: No Tx unless AN @ lumbosacral junction
o Fully segmented hemi 3 choices 1) ant and post fusion 2) hemiepiphysiodeseis + fusion 3)
hemivertebra excision (ideal for L5 with truncal imbalance)

Type of Deformity Progression Treatment

Unilateral bar w/ contra hemi Early, rapid, relentless PSF, add ASF girls < 10, boys < 12
Unilateral bar Rapid Same
Segmented hemi Steady ASF or hemi-epiphysiodesis (age<5,
curve<70, no kyphosis)
Partial hemi Less rapid Observe vs. excise
Incarcerated hemi Slow Observe
Non segmented hemi (block Little Observe
vertebra)

64. Infantile Idiopathic Scoliosis (better called Early-Onset)

 Traditionally, idiopathic scoliosis has been divided into 3 categories based on age of onset:
o Infantile (0-3 years)
o Juvenile (4-9 years)
o Adolescent (10 years -maturity)
 Arguably, growth velocity is increased in infancy and adolescence, but remains constant during the juvenile
period, and so it is probably not worth assigning a category to the juveniles
 Thus, it may make more sense to conceptually break it down into two groups:
o Early onset, referring to those in which the deformity arises before age 5
o Late onset referring to those in which the deformity arises after age 5
 The key is that if significant thoracic deformity is present before age 5, the patient is in the category
where he/she is at real risk of subsequent cardiopulmonary compromise down the road

Characteristics of “infantile” or “early onset” idiopathic scoliosis

 Males more commonly affected than females
 75% convex to the LEFT, unlike adolescent idiopathics where the majority are convex right
 Thoracic and thoracolumbar curves tend to resolve, but double structural curves with a thoracic component
have a definite progressive potential
 Initial curve size and amount of associated rotation are prognostic factors
 85% of the curves resolve spontaneously, 15% progress
 Mehta Rib Vertebral Angle Difference – a measure of rotation
o At the apical vertebrae, measure the angle of the neck of the rib against vertical on both sides (on
the convexity, the angle is more acute; on the concavity, the angle is more obtuse)
o The difference between these two angles is the rib vertebral angle difference (RVAD). If the
RVAD exceeds 20, the curve is likely to be progressive
o The RVAD greater than 20 is the single most important factor predicting progression

Approach
 Start searching for other reasons for the deformity:
o Dysraphism?
o Tethered cord?
o Syrinx?
o Congenital failure of formation or segmentation
 Detailed neurological examination
 Look for other visceral abnormalities

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 Xrays to see if this is a congenital curve
 Then measure the RVAD
 If any suspicion that this is not an ―idiopathic‖ curve, get an MRI

Treatment
 Most resolve on their own
 Serial casting (elongation derotation flexion casting) is the conservative treatment of choice
o The indications for casting are unclear, but any low-weight floppy child with a big curve and an
RVAD over 20 should be casted
o Casting is usually done in the OR under GA
o No point in casting past 5 years of age (growth velocity has plateaued.) Can be braced after
this
 Surgery when serial casting has failed to halt progression – requires anterior discectomy over four or
five apical segments, then growing rod posteriorly

65. Juvenile Idiopathic Scoliosis

 Technically speaking, juvenile refers to curve occurring between 4 and 9 years of age
 Represents a part of the continuum between infantile and adolescent scoliosis (two different entities)
 May resemble infantile or adolescent curves
 In the lower end (3-6 years) the female male ratio is nearly 1:1 (more like infantile)
 In the upper ends (7-10 years) the female to male ratio is nearly 4:1 (more like adolescent)
 Spontaneous correction is more likely in the younger age group
 Left thoracic and left lumbar curves are more likely to improve without treatment in the 3-6 year group
(like the infantiles tend to do as well)

 Approximately 70% of curves in juvenile patients progress to require some treatment – in 50% of these,
the curve progression requires surgery
 Curve progression is not surprising, seeing as how much spine growth is left ahead of the child
 Rib Vertebral Angle Difference
o Measured in this group as well, but tends not to be as good at predicting progression in the
juveniles (cut off is 20 degrees)
o Serial RVAD measurements, however, have been used to measure response to brace treatment in
this group
 Other predictors
o Curves >45 degrees at the beginning of brace treatment tend to require surgery eventually
o Curves >35 degrees at the beginning of brace treatment have a 50% chance of requiring surgery

Treatment
 Curves <25 degrees are observed
 Curves that progress >25 degrees are braced (Milwaukee brace)

Milwaukee brace
 Patients with curves < 35 degrees and RVADs < 20 tend to do well with brace
 Patients with curves > 45 degrees and RVADs > 20 tend to do poorly with brace
 Patients between 35 and 45 degrees were unpredictable

Surgery
 Try to delay as much as possible – may let a kid get to about 55-60 before pulling the trigger, to allow
for as much spine growth as possible
 Two periods of rapid spine growth – birth to 5 years, and 10 to 16 years
o Between 5-10 years: each spinal segment averages 0.05 cm growth per segment per year
o After 10 years: each spinal segment averages .11 cm per segment per year

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  A basic formula: cm of shortening = 0.07 x number of segments fused x number of years of
growth remaining
o So if you were going to fuse 8 segments in a 7 year old who has 7 more years to grow, the
predicted cm of shortening would be 0.07 x 8 x 7 = 3.92 cm

 Almost all will be Risser 0

 To avoid crankshaft, should do front and back if doing fusion
 Can try subcutaneous growing rod – tends to increase hypokyphosis, and needs changing every 6-
12 months though

66. Adolescent Idiopathic Scoliosis

1. Imaging
a. Xray – Risser stage, Cobb angle, Tri-radiate status
i. Note apex of deformity (thoracic apex left curves = significant association with
cord pathology (except infantile, < age 3, left thoracic common, male > female)
ii. Stable vertebrae = vertebrae bisected by central sacral line
iii. Stable zone = vertical lines through LS facets
iv. Neutral vertebra = least rotated vertebra
v. Neutral disc = disc that opens right and left on supine bending films
vi. Look for structural abnormalities (vertebrae and ribs)
b. Bending films
c. MRI – brain and spine if not idiopathic
d. Renal U/S and cardiac echo if congenital
2. Tx
a. Risk factors for progression idiopathic: female, age < 12, premenarchal, curve > 20 at
presentation (curve >50 at maturity progress 1 per year)

Curve Progression Skeletal Maturity Treatment

0-20 Immature Observation
20-30 5-10 Immature Brace (23/24)
30-40 Immature Brace (23/24)
> 40 Immature Surgery
> 50 Mature Surgery

67. ? Fusion levels in scoliosis

o must go stable to stable vertebra( that vertebrae most closely bisected by central sacral line)
when going posterior
o can go neutral to neutral( no rotation, pedicles symmetric) when going anterior

68. Neuromuscular Scoliosis

Spinal muscular atrophy and DMD, need to have good PFT‘s to do surg (FVC‘s>40), tx both as
neuromuscular scoli‘s w fixation to sacrum

69. Congenital Kyphosis

Congenital Kyphosis – uncommon, HIGH neuro impairment (most common cause of paraplegia after
infection), otherwise similar to other congenital
PSF < 50 & < 5 yrs, ASF + PSF > 50

Classification – Winter

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  Type I – failure of formation, Type II – failure of segmentation, Type III – mixed form
 Most vertebral malformations that cause spinal deformity occur between days 20-30 of fetal
development
 Natural history well known, with type I and II tending to be progressive with greatest progression during
adolescence
 Most common at T10-L1
 Type I produces a much more malignant type of kyphosis with rate of progression averaging 7
degrees/yr and higher incidence of neuro involvement and paraplegia because of the acute angular
kyphosis over a short segment
 Type II progresses an average of 5o /yr but rarely neuro involvement b/c involvement of several
segments produces gradual kyphosis and vertebral height usually maintained
 As in all congenital spine abnormalities, there is a high incidence of associated anomalies within (5-
18%) and outside the spine
 Spinal dysraphism (in 40%)
o Diastematomyelia
o Tethered cord
o Syrinx
o Arnold-Chiari malformation
o Diplomyelia
o Intraspinal tumour
 Look for hairy patches, cutaneous nevi, dimples or clefts, and neurologic signs
 Look for genitourinary and cardiac abnormalities, pulmonary, auditory, Klippel-Feil
 Congenital kyphosis is more common than lordosis, but much less common than congenital scoliosis

Patient Presentation
 May be detected before birth via U/S
 If mild, can be overlooked until growth spurt
 Physical exam reveals kyphotic deformity at TL junction or lower thoracic spine – should attempt to
determine rigidity in flexion/extension
 Detailed neuro exam
 Associated MSK and non-MSK anomalies should be sought
 High quality AP and lateral xrays + flex/ext laterals plus CT with 3D reconstruction
 MRI should be obtained in most cases because of the significant incidence of intraspinal
abnormalities

Treatment
 The treatment of congenital kyphosis is SURGERY
 NO ROLE for conservative management (braces) unless for compensatory curves
 If deformity is mild or diagnosis uncertain – close observation
 Surgical Options:
o Posterior fusion
o Anterior fusion
o Combined anterior/posterior fusion
o Anterior osteotomy plus posterior fusion

Treatment of Type I (3 stages)

Early treatment of mild deformities
 With known progression of 7/yr, best treatment is early posterior fusion
 If less than 50-55 degrees, younger than 5 yrs, posterior fusion alone one above and below with
hyperextension cast for 6/12
 May need second procedure after 6/12 to assess fusion mass and possible second fusion

Late treatment of moderate to severe deformities

 Older patients with type I, posterior fusion alone may be successful if <50-55 degrees

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  If > 55, anterior and posterior is more reliable
 Anterior alone will not correct deformity
 Correction of deformity requires anterior strut grafting with temporary distraction and posterior fusion
with or without posterior compression instrumentation
 If no correction is attempted, simple anterior interbody fusion combined with posterior fusion can be
performed
 May need kyphectomy

Late treatment of severe deformities with cord compression

 Anterior decompression is indicated
 Laminectomy has no role
 For associated scoliosis, anterior approach should be on concave side of the scoliosis to allow the
spinal cord to move both forward and into the midline after decompression
 After decompression, involved vertebrae are fused with anterior strut graft followed by posterior
fusion with or without stabilization
 Post op in cast, brace or halo

Treatment of Type II
 Divided into early treatment of mild and late treatment of severe
 If mild and detected early, posterior fusion with compression instrumentation but kyphosis must be
<50
 Fusion should include all involved vertebrae plus one above and below
 If severe and detected late, correction can only be obtained by anterior osteotomies and fusion
followed by posterior fusion and compression instrumentation

Complications
 Pseudarthrosis – minimized by performing anterior and posterior fusion for >50
 Progression – same as above and extend one level above and below
 Paralysis – lessened by not trying to correct deformity with instrumentation
 Low back pain – 38% secondary to increased lumbar lordosis

70. Scheurman‟s Kyphosis

Scheuermann‘s Kyphosis - >5 ant wedging at 3+ consecutive levels
45-75 = brace, physio; > 75 = ant release, PSF. Consider anterior release for large curves or if
curve does not improve more than 55 degree with bending.

71. Scenario of Complication in Scoliosis Surgery

o Big curve: stage the correction
o 1st. Anterior release disk and ribs, use ribs as graft into disk spaces
o then to halo-femoral traction with appropriate monitoring as there is Neuro risk
o then go back and do posterior instrumentation and fusion.
o Intra op she has no movement on wake up test.
o You take out all your hardware and let correction release. Recheck. No different. Close
up and talk to neurosurg also.
o Get MRI post op to look for hematoma – if present go back in now and decompress
o Else is might be an infact. Sucks !

72. Slipped Verebtral Apophysis

o Lateral radiographs may show a small triangular opacity posterior to the vertebral body.
o The inferior apophysis of L4 is most commonly involved.
o The treatment of a slipped vertebral apophysis without neurologic symptoms is similar to the
nonoperative treatment of herniated disks.

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 o If there is neurologic compromise, excision of the bone fragment with attached cartilage and
disk is the treatment of choice. A bilateral laminotomy is recommended to safely remove the
entire central fragment.

73. Idiopathic Juvenile osteoporosis

o 5 cardinal features:
1. Onset before maturity
2. Multiple fractures
3. Pain in the back and extremities
4. Metaphyseal compression fractures
5. Evidence of osteoporosis in new bone
o **Remember leukemia as the major differential
o they can get back pain and scoliosis.you should brace this for comfort.

74. Child with painless limp

 Go through the differential diagnosis of painless limp:
1. Congenital
2. Developmental: SCFE, Coxa Vara
3. Inflammatory
4. Neoplastic
5. Vascular: Perthes
6. Bony dysplasia
7. Infectious: but usually painful
8. Trauma: but usually painful
 Most of these have pain
 Perthes and SCFE are the classic painless limps

 Go through the history, looking for systemic signs, trauma, previous infections, other joints involved,

 On physical exam, look for:

o Height and weight (bony dysplasias)
o Gait
o Dysmorphic features
o Gait abnormalities (lurch), abductor weakness, leg length
o Signs of spinal dysraphism
o Endocrine abnormalities
o Wasting, neurology
o Limitations of motion - Perthes often have decreased internal rotation and abduction, DDH has
limited abduction, SCFE have obligatory external rotation with flexion

Now, for the x-rays: unilateral or bilateral sclerosis and fragmentation of the femoral epiphysis
 First thing, make sure you look at both hips!
 Don‘t jump to the conclusion that the kid has Perthes – Perthes is rarely bilateral
 The other possibilities include:
o Meyer‟s dysplasia (if really young <4 On radiographs ossification of the femoral heads appears
at approximately 2 years of age instead of at 6 months. In addition, multiple irregular centres
develop with an abnormal flattened appearance of the femoral capital epiphysis. Later serial
radiographs show consolidation of the granular ossific nuclei and a return of the femoral heads
to normal.)
o Hypothyroidism – readily treatable
o Septic arthritis and osteomyelitis – NEVER FORGET SEPSIS!
o Bony dysplasia – MED, SED, Morquio‟s (most common, presents by 18 months to 2 yrs with
waddling gait, knock knees, thoracic kyphosis, cloudy corneas, and normal intelligence. Bony changes
include thickening skull, wide ribs, anterior beaking of vertebrae, wide/flat pelvis, coax vara with

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 nd
unossified femoral heads and bullet-shaped metacarpals. C1-2 instability 2 to odontoid hypoplasia
presents with myelopathy and tx w decompress/fusion. This syndrome assoc with excretion of keratin
sulfate in the urine (whenever you say SED, also include Morquio’s – they are radiographically
identical and both need evaluation of C1-2 for atlantoaxial instability)
o Gaucher‟s disease - An autosomal recessive disorder caused by deficiency of the enzyme
glucocerebrosidase (see GLUCOSYLCERAMIDASE) featuring the pathological storage of
glycosylceramide in mononuclear PHAGOCYTES (Gaucher Cells). The most common subtype is the
non-neuronopathic form, a slowly progressive condition characterized by hepatosplenomegaly and
skeletal deformities. The neuronopathic forms are divided into infantile and juvenile forms. The infantile
form presents at 4-5 months of age with anemia, loss of cognitive gains, neck retraction, dysphagia, and
hepatosplenomegaly. The juvenile form features a slowly progressive loss of intellect,
hepatosplenomegaly, ATAXIA, myoclonic SEIZURES, and spasticity. The neuronopathic forms are
characterized by neuronal loss with neuronophagia, and accumulation of glucocerebroside in neurons
o Sickle cell
o Corticosteroid-induced AVN

Note on the x-rays

 Is there a widened joint space (from decreased bone growth, relatively increased articular cartilage
growth)
 How much of the epiphysis is involved; the lateral pillar classification is applicable only to Perthes
 Is there any involvement of the physis?
 Is there any involvement of the metaphysis?
 Is the neck broad and short (coxa breva)?
 Are there acetabular changes? YOU DO NOT SEE ACETABULAR CHANGES WITH EARLY
PERTHES
 Is there extrusion of the femoral head – how congruent is it?
 If you‘re pretty sure this is Perthes, grade it‘s lateral pillar stage, look for at risk signs (calcification
lateral to the epiphysis, lateral subluxation, Gage‘s sign, metaphyseal cysts, horizontal physis)

Note: Perthes can be bilateral, but it is rarely symmetric, and it may have metaphyseal cysts, which are not
present in MED. Also, MED may have some acetabular changes – these are not present in Perthes

** If you think this is a bony dysplasia, AND ON THE EXAM YOU BETTER BE THINKING THAT THIS IS
MORE THAN JUST PERTHES, do a skeletal survey, with particular attention to the knees, spine, feet/ankles
to look at other physes

 As an aside: this kid has MED; do abduction views to see if there is improved concentricity. Because they
may have extrusion of the femoral head, they often get hinged abduction
 You can consider a valgus intertrochanteric osteotomy if there is sufficient coverage, to get the extruded
part away from the acetabular lip

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75. Toe Walking
Important points: uni or bi, from birth or new onset (ie, early or late), neurological deficits, FH
Differential:
1. HABITUAL: 70% male, 70% +ve FH. Most be normal by 3 yr old. Can heel walk if wants.
2. STRUCTURAL
Fixed equinus – CTEV / arthrogryposis
Short / tight TA
SOL in calf
3. NEUROMUSCULAR
CP
Spinal dysraphism/tethered cord
DMD
CMT
Familial spastic paraplegia
4. SHORT LEG: Real, Apparent (knee or hip deformity)
Hx: Gestational, Brith, FH, Walking age, How long? How often? (all time?) CP?
Px: Gait & Running coordination (Toe walk/heel walk), Upper Limb (hemiplegia), Spine (pigmentation,
pits, hairy tufts, lipoma), Lower Limb (Trendelenburg, wasting, Active and passive ROM of ankle with
knee flexed and extended, sole of foot, reflexes, LLD, Gower sign)
Invx: CPK & muscle biopsy (R/O DMD), Spine X-ray and MRI, Pelvis X-ray (R/O DDH), EMG

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Tx: Neurology consult, Non-operative (TA stretches, serial casting, AFO, Botox in CP). Surgery: TA
lengthening or proximal gastorc recession (if isolated gastroc contracture). In CP, might consider
doing multiple levels at the same time to avoid Birthday Syndrome

76. CP
Rules of thumb:
 Quadriplegics: Think SPINAL DEFORMITY. When scoliosis affects seating balance,
consider long thoracolumbar (and possibly to sacrum) fusion.
 Diplegics: Think HIP INSTABILITY and contractures. May need hip surgery combined with
knee and ankle contracture releases at age 4-6.
 Hemiplegics: Think UPPER EXTREMITY and FOOT/ANKLE EQUINUS. Tendoachilles
lengthening after they reach age 4 (recurrence rate drops from 25% to 12%), possible tendon
transfers 1-2 years later, and upper extremity surgery at 10-12 years.
 Predictors of walking: ―Bleck‘s Criteria‖. Done after age of 12 months.
If 2 or more abnormal, child unlikely to ever walk
1. Persistence of neck righting reflex
2. Persistence of asymmetric tonic neck reflex
3. Persistence of symmetrical tonic neck reflex
4. Persistence of Moro reflex
5. Persistence of extensor thrust (rigidly straight when lowered to table)
6. Absence of parachute reflex
7. Absence of foot placement reflex (lifts foot to put it on table when held)
 In CP: spasticity  joint contracture  joint damage
 It is generally not possible to make these patients NORMAL; the goal of surgery is therefore to
make them BETTER, not just DIFFERENT
o Goals of lower extremity surgery: PAINLESS STABILITY
o Goals of upper extremity surgery: FUNCTIONAL MOBILITY
 Surgical indications: prevent complications (absolute); improve function (relative)
 In general, lower extremity surgery is optimally delayed IF POSSIBLE until a mature gait
pattern is established. In general, try to do all lower extremity surgery in one sitting, so as to
minimize repeat hospitalizations and periods of rehab.

CP Spine:
 Mainly scoliosis. Kyphosis and lordosis do occur.
 The actual curve patterns differ. with CP curves often being long, sweeping, unbalanced
thoracolumbar curves with significant pelvic obliquity
 Non-operative Management:
o Seating Support: For non-walkers, to optimize function, prevent pressure sores, and
assist in the nursing/caring of these children.
o Bracing: Temporary control using TLSO, but this is unlikely to succeed in the severe
quadriplegic kids.
 Operative Management
o For the severely handicapped spastic quadriplegic, when to fuse is controversial, but
deterioration in function (particularly seating ability) and development of pressure sores
are relative indications.
o In the long, thoracolumbar or lumbar curves, consider extending the fusion to the
sacrum, if the pelvis demonstrates obliquity and is part of the curve.
o Posterior fusion with Luque wires and Galveston pelvic fixation is probably optimal for
the soft, osteopenic bone.

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 o Combining anterior release and fusion with posterior fusion maximizes correction and
improves fusion rates.
 Complications
o Intraoperative blood loss is usually increased.
o In general, respiratory problems and pseudarthrosis are two major post-operative
issues.
o Ileus secondary to a retroperitoneal approach and/or narcotic use can compromise an
already under-nourished child.
o Watch for superior mesenteric artery syndrome.

CP Upper Extremity
 Start with non-op – physio, botox. Then operative.
 Elbow Contractures:
o If elbow contractures are mild – release lacertus, Z lengthen biceps and
musculotendinous lengthening of brachialis
o If >90 degrees, need to add extensive release of medial and lateral epicondyles, biceps
and brachialis and anterior capsule
 Wrist Contractures:
o Forearm hyperpronation and wrist flexion contracture – transfer of FCU (the main
deforming force) to the extensors is successful
o If there is more ulnar deviation than palmar flexion – transfer ECU to ECRB
 Thumb in palm – static contractures are treated with web space Z plasties and adductor
release
o Static contractures of FPL and FPB need lengthening or release
o Dynamic balancing with tendon transfers to weak abductors and extensors – donors are
PL, FCR and brachioradialis; recipients are EPL, EPB and abductor pollicis longus
o MCP joint needs to be stable post op – in most is achieved by muscle balancing – on
occasion, capsulodesis or arthrodesis

CP Lower Extremity
Equinovarus (usually hemiplegic)
 If the anterior tibialis muscle contributes to supination of the equinovarus foot, a Rancho
procedure is indicated, consisting of:
1. Posterior tibialis muscle lengthening above the malleolus
2. Achilles tendon lengthening
3. Split anterior tibialis tendon transfer. The lateral half of the anterior tibialis tendon is
detached from the base of the first metatarsal, split above the extensor retinaculum, routed
beneath the retinaculum, and inserted into a bony tunnel in the cuboid. The Y-shaped
tendon is then balanced medially and laterally so that activation of the muscle leads to
dorsiflexion without supination.

Equinovalgus (usually diplegic)

Orthotic. Surgery. Soft tissue is ineffective. Bony procedures (lateral column lengthening or fusion)
1. Lateral column lengthening: opening wedge osteotomy of calcaneal neck 1.5 cm proximal to
calcaneocuboid joint is supported with a structural graft, either iliac crest autograft or allograft
2. Arthrodesis: Grice extra-articular subtalar arthrodesis. A graft taken from either the fibula or
ilium is placed vertically in the sinus tarsi to provide structural support.
3. If there is coexisting valgus deformity at the ankle, supramalleolar osteotomy or
hemiepiphysiodesis should be considered.

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Crouch Knee
Surgical treatment consists of lengthening the hamstring muscle group.
 The medial hamstrings (ie, the gracilis and semitendinosus muscles) are Z-lengthened
 Semimembranosus and biceps femoris muscles undergo intramuscular lengthening by
sectioning of the overlying fascia.
Postoperatively, either knee immobilizers or long leg casts are used for immobilization.

Stiff Knee Gait

Treatment is rectus femoris muscle transfer. The rectus is detached distally from the patella and
rerouted into the medial hamstrings or sartorius. Care must be taken to preserve the attachments
of the rest of the quadriceps mechanism on the patella. The rectus theoretically then acts as a knee
flexor during the swing phase, although in reality this has not been found in the gait laboratory.
Simple distal release of the rectus does not provide the same improvements in swing-phase
knee flexion as does transfer of the tendon.
Although results of rectus transfer appear to be best when done concomitantly with hamstring
lengthening, some patients have hamstring lengthenings that do not require rectus transfers.
Delayed transfers can be done if limitations of swing-phase knee flexion develop after
hamstring surgery and are problematic.

Hip involvement
The hamstrings provide stance phase hip extension because they cross both the hip and knee.
Lengthening both the medial and lateral hamstrings in patients with crouch gait produces hip extensor
weakness, which commonly leads to an increase in the anterior tilt of the pelvis during gait. When a
hip flexion contracture coexists with hamstring spasticity, the iliopsoas muscle should be lengthened
concomitantly.

Hip Dysplasia in CP
 Summary:
o Start with soft tissue releases
o If you can‘t get 30 degree of abduction using botox, splinting, do adductor tenotomy
o Acetabular index above 25 degrees, do periacetabular osteotomy
o High valgus angle do femoral osteotomy
o Add open reduction and capsulorrephy (especially is subluxation is more than 50%)
o Want to get knees to 90 degrees with hamstring lengthening

 80% of the hip problems in CP occur with spastic quadriplegia. Usually have posterosuperior
acetabular deficit. In DDH, usually have anterior acetabular deficiency.
 Common problems are contractures, hip at risk, subluxation, and dislocation
 Pathoanatomy: combinations of muscle imbalance, acetabular dysplasia, pelvic obliquity,
excessive femoral anteversion (due to persistent hip flexion), increased femoral neck valgus
(due to persistent hup adduction), lack of weightbearing, and maldirected resultant force vectors
across the hip joint
 In all but the most severely involved children, hip dislocation should be prevented. Hip
subluxation is often painless but dislocation can lead to pain. Approximately 50% of CP kids with
dislocated hips will have pain - it is important to ask about pain in the history.
 For this reason it may be wise to obtain an annual screening supine AP xray of the hips in
children with spastic quadriplegia, and in patients with spastic diplegia who do not walk
 Clinical Signs: Limited abduction, Asymmetric knee height (Galeazzi sign), Windswept posture
(one hip adducted and other hip abducted), Asymmetric leg length, Hip flexion contractures,
Tight psoas leads to fixed flexion deformity of hip, lumbar lordosis and prominent bottom,

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 Hamstring contractures lead to lumbar kyphosis and small bottom, knee flexed at beginning of
stance phase, high patella, Adductor contractures lead to scissored gait if bilateral

Hip at Risk
 Increased valgus and anteversion, shallow acetabulum, but no subluxation, tightness and
contractures in the adductor and flexors
 Without treatment, hips at risk often progress to subluxation or dislocation, particularly if hip is
stiff. Natural History quite variable
 If hip is at risk and no contracture night splint
 If hip stiff  lengthening/weakening of the tight adductors and flexors (psoas tenotomy), physio
+/- night splint
 In the past, anterior branch, or even complete, obturator neurectomy performed; if child has
athetoid component, in addition to spasticity, obturator neurectomy should never be done 
severe, disabling abduction contracture.
 Never do obturator neurectomy in ambulatory child, and rarely indicated at all

Subluxation
 Uncovering of > 1/3 of the femoral head and a break in the Shenton‟s line. Often has
increased femoral valgus and anteversion
 Surgical treatment of a subluxation can prevent subsequent dislocation
 If child is young, soft tissue releases and prolonged splinting may be all that is needed
 Proximal femoral osteotomy often required to stabilize the hip joint
o Varus is usually reduced to about 115° in an ambulatory child, or even less in a
nonambulator
o Derotation of the excessive femoral anteversion to approximately 10 to 20 degrees (or
30 to 45 degrees of passive internal hip rotation) to prevent posterior subluxation
o The younger the patient, the more likely is the valgus and anteversion to recur
 If the magnitude of the subluxation > 50%  open reduction and capsulorrhaphy
 If acetabular dysplasia is present (acetabular index >25 degrees), it almost always should be
corrected surgically; an exception might be a child younger than 4 or 5 years with mild dysplasia
and corrected abnormal valgus and anteversion. In this situation acetabular remodeling may
occur.
o The dysplastic acetabulum in cerebral palsy is shallow. In nonambulators, the
acetabular deficit is superior, posterior, and usually more severe than in ambulatory
patients.
o Femoral anteversion is greater in ambulators
o The Salter, Steel, Sutherland, Pemberton, pericapsular, Dega, and Chiari
osteotomies, and shelf augmentation of the acetabular rim, all have been successful in
cerebral palsy when appropriate indications are met (depends on defect)
o If the acetabulum is found to be deficient superiorly and anteriorly, or purely
superiorly, an anterolateral rotational osteotomy, such as a Salter, Steel, or
Sutherland procedure, or a Pemberton osteotomy, is appropriate
o Often, there is superior and posterior deficiency, in which case, restoration of
lateral and posterior coverage by a shelf-augmentation procedure, an Albee shelf, a
Dega procedure, or a pericapsular osteotomy may be more appropriate (Devin does
the San Diego)
o The Chiari osteotomy can be performed if the superior acetabular rim has not been so
proximally eroded that the cut will enter the sacroiliac joint

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Dislocation
Common Procedures
 Accepting the dislocation
 Relocation procedures
 Proximal femoral resection

Uncommon Procedures
 Hip arthrodesis
 THA (mild spasticity)

 If the dislocation occurred within 1 year, and/or if the anatomy does not appear excessively
distorted, perform anterior open reduction and capsulorrhaphy, combined with appropriate soft
tissue releases and a VDRO with shortening, with possible acetabular osteotomy (Dega).

 Dislocated for longer than 1 year painless vs. painful

o painless: no treatment
o painful: proximal femoral resection with muscle interposition (gluteus medius / vastus
lateralis)
 This resection is performed at the subtrochanteric level, the thickened capsule
and gluteus medius muscle are sewn over the acetabular inlet, and a muscle
cuff of vastus lateralis is sewn over the beveled femoral stump
 NSAID‘s for HO
 hip spica cast for about 3 to 4 weeks
 physio
 Acetabular dysplasia is often present and it is wise to correct this at the same
time.
 Heterotopic ossification about the hip is almost universally seen after proximal
femoral resection, and single–dose radiation therapy should be considered to
minimize its magnitude
 Femoral head resection, combined with subtrochanteric valgus pelvic support
osteotomy, has been successful in relieving the pain of chronic hip dislocation

Osteoarthritis
 surgery indicated in painful, reduced hips that have failed medical mgt.
 arthrodesis and THA have both been successful
 for arthrodesisincorporate more flexion if pt is non-amb
 Arthrodesis is usually performed in a position appropriate for walking, sitting, and lying: 30
degrees of flexion, 5 to 10 degrees abduction, and neutral rotation for an ambulatory patient,
and 45 degrees of flexion for a nonambulator

Flexion Contracture of the Hip

 Usually caused by contracted iliopsoas.
 In severe cases involves all anterior muscles/soft tissues
 Most common cause of lumbar hyperlordosis
 Consider release when contracture is 20-25o and affecting function.

Extension Contracture
 contracted hamstrings
 cannot sit in wheelchair

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  botox injections
 proximal hamstring lengthening
 posterior capsulotomy of the hip and release of the external rotator muscles may be necessary
in refractory cases
 recurrence of common following proximal hamstring lengthening.

Extension Plus Abduction Contracture

 not common
 often iatrogenic following adductor and psoas release in children with athetosis
 OR if child has co-existing spasticity of hip extensors and abductors
 mild deformity  physio and proper seating in wheelchair
 Severe deformity surgical treatment is necessary.
 release of the proximal hamstrings, femoral and iliotibial band insertions of the gluteus maximus,
the external rotator muscles
 posterior capsulotomy of the hip joint PRN
 femoral shortening may be necessary to prevent overstretching of the sciatic nerve in chronic
cases
 intra-thecal baclofen controversial

77. Differential Diagnosis of Unilateral Hip Pain in Pediatrics

Congenital - congenital coxa vara (probably not painful until later)
- proximal femoral focal deficiency

Traumatic - Slip capital femoral epiphysis

- Femoral neck, intertrochanteric fracture or stress fracture
- LT or GT avulsions, ASIS avulsion
- Ischial, pubic, ilium fractures

Developmental - dislocation/dysplasia (probably not painful quite as yet, but may be)
- developmental coxa vara
- idiopathic chondrolysis

Vascular - Perthes disease

- post-traumatic
- sickle cell, Gaucher‘s, or idiopathic osteonecrosis

Inflammatory - toxic synovitis, bursitis, osteitis

- juvenile rheumatoid arthritis
- other seronegative spondyloarthropathies – Reiters, psoriatic, ank spond

Neoplastic - benign – UBC, ABC, EG, chondroblastoma, osteoid osteoma, osteoblastoma,

fibrous dysplasia, GCT (abit young for this)
- malignant – ostosarcoma, Ewings
- leukemia/lymphoma

Infectious - septic arthritis

- proximal femoral osteomyelitis
- psoas abscess

Metabolic - rickets??

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78. Hemophilia
Remember iliacus hematoma vs hip hemarthrosis in a kid. Present very similar. Femoral nerve palsy
more likely in the former.

Now, to tx the hip. Aspiration is needed and of course factor replacement. With the hematoma. Factor
replacement and compression dressings.

THE SERVERITY IS BASED ON FACTOR AVAILABLE:

MILD 5-25%
MODERATE 1-5%
SEVERE 0-1%

Levels:
Vigoourous PT - 20%
Tx of Hematoma – 30%
Acute hemarthrosis or soft tissue surgery ->50%
Skeletal surgery – 100% then try to maintain about 100% for 1st week and then 50-75% for week 2.

79. KID PRESENTS WITH AN IRRITABLE (PAINFUL) HIP:

1. INFECTION
2. JRA (most common joints are knee,ankle,hand/wrist, then hip and neck)
3. HEMOPHILIA
4. TRANSIENT SYNOVITIS

80. DDH
 Risk factors: Breech, 1st born, female, oligohydramnious, Torticollis, met adductus,
 Use pavlik up to 6/12. Tx w pavlik for 6/52, if stable, no further tx. If not stable, tx until stable
and then another 6/52.

Approach to DDH – Newborn – 6 months

The hip can be one of three things:
1. Barlow positive– hips flexed to 90 and downward axial force to dislocate hips dislocated, but reducible
2. Ortolani positive- the clunk or click upon re-entry into the acetabulum
3. Subluxatable

Any of the above gets:

 Pavlik harness and U/S to be sure that it is in, and reassessment in a week
 Hips should be flexed 90-100 (ICL says no more than 100 (incr fem. Nerve palsy), and the knees
should be able to be brought to within 4-5 cm of one another (ie – don‘t crank them too far into
abduction). Say should determine safe zone with the abduction and to NOT go beyond 60deg as this
incr‘s risk of ON of the head
 Basically, do a Barlow once the Pavlik is on to see at what point of adduction the hips dislocate
– then tighten up the posterior straps to prevent adduction to this point, but no more (anterior
straps control flexion)
 At 1/52, check motion, check femoral nerve, check stability, get an U/S
 Use of Pavlik contraindicated in:
o major muscle imbalance such as myelomeningocele (L2-4 level)
o major stiffness (arthrogryposis)
o ligamentous laxity (Ehlers-Danlos)

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 o should not be initiated in > 10/12 old (I‘m going to say >6/12(After 6 months of age the failure
rate for the Pavlik harness is greater than 50% because it is difficult to maintain the increasingly
active and crawling child in the harness.))
 Children 3/12 wear for 3/12, those > 4/12, wear for double their age, usually part time over last 2/12,
and some other form of bracing once walking age (consider abduction orthosis beyond 9/12)

Ultrasound Assessment
 Measure 2 angles:
o Alpha angle - measurement of the slope between the ilium and bony acetabulum (>60 is normal
– want lots of alpha)
o Beta angle – between the bony ilium and the labrum (cartilaginous component of acetabulum)
(normal <55)

FIGURE 23–16 A: Ultrasonography of a normal newborn. B: Anatomic drawing of

hip landmarks (after Graf): 1, femoral head; 2, iliac limb; 3, bony acetabular roof;
4, acetabular labrum; 5, joint capsule; 6, osseous rim. C: Ultrasonograph of a
newborn. Note the alpha angle and the beta angles.

Xray Assessment
 Increased acetabular index - good measure in <
8yrs with normal <30; after that use CEA – normal
> 25
 Disruption of Shenton‟s line
 Absent tear drop
 Dissimilar sizes of ossific nuclei (usually
smaller)

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  Location of ossific nucleus of femoral head superior and lateral with respect to acetabular roof (not in
the inferomedial quadrant)

Treatment Algorithm:
 If stable in a week – continue Pavlik for 6/52 – take off and if stable, leave off – bring back at 4/12 for
xray
 If not stable but reduced – continue Pavlik until they are stable, then 6/52 after that
 If not reduced within 2-3/52 in the Pavlik – give up and proceed with traction, adductor tenotomy, closed
reduction, arthrogram and spica cast in 100 flexion and 40-50 abduction (human position) –
occasionally open reduction required. Need to check if you attempt CR and tenotomy before you give
up and call it teratologic
 If not able to reduce and keep reduced within the first 2 months, even with a Pavlik or closed
reduction – may have a teratologic dislocation, and the acetabulum has never really formed. Back
off – aim for range of motion and plan for open reduction and acetabular osteotomy at 6-12/12
 Complications of Pavlik harness include inferior dislocation with too much flexion, femoral nerve palsy
with prolonged excessive flexion, and osteonecrosis (ON if > 60deg of abduction)

 Chest halter strap at the nipple line

 Shoulder straps are set to hold the cross strap at
this level
 Leg and foot stirrups must have their anterior and
posterior straps oriented anteriorly and posteriorly
to the child's knees
 Hip flexion 100-110 degrees and should be in the
anterior axillary line
 Posterior abduction strap should be at the level of
the child's scapula and adjusted to allow
comfortable abduction within the safe zone (arc
of abduction and adduction between redislocation
and comfortable, unforced abduction)
 Posterior strap acts as a checkein to prevent the
hip from adducting to the point of redislocation

Note: this algorithm works best in the NEWBORN. After 2/12, and up to 6/12, you can still try the Pavlik
even in the dislocated hip. But these need to be watched very carefully. U/S to confirm that the hips are
reduced. If you are starting late and are not totally reduced with the Pavlik within a couple weeks, back off.
The kid needs a closed reduction and a spica cast

Approach to DDH – 6 to 24 Months

 The pathoanatomy is getting tougher here. At this stage, no Pavlik harness.
 Consent for closed reduction, arthrogram, possible adductor tenotomy and spica cast possible
open reduction and spica cast, possible femoral shortening osteotomy, possible acetabular
osteotomy, postoperative CT

 Start with traction – this probably doesn‘t reduce AVN but it increases the chances of getting it closed
(traction has no role beyond 2 years). Skin traction is the most commonly used method, although
some physicians recommend skeletal traction. Skin tapes should be applied above the knee to
distribute the traction over a large area. The author prefers to wrap Elastoplast tape loosely over
tincture of benzoin from the ankle to the upper thigh. It is important not to stretch the Elastoplast tape at
all; it should merely lie on the skin in a circumferential manner, with each edge directly opposing the
preceding edge. Buck traction tapes are then applied from above the ankle to the thigh and to the foot
plate; weights may be added to both legs, so that the buttocks "lightly" touch the bed. (generally 1lb
per year of life – max 6 lbs)(gallie traction I think)
 Closed reduction of a hip dislocation (osteotomies of pelvis or femur are rarely needed
in this age group):

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 o One assistant to hold pelvis stable with the patient is supine
o Right hand over the knee, left hand under the hip – apply traction
o Then flex the hip up to 90, maintaining traction (so you‘re lifting UP on the leg)
o Then gentle abduction/external rotation once you‘re up at 90 to bring the hip into joint
o If you think you‘re in, then assess for zone of safety
o Determine amount of adduction that causes dislocation, then determine what the
maximum abduction is - you want to avoid these extremes by about 15o
o So if he dislocates at 10, and maximum abduction is 50 - his safe zone is only between
25 and 35 degrees (ie 10 degree safe zone) - this is no good
o Do an adductor tenotomy and check again - basically, you want a wide zone of
safety - 30 to 50 degrees and want to make sure that you are not too close to the
maximal abduction – risk AVN! Should not go beyond 60
o Then 0.5 cc Isovue into the joint, injecting medially just under the adductor longus
tendon (which is now cut)
o Look for a medial dye pool of less than 5 mm:
o if < 5 mm, the kid gets a spica cast and a CT before discharge home
o if > 5 mm, the kid gets an open reduction – medially if less than 1 year, anteriorly if
1-2 years
 If you forget consent for open reduction, back off, wake the kid up, talk to parents, then proceed
later.
 Medial approach (Morrissey p309)
o Designed to remove certain obstacles to closed reduction like tight iliopsoas, constricted
capsule, and transverse acetabular ligament
o Unlike the anterior approach, cannot do a capsulorrhaphy and difficult to deal with cranial
structures like the labrum
o Use this approach for < 1yr old
o Other indications mentioned are those who cannot maintain concentric reduction with less
than 60 degrees of abduction or persistent medial dye pool
o Interval - pectineus anteriorly and adductor longus and brevis posteriorly
o Supine with knee flexed and leg abducted then transverse incision 3-4cm in length 1cm
distal to the groin with 2/3 of incision superior to adductor longus tendon – similar to
incision used to release adductors in CP
o Open superior fascia of adductor longus and release close to its insertion and retract distally
exposing adductor brevis in the inferior part of the wound and pectineus in the superior part
o Branches of obturator nerve can be seen on the surface of adductor brevis
o Posterior border of pectineus is freed - similar to when performing an iliopsoas tenotomy –
and retracted superiorly (beware anterior branch of medial circumflex femoral artery
which runs posterior to pectineus)
o LT and iliopsoas can be felt but not easily seen because tendon is surrounded by fascial
layer that must be opened first, pull tendon into wound and sharply divide
o Now clear the fat off the capsule and divide – but be careful of the branch of the medial
femoral circumflex that crosses the capsule inferiorly which sometimes can be dissected and
spared – otherwise ligate
o Capsule is cut open in the direction of the femoral neck
o Transverse ligament readily identified and sectioned
o Ligamentum teres can be seen and followed to the true acetabulum
o Clear pulvinar from the acetabulum
o Additional release of the capsule if necessary to reduce hip – then check stability and
position for post-op casting noting degree of flexion that causes inferior subluxation
o Apply one and a half leg spica in similar to human position but with less flexion
o Maintain in cast same amount of time as closed reduction which varies with age
o Development of lateral edge of acetabulum is useful sign of stable reduction
o Remember you CANNOT do a capsulorrhaphy through a medial approach

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 Anterior Approach to a Developmentally Dislocated Hip (Morrissey p293)
o Advantage of exposing capsule and both the superior and inferior aspects of the acetabulum
allowing you to address all obstacles to reduction and to perform a capsulorrhaphy
o Only disadvantage is need for experience and expertise
o Lateral position with sand bag behind bag allowing patient to roll back
o Incision can be transverse or oblique centered 2cm below the ASIS permitting same exposure
as Smith-Peterson
o Incision carried down through superficial fascia exposing crest
o Sartorius-TFL interval identified just distal to ASIS and small stab wound made through fascia
then scissors to open it up full length staying toward TFL to avoid LFCN
o LFCN should be identified and protected 1-2cm distal to ASIS and taken medially with
sartorius while TFL is taken laterally
o Rectus forms the floor of this interval and exposing the tendinous portion of the straight head
allows identification of the AIIS
o At the inferior extent of the wound, passing deep between sartorius and TFL, ascending
branch of lateral femoral circumflex artery should be identified and divided
o When this interval is not divided beyond these vessels, there is insufficient exposure
o Proximally this interval needs to be opened to the ASIS
o Shift retractors to expose iliac crest and iliac apophysis is split open down to the bone
starting at the midportion down to the AIIS, then pulled off the crest and the periosteum is
elevated off the outer table pulling the tensor and abductor muscles laterally
o Rectus muscle is divided at its conjoined tendon and retracted distally
o Divide and clean fat and fibrous tissue off capsule
o If hip has been dislocated for any length of time, there is a false acetabulum and capsule
adheres to it – strip it off ilium down to true acetabulum
o Before proceeding, ensure capsule has been exposed adequately – inferiorly down to its
insertion on the pubis and ischium, beneath the superiorly displaced iliopsoas and superiorly
around to the posterior aspect
o Divide the iliopsoas as it crosses the pubic ramus just medial to the AIIS – and be careful as
femoral nerve is nearby
o Proper incisions in the capsule are important – first incision is parallel to acetabular rim
extending from most inferior to the posterosuperior aspect

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 o Transverse incision is then made over the femoral neck, dividing the capsule into superior
and inferior parts
o Ligamentum teres if present is identified and sectioned and excised providing an excellent
guide to the inferior acetabulum leading to the transverse acetabular ligament which also
should be divided
o Clear the pulvinar
o Femoral head should reduce easily
o Strong absorbable suture to repair the capsule, placed first medially on the acetabular side
including periosteum then through the capsule – in an effort to pull the femoral head inferiorly
and medially – excising the redundant superolateral flap
o Capsular repair should hold the femoral head in joint firmly
o Post operatively, spica cast in 30 flexion, 20 abduction, 15 IR and left in place for 6/52 then
bilateral cylinder casts in 15 flexion plus bar for 4/52 and then further bracing should not be
necessary

Approach to DDH – 24 Months and Older

 Goal is to safely reduce the dislocated hip and to surgically recreate normal anatomy that will maintain
reduction and allow rapid development of normal hip function
 Open reduction and femoral shortening for any child > 2 years
 Prevalence of AVN in very young – 10%, similar to described for older 9%
 Basic approach here is:
o Capsulorrhaphy
o Femoral derotational shortening osteotomy
o Acetabuloplasty
 As per ICL 53, they prefer an anterolateral (Salter) incision and a separate lateral incision over the
femur for the femoral shortening
 With femoral shortening, an adductor tenotomy is unnecessary
 Note: Give up on a unilateral dislocation after age 8; give up on the bilateral dislocation at age 6

Innominate Osteotomy of Salter

 Redirection of the entire acetabulum as a unit by performing a transverse osteotomy of the ilium just
above the acetabulum and opening the osteotomy anterolaterally by hinging and rotating the acetabular
segment on the symphysis
 Designed to preserve normal acetabular structures and shape while correcting the abnormal
anterolateral facing of the acetabulum seen in cases of DDH
 Provides about 15 degrees of lateral coverage and 25 degrees of anterior coverage
 Positioned as for open reduction through anterior approach, same incision and approach but if
open reduction is not to be performed, capsule does not need to be exposed
 Inner and outer table of ilium exposed, periosteum carefully elevated from sciatic notch and Gigli saw
pulled through notch with retractors on either side to protect soft tissues
 Saw emerges at or just above AIIS
 Tricortical bone graft to keep osteotomy open is taken from anterior iliac crest

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 Imperative to perform iliopsoas tenotomy at this time
 Distal fragment is manipulated with towel clip if capsule has been opened or simply by placing
leg in figure four position if not – to pull it down and forward
 Bone graft is tailored to fit tightly in the gap and should be relatively stable – and distal fragment should
not be displaced posteriorly
 2 heavy Kwires passed from proximal to distal lying medial and posterior to the acetabulum – taking
care not to enter the joint
 Check motion of hip, close wound over drain
 Reliable – 3 point partial weight bearing, no immobilization and early ambulation
 Unreliable – immobilized for 6/52

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Femoral Shortening Osteotomy (ICL 53)
 Separate lateral incision from tip of trochanter distally
 To prepare for derotation, existing femoral anteversion is estimated by grasping the proximal part of the
tibia with the knee flexed 90 (can also be determined by CT)
 In DDH, femur is usually anteverted 40-60, compared with the normal 10-20
 Neck shaft angle is near normal 130-140
 Only femoral shortening and derotation are required
 To avoid varus, initial guide pin is introduced transversely at the distal extent of the GT apophysis and
the inserting chisel for the bladeplate is placed parallel to and immediately below the pin
 Second transverse guide pin is placed in the distal part of the femur just above the femoral condyles –
introduced at a right angle to the femur in the frontal plane
 Saw cut 1cm below and parallel to the chisel
 Bone ends are allowed to overlap with the femoral head reduced into the true acetabulum, allowing the
surgeon to estimate the degree of shortening required
 Removal of 1.5 to 2.5 cm segment
 Osteotomy is fixed with appropriately sized blade plate (this is then followed by capsulorrhaphy)
 Spica cast flexed and abducted 30 degrees for 10-12/52

Approach to DDH – Acetabular Dysplasia

 After treating the dislocation, you must follow the kid to see if the acetabulum is developing normally
 Look to see what the pathology is:
o Is it dysplasia of the acetabulum with a shallow cup – acetabular index down, sharp angle
down?
o Is it a coxa valga with superior loading?
o Is it both?
 Is the dysplasia causing recurrent instability? Then you better get on with an osteotomy
 If reduced, it is somewhat controversial to decide when to do the osteotomy – wait for remodeling, or
just go ahead and do it to encourage better remodeling? Probably a more aggressive approach is
warranted – if the acetabulum is not developing normally after a couple visits to the clinic, pull the
trigger

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Reconstructive Osteotomy Principles
 Cannot have degenerative arthritis
 Should have a good range of motion (how good is debatable)
 Should check an abduction/internal rotation x-ray to assess two things:
o Congruency
o Coverage
 On this view the head and acetabulum should be CONGRUENT to proceed with a re-directional
osteotomy (Salter, Triple, Steel)
 If reduced but not completely congruent, consider acetabuloplasty – Dega, Pemberton (more in the
CMT or paralytic population)
 If not reducible – need a salvage procedure (Chiari or Shelf)
 Look at the femoral neck shaft angle:
o Is the deformity there?
o Does it need a varus osteotomy?
o Most have lots of anteversion and not that much valgus, so a varus osteotomy runs the risk of
elevating their GT and causing an abductor limp
o If doing a varus osteotomy, medialize the femur with the offset on the plate

From CORF
When to do salter??
Usually after 2 at least. Dr Keifer says if no progression of acet coverage in 2yrs of monitoring will do the
osteotomy (he does his from age 3-6)

Summary Treatment Algorithm:

 If stable in a week – continue Pavlik for 6/52 – take off and if stable, leave off – bring back at
4/12 for xray
 If not stable but reduced – continue Pavlik until they are stable, then 6/52 after that
 If not reduced within 2-3/52 in the Pavlik – give up and proceed with traction, adductor
tenotomy, closed reduction, arthrogram and spica cast in 100 flexion and 40-50 abduction
(human position – still need to be in safe zone) – occasionally open reduction required. Need
to check if you attempt CR and tenotomy before you give up and call it teratologic
 If not able to reduce and keep reduced within the first 2 months, even with a Pavlik or
closed reduction – may have a teratologic dislocation, and the acetabulum has never really
formed. Back off – aim for range of motion and plan for open reduction and acetabular
osteotomy at 6-12/12
 Complications of Pavlik harness include inferior dislocation with too much flexion, femoral
nerve palsy with prolonged excessive flexion, and osteonecrosis (ON if > 60deg of abduction)
 Closed reduction
o Adductor tenotomy
o Traction, flexion of hip, AB and ER to put hip in jt
o Then cast in human position (100deg of flex ~40deg abduction (need safe zone)
o Continue and change in 6/52 in OR for another 6/52
o CT or MRI post-operatively to check position
o Then 2/12 of abduction orthosis
o Then indefinite until acetab is developing normally
 6-24 months
o Open reduction w medial approach <1yr
 No capsulorraphy
 Check amount of inferior subluxation w flexion
 Cast in similar to human position w less flexion

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  Keep for 6/52 – change in OR and check stability
 Common block to reduction is teres, TAL, constricted anteromedial capsule
o Anterior approach w capsulorraphy
 Post operatively, spica cast in 30 flexion, 20 abduction, 15 IR and left in place
for 6/52 then bilateral cylinder casts in 15 flexion plus bar for 4/52 and then
further bracing should not be necessary

Anterior Approach to Dysplastic Hip

 For > 1 yr, Can address all obstacles to reduction and do capsulorrhaphy
 Position lateral and roll back, Incision centered 2cm below ASIS
 Incise through superficial fascia to expose crest
 Open interval between sartorius and TFL – protect LFCN
 Rectus forms the floor – direct head to AIIS
 Identify ascending branch of MFCA (actually it is the LCFA, med circ is posterior!!) seems like
a few sources (l&w) says med circ.
 Expose crest proximally and split apophysis down to bone
 Divide rectus and reflect distally
 Clear capsule
 Divide iliopsoas as it crosses the pubic ramus just medial to AIIS – watch for femoral nerve
 Incise capsule parallel to acetabulum from inferior to posterosuperior
 Then perpendicular incision along femoral neck
 Identify ligamentum teres, follow to true acetabulum and release
 Release TAL inferiorly
 Clear pulvinar from acetabulum
 Gently reduce hip
 Capsulorrhaphy taking inferior flap and suturing apex to superior acetabulum
 Excise redundant superolateral flap
 Spica cast in 30 flexion/20 abduction/15 IR for 6/52
 Change at 6/52 and D/C at 3/12
 Then abduction brace for nights and naps prn

81. Acetabular osteotomies

 What about in the older child or adolescent?
 Little controversy here - any significant degree of dysplasia in a patient over 8 is an
indication for surgical intervention if coverage can be achieved
 Start with finding out if the hip is or can be concentrically reduced – abduction/internal
rotation view (30 abduction, 15 internal rotation)
 If not reducible – then you‘re stuck
o They need a shelf or Chiari salvage osteotomy – and for this you might as well wait until
they‘re pretty symptomatic
 If reducible – then you‘ve got some options
o Ask yourself – Does the acetabulum need to be re-directed, or does it need to be
reshaped? Or is it the femur that needs to be osteotomized
o Where is the pathology – that is where you start
o And remember, if there is pathology on both sides, and you‘re not quite sure, you can
always do the acetabulum first and see what happens

If the acetabulum just needs to be re-directed:

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  Salter: not a terribly powerful osteotomy; you can gauge how much coverage you‘ll gain by
looking at how much coverage there is on the 30/15 AIR view
 Steel: triple osteotomy – much more powerful
 Sutherland: double osteotomy – more powerful, but prominence of the piece in the groin
makes it less popular
Ganz

If it needs to be re-shaped:
 Pemberton
o Acetabuloplasty; closes down the anterolateral aspect of the acetabulum by hinging it
on the open tri-radiate cartilage
o Make sure the tri-radiate cartilage is actually intact
 Dega
o Acetabuloplasty, closes down the posterolateral aspect of the acetabulum, again by
hinging it on the open triradiate cartilage
o Useful in the paralytic dislocation

82. Perthes
 Note the age group: usually 4-10 year olds, predominantly males (4:1)
 Most common presenting symptom is a painless limp
 Pain if present is activity related and located either hip/groin/thigh/knee
 Unproven (but possible) association with clotting abnormalities, thyroid disorders
 Goes through stages: blood supply is injured, ossific nucleus stops growing, cartilage widens, then
subchondral fracture, then fragmentation, then resorption and new bone formation (healing)
 The goal is to keep the hip as normal and supple as possible during the course of the disorder

Differential diagnosis of Femoral Epiphyseal Fragmentation

 Inflammatory/infectious etiologies
 Skeletal Dysplasia: MED, SED, Morquio‘s
 Meyer‘s dysplasia (if young <4)
 Sickle cell/thalassemia/Gaucher‘s
 Corticosteroid AVN
 Hypothyroidism

And if bilateral, think:

 MED: you may find some acetabular changes (unlike Perthes)
 SED
 Hypothyroidism (most common)
 Gaucher‘s Disease

Physical Examination
 May see antalgic or Trendelenberg gait
 Generally motion, primarily IR, is limited; check abduction too
 Mild hip flexion contracture (10-20) may be present
 May be apparent LLD because of adduction contracture or true shortening

If you think this is a bony dysplasia do a skeletal survey (esp knees, spine, feet/ankles)

Clinical at risk factors – older child, female, obesity, and marked restriction of motion
 The number one prognostic factor is their age of onset – less than 6 tend to do well; after 6 tend to do
more poorly

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Radiographic Evaluation
 AP and Lauenstein (frog leg) lateral
 Standing AP will give better info about extrusion or subluxation
 Look at Shenton‘s line, size and shape of the epiphysis, medial acetabular widening, changes in the
femoral neck (widened)
 Extrusion index is width of involved epiphysis lateral to the lateral margin of the acetabulum divided by
the uninvolved epiphysis
 AP in maximal abduction may allow early diagnosis of hinge abduction – can sometimes see a divot
in the head where the acetabulum is impinging
 In absence of changes on xray, bone scan may reveal avascularity
 MRI is also useful
 Radiographic stages based on Waldenstrom
o Initial – decreased size of the ossification center, widening of the medial joint space,
subchondral fracture, physeal irregularity
o Fragmentation – epiphysis appears fragmented, and areas of increased radiolucency and
radiodensity
o Reossification – bone density returns to normal during this or repair
o Repair
o Healed – once reossification is complete the shape of the femoral head is representative of the
healed phase

Herring lateral pillar classification (1992):

 Based on an AP pelvis x-ray – assesses the height of the lateral 15-33% of the involved epiphysis
compared with the contralateral normal epiphysis; applied in the early fragmentation phase:
 A – no involvement of lateral pillar
 B – lateral pillar >50% intact
 C – lateral pillar < 50% intact
 This classification has been found to be prognostic and have interobserver reliability

Catteral
I. Anterior head involvememt < ¼
II. Anterolateral head involvement with sequestrum < ½
III. ¾ head involvement
IV. whole head involved

Salter and Thompson

A - < ½ of head involved with subchondarl fracture (Cat I an II)
B - > ½ of head involved with subchondral fracture (Cat III and IV)

Catterall “Head at Risk” signs: having two or more is considered bad

1. Gage‘s sign (radiolucent V on the lateral side of the epiphysis)
2. Calcification lateral to the epiphysis
3. Lateral subluxation of the CFE
4. Horizontal physis
5. Metaphyseal cysts
The value or accuracy of these is controversial

Prognosis
 Most hips do well until the 5th decade
 At maturity, deformity and congruity are the key factors
 Age at onset is prognostic – younger than 6 do well because of increased remodeling potential Miller
says <6 do well

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Treatment
3 Goals of Treatment:
1. Relief of symptoms
2. Femoral head containment
3. ROM preservation

Options:
1. Observation or none
2. Intermittent symptomatic treatment
3. Containment – surgical or non-surgical – most controversial
4. Late surgery for deformity
5. Late surgery for arthritis

Operative
•mini open adductor tenotomy and Petrie casts in abduction and IR for 6 weeks.
•Never operate on a stiff hip.
•Surgery involves:
(1) innominate osteotomy
(2) femoral varus osteotomy (if no hinge abduction)
(3) combination or
(4) shelf or Chiari – salvage (whatever necess to get head in)
(5) VALGUS proximal femoral osteotomy specifically for hinge abduction

Containment
 Purpose is to contain the femoral head within the acetabulum to prevent deformity, permit
physiologic motion, and promote remodeling
 Current indications include:
o Age at clinical onset of 6-10 yrs
o Greater than ½ CFE involvement (Pillar C)
o Loss of femoral head containment (subluxation)
o With prerequisites of full ROM especially abduction in extension, minimal or residual hip
irritability and minimally deformed head

Proximal Femoral Osteotomy

 Varus osteotomy of the proximal femur is most common.
 Can be used in combination with pelvic osteotomy when containment cannot be obtained with femoral
osteotomy alone.
 In contrast, valgus extension osteotomy in later stages when the deformed extruded head causes
pain and an adduction deformity
 Effective method of containment in the early and fragmentation stages
 Can prevent femoral head deformity and restore spherical congruity provided that the femoral head can
be contained in the acetabulum and that growth remains to allow femoral head remodeling
 Limitations – worse when operating in healing phase, 9 yr old or older, and when femoral head
could not be contained by osteotomy
 Advantages
o Can be done even when there is flattening or incongruity of the femoral head as long as the
disease is in the early or fragmentation stages, head can be contained and in the presence of
mild to moderate limitation of ROM
o Pelvic osteotomies or shelf procedures are indicated when femoral head is still round and
without deformity and require full ROM preop
o Another theoretical advantage is increasing functional length and decreasing joint reaction
forces
 Disadvantages

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 o Failure of remodeling may result in persistent varus (usually 127-129), trochanteric prominence
(25%) and LLD (more than 2cm, 4-6%)
o Residual varus does NOT increase the risk of pain or later arthritis
 Technical Considerations
o Treatment for <6 yrs unlikely unless subluxation, rarely for 6-9 yrs with minimal
involvement, and most children older than 9 regardless of amount of necrosis because of
poor prognosis for all untreated
o 3 prerequisites for containment – early or fragmentation stage, fair to good preop ROM (30
abduction and < 10 FFD), and containment must be possible without hinged abduction
o Optimal amount of varus correction in most is usually 20 – neck shaft angle must be reduced
enough to contain the femoral head without creating too much varus (never below 105 and
Barnes says 115 in older than 9)
o Types of fixation – 90 blade allows medial displacement and 10-15 degrees of extension to
facilitate containment of the anterior femoral head but derotation is not necessary

Valgus Extension Osteotomy for Hinge Abduction

 Occurs in late stages when the extruded femoral head impinges on the lateral margin of the
acetabulum during abduction preventing containment and causing the medial surface of the femoral
head to pull away from the medial wall of the acetabulum
 Symptoms are increasing pain, limp, and loss of ROM
 Arthrography can confirm or AP in maximal abduction
 Presence of hinge abduction indicates a very poor prognosis unless treated
 Early stages while still in fragmentation stage, may be possible to restore motion and contain head with
preliminary traction, adductor tenotomy, iliopsoas recession, and medial capsulotomy to reduce the
femoral head follow by Petrie casts for 2-4/12 – hip can then be contained with surgical procedure like
varus osteotomy, Salter or both
 When hinge abduction is fixed, options are Shelf, Chiari, or valgus extension
 Shelf and Chiari are not designed to reduce lateral impingement but do improve coverage and pain
relief
 Valgus extension unloads the lateral aspect of the head – relief of pain and restoration of motion occur
in 80-90%

Pelvic Osteotomies
 Salter
 Shelf
 Chiari medial displacement

Patients Less than 6 years

 No evidence that ANY Rx alters the natural history – they do well
 Treat the symptoms only
 Home traction, avoidance of weightbearing, NSAIDs

Patients 6, 7, 8 Years
 Bone Age 6 or Less with Lateral Pillar A or B (at least 50% of lateral pillar intact)
o Outcome not altered by treatment – treat for symptoms only
 Bone Age 6 or More with Lateral Pillar B
o Do better with containment methods – you pick (cast, brace)

Lateral Pillar C
 Not clear if treatment alters natural history
 Treat with ROM and containment

Patients Age 9 or more – the most challenging

 Hard to get them to wear a brace

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  May have to do osteotomies to keep them contained (varus osteotomy or Salter osteotomy)

In Summary:
Lateral pillar A – treat symptomatically; keep up the ROM
Lateral pillar B in a kid with bone age 6 or less – treat symptomatically, ROM exercises
Lateral pillar B in a kid with bone age greater than 6 – treat symptoms, ROM exercises, and containment
Lateral pillar C – hard to know – treat symptoms, ROM, and containment

Valgus Osteotomy for Hinged Abduction Technique

 In addition to altering the relationship of the femoral head to the acetabulum, valgus osteotomy of
the hip lengthens the leg and lowers and lateralizes the greater trochanter
 To maintain the proper axis through the knee joint, it is desirable to lateralize the femoral shaft
 Many hips suitable for valgus osteotomy also have a short femoral neck, and the lateralization of
the shaft tends to lengthen the neck
 One common problem with this osteotomy in the older child and young adolescent is that there are
often not suitably sized fixation devices for these intermediate–sized bones and often requires
modification of existing devices by bending to avoid medialization of the femoral shaft or by
shortening of the blade of the blade plate devices used for adults
 Simplest technique is resection of a laterally based wedge. In this
procedure, a simple laterally based triangle of bone is removed from the
intertrochanteric area with the angle of the wedge being equal to the
desired correction. How the wedge is made depends on the type of
fixation used and is designed to produce interfragmentary compression:
o If the 130-degree angled blade plate is used, the base of the
osteotomy (the distal cut) is inclined and the proximal cut is
horizontal. Compression across the osteotomy site is provided
by the varus stress on the proximal segment.
o If a 90-degree blade plate is used, the base of the osteotomy is
horizontal and the interfragmentary compression is obtained by
prestressing the plate.
 The most difficult of the valgus osteotomies to perform is the osteotomy
that lateralizes the distal fragment and lengthens the femoral neck
 Although preoperative planning with templates can be used, a simpler
method, which is actually useful for most valgus or varus osteotomies, is
one that uses intraoperative positioning of the femoral head in the proper relationship to the acetabulum
while the osteotomy and fixation are achieved relative to the median and coronal planes of the patient
 Conceptually, the operation is performed with the following steps:
o Patient on a radiolucent table or a fracture table so that a good view of the hip joint is obtained
o Leg is adducted until the femoral head is in the desired relationship to the acetabulum
o A small amount of radiopaque dye in the hip joint may prove useful if there is a significant
amount of unossified femoral head
o Next, the chisel for the 90-degree fixation device is inserted perpendicular to the median plane
of the body
o Finally, an osteotomy is created that will allow the femoral shaft to be brought back into the
median plane of the body and secured with the plate

Details
 With the leg held in the desired position, a Steinmann pin is introduced into the most superior portion of
the greater trochanter to serve as a guide for the chisel
 This pin should be perpendicular to the median plane of the body and parallel to the floor of the
operating room, which should be the same as the coronal plane of the patient
 The position of this is verified on the image intensifier, and the chisel is driven in just below the guide
pin
 At this point, it is a good idea to loosen the chisel by driving it part way out so that it will not be difficult
to remove after the osteotomy is completed

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  The next step is to locate the site for the osteotomy
 This should be perpendicular to the shaft of the femur and at the level of the proximal margin of the
lesser trochanter
 A mark in the cortex crossing the osteotomy site or a Steinmann pin in the anterior cortex distal and at
right angles to the osteotomy should be placed as a reference for rotation
 A single osteotomy cut is made
 The chisel is removed and the blade of the fixation device inserted
 In an adult-sized patient, the condylar blade plate is an ideal device
 With the blade in place, the plate is rotated toward the shaft, while the shaft is pulled laterally with a
large forceps
 The idea of this is to drive the lateral edge of the proximal surface into the medullary surface of the
distal fragment
 This often proves difficult, however, and seems to make the femur too long
 It is at this point that removing a portion of the proximal fragment parallel to the blade aids in the
reduction and increases the contact of the two osteotomy surfaces
 If still more shortening is needed, additional bone is removed from the distal fragment
 The plate is now tensioned and secured to the distal fragment
 It is often desirable to add extension to the osteotomy, depending on the clinical and arthrographic
findings
 To achieve extension, the blade is not inserted at an angle perpendicular to the shaft of the femur as is
usually done but rather, it is rotated so that it will be perpendicular to the shaft after the desired
correction is obtained
 The chisel is guided with the slotted hammer to maintain the correct angle
 After the osteotomy is completed, the proximal fragment is allowed to go into flexion
 The distal fragment is brought into extension and translated posteriorly
 Any other corrections are made at the same time, and the shaft is then secured to the plate

Postop
 If the child is young or unreliable, may consider a spica cast for 6/52
 If older, partial WB for 6/52 and then reassess according to bony healing

So for the exam, Perthes:

 When you get a hip or knee problem in the right age group need to keep Perthes in your
differential – but make sure it‘s unilateral – if bilateral, think dysplasia/hypothyroidism
 Check ROM – they‘re be painful and have decreased abduction usually
 And xrays – is the head shape and size normal, is there extrusion, Shenton‘s line, height of
lateral pillar, metaphyseal cysts
 May consider blood work, MRI or bone scan to assess the head, rule out infection
 First priority is ROM and symptom control with physiotherapy and pediatric NSAIDs (stick with
ibuprofen)
 Follow them closely because they can get worse quickly – return to clinic 3-4/52 later
 If they‘re better, great
 If they‘re worse, repeat history and physical, get another xray to confirm diagnosis and rule out
something more sinister
 Next option in the algorithm is taking them to the OR and assessing their ROM under GA – if
it‘s better, it tells you that it‘s related to spasm and inadequate pain control, and if it‘s not,
perform an adductor tenotomy
 Then do an arthrogram (needle below adductor longus, 45 degree angle aimed at ipsilateral
shoulder) and check for congruency and hinge abduction
 So the hip is in, no hinge, and ROM is good – Petrie cast and follow up in 6-8/52

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  Invariably (on the exam anyway) they will return and be worse – at this point you have to
determine if you‘re going to do an osteotomy of the femur (usually a varus osteotomy but for
late hinge abduction with adduction deformity, valgus extension) – xray will show loss of lateral
height, increased lateral extrusion, subluxation (break in Shenton‘s line), coxa magna
 The other consideration is whether or not to do anything to the pelvis – may need a Salter or
some sort of salvage like a Chiari

Walsh LCP Summary

1. Hx: 4-10, boys>girls, blood dyscrasias
2. Exam: small for age,  IR & Abduction (early synovitis, late bony)
3. Imaging
a. Xray – AP pelvis, Frog – crescent, Herring Classification, at risk signs = subluxation (worst),
lateral calcification, Gage sign, metaphyseal cysts, horizontal growth plate
i. AIR view – assess containment
b. Left wrist xray to judge bone age (bone age < 6 good, > 8 poor)
4. Tx
a. Goal = decrease synovitis and pain – ROM – Containment
b. Peds consult – r/o hypothyroid, Gaucher, sickle cell, coagulopathy
c. 1st Stage = ROM – bedrest 2-3 days, pain control, physio, may go on to adductor tenotomy and
petrie cast
d. 2nd Stage = Containment
e. Treatment Summary
i. If age < 8 (6 bone age) only ROM treatment (possible adductor tenotomy if needed for
ROM)
ii. If age > 8 (bone age 6)
1. ROM for Herring A and C
2. Surgical containment for Herring B (VDRO  Salter)
a. Intra-op arthrogram to assess hinge
b. VDRO not > 120 or risk adductor lurch
3. Complications
a. Residual deformity
i. Coxa magna, plana, breva
ii. Greater troch overgrowth may require distal transfer
a. May go on to THA (by age 55 many with OA)

83. Coxa Vara

o The physis is more vertical: you measure this by the hilgenreiner- physeal angle.
o <45 deg – tends to improve
o 45-60 deg - GRAY zone
o >60 deg – tends to get worse – operate now ! (Intertroch abduction/derotational
osteotomy). Coxa vara is associated with femoral internal rotation, so you need to
address that during surgery by DEROTATING THE FEMUR in addition to abduction.
o Just remember femoral IR with coxa vara. Tibial internal rotation with tibia vara
(Blount‘s).

Coxa Vara
 Defined as any decrease below the normal values of the neck–shaft angle of the proximal femur (<
125). Normal 150 at birth, 142 at age 5.
 Comprises a group of conditions occurring during childhood with different causes and natural
histories that ultimately produce a specific deformity in the proximal femur

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  Three main categories: congenital coxa vara, acquired coxa vara, and developmental coxa
vara. (Weinstein more than three ACCDD)
 Acquired coxa vara:
o Includes all clinical entities in which the deformity of the proximal femur is secondary to an
underlying metabolic, tumorous, or traumatic condition:
 Rickets
 Renal osteodystrophy
 Hyperparathyroidism
 Hypothyroidism
 Perthes disease
 DDH
 Infection
 Trauma c early closure physis
 Tumour
 SCFE
 Congenital coxa vara:
o Present at birth, and is assumed to be caused by an embryonic limb–bud abnormality.
o Significant proximal femoral varus is present at birth, but usually shows minimal progression
in the degree of varus during growth
o Associated congenital musculoskeletal abnormalities and significant limb–length inequality,
secondary to femoral segment shortening, are common
o This category includes cases of proximal femoral focal deficiency, congenital short
femur, and congenital bowed femur
 Cretinism
 Dysplastic Coxa Vara:
o MED
o SED
o Achondroplasia
o Cleidocranial dysostosis
o Fibrous Dysplasia
o Morquio‘s
 Developmental coxa vara, also known as cervical or infantile coxa vara
o represents coxa vara not present at birth, but that develops in early childhood and produces
progressive deterioration of the proximal femoral neck–shaft angle during growth
o Classic radiographic changes accompany the physical findings
o There is no significant increase in associated musculoskeletal anomalies
o A minimal limb–length inequality develops secondary to the progressive varus deformity of
the proximal femur, but not because of a significant true decrease in the femoral segment
length
o Developmental coxa vara is a specific deformity of the proximal femur, manifesting in the
pediatric patient with characteristic behavior during growth and associated radiographic
findings that differentiate it from other forms of childhood coxa vara
o Developmental coxa vara is a rare entity with a reported incidence of 1 in 25,000
o Bilateral involvement occurs in 30 to 50%
o Familial pattern in a limited number of cases which is proposed to be AD

Etiology of Developmental Coxa Vara

 Remains unknown: metabolic, mechanical, vascular, developmental error of cartilage maturation
 Most widely accepted theory about the cause - the deformity in the proximal femur is the result of a
primary ossification defect in the inferior femoral neck, on which physiologic shearing stresses,
applied during weight bearing, cause fatigue of the local dystrophic bone, resulting in the
progressive varus deformity

Clinical Presentation
 Present sometime between the initiation of ambulation and 6 years of age

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  Most frequent complaint is a progressive gait abnormality; pain is rarely reported
 In patients with unilateral involvement, the gait abnormality is caused by combined abductor muscle
weakness and limb-length inequality
 As the neck–shaft angle of the proximal femur decreases in developmental coxa vara, the
articulotrochanteric distance between the femoral head and greater trochanter also decreases,
which affects normal hip joint mechanics
 As the articulotrochanteric distance decreases, the normal length–tension relation of the abductor
muscles is lessened, and the ability of the abductor muscles to control the pelvis in one-legged
stance is weakened
 The functionally weaker abductor muscles produce the gait abnormality seen in patients with
developmental coxa vara
 Patients with bilateral involvement present with a waddling gait pattern associated with increased
lumbar lordosis, similar to that seen in bilateral developmental hip dislocation
 Physical examination usually reveals a somewhat prominent and elevated greater trochanter, which
is often associated with an abductor muscle weakness and positive Trendelenburg testing
 An associated limb-length inequality is commonly identified, but this is usually mild and averages
only 2.5 cm. Galeazzi sign.
 ROM is usually restricted in all planes, with the most significant limitations occurring in abduction
and IR (THE LIMITATION IN IR distinguishes it from DDH, because both has limitation of
abduction)
 Loss of abduction is associated with a decrease in the neck–shaft angle of the proximal femur
 Loss of IR is secondary to the progressive decrease in femoral anteversion seen in developmental
coxa vara
 An associated hip flexion contracture is often identified
 Associated musculoskeletal anomalies are rare

Radiographic Findings
 Diagnosis of developmental coxa vara, and its differentiation from other forms of coxa vara,
depends on the identification of certain classic xray findings
 Classic radiographic features of developmental coxa vara:
1. Decreased femoral neck–shaft angle, often to values < 90 degrees
2. A more vertical position of the physeal plate
3. A triangular metaphyseal fragment in the inferior femoral neck, surrounded by an
inverted radiolucent Y pattern
4. A decrease in normal anteversion of the proximal femur, may become true retroversion
5. Coxa brevia
6. In some patients, mild acetabular dysplasia
 May need Internal Rotation view to accurately measure the Femoral Neck-Shaft Angle
 The more vertical position of the physeal plate is measured by the Hilgenreiner physeal angle,
which is defined by the angle subtended by the planes of the physeal plate and the Hilgenreiner line
-normally < 25 degrees, but in developmental coxa vara, usually 40-70
 The inverted Y pattern seen in the inferior femoral neck remains the sine qua non of this
condition - was once postulated to be a true double physeal plate - biopsy specimens and MRI
studies have shown that the radiolucent area actually represents a zone of widening of the inferior
portion of the physeal plate, with associated abnormal ossification and an interposed triangular
segment of dystrophic bone

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This measurement is useful in distinguishing coxa vara from post-traumatic or dysplastic coxa vara. The
distance should be 20mm.

Natural History
 Historically, untreated developmental coxa vara was viewed as a condition in which a pattern of
progressive varus deformity of the proximal femur ultimately resulted in the development of a stress
fracture–related nonunion of the femoral neck and premature degenerative arthritic changes within
the hip joint
 These changes led to progressive pain and disability for the patient, and were thought to occur
universally
 Recently been shown that not all patients follow such a progressive course - studies demonstrated
that the determining factor for progression of the varus deformity was the Hilgenreiner physeal
angle:
o < 45 degrees more commonly had spontaneous healing of the femoral neck defect
and an associated arrest in progression of the varus deformity
o >45 found to more commonly manifest the more classic progressive pattern

Treatment
 Concentrate on prevention of the secondary deformities of the proximal femur created by the
condition's natural history

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 Main objectives:
1. Correction of the varus angulation into a more normal physiologic range
2. Changing the loading characteristics seen by the abnormal femoral neck from shear to compression
3. Correction of limb-length inequality
4. Reestablishment of a proper abductor muscle length–tension relation
 Nonoperative treatment during childhood has historically been unsuccessful
 Surgical derotational valgus–producing proximal femoral osteotomy has been shown to be the most
effective
 Intertrochanteric–subtrochanteric osteotomies remain the treatments of choice
 Pauwels' Y–shaped osteotomy and Langenskiold's valgus–producing osteotomy are examples of
intertrochanteric corrective osteotomies that have produced good results
 Pauwels' Y–shaped osteotomy does not allow rotational correction
 Subtrochanteric valgus–producing osteotomies also remain well–proven forms of successful
therapy
 Additional principles of proper surgical treatment include:
o a concomitantly performed adductor tenotomy that allows less-forceful correction of the
bony deformity and improved stability at the osteotomy site, when the femur is put into
valgus
o A proximal femoral shortening procedure at the level of the osteotomy can be employed to
facilitate correction of the varus deformity and unload the femoral head, in situations in
which difficulty in reduction of the osteotomy and excessive femoral head pressure are
realized as proximal femoral valgus is recreated
 To prevent loss of the surgical correction achieved before healing of the osteotomy, firm internal
fixation, by a tension band technique, blade plate, or nail-plate system, is recommended
 Violation of the physeal plate by the internal fixation device should be avoided
 A spica cast may or may not be applied
 It is important to include internal rotation of the distal segment at the time of osteotomy, to
correct the loss of internal rotation seen in developmental coxa vara and reestablish more normal
rotational arcs at the hip, postoperatively
 The goal of surgical treatment is to produce a valgus overcorrection of the neck–shaft angle
of the proximal femur, regardless of the patient's age – to a value of 160 or greater, and
Hilgenreiner physeal angle to 30 to 40 degrees, to significantly decrease the potential for
varus deformity recurrence
 The criteria for surgical intervention, in a patient with developmental coxa vara, include one or more
of the following clinical and radiographic findings:
o Hilgenreiner physeal angle > 45-60
o Neck–shaft angle is progressively decreasing or < 90-100
o Patient develops a Trendelenburg gait
 Corrective osteotomy is best performed, not at a particular age, but as soon as the criteria
for surgical intervention are apparent

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Results
 The triangular metaphyseal defect in the femoral neck spontaneously closes by 3 to 6 months
postoperatively in the majority if adequate valgus has been created
 Between 50-89% demonstrate a premature closure of the proximal femoral physeal plate -
usually occurs within 12 to 24 months but is not related to surgical trauma, patient age, or
degree of valgus correction and more likely represents a possible surgically induced acceleration of
natural physeal plate closure
 May also be a manifestation of an inherently abnormal proximal femoral physis in developmental
coxa vara, which is stimulated to undergo closure as the stresses across the plate change from
shear to compression after surgical realignment of the proximal femur
 If premature closure of the proximal femoral physeal plate occurs, the patient must be
monitored closely for the development of a growth-related recurrent varus deformity of the
proximal femur, and for development of a significant limb-length inequality secondary to
closure of the proximal femoral physis, which accounts for approximately 13% of the growth
of the lower limb
 True varus recurrence, secondary to the underlying pathologic process, is rare if adequate proximal
femoral valgus is reestablished and maintained by stable internal fixation
 The proximal femoral physeal angle must be corrected to < 30-40 to facilitate conversion of shear to
compression forces
 Equally important that stable internal fixation be used to maintain the valgus correction until full
osseous healing has occurred, and that the internal fixation device does not violate the physeal
plate
 If premature proximal femoral epiphyseal plate closure occurs, it creates a situation of unbalanced
growth about the proximal femur, with secondary trochanteric overgrowth and recurrent coxa vara
and coxa brevia
 To prevent this recurrent deformity, it is recommended that after premature closure of the
proximal femoral epiphyseal plate has been documented, greater trochanteric
apophyseodesis, or advancement be performed
 If the varus deformity does recur, a repeat valgus–producing femoral osteotomy
 Proper and timely treatment of developmental coxa vara can result in a hip joint that is painless, has
a functional range of motion, and demonstrates a negative Trendelenburg gait at maturity
 Although most patients continue to show a mild residual limb-length inequality, it rarely is significant
enough to require a shoe lift

Type Facts Non-op Op – Operate as soon as pt meets

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 criteria, regardless of age
Developmental Mechanical overload, F/u q6 months, HEA < 45 Valgus subtroch osteotomy –
sclerotic calcar, bilateral unlikely progression, > 60 overcorrect to make physis
1/3 – 1/2 likely, 45-60 less clear horizontal
Congenital Short femur, PFFD, fem Will not correct, must f/u Valgus derotational  femoral
neck retroversion, knee and plot final LLD lengthening
valgus
Dysplastic Rickets, osteopetrosis, Wait until femoral head ossified,
fibrous dysplasia valgus osteotomies prn
Traumatic Perinatal SH I – SPICA,
typically do well
AVN Greater troch epiphysiodesis < age 5
(after age 8 only appositional so no
need)

Buzz Words for Intertrochanteric (or subtrochanteric) Valgus-Producing Osteotomy for

Developmental Coxa Vara:
 Consent: usual risks, especially, recurrence, growth arrest, needs for future surgery, LLD
 Aim for Neck Shaft Angle of >160, HE angle <16, restore the abductor lever arm
 Preoperative templating for the amount of lateral wedge to remove
 Avoid growth plate
 Fixed angle device (blade plate)
 Internal rotation of the distal fragment
 May need adductor tenotomy
 May need femoral shortening to avoid undue pressure on the femoral head
 Hip spica
 Observe closely for trochanteric overgrowth

84. Marfan‘s (PREOP CARDIAC)

Chrm 15 – Fibrillin
A) MSK - pectus deformities, long slender digits and long slim arms, SCOLIOSIS, SCOLIOSIS,
SCOLIOSIS, acetabular protrusio
B) Ocular – myopia superior lens displacement ( homocysteinuria-inf. Lens dislocation)
C) Cardiac – Ao Regurgitation , aortic dilatation, MVP

85. Friedrich‟s Ataxia -- PREOP CARDIAC

Triad of ataxia, areflexia, Babinski

Disorder of Frataxin, Normal CK

Orthopedic:
1. Gait Ataxia ( onset usually before age 20)
2. Proximal > distal muscle weakness
3. Pes Cavovarus( not treated well conservatively)
4. Scoliosis( tx much like idiopathic, can brace early)
5. Positive Romberg‘s sign
Neurologic
1. Dysarthria
2. Optic Nerve Problems
3. Nystagmus

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Preop Consideration: CARDIOMYOPathy!! Usually die of this in 40-50‟s

In Friedrich‟s: NCS - Marked dec sensory action potential

- only slight dec in motor conduction velocity
this differs from other motor and sensory neuropathies
- differs from HMSN (where motor conduction velocity sig dec)

86. CMT
o CMT – DON‘T FORGET 8% HIP DYSPLASIA AGE 5-15, examine the hands for ulnar/median
nerve abnormalities and intrinsic minus hands if they present with cavus feet. Send them to a
neurologist
o Neurologist, Cavus Foot, Hip Dysplasia (8%), Scoliosis (upto 50%, treat like idiopathic),
Intrinsic minus hand

87. Normal Knee Alignment in Pediatrics

1. Age 0-2 varus goes from 15 to ~0 (greatest at 6 months)
2. Age 2-3 goes 0 to 10 valgus (persistent genu varum beyond 2 years is abnormal)
3. Age 3-6 goes 10 - 7

88. D/D of Genu Varum:

1. Physiologic Genu Varum – MOST COMMON: NEVER after 2 years, Even large angulation can
correct, Concomitant internal tibial torsion typically corrects, Xrays = bowing of femur and tibia
(gradual), normal physes
2. Blount‟s Disease: see below
3. Rickets (Vitamin D resistance): Hypophosphatemic rickets (sex linked, inherited), Suspect if
patient short (most below 10th percentile), Distal femur and proximal tibia varus, Treat medically
(oral phosphates and Vitamin D), If need OR, may wait to maturity since chance or recurrence
without strict medical compliance
4. Renal Failure / Renal Osteodystrophy: May see varus or valgus depending on when renal
failure occurs (ie accentuates present alignment), Physis similar to rickets = widened, cupped,
femur and tibia, Postpone treatment until renal disease stabilized
5. Skeletal Dysplasias:
a. MED
b. Schmdit Metaphyseal Chondrodysplasia: Rare, inherited syndrome
c. Achondroplasia: Rarely symptomatic, proximal fibula physis is superior to tibial.
Treatment: proximal fibular epiphysiodesis done early and proximal tibial osteotomy if genu
varus is established.
6. OI: because of multiple fractures, treatment: Bracing in mild deformity. Bowing treated with
osteotomy + telescoping IM rodding
7. Focal Fibrocartilaginous Dysplasia: (unilateral, usually self limited by age 4), Cortical lucency
with surrounding sclerosis in proximal medial tibial metaphysis
8. Post trauma
9. Infection
10. Osteochondroma
11. Inflammatory arthritis

89. Blount‟s Disease

Hx: black, females in infantile, males in males, early walker, is deformity progressive, R/O personal
history of rickets, dysplasia, FH of bowed leg, short stature

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O/E: general, height and weight, gait (look for varus thrust), L/E: alignment, abrupt or gradual varus,
rotation (look for Internal Rotation)
Detailed Exam: general exam and vitals, height and weight and plot for age, inspect standing
alignment of legs in front and behind, observe child walking for thrust of knees, leg lengths,
foot progression angle, inspect knees for skin changes, swelling, alignment, palpate knees for
tenderness, ROM of knees bilaterally, examine patellas for subluxation, examine tibia for varus
and rotational abnormality (normal tibial torsion 20-30 ER), similarly femur for varus and
femoral torsion (position patient prone and check position of maximal prominence of greater
trochanter – normal 40 anteversion), knee stability, neurovascular exam of extremities
Inx: X-ray (hips to ankle, AP, with the knees pointing forward), MRI, if you are not sure this Blount‘s
 get skeletal survey to R/O dysplasia
X-ray stages of blount: Fragmentation  Depression and varus angulation  Beaking 
Osseus bridging

Early-onset (old name Infantile) Blount‟s: < 3yrs, Often difficult to distinguish from physiologic
bowing particularly when < 2yrs but nearly 60% bilateral. In physiologic bowing, varus occurs almost
equally in the distal femur and proximal tibia
Late-onset (old name Adolescent) Blount‟s > 8 yrs, Often easier to diagnose, Often unilateral

Assess the x-rays

 Note the metaphyseal diaphyseal angle (MDA) and the medial physeal slope
 Many children also have considerable internal tibial torsion so make sure the patella is
pointing forward – and weight bearing views once 3-4 yrs
 Previously recognized threshold of MDA to diagnose Blount‘s was 11 o it is probably more
accurate at approximately 16o
 Recommendations from St. Justine 2005:
o <11 normal
o 11-14 – watch closely with xrays q6/12 until progression/regression
o >15 – Blount‘s disease diagnosed and treat

General Indications for Bracing:

1. 2-3 yr old with MDA > 16
2. Children with MDA of 11 but risk factors for progression like obesity, female, or lig laxity
 Brace should be KAFO worn during weight bearing hours with brace‘s knee hinge locked
during walking (L&W says wear 23 of 24 hrs?? where did this info come from)
 Thigh cuff as high as possible with frequent evaluations and readjustments
 Ankle joint should allow free motion
 Usually one year in brace will correct the deformity, Bowing resolves in 65-90%
 Prognosis worse for bilateral
 Bracing is controversial – at St. Justine most of the staff said they brace these kids and then
osteotomy at age 3

General Indications for Surgery:

 Best results of osteotomy found in < 4 yrs old
1. First time visit > 36 months of age – you have no time to waste before the age of 4 to be
messing around with bracing.
2. Documented progression in the KAFO at any age
3. Metaphyseal diaphyseal angle of > 16 at any age
4. The <36 month old who will not tolerate bracing
5. In late-onset, varus > 10 to prevent OA.

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So, if they fail the bracing or they have an indication for surgery:
1. Repeat standing films
2. Make sure you have lateral x-rays to assess posterior slope as well
3. Reconsider the diagnosis – are you SURE it‘s Blount‘s?!??!
4. Draw out their mechanical axis and their tibial anatomic axis to determine what the correction
needs to be – you need to overcorrect them to valgus 10 degrees
5. If you have ANY SUSPICION of a bony bar – get an MRI! On the exam, get an MRI on any
Blount’s who you are taking to the OR, to rule out this possibility
6. Plan for closing wedge osteotomy laterally plus fibular osteotomy, prophylactic anterior
fasciotomy, K-wire fixation, cast
7. Be ready to add physeal bar resection if less than 30-50% for stage IV - VI
8. Some people advocate lateral staple hemi-epiphyseodesis for adolescents with significant
growth left– sometimes difficult to predict how much correction this will give you, and it is not
assured that if you want to back off, that the physis will start growing again on that side – only
considered in mild deformity
9. Recognize the high potential for recurrence if over age of 5 when you are starting, or if they
have Langenskiold V or VI, or if they have a bony bar

Possible Complications: compartment syndrome, neurovascular injury, LLD, recurrence,

overcorrection, growth arrest, nonunion, tubercle growth plate damage

How to address complications:

1. For traction on the peroneal nerve (more common with varus correction), remove the cast and
return the leg to the preoperative position. Then remove all pressure on the peroneal nerve and
loosen all dressings from the thigh to the toes and observe closely.
2. For anterior compartment syndrome, remove the cast and return the leg to the preoperative
position. Loosen all dressings from the thigh to the toes. If improvement does not occur
immediately, then fasciotomy without delay is mandatory.
3. For anterior tibial artery occlusion remove the cast and return the leg to the preoperative position.
Loosen all dressings from the thigh to the toes and observe closely. If immediate improvement is
not evident, consider arteriography followed by appropriate surgery

90. D/D Genu Valgum

1. Physiological valgus: (incl GLL): should max out at around 12+/-8o at 3-4 years of age
2. Physeal injury: trauma (Cozen fracture), tumor, infection
3. Inflammatory: JRA
4. Metabolic: nutritional rickets (Vit D def), Vit D resistant rickets (usually varus), Renal
osteodystrophy
5. Dysplastic: MED, SED, Psuedoachondoplasia, Kniest synd, OI
6. Neuro-muscular: CP, polio
7. Congenital : dislocation of the patella, hypoplasia of LFC
8. MPS: Morquio

Management
 in general, genu valgum is associated with more patellofemoral problems than genu varum
 if they are 30-36 months old and otherwise completely normal – observe; even if >20 degrees
 Indications: progressive deformity, thrusting gait

Physiologic knock knees

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 Age > 10, > 10 cm intermalleolar distance, or >15-20 degrees of valgus
 hemi-epiphysiodesis if you are confident you know how much length they are going to gain (ie
ensure you won‘t overcorrect)
 medial physeal stapling if unsure (you can take out the staple – but you are not guaranteed
that it will continue to grow once you take out the staple)
Note: genu varus – you want to basically OVERcorrect But in genu valgum, you want to just get
them about neutral, maybe slight valgus. DO NOT OVERCORRECT the valgus knee.

Post traumatic valgus

 Common after prox tib # without assc fibular #
 Spontaneous improvement usually occurs over 3 – 4 years, avoid early tibial osteotomy
 If persistent deformity after this, consider proximal tibial hemiepiphyseodesis or vaurs
osteotomy of the tibia, must also osteotomize the fibula, or it will recur

Skeletal Dysplasias (Morquio‘s, pseudoachondroplasia and metaphyseal dysplasias)

 Arthrography to assess joints above and below to determine the optimal position at osteotomy
 Morquio‘s – if progressive, the deformity requires osteotomy. Also consider atlanto-axial
instability as this is common, may be causing upper cord compression and this may be the root
of the gait disturbance. Always get flex/ext with this group.

91. Epiphysiodesis
 suitable for those children who have sufficient leg length data to enable a confident prediction
of the discrepancy at maturity, and who require correction of 2 to 6 cm
 growth loss is
o 27% for the proximal tibia plate
o 38% for the distal femoral plate
o 65% for combined epiphysiodesis of both plates
 prediction of the effect of surgery can be made accurately within 1 cm in almost all cases
 err on the side of undercorrection than overcorrection
 slight discrepancies are well tolerated, it is best to aim for 0.5 to 1.0 cm of undercorrection
 principle: produce a symmetric bony bridge that tethers the physis and prevents future growth

Techniques
 traditional open techniques involve removing a block of bone from the medial and lateral
aspects of the plate, extirpating the plate with a curette, and replacing the block of bone in
such a fashion as to produce a bony bridge
o Phemister - removal of a rectangular block, two–thirds on the metaphyseal side and
one–third on the epiphyseal side of the plate, and its replacement in the reversed
position .
o Blount - physeal arrest by placing three staples across the physis both medially
and laterally, producing a tethering effect resulting in arrest of growth. Growth arrest
was occasionally asymmetrical, and a second operation was sometimes necessary to
remove the staples.
o Percutaneous techniques
 drill or burr, through small medial and lateral incisions, under image intensifier
control
 Great care must be taken to line up the image intensifier beam perfectly to
ensure that the tool is in the plate
 wider excision of the plate
 may accompanied by excessive bleeding or hematoma formation

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 usually performed through two incisions, one medial and one lateral
Because the growth plates, particularly the distal femoral, are not perfectly flat,
there is a significant technical challenge in making sure that the tip of the tool is
in the plate, and that it stays there.
 In the distal femur, the intercondylar notch intrudes into the
posterior aspect of the plate, and the surgeon must be careful not to
inadvertently enter the notch by being sensitive to the feel of the tool
touching cortical bone
 Approximately 50% of the area of the plate should be removed in the pattern shown


o Obliteration of medial and lateral circular segments of the plate, leaving the central part
and the strong periphery, successfully stops growth, yet the bone retains sufficient
strength to forego immobilization
 Tibial epiphysiodesis should be accompanied by arrest of the proximal fibular physis, if
the tibial shortening is greater than 2.5 cm

92. Hemiepiphysiodesis
o Use Green and Anderson growth data (other charts available in the literature)
o Address surgery at site of pathology to preserve horizontal axis of joint line
o Distal femur preferred for idiopathic genu valgum
o Staple hemiepiphysiodesis
o Two to three reinforced "Blount staples" (Zimmer) may be placed extraperiosteally:
o critical to follow the patient closely with clinical and radiographic examinations to
monitor correction obtained, and possible staple displacement and/or breakage
o If complete deformity correction is obtained, staple removal is necessary to prevent over
correction
o Consider with staple removal, a permanent epiphysiodesis of the growth plate to
prevent rebound growth
o Typically, at least 15 to 18 months of growth remaining
o Follow every 3 months
o Leaving the staples in for a period of 3 to 4 years may cause permanent closure of the physis
o patient who is not a candidate for staple hemiepiphysiodesis, typically presents with a
history of progressive varus deformity and knee-joint pain. A dynamic lateral thrust is
often noted during walking. This severe, dynamically unstable deformity will predictably not
be significantly improved by the slow correction obtained with staple hemiepiphysiodesis

93. Tibial Bowing

Posteromedial Bowing:
 Clinical findings include:
o Calcaneovalgus foot with excessive ankle dorsiflexion with the dorsum of the foot often lying
on the anterior surface of the leg at birth and limited ability to plantarflex beyond neutral
o Apparent or real shortening
o Posteromedial bow at the junction of the middle and distal third
o Always unilateral

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 o X-ray: 20-60 degree bow, medial angulation, bone appear normal, no obliteration of the canal
 associated with calcaneovalgus foot. Long term issues with LLD.
 shortening of the affected tibia may not be readily apparent clinically in newborns, but is
expected to increase in these children.
 posterior angulation rarely persists, often producing a mild S–shaped tibia
 medial angulation is less likely to resolve completely, and residual valgus in the tibia may
be clinically significant
 growth inhibition is fairly constant, as the absolute leg–length difference increases with
growth
 Differential Diagnosis:
o Benign and common calcaneovalgus foot – similar foot position but no bow and corrects itself
with no sequela
o Fibular hemimelia – presents with valgus limb with some shortening but less dorsiflexion, and
absent fibula plus often hypoplastic lateral rays
o Distal motor paresis – such as seen in L5 myelomeningocele produces a very dorsiflexed foot
with slight valgus although the tibia is straight
 Treatment:
o passive stretching of the foot
o serial cast application may be used for severe deformities
o corrects rapidly in the first year. No correction after 4 years.
o rarely, extreme dorsiflexion and valgus persist, such that plantigrade weight-bearing
cannot be accomplished. Use of a solid AFO or SMO may be facilitate weight-
bearing for walking . As tibial length inequality increases, a shoe lift may be needed
to balance the pelvis. Gradual contracture of the plantar flexors is not uncommon.
Passive stretching is usually adequate treatment in young children.
o Limb discrepancy at maturity – 5-27% - and if no corrective procedure has been
performed, mean discrepancy is 4cm
o Close follow-up and limb-length inequality can be corrected with epiphyseodesis of
the contralateral side
o Because of the persistent tibial bow of 5-7 degrees with a posterior and medial apex,
limb lengthening with simultaneous deformity correction often is considered but early
osteotomy does not seem to affect ultimate growth inhibition

Anteromedial Bowing:
o associated with fibular hemimelia
o
Anterolateral Bowing:
Pseudoarthrosis, NF
Hx: Developmental hx – 50% learning disorder. Speech delay, late developing gross motor skills,
mental retardation, PMhx (hypertension, renal artery stenosis, pheochromocytoma in adults, CVAs),
FMhx – autosomal dominant (50% caused by new mutation).

Px:
Diagnostic Criteria (NF1 if 2+ present)– examine specifically for
o > 6 Cafe au lait spots >6.5mm in size in kids vs 15mm in adults
o Inguinal + axillary freckling
o Neurofibromas >2 (bluish and raised over skin surface)
 or 1 plexiform neurofibroma (ropy bag of worms) – if crosses midline likely tumor
originates from spinal cord and will be malignant. Plexiform neurofibroma has
potential for malignancy

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 o Optic glioma
o Lisch nodules (iris hamartomas)
o Distintive bone lesion
o 1st degree relative with NF-1

Inx:
X-ray of the involved limb
X-ray of C-spine, X-ray TLS spine, MRI spine

 rare(1:140000), occurring equally in girls and boys

 almost always unilateral
 acute # occur during first 2 yrs of life, usually shortly after birth
 neurofibromatosis is present in approx 40-50% of pts with pseudarthrosis, while approximately
10% of pts with neurofibromatosis will have pseudarthrosis of tibia
 can also have pseudarthrosis of the fibula, but this almost always occurs in association with
congenital pseudarthrosis of the tibia

Classification
Boyd System (Most widely used)
 I Fracture present at birth
 II Hourglass constriction of tibia often associated with neurofibromatosis
 III Bone cysts
 IV Sclerotic segment of tibia without constriction, stress fracture results
 V Dysplastic fibula
 VI Intraosseous neurofibroma
Anderson System
 Dysplastic type - characterized by narrowing, sclerosis, and obliteration of the medullary
canal
 Cystic type - no narrowing but instead has cyst-like areas which resembles fibrous
dysplasia microscopically. In this type, leg appears normal early in course, with # and
pseudarthrosis occurring after 5 years of age
 Sclerotic type
 Fibular type
 Clubfoot or congenital band type

 Other radiographic features include hindfoot positioned in calcaneus, diminished height of lateral
distal tibial epiphysis and variable shortening of the limb
 Differential diagnosis:
o Fibrous dysplasia
o OI
o Rickets
o Camptomelic dysplasia
 One distinguishing feature is that it is rarely bilateral

Non Operative Treatment

 Once the diagnosis of anterolateral bowing is made, full-time brace treatment is indicated
 AFO appropriate protection prior to walking
 KAFO is fit as the infant begins walking

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  Orthotic support is continued indefinitely during growing years with or without surgical
reconstruction of a pseudarthrosis
 Although very uncommon, anterolateral bowing occasionally does not progress
o Anteriorly bowed tibia, with or without a previous fracture (Boyd type IV), which actually
consolidates with immobilization
o Supplemental onlay bone grafting may be beneficial as patients seemingly carry less
chance of further progression and fracture following this procedure
 Electrical stimulation
o 55–80% union, Noninvasive, may be combined with other techniques
o Limited ability to correct deformity, long time in cast

Surgical Treatment Options

Once # ensues, operative treatment:
 Intramedullary rodding (Williams Rods) + pseudarthrosis excision + bone grafting
o 90–100% union
o Ideal choice because:
 the fracture may take a long time to heal, necessitating that the fixation serve its
purpose for years
 great tendency to refracture, avoids stress shielding that occurs under a rigid
plate and stress riser created by the screw holes that remain when the plate is
removed
 anterior and lateral bowing of the tibia that must be corrected as a part of the
treatment
 bone is small and osteopenic
 distal segment is often short, making fixation to it difficult and insecure
 soft tissue coverage in the leg of a small child is not great
 stimulus of weight bearing is preserved
 device can cross the ankle into the talus and os calcis with little morbidity to help
secure fixation of a short distal fragment
o Corrects deformity, provides long-term internal splint
o May cause ankle stiffness; does not correct severe, established shortening
 ORIF & bone grafting with autogenous graft with or with out electrical stimulation
 Vascularized fibular transfer
o 90–95% eventual bone union
o Provides excellent bone stock, may add slight length
o Requires specialized skill, relatively long operation, distal angulation hard to correct may
still leave the involved leg w/ potential for #, angulation, & growth disturbance
 External fixator (circular or monolateral frame)
o 90–100% union
o Corrects nonunion length, angulation
o High risk of refracture, bowing; long term follow-up not available
 Syme’s amputation
o Indicated for pseudarthrosis with limb length inequality greater than 5 cm and/or severe
foot deformity
o Decreases the level arm on the small distal fragment
o The Symes prosthesis protects the pseudarthrosis
o Recommended only in extreme cases when the ankle is nonfunctional or numerous
previous procedures
 Below knee amputation
o After all else has failed

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 o amputation through the pseudarthrosis may leave scars over the amputation stumps
and the over growth phenomena may end up requiring additional revision amputations
o in some cases, spontaneous union of the pseudarthrosis will occur (due to total contact
of the prosthesis and the beneficial effects of weight bearing

Complications: Malalignment, Refracture, LLD

Pre-op and acute care of Pseudoarthrosis of the Tibia

 Type and screen
 Spine imaging ok (C-Spine)
 Template for size and length of IM rod needed
 Consent
o Resection of pseudoarthrosis, bone grafting, and Rush IM rodding of tibia extending
trans-ankle into calcaneus
o Immdediate risks: generic including compartment syndrome
o Delayed risks: recurrence of pseudoarthrosis, refracture, ankle stiffness, growth
disturbance due to trans-ankle rodding, LLD, lateral plantar nerve entrapment
1. correction of angular deformity
2. resection of pseudoarthrosis
3. reconstitution IM canal blood supply by reaming
4. bone graft
5. stabilize pseudoarthrosis with IM rod

Post the case

o Radiolucent table, Fluoro, Osteotomes, Rongeurs, curretes, High speed burr
o Drill, Rush rod, Cast cart
Approach + fixation
 Williams technique – offer with fracture through pseudoarthrosis that‘s not healing with casting
o Abx: Yes
o Position: Supine
o Approach and Fixation
 Tourniquet
 Anterior tibial incision centered over pseudoarthrosis just lateral to crest
 Divide deep fascia of anterior compartment at this level
 Subperiosteally expose normal tibia proximal and distal to pseudoarthrosis
 Resect of psedarthrosis to bleeding bone edges
 Harvest ICBG
 Bone graft pseudoarthrosis site
 IM drilling both ends of pseudoarthrosis to reconstitute IM blood flow and ease
passage of IM device
 Correct bowing deformity of tibia by appropriate resection of pseudoarthrosis
 IM rush rod is placed through pseudoarthrosis site and driven distally through
ankle, talus, calc and out sole of foot. Make sure position of ankle and foot is
correct
 Approximate tibial fragments at pseudoarthrosis site and drive IM rod from sole
of foot proximal into tibial metaphysic
 Distal end of rod is left under heel pad but inside calc
 Close in layers
 Long leg splint – hip spica cast to remove motion
 Moulding for KAFO

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 o Splinting and immobilization
 Will need rod exchages as child grows and continuous bracing

Spinal Manifestation of NF
 X-rays of c-spine
o Kyphosis
o instability
 X-ray of spine
o Scoliosis Dystrophic changes
 Short segments with sharp angulation
 Scalloping of posterior vertebral margins
 Severe apical vertebra rotation
 Wedging
 Widened spinal canal: Allows for large angular deformity without neuro deficit
 Enlarged neural foramina
 Widened interpedicular distance
 Defective pedicles
 Paraspinal mass
 Spindling of transverse process
 Rotation of ribs – ―penciling‖ of ribs diagnosed when rib is smaller in diameter
than the midportion of the second rib
 Rib dislocations
o Scolisosis Nondystrophic changes (similar to idiopathic scoliosis)
 Wedging
 Angulation
 Rotation
 Curve progression likely if 3 pencilled ribs, 3 dystrophic features, or manifests
before age 7
o Kyphoscoliosis
 MRI spine
o Intrapsinal tumors
o Dural ectasia
 Circumferential dilation of dural sac with increased CSF and a brownish
proteinaceous material
 Expanding dura can erode surrounding osseous structures
o Meningoceles
 Expansion of dural extasia out through neural foramina
o Dumbbell lesions
 Neurofibroma exiting from spinal canal
 More rarely can be due to dural ectasia
 Seen as a single enlarged neural foramen on oblique Xray of spine
 MRI brain – optic glioma f/u

Treatment of Spinal Deformity in NF:

 Scoliosis
o Nondystrophic is treated as idiopathic scoliosis but with close follow-up for development of
dystrophic component.
 Curves apex right with longer curve
 Cobb < 20 observe q 6 months

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  Cobb 20 – 35 brace & Xray q 6 months
 Cobb > 35 posterior spine fusion with instrumentation
 Cobb > 60 anterior release and bone graft + posterior fusion and instrumentation
o Dystrophic
 Curves tend to have short segments, sharp curves, severe apical rotation. Usually
apex left
 Cobb angle < 20 observe with x-ray q 6 months
 Cobb angle 20-40 – Posterior spine fusion with instrumentation (even in young child
– minimal growth stunting will develop)
 Cobb >50 Anterior and posterior spine fusion
 Kyphosis
o < 50 degrees = bracing
o >50 degrees neuro intact = Anterior and posterior spine fusion + laminectomy
decompression.
o >50 degrees neuro deficit = Anterior decompression + anterior and posterior fusion
o > 70 degrees = anterior and posterior spine fusion + decompression + indefinite bracing
o F/U q 6months for pseudoarthrosis

Tumors associated with NF

o Neurofibrosacroma (think of this in any NF case with pain and increasing swelling in a
previous neurofibroma)
o Leukemia
o Rhabdomyosarcoma of urogenital tract
o Wilms tumor
o Parathyroid adenoma
o Sipple syndrome – NF, bilateral pheochromocytoma, medullary thyroid carcinoma

Acute Care of NF
o Goal of treatment of tibia is to prevent deformity and fracture. If fracture occurs goal is to
promote healing and prevent re-fracture
o Image spine including MRI esp C Spine prior to OR
o MRI brain
o Consult pediatrician and multidisciplinary team for management of non-orthopedic aspects of
NF
o Serial eye exams, ophthalmoloy
o Genetic counselling to parents

94. Clubfeet
 1/1000; male: female 2:1; bilateral 50%
 Do a thorough birth/pregnancy/delivery history.
 Family history – 2nd sibling 20-30x risk
 Look for associative disorders: oligohydramnios, arthrogryposis, diastrophic dysplasia, Larsen‘s, spinal
dysraphism, Goldenhar‘s syndrome, Pierre Robin syndrome, Streeter‘s dysplasia (congenital
constriction bands), spina bifida, CP, polio

Consider the pathoanatomy

Hindfoot
 Talar body is externally rotated (somewhat controversial) but the neck and head are medially and
plantarly rotated (ie – there is some intra-talar deformity)
 The external rotation of the body leads to an externally rotated bimalleolar axis

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  The calcaneus is equinus and varus, so that it is parallel rather than divergent with the talus
 The posterolateral capsular structures including the subtalar capsule, ankle capsule, calcaneofibular
ligament, and posterior talofibular ligaments are contracted
 The Achilles is contracted

Midfoot - Forefoot
 The talonavicular joint subluxes, with the navicular riding medially and dorsally on the talar head,
coming almost to lie adjacent to the medial malleolus; gives rise to the crease on the medial aspect of
the foot
 The calcaneocuboid joint similarly subluxes medially, with the cuboid riding medially and somewhat
plantarly on the calcaneus into a cavus type deformity
 The whole midfoot/forefoot complex is adducted and supinated, although the forefoot may actually be
relatively pronated with respect to the midfoot (according to Ponsetti)

Then, all the soft tissues that cross the hindfoot and midfoot get contracted:
 Long and short plantar ligaments contracted – maintain the arch normally, but sustain the cavus
in clubfoot
 Tib post, FDL, FHL are all contracted – enforce the varus and cavus
 Spring ligament contracted
 Plantar fascia contracted

Physical Examination
 Look for dysmorphic features
 Obviously, do a thorough physical exam: other joints involved? Hip? Knee? Arthrogryposis?
Neurological? Look at back, neck, hands
 Look: see hindfoot equinus, deep posterior crease, empty soft heel, hindfoot varus (apparent
supination of the foot), medial crease (midfoot cavus), convex lateral border (forefoot adducted)
 Feel: space between medial malleolus and navicular, the prominent lateral tarsal head (uncovered by
subluxation of the cuboid), emptiness of the heel (calcaneus in equinus) and interval between fibula
and Achilles (calcaneus is pulled up into equinus and the posterolateral capsular structures are tight)
 Move: how much dorsiflexion is there (ie. how rigid is the equinus?), how rigid is the midfoot adductus
(can you straighten the lateral border)? And how tight are the long toe flexors?

Xrays
 Get an xray before going to the OR to rule out associated coalitions in the rigid foot
 Look at Kite angle (talocalcaneal angle) on the AP: should be 20-40 normally
 Look at talocalcaneal angle on lateral: should again be about 20-45

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Treatment
Goals
 Plantigrade, flexible, painless, normal shoe wear, functional, close to normal looking
 Begin treatment of the newborn with above knee casting, even if arthrogrypotic (anticipate that you‘ll fix
these later on)

 Ponsetti Principles
o Manipulation prior to each casting
o Serial casting – weekly changes
o Above knee cast to maintain external rotation
o Sequential correction – ―CAVE‖
o Gentle stretch
o Residual equinus – percutaneous Achilles tenotomy
o Foot abduction orthosis for 3-4 years to maintain correction
o Late tibialis anterior transfer for some
 Cast #1 (Cavus correction)
o Elevate the 1st MT to supinate the forefoot (corrects the midfoot/forefoot deformity by
reducing the navicular back onto the talus and cuboid back to calcaneus)
o From ponseti video, must keep pressure on the lateral aspect of the talar head when
doing this manipulation
o This eliminates the medial crease and reduces cavus

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 o Never pronate the foot
o Ignore equinus
o Cast extended above knee
 Cast #2 (Adduction correction)
o Keeping foot supinated, begin pure abduction of the foot
o Counter pressure against the lateral part of the talus (NOT calcaneus)
o Don‘t pronate
o Ignore equinus
o Mold the arch
o Mold above the heel
o Cast extended above knee to maintain ER
 Weekly cast changes (average 5 sets of casts) (Adduction and hindfoot Varus)
o Keeping the foot supinated, progressively increase abduction of the foot
o Counter pressure against the lateral talus (NOT calcaneus)
o Until 70 of external rotation
o Cast extended above knee to maintain ER
o Hindfoot varus corrects as foot is fully abducted
 When forefoot is abducted and hindfoot is in valgus, address Equinus last
o Casting if there are signs of flexibility (10-15%) OR
o Percutaneous Achilles tenotomy (do this at the 10wk mark if don‟t have 10deg of dorsiflex)
o Technique – local or GA, 1cm above insertion, Beaver blade inserted medial to tendon and
directed laterally to complete tenotomy, 10-20 dorsiflexion, long leg cast for 3/52 well molded
with 20 dorsiflexion and 70 abduction
 Foot abduction orthosis
o Denis Browne bar – 70 ER on affected side, 45 normal side – full time for 3/12 and nighttime
use for 3-4 years
 Recurrence
o Serial casting, repeat tenotomy, resume bracing
o Late recurrence – tibialis anterior transfer to 3rd cuneiform/cuboid and TAL if equinus;
rarely posterior release
o Medial cuneiform opening wedge, lateral cuboid closing wedge as well
Generally, casting process is 5-10/52 depending on the degree of deformity needed to be corrected

Complications of closed treatment include:

 Increased cavus deformity
 Rocker-bottom foot (from trying to correct equinus too soon)
 Longitudinal breach
 Flattening of the proximal surface of the talus (flat-top talus)
 Skin breakdown
 Increased stiffness

Surgical Management
 Limited indications:
o Failed non-op (5%)
o Late referrals – neglected or older clubfoot
o Recurrent clubfeet (post surgical)
 No consensus on when it should be done
 Probably initiate between 4-12 months of age (some time before the kid is walking)
 Indicated for failure of casting/manipulations – do not continue with forceful manipulations if you are
getting nowhere!
 As there is disagreement on the pathoanatomy, there is disagreement on what the surgery
should accomplish
 In general:
o < 4 yrs - soft tissue procedures

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 o 4 - 12 - both soft tissue and bony procedures
o Adolescent/teens get bony procedures
 In the neglected or older clubfoot, initial serial casting still helpful using Ponsetti principles, repeat
tenotomy up to 18 months then surgical correction

Approach to Complete Posteromedial Release

 Prone, antibiotics, tourniquet and have K-wires ready
 Cincinnati incision:
o ―my incision begins on the medial side of the foot over the naviculocuneiform joint passing
posteriorly to cross just beneath the tip of the medial malleolus continuing across the back of the
foot over the Achilles at the level of the tibiotalar joint and continuing laterally to pass over the
lateral malleolus ending at the sinus tarsi‖
 Identify and protect all neurovascular bundles:
o Laterally – sural nerve and short saphenous vein
o Medially – tibial nerve, long saphenous vein, posterior tibial artery, saphenous nerve
 Posteromedial/circumferential release: (a la cart release)
o TAL
o Posterior talofibular and tibiofibular ligaments
o Posterior ankle capsule
o Subtalar release (often complete)
o Tibialis posterior lengthening
o Talonavicular joint release
o Plantar release
o FHL/FDL (conjoint) lengthening
o Calcaneocuboid release
o Preserve some of interosseous ligament
o Preserve deep deltoid ligament
o Fixation with pins

Start posteriorly:
 Laterally identify sural nerve and short saphenous vein – protect these
 Then go after Achilles and Z-lengthen
 Then identify posterolateral structures – calcaneofibular ligament, posterior talofibular ligament – and
release them
 Then go medially and identify the neurovascular bundle behind the medial malleolus and protect it
(tibial nerve, posterial tibial artery) – saphenous vein and nerve are anterior to the medial malleolus
 Now safe to go open the posteromedial and posterolateral capsule to the subtalar joint and ankle joint
so that you release these – you cannot correct the equinus by just cutting the Achilles, because of
these contracted capsular structures
 Releasing the interosseous ligament is controversial

Then go medially:
 Find abductor hallucis brevis and release its origin off the calcaneus, dissecting both plantarly and
dorsally around the muscle. The dorsal edge of this muscle is then identified and detached all the way
back to its insertion on the medial tuberosity of the calcaneus. This muscle is hinged downward with a
small periosteal elevator that dissects it off the underlying fascia. Be careful when detaching the
posterior insertion of the abductor hallucis because the neurovascular bundle will run beneath the
muscle in this region.
 Beneath the NV bundle is the lancinate ligament under which the medial plantar nerve dives; cut the
ligament, and then find the lateral plantar nerve diving beneath the calcaneus
 The medial plantar nerve from the posterior tibial nerve will run almost parallel to the flexor digitorum
longus tendon in the sole of the foot and will be just volar to it. The medial plantar branch of the
posterior tibial nerve can be followed proximally to help identify the neurovascular bundle just posterior
to the flexor digitorum longus tendon behind the medial malleolus.

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  At the completion of this stage of the dissection, the following structures are visible:
o most volar is the medial plantar branch of the posterior tibial nerve,
o just dorsal to it and paralleling its course is the flexor digitorum longus,
o crossing this tendon transversely at the master knot of Henry is the flexor hallucis longus tendon
o splaying out over the tuberosity of the navicular is the insertion of the posterior tibial tendon.
 If the flexor digitorum longus tendon is retracted, the plantar ligaments, the peroneus longus tendon
coming to insert on the base of the first metatarsal, and the medial side of the calcaneocuboid joint can
all be exposed.
 Find tib post, FDL, FHL, and z-lengthen them all.
 One way to lengthen FDL and FHL is to suture them to each other both proximally and distally and then
divide them near the knot of Henry (called conjoint lengthening) – one just proximally to where they are
suture together and one just distally – then sew together the cut ends
 Find peroneus longus, protect it, and cut the long and short plantar ligaments to reduce the cavus
 Open the talonavicular joint and calcaneocuboid joint from the medial side – release the capsule and
structures on the plantar surface to be able to reduce them
 In a child > 8 months, the calcaneocuboid may have to be opened laterally
 Small smooth K-wire through the posterolateral corner of the talus, through the head and into the
navicular with the navicular reduced, and even across into the medial cuneiform and 1st metatarsal

Post-op
 Cast for 6weeks
 AFO for a year

Late or Recurrent Deformity

Residual Deformity
 Most commonly secondary to incomplete release, especially of the plantar fascia and short/long
plantar ligaments
 Make sure it is not neurologic in origin – tethered cord?
 Was post-op casting and orthotic use sufficient?
 Is there motor imbalance around the foot?
 Where is the anatomic pathology? Hindfoot equinus? Hindfoot varus? Forefoot/Midfoot
adduction/supination?

Management – Stiff deformity

 If young (less than 4 yrs) you can probably get away with repeating the posteromedial release (or
whatever parts of it that you think are necessary to address the anatomic pathology)
 If older you need to think about osteotomies to help with the alignment
 If curved lateral border, think about trying to shorten the lateral column with a Dwyer lateral closing
wedge osteotomy with a release of the scar tissue that holds the cuboid medially OR a cuboid
decancellation
 Alternatively, if the hindfoot is still in a fair amount of fixed varus, you can do a medial opening wedge
osteotomy of the calcaneus (if you don‘t want to shorten the foot any more with a Dwyer)

Technique Double Tarsal Osteotomy To Correct Forefoot Adduction

Usually done in children >4 with residual supination and adduction after operative soft tissue
treatment
 Can either lengthen medial side, shorten the lateral side, or both

 Started on the lateral side of the foot

 Bolster is placed beneath the buttocks, turning the leg internally to facilitate the approach to the cuboid
 Incision may be either oblique, following the skin lines directly over the cuboid, or curvilinear over the
bone
 After opening the skin, peroneal tendons are identified, freed from their sheath, and retracted
plantarward

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 Soft tissues are freed dorsally and plantarward to expose the cuboid bone, keeping the joint capsules
intact
 Periosteum of the cuboid is incised from the dorsal to plantar side and elevated toward the joint
surfaces exposing the section of bone to be removed
 Using a microsagittal saw, laterally based wedge of the desired size is removed
 Important to go through the medial cortex of the bone so that the osteotomy will be mobile and
easy to close
 Wound is left open and bolster removed to provide better access to the cuneiform bone on the medial
side of the foot
 Straight linear incision is made directly over 1st cuneiform
 As the dissection is deepened, the anterior tibial tendon will be identified coursing over 1st cuneiform
 This tendon can be dissected free without disturbing any of its essential attachments – starting on the
inferior aspect of the tendon and reflecting it dorsally usually allows adequate exposure
 Continue to dissect the cuneiform bone (subperiosteally if and where possible) until both the proximal
and distal joints are identified positively, while trying to preserve intact the joint capsules and while the
plantar and dorsal aspect are exposed
 Check the path of the proposed osteotomy with fluoro
 Using the microsagittal saw, make a single osteotomy cut in the 1st cuneiform
 Be aware of the sloping joint surface, and if necessary, pass a small dissector into the
naviculocuneiform joint to mark its plane
 After completing the osteotomy, insert a blunt instrument to spread apart the fragments and ensure
their mobility
 Graft that was taken from the cuboid is now inserted into the osteotomy of 1st cuneiform
 If there is difficulty opening this osteotomy sufficiently to insert the graft, place a Kwire into each
fragment to open the osteotomy
 May be necessary to release the abductor hallucis tendon if it is tight or produces adduction of the great
toe after the graft is inserted
 If the bone is large enough, a small lamina spreader will work well
 When the bone is in place, it should be relatively secure; however, with any activity, there is the danger
that it may extrude so secure it with a Kwire passed through the base of the 1st metatarsal, the distal
fragment, the graft, and the proximal fragment
 The cuboid osteotomy is inspected
 If this osteotomy has not closed, it can be manipulated closed and held with one or two small staples or
a Kirschner wire

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Management – Dynamic deformity
 If there is a dynamic adductus and supination that is reducible passively try tendon transfer – seen
during swing phase of gait
 This is often due to incoordination of tib ant and tib post
 Options include:
o Split tib ant transfer to base of 5th MT
o Whole tib ant transfer
o Bring tib post through interosseous membrane to third cuneiform

Remember: the key is the age (and therefore the correctability) and the identification of what the
pathology is (either dynamic or fixed)
Above 4 years, really think about doing osteotomies

95. Approach to Congenital Vertical Talus (Congenital Convex Pes Valgus)

Definition
 Fixed congenital dorsolateral dislocation of the talonavicular joint, and occasionally calcaneocuboid,
with hindfoot equinus
 Talus is plantarflexed in a vertical posture with the dorsally dislocated navicular pressing down on
the talar neck
 Associated with subtalar eversion and fixed dorsiflexion of the mid and hindfoot
 This is at the extreme spectrum of flatfeet - ie. the ultimate flatfoot
 Causes:
o Idiopathic 60%
o Associated with conditions like chromosomal abnormalities (trisomy 13/15/19),
arthrogryposis, multiplex congenital syndrome, Larsen‟s, neurofibromatosis, nail-patella
syndrome, , and certain neurologic conditions (myelomeningocele, tethered cord,
lipoma, sacral agenesis) THIS IS A COMMON QUESTION IN ORAL AND MCQ
o DDH and contralateral clubfoot may occur with increased frequency
o Iatrogenic (overcorrection of a clubfoot)

 In many patients a neuromuscular imbalance results in contracture of the posterior, lateral and anterior
muscles causing the talonavicular joint to dislocate dorsolaterally, forcing the navicular to rest on the
dorsolateral talar neck and subsequently plantarflexes the talus in the mortise; the os calcis laterally
rotates from under the talus and the lateral column of the foot is deformed into valgus
 Calcaneocuboid joint may also be subluxed dorsally – the whole midfoot and forefoot are swung way
out into abduction
 Differential diagnosis includes:
o Oblique talus (TN joint is subluxated but reduces with plantarflexion)
o Calcaneovalgus foot
o Flexible flatfoot with midfoot sag and short Achilles

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 o Rigid flatfoot associated with tarsal coalition
o Peroneal spastic flatfoot

Clinical features
 Rigid convex plantar surface (Persian slipper) – rocker bottom flatfoot
 Contracted Achilles
 Hindfoot fixed equinovalgus with few posterior heel creases
 Head of talus palpable in plantar/medial midfoot
 Midfoot dorsiflexed and abducted on hindfoot - cannot be plantarflexed
 Crease overlying sinus tarsi (lateral)
 Hallmark – none of the deformities are correctable

Xrays
AP plus lateral with maximal plantar (to check correction) and dorsiflexion (to assess Achilles
contracture) to confirm diagnosis
Talus/calcaneus/MT‟s are ossified at birth, cuboid in 1st month
AP demonstrates midfoot valgus and increased talocalcaneal angle (decreased in clubfoot) (usu 20-40o)
In max dorsiflexion, persistent plantarflexed talus and calcaneus (contracture of Achilles and posterolateral
capsule) and dislocation of navicular on talar neck
 Increased talocalcaneal angle confirms hindfoot valgus (on lateral usu 25-50o)
 Usually talus dorsiflexed 90 degrees on tibia and calcaneus 20 degrees beyond
 Persistent dorsal translation of forefoot (TN dislocation is not reducible) on maximal
plantarflexed view (normal axis of talus-MT is almost a straight line)

Natural history
 It persists and causes disability if untreated – plantarflexed head becomes weightbearing surface
and callous develops, and no push-off and ultimately degenerative arthritis at the dislocated TN joint

Treatment
 1st manipulation and casting in plantarflexion and inversion mostly to stretch because nearly 100% will
need OR

Operative Options
 One or two stage circumferential release, talectomy, naviculectomy, subtalar arthrodesis, triple
arthrodesis, lateral column lengthening
 One stage circumferential release – 1st choice under 2 yrs – lengthen Achilles and peroneals,
releasing dorsolateral capsule possible split transfer of tib ant to head/neck of talus
 Medial column shortening +/- lateral column lengthening (the reverse of what you usually do in clubfoot)
 Fusion reserved for salvage (talectomy also salvage) – for residual or untreated deformity of the vertical
talus in the older child

OR
 Cincinnati incision:
o ―my incision begins on the medial side of the foot over the naviculocuneiform joint passing
posteriorly to cross just beneath the tip of the medial malleolus continuing across the back of the
foot over the Achilles at the level of the tibiotalar joint and continuing laterally to pass over the
lateral malleolus ending at the sinus tarsi‖
 Identify and protect all neurovascular bundles:
o Laterally – sural nerve and short saphenous vein
o Medially – tibial nerve, long saphenous vein, posterior tibial artery, saphenous nerve
 Reduce talonavicular dislocation held with Kwire(s) (from posterolateral talus through navicular, medial
cuneiform into 1st MT)
 Derotate subtalar joint
 Lengthen posterior, lateral and dorsal tendons (for sure Achilles)

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  Posterior and subtalar capsules must be lengthened/released as needed, as well as calcaneofibular
ligament (posterolateral) +/- interosseous ligaments
 Don‘t forget the extensor tendons, may need to be released (see case from sarah below)
 3/12 casting post op

Drennan: single stage

 Posterolateral release (calcaneofibular ligament), release Achilles, expose NV bundle, open reduction
of TN joint, cut interosseous talocalcaneal ligaments, then K-wires in the joint

Case (from Sarah)

18/12 child referred to you after being treated with serial casts from age 3 to 6/12 for clubfoot. Mother
is unhappy because now that child is walking, she says the child cries when she walks and the gait is odd. So
you take a full history asking about past medial and surgical history, meds, allergies, immunizations, birth and
developmental history, siblings and similar foot problems, as well as any family history of foot problems or MH
or bleeding disorders. All normal.
Proceed to physical exam, full head to toe looking for dysmorphic features, checking neck, listening to
heart, lungs and feeling abdomen. Check spine. Then lower extremity looking for signs of hip instability or
associated contralateral foot problems. Then the foot. Check gait and you notice that the foot is pronated.
Mild valgus hindfoot alignment. No skin creases. Ask specifically about rocker bottom foot – which this kid
has. Bony prominence plantarly. Neurovascularly intact. Normal passive ROM of ankle – difficult to assess
subtalar in patient this young. You ask for old notes from other orthopod and then you ask for xrays thinking
this is CVT. So you order AP and lateral as well as maximum plantarflexion view (to see if the vertical talus
corrects – if it does, then it‟s an oblique talus; if not, CVT). Lovell and Winter also says you should order
maximum dorsiflexion view which helps assess Achilles contracture (you should also get an idea of this from
the physical exam of ROM). So the xray shows a vertical talus with increased talocalcaneal angle that doesn‘t
correct on maximum plantarflexion view (meaning persistent dorsal translation of the forefoot and navicular on
top of the talus). The maximum dorsiflexion view shows persistent plantarflexion of the talus secondary to
contracted Achilles and posterolateral capsule.
So this is a difficult problem. Definitely refer to pediatric orthopedic surgeon and get pediatrics involved
to ensure there is not an associated syndrome. You can mention casting in plantarflexion and inversion to
stretch the soft tissues but this will likely need an operation. Before proceeding to the OR you need to
decide if you are going to have to do anything with the extensor tendons. If you are, then you need to do
an anterior incision as well as a Cincinatti. If you can get the foot down enough, may be able to release
enough posteriorly and laterally and reduce the TN joint through only the Cincinatti. May need to lengthen the
Achilles and/or the extensors. Get xrays in the OR to confirm reduction of the talocalcaneal angle and Meary‘s
angle (first metatarsal axis). Leave the pins in for 6/52. Cast for total of 3/12.
Potential complications – pin backs out. Check xray and if still doing something, cut it and leave it in. If
the reduction is lost, back to the OR. Compartment syndrome is unlikely in this setting.

CORF
Need to read about the grice extraarticular subtalar fusion

96. Causes of Cavus Foot

Bilateral Cavus
 CMT most common
 Friedrich‘s
 Tethered cord (MRI: cord extends below L1 and sits posterior in canal on axial cuts)
 All other dysraphism
 Diabetic neuropathy

Unilateral
 Trauma (crush injury - compartment sydrome missed)
 Polio

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  Incomplete SCI

Approach to Pediatric Cavus Foot

1. Hx: rare < age 3, ask re: bowel/bladder, FMHx + PMHx (CMT, Freidrich‘s ataxia, CP, polio)
2. Exam: Apex of deformity, flexibility, equinas, NV exam (strength – weak peroneals, tib ant,
intrinsics [flexors nl]), Coleman block
3. Imaging:
a. Xrays – STANDING AP, lateral foot, scoliosis xrays
i. Meary‘s angle, calcaneal pitch
b. MRI spine and brain (ask for this in all cases)
4. Diff (idiopathic is Dx of exclusion)
a. Brain – CP, Freidrichs ataxia (present in teens)
b. Spinal Cord – Myelodysplasia, syringomyelia, diastomatomyelia, polio, intrathecal
lipoma (or other tumor)
c. Peripheral nerves – CMT most common
5. Tx – Goal is mobile, plantigrade foot
a. Non-op for mild, non-progressive = shoe modification with lateral column support
b. Cavus and Cavovarus
i. Soft tissue releases (may be enough if all deformities flexible)
ii. Forefoot – midfoot – hindfoot osteotomies
iii. Tendon transfers (absolute in CMT)
1. Tib post – lateral cuneiform; peroneus longus - brevis
iv. Arthrodesis (triple)
1. Salvage, still perform releases, osteotomies, etc to de-tension for higher
fusion rate
c. Calcaneocavus
i. Progresses rapidly with growth so be aggressive
a. < 8 = TA and FDL transfer thru interosseous membrane to calcaneus
b. 8 – 12 = crescent posterior displacement calcaneal osteotomy
c. > 12 = 2 stage triple arthrodesis, fuse forefoot to hindfoot, wait 6 week, then subtalar fusion

97. Myelomeningocele
 watch out for latex allergy, blocked shunts, and tethered cord especially if sudden
change in neurology or function
 associated with hydrocephalus and Chiari malformation (caudal displacement of posterior
lobe of cerebellum
 hydormyelia is accumulation of fluid in the central canal of cord – often leads to scoliosis
 Occulta – midline defect in lamina, hairy patch indicates more serious problem
 Cystica
o Meningocoele: prolapse of CSF filed meningeal sac
o Lipomeningocele: lipoma in sac with neural elements entwined
o Myelomeningocoele: prolapse of sac containing cord and nerve roots
o Rachischisis: open myelomeningocoele
Ortho Concerns:
SPINE
 86% have a spine abnormality, scoliosis most common, 10% get severe kyphosis especially
lumbar
 scoliosis usually is uncompensated and progressive (large C-shaped curves)
 yearly x-rays

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HIPS
 most deformities related to muscle imbalance
 often flexion/adduction contractures leading to dislocation
 unless muscles can be transferred to the hip or it is already functional in walking, attempts to
reduce a dislocated hip are probably not warranted
 L3 level most likely to have dislocated hips

KNEES
 Most have flexion contracture
 >20° leads to crouched gait
 KAFO‘s important
 Nighttime splints
 A-frame
 Reciprocating gait orthoses

FEET
 almost all will have foot deformities which are generally non-responsive to casting as neonate
brace flexible feet
 very rigid clubfoot, usually has a supination deformity (tib ant is unopposed when peroneals
paralyzed)
 operate at 10-12 years old
 radical postero-medial release
 excise, don‘t lengthen tendons
 tenotomy of tib ant to correct the supination
 release subtalar, calcaneocuboid and talonavicular joints and rotate talus medially and pin to
navicular
 most fixed deformities require surgical correction and the specific deformity depends on the level
 valgus ankles
 most clubfoot recurrences are adduction of forefoot due to growth imbalance between medial
and lateral comluns
 try bracing, but will need closing wedge osteotomy of cuboid and opening wedge of medial
cuneiform at 5 years old

FRACTURES
 between ages 2-12, very prone to lower extremity fractures
 because of lack of sensation they don‘t usually complain of pain
 usually present with redness and swelling and have a fever up to 39 degrees and is often
confused with infection
 treatment is with soft splints only because casting leads to stress risers and worsening
osteoporosis
 generally heal well

Level Hip Knee Feet Orthosis Ambulation

L1 ER/flex - equinovarus HKAFO non

L2 Ad/flex flex ― ― ― ― HKAFO non
L3 ― recurvatum ― ― ― ― KAFO household
L4 ― extension cavovarus AFO household plus

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L5 flex dec flex calcaneovalgus AFO community
S1 - claw toes shoes normal

Intervention
 Close defects
 Shunt for hydrocephalus
 Stretching and strapping at 3 weeks if child well
 IVP to look for urinary problems
 LATEX ALLERGY!
 Stretching for 6-12 months
 Watch back closely
 Look for bars, hemivertebrae, kyphus
 S1 has flexion deformity of hips – psoas lengthening
 Dislocation of hips: closed reduction and adductor tenotomy and psoas transfer from lesser to
greater trochanter
 Older children: varus osteotomy, inominate osteotomy
 Want straight knee with hamstring release and or soft tissue release
 Want plantigrade foot

Teathered Cord
 At birth at L3
 By 2 months old at L1-2
 Signs include loss of muscle function, development of spasticity in lower limbs, scoliosis, back
pain, increased lordosis, bowel/bladder changes
 Unteathering may improve scoliosis (esp if curve is <45°)

Hydromyelia
 Accumulation of fluid in the enlarged central canal
 May lead to scoliosis, which may improve after hydromelia is treated

Arnold-Chiari Malformation
 Caudal displacement of posterior lobe of cerebellum
 Weakness or paralysis of vocal cords
 Problems with crying, feeding and breathing
 Cyanotic attacks, bradycardia
 Ocular problems

98. Spinal Muscular Atrophy

 Group of disorders characterized by degeneration of the anterior horn cells of the spinal cord and
occasionally the neurons of the lower bulbar motor nuclei, resulting in muscle weakness and atrophy
 Autosomal recessive
 Loss of anterior horn cells is considered to be an acute event without progression
 Neurologic deterioration may stabilize and remain unchanged for long periods
 Progression of muscle weakness is a reflection of normal growth that exceeds muscle reserve
 Respiratory function is compromised, and atelectasis and pneumonia are the usual causes of death
 Clinical features of spinal muscular atrophy vary widely and are based on the age at onset and the
functional capacity of the child at the time of diagnosis

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Classification

Type I, Acute Werdnig-Hoffman Disease

 Characterized by clinical onset between birth and 6 months of age
 Typically have severe involvement with marked weakness and hypotonia
 Usually die from respiratory failure between 1 and 24 months of age
 Pathologic multiple fractures may occur due to in utero osteoporosis secondary to decreased
movement at birth and suggest osteogenesis imperfecta -heal rapidly with immobilization

Type II, Chronic Werdnig-Hoffman Disease

 Onset of type II SMA varies between 6 and 24 months of age
 Less involved than those with type I SMA, but are never able to walk
 They may, however, live into the fourth and fifth decades

Type III, Kugelberg-Welander Disease

 Onset of type III SMA occurs after 2 years of age and usually before age 10
 Walking is usually possible until late childhood or early adolescence - usually are not able to run
 Motor capacity decreases with time, however, and they have difficulty rising from the floor because of
weakness of the pelvic-girdle muscles; this is known as the Gower sign
 There is atrophy of the lower limbs, with pseudohypertrophy of the calves
 Cranial nerve muscles are usually not affected
 Normal intelligence and may function effectively in society
 Both the quality and quantity of life may be extended in type II and type III spinal muscular atrophy by
the use of nighttime or full-time assisted ventilation

Functional Classification
Group I
 Never sit independently, have poor head control, and develop early progressive scoliosis
Group II
 Have head control and the ability to sit if placed in a sitting position but are unable to stand or walk,
even with orthotics
Group III
 Have the ability to pull to stand and to walk with external support, such as orthoses
Group IV
 Have the ability to walk and run independently

Genetic and Molecular Biology Studies

 Chromosome 5q

Clinical Features
 Clinical features vary according to the clinical classification
 Clinical characteristics common to all groups are relatively symmetric limb and trunk weakness and
muscle atrophy that affects the lower extremities more than the upper extremities and the proximal
muscles more than the distal muscles
 Hypotonia and areflexia are present
 Sensation and intelligence are normal
 In infants, gross fasciculations of the tongue and fine tremors of the fingers are commonly present
 The only muscles not involved are the diaphragm, sternothyroid, sternohyoid, and the involuntary
muscles of the intestine, bladder, heart, and sphincters

Diagnostic Studies
 Initial diagnosis - laboratory studies, EMG, nerve conduction studies, and muscle biopsies
 Hematologic studies in spinal muscular atrophy are not particularly useful -CPK and aldolase levels are
normal to only slightly elevated

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  Electrophysiologic studies, such as EMG, in patients with spinal muscular atrophy show typical
neuropathic changes, such as increased amplitude and duration of response
 Nerve conduction studies in spinal muscular atrophy are typically normal
 Muscle biopsies are usually diagnostic, demonstrating muscle fiber degeneration and atrophy
of fiber groups -however, with the recent advent of genetic testing for this disorder muscle
biopsy is usually not necessary

Radiographic Evaluation
 No specific radiographic characteristics that are useful in making the diagnosis
 Most common radiographic abnormalities are nonspecific and include hip subluxation or dislocation and
progressive spinal deformity

Treatment
 Major orthopaedic abnormalities associated with spinal muscular atrophy include the presence of soft
tissue contractures of the lower extremities, hip subluxation and dislocation, and spinal deformity

Lower Extremity Soft Tissue Contractures

 Result of progressive muscle degeneration and replacement with fibrous tissue
 Ambulation may be promoted and soft tissue contractures delayed by the use of orthoses, such as
KAFOs
 Contractures tend to occur most frequently after the child becomes wheelchair-bound
 The prolonged sitting posture enhances hip and knee flexion contractures
 Hip soft tissue contractures may also result in abnormal growth of the proximal femur and predisposes
the patient to coxa valga and progressive hip subluxation
 Soft tissue contractures without an associated osseous deformity usually do not require treatment
 Even when they are released, the sitting posture of the child enhances their recurrence

Hip Subluxation and Dislocation

 Progressive hip subluxation leading to dislocation occurs predominantly in spinal muscular atrophy
types II and III
 Important that this be prevented to provide comfort, sitting balance, and maintain pelvic alignment
 Periodic AP xrays of the pelvis, beginning in midchildhood to late childhood, are important to
allow early recognition of coxa valga and subluxation
 Once diagnosed, usually progressive because of the continued muscle weakness and soft tissue
contractures
 Procedures that have been used with some success in the past include soft tissue releases, such as
adductor tenotomy, iliopsoas recession, and medial hamstring lengthening - this restores some balance
to the proximal musculature
 Most children will benefit by varus derotation osteotomy if the hip is severely subluxated
 If the hip is dislocated, an open reduction with capsulorrhaphy and pelvic osteotomy of the
Chiari type may be beneficial
 The usual rotation osteotomies (e.g., Salter, Sutherland, Steel) sacrifice posterior coverage to
gain lateral (superior) and anterior coverage – but in the child who will be predominantly in a
sitting position, this lack of posterior coverage may predispose the patient to a posterior
subluxation
 Therefore, the pelvic osteotomy method chosen must allow improved posterior coverage - usually
accomplished with the Chiari osteotomy or perhaps a shelf procedure
 Even after satisfactory alignment of the hip, resubluxation and dislocation can occur due to the
progressive degeneration of the proximal muscles

Spinal Deformity
 Most children who survive into adolescence develop a progressive spinal deformity
 Occurs in 100% of the spinal muscular atrophy children and adolescents with type II and most of those
with type III, especially when they lose their ability to walk

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  As in other neuromuscular disorders, as the curve progresses there is an adverse effect on pulmonary
function
 Deformity typically begins in the first decade due to severe truncal weakness
 Once the deformity begins, it is steadily progressive and can reach severe magnitude unless
appropriately managed
 The thoracolumbar paralytic C-shaped and single thoracic patterns, usually curved to the right,
are most common - 30% of children also have an associated kyphosis, which is also
progressive
 In type II , the mean expected increase in scoliosis is 8.3 degrees per year, whereas in type III it
is 2.9 degrees per year.

Orthotic Management
 Bracing is ineffective – but can be effective in improving sitting balance and slowing the rate of
progression in young ambulatory children and has the advantage of allowing them to reach an older,
more suitable age for undergoing surgical intervention
 Orthotic treatment to help maintain posture or slow curve progression in a child 9 years of age or
younger with a deformity between 20 and 40 degrees
 TLSO is the most common orthosis used - must be carefully molded to distribute the forces over a large
surface area to prevent skin irritation and breakdown, a major problem for children with neuromuscular
diseases
 Occasionally, wheelchair modifications can also be effective in controlling truncal alignment and
improving sitting posture

Surgery
 Criteria for surgical spinal stabilization in spinal muscular atrophy include:
o Curve magnitude > 40 degrees
o Satisfactory flexibility on supine lateral bending radiographs
o FVC > 40% of normal
 When these criteria are met, posterior spinal fusion using segmental spinal instrumentation techniques,
such as Luque rod instrumentation and sublaminar wires
 Spine is usually osteopenic, and there is a risk for bone failure unless the forces of instrumentation are
minimized through extensive distribution
 Fixation to the pelvis using the Galveston technique is common (T2 – sacrum)
 In most children who are nonambulatory and have pelvic obliquity, fusion to the pelvis provides
improved spinopelvic stability and alignment
 Anterior spinal fusion and instrumentation are rarely indicated because of the compromised pulmonary
status of these children and may predispose the patient to pulmonary complications postoperatively
 When performed, it is combined with a simultaneous or staged posterior spinal fusion, usually with
Luque rod instrumentation
 Important that no postoperative immobilization be necessary; this enhances sitting balance and
pulmonary status and makes transfers easier
 Decreased function has been observed after spine fusion - loss of spinal mobility decreases the
function of the upper extremities and activities of daily living, such as performing transfers and personal
hygiene
 Operative complications are similar to other neuromuscular disorders including:
o Excessive blood loss
o Pulmonary complications
o Neurologic injury
o Wound infection
o Loss of fixation due to osteopenia
o Pseudarthrosis
o Death

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99. Osteogenesis Imperfecta
 Defect in type I collagen

4 types Inheritance Sclera Features

I AD blue preschool age (tarda), hearing loss
IA= teeth involved, IB = teeth not affected
II AR blue lethal
III AR Normal fractures at birth, progressive short stature
IV AD Normal milder form, normal hearing
IV A = teeth involved
IV B = teeth not involved

Clinical features
 Fragility of bone
 short stature
 scoliosis
 defective dentinogenesis of deciduous or permanent teeth or both
 middle ear deafness
 laxity of ligaments
 blue sclerae and tympanic membranes.

Radiographs
 thin cortices and osteopenia
 normal # healing with limited remodeling
 #’s decrease with incr age
 spinal compression #’s (codfish vertebra) are common
 scoliosis is common, bracing ineffective, needs fusion if >50 deg (like idiopathic)

Management
 early extremity bracing (prevent deformity and minimize #’s)
 Sofield’s osteotomies (shish kebab of multiple long bone osteotomies for significant deformities –
typically use fixed length rush rods or telescoping bailey-dubow IM rods.
 Fractures in;
 <2 tx like normal
 >2 tx with telescoping rods (L&W says use corrective osteotomies and rods >5yrs)

pic of Bailey Dubow rods (lengthen with growth)

**more prone to MH** as well as turners and DMD
Medical tx;
 According to L&W, although no good clinical trials, bisphosphonates are currently being used

100. Approach to Adolescent Hallux Valgus

 Anatomically defined by a hallux valgus angle > 16, intermetatarsal angle > 9.
 Usually family Hx positive; females > males
 May have slightly different pathoanatomy than adults, may have:
o increased metatarsus primus varus,
o an oblique 1st TMT joint articulation,
o a long first MT,

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 o generalized ligamentous laxity.
 Note the metatarsus primus varus = incr IMA angle – if undertaking surgery, this must be corrected

Things to consider:
 Is the MTP congruent? Is the MTP passively correctable?
 What is the IMA?
 What is the hindfoot like? Any equinus?
 What is the age of the patient and skeletal maturity – there is a high rate of recurrence if you
operate before the closure of the growth plates (the other reason for recurrence is failure to deal
with the metatarsal primus varus)

Soft tissue procedures

 Medial capsular reefing and realignment of abductor hallucis so that it is not a deforming force
 Lateral capsular release, adductor hallucis release from proximal phalanx and metatarsal head, division
of transverse metacarpal ligament

Bony procedures
 Proximal phalangeal closing wedge osteotomy with medial eminence excision and medial capsule
reefing (Akin)
 Distal osteotomy (Chevron)
 Diaphyseal osteotomy (Mitchell)
 1st TMT fusion (Lapidus)

Approach
 Make sure they have no Achilles tendon contracture, neuromuscular abnormalities, or spasticity
 Look for ligamentous laxity, pes planus, hindfoot valgus, and other postural deformities
 Try to temporize them as much as possible to get them to skeletal maturity
 Be very wary about operating on one before growth plates close
 Look very closely at their IMA and their first TMT – they often have an oblique first TMT which causes
metatarsus primus varus – you need to correct this either with a first TMT fusion (lapidus), or an
opening wedge osteotomy of the cuneiform
 Look at their MTP joint - most adolescents the joint is incongruous and you can pull the proximal
phalanx over with a soft tissue reefing medially

My approach is going to be fairly simple. I will do a Lapidus (first metatarsocuneiform arthrodesis), or

modify the Lapidus by doing an opening wedge osteotomy of the cuneiform

101. Congenital Hallux Varus

Definition
 Medial deviation of the hallux on the 1st MT that is present at birth
 May be an isolated deformity, but very often it is associated with other malformations of the foot:
o Short and thick first metatarsal
o Longitudinal epiphyseal bracket of the first metatarsal
o Accessory metatarsals and phalanges
o Duplication of the hallux
o Fibrous band that extends from medial side of hallux to the base of first metatarsal

Epidemiology : Rare condition, but the incidence has not been reported

Pathogenesis
 Reported to be associated with multiple malformations
 There are probably multiple causes, none of which have been identified

Clinical Features

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  The hallux is adducted by as much as 90 degrees, and cannot be aligned by passive manipulation
 There is a broad web space between the hallux and the second toe
 A firm subcutaneous band of fibrous tissue may be palpable along the medial forefoot
 There may be duplication of the hallux as a separate toe, or it may be associated with simple or
complex syndactyly
 Congenital hallux varus with complex polysyndactyly is commonly seen in Apert
syndrome

Radiographic Features
 AP xray will provide only partial anatomic detail of the abnormalities
 The varus alignment will be obvious
 Duplication of the phalanges in a hallux associated with polysyndactyly will also be apparent
 A rudimentary metatarsal duplication at the base of a fibrous band may not be visible because of
the lack of ossification at birth
 A longitudinal epiphyseal bracket will be suggested by the "D" shape of the metatarsal, with no
cortical differentiation along the convex medial border of the diaphysis.

Pathoanatomy
 A possible explanation for a single toe varus deformity is that two great toes, and perhaps a
metatarsal, originate in utero, but the medial or accessory one fails to develop
 The rudimentary medial structure forms a fibrous band that acts as a taut bowstring and pulls the
more fully developed hallux into a varus position, creating an incongruous first MTP joint
 In the foot with a longitudinal epiphyseal bracket, there is a varus deformity of the metatarsal,
creating the varus alignment of the hallux with the foot
 The MTP joint may be congruous, although there have been no published anatomic studies on this
aspect of the deformity
 The MTP joint congruity is similar to that seen in the opposite direction with juvenile hallux valgus,
and, as with the latter condition, it requires an operative approach that preserves joint congruity

Natural History
 Shoe fitting would be difficult or impossible without treatment

Treatment
 No role for conservative management
 Surgical management is mandatory, and depends on the individual pathoanatomy
 The literature is not particularly helpful in providing direction
 Soft tissue release and resection procedures with or without syndactylization to the second
toe are appropriate when the metatarsal is normal
 Unsatisfactory surgical results using these techniques were generally caused by the shortness of
the first metatarsal and rarely by symptoms or recurrent deformity
 Longitudinal epiphyseal bracket was not recognized at the time of that study, as indicated by the
radiographic images in the article
 Resection and interposition grafting of a longitudinal epiphyseal bracket is an effective technique
that leads to gradual correction of the varus deformity of the first metatarsal, and allows longitudinal
growth of the bone
 Interposition material can be fat, Silastic, or methyl methacrylate
 With adequate resection of the abnormal epiphysis and good anchoring of the graft, fat is an
excellent choice, and avoids the risks and potential complications of the foreign materials
 This procedure is combined with distal soft tissue release and resection of duplicated parts, as
indicated
 Hypercorrection of the first MTP joint should be avoided to prevent joint incongruity and progressive
hallux valgus

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  Late onset of degenerative arthrosis of the first MTP joint can be managed by arthrodesis
 Residual shortening of the metatarsal, with pain, callosities, or metatarsalgia, can be addressed
with metatarsal lengthening or amputation

102. Disorders associated with scoliosis

1. Freidrich‟s ataxia: scoliosis 100% of the time and kyphosis 66%, similar to idiopathic scoli, same
parameters for surgical correction/bracing
2. Klippel Feil: both congenital and idiopathic. Treat accordingly.
3. Marfan‟s:
 Scoliosis may be present and is relatively indistinguishable from that in other patients, but
in some patients, the vertebral height is notably increased
 Curve pattern frequently is either single right thoracic or double right thoracic and
left lumbar
 Tx same as idiopathic scoli
4. OI: Tx like idiopathic
5. CP:
 Usually in quadriplegic non-ambulators. The actual curve patterns differ. with CP curves
often being long, sweeping, unbalanced thoracolumbar curves with significant pelvic
obliquity. Mainly non-operative with seating support and bracing (temporary control).
 For the severely handicapped spastic quadriplegic, when to fuse is controversial, but
deterioration in function (particularly seating ability) and development of pressure sores are
relative indications.
 In the long, thoracolumbar or lumbar curves, consider extending the fusion to the sacrum, if
the pelvis demonstrates obliquity and is part of the curve. Posterior fusion with Luque wires
and Galveston pelvic fixation is probably optimal for the soft, osteopenic bone.
6. NF:
1. Nondystrophic is treated as idiopathic scoliosis but with close follow-up for development of
dystrophic component.
1. Curves apex right with longer curve
2. Cobb < 20 observe q 6 months
3. Cobb 20 – 35 brace & Xray q 6 months
4. Cobb > 35 posterior spine fusion with instrumentation
5. Cobb > 60 anterior release and bone graft + posterior fusion and instrumentation
2. Dystrophic
1. Curves tend to have short segments, sharp curves, severe apical rotation. Usu apex left
2. Cobb angle < 20 observe with x-ray q 6 months
3. Cobb angle 20-40 – Posterior spine fusion with instrumentation (even in young child –
minimal growth stunting will develop)
4. Cobb >50 Anterior and posterior spine fusion
7. Duchenne

103. Disorders of Cardiomyopathy

 Freidrichs ataxia
 Klippel Feil
 Marfan‘s: aortic regurgitation, aortic dilatation, aneurysms, and mitral valve prolapse
 Duchenne Muscular Dystrophy
 Down Syndrome
 Noonan Syndrome: mainly pulmonary valve stenosis

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BACK TO TOP

Spine
104. Important history aspects
Do not forget these two sentences. Remember them as a sentence.
1. Any constitutional symptoms: loss of weight or appetite, fever, chills, rigor, night sweats
2. Back pain: any radiation down the leg, any worsening with coughing or sneezing, any unsteady
gait, any bowel or bladder problems, saddle anesthesia, erectile dysfunction

105. Spiel for neurological examination (SPINE)

1. GAIT: I would start by inspection of the patient‘s gait checking for wide based or ataxic gait. I
would have the patient heel walk and then toe walk and then perform a tandem gait.
2. SPINE: LOOK, FEEL and MOVE
1. I would then inspect for alignment and posture and look for any hairy patches, dimples,
masses or bruises
2. I would then palpate down the spine looking for step deformities or tenderness, and for
paraspinal tenderness and spasm
3. I would put the patient thru a ROM including flex/ext, rotation and lateral bending.
3. NEUROLOGICAL EXAMINATION: motor, sensory, tone, reflexes, special tests, rectal
1. I would then perform a detailed motor and sensory exam in both the upper and lower
extremities and the trunk grading all muscle groups on the MRC scale and testing both
light touch and pin prick sensation according to the dermatomes and myotomes.
2. I would then check for general tone and clonus.
3. I would perform tendon reflex examinations including Hoffman, Babinski and abdominal
reflexes
4. I would then do SLR testing and femoral stretch test, test for Hamstring tightness
5. Rectal exam as appropriate for: rectal tone, voluntary contraction, pinprick sensation,
perianal sensation, and bulbocavernosus reflex
4. VASCULAR EXAM: of lower extremities
1. LOOK: I would inspect the feet and legs for color, hair distribution, nail changes, dry
skin
2. FEEL: I would check the peripheral pulses and check the capillary refill.

Root Sensory Motor Reflex

C1 -
C2 -
C3 -
C4 Top of shoulders -
C5 Regimental patch Elbow Flexion Biceps
C6 Radial forearm, thumb & index Wrist Extension Brachioradialis
C7 Middle finger Elbow Extension Triceps
C8 Ring & little fingers Finger Flexion (DIP of middle) -
T1 Ulnar forearm Finger Abduction (Little Finger) -
L1 Groin near inguinal ligament -
L2 Anterior upper thigh Hip Flexion -
L3 Anterior lower thigh Knee Extension -
L4 Medial aspect of foot Ankle Dorsiflexion Patellar
L5 Dorsum of foot Big Toe Extensor -

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 S1 Lateral aspect of foot Ankle Plantarflexion Achilles
Toe Abduction
S2 Posteromedial lower leg, thigh & buttock Bladder Sphincter -
S3 Perianal Anal Sphincter -

106. Dural Leak Spiel

1. I will alert the anesthetist about the tear and ask him/her to put the patient in Trendelenberg
position to decrease the amount of leakage
2. I will fully expose the durotomy (dural tear) by possibly extending my laminotomy proximally
and distally.
3. I will probe the tear with Penfield 4 to identify the extent of the tear and fully expose it.
4. I will cautiously use cottonoids and suction away from the nerve roots to obtain a dry field
5. I will use a 6-0 Nylon under Loupe magnification to obtain a running watertight seal starting
1mm proximal to the dural tear and extending 1mm distal to it, followed by a second pass back
to the proximal end of the tear and tie it.
6. I will ask the anesthetist to perform Valsalva maneuver and reverse Trendelenberg to
ensure that there is no leakage from my repair.
7. I may have to supplement the repair with Fibrin Glue (Tisseel).
8. I will close the wound layer by layer in a watertight fashion using non-absorbable sutures.
9. I will ask the anesthetist to ensure a smooth reversal of anesthesia so that coughing and
wretching on the endotracheal tube is kept to an absolute minimum.
10. I will keep the patient on supine bed rest for 1-2 days on IV antibiotics, mild narcotics,
laxatives and Foley catheter (to minimize straining)
11. I will observe the patient closely for any drainage from the wound or symptoms of dural leak
(e.g., headache)
12. If there is any drainage, I will send it for beta-2-transferrin in addition to gram stain and culture
and sensitivity.

If detected postoperatively:
1. D/D: CSF leak, infection, abscess, seroma, liquefied hematoma
2. Options: 1. re-operation and obtain a watertight seal repair, 2. subarachnoid drain, 3.
epidural blood patch, 4. percutaneous CT-guided fibrin glue injection.

107. Complications after neck surgery

 for laryngeal nerve palsy ENT consult, swallowing study, observe
 for vertebral artery injury pack, control, possible coil if stable to go to interventional, if can‘t
control, call neurosurgery for proximal and distal control
 for carotid artery injury needs stent by vascular
 retropharyngeal injury airway control, drain hematoma
 esophageal rupture Thoracics consult, ICU, NPO, ABx, debridement, ENT to pass NG-tube
 acute airway compromise stridorous on exam, laboured breathing  Intubate patient, fails
after multiple attempts

108. Indications for surgery in spinal metastases

o requirement of tissue for diagnosis
o treatment of an isolated lesion
o treatment of a fracture causing instability, pain, or spinal canal compromise
o radio resistant tumors, which usually include gastrointestinal and kidney metastases

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 o recurrent tumor in a previously irradiated field
o neurological symptoms that are progressive despite adjuvant measures
o potential instability.

109. Gun Shot Wounds Spine

1. removal of bullet in complete or incomplete for t1-t11, no difference
2. only if there is progressive deficit
3. or if there is an infection secondary to going through bowel that is causing either progressive
neuro, meningitis or septicemia

110. Spinal Infection (discitis/OM)

Pyogenic Vertebral OM
 thought to originate from the vertebral endplate.
 avg age 66 for vert and 16 for appendicular skeleton
 staph most common bug (in IV drug, most common pseudomonas)

Clinical
 neck or back pain, frequent night/rest pain
 Dx typically made > 3/12, getting better w more sensitive Dx measure
 meningismus common (can get in epidural abscess – kernigs)
 c-spine 10%, thoracolumbar the rest
 IV drug have more c-spine involvement
 Abscesses rare, epidural much more common than subdural
 Dx – ESR/CRP – MRI best (bright T2), bone scan also helpful
 Radiographs need 2-4/52 to show it.
 If disc space affected, almost always infection (miller CD)
 CT guided for tissue Dx or transpedicular biopsy

Non pyogenic infection (TB-Pott‟s)

 3 subtypes; anterior/peridiscal,central
 prediscal most common and starts in metaphysis and spreads under the ALL – can see
vertebral scalloping
 disc spaces relatively resistant to TB infection
 usually isolated in one body, resembles tumor (can be calcified)

Treatment
 goals of tx;
o eradicate dz
o pain relief
o preserve/improve neuro
o maintain/restore stability

 majority is NON surgical

o includes IV abx
o follow ESR/CRP
o brace for pain control
o 75% are cured with non-op
o TB tx w RIPE: Rifampin, Isoniazide, pyrazinamide, Ethambutamol for 12-18 months

 surgical indications;
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 o inability to get tissue closed
o presence of instability/deformity/fracture
o progressive neuro deficit (unless complete for >72hrs)
o sepsis (from vertebral focus)
o failure of medical management

 Almost always done anterior with tricortical iliac crest BG for 2 or less segments, can use fibula
for >2segments
 Fixation is controversial, most fix posteriorly after anterior I&D – some do fix anteriorly however

Iatrogenic infections (post op)

o Occur in 2-3% of procedures
o Discectomy 1% and fusion/instrumentation 4-8%
o Must be treated aggressively when recognized
o Layer by layer debridment
o Remove all bone wax and gelfoam
o Removal of bone graft controversial
 Most will remove loose pieces and leave the rest
o Retain hardware if acute and solid
o Remove hardware if;
 Failed and loose
 Recurrent/resistant infection
 Fusion is solid
o Meticulous hemostasis to avoid hematoma for nidus
o Strict deadspace closure

111. RA C-spine
o Frequency of Cspine involvement in RA – 34-86%
 Clinical variable that correlates most closely with Cspine involvement is presence of deformities in
the hand, particularly MCP subluxations
o Remember the articulations b/t O-1 and 1-2 are synovial and axial so no inherent stability is
provided by the articulations but rather by the ligaments such as the TAL
 Three RA deformities of the Cspine exist:
o Subluxation of C1 on C2 – result of either incompetent transverse ligament or erosion of the
dens – usually occurs as anterior subluxation but can be posterior or lateral
o Decrease in longitudinal distance between the dens and the brainstem - may be caused by
erosion of the O-1 or C1-2 joint or both – variably described as pseudobasilar invagination,
vertical settling, atlantoaxial impaction, cranial settling, or superior migration of the odontoid
o Subaxial subluxations (levels below C2) – caused by facet joint erosion and ligament
incompetence
o Progressive neuro deficits in 15-36%

Clinical findings
o Occipital neuralgia, ear pain (greater auricular branch)(both from C2 compression), facial
pain (trigeminal nucleus from settling), visual/equilibrium probs (vertebrobasilar insuff)
o Retention and incontinence
o Long tract signs
o Ranawat
o I – no neural
o II – subjective weakness w hyper-reflex and dysesthesia
o IIIa – objective weak w long tract signs – ambulatory

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 o IIIb – ‗ ‗ – non ambulatory

Imaging
AADI – N < 3mm, can be incr if transverse and alar ligs disrupted >1cm, all ligs disrupted
PADI – if <14mm – need flex/ext MRI to measure SAC & pannus, must fuse if PADI <14mm (PADI
preop of <10mm showed not recover w Sx)
SAC - <13mm critical value, must fuse if so
Use Ranawats measurement for cranial settling, >13mm N

Cervicomedulary angle of <135deg is pathologic of vertical settling

Surgical
Indications for surg
Neuro compromise (weakness/spasticity)
Impending neuro compromise
Cord compression on MRI
PADI < 14
SAC < 13
Intractable occipital headaches with proven instability
Procedures (depends on problem)
Reducible subluxation w/o neuro
Can do C1-2 via brooks/gallie or transarticular screws
Fixed subluxation w neuro OR partially reducible w PADI < 14mm
Decompression via C1 laminectomy with fusion (transarticular) – should not do brooks or gallie if
neuro symps present, as well can‘t do it here b/c have taken the lamina
Vertical settling
If Ranawat <12mm, need to do O-C2 fusion with lateral mass screw/plate or bars
Pannus resolves with stable fixation
Subaxial subluxations
Should be fused if SAC <13 or intractable pain or neuro deficit
Need to do posterior fusion +/- decompression
High risk of post of kyphosis if do an anterior procedure
Outcomes
Good pain relief
Less predictable neuro recovery, related to preop deficit
Class II – 60-100%
Class III – 20-60%
Preop PADI > 10mm is predictive of recovery from atlantoaxial subluxation
Preop PADI > 14mm is predictive of recovery if there was any vertical settling

112. Harvest of Posterior iliac crest bone graft

 straight longitudinal incision is made over posterior superior iliac spine;
 transverse oblique incisions are to be avoided because of the superior
clunial nerves which usually cross the crest 8 cm lateral to the PSIS;
 an alternative incision is an oblique incision from proximal-medial to distal-lateral, which is
parallel to the clunial nerves, and which is perpendicular to the posterior crest;
 as noted by Colterjohn et al 1997, this approach will improve superficial incision
tenderness, but will not affect deep tenderness;
 incise thru the subcutaneous tissues, and identify the fascia of glutues maxiumus which
blends in with the fascia of the external oblique;
 incise the maximus subperiosteally off of its origin;

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  using a key elevator, subperiosteally elevate the crest along the superior and lateral
surfaces;
 avoid incising thru or stripping the posterior ligamentous complex of the SI joint, since this
may lead to SI joint instability;
 inferiorly, the greater sciatic notch should be palpated prior to instrumenting in this area;
 injury to the superior gluteal artery is a potential complication of posterior crest harvest;
 in cases of superior gluteal vessel injury, also look for possible injury to the adjacent
ureters;
 bone graft can be harvested to within 1 cm of the notch;

113. Failed Back Surgery

o IN ORDER TO DISTINGUISH RECURRENT HERNIATED DISC FROM EPIDURAL
FIBROSIS, YOU GIVE CONTRAST. DISC WILL SHOW NO UPTAKE AND EPIDURAL
FIBROSIS IS ACTIVE INFLAMM SO IT WILL LIGHT UP WITH GADOLINIUM.
o MRI is also extremely sensitive for identifying inflammatory processes such as discitis, and in
fact, it is the test of choice when a postoperative disc space infection is suspected.
o Decreased signal intensity in the disc on the T1-weighted images and increased signal on the
T2-weighted images, particularly with enhancement following Gd-DTPA injection, all suggest
an inflammatory process

114. Paraplegia care: pre and postoperative care

 Airway : ensure that pt is in ICU for close monitoring of airway
 Breathing: arterial line for frequent ABG, watch for atalectasis by CXR
 Circulation: central line to assess JVP (must avoid hypotension), renal dose Dopamine
 Disability : think CNS/neuro for associated head injury (epidural hematoma)
 Every other system:
o Endo: Steroids? I‘m saying NO, but must mention your stance!
o MSK: needs frequent turns
o Hematologic: DVT prophylaxis
o GI: PUD prevention (especially if using steroids), stool softener (to avoid autonomic
dysrelfexia)
o GU: Foley catheter

BACK TO TOP

Upper Extremity
115. Spiel for Shoulder Arthroscopy

116. Subscapularis Lengthening

 Subscap lengthening for decr rom and glenohumeral wear secondary to previous non-
anatomic repair
 described in campbells as a coronal subscap lengthening:
 We cut the superficial lateral aspect of the tendon at the lesser tuberosity near the long head of
the biceps. We then split the tendon medially in the coronal plane. Finally, we complete the
medial aspect of the cut by transecting the remaining tendon and capsule adjacent to the
glenoid labrum. At the conclusion of the procedure we will suture the lateral end of the

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 superficial flap to the medial end of the deep flap. 20-30 deg of ER equals ~ 1cm of
lengthening.

117. Cuff Tear Arthropathy

o Do a delta if flexion is only to 70 deg and CTA if can flex preop greater than 70 deg.
o If deltoid is paralyzed, fuse the shoulder

118. Approach to Brachial Plexus Injury

Patterns
ERB‘s C5,6
Total c5-T1
Klumpke‘s c7-T1

Risk factors for poor outcome:

1. no biceps return by 3 months
2. Horner‘s syndrome ( so examine the kids eyes) – Ptosis ( droopy eyelid) miosis ( dilated pupil) and
anhydrosis( lack of facial sweating )
3. Total plexus involvement.

Associated injuries:
Clavicle fracture
Humerus fracture
Septic Shoulder

Treatment
Initially non–op: maintain passive ROM shoulder, elbow, wrist but ESPECIALLY EXTERNAL
ROTATION OF SHOULDER

Surgical
o IF no return by 3-6 months: Microsurgical repair of plexus. No role for neurolysis alone at any
age. Exploration of the plexus and reconstruction of avulsion and nonconducting rupture
injuries. Consider sural nerve grafts, intercostals or spinal accessory nerve transfers.
o IF you have flail arm AND A HORNERS then go for surgery 1-3 months.
o Shoulder Surgery
o Persistent IR contracture will lead to glenoid deformities and humeral head
abnormalities and even to frank dislocation.
o IF there is only mild increase in glenoid retroversion or slight posterior subluxation : can
do anterior musculotendonus lengthening of pec major and post lat dorsi and
teres major transfer to the rotator cuff.(l”episcopos)
o If there is more severe post glenoid flattening or even development of false glenoid soft
tissue procedure is no good but humeral derotation osteotomy is indicated.

o UPPER PLEXUS LESIONS ARE MORE LIKELY NERVE RUPTURE AND LOWER TRUNK IS
MORE LIKELY ROOT AVULSION
o Coexisting Horner‘s syndrome and diaphragmic paralysis are adverse prognostic factors, as is
o flaccid paralysis of the entire limb. The absence of a history of shoulder dystocia may be an
adverse prognostic factor as well.

o Adjunctive investigations such as MRI and EMG provide much less dependable prognostic
information than sequential clinical assessment and do not weigh directly on the decision to
intervene. They may have some role in planning the surgical exploration. MRI has supplanted

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 myelography as the imaging technology of choice for demonstration of pseudomeningoceles.
When traction on a nerve root causes a tear in the dura of the nerve root sleeve, a collection of
cerebrospinal fluid can form adjacent to the root, and if this collection persists and becomes
contained by a fibrotic membrane, the resulting cystic lesion is a pseudomeningocele. Traction
sufficient to tear the nerve root sleeve often causes avulsion of nerve rootlets from the spinal
cord, but the predictive value of pseudomeningocele detection as an indicator of root avulsion
is not perfect

Postganglionic
o Once a postganglionic lesion is diagnosed, a proximal donor nerve root will be available for
repair, or grafting.
o A nerve repair is performed when the nerve ends may be sutured without undue
tension.
o A nerve graft is indicated in a nerve rupture where the distance between the two stumps
does not allow tension-free cooptation.
 Standard fascicular grafts, using donors such as sural nerves, medial brachial or
medial antebrachial cutaneous nerves may be undertaken.
 Occasionally, Vascularized nerve grafts are used to maximize the amount of
nerve-graft material. A common indication is C8 and T1 avulsion in association
with large root stumps of the remaining plexus. The avulsion of the C8—T1 roots
makes the ulnar nerve, based on the superior ulnar collateral artery, an ideal
donor, as nerve repair or grafting will not reinnervate these distal muscles.

Preganglionic
o If a diagnosis of preganglionic lesion is made, there is no need to explore the brachial plexus
and the surgeon may proceed to neurotization.
o An uninjured, less important nerve is separated from its muscular insertion and then coupled
directly, or via free grafts, to the distal stump of a nonfunctioning nerve.
o Neurotization is only useful in avulsion injury to the upper roots, or if grafting is unsuccessful.
o Shoulder abduction is best performed with a spinal accessory to suprascapular nerve transfer.
o Elbow flexion is restored with an intercostal to musculocutaneous nerve transfer, preferably
without the use of an interposition graft.

119. Posterior shoulder dislocation

Treatment options
 Leave if little pain, elderly, etc, attempt gentle closed reduction if < 4 weeks (some
sources say can attempt CR if < 6/52, for missed anterior dislocations, NO CR >
4/52)(OR best) then immobilize 6/52; if unsuccessful either open or leave (cambells says no
CR for either beyond 3/52, risk of NV injury or # too high
 Pre-op CT to assess glenoid and humeral head deficiencies
 >30% glenoid deficient, need coracoid transfer or bone graft augment w screws
 If head defect 20-40% - open and Neer procedure or McLauglin
 If more than 40% - osteochondral allograft in <45 yrs and replace in older
 Allow glenoid erosion to guide graft vs TSA

120. Detailed Treatment of Posterior Shoulder Dislocation

 If interval between dislocation and diagnosis has been prolonged, sometimes preferable not to treat the
dislocation – frail, elderly, demented, unstable epilepsy or minimal functional impairment
 Active treatment for all other patients with the aim of achieving a congruously relocated, stable,
functional and pain-free shoulder

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Dislocations with Involvement of <40-50% Humeral Head Articular Surface and No Deformity or
Degenerative Changes
 Usually recognized in dislocations diagnosed immediately or within 6/52
 Most require reduction under conscious sedation or GA followed by assessment of stability
 Attempted closed reduction for dislocations with small humeral head defect that are diagnosed within
6/52
 Impression fracture is disimpacted and is cleared from the posterior glenoid lip with use of gentle
manipulation while the arm is flexed 90 and adducted
 ER at this stage will relocate the shoulder but should not be attempted until the defect has been fully
disengaged because of risk of fracturing the humerus
 Open reduction is indicated if attempted closed fails which is typical if the diagnosis is delayed and/or
there is a large humeral head defect
 Deltopectoral approach is most commonly used but provides limited access to the posterior glenoid
 Separate posterior approach is sometimes required
 Deltoid splitting superior approach is preferred by some surgeons
 Regardless of the approach, following arthrotomy of the rotator interval and prior to relocation, the
impression fracture should be disengaged from the glenoid rim under direct vision
 Following reduction, stability is assessed by internal rotation to establish the point at which
dislocation occurs
 Degree of instability is usually determined by the size of the anterior humeral head defect as it re-
engages
 If reduction is stable through full ROM (usually <25% head defect), immobilization in neutral or ER for
4/52
 If redislocates with IR, two choices: adjunctive stabilization or immobilization in more stable position of
ER with operative stabilization becoming more popular
 Aim of adjuctive stabilization procedures is to restore stability throughout a functional ROM thereby
preventing an acute redislocation
 Transposition of the subscap (McLaughlin) or with the LT (Neer modification) for larger defects - Neer is
preferred if there is a fracture of the LT
 Despite mention in all textbooks, this is falling out of favor because of the abnormal mechanics it
creates by altering the subscapularis function
 Rotational osteotomy has been described but rarely used
 These techniques are less successful when 33-50% of the head is involved – additionally there is a risk
of subscap dysfunction, leading to weakness of IR or contracture
 Disimpaction, elevation and autogenous bone grafting has been used more recently
 When remaining articular surface is not osteoporotic, deformed or arthritic, a sculpted osteochondral
humeral allograft may be preferable for large defects occupying up to half of the articular surface (this
is becoming the procedure of choice if you‟re not going to do a hemiarthroplasty)
 These are fixed with headless screws
 Functional results similar to subscap transfer
 Stability should be reassessed after the adjunctive procedure
 Inadequate restoration of stability may be due to posterior capsulolabral disruption or a displaced
glenoid fracture which may require stabilization

Dislocations with Involvement of > 40-50% of the Humeral Head Surface or with Deformity or
Secondary OA of the Humeral Head
 Most commonly seen when the diagnosis has been delayed or in older patients who have really soft
bone
 Open reduction and stabilization of the humeral head has been used to treat carefully selected,
younger patients with >50% defect
 Arthroplasty is more commonly used – both hemi and TSA – never directly compared for outcome
 Recognized technical problem is predisposition to posterior subluxation or dislocation due to capsular
and subscapularis contracture

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  To overcome this, do a capsular release and place the component in neutral amount of version
(rather than retroverting the component)
 Rarely excision or arthrodesis is considered for large defects

Fracture-Dislocations
 Dislocations with undisplaced LT treated like simple dislocations
 But ORIF is recommended for displacement
 LT can be fixed either anatomically or into the humeral head defect
 2/3/4 part – treated either with ORIF or arthroplasty determined by age and medical status
 Arthroplasty generally favored for multipart fractures in the elderly
 May be difficult to judge the appropriate prosthetic soft tissue tension and to obtain stable fixation of the
fractured tuberosities
 Head salvaging reconstruction for young adults with good bone
 ORIF is usually preferred
 Temporary transfixation wires may prevent displacement of undisplaced neck fractures during open
relocation
 Fixation
 2 part – simple interfragmentary screw
 Multipart – more complex tension band, buttress plate, or IM fixation
 Stability should be assessed intraop after fixation
 Neglected fracture-dislocations may be difficult to relocate and malunion makes things difficult
 If attempting arthroplasty, best to avoid osteotomy and realignment of the tuberosities as this can be
associated with nonunion, secondary displacement, and a poor functional outcome
 In many cases, joint excision or fusion may be the only technically feasible option

Outcome and Complications

 Risk is high and worse when late diagnosis, large humeral head defect, secondary humeral head
deformity and arthrosis, or when fracture is associated with dislocation
 May redislocate after reduction
 Osteonecrosis has been reported following simple dislocation but more often after internal fixation
 Risk increases with increased fracture displacement and extent of involvement of the tuberosities
 Following anatomic reconstruction, head may continue to be perfused by intact posteromedial vessels
or alternatively by creeping substitution
 AVN may be associated with satisfactory function
 Symptomatic patients treated with arthroplasty
 Stiffness often develops and can be debilitating

121. Approach To Posterior Recurrent Instability of the Shoulder

Indications/Contraindications
 Not as common as anterior and usually young, athletic presenting as recurrent posterior subluxation
rather than dislocation
 Not in and of itself an indication for surgery – 2/3 respond to physio of ER and scapular stabilizers
which usually decrease symptoms but instability may remain
 No patient with instability should have surgery who has not had 6/12 rehab
 Surgical procedures aimed at returning athletes back to their sport are usually unsuccessful and repair
in the athlete should be done for pain and instability with the primary indication being recurrent,
symptomatic, unidirectional subluxation that has failed to respond to a comprehensive non-operative
program
 Two other clinical syndromes need discussion:
o MDI needs to be ruled out and if present, rehab in all directions and if this fails, need
stabilizing in all directions and may require extensive inferior capsular shift from posterior or
combined approaches

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 o In addition, some patients with overly tight anterior repair may lead to gradually increasing
symptomatic posterior instability – in these patients, anterior subscapularis lengthening may be
more effective (coronal Z lengthening described in Campbells)
o Second syndrome, suprascapular nerve injury and weakness of infra and supraspinatus with
posterior subluxation secondary to weakness – so attention to the nerve injury and rehab rather
than posterior capsule
 Posterior capsular repair is contraindicated in ligamentously lax or MDI
 If surgery is indicated, need a capsular shift procedure
 Bony abnormalities are rare
 With significant arthritis, capsular repair can make symptoms worse
 Relative contraindication – although lax and able to posteriorly sublux, does not have enough
symptoms to warrant surgical repair/patient hasn‘t done physio

Preoperative Planning
 Typical patient has injury occurring while arm is in a position below shoulder level – often with direct
blow from AP direction followed by recurrent symptomatic subluxation
 Feels shoulder slip, pop or click in and out
 Episodes often occur with the arm in the frontal plane
 Dynamic subluxation occurs as the patient begins to raise the arm upward, it reaches a point in
the arc where the shoulder slips posteriorly and as the arc of elevation is continued, relocation occurs
 May or may not be painful
 Most important preoperative assessment is to document that the patient has an isolated posterior
instability rather than MDI
 Try to elicit ligamentous laxity
 Attempts should be made to center the humeral head in the glenoid by a load and shift test and to
subluxated the shoulder anteriorly, posteriorly, and inferiorly
 Hallmark physical finding of MDI is a sulcus sign
 Isolated posterior instability often can be subluxated in a posterior direction by the examiner who
grasps the humeral head and pulls directly backward
 Load and shift/posterior drawer +ve in posterior direction but -ve in all other
 May also be able to demonstrate posterior subluxation as the arm is brought into the frontal plane at 90
degrees and internal rotation force is applied
 Posterior apprehension, though rare, should be tested with arm forward elevated and internally rotated
followed by posterior stress causing sense of instability, pain or painful subluxation
 ROM usually normal as is strength but may see external rotation weakness
 Xrays to include AP in IR and ER, lateral and axillary
 Rarely show bony changes but may see bony reaction along the posterior rim but unusual to have
reverse Hill-Sachs
 Rarely CT arthrogram or MRI
 If there is any doubt about the diagnosis – EUA or arthroscopy

Surgery
 GA, lateral decubitus
 Arthroscopy with 10lb traction on the arm to first assess articular cartilage and rule out associated
anterior Bankart – after, release traction
 Landmarks for incision – posterior aspect of AC (just medial to posterolateral corner of acromion) and
the posterior axillary fold
 10 cm saber cut made beginning posterior to the AC joint 2cm medial to posterolateral acromion and
continue inferiorly to axillary fold
 Skin flaps are raised exposing underlying deltoid, deltoid split in line with fibers from the spine in an
area 2-3cm medial to the posterior corner of the acromion distally about 5cm
 Not necessary to detach any deltoid but is retracted exposing underlying infraspinatus and teres minor
and heavy overlying fascia which is divided

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  This interval is poorly defined so easier to open between two heads of infraspinatus identified by
stripe of fat and opened from it‘s lateral tendinous insertion to just medial to the glenoid (taking care not
to go further than 1.5cm medial to glenoid because of risk to suprascapular nerve)
 Infraspinatus dissected free from capsule medially and laterally
 Capsule is divided from lateral to medial in its midportion to the edge of the posterior glenoid
labrum – in 95% labrum intact and if so, can be used to hold sutures when advancing the capsule
(transverse)
 Next a T incision made in the capsule medially along the edge of the glenoid labrum creating a
superior and inferior flap which are tagged
 If labrum is damaged and reverse Bankart present, similar to conventional repair except that the labrum
is resected
 Three or four #1 ethibond passed through the labrum from inferior to superior
 Inferior capsular flap is advanced superiorly and medially and sutures are mattressed through the
capsule beginning inferiorly and proceeding superiorly
 Sutures are tied with arm in neutral
 Superior flap is brought over the inferior flap and advanced distally and medially
 Then previously tied sutures are mattressed through the superior flap to make a double layer at the rim
of the glenoid
 Lateral split in the capsule is repaired in a side-to-side fashion with #1 absorbable and if necessary the
split in infraspinatus is repaired
 Split in deltoid is closed with absorbable #1 then subcutaneous tissue and skin
 Sterile dressing and abduction pillow with elbow kept posteriorly to coronal plane

Postoperative Management
 Abduction pillow for 3/52; at 3/52, brought down to side and allowed IR
 Gentle ROM with an overhead pulley
 Active ER within 3/52 initially with submaximal isometric and then progressing to more resistive
exercises but no forward flexion until 6/52

Summary of Recurrent Shoulder Posterior Instability

 Make sure it‘s not MDI
 Adequate trial of rehab
 Posterior approach between infraspinatus and teres minor
 Dissect capsule but not too far medial (suprascapular nerve)
 T capsulotomy with horizontal limb at the mid-glenoid and the ver
limb and the margin of the glenoid
 Take the inferior flap and bring it superior and medial
 Then take the superior flap and bring it inferior and medial
 Close the horizontal limb
 Abduction pillow for 3/52 with gentle ROM overhead
 No forward flexion until 6/52

122. Distal Biceps Two Incision Technique

Boyd and Anderson Technique (modified)
 Make a 3- to 4-cm incision over the anterior aspect of the elbow (but proximally anterolateral, crossing
obliquely and extending medial and distal if needed)
 Incise the deep fascia and locate the distal tendon of the biceps; usually it is retracted 5 to 7.5 cm
proximal to the elbow
 Protect the LABC during this dissection, identified between brachialis and brachioradialis (most
commonly injured)

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  Pass a heavy nonabsorbable (#2 Fiberwire) suture through the tendon so that its ends emerge on
the avulsed surface
 Then with a hemostat locate the tunnel between the radius and ulna through which the tendon
originally passed
 Flex the elbow and make a second incision on the posterolateral aspect of the elbow
 Incise over the hemostat through the deep fascia overlying the CEO
 The CEO and supinator are then split down to the radial tuberosity with the arm in full pronation to
protect PIN
 Then pronate the forearm and bring the radial tuberosity into view
 Now use a high speed burr to make a trapdoor in the tuberosity to accept the tendon and drill two
(or three) holes opposite the cavity
 With a tendon carrier or a hemostat pass the ends of the nonabsorbable suture in the biceps
tendon between the radius and ulna and bring them out through the second incision
 Use traction on the sutures to pull the tendon through into the posterolateral incision
 Now thread the ends of the suture into the trapdoor and bring them out through the holes in the
bone
 Flex the elbow and insert the end of the tendon into the cavity; hold it in position with forceps and
securely tie the suture
 Place reinforcing sutures through the tendon into the adjacent soft tissues and close both incisions

Post Op
 With the elbow flexed to 110 degrees and the forearm in moderate supination, a posterior plaster splint
is applied
 After 2/52 splint and the sutures are removed and new posterior plaster splint is applied for 3-4/52 after
which gradually increasing active exercises are started
 Full ROM should be possible by 6-8/52 but return to full activities should be delayed for at least 12/52

123. Stiff Elbow

Surgical Treatment Options
 Open, arthroscopic or combo
 Indications for surgical release of contractures:
o Impairment of function with usually > 30 FFD or < 120 flexion (negotiable)

Lateral Column Approach

 After raising a fasciocutaneous flap, lateral column of the elbow is exposed
 Starting proximally, the lateral supracondylar ridge is exposed proximally to the epicondyle by
subperiosteally reflecting the ECRL anteriorly off the humerus and the lateral triceps off
posteriorly
 Dissection is continued 2-3cm distally through the CEO from the epicondyle (in a line toward
Lister‘s)
 This generally passes in the interval between ECRL and ECRB along the anterior edge of EDC
 The entire anterior soft tissues are then reflected anteriorly off the capsule, which can then be
excised
 The release should continue down to the level of the collateral ligaments
 When elevating brachialis off the scarred anterior capsule, it is safer to dissect proximal to distal to
avoid crossing a nerve embedded in the scar tissue
 Also technically easier to dissect between brachialis and capsule rather than to dissect it off and then
try to separate it
 Posteriorly, triceps is raised off the back of the humerus and dissected off the posterior capsule (see
diagram below)
 Capsule is then elevated from the humerus and olecranon fossa which is cleared off scar tissue and
osteophytes

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  When dissecting medially, the ulnar nerve is at risk – safer to expose the nerve either through a
separate medial approach or underneath the triceps from the lateral side
 Nerve runs along the medial border of the triceps adjacent to the intermuscular septum – nerve can
then be exposed along its course and protected – anterior transposition may be required

Medial Column Approach

 Dissection is conceptually similar
 After transposing the ulnar nerve, the pronator teres muscle origin is reflected from the medial
supracondylar ridge down to the level of the medial epicondyle
 The common flexor-pronator tendon is split longitudinally for 2cm distally
 The brachialis and the anterior portion of the flexor-pronator group are dissected subperiosteally off
the anterior humerus and capsule – proximal to distal
 Capsule is then excised
 If there is any concern about the radial nerve, a separate limited exposure can be made on the lateral
side, so that the lateral capsule can be excised under direct vision
 Posterior release from the medial side is identical to lateral BUT ulnar nerve must first be transposed
 Collateral ligaments are preserved with both along with the common extensor and flexor-
pronator tendons
 Collateral ligament release is required to subluxate the elbow and thereby release intra-articular
adhesions or to perform an interposition arthroplasty
 In long standing contractures, may be necessary to release the posterior band of the MCL if
decreased flexion after initial release
 Upon completion, CFO and CEO tendons are reattached to the epicondyle and supracondylar ridge
through drill holes – if sufficient tissue is left on the bone, drill holes are not necessary
 Skin is closed over drains

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*collateral ligaments are not released in either column procedure. They are released when intraarticular
adhesions need to be released or for interposition arthroplasty (>50% articular surface destroyed)
Post Operative Care
 Lightly wrapped in bulky dressing with anterior slab from shoulder to hand
 Once neuro status is confirmed, indwelling axillary catheter is placed and CPM is started from full
flexion to extension
 1st 24 hours, out of CPM for no longer than 5 minutes at a time
 Usually hospitalized for 3 days
 CPM for 3-4/52
 May continue using splits after that
 Indomethacin is recommended for high risk (with cytotec)

Results
 Patients regain about 50% of lost motion
 95% gain 10 degrees or more
 80% gain functional arc

Complications

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  For open, 10-30%
 In order of frequency: wound infection, neuritis or neuropathy, HO, excessive scar and pain
 Delayed onset neuropathy in patients whose loss of flexion is acutely increased with procedure causing
compression in the cubital tunnel – occurs in first couple days
 Should transpose in all < 100 flexion
 Nerve injuries in arthroscopic release can be decreased by:
o Use of retractors
o Avoiding the use of suction around nerves
o Use of shaver instead of burr around nerves
o Knowledge of where nerves are and/or visualizing them
o Recognizing limits of surgical expertise

Hetertopic Ossification of the Elbow

 3% of simple elbow dislocations
 20% of fracture-dislocations
 Then most often seen in neural axis trauma, below the level of the spinal cord
 5-10% of closed head injury and most commonly on side of hemiplegia
 Greatest risk (76-89%) head injury and elbow trauma
 Thermal or electric burns
 Secondary to Boyd approach for distal biceps repair
 When it develops anteriorly is usually beneanth brachialis muscle
 When it forms posteriorly it is in line with the jt beneath the triceps, most common site to cause jt
ankylosis

Prevention
 NSAIDs
 External beam radiation 700 cGy

Clinical Presentation
 Clinically presents as local soft tissue swelling, tenderness, warmth and progressive loss of
elbow motion – and can be mistaken for infection
 Pain is not usually the predominant symptom
 Can occur any time between 2-12 weeks
 Labs – transient fall in Ca, rise in PO4, alk phos rise within 2-4/52 and peak at 3-4x normal at 3-4/12
 Bone scans can reveal abnormal uptake in first several weeks and remain abnormal for up to 1 year
 Follow with xrays
 Initially fluffy, ill defined periarticular density
 With time, margins become more distinct
 Radiographic maturity defined as the ability to identify sharp cortical margins commonly takes 3-5/12
– and it is now recognized that surgical intervention can safely proceed at this time (in children may be
prudent to wait, at least until physes close to prevent premature closure as well as possibility of
spontaneous resolution)

124. Elbow instability (terrible triad – coronoid/rad head #/elbow dislocation)

 Usually secondary to posterior dislocation
 Reduce and get preop CT
 Posterior incision and develop flaps, start lateral
 Interval usually done for you, if not, use kocker distal and BR/lat triceps proximally
 Assess radial head, if sig communution, plan to excise, if not, fix w headless screws to buried
small frag in safe zone (100deg arc defined by bisecting the rad head when forearm in neutral
rotation)
 If rad head is screwed then resect and plan for replacement

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  For coronid #, decide how best to fix, either retro screws through ulna or suture w fragment
and capsule through ulna bone tunnels.
 Then fix LUCL to isometric pt of lat epicondyle in center of capitellum w suture anchors or bone
tunnels
 Next test stability, should have arc of 20-130 of stability. If unstable to valgus on medial side,
this is OK
 If still unstable either posterior or posterolateral the must;
o Check all reductions
o If OK, decide to open and fix medial side or hinge fixator
o The McKee paper uses fixators only for revision settings and will fix the medial side if
still unstable

125. DRUJ pathology

Differential of Ulnar Sided Wrist Pain:
ulnocarpal impingement, TFCC tear, DRUJ incongruity, DRUJ instability, hamate #, pisiform #,
pisotriquetral OA, ECU tendonitis, FCU tendonitis, ulnar styloid #

 Three of the most common are:

o Malunited Colles fracture
o Malunion or nonunion of the radius
o Cessation or abnormality of growth of the distal radius
 Discrepancy in length can be treated in one of three ways:
(1) the length of the radius can be restored
(2) the ulna can be shortened
(3) the distal ulna can be resected, either partially (hemi-resection arthroplasty) or entirely (Darrach
procedure)

 Dysfunction of the DRUJ is a frequent source of persistent complaints after distal radial malunions
 Characteristic symptoms include pain, decreased forearm rotation, decreased grip strength, and instability
 Can be caused by malunion of fractures into the sigmoid notch, injuries to the TFCC, and palmarly
displaced malunions of ulnar styloid fractures
 In a kinematic study, radial shortening produced the most profound changes, decreased radial
inclination and dorsal tilt led to moderate changes, and dorsal displacement caused minimal changes in
joint kinematics - 6 mm of radial shortening caused DRUJ dysfunction****
 If the radial deformity is unacceptable, a distal radial osteotomy alone frequently realigns the DRUJ,
especially if radial shortening is 6 mm or less
 If a positive ulnar variance remains after distal radial osteotomy, an ulnar-shortening procedure can
be done as well
 Three types of ablative procedures:
 Complete ablation of the distal ulna (Darrach procedure)
 Partial resection of the distal ulna (Bowers and Watson arthroplasties)
 DRUJ fusion with proximal ulnar pseudarthrosis (Sauvé-Kapandji procedure)
 Darrach procedure most commonly recommended for symptomatic DRUJ problems in patients who are
elderly, debilitated, or have low functional demands, or to salvage other failed DRUJ procedures
(performed 2.5cm prox to ulnar styloid)

For the exam approach to the DRUJ: Need to determine if there is:
1. Ulnocarpal impaction
2. DRUJ arthritis
3. DRUJ instability

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 If isolated instability, don‘t go chasing the malunited distal radius with an osteotomy or try to
shorten the ulna, use split ECU for volar instability and split FCU for dorsal instability, if both
volar and dorsal instability use the brian adams procedure (see diagram below)
 If they have ulnocarpal impaction, decide if you can restore radial length with an opening wedge
osteotomy with tricortical ICBG or if you need to shorten the ulna
 If they have arthritis and they are young, do a Bowers hemiresection and PL interposition – the
other choice is a Sauve–Kapandji
 If they are older, you can do a Darrach but be aware that the entire carpus can fall off the side
once you have removed this restraint and they‘ll be weak – don‘t do a Darrach in a young person
 If they have advanced wrist arthritis, you‘ll need to do a wrist fusion and you could incorporate a
Sauve-Kapandji to restore some prosupination

Clinical Scenarios:
Ulnar impaction syndrome – chronic TFCC tear, ulnar shortening osteotomy  arthroscopic TFCC
debridement
Acute instability
ulnar styloid # - ORIF if large fragment (k-wire and tension band wiring)
ORIF associated # (eg Galleazzi) and reassess DJUJ, soft tissue/bony stabilization, immobilize in
above elbow cast in reduced position (supination), consider open reduction if irreducible and soft
tissue repair, consider K-wire across DRUJ
Essex-Lopresti lesion- radial head, interosseus and DRUJ injury: treat with ORIF radial head, if
unreconstructable-replace with titanium prosthesis
Nonunion/malunion distal radius- may cause ulnar impaction/TFCC tear-consider osteotomy of radius
with ICBG or ulnar shortening osteotomy (correct pathologic anatomy)

Summary
Impingement
Darrach – Low demand patient or previous wrist fusion – stabilize stump with volar capsule: Resect
about 2 cm of distal ulna
Feldon wafer procedure – less than 4 mm positive
Ulnar shortening osteotomy – more than 4 mm positive

Instability
TFCC repair - if peripheral TFCC tear
FCU /ECU/ Pronator quadratus stabilization if reconstructible
Sauve Kapandji procedure if not reconstructible
Kleinman-Greenberg (ECU and P. quadratus stabilization ) - For Post Darrach

Incongruity
Synovectomy
Resection Hemiarthroplasty (need intact TFCC): Dorsal approach, preserve ECU sheath, reshape distal ulna,
ablating DRUJ, may need to shorten ulnar styloid
Sauve-Kapandji for Rheumatoids: Dorsal approach,protect sensory branch of ulnar nerve, decorticate DRUJ,
stabilize with pin, ostetomize 15 mm, preserve ECU sheath, stabilize stump with Pronator quadratus, , fix DRUJ
with two 3.5mm screws.

Brian Adams procedure (Moro uses this)

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For the Brian Adams the graft used is PL, dorsal approach is through 5 th compartment and volar b/t
N/V bundle and flexor tendons

DETAILED DRUJ PROCEDURES: DARRACH, BOWERS, SAUVE-KAPANDJE

Darrach Resection of Distal Ulna

Operative Technique
 Expose the distal ulna through a medial longitudinal incision
 Incise the periosteum longitudinally and reflect it from the distal ulna with care to avoid
otherwise perforating it
 About 2.5 cm proximal to its distal end, drill holes transversely through the ulna and complete
the division of the bone with bone-biting forceps and lift the distal fragment outside the wound
 Divide the capsule of the joint close to the articular cartilage
 Divide the styloid at its base and leave it attached to the ulnar collateral ligament
 Then reef and plicate the periosteal envelope and ligament to stabilize the end of the bone

Postoperative: No immobilization is necessary and active exercises are allowed POD#1

Indications:
Symptomatic DRUJ problems in patients who are elderly, debilitated, or have low functional
demands, or to salvage other failed DRUJ procedures

Advantages
 Rotary motions of the forearm usually are restored, and pain is relieved within a few weeks after
surgery
 Motion in the wrist was improved, especially pronation, supination, and ulnar deviation, and in some
cases dorsiflexion
 All patients had improvement in grip and function of the hand and had less than 30 degrees of
restriction in pronation and supination
 May be useful for some malunions and nonunions of the radial shaft with DRUJ incongruity - in
nonunions of the radius or malunions with overlapping of the fragments without fracture of the ulna,
radial shortening produces a derangement of the articular surfaces of the distal radioulnar joint and if
shortening is marked, the joint can become dislocated secondarily
 If the malunion or nonunion is of long duration, the soft tissues may have so contracted that length of
the radius cannot be restored at surgery, even after the fragments have been thoroughly mobilized
 Rather than attempting to bridge the defect and restore the length of the radius, resecting the distal
ulna and grafting the shortened radius with the two fragments in apposition may be the best alternative

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Disadvantages
 Resection of the distal ulna results in loss of the ulnar support of the carpus and alters axial loading
characteristics of the wrist
 Decreased grip strength, pain, and instability of the ulnar stump (usually caused by excessive
resection) are all potential complications
 If the ulna has been resected at a level proximal to the pronator quadratus, the distal ulna may
subluxate dorsally on pronation and cause pain and disability; if the disability warrants surgery, a
tendon graft can be looped around the ulna and the tendon of the flexor carpi ulnaris (Bunnell) with the
tendon graft then joined to itself by a removable running suture of stainless steel wire holding the ulna
anteriorly (FCU for dorsal, ECU for volar instability)

Bower‟s Hemiresection of Distal Ulna POSSIBLE ULNAR SHORTENING:

Indications
(1) unreconstructable fractures of the ulnar head
(2) ulnocarpal impingement syndrome with incongruity of the DRUJ
(3) RA involving the DRUJ
(4) posttraumatic arthritis and osteoarthritis of the DRUJ
(5) chronic painful TFC tear

Contraindicated:
if there is no reconstructable TFCC because without the TFCC, hemiresection interposition technique is not
believed to have a significant advantage over ulnar shortening techniques

TECHNIQUE 66-20 (Bowers)

 Begin the incision 5-7 cm proximal to the ulnocarpal joint on the dorsal aspect of the distal ulna
 Extend the incision distally and at the level of the ulnocarpal joint curve or angle palmarward for about 1
to 2 cm
 Carefully protect the cutaneous nerves to the skin in the area and expose the extensor retinaculum
and the distal ulnocarpal area to the fascia
 Elevate retinacular flaps, raising a proximal flap based laterally and a distal flap based medially
 Develop these flaps for exposure and for tissue for ECU or TFC augmentation
 Otherwise, reattach the flaps, use them for coverage of the arthroplasty, or excise them
 If ECU is stable, reflect it laterally with subperiosteal dissection to expose the distal ulna
 If ECU is unstable, mobilize it distally to its insertion on the 5th metacarpal
 Use the proximal flap to fashion a sling, pass it around ECU, and suture it to the 4th extensor
compartment
 After the retinacular flaps have been elevated, detach the radioulnar joint capsule distally, laterally
(radially), and proximally, and reflect it medially (ulnarward) to expose the articular surface
 Remove the synovium, the ulnar head articular surface, and subchondral bone with osteotomes
and rongeurs
 Remove osteophytes around the sigmoid notch and remove all subchondral bone of the ulnar
head
 Leave the styloid axis and ulnar shaft resembling a tapering, 1-cm dowel
 Carefully inspect the TFCC - central perforation repairs are not necessary
 With the wrist in ulnar deviation, compress and rotate the radial and ulnar shafts and if there is
ulnocarpal abutment or impingement, consider ulnar shortening
 If it cannot be determined preoperatively or during surgery, fill the radioulnar space with a ball of tendon
or muscle and stabilize the tendon to dorsal and volar capsules with sutures
 Use tendon from PL, ECU, or FCU (other choices include plantaris, long toe extensor)
 This interposition helps prevent radioulnar shaft approximation and stylocarpal impingement
 Close the wound by first replacing the ECU compartment or use a retinacular flap
 If shortening is not required, close the wound and apply a short arm bulky dressing with dorsal and
palmar splints

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  If ulnar shortening has been done, use a sugar-tong splint to control rotation

After Treatment
 Splint and sutures are removed at 2/52
 Wrist splint is worn for an additional 2/52, and finger motion is encouraged
 If ulnar shortening was done, a short arm cast is worn for another 2/52, and then a short arm wrist splint
is worn until healing is complete
 If shortening was done in the ulnar shaft, a splint or cast is worn for 8-12/52

Sauve-kapandji

Fernandez recommended this technique for patients with fixed DRUJ subluxation and concomitant
joint destruction associated with intraarticular fractures of the distal radius

Technique
 incision is made between the ECU and EDQ, beginning 5 cm above the ulnar head and ending
distal to the ulnar head
 care is taken to avoid cutting the dorsal ulnar sensory nerve;
 care is taken to avoid disturbing the ECU tendon sheath, and instead the dissection proceeds
thru the tendon sheath of the EDQ;
 ulnar neck and proximal aspect of ulnar head are exposed;
 The surface of the ulnar head and the sigmoid notch of the radius were debrided of any
remaining articular cartilage using rongeurs and osteotomes, taking care to achieve
appropriate rotation of the head.
 The shaft and neck of the distal ulna were exposed between the tendons of the extensor
(ECU) and flexor carpi ulnaris (FCU) muscle
 The length of the resection is equal to the required ulnar shortening plus 10 to 12 mm which is
the desired length of the pseudarthrosis.
 Resection was done with an oscillating saw without cooling the blade.
 The prepared surfaces of the distal radio-ulnar joint were opposed, and the guide wire of an
AO 3.5 cannulated screw positioned centrally from the ulna into the distal radius.
 Only the first cortex, the ulnar cortex of the ulnar head, was drilled and tapped and a partially-
threaded screw, of correct length, with a washer was inserted.
 There was usually good compression and a graft was not required, but cancellous bone from
the ulnar resection can be added in or around the fusion site.
 A Kirschner wire of 1.6 or 2.0 mm diameter was passed through all four cortices from the neck
of the ulna into the distal radius to achieve rotational stability.
 Mobilize the pronator quadratus into the defect left by the resected ulnar shaft to prevent bone
bridging;
 Pronator is achored by drill holes made in the dorsal side of the ulnar stump;
 The capsule was closed with absorbable sutures.

Distal Ulna Resection

 preop get x-rays of contralateral wrist to template,
 plan resection of 2-3 mm wafer of ulna.
 Risks include infection, non-union, neurovascular injury to dorsal cutaneous branch of ulnar
nerve or ulnar nerve proper, ulnar artery.
 Consent for ulnar shortening osteotomy, possible DRUJ debridement or hemiresection
 Need small fragment set, arthroscope.

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  Arthroscopist to repeat arthroscopy to debride any further flaps if necessary.
 Position patient supine, arm on arm-board, tourniquet and pre-op antibiotics.
 Longitudinal dorsal approach over ulna to allow exposure of DRUJ if necessary,
 Find and protect dorsal cutaneous branch of ulnar nerve (at level of retinaculum)
 Perform z-plasty of extensor retinaculum over 5th dorsal compartment (EDM),
 retract EDM and ECU,
 plan osteotomy 3-4 cm proximal to metphyseal-diaphyseal junction,
 select 6 hole LCDCP,
 Should mention that homens should be placed around ulna during drilling and sawing to
protect ulnar nerve
 apply to ulna and drill, measure and tap holes proximal to osteotomy,
 remove plate,
 mark rotation of ulna,
 perform transverse (or oblique) osteotomy approx 2-3 mm in width (width of saw blade),
 appose bone ends and affix plate to distal fragment,
 place resected bone around as bone graft,
 repair retinaculum.
 If necessary open DRUJ to debride.

Post-op ulnar nerve palsy. Should mention that homens should be placed around ulna during drilling and sawing
to protect ulnar nerve. Repeat history and physical including neurological exam and vascular exam including
Allen’s test if possible. Try to differentiate between whether this was an ulnar nerve palsy at elbow or at wrist.
Examine extrinsic ulnarly innervated muscles (FDP to D4 and D5 and FCU). If these are affected, assume
compression neuropathy at elbow and manage expectantly. If these are normal, then assume distal complete
ulnar nerve palsy, as this was not visualized during surgery, and plan decompression. Position supine, forearm
supinated, tourniquet in place, pre-op antibiotics. Volar approach along radial side of hypothenar eminence,
curving across flexor creases and proximally in line with FCU tendon. Mobilize FCU tendon ulnarly, revealing
ulnar nerve and artery (nerve is more ulnar). Dissect distally, dividing volar carpal ligament, the roof of
Guyon’s canal. This passes between pisiform ulnarly and hamate radially. Just distal to Guyon’s canal,
superficial branch to palmaris brevis and sensation to ulnar 1 ½ digits separates from deep branch to remaining
intrinsic muscles.

126. TFCC Tears

o if ulnar positive variance, then the TFCC tear is aggravated by ulnocarpal impingement and
you should shorten the ulna in addition to debriding the TFCC tear. You can shorten it by
doing an arthroscopic Feldon procedure (where you shave down 2-3 mm of the distal surface
through a hole in the TFCC) or doing a formal open shortening osteotomy of the ulna. When
you do the shortening, you can actually extend the incision distally and open the DRUJ and
look at the TFCC, debriding it open.

o if ulnar negative or neutral variance, then all you can really do is debride the TFCC tear

127. Hook of Hamate Fractures

o on physical exam, resisted FDP to little finger often reproduces their pain because it goes
right beside the hook.
o look for it on carpal tunnel axial view
o treatment is a cast, and if it doesn‘t unite, excision.
o when doing the excision, you have to start back in Guyon‘s canal, expose the ulnar nerve
and artery, then follow them distally. If you just go digging in at the hook, you‘ll likely cut
the nerve, as it goes right around the hook.

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128. Complex MCP Dislocation
o The approach to getting them reduced is VOLAR.
o Zig zag approach.
o You have to be aware the neurovascular bundle is pulled down and is draped over the
metacarpal head – so you have to be very careful that you just cut through skin and nothing
deeper to that.
o Then, to help you reduce it, you can release the A1 pulley – this allows you to move the flexor
tendon around abit more.
o Insert a howarth elevator to try to pry the proximal phalanx back. Reduce the volar plate – this
will help.
o Then, if necessary, you can cut the volar plate longitudinally if you still can‘t get it reduced.

129. Scaphoid Fracture

o Acute: 6 weeks long arm thumb spica, then 6 weeks short arm (for waist) – then X-ray and CT
o When doing waist nonunions, do from volar side with intercalary graft and Herbert bone screw.
o Do proximal pole fractures from the dorsal side
o remember: if you approach from the volar side ( Russe approach – incision starts proximally
over the FCR tendon and curves radially over the volar tubercle of the scaphoid along the
margin of the glaborous skin of the thenar muscles.) Bite off the volar lip of the trapezium to
obtain a better line for your screw.

Approach To Scaphoid Non-Union

 Full history and physical
 Xrays to include AP and lateral
 Additional dedicated scaphoid views include PA in ulnar deviation (which elongates the scaphoid) and a
grip PA which will assess SL ligament
 If fracture suspected, thumb spica for 2/52 then rexray out of cast or MRI (or bone scan)
 If fracture treated and persistent pain, CT best way to assess union
 MRI or bone scan best way to assess AVN

Mack Classification of Non Unions (5 types)

Type I Stable Nonunion
 Require volar Russe approach which allows better correction and preserves dorsal blood supply
 Russe is volar approach centered over the scaphoid tubercle longitudinal interval b/t fcr and radial
artery.
 Autogenous tricortical iliac crest first
 Vascularized if this fails
 Internal fixation with Kwires or with differential pitch (Herbert or Accutrak screw)
 In the absence of cyst formation, collapses or sclerosis, may benefit from percutaneous screw fixation
without bone graft (this is usually done dorsally)

Type II Unstable Nonunion

 Require correction of deformity and grafting
 Show carpal collapse or scaphoid fragment displacement
 On lateral see VISI and radiolunate angle > 15
 CT helps with planning
 Angulation and shortening can be addressed simultaneously as intrascaphoid angles, lateral and PA,
can be assessed on plain xray
 Normal lateral angle is < 35, PA angle should be > 35
 Significant bone loss is noted from the volar and ulnar side of the scaphoid
 Placement of a wedge graft corrects the humpback deformity and realigns the scaphoid

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  Take bone from the crest – trapezoidal graft combined with internal fixation
 Again, volar approach with Herbert screw

Type III Scaphoid Nonunion with Mild Carpal Arthritis

 Unstable nonunions show degenereative changes between the distal scaphoid segment and the radial
styloid
 Presence of arthritis can be assessed with CT
 First evidence is beaking of the styloid and joint space narrowing between the radial styloid and the
distal pole
 If only styloid, can do a short oblique styloidectomy (but no more than 4mm because it will affect the
intercarpal ligaments) combined with grafting
 Another option is excision of the distal fragment with preservation of the ligaments
 An unstable scaphoid fracture in the presence of moderate arthritis involving the radial styloid
and the scaphoid fossa mandates salvage – either with four corner fusion and scaphoid
excision OR PRC
 These maintain motion, carpal height and strength
 Pain relief is variable
 Radial styloidectomy should still be performed if there is impingement when the wrist is taken through a
ROM
 If the presence of capitolunate arthritis, no PRC
 Carpal alignment should be corrected when performing a four corner fusion – use the spider or
hubcap plate – lunate tilt should be reduced
 Bone graft from the excised scaphoid and styloid can be used

Type IV and V Scaphoid Nonunion with Carpal Arthritis

 Development of midcarpal arthritis distinguishes type III from IV/V and mandates salvage
 Type IV differs from type V in the development of radiolunate arthritis
 Wrist arthrodesis is the procedure of choice
 Dorsal approach between 3rd and 4th, Z lengthen extensor retinaculum, don‘t violate the DRUJ, PIN
neurectomy, decorticate all bony surfaces, 10 degree extension plate from Synthese onto the 3rd
metacarpal +/- proximal row carpectomy

Special Considerations
 AVN most commonly occurs with proximal pole
 Look for punctuate bleeding when debriding nonunion site
 Get a preop MRI
 One option is a vascularized bone graft from the distal radius using a 1,2 intercompartmental
supraretinacular artery graft
 The artery branches from the radial artery proximally and rejoins it in the snuff box
 Graft comes from the radius between the 1st and 2nd extensor compartments with the pedicle based
distally

Post Op
 Immobilize in spica cast for minimum of 4/52 then thumb spica splint
 CT to assess union – some say 50% bridging bone while others use 75%

130. Perilunate injuries

Typical scenario is type 4, complete lunate dislocation w transcaphoid # and median nerve
compression
 Try to reduce in ER (traction, extension then flexion w thumb on lunate)
 If not, must reduce in OR open (use CTR incision in line w 4th MC just ulnar to thenar crease)

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  Dissect to ulnar side of PL and identify the flexor tendons beneath. Median nerve is medial in
the carpal tunnel. Must take transverse carpal ligament to expose the tunnel, can then reduce
lunate and repair volar capsule
 Must then use russe incision to fix scaphoid unless you can do it dorsally when you go b/t 3 rd
and 4th to fix the dorsal ligs.
 Must fix scaphoid first, pin it to capitate and lunate and then examine any other torn structures
and fix them primarily.

Approach To Perilunate Injuries

 Lunate is connected to the scaphoid and the triquetrum by strong interosseous ligaments which allow
the proximal row to move in synchrony
 Disruption leads to dysynchronous motion within the proximal row – ―dissociative carpal instability‖
 Proximal row is attached to the distal row by capsular ligaments
 Disruption of the capsular ligaments causes incongruity and abnormal motion between the proximal
and distal rows – ―nondissociative carpal instability‖
 Mayfield described the sequence of perilunate disruption by placing cadaver wrists under extreme wrist
extension resulting in four stages of instability:
o Stage I - Disruption of the SL ligament
o Stage II – Force propagates through the space of Poirer and interrupts the lunocapitate
connection
o Stage III – LT connection is violated and the entire carpus separates from the lunate but the
lunate remains aligned with the radius the remainder of the carpus dislocates – usually dorsally
o Stage IV – most severe, lunate dislocates from its fossa into the carpal tunnel – lunate rotates
on its intact palmar ligaments and the capitate becomes aligned with the radius
 Prefix ―trans‖ is applied to any fractures
 Lesser arc injury – purely ligamentous disruption
 Greater arc injury – fractures of the osseous structures around the lunate

Diagnosis
 May complain of median nerve symptoms
 Get good xrays
 Definitive finding is loss of colinearity between the radius, lunate and the capitate
 In stage III, capitate is dislodged from the lunate, usually dorsally
 In stage IV, lunate is dislodged from the radius, usually volar, rotating on its intact volar ligaments with
the concavity facing downward (―spilt tea cup sign‖)
 Carpal bones of the proximal and distal rows will appear crowded
 Lunate which is normally trapezoidal, will appear triangular or wedge shaped
 CT, MRI and arthrogram play limited role

Treatment
 Try a closed reduction early by applying 10-15lb traction plus some sedation and after 5-10 minutes of
traction, thumb on the lunate, hyperextend the wrist and then flex it over the lunate – may hear a pop
 Get post-reduction xrays and assess carpal tunnel symptoms
 Look for associated fractures, SL widening, scaphoid flexion, measure SL angle (usually 30-60) and will
often be >70 as the scaphoid flexes and the lunate goes into DISI
 Plan for operative treatment urgently if closed reduction unsuccessful and relatively soon if successful

Operative Treatment
 Some talk about percutaneous but this has limited role
 Open is preferred – either volar, dorsal or combined
 If lunate is reduced, start dorsal with standard longitudinal incision between 3rd and 4th compartments
 Expose capsule and extend the tear longitudinally with elevation of flaps

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  Assess carpus for chondral damage and adequacy of lunate reduction (capitate head should be
completely covered by lunate)
 LT ligament is usually too torn for primary repair
 SL often is avulsed from scaphoid and may be able to be reattached
 First pin the SL joint with 0.045 inch Kwire
 Non absorbable 3-0 polyester sutures placed through the torn interosseous ligament for
reattachment to the scaphoid and sutured to remaining cuff or placed through drill hole OR use suture
anchors
 Add Kwire across scaphocapitate joint
 After SL ligament repair, LT joint is reduced and pinned
 Now turn attention to volar side and do an extended carpal tunnel incision, through the transverse
carpal ligament and antebrachial fascia
 Retract flexor tendons and median nerve and visualize the volar wrist ligaments as well as the tear
across the midcarpal joint – repair this rent with 3-0 non-absorbable
 After closure, sugar tong in slight extension
 Remove sutures at 2/52 and place in long arm cast, converted to short arm at 4/52 and remove wires at
3/12
 If trans-scaphoid fracture, fix with Herbert screw first and proceed as above (the difficulty is determining
where to fix it from, plan volar incisions carefully if you have to release the carpal tunnel as well, can
make two volar incisions or try and fix scaphoid from dorsal, probably best to make two volars)

131. Carpal Metacarpal OA

Classification (Eaton)
 I – prearthritis (slight joint space narrowing)
 II – slight narrowing of CMC joint
 III – marked narrowing CMC joint (STT not involved)
 IV – pantrapezial arthritis

Treatment
Non-Operative
 NSAIDs, splints and steroids

Operative
Arthrodesis (for stages II and III) of CMC is good choice for laborers
o Advantages – good pain relief, stability and length preservation
o Disadvantages – decreased ROM, non-union 12%, and STT joint not treated
Technique
 Supine, hand supinated on hand table, tourniquet
 Palmar curved incision exposing the proximal 2/3 of the thumb metacarpal and the dorsal and palmar
sides of the trapeziometacarpal joint
 Identify and protect the branches of the superficial radial nerve and EPB tendon
 Detach the abductor pollicis longus tendons with a portion of the joint capsule for later reattachment
 Reflect the thenar muscles distally
 Incise the dorsal and palmar capsule and expose the joint
 Use a burr to remove the articular cartilage and the subchondral bone down to cancellous bone
 Slightly round the base of the thumb metacarpal and make a matching shallow concavity in the
trapezium
 Preserve the overall shape of the joint to avoid undue shortening of the thumb
 Use a small osteotome to make small, shallow cuts in the bone surface
 Insert crossed K wires to firmly hold the joint in about 30-40 degrees of palmar abduction and about 30-
35 degrees of radial abduction ("clenched fist")
 Using a small drill point or a Kirschner wire, make drill holes to outline a rectangular corticocancellous
graft on the dorsum of the thumb metacarpal

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  Connect the drill holes with a small osteotome to mobilize the corticocancellous "sliding graft"
 Make a rectangular recess in the dorsum of the trapezium to receive the graft
 Move the graft proximally into the trapezial recess and impact the graft
 If needed, stabilize the graft with an additional Kirschner wire or screws to avoid graft displacement
 Reattach the abductor pollicis longus tendon to the joint capsule and close the skin
 Over a non-adhering dressing apply a cast padding and a thumb spica

Options for stage II and III include:

 Metacarpal extension osteotomy – gained popularity with 93% improvement at 7 yrs
 Trapezial resection and ligament suspension (or suspension arthroplasty) has emerged as the favored
approach in most patients (aka LRTI)(ligament reconstruction and tendon interposition)

Technique
 Expose the thumb CMC through an incision along the radial border of the MC, curving ulnarly in
the distal wrist flexion crease as far as the FCR tendon
 Reflect the thenar muscles extraperiosteally from the metacarpal and volar aspects of the trapezium
 Reflect the APL palmarward
 If xrays reveal only trapeziometacarpal arthrosis, excise distal half of trapezium
 If pantrapezial arthrosis or severe thumb-web contracture, excise it all – but don‘t damage FCR in the
process
 Remove a portion of the trapezoid if needed
 Excise only the articular surface of the thumb metacarpal
 Make the hole in the base of the radial cortex of the thumb metacarpal with a 6mm gouge
 Split the FCR longitudinally for 10-12 cm leaving it attached distally
 Seat the metacarpal in a medial direction toward the index metacarpal and stabilize it in the abducted
position with a longitudinal Kwire
 Pass the free end of FCR into the canal and out the metacarpal hole
 Pull the tendon slip tight and suture it to the lateral periosteum then onto itself
 Fold the remainder of the tendon to act as a spacer and suture it to itself and the deep palmar capsule
 Transfer the EPB proximally and insert it on the metacarpal shaft to augment the metacarpal
abduction and remove the hyperextension-deforming force
 Thumb spica post op

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132. SLAC
Five key radiographic features of SL lig disruption
1. Scaphoid is flexed
2. Scaphoid ring sign
3. Distance between proximal aspect of the ring to the proximal pole of the scaphoid is <7mm
4. SL gap >3mm
5. Lunate and triquetrum are dorsiflexed

Dynamic SL instability
 Apparently very common cause of young adult wrist pain
 Normal xray findings but + watsons
 Tx 90% pain relief w blatt capuslodesis (uses slip of dorsal capsule to attach to dorsal distal pole of
scaphoid to help extend and stabilize scaphoid
 SLAC stages
o Stage I - joint space narrowing between the styloid of the radius and the distal outer aspect of
the scaphoid
o Stage II – degenerative changes along the entire articular surface between the radius and the
scaphoid
o Stage III –narrowing of the capitolunate joint
o Stage IV – pan carpal degeneration

Treatment
Operative Treatment
 Stage I
o Intercarpal arthrodesis either STT or SC maintaining alignment of scaphoid to longitudinal axis
(50-55 degrees)

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 o Radial styloidectomy performed simultaneously and consisting of removal of 7mm dorsal and
4mm volar improves wrist motion
 Stage II or III
o Motion preserving reconstructive procedure, either 4 corner fusion (CLHT) with scaphoid
excision or PRC
o 4 corner causes 15-20 degrees more loss of wrist ROM than PRC
o 4 corner failure in 30%

 For these fusions, the majority of the procedure is very similar to a wrist fusion with the exception of the
extent of the incision, the amount of decorticating necessary and the implant itself

STT Fusion

 Make a transverse incision in the skin on the dorsum of the wrist over the area of fusion (can also be
longitudinal)
 Retract the branches of the superficial radial nerve and the veins
 Open the extensor retinaculum along the tendon of EPL
 Approach the wrist between ECRL and ECRB or, as recommended by Kleinman, expose the wrist
capsule between the 1st and 2nd compartments, exposing the adjacent surfaces of the STT joint and
retracting the radial artery
 Open the STT joint and open the capsule to expose the proximal articular surface of the scaphoid
 STT fusion is contraindicated in the presence of significant radioscaphoid arthritis
 If this is found, SLAC wrist reconstruction should be done
 Observe the following principles as recommended by Watson:
o Careful planning is essential
o Minimum necessary joints should be fused
o Packed, cancellous bone graft arthrodesis with sufficient graft
o External dimensions of the fused unit must equal the external dimensions of the same bones in
their normal state
o Only the joints to be fused should be pinned

 Careful attention to the reduction of the scaphoid is required to avoid fixing the scaphoid in an
excessively longitudinal or dorsiflexed position
 Insert 0.045-inch K-wires through the scaphoid into the carpus to maintain this reduction and correlate
the reduction by inspecting the reduced dorsal surface of the proximal pole of the scaphoid and the
dorsal aspect of the lunate
 The longitudinal axis attitude of the scaphoid should be 30 degrees or more to avoid excessive
longitudinal orientation of the scaphoid and subsequent radioscaphoid impingement
 Remove articular surfaces of the trapezium, trapezoid, and scaphoid
 Kleinman's modification of removing only the dorsal two thirds of the articular surfaces allows
preservation of the carpal height, maintaining the contact surfaces of the palmar one third
 Obtain AP and lateral xrays to confirm acceptable reduction of the scaphoid and closure of the
preoperative SL diastasis
 Usually three 0.045-inch Kirschner wires are used to secure the scaphoid, trapezium, and trapezoid
 Two pins pass from the trapezoid toward the scaphoid, and one passes across the trapezium-
trapezoid joint
 Remove all hyaline cartilage and subchondral bone
 Bone graft can be obtained from the distal radius or from the iliac crest (I‘m going to use crest, it‘s just
easier)
 Control bleeding and close the donor site wound and pack the cancellous bone into the defect left in
the STT joint
 Watson recommends placing pins by passing 0.045-inch Kirschner wires retrograde out through the
raw bony surfaces

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  After the scaphoid, trapezium, and trapezoid are positioned for fusion, the pins are then drilled across
the fusion site in an antegrade direction
 To maintain the proper position of the scaphoid with the proximal pole depressed into the radial
articular surface, the distal pole is elevated, as noted previously, and two pins can be used to secure
the scaphoid to the capitate for temporary maintenance of reduction
 Avoid passing the pins from the intercarpal arthrodesis into the radius or ulna
 Ascertain that the spaces between the bones have been thoroughly packed with bone graft and that
the external dimensions of the fusion unit are the same as the external dimensions of bones in the
normal wrist
 As an addition, cortical bone graft can be used to bridge the fusion site on the dorsal surface and
requires mortise fitting or notching into position
 Pins are driven across the surfaces previously prepared
 Check wrist motion to be sure that no pins obstruct radiocarpal motion and cut the pins off just
beneath the skin
 Deflate tourniquet, obtain hemostasis, insert drains as needed, and close wound
 Apply a bulky compression dressing with a long arm plaster splint

So in summary:
 Acute SL dissociation – repair with suture anchors and pin scaphoid to capitate and lunate plus cast
8/52 (may do this up to 6/12 or so) – similar to perilunate
 Late SL dissociation – treatment depends on presence of arthritis:
o No arthritis – Blatt
o Stage I – STT with styloidectomy
o Stage II/III – 4 corner with scaphoid excision and styloidectomy or PRC

133. Wrist Fusion

 Supine with tourniquet
 Prep the forearm and the crest if you‘re using autograft
 Standard dorsal approach from the distal aspect of the 3rd metacarpal extending proximally on the ulnar
side of Lister‘s tubercle and stopping 5-7 cm proximal to the radiocarpal joint
 Incise down through skin carefully and cauterize any bleeders as they appear
 You will be in the area between the tendons of the 3rd and 4th compartments
 You will need to raise full thickness flaps on either side of the incision and will have to carefully incise the
epitenon off the tendons
 Be very careful as you are coming proximally down the 3rd metacarpal to encounter the extensor
retinaculum – you must not cut this in advertently
 Continue raising your flaps, expose the tendons of the 2nd, 3rd, 4th and 5th compartments as well as the
proximal and distal aspects of the extensor retinaculum
 You will be able to use your finger laterally to develop the plane – and will have to get way radial to expose
the styloid and scaphoid
 Take any fat on the tendons off with the flap
 Extend up onto the distal radius just ulnar to Lister‘s tubercle and 3cm or so proximal – but DON‟T enter
the DRUJ
 Now you are ready to make a Z lengthening type cut in the extensor retinaculum (which will later allow you
to close it primarily over your plate)
 Once you have your retinacular flaps isolated and retracted ulnarly and radially, isolate the contents of
each of the four extensor compartments and place fine piece of rubber around each to use as retraction
(take 4th and 5th ulnarly, and 2nd and 3rd radially)
 Now you are looking at capsule
 And just sitting on capsule, under the 4th compartment tendons, above capsule, is the PIN with its
accompanying veins – dissect it out, use some cautery, and resect 2cm of the nerve – this functions to
denervate the joint and is a billable code (PIN neurectomy)

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 Starting distally on the 3rd metacarpal, start raising your medial and lateral flaps subperiosteally – make
sure you are on the center of the 3rd metacarpal and distal enough to get three screws in it, continue
proximally along the capitate, lunate, and onto the distal radius, just ulnar to Lister‘s and proximal to it
 Now that you have those flaps raised, you are looking at the 3rd metacarpal, your first and second carpal
rows and the distal radius (better not see the DRUJ or the TFCC which are both close by)
 If you are performing a proximal row carpectomy, do it now – do this by hyperflexing the wrist and start with
the scaphoid (the procedure would be the same at this point if you were doing a 4 corner with a scaphoid
excision except you wouldn‘t need to get so far onto the 3rd MC and not so far proximal)
 If you can take it out in one piece, great – if not, use a rongeur – but be careful volarly as your median
nerve isn‘t too far away, especially with the wrist flexed
 To get the scaphoid out, release all of the intercarpal ligaments with a 15 blade
 Once the scaphoid is out, take the lunate and then the triquetrum – if you‘re really good, they will all come
out in one piece and you could actually assemble the first row on the back table
 And remember when taking these out, be careful volarly as you would like to preserve the volar capsule
 Now check with your finger that you haven‘t left any bony bits in
 Perform your radial styloidectomy (you would do this for an STT too)
 Then decorticate all of your joint surfaces with a burr which include – the 3rd MC/capitate, capitate/hamate
(careful here to only decorticate the dorsal half the proximal hamate), capitate/trapezoid, the old
capitate/lunate, the distal radius (but being careful over on the ulnar side near the DRUJ and TFCC)
 Use an osteotome slightly wider than the plate to dig a very shallow trough in the distal radius to accept the
plate – but don‘t go too deep because you want that strong cortical bone for support
 So now you‘re ready to check your position, bone graft and plate
 You want to make sure that the hand is aligned in 5 degrees ulnar deviation and neutral flexion/extension
(and usually this will require a slight ulnar translation of the 2nd carpal row)
 Harvest your bone graft and make it into very small pieces – pack it between the carpal bones, the 3rd MC
and the distal radius but keep graft away from the DRUJ
 Now the plate – hold it in place so you can get 3 of the 2.7mm screws in the 3rd MC, hopefully 1 into the
capitate and 3 into the distal radius which are 3.5mm (if you don‘t take out the proximal row, you may only
be able to get 2)
 The first hole that you drill is in the 3rd MC – hold the plate in the middle (checking on either side of the
bone to ensure you are centered because it is small, and if you are off to one side, you could crack it),
mark it with cautery or preferably a marking pen, remove the plate and drill – then put the plate back on,
and depth gauge
 Place the 2.7 mm self tapping screw
 Now drill one of your distal radius screws (which are 3.5mm) through the plate and place the screw
 Now beware that despite having a screw proximal and distal, it can still shift through the middle so be sure
that you are happy with your alignment before you place your third screw
 Check alignment and screw length with fluoro
 Pack in any extra graft under the plate if possible
 Let down the tourniquet and cauterize any bleeders
 Place a drain through the apex of the proximal part of the incision
 Close the periosteal flaps over the plate with 3.0 vicryl and the extensor retinaculum with #1 vicryl (cover
the retinaculum over the plate but under the tendons, otherwise much higher incidence of tendon rupture)
 Try to get as much plate coverage as you can
 Interrupted 2.0 vicryl to close subcutaneous tissue followed by running subdermal 3.0 monocril and staples
 Volar and dorsal slabs
 Case done.

134. Radius Malunion

 Know volar approach cold
 Has been a common question on the FRCS exam for last few years
 Principles are

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 o Volar approach for volar malalignment – correct to 10deg volar tilt w tricortical BG and
plate
o Dorsal approach for dorsal malalignment – correct to 5-10 deg of volar tilt w posterior
open wedge tricortical and plate
o Check ulnar variance when done, may need ulnar shortening

135. Scaphoid #
 Many different scenario‘s of scaphoid non-union
Scenario 1
 Waist non union w no deformity and no avn
 Russe w bone graft
Scenario 2
 Waist w some humpback and no avn
 Same
Scenario 3
 Prox pole nonunion w avn
 Can excise fragment and interpose some dorsal capsule (like a blatt I think)
Scenario 4
 Waist # w avn of prox frag
 Here can think about vasc bone graft (1,2 supraretinacular artery vasc BG)
Scenario 5
 Signs of SNAC – same as SLAC but usually radio-scaph is preserved, is this actually true?
 Do same procedures as in SLAC section above

136. Keinbock‟s
Local pain, tenderness, and decreased grip strength; slightly larger wrist circumference

ddx – Keinbock‘s, subtle carpal instability, ganglion, tenosynovitis

What are the associations to Keinbock‘s?

- trauma – repetitive or single; although, severe trauma (perilunate dislocations) often do not get this
- ulnar variance – the ulnar negative wrist
- vascular anomalies in supply – having only one feeding vessel rather than two
- shape

- it is bilateral in 15%

X-rays: remember that to assess ulnar variance (the ulnar variance view) the forearm must be in
neutral rotation. The easiest way to do this x-ray is with the patient seated, shoulder abducted to 90,
elbow flexed to 90, and the forearm in neutral rotation, and the x-ray aimed right at the wrist joint, not
at the forearm or hand.

What is ulnar minus? 3 millimeters is considered pathologic.

4 stages:
1 – pre-radiographic
2 – sclerosis
3A – fragmentation and early collapse without scaphoid rotation
3B – fragemetation and early collapse with scaphoid rotation

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4 – collapse and arthritis

- assess collapse with carpal height ratio – carpal height / 3rd metacarpal height

There are a number of scenarios. The first differentiation is the EARLY vesus ADVANCED
Keinbock‘s – based on the scaphoid rotation.

- ie. Stages 1 to 3A versus 3B and 4

In stages 1 to 3A (pre-scaphoid rotation) and the ulna is short (ulnar minus), then start with a radial
shortening, which seems to be simpler than the ulnar lengthening. Favero favors a volar approach
to the distal radius through FCR sheath. Cuts the radius near the metaphyseal/diaphyseal junction so
that he can get a plate with a few good screws in the distal fragment. Often you only need a few
millimeters of shortening. Apply the plate and compress across the osteotomy.

In stages 1 to 3A (pre-scaphoid rotation) and the ulna is NOT short (ulnar neutral), then you cannot
do a radial shortening. In this case, probably best to start with an intercarpal fusion – ie. STT fusion,
or try to change the joint biomechanics by doing an osteotomy to increase the radial inclination (ulnar
closing wedge or radial opening wedge). Other possibility would be a revascularization procedure,
but these sound pretty experimental.

In stages 3B (post-scaphoid rotation), basically, you have some collapse of the carpus. The scaphoid
rotates (flexes) as the capitate collapses. You‘re kinda screwed here. At this stage, you can excise
the lunate and do a limited carpal fusion (either an STT or scapho-capitate), or do a proximal row
carpectomy if the proximal pole of the capitate is not severely degenerative.

NOTE: the prerequisites for doing a PRC are 1. an intact lunate fossa, and 2. an intact
proximal pole of the capitate (although some say that mild degenerative changes on the
capitate are not a contraindications to PRC).

In stage 4, there are fairly advanced degenerative changes. The choices here are pretty limited, and
basically come down to the patient‘s functional demands.
- If active and want some wrist motion – lunate excision and scapho-capitate fusion
- If just want pain relief and don‘t mind the idea of a stiff wrist – wrist arthrodesis

137. Carpal Tunnel Release

 Curved incision ulnar (5mm) to and paralleling the thenar crease and extend this proximally to the flexor
crease of the wrist, where it can be continued farther proximally if necessary
 Angle the incision toward the ulnar side of the wrist to avoid crossing the flexor creases at a right angle
but especially to avoid cutting the palmar sensory branch of the median nerve, which lies in the
interval between PL and FCR
 Maintain longitudinal orientation so that the incision is generally to the ulnar side of the long finger axis
or aligned with PL
 Incise and reflect the skin and subcutaneous tissue
 Identify the deep fascia of the forearm proximal to the carpal tunnel by subcutaneous blunt dissection
proximally and incise it, taking care to avoid the median nerve beneath it
 Place a blunt dissector beneath the fascia to dissect the carpal tunnel contents from the transverse
carpal ligament
 Identify the distal end of the transverse carpal ligament

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  Carefully divide the transverse carpal ligament along its ulnar border to avoid damage to the median
nerve and its recurrent branch, which may perforate the distal border of the ligament and may leave
the median nerve on the volar side
 The strong fibers of the transverse carpal ligament extend distally farther than is generally expected
 As emphasized by Cobb et al., the flexor retinaculum includes the distal deep fascia of the forearm
proximally, the transverse carpal ligament at the true carpal tunnel, and the thick aponeurosis between
the thenar and hypothenar muscles
 Take care to release all components of the flexor retinaculum
 Be aware of anomalous connections between FPL and the index FDP, anomalous FDSs muscle
bellies, as well as anomalies in the PL, hypothenar muscles, lumbrical muscles, and in the median and
ulnar nerves
 Avoid injury to the superficial palmar arterial arch, about 5 to 8 mm distal to the distal margin of the
transverse carpal ligament
 Inspect the flexor tenosynovium
 Tenosynovectomy occasionally may be indicated, especially in patients with RA
 Close skin with 4-0 nylon
 Compression dressing and volar splint but hand is actively used ASAP, sutures out at 14 days and
splint off at 2-3/52

138. PIP Joint Fusion

- place the PIP joint in maximal flexion, and remove the distal end of the proximal phalanx w/ a
volar slope;
- articular cartilage is removed from the base of the middle phalanx;
- as the finger is brought from a hyperflexed to a slightly flexed position, the transected bone ends
are brought under tension;
- position of fusion:
- 20-25 deg of flexion in the index finger;
- 30 deg of flexion in the long finger;
- 40 deg of flexion in the ring finger;
- 40-50 deg of flexion in the little finger;
- fixation:
- longitudinal K wire is placed across the joint;
- oblique K wire is placed across the joint;

needs to be fused in 10-20 deg flexion, 20 deg pronation, and 20 deg of abduction;
- tension band can neutralize the distraction force of the finger flexors (which are stronger than
extensors and therefore cause distraction);
- dorsal incision is made over the joint;
- extensor tendon is split longitudinally and halves are retracted;
- joint surfaces are molded into opposition;
- because of the cam shape of the phalangeal (or metacarpal heads) more molding is required on
the volar surface (where visualization is difficult);
- transverse drill hole is made thru dorsal surface of distal bone segment;
- stainless steel wire is then inserted thru the hole;
- it is easier to perform this now, rather than after transected bone surfaces have been
reduced and fixed;
- two parallel K wires are placed across the joint to provide rotational stability;
- wires are first inserted retro-grade thru the proximal bone segment's dorsal bone surface at
the mid point;
- joint is reduced in desired position of flexion;
- wires are then driven down meduallary canal of distal fragment;

160
 - angle is fusion is controlled by flexing the digit (to appropriate level) and driven wires parallel
to dorsal phalangeal surface;
- tension band wire is then figure of 8 wrapped over dorsal surface of bone, and wrapped around
protruding K wires of proximal fragment;
- K wires are bent, cut, and rotated;
- tension wire is tensioned w/ needle driver;
- wire is cut, and bent;
- after one week, the other digits can resume normal ROM;
- fusion usually occurs at 4-6 weeks;

139. Rheumatoid Wrist

Distal Ulna instability:
1. synovitis and attenuation in pre styloid recess of ulna and attenutation of stabilizing ligaments
2. DRUj synovitis
3. Synovitis of ECU sheath

Patients with persistent synovitis, despite a 6-month trial of disease-modifying antirheumatic drugs
and anti-inflammatory medications supervised by a rheumatologist, may be considered for
prophylactic surgery. Options include tenosynovectomy, wrist synovectomy, and DRUJ stabilization.
Surgery to prevent wrist deformity, such as tendon transfer of the
extensor carpi radialis longus to the ECU, also should be
considered.

risk factors for tendon rupture include:

1. persistent tenosynovitis,
2. dorsal dislocation of the ulna,
3. the so-called scallop sign (ie, bony erosion over the ulnar
side of the distal radius).

Patients with two or three of these risk factors were given the
option of prophylactic
surgery, which seemed to prevent tendon rupture in most patients.

If you have an EDM rupture, it may be clinically silent b/c of EDC5

or the juncturae tendinae however it is a sign of impending tendon
ruptures…like EDC 5. Get on with some surgery !

Can‘t extend fingers?

1. Ext tendon ruptures
2. MCP subluxation
3. Extensor tendon subluxation into valleys ( sagittal band rupture)
4. PIN compression at elbow from synovitis

On full passive wrist flexion, the tenodesis effect of intact extensor tendons normally causes MC P
joint extension. When the finger can actively be held in full extension once it has been passively
positioned, then tendon subluxation caused by sagittal band attenuation is likely.

Tenosynovectomy is unlikely to be of value when the associated joints are stiff or ankylosed
because of arthritis or deformity. With tenosynovectomy you remove all bony prominences such as
ulnar head, listers tubercle

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For the unstable distal ulna, a distal ulna resection (Darrach procedure) or a distal radioulnar joint
fusion proximal resection (Sauvé-Kapandji procedure) is indicated to prevent further tendon
abrasion.

Flexor tendon ruptures

Most common is FPL ( mannerfelt – Norman) and then FDS to index

The Mannerfelt lesion occurs when the distal pole of the scaphoid
and trapezium pierce the volar wrist capsule, causing FPL tendon rupture.

**Extensor tendons usually rupture ulnar  radial, Flexor tendons rupture Radial  ulnar.

FPL rupture: treatment options

1. IP fusion of thumb **Most reliable option

2. Palmaris longus transfer – since usually ruptured in carpal tunnel
3. FDS ring transfer to FPL

FDP index rupture:

1. DIP fusion
2. side to side FDP transfer

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140. Rheumatoid Wrist (Vaughan Jackson)
History
 Patients usually present reporting sudden inability to actively extend the MP joint of the small finger
 This is seldom associated with significant discomfort, although symptoms of pain, instability, or catching
of the DRUJ may be present
 Often, a history of swelling is reported on the dorsum of the hand and wrist due to extensor
tenosynovitis and underlying joint synovitis that may have been present for months to years
 If medical attention is not sought in a timely fashion, patients may note that active MP extension of the
ring, long, and, finally, index fingers is lost in succession
 It is important to elicit a history of wrist and MP joint pain or dysfunction that preceded the inability to
extend the digits
 Anatomic abnormalities of these articulations may influence the choice of available methods of surgical
reconstruction

Physical
 In patients with RA who have relatively normal MP joints, loss of active extension is clinically obvious
 The MP joints are among the most commonly affected articulations in patients with RA
 Subluxation of the extensor tendons and the joints are particularly common deformities
 Extensor tendon subluxation is usually visible, and these patients are often able to maintain MP
extension once the joint is passively positioned, further distinguishing them from the patient with tendon
rupture
 The presence of fixed deformity that cannot be passively corrected and radiographic findings confirming
MP joint subluxation or dislocation suggests that treatment of the joints is required, in conjunction with
treatment of the tendon rupture
 The DRUJ usually requires reconstruction at the time tendon continuity is restored
 ROM, pain, synovitis, and instability of this joint must be documented
 Evaluate wrist motion and stability, as these findings may impact the choices made for surgical
reconstruction of the DRUJ
 Volar and ulnar radiocarpal subluxation often accompanies pathology involving the extensor tendons
and the DRUJ
 PIN palsy due to synovial proliferation at the elbow may also result in the loss of active MP extension
 Nerve palsy does not usually produce the same pattern of loss of extension, beginning with the small
finger and progressing radially
 If selected digits are affected, the ring and long fingers tend to lose extension first when the PIN is
involved
 The tenodesis effect of wrist flexion resulting in MP extension is still present in cases of PIN palsy

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  This finding can sometimes be difficult to demonstrate in the rheumatoid limb in which wrist motion or
passive ROM of the MP joints may be limited by underlying disease
 Even following tendon rupture, associated synovitis may fix the distal tendon stump to adjacent soft
tissues, resulting in an apparent tenodesis effect and further confounding efforts to distinguish these
processes

Surgical Treatment of Vaughan Jackson Syndrome

 Surgical efforts to restore tendon continuity must always include thorough dorsal tenosynovectomy with
retinaculum transposition and resection or reconstruction of the DRUJ sufficient to remove the bony
prominences that produced tendon rupture
 Small finger MP joint extension
o May be lost following isolated rupture of the EDM in the patient without significant EDC tendon
contribution to this digit, or it may follow rupture of both the EDM and a slip of the EDC
o The distal tendon stump that produces strong MP joint extension of the small finger
(usually EDM) may be transferred to the adjacent EDC to the ring finger
o Occasionally, the distal stump is so short that such side-to-side suture tends to produce
unacceptable abduction of the small finger. In these instances, the EIP may be
transferred to the EDM
 Loss of ring and small finger MP joint extension
o Usually best treated by using the EIP to motor both the EDM and EDC ring. Alternatively, the
EIP may be transferred to the EDM, and the EDC ring may be sutured side-to-side to the
intact EDC long
 Loss of long, ring, and small MP joint extension
o Usually treated by transfer of the EIP to both the EDM and EDC ring and side-to-side suture
of the EDC long to the intact EDC index
o If the EIP is the only remaining extensor to the index finger, a flexor digitorum sublimis
(FDS) tendon may be used to motor the ring and small MP joint extension in place of the
EIP
o Although one of the radial wrist extensors (preferably ECRL) can be considered as a motor
tendon in this circumstance, it is often not long enough to reach the distal stumps of the
ruptured tendons and does not have sufficient excursion to restore normal MP joint motion
 Loss of MP joint extension of the index, long, ring, and small fingers
o Constitutes the final stage of this process and should only be seen in neglected cases
o Although one hesitates to remove power and joint stability from the volar surface of the
rheumatoid hand, transfer of the FDS tendons to provide MP joint extension, as originally
described by Boyes in the treatment of radial nerve palsy, is often the best alternative
o Many patients actually feel that flexor function is improved as a result of decompressing the
digital flexor sheaths by tendon harvest
o Most authors use the FDS ring to motor the ring and small fingers and the FDS long to
motor the index and long fingers
o The classic Boyes transfer routed these tendons through a window in the interosseous
membrane - however, adhesions may be limited in the rheumatoid hand by using the alternative
of a subcutaneous tunnel around the forearm
o The radial route of passage is preferred, as it tends to counteract the tendency for ulnar
subluxation of the digital extensors on the dorsum of the MP joints

Consultations
 Appropriate hand therapy and splinting are crucial to the success of these procedures
 In the absence of supervised therapy, limitation of motion due to scarring and adhesion formation may
exceed that which was present preoperatively
 Joints adjacent to those that are being surgically treated are seldom entirely normal in the rheumatoid
hand, and early motion is necessary to prevent stiffness and functional deterioration
 Although many authors advocate immobilization of the MP joints in a position near full extension for 3-4
weeks following extensor tendon reconstruction, the author favors a program of graduated dynamic
extension splinting in an attempt to maximize motion

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  Therapy is usually initiated on the third or fourth postoperative day after edema has declined and the
wounds have settled
 Patient disease and medical regimen may dictate the choice of postoperative therapy

141. Tendon Transfer Details for Radial Nerve Palsy

Transfer of PT to ECRB, FCR to EDC, and PL to EPL
 Gently curved incision in the middle third of the dorsal forearm to expose the EPL and common
extensor tendons and EIP proximal to the extensor retinaculum
 Fully flex the fingers and hold the wrist in extension
 Sequentially secure the EDC and EIP tendons together under equal tension just proximal to the
extensor retinaculum using 2.0 non-absorbable braided sutures
 Place the wrist in neutral and evaluate synchronous MCP joint extension by placing traction on a
Kocher clamp that has been placed proximal to the sutured region of the EDC and EIP tendon
composite
 Additional extensor tendon balancing may need to be done by adjusting tension with additional
mattress sutures
 Inclusion of the small finger proprius tendon may be necessary
 Make a gently curved volar incision, extending from the junction of the proximal-middle third of the
forearm to 4 cm proximal to the distal wrist flexion crease to expose the PT, FCR, and PL
 Locate the interval between BCR and PT and trace PT to its insertion (midway along the lateral aspect
of the radius)
 Sharply free PT from the radial shaft and remove a 2- to 3-cm periosteal extension in continuity with its
tendinous insertion
 Trace FCR distally and with wrist flexed transect it at the distal wrist crease level
 Verify presence of PL and trace its tendon distally, dividing it at the distal wrist flexion crease
 Take care to avoid mishandling the median nerve
 Elevate and dissect these 3 motor units of their fascial attachments proximally to allow them co-linear
alignment with their intended insertions
 Transect EPL at its musculotendinous junction (via your dorsal incision) and make a 2-cm incision
dorsally just proximal to the thumb MCP
 Deliver EPL to this wound with a Kelly clamp
 Release any fascial attachments
 Make another 2-cm transverse incision in the distal wrist flexion crease at the base of the thenar
eminence
 Make a tunnel with a Kelly clamp to pass EPL volar and radial to the thumb CMC joint
 Likewise, tunnel EPL to the volar wound by free passage of the Kelly clamp
 Free EPL passage and effortless excursion is achieved by releasing again any fascial attachments
 Assess the desired thumb radial abduction and extension by placing traction on the free rerouted EPL
tendon in line with the PL towards the medial epicondyle
 Wrap the tendon in a moist 4 × 4 sponge
 Develop subcutaneous tunnels from proximal-volar to distal-dorsal, keeping a straight line approach to
the destined tendon attachment sites for the PT and FCR motors
 The tunnels should be just superficial to BCR and ECRL, leaving no potential for compression of the
superficial sensory nerves
 Place FCR through the EDC and EIP composite in a proximal-radial to distal-ulnar direction, using a 15
blade and mosquito hemostat
 Adjust the tension so that with full passive wrist flexion the MCP joints extend fully and with full wrist
extension the fingers can be passively flexed
 A Pulvertaft type weave is not possible; however, multiple horizontal mattress sutures should be used
to anchor the FCR to each individual tendon in the EDC and EIP composite
 Weave the PT and periosteal slip through the more centralized wrist ECRB
 The PT and ECRB tendons can be joined by several passages of the PT tendon and its periosteal
extension through the recipient ECRB

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  This procedure can be simplified with the use of a 15 blade and a mosquito hemostat - hold the 15
blade parallel to the tendon fibers and pass through the tendon
 Grasp the blade with the mosquito hemostat and pass the mosquito hemostat back through the tendon
with the blade and grasp the free tendon end
 This procedure is repeated three or more times, and each time the blade is passed 90 degrees to the
previous pass
 Using multiple 2-0 braided non-absorbable sutures in horizontal mattress fashion, secure the tendon
weave with the wrist held in 40 degrees of extension with the PT under near maximal tension
 Weave the EPL tendon through the PL in a 90-90 fashion
 Place traction on the tendon in line with the PL and check for the desired thumb palmar abduction and
IP joint extension
 The tension should be such as to maintain slightly more than half maximal PL excursion, which should
balance the thumb in abduction and extension
 Achieve hemostasis after tourniquet deflation, and close wounds in routine fashion
 When the FCU instead of the FCR is used for digital extension, a volar forearm incision should extend
to the distal wrist flexion crease
 The FCU tendon is detached near the pisiform
 The procedure is analogous to that described for the FCR motor except for the details concerning
proximal dissection of the FCU muscle and passing the tendon around the ulnar shaft
 The FCU is muscular throughout and in thin arms removal of the middle and distal muscle portion may
make this motor less visible

Post Op Management
 Sutures may be removed 10 to 14 days postoperatively, the wrist is kept in 40 degrees of extension,
the MCP joints in full extension, and the thumb radially abducted and extended for 3 weeks
 Supervised physical therapy is begun at this time
 A removable custom-molded splint keeping the wrist, fingers, and thumb in the postoperative position is
worn at night and between therapy sessions for approximately 3 months postoperatively

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Transfer of PT to ECRB, FCR to EDC, and PL rerouted to EPL. A/B Volar and dorsal incisions used in combination of
transfers. Note short transverse incisions over thumb MP joint dorsally and wrist volarly used in rerouting EPL. C, Transfer
of PT into more centralized ECRB. Note that PT insertion is harvested with a 2- to 3-cm periosteal extension strip. D, FCR
transfer to EDC. Note that FCR motor tendon attachment at 45-degree angle into recipient tendon. E and F, Transfer of
PL to rerouted EPL. By rerouting EPL out of its third extensor compartment a combination of thumb abduction and
extension can be achieved.

Thumb CMC OA
radius malunions
TFCC tears
Keinbock's

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Shoulder OA and cuff tear arthropathy
Large cuff tears
Hill-Sachs lesions
AC separation (hook plate, weaver dunn sort of ones)
Elbow terrible triad

BACK TO TOP

Sports
142. Spiel for Knee Arthroscopy

143. Spiel for ACL (Hamstring) Reconstruction

1. Diagnostic scope of knee (high anterolateral portal, and the low anteromedial portal)
2. Identify/debride meniscal pathology (if repair, do at end)
3. Debride remnant ACL, tunnel sites
4. Harvest graft:
1. oblique incision over pes anserinus (1 cm medial to tibial tubercle, 5 cm below jt line)
2. Identify upper border with finger/vessels
3. Incise sartorial fascia
4. Hook semi-T and gracilis tendons with Luer clamp
5. Identify bands to gastrocnemius and cut them (look for dimpling)
6. Pass tendon stripper for each tendon
7. Detach at distal insertion
8. Remove muscle from graft
9. Fold tendons over endobutton (with #5 & #2 ethibond)
10. Suture ends using Krackow-style technique with #2 ethibond
11. Measure graft, then wrap in damp gauze;
5. With knee at 90 degrees, place femoral guide at 10:30 (for right knee)/1:30 (for left) position at
back of femur (not resident‘s ridge)
6. Insert guide pin until it pierces anterolateral thigh
7. Ream appropriate size over guide pin to depth 30mm (mark same on graft)
8. Proceed to tibial tunnel
9. Place tibial tunnel guide 5 cm distal to joint and 2 cm medial to crest in incision & set to 55
degrees
10. Place guide for appropriate tunnel in joint (see below)
11. Insert guide pin & advance to check it passes by PCL
12. Ream appropriate size, then use reverse reamer to smooth entry into joint
13. Use guide pin and sutures to pass graft into tunnels
14. Ensure endobutton deployed; tension graft with 20 cycles or tensioner
15. Ensure isometry
16. Insert interference screw fixation for tibia in extension, while maintaining tension
17. Wash out knee
18. Close

144. Lack of full extension 8 wks following ACL

1. Arthrofibrosis- 3 stages and tx accordingly
2. Cyclops lesion from inadequate notchplasty
3. Impingement from tibial tunnel being too far anterior
4. Scarring of MCL from injury

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 5. Missed bucket handle meniscal tear
6. Infection

145. Meniscal Repair Spiel (INSIDE-OUT TECHNIQUE)

YOU CAN ASSESS VASCULARITY OF THE TEAR ONLY WITH THE TOURNIQUE DOWN

Stable Tears Less than 1cm do not require repair, tears that are considered stable include:
 partial-thickness tears measuring less than half the height of the meniscus
 full thickness oblique or vertical tears that measure less than 7 to 10 mm in length if the
inner portion cannot be displaced more than 3 mm with probing.

Tricks to improve healing of meniscal repair:

1. Rasping the synovium of the menisco-capsular junction to achieve bleeding on both the
femoral and tibial side of the meniscus.
2. Trephination: a series of horizontally oriented holes is made using a spinal needle or small
trephine through the peripheral aspect of the meniscus.
3. Fibrin clot

Indications:
1. Any peripheral non-degenerative longitudinal tears < 3 cm: If tear is w/in 3 mm of the
periphery, it is considered vascular; area 3-5 mm from periphery is grey zone, & > 5 mm from
periphery is considered avascular
2. Unstable tears or tears within vascular zone that are > 7 mm are repairable
3. Mobile, single, vertical, longitudinal tear of the meniscus limited to vascular outer one-third of
the meniscal substance
4. Note that instability in full extension suggests concomitant POL tear, which by itself is an
indication for operative repair (w/ the same incision being used to repair the meniscus)

Relative contra-indications:
1. Tears greater than 3 cm do not seem to heal, following surgery;
2. Transverse tears, even in the periphery, do not seem to heal;
3. Do not repair flap tears, radial tears, cleavage tears, or vertical tears with secondary lesions
that extend into avascular inner 2/3 of meniscus, except in young teen agers;
4. Ligamentous instability is a relative contraindication to repair: w/ ACL insufficiency, the rate or
re-tearing approaches 40%, especially in younger acitve individuals, and therefore ACL
reconstruction should be performed at the same surgery

MEDIAL
1. Place patient supine, with ability to flex knee (holder, table bent); pad both legs well
2. Diagnostic arthroscopy; reduce bucket handle tears as necessary
3. Approach (almost identical to popliteal artery approach mentioned above)
1. The incision parallels the anterior border of the sartorius.
2. The sartorial fascia is incised along the anterior edge of the sartorius.
3. Retract sarotrius posteriorly
4. Incise fascia posterior to superficial medial ligament
5. Now, retract the sartorius, gracilis and semitendinosus posteriorly.
6. Use a retractor to pull the medial head of gastroc posteriorly from semimembranosus
inferiorly
7. Your working triangle will be between the posterior knee capsule anteriorly, the deep
tendon of gastroc posteriorly and semimembranosus inferiorly.

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 8. must release semimembranosus and medial head of gastrocnemius to identify the popliteal
artery which lies lateral to medial head of gastrocnemius
9. Dissect down to capsule, taking care to protect saphenous n (palpate attachment of
semimembranous to posterior tibia and dissect anterior to it)
10. Dissect along capsule posteriorly; place retractor to protect neurovascular structures and
direct needles to incision
4. Rasp the meniscal tear and perimeniscal synovium
5. With tear reduced, pass 2-0 (absorbale or non-absrobable) meniscal sutures in vertical mattress
configuration 3mm apart, alternating inferior and superior surfaces knots
6. Use anterolateral portal for most tears and anteromedial port for posterior (bent guides or arrows)
7. Use double barrel guide to direct sutures away from posterior neurovascular structures
8. May need arrows for posterior horn
9. After sutures are placed, flex and extend the knee to ensure that the posteromedial corner has
not been reefed (generally reefing the pouch will limit extension)
10. With sutures pulled tight, ensure good reduction of tear; proceed to tie sutures against capsule
under direct visualization (if ACL reconstruction at same time, tie sutures after reconstruction)
11. Make sure that branches of saphenous nerve are not caught in the sutures
12. Close

LATERAL
1. Place patient supine, with ability to flex knee (holder, table bent); pad both legs well
2. Diagnostic arthroscopy; reduce bucket handle tears as necessary
3. Knee flexed to 90 degrees to relax peroneal nerve behind biceps
4. 6cm vertical incision at the posterolateral corner of knee, incision just posterior to LCL
5. Interval between ITB and biceps
6. Longitudinal incision made in deep fascia along posterior border of IT band
7. Blunt and digital dissection down to posterolateral femur
8. Split the biceps from ITB and retract posteriorly, thus protecting peroneal nerve, which lies
behind it
9. Identify lateral head of gastrocnemius and dissect it free off posterior capsule, starting
inferiorly and working up
10. Rasp tear and perimeniscal synovium
11. Place meniscal sutures from anteromedial portal, with retractor/spoon/speculum protecting
posterior neurovascular structures and guiding needles to incision;

POST-OP ORDERS FOR MENISCAL REPAIR

 Touch weight-bearing for 2 weeks in hinged knee brace 0-90 degrees
 Partial weight-bearing for 2 weeks
 After 4 weeks, progress to WBAT
 Running can start at 5 months, sports at 6 months

BACK TO TOP

Arthroplasty
146. Hip Pain History in the young (AVN, FAI, Dysplasia, Labral Tear, Infection, Tumor)
In addition to your usual pain questions:

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  History of pain aggravated by FLEXION type activity (think femoroacetabular impingement)
 Sudden onset of pain after a precise incident of trauma (sudden abduction) in addition to
mechanical symptoms (think traumatic labral tear, notice that labral tear may accompany
advanced femoroacetabular impingement)
 Feeling of unsteadiness at the end of the day (more dysplastic picture)
 Any mechanical symptoms: catching, clicking or sense of instability
 Any history of hip problems during childhood
 Any constitutional symptoms: loss of weight and appetite, fever, chills, night sweats
 History of smoking and alcohol (how much alcohol in details, more than 7 beers/day for 7
years (400 ml of alcohol is a risk)
 Any personal of family history of bleeding dyscariasia, sickle cell, Protein C and S, storage
disease (Gaucher‘s)
 Any history of diving as leisure activity

147. Gait in relation to arthroplasty: Trendelenberg for hips, Lateral or medial thrust for knees

148. Steps to deal with intraoperative instability of THA

1. impingement – remove impinging osteophytes or cement
2. acetabular component position
i. check version of acetabulum
ii. check for medialization of acetabulum (if uncemented cup, correct orientation
and lateralize if necessary (bone graft medial wall or use lateralized liner)
3. femoral component position – check version of femoral component
4. femoral offset – use increased offset femoral prosthesis if possible
5. neck length – increase neck length, but try to avoid collar as this will lead to
impingement
6. larger head
7. lipped liner – rotate to cover unstable area but prevent impingement
8. constrained cup – better in older patients due to high risk of acetabular component
loosening
9. trochanteric advancement

149. THA after DDH – Issues

1. Pre-op:
a. History:
i. Amount of disability
ii. Limping (Trendelnberg gait)
iii. Make sure that all non-operative options have been tried
iv. Any operations in the past: details of operation, operative notes, complications
after those operations, was it acetabular vs femoral operation. Acetabular will
make your life easier (better coverage), femoral will make it worse (you will have
difficulty in reaming, version).
b. Physical exam:
i. Limb length discrepancy
c. Discussion with patient:
i. Plan for THA – it is difficult  ask for arthroplasty surgeon
ii. Discuss with the patients the risks: higher failure (loosening, dislocation),
possibility of wake-up test
iii. Discuss with him high possibility of not correcting the gait completely to normal
but definitely controlling the pain

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 d. Pre-op arrangement:
i. Discuss with anesthetist possible need for wake-up test if you need to stretch the
nerve
ii. Special instruments (smaller stems, allografts for shelf graft, strut graft and cable
if you are doing shortening osteotomy, smaller cups, x-ray to check the hip center
if difficult to visulaise).
2. Operative Issues:
a. Approach: Trochanteric osteotomy (anterior sliding vs others) vs modified hardinge
(conventional)
b. Cup
c. Stem

1. Issues in the approach: Advantages and disadvantages of troch osteotomy.

Proximal migration of femur  stretching of tissues , difficult approach. Discuss the
modified sliding troch osteotomy (i.e., keeping the posterior 1cm intact).

2. Issues with cup: Mention that in DDH will be issues with hypoplasia of the
acetabulum. There will be true acetabulum and pseudo-acetabulum. Decision
between low (the pseudo-acetabulum is touching the true one) and high hip centers.
Advantages and disadvantages for each.

a. You will need shelf bone graft (auto or allo), if there is less than 70% coverage
of the cup with host bone. This should be fixed with 2 cancellous screws (4.5)
and supplemented with flying bridge bone graft.
b. You may need x-ray to locate the hip center if it is difficult to visualize
c. You limit to stretch the sciatic nerve is 4cm. Mention that you will expose the
nerve and feel it to avoid over stretching. If you cannot reduce the hip down to
the low hip center, consider shortening osteotomy.

3. Issue with stem (femur): With DDH, there is severe anteversion of the femur and
the canal tend to be narrow. Thus you will use smaller straight stems or modular
stems to adjust for anteversion. You may want to cut the femur at the level of lesser
trochanter (rather than 1 cm above it) to give you more room to adjust the version.
Cemented vs uncemented.

3. Postoperative protocol:
a. Close observation
b. Non-weight bearing for at least 6 weeks. Repeat x-ray to assess the graft take

150. THA after DHS

oR/O Infection
oGet OR notes (may be Ambi plate instead of DHS)
oWarn patients of intraoperative fractures, instability, risk of infection
oDislocate hip with hardware in, then reduce, then remove hardware
oUse extensively coated stems
oGraft holes
oGet intraoperative X-ray or in RR (to make sure you have not cracked at the distal hole)
oGo east on the acetabulum because it is probably soft and could easy fracture if you under
ream and tried to smash it in.
o Protect weight bear

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151. Spiel for TKA
1. I would use a cemented PCL-substituting total knee replacement, with intra-operative assessment
of the patella for possible resurfacing
2. I would template the femorotibial valgus angle and component size pre-operatively
3. Inflate Tourniquet
4. Midline anterior incision from hand above patella to just past tibial tubercle
5. Flex knee and make a medial parapatellar arthrotomy; caution taken with patellar tendon insertion
(can pin prophylactically)
6. Elevate capsule and MCL off tibia subperiosteally to posteromedial corner of knee
7. Extend knee and evert patella, watching insertion of PT; release adhesions and lateral
patellofemoral plicae; do minimal lateral release if necessary (obese patients)
8. Assess the patella and decide if needs resurfacing or not.
9. Flex knee; excise ACL and anterior portion of menisci; excise osteophytes
10. Sublux tibia anteriorly and externally rotate to relieve pressure on PT insertion
11. Excise patellar fat pad partially; place retractors against tibial bone and retract extensor
mechanism, medial soft tissues
12. Drill hole in center of intercondylar notch of femur with starter drill; insert IM femoral alignment
guide set to 5 (men) or 7 (women) degrees valgus
13. Determine rotational alignment using 3 degree external rotation guide ; Check rotation using
epicondylar axis;
14. Secure alignment guide in appropriate rotation using pins; attach stylus to the anterior resection
guide and insert into femoral alignment guide; adjust stylus to determine anterior skim cut,
referencing off the high point of the anterior lateral cortex; secure anterior resection guide; check
with nosepicker; make anterior skim cut
15. Insert distal resection guide (8mm) and secure with pins in neutral holes and cross pin
16. Remove IM guide assembly; make distal cut;
17. Size femur with posterior-anterior sizing guide (if off-size, use smaller)
18. Position appropriately sized femoral cutting guide on distal femur and secure with 2 serrated pins
and pointed towel clips; complete femoral bony cuts (posterior condyles, posterior chamfer,
anterior cortex, anterior chamfer)
19. Remove cutting guide
20. Place femoral notch block in holes from cutting guide pins, flush against bone; secure with pins
21. Perform notch cut; next, place notch punch in tracks on notch guide; impact punch until fully
seated; check with notch compactor;
22. Trial femoral component
23. Drill fixation lug holes through trial component
24. With knee flexed, place Hohmann retractor in front of PCL and sublux tibia anteriorly; complete
resection of soft tissues from tibial plateau
25. Place external alignment guide over tibia, centered on ankle joint distally and secure proximal
portion centered over the tibial eminence
26. Alignment guide should lie over medial 1/3 of tibial tubercle and in line with 2nd MT
27. Place tibial resection guide over alignment apparatus
28. Use stylus to select either 2mm off bad side or 8mm off good side; check with nosepicker; secure
tibial resection guide with pins;
29. Remove external alignment guide;
30. Respect proximal tibia taking care to protect MCL, LCL, patellar tendon and posterior structures
31. Remove resection guide
32. Flex knee and size tibial component; replace trial femoral components and insert trial tibial
component with insert; take knee through ROM with patella reduced, watching for lift-off; assess

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 for ligamentous stability; adjust as necessary (minimum 8mm poly); mark correct tibial rotation
using electrocautery; check overarll leg alignment with alignment rods;
33. Remove trial components
34. Place tibial baseplate in proper rotation; secure base plate with pins; insert keel punch of
appropriate size
35. Wash and dry bony surfaces;
36. Prepare cement; apply cement to underside of tibial component and press cement into cancellous
tibial surface;
37. implant tibial component, removing any excess cement;
38. insert polyethilene liner;
39. place cement on underside of femoral component and push cement into cancellous surfaces (not
too much cement posteriorly as it is hard to remove excess);
40. implant femoral component and remove excess cement;
41. extend leg to apply continuous pressure on components while cement cures
42. Take knee through ROM, hemostasis, close over drain (note this does not address patella)

152. Unable to Evert the Patella During TKA (SOLUTIONS)

1. medial parapatellar arthrotomy
2. release adhesions on the undersurface of the patellar tendon and excise the fat pad
3. clear lateral gutter
4. if there are substantial patellar osteophytes, remove them
5. lateral release
6. quadriceps snip (remember veering oblique and lateral) – no turn down due to increased risk
of AVN
7. tibial tubercle osteotomy (7cm long) fixation w luque wires

153. Patellar Mal-tracking During TKA (REASONS)

1. Check that femur is in 3degree external rotation
2. Check that the femur is not oversized
3. Check that the tibial tray is centered over the medial 1/3 of the tubercle and is externally rotated
4. Check that both components are slightly lateralized
5. Check that the patellar button is slightly medialized and not overstuffed. (remember, the
anatomic median ridge of the patella actually sits 3-4 mm MEDIAL to the anatomic midline
of the patella – if you put it in the anatomic midline, you will be too far lateral)
6. Release the tourniquet
7. Lateral release (avoid injury to the lateral superior geniculate artery)
8. Tibial tubercle medialization (Elmslie-Trillat)

154. Treatment Options for Unicompartment Arthritis of the Knee

Non-Operative
 NSAIDs
 Glucosamine/chondroitin
 Viscosupplementation
 Weight loss
 Exercise/physio
 Bracing (sleeve, hinged braces, unloader braces)
 Heel and sole wedges

Operative

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  Arthroscopy
 HTO (for medial compartment: medial opening wedge/lateral closing wedge)
 UKA
 TKA
 ? osteochondral allograft

155. UKA
Indications
Older, less active
Isolated medial compartment and well preserved lateral compartment (intact meniscus)
Osteoarthritis/osteonecrosis
Minimum ROM 15-110
Deformity correctable to neutral

Contraindications
Deficient ACL or PCL
Medial or lateral subluxation or posterior tibial bone loss on X-ray (indicative of ACL deficiency)
Varus >15
FFD >15
Additional lateral involvement
Inflammatory +/- Chondrocalcinosis
Anterior knee pain
Isolated lateral (relative)
PF arthritis: not as strong contraindication as before

Operative Procedure for UKA

Principles:
 With medial compartment arthritis: correct to neutral or slight varus.
 Femoral component should be centred on the condyle and parallel to the tibial component.
 Tibial component should cap but not overhang the cortex to prevent irritation of the pes
anserinus.

156. TKA after HTO (issues)

1. R/O Infection
2. Ligaments:
1. Ligamentous laxity (MCL, LCL) may also be seen in these knees, particularly those that are in
significant valgus. Soft-tissue balancing may require releases and/ or ligament advancement
and/or constrained components.
2. Extensor mechanism
3. Hardware:
1. Old report for details of hardware used.
2. If retained hardware cannot be removed without extensive operative dissection at the time of
the knee replacement then it may be advisable for the hardware to be removed through the
previous incision and the TKR performed after the wound has healed.
3. Remove hardware with minimal bone loss and avoid fracture
4. Skin Incision: The optimal skin incision should be a midline longitudinal incision, regardless of
the previous incision used. ?Make sure you have at least 7cm bridge.
5. Exposure:

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 1. With soft-tissue scarring following a HTO the subperiosteal exposure of the tibia is often more
difficult.
2. Patella eversion may also be difficult particularly in the presence of patella infera.
3. A lateral retinacular release early in the procedure may facilitate exposure.
4. With severe scarring and patella tendon shortening, a quadriceps snip or quadriceps
turndown may be necessary.
6. Bone Stock (FOR CLOSING WEDGE): The predominant abnormality in the proximal tibia is the
loss of lateral bone stock. This can often be dealt with by a minimal lateral resection. Have bone
graft, metal augments, stemmed component, different levels of constraints.
7. Proximal Tibial Deformity: Address with extramedullar tibial guide and offset tibial tray
8. Joint Line: reconstitute joint line to avoid patella baja (or infra).
9. Instruments available: bone graft, metal augments, large fragment screw, stemmed prosthesis,
different level of constraints (PS, CCK, Hinged).

157. TKA post UKA (issues)

1. R/O Infection
2. Ligaments
3. Skin Incision
4. Exposure
5. Bone Stock
6. Instruments: bone graft, metal augments, stemms, different constraints (PS, CCK, Hinged)

158. Patellar Fractures in TKA

Keep at least 15mm of remaining bone in the patella to decrease risk of fracture.
1. Type I – patellar fractures with a well-fixed implant and intact extensor mechanism – treated non
surgically
2. Type II – patellar fractures associated with disruption of the extensor mechanism in a knee with a well-
fixed patellar implant – typically requires OR with options including ORIF vs partial or complete
patellectomy with repair of the extensor mechanism – high rate of complications esp with ORIF
3. Type III – patellar fractures associated with loose patellar component; if symptomatic, surgery may be
necessary
1. Type IIIa – involve good remaining bone stock and may be managed with revision
2. Type IIIb – poor remaining bone stock and may be treated by removal of the implant and
possible partial patellectomy

159. Revision TKA

 Are the components loose?
o Definite (fracture, migration/subsidence)
o Probable (>50% lucent lines of 2mm or more)
o Possible (<50% lucency of 2mm or more)

ISSUES WITH REVISION TKA

1. Infection (BW, Aspirate, Bone-Indium, Frozen Section)
2. Old Operative Report: the make of the implants
3. Company Representative: if not familiar with instrumentation in situ
4. Skin (healthy, previous incisions, post-op gastrocs flap for ANY necrosis)
5. Exposure (quads snip, lateral release, tubercle osteotomy OR VY-turndown)
6. Removal of components (Gigli saw, cement osteotomes and currettes)
7. Bone stock (5mm=PMMA, 2cm=wedges, >2cm = allograft); another way to think about it if bone
loss extends past epicondyle proximally OR below tibial tubercle, structural
allograft & stemmed components will be needed OR tumour prosthesis
8. Components (bone graft, metal augments, stemmed components, constrained components)
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 9. Reconstruct the Joint Line
10. Cement (use Antibiotic impregnated PMMA for revisions)

BACK TO TOP

Foot and Ankle

160. Tib Post Deficiency
 Tib post deficiency  valgus but correctable passively: FDL transfer and calc slide osteotomy (if you
do the slide then you don’t need to lengthen the Achilles according to J. Lau)
 if they can invert past midline, tendon is functional and NOT disrupted
 medial cuneiform to floor normally > 15mm

Incidence/Epi
 A correlation between PTT dysfunction and sedentary middle-aged/elderly females has been observed
 Higher incidence also been observed in patients with HTN, obesity, RA and seronegative inflammatory
arthropathies
 >50% of patients recall a traumatic event but traumatic ruptures have been reported in athletes and
associated with ankle fractures

Clinical & PE
 insidious onset of unilateral flatfoot and medial/plantar pain
 different findings depending on stage of dz
 key exam features;
o too many toes sign
o ability to do single heel rise and repeated heel rise
o does the arch restore with heel rise?
o T @ TP insertion (accessory navicular?)
o Subtalar motion (gone with stage III-IV)
o Lateral fibular impingement pain (greater with fixed severe deformity)
Imaging
 AP, uncovering of talar head
 Incr talar 1st MT angle
 Divergence of talus and calc (meary incr)
 On lat, lower arch, plant flex talus, incr talar 1st MT angle
 MRI for status of PT
Staging – by Myerson
o Stage I: Tenosynovitis with minimal deformity
o Stage II: PTT insufficiency with flexible flatfoot deformity
o Stage III: PTT insufficiency with rigid flatfoot deformity
o Stage IV: Stage III with valgus talar tilt in ankle mortise

Treatment
 Stage I
o Nonop – NSAIDS, rest, act mod, immobilize w short leg walk cast 6-8/52 followed by
molded orthotic/brace
o If persists, tenosynovectomy (esp important for inflammatory conditions)
 Stage II

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 o Significant TP pathology but flexible foot, can use AFO and accommodative
bracing/orthotics.
o Many times need Sx b/c of progression and pressure in medial foot
o Many procedures to do, best choice for exam is FDL tendon transfer and medial
displacement calc osteotomy
o Osteotomy done laterally and FDL transfer done from medial side. FDL identified at
knot of henry and released. Attached to navicular through bone sutures.
 Stage III – fixed deformity
o Exhaust conservative
o Likely will need triple arthrodesis, limited TN fusions have been shown effective in older,
lower demand pts – otherwise, triple
 Stage IV
o Typically need pan talar fusion if the tib/talar degen is significant.
o If tib/talar OK then triple with medial calc displace osteotomy with repair of the deltoid
can also be done.

161. Hallux Rigidus

Non-op: NSAIDs, Orthosis to incr medial forefoot rigidity (Morton‘s extension), Injections, Extra-depth
shoe with stiff soled rocker bottom or metatarsal bar

Surgical Treatment
1. Cheilectomy with or without dorsiflexion osteotomy of proximal phalanx
 Dorsal or medial approach, resect to get 70-90 dorsiflexion intraop
 Probably best for grade 1, maybe 2 (minimal changes)
 Dorsal closing wedge osteotomy of the proximal phalanx can be added if adequate dorsiflexion is not
obtained intraoperatively
2. Resection arthroplasty (keller)
 Consists of removal of the base of the proximal phalanx and destabilizes the joint by removing the
attachment of the plantar plate and the FHB which can lead to a cockup deformity, instability of the 1st
ray, weakened pushoff, excessive shortening of the hallux, and transfer metatarsalgia
 Usually reserved for elderly, more sedentary
 Can modify it and interpose EHB and dorsal capsule
3. Arthrodesis
 Most commonly used for grade 3 and is the definitive procedure for pain relief
 Fused in 15 valgus and should not touch 2nd toe
 20-30 dorsiflexion relative to 1st MT, 10-15 dorsiflexion relative to plantar foot
 Use of flat cuts and cup and cone technique both have high success
 Fixation with compression screws, pins, staples, dorsal minifragment plate
 Complications include malalignment, nonunion, IP arthritis (up to 15% but most not symptomatic)
 Excessive dorsiflexion is better tolerated than plantarflexion

162. Rheumatoid Foot

General
 Forefoot>midfoot>hindfoot
 WB films to r/o tib-talar valgas rather than tib pst deficiency

Pre-op Medicine (RA drugs/steroids), anesthesia (c-spine/steroids)

Conservative
 Wide toe box, metatarsal bar, moulded insert for boney prominences
 If tib/tal involved, moulded AFO

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Forefoot
 Earliest – MTP synovitis w intrinsics pulling PIP into flexion on dorsal sublux of phalanges on
MTP‘s
 In seroneg arthropathies, hammer toes in isolation, in RA, rare in isolation
 Skin problems – Fat pad atrophy under MTP‘s, plantar calluses/ulcers/dorsal P/DIP corns
secondary to PIP flexion

Forefoot reconstruction
1st MTP Fusion For Hallux Valgus Deformity In RA (Mann)
 Dorsal longitudinal incision medial to EHL, preserving dorsal branch
of superficial peroneal nerve to medial side of incision
 Capsular incision in-line with skin incision, Synovectomy
 Sharply dissect soft tissues circumferentially from distal MT and PP
 With toe in 15° dorsiflexion resect (WRT floor) 5mm of MT and 5mm of PP
 Appose ends of bone and skewer with K-wire 10-15deg of valg
 If bone stable enough can use interfragmentary screw at 45° and
supplement with 6-hole ¼ tubular dorsal plate

Lesser Toe Resection Arthroplasty (Mann)

 Dorsal 2nd and 4th interspace 2-3cm long incisions to webspace
 Identify and protect common digital nerves & arteries by staying on bone
 Identify and transect EDL tendons (superficial and medial to EDB tendons) at PIP
 Capsular incision medial to EDL tendon, circumferential release @ MTP
 Resect metatarsal head to level of diaphysis, place cut ends of EDL
tendons and skewer with K-wire retrograde through medulla (Anchovy), remember to cascade
the resections
 Address any PIP contractures with osteoclasis or resection before wire
 Compression dressing (remove it and pin if toes cyanotic 2h postop)
 Postop shoe at 24h, pins out at 5/52, postop shoe for another 6 weeks

Hindfoot
Causes of pain
 Tib pst dysfunction
 Sub T synovitis
 Results in hindfoot valgus

Conservative
 Same stuff, arc support w heel cup +/- AFO w T strap

Sx
 Triple arthrodesis. Can also do isolated fusions (i.e. if just TN jt burnt).

Procedure
Lateral incision for subtalar and CC Arthrodesis
 1cm distal to tip of fibula extending distally in line w 4th MT
 Protect peroneals and sural nerve proximally (will be in inferior pt of incision)
 find CC & STJ
 Elevate EDB and EHB to identify sinus tarsi and CCJoint in distal 1/3 of EDB muscle belly

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  Debride joint esp. medially and inferiorly and drill holes on either side
 Clear sinus tarsi of soft tissue including inferior extensor retinac. & T-C interosseous ligament
 Laminar Spreader or Hohmann in sinus tarsi (or if fibrosed will have to drill it out)
 Curet or osteotomize articular cartilage from posterior facet (beware FHL tendon on medial
side) to bleeding cancellous bone
 Reduce with ankle at neutral and STJ in 10° valgus

Medial incision for TN Arthrodesis

 curved incision from distal / anterior medial malleolus to insertion of Tib Ant
 Identify and divide branches of saphenous vein and nerve if required for exposure
 Find TN Joint and subP. dissect around this
 Deep Peroneal N. & Dorsalis Pedis in anterior flap !
 Debride with curets / Osteotomes across to lateral side of TNJ

Reduction And Fixation Of Triple Arthrodesis

 Avoid supination and varus – Ankle Neutral, Hindfoot 10° valgus – symmetric ER w other foot
(or 15 deg if other foot is crap)
 Fix TNJ with COUNTERSUNK 6.5mm cannulated screw from
medial-plantar to lateral-dorsal
 Fix CCJ through separate dorsal incision between base of 4th and 5th MT / Rongeur top of distal
cuboid and use COUNTERSUNK 6.5mm cannulated screw from distal-dorsal to
proximal-plantar
 Subtalar screw starts 1cm lateral to midline at junction of Glaborous / Nonglaborous skin and
just exits dorsal talus (↑ bite)
 If bone is poor substitute cannulated screws for Steinmann Pins & graft STJ as required
(Fixation not required but use it)
 Order of fixation should be ST first then either of the other two. Fixing TN first locks the rest of
the jts.

163. Cavovarus Foot (peds and adult)

Assessment
 It may not be initially clear what the initial diagnosis is
 Consider the differential:
o Neuromuscular (2/3 will have a NM disorder and ½ of these will be CMT)
 Muscular – muscular dystrophy
 Long Tract and Central Disease – Friedrich‘s, spinocerebellar degen‘n, CP,
syrinx, tumour, tethered cord, dysraphism, diastematomyelia
 Anterior Horn Cell – polio, SMA
 Peripheral Nerves – CMT, tumour
o Congenital
 Arthrogryposis
o Traumatic
 Compartment syndrome, crush injury, burn.
 Most commonly: CMT, polio, Friedrich‘s, spinal cord tumor, dysraphism, diastematomyelia,
tethered cord
 Bilateral or unilateral
o Bilateral: CMT, diabetic neuropathy, Friedrich‘s ataxia, spinal cord tumour, spinal
dysraphism, diastematomyelia, tethered cord
o Unilateral: polio, trauma, incomplete spinal cord injury, crush
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Don‟t forget;
 Additional useful tests: CK, EMG, nerve conduction studies, nerve (sural biopsy for CMT) or muscle
biopsy (for muscular dystrophy)
 Assoc w DDH
Is the cavus deformity hindfoot or forefoot?
Calcaneal pitch (calcaneal tuberosity moved more distally - dorsiflexed) of >30 is more suggestive of gastrocs
weakness secondary to polio, cauda equina, incomplete spinal cord injury, or meningomyelocele
Calcaneal pitch of < 30 is more suggestive of CMT - more forefoot cavus with the plantarflexion of the first ray.

Approach to Pes Cavus – CMT

 The pes cavus associated with CMT is caused by progressive weakness of intrinsics, peroneus
brevis, and tib ant
 The first ray is pulled down by peroneus longus
 The hindfoot swings into varus by the force of tib post to stabilize the weightbearing foot (tripod), and
the long toe extensors try to work as ankle dorsiflexors, eventually causing clawing
 So the typical deformities in CMT eventually are: hindfoot varus, cavus deformity (mainly through
the forefoot), and forefoot valgus
 Every patient with pes cavus needs a thorough neurological exam and possibly an MRI to make sure it
is not coming from the cord

Are the deformities fixed or flexible?

o Forefoot: look for passive motion at the TMT, and MTP
o Hindfoot: look at the Coleman block test – does the hindfoot varus correct? (this test has pt
stand on block 2.5-4cm off ground with the heel and lat foot on the block and 1st – 3rd MT‘s
hanging off the block. If varus corrects, ST jt is supple and likely only soft tissue procedures
needed, if not, then likely need boney and soft tissue)

Orthotics
 AFO to prevent equinus contracture
 Orthotics to accommodate for the plantarflexed first ray and to support the hindfoot

Treatment Principles - Get the foot stable, plantigrade, and painless

 Do what needs to be done – if there are soft tissue problems that are flexible/correctable – do soft
tissue procedures
 If there are inflexible deformities/bony deformities – do bony procedures
 Basically, start with soft tissue procedures, then do osteotomies if you can‘t get it fully get it corrected
with the soft tissue procedures
 Then do tendon transfers to balance the foot

Surgery
 Because CMT is an evolving disease, the younger you do them, the more risk of recurrence

Soft Tissue Procedures

 In general, when the deformities are still supple and correctable:
 Release plantar fascia (complete) and medial structures (abductor hallucis, long and short plantar
ligaments (calcaneonavicular ligs), quadratus plantae)
 Transfer peroneus longus (strong – pulls down on 1st ray) to peroneus brevis (weak – lose inversion)
 Jones IP fusion and transfer of EHL to metatarsal neck for the clawing of the hallux. (This is key to
preventing the EHL from continuing to plantarflex the first metatarsal)
 Girdleston-Taylor flexor to extensor transfers for the lesser toe clawing; or EDL tenotomies + IP
fusions(I am using this for the exam)

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  Lengthen heel cord after you‘ve done the other soft tissue procedures

Bony Procedures
 In general, for rigid, uncorrectable deformities
 Rigid first ray plantarflexion requires dorsal closing wedge osteotomy (think its called a moberg)
 May require multiple dorsal closing wedge osteotomies if other metatarsals are flexed down, if
correctable, can do a Jones procedure which entails a release and transfer of EHL to MT head with an
IP athrodesis. This relieves the clawing of the first toe and decreased the amount of plantar flexion of
the 1st MT that the claw is causing (good pic in OKU F&A)
 Hindfoot varus that is rigid can be corrected by a lateral wedge osteotomy (Dwyer) and/or a Samilson
osteotomy that dorsally translates the calcaneus, this is considered a triplane osteotomy that can
correct for the varus and increased calcaneal pitch.
 Finally, triple arthrodesis that addresses both the hindfoot and forefoot deformities
 Don‘t forget that if the apex of the cavus is in midfoot with high calcaneal pitch (pitch usually <30deg in
CMT cavus) will need to do osteotomies of either metatarsals or TM jts w fusion

Tendon Transfers
 Transfer tib post to dorsum of foot through interosseous membrane (route tendon beneath flexor
retinaculum anteriorly) or around the ankle to the cuboid (tib post contributes to the varus hindfoot
because its inversion moment is not countered by the eversion moment of the peroneus brevis
 Consider transferring tib ant to the lateral side of the foot – BEWARE – tib ant is usually pretty weak
and may not be eligible for transfer
 Remember in adult cavus foot, can have lateral instability and may need a lateral ligament
reconstruction. Can use peroneus brevis (Chrisman-Snook uses split PB to recon ATFL and CFL
(distal PB insertion stays attached)

164. Charcot Foot

 Repetitive microtrauma theory secondary to neuro changes. Occurs in 7.5% of diabetics
 Development of this condition requires a well perfused foot (precludes those sig vasc dz of the
LE)
 Classification (Eichenholtz)
o Stage I – Fragmentation: Periarticular # & jt subluxation
o Stage II – Coalescence: Resorption of bone debris and ST homeostasis
o Stage III – Consolidation: Restabilization of foot with bone or fibrous of the involved jts
 Exam/Dx:
o Usually warm/dry/erythematous/swollen foot, redness usually disappears with
prolonged elevation (can help differentiate from infection)
o Infection is main dz on ddx – MRI and white cell scan are best tests to rule out infection
 Management
o Very challenging to tx
o Tx with total contact casting (TCC) and change frequently for wound checks and re-
fitting b/c of swelling improvement.
o TCC may be needed for up to 9 months for some, typically ~4/12
o If ulcerations develop, debridment of Wagner 3-5 w abx should occur with cast changes
o Typically pts are left with no or mild deformity after the consolidation phase (75%).
o Can then be managed with accommodative AFO‘s and orthotics.
o Surgical intervention for deformity best performed in consolidation phase, very high
complication rate if Sx in stage I or II
o Occasionally may need to operate if significant deformity with secondary ulceration in
fragmentation phase (CORF 2006)

165. Plantar Fasciitis

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H&P
 Gradual onset plantar heel pain, Overwt female, Aggravated by activities and relieved by rest
 ‗first steps‘ in morning the worst (foot posture overnights relaxes PF and thus contracts while
sleeping)
 DDx of plantar heel pain
o Plantar fasciitis
o Calcaneal stress # (pain when squeeze med-lat calc @ same time)
o Fat pad atrophy (central heel pain), can be 2 to steroid injections or elderly
o Compressive neuropathy – lat. Plantar nerve most common
o Inflammatory arthropathies
o Infection
o Neoplasm
o Trauma (tib pst tendon rupture/dysfunction)
 PE-usually T when put PF on stretch and deep palp medial tuberosity of calc (PF origin, it
inserts on FDL tendon sheathes and the bases of the prox. Phalanges)
 Pain more medial over the origin of the AbHL is more indicative of lat.plant.nerve compression
Imaging
o Nothing really that helpful
o Xrays show calc spur in 50% but not indicative of Dx as the occurrence in general
population is high
o MR and bone scan not too useful unless another Dx is being entertained
Non operative
o Effective in 85-90% of pts, can take 6-12/12 to resolve.
o RICE with PF and Achilles stretching (can inflame in first 2-4/52)
o Soft heel cup inserts over the counter
o NSAIDS
o Act mod.
o If no better at 2/12, night splint to keep PF on stretch
o If no better can do steroid injection
o If no better can use WB casting for 6/52 – then restart stretching – cure rate of 42%
o If fail all conservative for 1yr, search for another Dx (inflammatory)
o If none, then surgical

Extracorporeal shockwave therapy

o newest therapy, 54% better than placebo w 4-6/52 Tx

Surgical
o 80-90% good results
o partial release (50%) from medial approach – can also do distal tarsal tunnel release if having
lateral plantar nerve symptoms (the PF and this can overlap)

166. Chronic achilles tendon rupture.(OKU F&A)

o defined as rupture >3/12 from time of injury

H&P
o pain at tendon
o gap and tendon continuity may feel normal as has filled w scar
o forced dorsiflex compared to N leg is > in rupture leg
o tendon thickening/calf atrophy/gait abnormality
o Thompson‘s equivocal

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 o Repetitive heel rise not possible (single rise can be possible)

Surgical Tx (extensive dissection – incr risk of infection)

o Not indicated for anyone with medical or limb problems (neurovacular/infection problems in
affected extremity)
o Tx depends on size of defect

1-2cm defect
o End to end repair possible – do not overtighten!

2-5cm
o V-Y myotendinous lengthening, tendon transfer or both
o Inverted V in gastrocs fascia, arms of release should be twice as long as defect
o Reconstruction choice is tendon transfer of FHL
o Is attached to calc anteromedial to native Achilles insertion

>5cm
o Turndown procedure with or without FHL transfer
o 1cm wide strip of tendon to overlap defect 2cm prox and dist is needed
o need long incision to get the tissue right up to gastrosoleus myotendinous junction.
o Problem with adherance, get moving early

167. Hallux Valgus

o Congruent deformitites
o Tx w chevron, akin or combo of the two – NO DSTP!
o To tx incr DMMA – can do biplanar medial closing wedge chevron osteotomy +/-
Akin
 Incongruent deformities is based on the severity
o Mild (HVA <30, IMA < 13)
 Distal Chevron
 Distal soft tissue procedure (DSTP - modified McBride)
o Moderate (HVA 30-40, IMA 14-18)
 Distal chevron +/- Akin as needed
 DSTP + a proximal metatarsal osteotomy
o Severe (HVA >40, IMA >18)
 DSTP + proximal metatarsal osteotomy
 DSTP + 1st MTP fusion

 First ray hypermobility or instability of the 1st MTC can be corrected by a DSTP + 1st MTC
fusion (Lapidus) – present in 5-10%
 No good way of determining hypermobility, mann‟s book says the best way is to have
the pt WB on the foot and watch for the first ray to excessively dorsiflex???
 Inflammatory arthritis of the 1st MTP is typically treated with fusion and degenerative arthritis
with fusion or Keller resection arthroplasty (resection of base of phalanx) in the elderly
 Callus under the 2nd MT head is also sign of hypermobility (is a transfer metatarsalgia b/c of
the excessive mov‘t)

168. Hallux Varus

Tx of hallux varus
 Release imbricated medial side and transfer EHL to lateral base of phalanx

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  Can also do fusion

BACK TO TOP

Oncology
169. Principles of Biopsy Spiel
I prefer the biopsy to be done by the MSK oncologist to decrease the risk of complications (5-12
times more if done by the non-treating MSK oncologist), however, the principles of biopsy are:
1. I will make sure that all the local and systemic staging have been done
2. I will discuss the patient the possible complications: infection, neurovascular injury,
inadequate tissue for diagnosis & pathological fracture
3. I will review the imaging findings (especially cross-sectional imaging) with an MSK radiologist
to confirm my findings and plan the path for the biopsy
4. I will make sure that there is an MSK pathologist available for frozen section
5. I will discuss the proposed incision with the MSK oncologist taking into consideration the
definitive reconstructive procedure
6. I will make sure that I have available instruments: curettes, drills, osteotomes, trephine, burr,
bone wax, and gelfoam.
7. I will take the patient to the OR, under general anesthetics without pre-operative antibiotics.
8. I will apply a tourniquet without exsanguinating the limb. I will inflate the tourniquet only if
needed for hemostasis control during the procedure.
9. I will make a longitudinal incision centered over the lesion in fashion such that to excise it and
incorporate it into the definitive incision as discussed with the MSK oncologist
10. I will use a direct muscle splitting approach going through one compartment only directly
down to the tumor, avoiding any intercompartmental plane.
11. I will make sure that my soft tissue dissection is minimal to avoid contamination of normal
tissue and avoiding raising any flap.
12. I will make sure to avoid exposure of the neurovascular bundle and stay away from the nearby
joint.
13. I will send sample from soft tissue mass, if available; otherwise, I will make an oval window in
the bone, and send the sample for frozen section and ask pathologist:
a. Is there adequate lesional tissue and whether it is representative.
b. Is it consistent with the differential?
c. Is it necrotic?
d. Is there infection?
14. I will send the tissue for pathology, gram stain, culture and sensitivity (aerobic, anaerobic,
fungi and TB). I will use the following preparation:
a. B5 (if suspicious of lymphoma)
b. glutaraldehyde for EM in case of Ewing‘s,
c. culture medium for flow cytometry
d. snap frozen in liquid nitrogen for molecular analysis.
15. I will fill the bone defect with cement as needed.
16. I will maintain meticulous hemostasis throughout the procedure by deflating the tourniquet
prior to closure and burying the hematoma inside the muscle
17. If I need to use a drain to prevent any postoperative hematoma and contamination of the field,
I will bring the drain at the distal end of the incision within few millimeters or just at the distal
end of the incision to incorporate it with the definitive incision.
18. I will close the wound in multiple water-tight layers

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 19. I will apply pressure dressing.
20. I will protect the lower extremity with back slab and non-weight bearing to prevent fracture
through the biopsy site. (crutches)
21. Involve multi-disciplinary team: MSK pathologist, Medical oncologist, Radiation Oncologist
and Orthopaedic oncologist

170. SEVEN QUESTIONS of tumor X-ray description

1. Site?
2. Size?
3. What is the lesion doing to bone?
4. What is the bone doing in response?
5. Matrix?
6. Cortex eroded?
7. Soft Tissue mass?

171. Principles in Osteosarcoma and Ewing‟s Sarcoma:

1. Local and Systemic Staging
2. Biopsy and confirm diagnosis
3. Refer
4. Neoadjuvant Chemotherapy: 6-8 weeks
5. Re-staging
6. Limb Salvage (wide resection and reconstruct) or Amputation
7. Chemotherapy: 6-8 months

172. Local and Systemic Staging for Bone Tumor

 Local:
1. Imaging – xrays in 2 planes whole bone
2. MRI or CT of the whole extremity

 Systemic:
1. Bone scan helpful in determining extent of involvement – remember can be cold in myeloma
(30% of the time)
2. Skeletal Survey: if suspecting MM
3. CT chest, abdomen and pelvis
4. Mammogram
5. Lab studies – CBC with smear, ESR, CRP, lytes, BUN, Cr, calcium, phosphate, albumin,
alkaline phosphatase, LDH, liver function tests, PSA, CEA, AFP and CA125, serum and
urine protein electrophoresis
6. Urinalysis may detect blood in renal cell, Bence Jones Protein

173. Metastatic Lesions in the Bone

Impending Fractures
 Historically, patient was at risk for fracture if lesion was painful, > 2.5cm and > 50% cortical involvement
 Mirels scoring system to predict risk of pathologic fracture (out of 12, >8 fix)
 Criteria involved:
o Image – blastic (1), mixed (2), lytic (3)
o Size - <1/3 (1), 1/3-2/3 (2), >2/3 (3)
o Site – UE (1), LE (2), peritrochanteric (3)
o Pain – mild (1), moderate (2), mechanical (3)
 Pathologic fractures heal slowly if at all
 Undergoing prophylactic fixation improved outcome
 Goals of surgical treatment:

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 o Alleviate pain
o Reduce narcotic use
o Restore skeletal stability
o Regain functional independence
 Decision to proceed to OR:
o Life expectancy
o Comorbid disease
o Extent of disease
o Histology
o Anticipated future oncologic treatments
o Degree of pain

General Operative Treatment Principles

 Open curettage of as much of the tumor as possible if site permits without violating cortical bone which
is required for support – pure closed treatment OK for radiosensitive tumors
 Rigid fixation (typically IM but sometimes plates) augmented with PMMA for increased stability where
possible
 Always lock proximally and distally
 Otherwise long stemmed cemented arthroplasty
 All of these get post-op radiation to prevent progression of disease once the wound has healed (at 10
days or so)

Treatment Of Specific Sites

Upper Extremity
 Proximal humerus
o Long stemmed cemented hemiarthroplasty
o If more extensive, endoprosthetic replacement
o Allograft prosthetic composite in rare cases
 Humeral diaphyseal lesions – IM nail or plate
 Distal humeral lesions – flexible IM nails, 90/90 plating, or resection with endoprosthetic replacement
 Forearm and hand lesions
o Distal to elbow are rare (lung, breast, renal cell most common; lung for hand)
o Radius and ulna treated with IM nails or plates or functional bracing
o If distal or extensive, amputation

Lower Extremity
 Pelvic/acetabular lesions
o Get a CT and xray entire femur
o Depending on extent of disease, standard cemented cup, antiprotrusio device or cage with
Steinmann pins or screws to get good bony purchase
 Femoral head and neck – cemented hemi vs THA with long stemmed femur with venting
 Peritrochanteric lesions
o IM better than screw and plate
o Be prepared to use calcar replacing prosthesis for extensive or radioresistant lesions
 Subtrochanteric lesions
o Substantial number won‘t heal because of 4-6x body weight through this area
o No screw and plate
o Statically locked reconstruction nails and endoprosthetic replacement for extensive disease
 Femoral diaphyseal lesions
o Statically lock IM nail +/- open curettage and PMMA
o Consider recon nail
 Supracondylar lesions
o Internal fixation with cement augmentation
o For advanced local disease, distal femoral replacement

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  Tibial lesions
o Far less common
o Proximally treat like a supracondylar – ORIF with cement
o Diaphysis – statically locked nail
o Distally – large fragment internal fixation with PMMA
 Foot lesions
o <1%
o Most common – lung, kidney and colon
o Treat with combo of radiation, orthotics and limited surgery
 Spine
o Delay in diagnosis may lead to neuro deficit and possible permanent loss of function
o If no known primary, CT guided biopsy, MRI and bone scan and check for hypercalcemia
o Myeloma and lymphoma are particularly radiosensitive so can use it emergently
o Operatively vertebro/kyphoplasty or decompression and internal fixation (remember to embolize
preop)

Radiation Treatment
 Myeloma and lymphoma – good
 Renal cell – bad
 Typical regimen 3 Gy in 10 fractions

174. Soft Tissue Lesions

Approach to Soft tissue lesions

If size is ,< 5cm or superficial then more likely benign. Deep > 5 cm or causing symptoms is more likely to be
malignant.

So if patient presents with signs of benign lesion you get an xray which may not show you much or may show
phlebolith ( hemangioma) or calcification:
1. Abnormal infection ( parasitic)
2. Synovial sarcoma
3. myositic ossficans

get an U/S which will show you if it is cystic( more likely benign) or solid. Or if there is a vascular nature to it.

If all signs are benign you can follow the patient closely and if they get symptoms of the mass grows then get
the MRI.

the most common site of metastases from soft-tissue sarcomas is to the lungs. In comparison to plain
radiography, CT has superior resolution in the imaging of Metastatic disease in the lungs. Perform a CT scan of
the retroperitoneum in the evaluation of extremity myxoid liposarcomas because, on occasion, patients will
have concomitant disease in the retroperitoneum and extremities.

esia required, and the greater cost of an open biopsy, it is the most reliable method for obtaining representative
tissue. Open biopsies may be excisional or incisional. However, because of the technical difficulty in
performing an incisional biopsy in the case of very small tumors, an open excisional biopsy is indicated for
these tumors. In very small tumors, take a small cuff of surrounding tissue en bloc with the tumor (primary
wide excision) because additional surgery may not be necessary, even in cases of malignancy.

Common benign deep soft-tissue tumors include intramuscular lipomas, extraabdominal fibromatosis (desmoid
tumors) hemangiomas, and benign nerve sheath tumors.

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175. Hypercalcemia
Symptoms
 Mild elevations in calcium levels usually have few or no symptoms
 Increased calcium levels may cause the following:
o Nausea, Vomiting, Abdominal or flank pain (The workup of patients with a new kidney
stone occasionally reveals an elevated calcium level, Constipation, Polyuria
o Alterations of mental status, Lethargy, Depression, Headache, Coma
o Weakness and vague muscle/joint aches
Physical
 Few physical examination findings specific to its diagnosis
 Primary malignancy may be suggested by lung findings, skin changes, lymphadenopathy, or
liver or spleen enlargement
 Hypercalcemia can produce a number of nonspecific findings, as follows:
o HTN and bradycardia may be noted but this is nonspecific
o Abdominal examination may suggest pancreatitis or the possibility of an ulcer
o Proximal muscle weakness that is more prominent in the lower extremities; they also
may have bony tenderness to palpation
o Hyperreflexia and tongue fasciculations may be present
o Polyuria and dehydration are common
o Lethargy, stupor, or even coma may be observed
Lab Studies
 Confirmatory tests: Changes in serum protein concentrations alter the total serum calcium
level but do not affect the unbound fraction so must calculate the actual level as follows:
Corrected total calcium (mg/dL) = (measured total calcium mg/dL) + 0.8 (4.4 - measured
albumin g/dL)
The average normal albumin level is 4.4. The reference range for corrected value of calcium is
approximately 9-10.6 mg/dL.
o The corrected calcium value is useful in most situations, but individual variation can
occur
o If the corrected serum calcium level still is not accurate, it is possible to measure the
free calcium ion activity (ie, ionized calcium level)
 Other nonspecific laboratory abnormalities commonly found in patients with hypercalcemia
result from disordered renal function. Patients commonly have significant azotemia at
presentation
 Hypercalcemia may produce ECG abnormalities related to altered trans-membrane potentials
that affect conduction time. QT interval shortening is common, and, in some cases, the PR
interval is prolonged. At very high levels, the QRS interval may lengthen, T waves may flatten
or invert, and a variable degree of heart block may develop. Digoxin effects are amplified.
 After a diagnosis of hypercalcemia is established, the next step is to determine the cause.
Initial testing is directed at malignancy, hyperparathyroidism, and hyperthyroidism, the most
common causes of hypercalcemia.
o PTH is the most direct and sensitive measure of parathyroid function
o Parathyroid hormone-related peptide (PTHrP) is thought to mediate the hypercalcemia
that develops with many malignancies. Assays to measure this peptide are available.
o Measurement of calcitriol is difficult but can be accomplished. This laboratory value is
useful in diagnosing hypercalcemia secondary to a granulomatous disease such as
sarcoidosis.
o Other electrolytes also may be disturbed in hypercalcemia. Serum phosphate levels
tend to be low or normal in primary hyperparathyroidism and hypercalcemia of
malignancy. Phospate levels are elevated in hypercalcemia secondary to vitamin D–

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 related disorders or thyrotoxicosis. Serum chloride levels usually are higher than 102
mEq/L in hyperparathyroidism and less than this value in other forms of hypercalcemia.
Goals of treatment
Principles
1. Stabilization and reduction of the calcium level
2. Adequate hydration
3. Increased urinary calcium excretion
4. Inhibition of osteoclast activity in the bone
5. Treatment of the underlying cause (when possible)
Steps:
1. Initial step is hydration with saline helping to decrease the calcium level through dilution
and increase the renal calcium clearance
2. Rate of fluid therapy is based upon the following:
o Degree of hypercalcemia
o Severity of dehydration
o Ability of the patient to tolerate rehydration
3. Hydration is ineffective in patients with kidney failure because diuresis is impossible so
dialysis is necessary
4. Loop diuretics (furosemide) may be used with hydration to increase calcium excretion –
but avoid thiazides because they increase the reabsorption of calcium
5. Calcitonin 2-8 U/kg IM/SC q6-12
6. Pamidronate 60 mg IV over 4 hours (if severe, 90 mg IV over 24 hrs)
7. Potassium phosphate 8 mmol IV q6h but more of a last resort

176. Small round blue cells (LIME E)

o Lymphoma
o Infection
o Myeloma
o EG
o Ewings

177. Myeloma and Lymphoma: treat with chemotherapy and radiotherapy

178. Five things that can look like anything:

1. Infection
2. EG
3. Fibrous Dysplasia
4. Chondroid Lesions
5. Metastatic Disease

179. Causes of pathology on both sides of the joint

2. Pannus (Inflammatory Arthropaty – RA)
3. PVNS
4. Infection
5. Blood ( hemophilia)
6. OA
7. TB

180. Fibrous Dysplasia

 Lesions can cease to grow after adolescence – new lesions can develop and grow after
maturity however

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  Monosotic – late childhood, early adult
 Poly – younger. Poly w endocrine – even earlier.
 Assoc syndrome is McCune-Albright
1. Skin and endocrine abnormalities
2. Café au lait spots – found midline, rough borders (NF smooth borders)
3. Multiple myxoma‘s of ST
4. Numerous endocirine
5. Cushings/hyperthyroid/acromegaly
6. Precocioius puberty and short stature
 DDx for polyostotic
1. Ollier‘s multiple enchondromatosis
2. Pagets
3. Brown
 Dx and Tx
 Biopsy typical for monostotic but not for classic poly (I disagree)
 Very difficult to eradicate w surg
 Try to live w lesion
 Options are resection and BG w cancellous, cortical struts (can also use as
intramedulary)
 Valgus osteotomy may be req‘d for prox femoral varus.
 Heals w fibrous dysplasia
 Is third most common cause of secondary o.sarc arising from bone behind pagets and
radiation

181. UBC
 80-90%<20yrs
 aspiration, high ALP
 central medullary lesion
 80% prox hum/femur
 calc and talus (usually a bit older (colterjohn case of 16yr old w big calc lesion)
 fallen fragment sign (when # in the bone)
 MRI of ABC vs UBC
o UBC: no fluid/fluid unless # present, Not as expansile
o ABC: multicystic w fluid fluid and more expansile, usually eccentric and not central
 Tx
o Observation or aspiration for Dx
o Should be green/yellow fluid
o If no fluid or is hemorrhagic, open biopsy
o Can tx w repeated asp/injection w steroid/bone marrow (do this if no # present)
o #‘s heal normally, do not inject # until healed
o curettage and bg if structural integrity of bone compromised, high recurrence rate
however

182. Aneurysmal Bone Cyst

 Be sure to say extensive intralesional curettage w burr and adjuvant therapy (water most
common, phenol, nitrogen, etc)
 Can be primary (from AV fistula that results in bone lesion) or from secondary degen of
chondroblastoma/osteoblastoma/gct/fibrous dysplasia
 80%<20yrs, rare > 30 (same as UBC)

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  spine (post elements) & femur most common sites
 both ubc and abc can but rarely cross physis
 DDX
o Ubc
o Gct (may coexist)
o Telangiectatic
 Tx
o Biopsly usally req‘d as aspiration only yields undiagnostic blood
o Curette and bg or cement to fill defect
o 10-20% recurrence
o excise expendable bones, also consider in recurrence

183. EG (histiocytosis x)
 Ages 5-10 most common, rare >30
 Associated syndromes
o Hand-schuller-christian – DI/exopthalmous/rarefied skull defects
o Litterer-Siwe – fatal <2yrs
 Spine common site (vertebra plana)
 Multiple lesions common
 Ddx
o UBC
o O.myelitis
o Ewings,
 Tx
o Once dx made, can observe, usually go away
o Indications for sx
 Determine dx
 Persistent pain
 Prevent and tx path #
o Curettage and BG is tx
o Radiation only for resistant or recurrent lesions

184. Ossifying Fibroma (osteofibrous dyslplasia or kemson-campanacci lesion)

o very rare, occurs in 1st and 2nd decades
o bowing or anterior expansion of tibia most common presentation
o lytic w sclerosis. Geographic, metaphyseal
o DDx
o Adamantinoman (only clinical/radiographic difference is this one occurs in older people),
need biopsy
o Fibrous dysplasia
o Nonossifying fibroma
o Osteoblastoma
o ABC
o Nat hist
o <5yrs, little progression
o after maturity, little progression
o may change to adamantinoma
o Tx
o Asymptomatic, observe
o If <10, delay excision, much higher recurrence if take in this age group

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185. Giant Cell Tumour
 80% occur >20yrs
 5% can met to lung
 can occur anywhere, 75% in epiphysis/metaphysis of long bones, eccentric
 Campannaci classification
o Stage I – initial stage
o Stage II – more aggressive, no breakthrough (60% in this stage)
o Stage III – aggressive w breakthrough (30% of lesions)
 MR, shows focal signal changes due to hemosiderin (aids in dx)
 DDx
o Brown tumor (must do serum Ca/PTH to differentiate the two
o All the other stuff as well as telangiectatic
 Tx
o Expendable bones, en bloc
o Non-expendable
 Extensive intralesional curettage w burr and water (adjuvant thereapy)
 Ferguson says: One study utilizing a combination of hydrogen peroxide,
electrocautery, phenol and sterile water has reported a local recurrence rate
of 6%
 Can BG or cement
 10-25% recurrence

186. Chondrosarcoma
 2/3 occur as primary tumor and 1/3 devel from enchondroma or osteochondroma (the
secondary ones are usually low grade)
 secondary chondro occurs in younger pts 20-40
 normally b/t 30-70
 cartilage tumors in hands and feet are typically benign
 low grade and enchondroma difficult to tell on biopsy
 tx is wide resection
 rad/chemo, no good , rad only used for residual margins in spine/pelvis

special notes
 clear cell chondro (is the malignant version of chondroblastoma)
o rare, age 20-40, low grade
o within epiphysis/metaphysis
 dedifferentiated chondro
o rare, very high grade, very poor prognosis

187. Chondroblastoma
o 95% from 5-25yrs
o most commonly epiphyseal
o DDx
o Enchondroma
o Clear cell chondrosarc
o GCT
o FD
o Infection
o Pelvic lesions are more aggressive

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o Femur>tibia>humerus>pelvis>tarsal
o Tx
o Intralesional curettage and BG
o Recurrence is 10-30%

188. Enchondroma
o Age 15-40
o Assoc syndromes are;
o Ollier‘s: Multiple enchondromatosis, Incr risk of malignancy
o Maffucci‘s: Multiple w evidence of hemangioma‘s, V. high risk of malignancy, Can see calcified
phleboliths in the hemangioma‘s on xray
o Common in hand, many other areas are asymptomatic
o V difficult to distinguish from chondrosarc sometimes
o Bad signs: Endosteal scalloping/erosion in long bone lesions (more common hand
without being c.sarc‘
o Popcorn calcifications
o DDx
o Bone infarct
o Gct
o FD
o Ubc
o C.sarc
o Tx
o Avoid biopsy in classic, asymptomatic lesions (xray in 3/12)
o Should biopsy when;
 Lesion changes
 Persistent pain
 Worrisome xray findings, erosion, permative lysis
o If symptomatic, curettage and BG

189. DDx for onion skinning:

 EG
 Non-Hodgkin's lymphoma
 Ewing's sarcoma
 Osteomyelitis
 Osteosarcoma

190.
191. Common Syndromes in Orthopaedic Oncology
o McCune Albright Syndrome:
o **Presents with short stature and precocious puberty
o Polyostotic fibrous dysplasia, midline and smooth café au lait spots, endocrine (
hyperthyroid,cushings, acromegaly,)
o Ollier‟s: multiple hereditary enchondromas
o Maffuci‟s: Ollier‘s with visceral, GI malignancies and soft tissue hemangiomas
o Letterer-Siwe: fulminant, lethal form of EG
o Hand Schuller Christian: classic triad of DI, exopthalmus, and lytic skull lesions in EG.
o Gardners‟s syndrome: Osteomas, Intestinal polyposis, ST fibromas, Sebaceous cysts
o

192. RADIOTHERAPY

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  dose measured in Gray: 1 rad=1centigray (cGy), therefore 1 Gray = 100 rads
 total dose delivered in fractions (smaller doses) to avoid exceeding tissue tolerance and allow
cells to be in phase to maximize effect
 esp. good for round cell lesions (Ewings, MM, Lym), mets and adjuvant for STS
 usually ~ 180-200cGy/d, 5D/wk

Doses
mets: 25-30 Gy
STS: 45-60 Gy
Bone Sarc: 60+ Gy
Post-op Margins 45-60+ Gy
Benign Aggressive (i.e. GCT, ABC) 40-50 Gy

Previous Radiotherapy
-if pt has hx of radiation with 45 Gy or less it is O.K. to operate through tissue, if 45-50 Gy there will
probably be delayed or complicated wound healing, and if 60 or more then wound will not heal

193. Benign and Malignant Bone Tumor Treatment Summary

Osteoid osteoma
 Start with NSAIDs
 Percutaneous radioablation (not in spine!! Dura !!)
 Percutaneous curettage
 En bloc resection +/- internal fixation

Osteoblastoma
 En bloc excision in expendable bones
 Lytic lesions treated with curettage and bone graft or cement
 Spinal lesions may require rads if soft tissue mass and epidural disease is extensive
 Risk of recurrence after curettage and bone graft 10-20%
 Differentiation to osteosarcoma

Osteoma
 Complete excision if symptomatic, or for diagnosis is large
 Complete removal is curative

Osteochondroma
 Ceases growth after maturity so if asymptomatic – leave it
 Excise if locally painful or NV compromise or if change in cartilage cap
 Pain is acceptable indication for excision in skeletally immature however may lead to deformity or
recurrence

Famililial Osteochondromatosis
 Deformity in upper and lower extremities may require correction
 Monitor for malignant change and investigate or biopsy for pain, enlargement after maturity and new
areas of lysis within pre-existing lesion
 Recurrence after excision is suspicious for malignancy

Enchondroma
 Pathology can be confusing so avoid performing biopsy except when:
o Lesion changes over time

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 o Persistent pain
o Worrisome xray findings of endosteal erosion or permeative lysis
 If lesion appears benign, watch it; wait 3/12 and re-xray; if no change repeat at 6/12 and 1 year
 If symptomatic, curettage and bone graft and usually curative

Bell
Enchondroma
Ages 15-40
 Usually discovered as incidental lesions in metadiaphyseal long bones
 Also hands (prox phalanx>metacarpals>mid phalanx>distal phalanx) and feet
 Usually geographic with little endosteal response (more erosive features in the hand)
 Must watch for endosteal scalloping and permeative lucency within or around an established
enchondroma (these are signs of chondrosarcomatous degeneration)
 Usually lucent in hand and calcified (popcorn or stippled) in long bones
 Very rarely ST mass
 Cartilage bright on T2
 DDx –
o Bone infarct (smoke rising from chimney)
o GCT
o Fibrous dysplasia
o UBC
o Chondrosarc
 Usually do not biopsy, only do so if;
o Lesion changes
o Persistent pain
o Worrisome xray findings
 Tx w curettage and BG
 Olliers is multiple enchondromatosis – 25-30% malignant transformation
 Maffucci’s – is olliers with multiple ST hemangiomas – very high risk of malignancy

Ollier‟s Disease (Multiple enchondromatosis)

 25-30% risk of malignant degeneration to chondrosarcoma – usually low or intermediate grade

Maffucci‟s Syndrome (above with multiple soft tissue hemangiomas)

 Risk of developing chondrosarcoma higher than Ollier‘s

Chondromyxoid fibroma
 Open biopsy is usually necessary
 Curettage and bone graft or marginal excision
 Consider en bloc excision if location permits removal without significant associated morbidity
 Recurrence < 20%

Chondroblastoma
 Lesion must be well visualized at removal – opening joint capsule is usually required
 Curettage is treatment of choice and must be thorough
 Phenol and liquid nitrogen generally NOT used for fear of growth plate or cartilage damage
 Defect is packed with autograft/allograft
 Recurrence 10-30%

Periosteal chondroma (Juxtacortical chondroma)

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  En bloc resection with an intact narrow rim of normal bone is the treatment of choice
 Curettage has high risk of recurrence
 Spilling cartilage into soft tissues increases risk of local relapse

Synovial chondromatosis
 Diagnose with xrays, arthrogram, MRI or arthroscopy
 Removal of loose bodies with total synovectomy in early or transitional stages

Fibrous cortical defect

 Plain xrays are usually diagnostic
 Observation only with repeat xrays at 3-6/12 intervals for 1 year if atypical appearance
 Usually heal spontaneously
 Treatment for progressive painful lesion is curettage and bone graft
 Risk of recurrence is low

NOF
 Essentially a big fibrous cortical defect
 Treat surgically with curettage and bone graft if:
o Atypical location
o Intractable pain
o Pathologic fracture
o Impending pathologic fracture
 Most lesions undergo spontaneous healing

Fibrous dysplasia
 Biopsy may be needed if the lesion is monostotic but rarely for polyostotic
 Difficult to eradicate extensive lesions without a major bone resection – this is usually not appropriate
for a dysplastic (as opposed to neoplastic) lesion
 Goal of therapy is to permit the patient to live in mechanical symbiosis with the lesion – so treatment
determined by age, activity of the lesion, extent of fracture risk and mechanical deformity
 Surgically treated lesions often recur rapidly in skeletally immature
 Conservative therapy includes bracing, activity modification
 Surgical treatment includes replacement of dysplastic fibro-osseous tissue with autograft, cancellous
allograft, and/or allograft cortical struts
 Allograft cortical struts may be used as intramedullary splints or only struts
 Internal fixation is often necessary to supplement grafts
 Consideration should be given to correction of deformity to decrease risk of further fracture
 Valgus osteotomy and instrumentation often required for proximal femur to prevent progressive
shepherd‘s crook deformity

Ossifying fibroma (osteofibrous dysplasia)

 If asymptomatic, observe
 Delay excision and bone graft until age 10 if possible since excision before this associated with high
recurrence rate

GCT
 Expendable bones (fibula, rib):
o Should be resected with wide en bloc resection reducing risk of recurrence.
o May be wise to excise distal radius en bloc if cortex is extensively eroded with a soft tissue
mass.
 Non-expendable bones
o Intralesional curettage through a large cortical window with extensive burring back to normal
bone
o Adjuvant treatment with phenol or liquid nitrogen may low recurrence risk

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 o Defect should be filled with bone graft and/or cement
o Consider internal fixation if lesion is extensive
 Spinal lesions – if patient has a deficit, decompression
 Radiation may be used after partial removal of axial (spine, sacrum) lesions
 Recurrence after intralesional treatment is 10-25% and most dependent on the completeness of tumor
removal but can be decreased with use of phenol or cement
 <%5 develop metastases usually to lung
 Rare malignant transformation

ABC
 Open biopsy is often necessary
 Curettage and bone graft or cement
 Recurrence in 10-20%
 Nonessential bones (rib or fibula) en bloc excision is appropriate and also for recurrent aggressive
lesions

UBC
 Plain films and aspiration are usually diagnostic yielding green/yellow fluid
 If no fluid or hemorrhagic, proceed to open biopsy
 Repeat aspirations and injections of steroid or autologous bone marrow are treatments of
choice for lesions without pathologic fracture. May take 6-12/12 to heal
 Pathologic fractures heal without undue delay and are unaffected by steroid injection
 Generally delay injection into fracture cyst to prevent leakage
 Curettage with bone graft may be indicated if structural integrity of bone is at risk
 Local recurrence rate is high and increases with incomplete excision

EG
 Indications for surgery:
o Determine diagnosis
o Persistent pain
o Prevention or treatment of pathologic fracture
 Once diagnosed, may be observed and usually heal spontaneously
 Curettage and bone graft are especially indicated for lower extremity lesions and are
supplemented with internal fixation if at risk for fracture
 Low dose radiation is effective in most lesions but usually reserved for recalcitrant nonhealing
or recurrent lesions
 Multiple lesions or visceral involvement may respond to chemotherapy
 Vertebra plana in kids

Letterer-Siwe Disease
 Acute fulminant disease affecting infants and children <2 with less skeletal involvement
 Systemic disease and potentially fatal
 Treatment includes steroids and chemotherapy

Hemangioma
 For spinal lesions, CT or MRI to confirm diagnosis
 Once vertebral collapse, xrays may no longer be diagnostic
 If lesion is asymptomatic, no treatment
 Tumor is usually resected anteriorly if:
o Neuro deficit
o Collapse with neurologic change or chronic painful kyphosis
 Preoperative embolization should be considered

Osteosarcoma

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  Biopsy in consultation with tumor surgeon
 Chemo and surgery for usual high grade lesion
 Neoadjuvant chemo prior to limb salvage
 Thoracotomy and removable of respectable pulmonary lesions prolongs overall survival and results in
long-term disease free survival in 20-30%
 Prognosis dependent on presence of mets and extent of necrosis after chemo
 Large tumor, axial location, and positive margins after resection are also risk factors
 5 yr survival 50-85%
 Radiation for unresectable lesions – rarely alters local disease progression

Chondrosarcoma
 Biopsy in consultation with tumor surgeon
 Differentiation of low grade chondrosarcoma and benign enchondroma can be difficult
 Treatment is surgical excision with wide margins
 Radiation and chemo are NOT effective
 Radiation for palliation or surgically inaccessible lesions
 Radiation before or after microscopically incomplete resections in spine or pelvis
 Disease free survival at 5 yrs 30% for high grade; 90% for low grade

Fibrosarcoma of bone
 Biopsy in consultation with tumor surgeon
 Wide resection is required
 Amputation may be required to achieve adequate margins
 No definite evidence for adjuvant chemo but many centers recommend for high grade
 Radiation for surgically inaccessible lesions or palliation

MFH
 Biopsy in consultation with tumor surgeon
 Although surgery is the mainstay of treatment, neoadjuvant and adjuvant chemo are often used but
efficacy not well documented

Myeloma
 Serum or urine immune electrophoresis is generally diagnostic
 Stage and renal function are combined to predict survival
 Chemo is the mainstay +/- bone marrow transplant
 Pamidronate is effective in managing hypercalcemia and controlling bone symptoms
 Radiation can be effective to control painful lesions
 Surgery may be required for impending pathologic fractures or spinal cord compression
 With standard chemo, 15% die within 6/12, and from this point onward 15% per year
 Bone scan cold 30% of the time

Solitary Plasmacytoma
 Rare, only 3% of myeloma
 2/3 will get myeloma usually within 3 years
 May be resected or more commonly treated with radiation

Lymphoma
Hodgkin‟s
 Biopsy is required – gallium scan may demonstrate nodal tissue that may be biopsied in preference to
bone
 Treatment is multiagent chemo and radiation
 Radiation may be given to control bone pain or attempt to avert impending pathologic fracture

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  Surgery is usually reserved for osseous complications like treatment of fracture or impending
fracture

Non Hodgkin‟s
 Prior to bone biopsy, evaluate whether there is some soft tissue that could be biopsied with less
morbidity
 Lymphoma is radiosensitive and bone resection is generally not needed
 Solitary lesions get radiation with chemo
 In rare case of local recurrence, resection may be necessary for local symptoms
 5 yr survival for solitary bone lesions >50%
 For disseminated disease, need chemo
 Pathologic fracture often requires ORIF

Leukemia
 Diagnosis with CBC with peripheral smear and bone marrow aspirate
 If negative, biopsy the lesion
 Treatment is by hematology/oncology

Ewing‟s
 Chemo is effective to shrink the tumor and manage micromets
 Role of surgery and radiation for local disease is controversial
 Lesions arising in expendable bones should be excised
 Radiation for local treatment has risks of local recurrence (as high as 30%), pathologic fracture,
secondary osteosarcoma, fibrosis affecting function, and growth distrurbance in children
 No evidence of survival advantage with surgery
 Many centers advocate resection after neoadjuvant chemo
 Unresectable lesions get radiation and chemo

Adamantinoma
 Biopsy in consultation with tumor surgeon
 Wide resection with reconstruction using allograft, autograft or vascularized fibula
 Amputate if lesion cannot be resected with negative margins
 15% will metastasize

Chordorma
 Biopsy in consultation with tumor surgeon
 Total resection with clear margins is required
 First resection is best chance for cure
 Radiation may be used for microscopically positive margins or for palliation (but often short lived)
 Cure is dependent on completeness of resection – if wide negative margins, > 80% chance of cure

Stress fracture
 Rest and avoidance of activity that caused the fracture
 Immobilization and splinting useful in acute phase

Enostosis
 If lesion is thought to be a bone island, follow with serial radiographs

Hyperparathyroidism
 Looks like a GCT
 Treat by rectifying emergently life threatening electrolyte disturbances and identify and treat the cause
of the increased PTH

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Paget‟s

 Treatment aimed at controlling osteoclastic activity and include bisphosphonates, calcitonin and
mithramycin

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