ORTHO NOTES BY JOACHIM & LIYANA (EDITED BY WAI WAI) 5 ELBOWS & FOREARMS 36

 Cubitus Varus (Gunstalk Deformity)

TABLE OF CONTENTS  Cubitus Valgus
NO. TITLE PAGE  Rheumatoid Arthritis
 Osteoarthritis
1 INTRODUCTION TO ORTHOPAEDICS 4
 Olecranon Bursitis
 History-Taking
 Tennis Elbow (Lateral Epicondylitis)**
 Analgesics Ladder (by WHO)
 Golfer’s Elbow (Medial Epicondylitis)**
 Post-Op Management (fever/oliguria/dyspnoea/shock)
 Cubital Tunnel Syndrome**
 Plaster Techniques
 Supracondylar Fractures
2 FRACTURES – GENERAL PRINCIPLES*** 8
 Elbow Dislocations
 Definitive treatment  Medial Condylar Injury
 Open Fractures  Radial Head Fracture
 Emergency Care  Radial Neck Fracture
 Irrigation & Debridement  Forearm Fracture/Dislocations
 Stabilisation of Fracture  Nightstick Injury
 Wound Coverage  Causes of Tardy Ulnar Nerve Palsy
 Delayed Union & Non-Union 6 HANDS & WRISTS 39
 Management of Bone Loss
 Types of Cases
 Fracture Healing
 DDx of Painful Elbow & Hand
 Compartment Syndrome
 Hands
 Avascular Necrosis
o Acute Infections
 TipBits for Fractures
o Skin
3 SHOULDERS 17 o Muscle/Tendon Disorders
 Approach to Shoulder Problems o Lumps
 Rotator Cuff Impingement  Wrists
 Calcification of the Rotator Cuff o Joint Disorders
 Biceps Tendonitis o Lumps
 Rupture of Biceps Tendon o Muscle/Tendon
 Frozen Shoulder*** o Nerves
 Shoulder Joint Instability & Dislocations  Hands & Wrists
 Other Disorders of the GH Joint o Rheumatoid Arthritis
 Disorders of the Scapula o Osteoarthritis
 Fractures of the Clavicle o Bone Disorders
 Fractures of the Scapula  Colles’ Fracture
 AC Subluxation/Dislocations  Smith’s Fracture
 Scaphoid Fracture
 SC Dislocations
 Complications of Wrist Fractures
4 ARM 29
 Lunate Dislocation
 Fractures of the Proximal Humerus  Perilunate Dislodation
 Fractures of the Shaft of Humerus  Scaphoid Dislocation
 Fractures Around the Elbow in Children o Brachial Plexus Lesions
 Fractures & Dislocations Around the Elbow in Adults o Zones of the Hand
7 HIP 51  Danis Weber Classification
 Pelvic Fractures  Lauge Hansen Classification
 Approach to Hip Pain  Ligamentous Injuries
 Congenital Dislocation of the Hip (CDH) /  Recurrent Knee Subluxation
Developmental Dysplasia of the Hip (DDH) 11 FOOT 77
 Hip Dislocation  Evaluation of Foot Complaints
 Perthes’ Disease (Coxa Plana)  Congenital Talipes Equinovarus (Congenital Club
 Slipped Capital Femoral Epiphysis (SCFE) Foot)
 Pyogenic Arthritis  Hallux Valgus
 Transient Synovitis  Ruptured Tendo Archilles
 TB Hip  Hallux Rigidus
 RA Hip  Pes Planus
 OA Hip  Footballer’s Ankle
 AVN of the Hip***  Archilles Tendonitis
 Proximal Femoral Fractures – Summary  Talar Fracture
8 KNEE 64  Calcaneal Fracture
 Knee – DDx  Plantar Fasciitis
 Common Knee Symptoms  Bunions
 Meniscal Tears  Metatarsal Fracture
 Meniscal Cysts 12 SPINE 82
 Chronic Ligamentous Instability  Approach to Back Pain
 Osgood-Schlatter Disease  Prolapsed Intervertebral Disc (PID)
 Osteochondritis Dessecans  Scoliosis
 Patellar Fracture  Adolescent Idiopathic Scoliosis
 Recurrent Dislocation of the Patella  Lumbar Spondylosis
 Patellar/Quadriceps Tendon Rupture  Spinal Stenosis
 Dislocated Knee  Spondylolisthesis
 Chondromalacia Patellae  Cauda Equina Syndrome
 OA Knees***  PID vs. Spinal Stenosis
 RA  Lumbar Spine Fractures
 Baker’s Cyst (Popliteal Cyst)  Cervical Myelopathy
 Housemaid’s Knee (Prepatellar Bursitis)  Cervical Spondylosis
 Clergyman’s Knee (Infrapatellar Bursitis)  Cervical Lesions
 Semimembranous Bursa  Cervical Spine Trauma
 Charcot’s Joint 13 DM FOOT (ORTHO) 93
9 TIBIA 72 14 POLYTRAUMA 98
 Tibial Plateau Fracture 15 FRACTURES 104
 Tibial Diaphysis Fracture 16 BONE & JOINT INFECTIONS 108
10 ANKLE 74
 Acute Haematogenous Osteomyelitis
 Evaluation of Ankle Complaints  Subacute Haematogenous Osteomyelitis

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  Post-Traumatic / Operative Osteomyelitis
 Chronic Osteomyelitis
 Acute Suppurative Osteomyelitis
 TB
17 OSTEOPOROSIS*** 111
18 RHEUMATOID ARTHRITIS*** 113
19 ANKYLOSING SPONDYLITIS 117
20 GOUT*** 118
21 BONE TUMOURS & CYSTS (OSCES-ORIENTED) 120
22 PAEDIATRIC ORTHOPAEDICS 124
 Fractures
o Ossification Centres
o Ligamentous Laxaties
 Congenital, Developmental & Physiological
Conditions
o Torticollis (wry neck)
o Approach to Limping Child
o DDH
o Clubfoot (Congenital Talipes Equinovarus)
o Flatfeet (Pes Cavus)
o LL malalignment
o Scoliosis
o Cerebral Palsy (CP)
23 IMPORTANT CLASSIFICATIONS FOR ORTHOPAEDICS 139
24 DISEASE MNEMONICS 142

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INTRODUCTION TO ORTHOPAEDICS PAST MEDICAL HISTORY
HISTORY TAKING - Comorbidities (fitness for op)
- Medication history
PRESENTING COMPLAINT - Any drug allergies
Pain
- SOCRATES
SOCIAL HISTORY
- For timing/frequency - Alcohol/smoking
o Early morning pain – hallmark of inflammation - See ‘activity’
o Relieved at night – often mechanical in nature - Any caregiver support
o Night pain – indicates severity of pain, ?underlying malignancy
- For relieving factors: include analgesics & TCM
SYSTEMIC REVIEW
- Any recent history of trauma/falls
Activity For upper limb
- The usual systemic review questions (especially to rule out extra-articular
Loss of function – for lower limb - Hand dominance
manifestations of certain diseases such as rheumatoid arthritis)
- Going to shops - Washing, dressing, combing,
- Red flags for lower back pain
- Use of walking aids (community ambulant?) feeding, writing
o Metastasis: LOW, LOA, night sweats, history of malignancy, night pain
o Any lift landing? - Use of chopsticks (assess fine
o Infection: fever, history of TB / toe gangrene
- Walking distance motor skills)
o Neurological deficits: BO, PU (continence), whether neuro deficits are
- Use of stairs progressive
Also assess pre-morbid ADL status (dressing, eating, ambulating, toileting, hygiene) o History of trauma
o Hairy patch / cafe-au-lait spots (especially in paediatric population)
Specific to lumbar spine
- History of injury
- Radiation of pain (look for dermatomal distribution) ANALGESIC LADDER (BY WORLD HEALTH ORGANISATION)
- Associated neurological symptoms (numbness/paresthesia) & their distribution
- Any sphincter disturbance (bladder & bowel symptoms secondary to cauda equina  Mild pain: Step 1: Simple analgesics (non-opioid)
syndrome) o Initiate topical and/or simple oral non-opioid analgesics (e.g. paracetamol,
NSAIDs)
Specific to the hip o + adjuvant e.g. tricyclic antidepressants, anticonvulsants (pregabalin or
- Stiffness & pain arising from hip joint gabapentin) for neuropathic pain.
- Whether patient is able to care for their feet / pedicure
 Moderate pain: Step 2: Weak opioid
Specific to the knee o Weak opioid (e.g. tramadol, codeine phosphate or dextropropoxyphene)
- Locking (due to jamming by torn meniscus or loose body) o + adjuvant e.g. tricyclic antidepressants, anticonvulsants
- Giving away (due to patellofemoral problem, loose bodies, torn flap of meniscus,
ligamentous laxity)  Severe pain: Step 3: Strong opioid
o Opioids (e.g. morphine, oxycodone)
Specific to the feet
- Back pain (referred pain) o + adjuvant e.g. tricyclics, anticonvulsants
- Pins & needles (lumbar spine pathology/nerve entrapment/peripheral neuropathy)
- Footwear

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POST-OPERATIVE MANAGEMENT then reabsorbed, with collapse of the supplied lung segments, usually the basal lobes.
The collapsed lung may become secondarily infected by inhaled organisms.
1. Life Threatening – vital signs Predisposing factors
2. Limb Threatening – circulation  obesity
3. Post op pain  smoking
 wound pain
4. Post op urine output
 opiates and drowsiness
5. Post op nutrition  pregnancy
6. Rehabilitation – independent, dependent in ADL, WB  muscular weakness
7. Discharge  nasogastric tube
 abdominal distension
Days 3-5  bronchopneumonia
Postoperative Management Related to Surgery  developing sepsis, which may be:
1. Postop consciousness – post sedation and anaesthesia, CVA, hypoxia, o wound infection
o drip site or drain infection
hypovolemia o abscess formation, e.g. subphrenic or pelvic, depending on type of
2. Post op airway – aspiration, pneumonia surgery performed.
3. Post op circulation - Hypovolemic shock, PE/DVT Indications for prophylactic antibiotics
4. Local circulation - , vascular injury or compromise, Compartmental symptoms • patients at risk of subacute bacterial endocarditis, for example with mitral
5. Nerve compression valve disease or prosthetic valves
6. Post op GI • patients undergoing prosthetic joint or vascular components
7. Postop urine • operations which involve contamination to some extent, for example colon
8. Postop fever or oesophageal resection
• patients who have some other type of indwelling prosthesis, for example
9. Post op wound infection
total hip replacement
As a general rule prophylactic antibiotics should be given in the perioperative period
and then discontinued. It is best if the first dose can be given on induction of
Post-Op Fever anaesthesia. Prolonged administration of antibiotics is accompanied by undesirable
Days 0-2  mild pyrexia side effects, such as the emergence of antibiotic resistant organisms, or the
o tissue damage and necrosis At the site of the operation development of pseudomembranous colitis; it is for this reason that duration of therapy
o haematoma
 higher persistent pyrexia should be stated.
o postoperative atelectasis
Postoperative wound infection
o specific infections related to the surgery
 biliary infection after biliary surgery Postoperative wound infection is a potentially hazardous complication of surgery. It is
 urinary tract infection after urological surgery important to consider the risk of it occurring, and to give prophylaxis if appropriate.

Note that fever due to blood transfusion may occur in this initial post-op period. Risk factors
- senility, diabetes, ischaemia, malnutrition, vit C & Zn deficiency
Postoperative atelectasis generally occurs within 48 hours. - steroids and cytotoxic drugs, radiotherapy
It is an extremely common post-operative complication with some degree of
pulmonary collapse occurring after almost every abdominal or trans-thoracic
- long preoperative hospital admission
procedure. - shaving the operative site the night prior to surgery
- rough handling of the tissue
Mucus is retained in the bronchial tree, blocking the finer bronchi; the alveolar air is - poor blood supply, for example sutures too tight

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 - failure to debride devitalised tissues IN SUMMARY
- large dead space  wind -- atelectasis within 48 hrs, aspiration, pneumonia
- contamination of wound  water -- UTI's, especially if catheterized
 wound -- check for wound infection.
Wound irrigation
• removal of foreign bodies  veins -- (OK, it's a "V") DVT, phlebitis from IV's
• reduction of pathogen numbers  drugs -- drug reactions (uncommon)
• removal of blood, clot and dead tissue
• removal of free cancer cells Fever within 48 hours is usually atelectasis. After 48 hours, atelectasis is less likely.
• moistening of tissue
After 5 days: wound infection
The solution used to irrigate may be: intraabdominal abscess (CT abdo and pelvis)
 physiological saline; its low osmolarity may aid in free tumour cell lysis DVT
 topical antiseptic, e.g. chlorhexidine and iodine; both may cause undesirable
cell death of host tissue. Alternatives include spraying dry povidone-iodine
spray onto the wound - this has been shown to reduce infection rates - or Post-op Dyspnoea
local injection of antibiotic peroperatively. 1. Atelectasis -- usually within 48 hours, more likely in elderly, COPD, smokers, obese
Days 5-7  venous thrombosis, in the limbs or pelvis
 causes related to specific op’s, e.g. failure of bowel anastomosis with fistula
patients, and those with upper abdominal incisions. Treatment is to mobilize,
formation & leakage encourage deep breathing and coughing, chest physiotherapy
>7 days Causes are less likely to be directly related to the specific operation undertaken. 2. Aspiration -- risk factors include GERD, food in the stomach, intestinal obstruction,
Causes include:- and pregnancy (delayed gastric emptying). Prevent via preoperative fasting in elective
 wound sepsis
patients, 'rapid sequence" induction in emergency patients, and those at high risk.
 distant sites of sepsis eg cerebral or hepatic abscess
 thrombotic disease 3. Pneumonia -- atelectasis, aspiration and copious secretions are predisposing factors.
 postoperative atelectasis Often gram-negative, and or polymicrobial.
 postoperative pneumonia 4. Heart failure -- caused by fluid overload in patients with limited myocardial reserve,
 wound infection post op MI, or dysrhythmias (most commonly a fib).
 intravenous phlebitis
5. Pulmonary embolus -- most clinically significant pulmonary emboli arise from the iliac
 urinary tract infection
 prostitis and femoral veins.
 gout
 central line sepsis
 parotitis
 drug reaction
Post-Op Oliguria
 transfusion reaction
o non-haemolytic transfusion reactions • Pre-renal -- COMMONEST CAUSE OF LOW URINE OUTPUT
o febrile transfusion reactions o external fluid loss (hemorrhage, dehydration, diarrhea)
 complications of specific operations, for example pericarditis after cardiac o internal, third space loss -- bowel obstruction, pancreatitis
surgery • Renal -- nephrotoxic medications
o Untreated pre-renal causes leading to acute tubular necrosis
• Post renal -- prostatic hypertrophy, blocked foley, stone in solitary kidney

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Post-Op Shock o Inadequate resuscitation
- Basic haemodynamics: CO = SV x HR  Patients are NPO for several hours prior to surgery
- Recognising shock  Patients with intraabdominal processes (especially infection and SBO)
o Easy signs to find: have tremendous fluid losses.
 Urine output  The best prevention of postoperative resuscitation problems is
 The best CVP is if you see pee preoperative resuscitation.
 Think Foley - Post-op septic shock
 Blood pressure o Utilize Rivers goal directed protocols (N Engl J Med 2001; 345:1368-1377,
 Skin temperature Nov 8, 2001 )
 Mental status  CVP 8-12
 Drain saturation  Urine output > 0.5 cc/kg/hr
o Lab investigations  SvO2 > 70
 FBC  Hgb to 10, Dobutamine
 Serial FBC for any patient with bleeding risk  MAP>65
 Lactate  Norepinephrine or Dopamine
 BUN / Cr - Post-op cardiogenic shock
 Coagulation profile o Patient may not complain of chest pain although there may be clues on exam.
 Electrolytes (specifically bicarb) o EKG/Echo/Swan/enzymes, etc.
- Resuscitation fluids o Must weigh risk of bleeding (ASA, thrombolytics, cath) vs. benefit
o No evidence to show that one type of fluid is superior to another in  Usually benefit of treating heart outweighs risk
resuscitation o Inotropic support
o Ensure that you use enough crystalloid. - Abdominal compartment syndrome
- General principles o Post op laparotomy patients can be at risk for this as well as cirrhotics
o Resuscitation with appropriate and o EASY to measure. Basically stick a foley catheter to a CVP monitor
enough fluids o Abnormal is over 20 cm water. Dangerous over 30.
o Give blood if bleeding or evidence of o Treatment is decompression
oxygen delivery problem o You only find it if you THINK about it.
o Pressors to mitigate hypotension - Summary
o Stress dose steroids if indicated o Resuscitation, resuscitation.
o Intensive insulin o Think about hypovolemia
o Normothermia o Think about bleeding.
- Hypovolaemic shock o Think about sepsis.
o Bleeding o Think about abdominal compartment syndrome
 Think about the surgery and everything that could go wrong o Get an EKG in high risk patients.
 Surgical bleeding vs. postoperative “oozing” o And remember… The best treatment is PREVENTION
 Support with fluids and blood products.
 Treat hypothermia

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PLASTER TECHNIQUES INITIAL MANAGEMENT
 ABCDEs
Basic Principles  Limb - attend to neurovascular status (above and below)
1. One joint above and below the fracture  Rule out other fractures/injuries (especially joint above and below)
2. Cast is well molded with no pressure points  Rule out open fracture
3. Always place a backslab/U slab even if patient is just admitted for pain control.  Take an AMPLE history - A llergies, M edications, P ast medical history, L ast
4. All hand fractures have a standard functional hand position cast meal, E vents surrounding injury
 Analgesia
Indications
 Splint fracture - makes patient more comfortable, decreases progression of soft tissue
• Fractures that can reduced and be stably maintained injury, decreases blood loss
• No major soft tissue injury  Imaging
• No suspicion of compartment syndrome
• No vascular compromise RADIOGRAPHIC DESCRIPTION OF FRACTURES
 Rule of 2s
Types of Plaster Casting • 2 sides: bilateral
• 2 views: AP and lateral
» Forearm U slab: Forearm fractures
• 2 joints: above and below the site of injury
» Shoulder U and O slab: Proximal and midshaft humerus fractures • 2 times: before and after reduction
» Intrinsic plus hand slab: Hand fractures  Identify view + date + patient identification (“This is an AP X-ray view of the knee
» Above knee cylinder slab: Knee injuries joint taken on 1/12/10 for Mdm. Gee”)
» Above knee slab: Tibia/Fibula fractures  Anatomy
» Below knee slab: Ankle fractures • Which bone
• If diaphyseal decribe by thirds : proximal/middle/distal
• Type
 spiral # - rotational force, low energy (# line > 2x bone width)
FRACTURES—GENERAL PRINCIPLES  oblique # - angular and rotational force
Mechanism: remember the process leading to the fracture  transverse # - direct force, high energy
• Traumatic  comminuted # (> 2 pieces) - direct force, high energy
• Pathologic – remember O M I T: osteopenia/osteoporosis, metabolic bone  compression #
disease (hyperparathyroidism, hyperthyroidism, osteogenesis imperfecta,  avulsion # - strong muscle inserting into small bone e.g. quads to
rickets), infection, tumour patella, triceps to olecranon, peroneus tertius to 5th metatarsal head
• Stress – repetitive mechanical loading, periprosthetic  butterfly # - 2 lines break out obliquely from point of contact of blow
producing a free-floating ‘butterfly fragment’
CLINICAL FEATURES OF FRACTURES  Articulation
 Pain and tenderness • Extra-articular: diaphysis/metaphysis
 Loss of function • Intra-articular  salter-harris classification (for children)
 Deformity  Apposition (% displacement) – any shortening? [i.e. bayonet #]
 Abnormal mobility and crepitus (avoid)  Angulation
 Altered neurovascular status (important to document)  Apex
 Associated structures (aka soft tissue): calcification, gas, foreign bodies

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 » N - N on-union
» O - O pen fracture
» C - neurovascular C ompromise
» A - intra- A rticular fractures (require anatomic reduction)
» S - S alter-Harris III, IV, V and/or special situations depending on site
» T - poly T rauma
» Others
 failure to reduce using closed reduction
 cannot cast or apply traction due to site (e.g. hip fracture)
 pathologic fractures
 fractures in paraplegics for nursing access
 potential for improved function with ORIF
 infection
 new fracture through screw holes
 implant failure
DEFINITIVE MANAGEMENT
 Goals – “Obtain and Maintain Reduction” Stabilization
• reduce Stabilize the fracture site but do not completely immobilize the limb if possible
• stabilize
• rehabilitate External stabilization
 Attempt closed reduction 1. splints/tape Non-rigid fixation – risk of loss of
• if successful 2. casts
reduction but stimulate rapid callus
 Then stabilize formation
3. traction
• if unsuccessful 4. external fixator
 Open reduction
Rigid fixation –
 Then stabilize-- usually internal fixation Internal fixation immediate loading but
 Rehabilitate 1. percutaneous pinning (Kirschner or K-wires) does not stimulate
2. extramedullary fixation (screws, plates, wires) callus formation
Reduction 3. intramedullary fixation (rods) - biomechanically advantageous
 Is reduction necessary?
• may not be for clavicle, fibula, vertebral compression fractures Rehabilitation
 reduce when amount of displacement is unacceptable  To avoid joint stiffness
 imperfect apposition may be acceptable while imperfect alignment is rarely  Isometric exercises to avoid muscle atrophy
acceptable  Range of motion (ROM) for adjacent joints
 Closed when possible  Continuous Passive Motion (CPM) following rigid fixation of fracture allows joint
 Closed reduction motion to prevent stiffness for intra-articular fractures
» Minimise damage to blood supply  After cast/splint removed and fracture healed  resistive muscle strengthening
» Rely on soft tissue attachments  Evaluate bone healing (clinical, x-ray)
» Rarely adequate for intraarticular #
» Difficult in babies whose bones cannot see in X-ray
 Open reduction: indications – remember NO CAST

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OPEN FRACTURES
EMERGENCY!
 Definition: A fracture or its haematoma that communicates with the environment.
 Gustilo-Anderson Classification of Open Fractures*****

Superficial to deep
Gr Laceration Soft tissue Fracture Contamination Comments
I <1cm long Little damage, Usually Clean puncture Simple #
no crush transverse, (compound [5% chance of amputation]
short oblique, from within)
little

More energy, higher velocity trauma

comminution
II 1-10cm Moderate Moderate Moderate Butterfly #
crushing, no comminution contamination [10% chance]
flap/avulsion
IIIa >10cm Extensive Extensive Severe Adequate soft tissue coverage (NOT SKIN) despite
damage to skin, comminution contamination extensive laceration/flaps
muscle, neuro- & instability - Segmental # (= # at 2 levels)
vasculature - Farm injuries / any injury occurring in a
highly-contaminated envt
- GSW
[20% chance]
IIIb Extensive soft tissue injury/loss
Periosteal stripping & exposure of bone
[30% chance]
IIIc Any open # a/w arterial injury that requires repair
regardless of wound size/soft tissue injury
- Prophylactic fasciotomy always done to
prevent post-op compartment syndrome
[>40% chance]
NB. can only differentiate Gr III into a, b and c ONLY AFTER SURGICAL INTERVENTION
(i.e. debridement)

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EMERGENCY CARE  Sterile scrub: use scrubbing brush and scrub the site to debride all necrotic
Approx. 30% of patients with open fractures are polytrauma patients who have suffered tissues (dead muscle/fat/other tissues) --- how to tell if muscle is dead or not?
damage to 2 or more systems. Manage according to ATLS. Only manage the fracture 4C’s Dead Live muscle
when the patient is stable. [In grey: for open #s] muscle
Consistency Mushy Turgid
1. ABCDE Colour Pale pink Pink/bright
2. Neurovascular status of the limbs (above & below) red
 Control any haemorrhage with direct pressure. Set IV line & start IV fluids. Contraction (most important) Absent Present
 Don’t reduce any # unless there is apparent neurovascular compromise from Capillary No bleed Bleeding
position of #.  Repair vascular injury if present (i.e. re-anastomose the vessels)
 Dressings & splints that might have been put on at the accident site should be  For crushed injuries involving both vascular & nerve injury  amputate
removed partially to assess soft tissue conditions and neuromuscular function.  Remove comminuted fragments (anything that’s dead and without soft tissue
All sterile wound dressings should be left in place because redressing wounds attachments  discard)
in the emergency room increases the infection rate  Wash with 10L of saline (to dilute bacterial load)
3. Any other #/injuries (above & below) – remove gross debris, i.e. turf, rocks  Take wound cultures at the end of the procedure
4. Rule out open #  THEN reduce
5. Take an AMPLE Hx  THEN maintain
6. Analgesia – 75mg I/M pethidine  External fixation preferred – can be temporary (for 2/52 until you’re
7. Start IV antibiotics [after wound c/s samples are taken] in all open # during the first sure there’s no infection at site, then internal fixation) or permanent
3-5 days (empirical NOT prophylactic!) Use broad spectrum antibiotic (e.g. 1st (for 3-6 months until # unites)
generation cephalosporins); in grade 3 #, add gentamicin +/- metronidazole, and  Disadvantage of internal fixation: must strip soft tissue :. Avoided for
monitor for toxicity. grade 2 & above
8. Tetanus toxoid booster (TTB) – 0.5mL  Disadvantage of intramedullary nail: may spread infection (even
Human anti-tetanus immunoglobulin (HATI) – 250 units though in this case needn’t strip soft tissue)
Simple wound Tetanus-prone  Wound usually left open to drain
wound  48h later,
Full course + booster within - TTB
 ‘relook operation’ – see if repeat I&D is necessary
10y
Full course + booster 10y ago TTB TTB + HATI  Ensure soft tissue coverage over exposed area by 48th hour –
Non-immunised / unknown TTB TTB + HATI exposed tendon will not survive for long... Need flap!
 4-6 weeks later: bone graft/transport
9. Splint – to decrease pain, progression of soft tissue injury, blood loss  THEN skin graft (after swelling subsides; if not, compartment syndrome may
10. Imaging (X-rays) occur after grafting)
11. NBM and prepare for EOT
 Must get into OT within 6h (‘golden hours’) since risk of infection increases
after this time
 Done under LA/GA

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Complications of open #s Early Late
 Bone Local Neurovascular injury Malunion
» Osteomyelitis Swelling Nonunion
» Mal-union (NB. healing will always take place, it’s only a matter of how Compartment syndrome AVN
good the healing is) Infection Post-traumatic arthritis
» Non-union (healing has ceased, both pieces not united by 6 months) Implant failure Osteomyelitis
 Certain bones are prone, e.g. tibia (due to poor muscle coverage), Soft tissue blisters (infection) Heterotopic ossification
scaphoid, NOF (due to poor blood supply) Growth disturbance in children
 Also depends on severity of injury Joint instability
 Types Joint stiffness
 Hypertrophic: insecure fixation / premature wt bearing Nerve compression /entrapment
 Atrophic: poor blood supply, ends osteoporotic (e.g. in Reflex sympathetic dystrophy (RSD)
DM, vasculopathy, infection, sig tissue damage) --- Mx: System Hemorrhagic shock Multi-organ failure
open decortications & cancellous bone graft -ic Sepsis Renal failure
» AVN Fat embolism Shocked lung
» Arthritis DVT / PE PTSD, depression
 Regional ARDS
» Neurovascular injury
» Soft tissue blisters
 Types: haemorrhagic and non-haemorrhagic IRRIGATION AND DEBRIDEMENT
 Mechanisms of injury: shearing of skin (may become infected if
operated on), ischaemia (can be due to compartment syndrome!)  Irrigation and debridement (most important steps in treatment of open #)
» Compartment syndrome*****  To be done within 8h of the injury, otherwise wound is considered infected.
» Complex regional pain syndrome1  Done in the OT under LA/GA
» Heterotopic ossification  Only now are all the splints and bandages removed
» Joint stiffness  Reexamine thoroughly for neurovascular function.
 Systemic  Fluids are delivered under pressure and under a pulsed system to remove any blood
» Hypovolaemic shock clots and foreign bodies.
» Fat embolism  Isotonic saline or water is used for irrigation.
» Venous thrombo-embolism (DVT/PE) from immobility  Dilutes the degree of bacterial contamination. Repeat the irrigation at regular
» Multi-organ dysfunction syndrome intervals once the wound is open as there is a higher chance of removing
» ARDS (especially in polytrauma patients) contaminated material.
 Ensure that the whole wound is exposed to the fluids.
 There is a debate as to the usefulness of adding antibiotics to the fluids. If
proper debridement is done then only vascularised tissue should remain and
NB. Can also be classified as early & late complications
adequate tissue levels can be achieved with systemic antibiotics. However,
1
some studies have shown lower infection rates with added antibiotics.
Complex Regional Pain Syndrome (CRPS): a chronic pain state induced by Ultimately, the effect of irrigation is still mechanical.
- Soft tissue / bone injury (CPRS I aka reflex sympathetic dystrophy aka Sudeck’s atrophy)
- Nerve injury (CPRS II aka causalgia)  Ensure wound incision is large enough to facilitate exposure and inspection of
In which pain is a/w autonomic changes (e.g. sweating or vasomotor abnormalities), and/or trophic changes (e.g. wound site, including the joint.
skin/bone atrophy, skin loss, joint contractures). Aetiology unknown. Treatment: no cure; pain relief only.

12
 Meticulous removal and resection of all foreign and dead material from the wound.
 All non-viable, mutilated or macerated skin removed. Dead, frayed skin edges
are excised. Skin colour is a good determinant of viability of skin. When a cut
skin edge does not bleed then it is dead.
 Fasciae are expendable so it can be safely removed without fear of functional
deficit.
 Difference between dead & live muscle (see ‘emergency care’)
 Free fragments of bone are removed. Fractured bone ends must be exposed so
that they can be cleaned with brushes or removed.
 Exposed tendon will not survive for long. Early skin coverage, skin grafting or a
muscle/skin flap may be necessary to preserve its viability.
 Wound cultures should be taken at the end of the procedure.
STABILISATION OF FRACTURE
 Immobilisation of the fracture is crucial for the healing of soft tissue and bone.
 Stabilisation prevents further injury to the surrounding soft tissue, limits
intensity and duration of inflammatory response, diminishes spread of bacteria,
facilitates tissue perfusion and encourages early wound repair.
 Should still provide free wound access for repeated debridement and placement
of local or distant flaps and bone grafts.
 Should not interfere with blood supply of fracture segments and should be
sufficiently rigid to allow early joint motion and at least partial weight bearing.
 Slings, splints, casts and traction may be used as definite care of simple grade I and
grade II injuries and as temporary methods for more complex fractures.
 Slings can be used in fractures of humeral shaft or to provide additional support for
internally or externally stabilized forearm lesions. Splints can provide initial
stabilization of fractures below the elbow and knee.
 Circular castshave no place in early Mx as they cannot accommodate swelling.
 May prevent the detection of further soft tissue damage, circulatory impairment
and/or increase in compartment pressures.
 Casts can be used as subsequent care of stable grade 1 and 2 tibial fractures after the
wound is closed and swelling subsided.
 Can also be used as a secondary method of immobilization after removal of an
external fixator.
 Traction may be indicated for pelvic fractures, acetabular lesions and femoral
fractures. But rarely used in the upper extremity.
 External fixation is indicated for most contaminated grade 3b and c fractures.
 Advantages: 1) No foreign material in the wound. 2) Applied without any
additional soft tissue dissection. 3) Provides easy access to the wound 4) Easily
dismantled if further debridement needed.
 Disadvantages: 1) Potential for pins to injure neurovascular structures and tie
down muscle-tendon units interfering with joint motion and rehabilitation. 2)
Possible interference of the pins in reconstructive procedures as well 3) Pin
loosening 4) Secondary infection.
 Usually removed or replaced by casts, braces or internal fixation as soon as soft
tissue lesions have healed.
 Internal fixation provides excellent stabilization, allows early limb and patient
mobilization and facilitates fracture consolidation while preventing malalignment.
 However, procedure requires additional exposure and can cause partial loss of
periosteal, cortical or intramedullary blood supply  ↑es risk of infection.
 Screws are usually used in combination with a plate or external fixator for intra-
articular and peri-articular fractures. Plates may be used in treatment of less severe
diaphyseal, periarticular and intraarticular fractures of the upper limb.
 In the LL, plates are useful around joints. However, they must be covered well.
 Intramedullary nails are used for femoral fractures. They may be used as a
secondary method after external fixation but carries a risk of infection. Therefore
contraindicated if there is a history of local or pin track infection.
 Recent studies show that internal fixation for femoral shaft fractures and even tibial
shaft fractures result in faster union times as well as decreased risks of reoperation,
malunion and superficial infection. External fixation has also shown to be
associated with severe pin track infection, longer union times and a higher number
of surgical procedures to promote union.
WOUND COVERAGE
 The timing of wound coverage is important.
 Primary closure of wound associated with significant risk of infection.
 Therefore, keep wounds open after initial debridement and decide again at the
second inspection.
 Aim to close the wound within 3-5 days.
 Keep moist meanwhile.
 Once wound is clean and tissues are viable, delayed primary closure or skin
grafts can be done.
 Aims of wound coverage: 1) Achieve a safe early closure 2) Avoid nosocomial
infection 3) Obliterate dead space 4) Facilitate future reconstruction.
 Direct closure done for fresh tidy wounds free from infection and contusion.
13
 Skin grafts are transplanted completely by detaching a portion of skin from a donor
site and transferring it to a raw bed-- has to achieve a new blood supply within 2-3
days to ensure viability.
 Often used as in intermediary measure before a flap.
 There are 2 kinds of skin grafts.
 Partial/split-thickness skin graft consists of epidermis and part of the dermis.
Can tolerate less ideal conditions and less vascularity than full thickness skin
graft. The donor site must be able to heal spontaneously by epithelialisation and
if necessary, more grafts may be taken from the same place. Good for covering
large skin defects overlying viable tissue such as muscle, for large size wounds
or those of questionable circulation. Grafts contract, have poor growth in
children and have abnormal pigmentation. Partial thickness skin grafts are
taken from inner thigh or lateral buttock.
 Full thickness is composed of the full thickness of the skin. Generally used for
fresh, non-contaminated wounds of small size. Full thickness skin grafts are
taken from groin or postauricular area, supraclavicular area.
 Flaps contain a pedicle attachment to the body receiving it’s sustenance via a
network of blood vessels.
 Because of their own blood supply, they can be used to reconstruct skin and
soft tissue defects irrespective of their vascularity.
 Choice of flap coverage must take into account patient’s age & needs, location,
size & condition of the defect, likelihood of subsequent reconstructive surgery
& associated zone of injury, tissues available for the flap.
 Flaps can be classified as skin, fasciocutaneous, muscle and musculocutaneous.
 Used for defects with poor vascular beds such as wounds overlying the tibia,
exposed metal plates, bare bones and tendons, bone defects and open joints.
Delayed bone or soft tissue reconstruction is proposed, especially if bone graft
or tendon transfer is being planned.
 An example of a local flap is the gastrocnemius. Used around the knee and
proximal third of the tibia, one of the 2 heads of the gastocnemius is used and
there must be a functional soleus. The soleus is sometimes used for mid-tibial
defects or sometimes even the distal third of the tibia
 Free microvascular flap is used for large defect.
 Helps prevent multiple reoperations. Provide durable coverage of the fracture
site, diminishes the infection rate and shortens the healing time. E.g. latissimus
dorsi and vertical rectus abdominis.
DELAYED UNION AND NON-UNION
 Delayed union and non-union are common in open fractures.
 Delayed union is when healing has not advanced at the average rate for the location
and type of fracture. I.e. reconstitution of mechanical stability but over a prolonged
period of time and with associated morbidity.
o Rx: adequate immobilization, internal fixation or even bone grafting.
 In non-union, there is evidence, clinically or radiologically that healing has ceased.
I.e. failure of reconstitution of mechanical stability after appropriate time intervals.
o MCQ: commonest site = junction of distal 1/3 and proximal 2/3 of tibia
o Can be classified as hypervascular (elephant foot, horse hoof or
oligotrophic pattern) or avascular (torsion wedge, comminuted, defect or
strophic pattern).
o Treated by stable internal fixation, bone grafting, bone transport or free
composite tissue transfer.
MANAGEMENT OF BONE LOSS
 Bone injury occurs during initial injury or from subsequent repeated debridement.
 Any bone replacement methods should only be done after adequate soft tissue
coverage and revascularization.
Bone grafts
 Work via 3 mechanisms: osteoconduction, osteoinduction and osteogenesis.
 Osteoconduction is the process whereby transferred bone acts as a scaffold for new
bone to grow. (+ neovascularisation)
 Osteoinduction occurs when undeveloped tissue is transformed to bone by one or
more inducing agents.
 Osteogenesis is new bone formed from live osteoblasts in the transplanted autograft.
Bone transport
 Used for large gaps (Ilizarov’s principle of distraction osteogenesis: induction of
new bone between bone surfaces that are pulled apart in a gradual, controlled
manner. Distraction gives rise to neovascularisation hence stimulating new bone
formation.)
 A segment of bone is created by corticotomy or osteotomy through normal bone in
one of the fragments of the fracture. This segment is transported by wires and new
bone forms in the gap by gradual distraction. The segment is moved by 1mm a day.
This technique of callostasis allows simultaneous restoration of a bony defect,
correction of limb length and deformity, improvement in the condition of local soft
tissues and the treatment of infection.
14
  Venous obstruction
Free composite tissue transfer  Increased venous pressure
 Example: fibula, which is mainly a cortical bone that provides excellent strength  Constrictive dressing, cast, splint
and length for large segmental bony defects. It is used together with muscle and
skin with its pedicle. Diagnosis
 Tibial compartments (common) and forearm flexor compartment
• may lead to Volkmann’s ischemic contracture
FRACTURE HEALING  Clinical signs and symptoms
Normal Healing • Early
 Pain out of proportion to injury & not relieved by analgesics**
1 0h Hematoma formation.  Increases with Passive stretch of compartment muscles
2 Within 8h Inflammatory reaction with proliferation of the cells under  Paresthesias
periosteum and within the medullary cana. Macrophages,  Pallor
undifferentiated stem cells and platelets surround fracture site.  Palpable tense, swollen compartment
3 3-6 wks Osteoclasts remove sharp edges (thus # more visible on • Late
radiographs), Callus forms within hematoma  Paralysis (inability to move limb - late)
6-12 wks Bone forms within the callus, bridging fragments. Forming  Pulses are usually still present (CRT normal)
woven bone.
 Compartment pressure monitoring
4 6-12 mths Consolidation—woven bone is replaced by lamellar bone
• In unresponsive or unreliable patients
5 1-2 yrs Normal architecture is achieved through Remodelling
• Normal tissue pressure is about 0 mm Hg
Evaluation of Healing - Tests of Union • Pressure increases markedly in compartment syndromes.
 Clinical - no longer tender to palpation or angulation stress • When intra-compartmental pressure rises to within 10-30mmHg of patient's
 X-ray - trabeculae cross fracture site, visible callus bridging site diastolic blood pressure, inadequate perfusion and/or ischemia results
• Fasciotomy usually indicated when the tissue pressure rises to 40-45mmHg
in a patient who has any signs or symptoms of a compartment syndrome-
COMPARTMENT SYNDROME even if distal pulses still present

Definition Signs of Compartment Syndrome in Anterior Leg and Forearm

 Condition where pressure within an enclosed anatomical compartment rises Anterior leg Volar forearm
sufficientto occlude the microvascular circulation causing tissue ischaemia and, if Fracture Type Tibial fracture Supracondylar (humerus)
untreated, tissue necrosis. Weakness Toe, foot extension Finger, wrist flexion
 Intracompartmental pressures over 30 mm Hg or over diastolic pressure requires Pain Toe, foot flexion Finger, wrist extension
intervention Sensory 1st dorsal web space Volar aspect of fingers

Etiology Treatment
 Fracture, dislocation  Remove constrictive dressings
 Soft tissue damage & muscle swelling  Bivalve casts down to skin and spread open
 Crush injury  Place limb at level of heart
 Arterial compromise  Emergency fasciotomy if difference between diastolic BP and compartment
 Muscle anoxia pressure is greater than 30 mmHg (treat within 4-6h of onset symptoms)

15
 AVASCULAR NECROSIS TIPBITS FOR #S
Aetiology 1. Arm fractures: nerves affected by humerus fracture location ARM fracture:
 Steroid use --- NOT dose related – idiosyncratic From superior to inferior: Axillary: head of humerus / Radial: mid shaft/ Median:
 Alcohol supracondular
 Post-traumatic fracture/dislocation
 Septic arthritis 2. Fractures: principles of management FRIAR: First aid, Reduction,
 Sickle cell disease Immobilisation, Active Rehabilitation
 Gaucher’s disease
 Caisson’s disease – deep sea diving/the bends 3. Forearm fractures: bone in Monteggia vs. Galeazzi "Break the forearm of the
MUGR (mugger)": Monteggia=Ulna, Galeazzi=Radius
 Perthe’s disease
 Idiopathic 4. Salter Harris fracture classification Salter Harris, modified to SALTR:
 type 1: Slipped epiphysis
AVN Classification
 type 2: Above the eiphyseal plat
Stage Clinical Features X-ray Features
 type 3: Lower than the eiphyseal plate
1 Preclinical phase of No plain x-ray abnormality; may be detectable on MRI
ischemia and  type 4: Through both above and below eiphyseal plate
necrosis; no pain  type 5: Raised epiphysis, as in a compression injury
2 Painful Early radiographic changes i.e. fragment appears dense, Salter Harris classification utilises visualising long bone distal portion with
normal bone contour diaphysis superiorly placed and epiphysis inferiorly placed.

3 Painful Radiographic changes obvious, abnormal bone contour 5. Bryant's traction: position BrYant's traction: Bent Y.
4 Very painful Collapse of articular surface and signs of arthritis on both Patient's body is the stem of the Y lying on the bed, and legs are the ends of the Y
sides of the joint up in the air.

Mechanism 6. Differentials for non-union of #s --- you need a SPLINT:

 Occurs following disruption of blood supply to bone  Soft tissue interposition
 Occurs especially in those bones extensively covered in cartilage which rely on  Position of reduction (too much traction, immobilization, or movement)
intra-osseous blood supply and distal to proximal blood supply, e.g. head of femur,  Location (eg. lower third of tibia slow to heal)
proximal pole of scaphoid, body of talus  Infection
 Results in ischemia  Nutritional (damaged vessels or diseased bone)
 Pathologic changes include resorption, subchondral fractures and loss of cartilage  Tumor (pathological fracture)

16
IMPORTANT ORTHOPAEDIC CONDITIONS IN THE SHOULDERS CAUSES OF SHOULDER PAIN
APPROACH TO SHOULDER PROBLEMS Tendon (rotator cuff disorders) Tendinitis
Rupture
IMPORTANT HISTORY TO TAKE FOR SHOULDER PAIN
Frozen shoulder
- Duration (time course of frozen shoulder – pain and stiffness for first 6 months, less
pain but persistent stiffness for next 6 to 12 months, and recovery of joint mobility Joint disorders Glenohumeral arthritis
18 months after start of symptoms). Acromioclavicular arthritis
- Any preceding trauma (frozen shoulder and rotator cuff tear often follow minor Referred pain Cervical spondylosis
precending injury). Cardiac ischaemia
Mediastinal pathology
- Neck pain – shoulder pain may be due to cervical pathology; shoulder pain is
typically located over the deltoid insertion and tip of shoulder, not along the Instability Dislocation
trapezius or neck. Subluxation
- Shooting pains travelling down arm, numbness and/or weakness of hand – Bone lesions Infection
indicative of cervical spine pathology or nerve problem. Neoplasm
- Pain on lying on shoulder while sleeping. Nerve lesions Suprascapular nerve entrapment
- Function of shoulder (see below).
Think 4 Ss for Shoulder: Stiffness, Stability, Strength, Smoothness
- Diabetes (very important as diabetes is a cause of idiopathic frozen shoulder).
Stiffness: Frozen Shoulder, Post-traumatic/post-surgical stiff shoulder.
- Heart disease – may result in referred pain to shoulder. Strength: Rotator cuff tears
Stability: TUBS vs AMBRII
FUNCTIONAL ASSESSMENT IN SHOULDER PROBLEMS Smoothness: Subacromial abrasion, primary degenerative joint disease, AVNs,
Recurrent dislocations, post-surgery arthritis, RA.
- Ability to reach for objects placed in overhead positions
- Ability to comb hair
- Ability to touch opposite shoulder and back (for personal hygiene)***
- Ability to wear top e.g. shirt, T-shirt, blouse

INVESTIGATIONS:
No blood investigations are required usually; shoulder X-ray is the most useful invx

Important features to look out for on shoulder X-ray:

- Narrowing of subacromial space
- Bony spur on inferior aspect of acromion or acromioclavicular joint
- Calcification of supraspinatus tendon (acute calcific tendinitis)
- Narrowing of joint spaces esp. glenohumeral joint
- Osseous lesion(s) if any

17
SHOULDER PAIN – likely OSCEs scenarios
Young Instability
AC joint injuries
Middle-aged Impingement syndrome
Frozen shoulder (women) – primary cause
Old Rotator cuff tears
Degenerative arthritis
Frozen shoulder – primary/secondary cause

Rotator cuff Frozen shoulder Shoulder instability

Stem
Pain
Any preceding trauma
Past medical history + any
drug allergies
Rule out cervical pathology
Functional assessment
Elderly gentleman Old gentleman / middle-aged lady Young gentleman
S: shoulder +/- lateral aspect of S: shoulder S: shoulder
arm (confused w radiculopathy) O: <18months ago O:
O: insidious/sudden after freq use C: C:
C: R: none R: none
R: none A: A:
A: T: T:
T: worse at night E: lying on shoulder while sleeping / night E:
E: cannot lie on affected arm pain because ‘I’m not conscious of where S:
S: my hands & arms go when I’m asleep’
S: TUBS vs. AMBRII
a/w weakness
a/w stiffness if post-traumatic a/w shoulder stiffness
If yes,
- check if patient had dislocated shoulder back then
- any pain before the trauma (patient may already have rotator cuff tear of which the pain was accentuated by
the trauma – in which case, surgical outcome may be poorer [attaching fat to bone instead of muscle to
bone, hence no function!])
Diabetes Have you been told by
(cause of idiopathic frozen shoulder) doctors previously that you
have ligamentous laxities?
- Shoulder pain typically located over the deltoid insertion and tip of shoulder, not along trapezius or neck
- Shooting pains travelling down arm, numbness and/or weakness of hand – indicative of cervical spine
pathology or nerve problem
- Ability to reach for objects placed in overhead positions
- Ability to comb hair
- Ability to touch opposite shoulder and back (for personal hygiene)
- Ability to wear top e.g. shirt, T-shirt, blouse

- Occupation & hobbies, whether those are affected

OTHER DIFFERENTIALS FOR SHOULDER PAIN

Tendon (rotator cuff disorders), Joint disorders, Referred pain, Instability, Bony lesions, Nerve lesions

What are the important steps in the shoulder exam that you would like to elicit?
I would still follow the LOOK, FEEL, MOVE sequence.
Rotator cuff Frozen shoulder Shoulder instability
LOOK Any post-traumatic/post-surgical scars
FEEL Tenderness
MOVE - Painful arc (tendinitis) Decreased active AND passive
- Drop arm sign (tear) ROM in ALL directions
- Difficulty initiating abduction (tear)
but NO muscle wasting
SPECIAL TESTS - For supraspinatus tendinitis: Jobe’s, Apprehension tests for
Hawkin’s, Neer’s shoulder instability

Describe what you mean by impingement syndrome / frozen shoulder / shoulder instability.
Impingement syndrome Frozen shoulder Shoulder instability
Definition “impingement position” where the Known also as adhesive capsulitis, it is a - Shallowness of the
glenohumeral joint is in abduction, slight well-defined disorder characterised by glenoid fossa of the
flexion and internal rotation progressive pain and stiffness which scapula & lack of support
usually resolves spontaneously after 18 provided by weak lig (3
- Site of impingement is usually the months. GH ligaments—Medial,
“critical area” of decreased vascularity Inferior, Superior;
in the supraspinatus tendon 1cm ‘Freezing’  6-12 weeks transverse humeral lig;
proximal to its insertion into the greater ‘Frozen’  3-4 months coracohumeral lig) make
tuberosity ‘Thawing’  up to 18 months the GH joint unstable
- strength mainly depends
on the rotator cuff
muscles
Aetiology +/- Repetitive rubbing of rotator cuff tendons PRIMARY ADHESIVE CAPSULITIS Classification of patients with
risk factors under coracoacromial arch (coracoacromial - Idiopathic in cause recurrent shoulder
ligament forms the roof, runs between - a/w DM, Dupuytren’s contracture, instability:
coracoid process & acromion) hyperlipidaemia, hyperthyroidism, - TUBS: Traumatic, Uni-
- Bone: OA (osteophytes) cardiac disease directional (unilateral),
- Tendon: rotator cuff tendinitis (in - Global contracture of the shoulder Bankart lesion, Surgery.
inflammatory conditions, e.g. RA, gout) joint, but maximally in the rotator - AMBRII: Atraumatic,
- Bursa: subacromial bursitis (also in interval area and around the Multi-directional,
inflamm. conditions) coracohumeral ligament Bilateral,
Rehabilitation, Inferior
Pathogenesis SECONDARY ADHESIVE CAPSULITIS Capsular Shift, Interval
- Friction leads to localised oedema and Intrinsic causes Closure
swelling (tendinitis) – “wear”  Chronic rotator cuff injuries
- Tendinitis is usually self-limiting but  Post-traumatic scarring following
with prolonged or repetitive injuries at the shoulder e.g. fracture of
impingement minute tears can occur, the surgical neck, greater tuberosity.
especially in elderly – “tear” Extrinsic causes
- Tears can be complicated by scarring,  Painful disorders resulting in
fibrocartilaginous metaplasia or decreased movements of the shoulder:
calcification in the tendon referred pain from cervical
- Vascular reaction occurs in an attempt radiculopathy, post-hand, wrist or
to repair a torn tendon or to elbow surgery, post-MI
revascularize a degenerate area. New
BVs grow in & calcium deposits are
resorbed. This vascular reaction causes
congestion & pain. Pain is caused by
wear, tear & repair of the tendons! All 3
happen in varying levels across the
ages.
Investigations: - Usually normal in early impingement X-rays usually normal – useful in To see if dislocation is present
X-ray - +/- erosion, sclerosis or cyst formation excluding other causes of painful shoulder, upon visit & to see if there is
at the greater tuberosity (insertion of such as infection, post-traumatic stiffness, Bankart lesion / Hill Sacks
the supraspinatus tendon) in chronic diffuse stiffness and reflex sympathetic lesion.
tendinitis dystrophy when patient 1st presents
- May see calcification of the supra-
spinatus tendon (incidental and not the
cause of pain)
- May see narrowing of the space
between AC joint & humeral head
- May see signs of AC joint arthritis –
osteophytes
Management TENDINITIS Aim of conservative treatment is to relieve Anterior instability
Conservative: pain and prevent further stiffening while - For acute dislocations:
- Eliminate aggravating activity, and waiting for recovery (since natural course Manipulation and
avoid “impingement position” is recovery in 12-18 months) reduction followed by
- Physiotherapy immobilisation in a
- Short courses of analgesia e.g. NSAIDs Analgesia (NSAIDs), H&L (at shoulder bandage or sling for
- Subacromial Hydrocortisone & joint), local heat. several wks
Lignocaine / Triamcinolone & - Recurrent dislocations:
Xylocaine injections at subacromial Physiotherapy: Indications for surgery
joint for pain relief (LA takes effect - Repeated circular movement of include frequent painful
immediately, lasts 1 day; corticosteroid shoulder dislocation and recurrent
takes effect 3-5 days later) - Assisted abduction – use towel or subluxation
Surgical rope, loop it over an overhead bar like
- Open or arthroscopic subacromial a pulley system, and hold on to each Posterior instability
decompression (acromioplasty) end with one hand. Patient uses - M. strengthening
o Excise coracoacromial downward pull of normal arm to exercises
ligament & anteroinferior part passively abduct painful arm - Surgery considered when
of acromion overhead. condition is disabling &
o Remove acromioclavicular - Assisted internal rotation – both hands there is no gross joint
osteophytes if present gripping either end of a towel slung laxity
TEAR across the patient’s back diagonally;
Conservative the hand on the painful side holds the Anterior dislocation
- Physiotherapy to improve strength lower end while the hand on the - M & R with sedation /
- Heat therapy normal side holds the end above the GA
- Local anaesthesia if necessary shoulder. Patient uses hand on normal - Hippocratic method:
Surgical side to pull upwards on towel, increasing traction
- If amenable to repair, open or passively internally rotating the applied to the arm with
arthroscopic cuff repair followed by painful shoulder. the shoulder in slight
subacromial decompression. Especially - Wall-crawling – patient uses fingers abduction while an
for young active individuals. With to “crawl” up a wall slowly, assistant applies firm
complete tears. Partial tears do not increasing flexion movement. counter traction to the

19
 require surgery unless persistent pain or body; e.g. using a towel
considerable instability. slung around the chest
- If not amenable to repair, open or under the axilla
arthroscopic debridement of degenerate - X-ray post-reduction to
cuff tissue and subacromial check position and
decompression. exclude fracture.
- Exclude an axillary nerve
injury, rotator cuff tear,
median, radial, ulnar and
musculocutaneous nerve
injuries after reduction
- Rest the arm in a sling for
3 wks, 1 wk for
those>30yrs old due to
risk of stiffness
- Avoid abduction and
lateral rotation for 3 wks
- Elbow and finger
movements

Posterior dislocation
- M & R by pulling on the
arm with shoulder in
adduction followed by
lateral rotation while
humeral head is pushed
forwards.
- Immobilisation in a sling

20

ROTATOR CUFF IMPINGEMENT
AETIOLOGY
- The cuff is made of subscapularis in front, supraspinatus above and infraspinatus
and teres minor behind.
- Repeated rubbing of the rotator cuff tendons under the coracoacromial arch (the
roof of which is formed by the coracoacromial ligament running between the
coracoid tubercle anteriorly to the anterior third of the acromion posteriorly)
- The greatest amount of wear occurs in the “impingement position” where the
glenohumeral joint is in abduction, slight flexion and internal rotation
- Site of impingement is usually the “critical area” of decreased vascularity in the
supraspinatus tendon 1cm proximal to its insertion into the greater tuberosity
- Vascular reaction occurs in an attempt to repair a torn tendon or to revascularize a
degenerate area. New blood vessels grow in and calcium deposits are resorbed. This
vascular reaction causes congestion and pain. Pain is caused by wear, tear and
repair of the tendons! All 3 happen in varying levels across the ages.
- Contributing factors to impingement
 Bone: OA thickening of AC joint, osteophytes along anterior edge of acromion
 Tendon: rotator cuff swelling (in inflammatory disorders such as RA & gout)
 Bursa: subacromial bursitis (in inflammatory disorders)
PATHOPHYSIOLOGY
- Pathological processes can be summed up into “wear, tear and repair”
- Friction leads to localised oedema and swelling (tendinitis) – “wear”
- Tendinitis is usually self-limiting but with prolonged or repetitive impingement
minute tears can occur, especially in elderly – “tear”
- Tears can be complicated by scarring, fibrocartilaginous metaplasia or calcification
in the tendon
- Healing is accompanied by a vascular reaction and local congestion which is
painful, and this may contribute to further impingement
- Healing is more rapid in younger patients (but also more painful) and less vigorous
in the elderly (less pain, chronic tendinitis that doesn’t heal completely).
- Deposits of calcium hydroxyapatite appear in the supraspinatus tendon in acute
(calcific) tendinitis. Although these calcifications are not painful, the florid vascular
reaction which produces swelling and tension causes severe symptoms. The
calcium usually resorbs quickly and disappears in a few months.
HISTORY
(SUB)ACUTE TENDINITIS
- Patient <40 years old
- Shoulder pain occurs after a bout of vigorous unaccustomed activity
- Patient complains of a “painful arc” (60-120 deg) on abducting the arm
- Complains of pain of increasing severity, reaching a climax after a few days.
- After which, the pain subsides and shoulder returns to normal.
CHRONIC TENDINITIS
- Patient 40-50 years old
- Patient has a history of recurrent attacks of subacute tendinitis
- Pain settles with medications (NSAIDs) or rest but recurs when doing more
demanding activities
- Pain characteristically worse at night, and patient cannot lie on affected side
- Pain and stiffness restrict daily activities
CUFF TEAR
- Partial or full thickness tear occurs with progressive fibrosis & disruption of the
rotator cuff
- Usually >45yo with refractory shoulder pain with increasing stiffness and weakness
- Partial tears are hard to detect as they present with painful arc but still normal
motion of the shoulder. Patient can abduct the shoulder upon giving LA because
pain is the limiting factor usually. Intact tendon fibres provide continuity for
vascular ingrowth and repair.
- Complete tears occur spontaneously after a sprain or jerking injury of the shoulder,
and the patient complains of acute pain and inability to abduct the arm. To
distinguish from partial tear: No abduction despite LA. There is little or no reaction
and no repair; proxial fibres may retract and become stuck down.
PHYSICAL EXAMINATION
SIGNS OF SUPRASPINATUS TENDINITIS
- Pain at the point of insertion of the supraspinatus along the anterior border of the
acromion, best felt with the arm held in extension
- Painful arc: Pain on active abduction between 60 and 120 degrees of motion, with
disruption of scapulohumeral rhythm.
- Impingement sign: Pain elicited when affected arm is passively flexed, abducted
and internally rotated (the greater tuberosity is brought under the coracoacromial
arch impinging the supraspinatus)
- Impingement test: Pain on doing the above procedure is reduced after injection of
H&L into the subacromial space
SUPRASPINATUS TEAR
- Difficulty in initiating abduction
- Ability to actively abduct the arm after passively abducting it above 90 degrees – TEAR
the abduction paradox, as supraspinatus initiates abduction but deltoid can abduct Conservative
the shoulder the rest of the way - Physiotherapy to improve strength
- “Drop sign”: the abducted arm suddenly drops to the side when it is lowered past a - Heat therapy
certain angle of abduction - Local anaesthesia if necessary
Surgical
INVESTIGATIONS - If amenable to repair, open or arthroscopic cuff repair followed by subacromial
1. X-ray decompression. Especially for young active individuals with complete tears. Partial
- Usually normal in early impingement tears do not require surgery unless persistent pain or considerable instability.
- May be erosion, sclerosis or cyst formation at the greater tuberosity (insertion - If not amenable to repair, open or arthroscopic debridement of degenerate cuff
of the supraspinatus tendon) in chronic tendinitis tissue and subacromial decompression.
- May see calcification of the supraspinatus tendon (incidental and not the cause
of pain) CALCIFICATION OF THE ROTATOR CUFF
- May see narrowing of the space between the acromioclavicular joint and the
humeral head (i) Acute calcific tendinitis
- May see signs of acromiclavicular joint arthritis – osteophytes
- Acute shoulder pain due to deposition of calcium hydroxyapatite crystals in the
2. Ultrasound critical zone of the supraspinatus tendon just medial to its insertion
- May detect large tears, but operator-dependent - Usually affects those btw 30-50yrs old
3. MRI - Investigations – X-ray shoulder jt: calcification seen just above greater tuberosity
- Accurate delineation of anatomy - Treatment – rest arm in a sling, NSAIDs, H&L and LA injection if necessary
- Can help determine site and size of a tear if present
(ii) Chronic calcification
MANAGEMENT - common, usually asymptomatic
TENDINITIS
BICEPS TENDONITIS
Conservative:
- Eliminate aggravating activity, and avoid “impingement position”
- Impingement syndrome.
- Physiotherapy - Pain and tenderness sharply localised to the bicipital groove.
- Short courses of analgesia e.g. NSAIDs - Rest, local heat and deep transverse frictions. Consider a local corticosteroid
- Subacromial Hydrocortisone & Lignocaine / Triamcinolone & Xylocaine injections injection if healing is delayed.
for pain relief (LA takes effect immediately, lasts 1 day; corticosteroid takes effect
3-5 days later) RUPTURE OF BICEPS TENDON
- Patient usu >50yo, can be part of rotator cuff lesion
Surgical
- Presentation: upper arm becomes painful and
- Open or arthroscopic subacromial decompression (acromioplasty)
bruised after patient lifted something and he/she
o Excise coracoacromial ligament & anteroinferior part of acromion
feels something snap in the shoulder
o Remove acromioclavicular osteophytes if present
- Signs: prominent lump in the lower part of the arm
(detached belly of the long head of biceps) upon
flexion of the elbow

22
 - Physical findings: shoulder appears normal with no wasting; most marked feature is
Treatment: decreased active and passive movement in all directions
- No treatment in the elderly if isolated lesion.
- If part of a rotator cuff lesion esp if patient is young, may need anterior INVESTIGATIONS
acromioplasty with reattachment of the tendon (splint the arm with the elbow - X-rays usually normal – useful in excluding other causes of painful shoulder, such
flexed for 4 wks) as infection, post-traumatic stiffness, diffuse stiffness and reflex sympathetic
dystrophy when patient 1st presents
Biceps:
Origin - long head from the supraglenoid tubercle and lies in the bicipital groove, short head is from MANAGEMENT
the tip of the coracoid process of the scapula;
Insertion - posterior part of the tuberosity of the radius and deep fascia on medial aspect of forearm Conservative
via bicipital aponeurosis - Aim of conservative treatment is to relieve pain and prevent further stiffening while
Action- supinator of the forearm, flexor of the elbow jt and weak flexor of the shoulder jt] waiting for recovery (since natural course is recovery in 12-18 months)
- Analgesia (NSAIDs), corticosteroid injections, local heat.
- Physiotherapy:
FROZEN SHOULDER (ADHESIVE CAPSULITIS) o Repeated circular movement of shoulder
o Assisted abduction – use towel or rope, loop it over an overhead bar like a
AETIOLOGY pulley system, and hold on to each end with one hand. Patient uses downward
The term frozen shoulder should be reserved for a well-defined disorder characterised pull of normal arm to passively abduct painful arm overhead.
by progressive pain and stiffness which usually resolves spontaneously after 18 months. o Assisted internal rotation – both hands gripping either end of a towel slung
PRIMARY ADHESIVE CAPSULITIS across the patient’s back diagonally; the hand on the painful side holds the
- Idiopathic in cause lower end while the hand on the normal side holds the end above the shoulder.
- Associated with DM, Dupuytren’s contracture, hyperlipidaemia, hyperthyroidism, Patient uses hand on normal side to pull upwards on towel, passively
cardiac disease internally rotating the painful shoulder.
- Global contracture of the shoulder joint, but maximally in the rotator interval area o Wall-crawling – patient uses fingers to “crawl” up a wall slowly, increasing
and around the coracohumeral ligament flexion movement.

SECONDARY ADHESIVE CAPSULITIS Surgical

- Poorly defined role, only for patients who fail conservative management
- Intrinsic causes
- Manipulation under anaesthesia (least invasive) – passive stretching of the capsule
 Chronic rotator cuff injuries
while patient is under anaesthesia, but be careful of causing fractures especially in
 Post-traumatic scarring following injuries at the shoulder e.g. fracture of the
the elderly.
surgical neck, greater tuberosity.
- Distend the joint by injecting a large volume of sterile saline under pressure
- Extrinsic causes - Fibrolysis/ division (open or arthroscopic) of the supraspinatus and infraspinatus
 Painful disorders resulting in decreased movements of the shoulder: referred may dramatically improve ROM. Must be followed by aggressive physiotherapy
pain from cervical radiculopathy, post-hand, wrist or elbow surgery, post-MI post-op.

CLINICAL FEATURES PROGNOSIS

- Patient aged 40-60 years - Better in younger patients with post-traumatic frozen shoulder; the idiopathic frozen
- Aching in the arms and shoulder after trauma, often trivial shoulders that occur in diabetics tend to recur and not improve.
- Pain gradually increases in severity and prevents sleeping on the affected side
- Subsides after several months with increasing stiffness that continues for 6-12mths
- Movement is regained gradually but may not return to normal

23
SHOULDER JOINT INSTABILITY AND DISLOCATIONS Bilaterally, and the instability usually responds to a Rehabilitation
program.
ANATOMY OF THE SHOULDER JOINT - Surgery rarely indicated. When surgery is necessary, it involves
- Articulation: occurs btw the rounded head of the humerus and the shallow pear- tightening of the Inferior capsule – inferior capsular shift, or Interval
shaped glenoid cavity of the scapula Closure.
- Movements: flexion, extension, abduction, adduction, lateral/medial rotation,
circumduction
- Relations:
1. ANTERIOR DISLOCATION OF THE SHOULDER
Ant: subscapularis, axillary vessels, brachial vessels
Post: infraspinatus, teres minor
MECHANISM OF INJURY
Sup: supraspinatus, subacromial bursa, coracoacromial lig, deltoid
Fall on the hand, driving humerus forwards, tearing the capsule or avulsing the glenoid
Inf: long head of triceps, axillary nerve, posterior circumflex humeral vessels
labrum
- Shallowness of the glenoid fossa of the scapula and lack of support provided by
weak ligaments(3 glenohumeral ligaments—Medial, Inferior, Superior; transverse
CLINICAL FEATURES
humeral ligament; coracohumeral ligament) make the shoulder joint an unstable
Severe pain, shoulder deformity
structure
- Strength mainly depends on the rotator cuff muscles
- Least supported part of the jt lies in the inferior location where it is unprotected by Lateral outline of the shoulder may be
the muscles flattened; bulge may be felt just below
- Shoulder laxity is not equivalent to instability!!! the clavicle

X-RAY FEATURES
ANTERIOR SHOULDER DISLOCATION – TYPES OF X-RAY VIEWS
AP VIEW Y-SCAPULAR (LATERAL AXILLARY VIEW
SCAPULAR) VIEW

- Classification of patients with recurrent shoulder instability:

a. TUBS: Traumatic, Uni-directional (unilateral), Bankart lesion,
Surgery.
- instability related to a clear Traumatic event that presents as
Unidirectional instability, usually involves a Bankart lesion (tear in the
glenoid labrum), and frequently requires Surgery
b. AMBRII: Atraumatic, Multi-directional, Bilateral, Rehabilitation,
Inferior Capsular Shift, Interval Closure
- Instability that arises Atraumatically, occurring in patients prone to
Multidirectional instability who have excessive shoulder laxity

24
AP-overlapping shadows of the humeral head and glenoid fossa with the head lying shoulder may reduce after 15-20mins
below and medial to the socket. Look out for Hill-sachs lesion which may indicate (iii) Hippocratic method: increasing traction applied to the arm with the shoulder
recurrent anterior dislocations in slight abduction while an assistant applies firm counter traction to the body;
e.g. using a towel slung ard the chest under the axilla – know at least this one!

Normal shoulder jt Anterior dislocation of the shoulder - X-ray post-reduction to check position and exclude fracture.
- Exclude an axillary nerve injury, rotator cuff tear, median, radial, ulnar and
COMPLICATIONS musculocutaneous nerve injuries after reduction
Early - Rest the arm in a sling for 3 wks, 1 wk for those >30yrs old due to risk of stiffness
(i) Rotator cuff tear: occurs usu in older people, difficulty in abducting the arm - Avoid abduction and lateral rotation for 3 wks
after reduction - Elbow and finger movements
(ii) Axillary nerve injury: patient unable to contract the deltoid (can inititate
abduction but difficulty in abduction beyond a certain angle) and small patch of
anaesthesia over the muscle (regimental badge area); usu a neuropraxia 2. ANTERIOR INSTABILITY
[course of axillary n.: arises from posterior cord of the brachial plexus (C5,6) in - most common type, accounts for 95% of instability
the axilla, passes through quadrangular space then comes into close relationship - Mechanism of injury: arm is forced into abduction, external rotation and extension
with the inf aspect of the capsule of the shoulder jt and medial side of the - In recurrent dislocations: labrum and capsule often detached from the anterior rim
surgical neck of the humerus] Radial n., median n., ulnar n, musculocutaneous of the glenoid(Bankart lesion) and there is the presence of an indentation on the
n. may be injured sometimes posterolateral aspect of the humeral head (Hill-Sachs lesion)
(iii) Axillary artery injury: examine for ischaemia before and after reduction
(iv) Fracture-dislocation: associated fracture of the humerus-ORIF. Greater CLINICAL FEATURES
tuberosity may be sheared off - Patient may describe his shoulder as ‘coming out’ after a sporting event in an acute
Late dislocation
(i) Shoulder stiffness - Complain that shoulder dislocates with relatively trivial actions and often he/she
(ii) Unreduced dislocation: closed reduction can be attempted up to 6wks after can reduce the dislocation himself
injury - In recurrent subluxation: patient may describe a catching sensation followed by
(iii) Recurrent dislocation: common if the glenoid labrum is detached or the numbness or weakness
capsule is stripped off the front of the neck of the glenoid; more common in - ROM full btw episodes of dislocation
younger patients – 90%, 50% in older patients - Apprehension test: examiner lifts the arm into abduction, external rotation and
then extension, patient’s body tautens in apprehension when he senses that the
TREATMENT humeral head is abt to slip anteriorly. Repeat test by applying pressure to the front
M & R with sedation or sometimes GA of the shoulder at the same time, patient will feel more secure now
(i) Kocher’s method: not recommended due to risk of nerve, vessel & bone injury - Drawer test: scapula is stabilised with one hand while examiner grasps the upper
(ii) Stimson’s technique: patient lies prone with arm hanging over side of bed; arm with the other hand to manipulate the head of the humerus forwards and
backwards with the patient supine

25
- Fulcrum test: patient lies supine and examiner places one hand behind the patient’s X-RAY FEATURES
shoulder to lever the humeral head forward by extending and laterally rotating the - AP view –humeral head looks abnormal in shape as it is medially rotated(light bulb
arm, patient becomes apprehensive. sign); humeral head stands somewhat away from the glenoid fossa (empty glenoid
sign)
INVESTIGATIONS
- X-ray shoulder jt: AP, lateral and axillary views:
 Hill Sachs lesion best shown on AP with arm internally rotated

AP view transcapular view axillary view

Lat view- posterior subluxation, dislocation and sometimes deep indentation on the ant
aspect of humeral head, may have accompanying fractures of the humeral neck,
posterior glenoid rim or lesser tuberosity

- CT shoulder COMPLICATIONS
- Arthroscopy (i) unreduced dislocations
- Examination under anaesthesia (EUA) to determine direction of instability (ii) recurrent dislocations

TREATMENT TREATMENT
- For acute dislocations: Manipulation and reduction followed by immobilisation in a - M & R by pulling on the arm with shoulder in adduction followed by lateral
bandage or sling for several wks rotation while humeral head is pushed forwards.
- Recurrent dislocations: Indications for surgery include frequent painful dislocation - Immobilisation in a sling
and recurrent subluxation

4. POSTERIOR INSTABILITY
3. POSTERIOR DISLOCATION OF THE SHOULDER - Recurrent instability almost always a posterior subluxation with the humeral head
- rare, <2% of shoulder dislocations riding back on the posterior lip of the glenoid
- Subluxation when the arm is in flexion and internal rotation
MECHANISM OF INJURY - Posterior drawer test positive: humeral head pushed backwards while the scapular
- Indirect force producing internal rotation and adduction; occurs most commonly spine and coracoid process are held by the other hand
during a epileptic fit or electric shock; can also be due to a fall on to the flexed, - Posterior apprehension test positive: forward flexion and internal rotation of the
adducted arm, direct blow to the front or fall on the outstretched hand. shoulder with a posterior force on the elbow
- Treatment: muscle strengthening exercises, surgery considered when condition is
CLINICAL FEATURES disabling and there is no gross joint laxity
- Arm is held in medial rotation, front of shoulder looks flat with a prominent
coracoid

26
5. INFERIOR DISLOCATION OF THE SHOULDER
- Occurs when the arm is hyperabducted
- Humeral head is levered out of its socket and pokes into the axilla
- May have severe soft tissue injury with avulsion of the capsule and surrounding
tendons, rupture of muscles, fractures of the glenoid or proximal humerus and
damage to the brachial plexus and axillary artery
- Patient’s arm will be locked in abduction and head of the humerus may be felt in or
below the axilla
6. MULTI DIRECTIONAL INSTABILITY
- Same as AMBRII
X-RAY FEATURES
- Humeral shaft points upwards with the head sitting
below the glenoid
TREATMENT
- M&R: Pull upwards in the line of the abducted arm with
counter-traction downwards over the top of the shoulder. Examine for
neurovascular damage post-reduction. Rest arm in sling for 3 wks.
- If this doesn’t work then open reduction may be needed.
OTHER DISORDERS OF THE GLENOHUMERAL JOINT
- Tuberculosis
- Uncommon
- Starts as osteitis, rarely diagnosed till arthritis supervenes.
- May proceed to abscess and sinus formation, and possibly fibrosis ankylosis.
- X-ray shows generalized rarefraction of bone in early stages with erosion of
joint surfaces. Late cases may have cystic destruction of the joint.
- Treatment: Anti-TB meds and rest the joint until acute symptoms settle.
- Rheumatoid Arthritis
- AC joint, shoulder joint and various synovial pouches usually involved.
- X-ray shows progressive loss of articular space and peri-articular erosions
- Treatment: Methylprednisolone may be injected into joint & subacromial bursa.
- Osteoarthritis
- Usually secondary to other fairly obvious disorders: congenital dysplasia, local
trauma, long-standing rotator cuff lesions, RA or AVN of head of humerus.
- X-rays show characteristic OA picture.
- Milwaukee Shoulder
- Patient presents with swelling of the shoulder and x-rays show a bizarrely
destructive form of arthritis. Similar conditions are encountered in other joints.
- Largely crystal-induced rapidly progressive arthropathy; sometimes associated
with massive rotator cuff tears.
- No satisfactory treatment
DISORDERS OF THE SCAPULA
- Congenital Elevation of the Scapula (Sprengel’s Shoulder)
o Scapula normally descends from neck by third month of fetal life. One
remains high in this case.
o Affected side is elevated, smaller and somewhat prominent.
o Usually painless but associated with other abnormalities like fusion of
cervical vertebrae, kyphosis/scoliosis.
- Klippel-Feil Syndrome
o Bilateral failure of scapular descent and fusion of several cervical vertebrae.
Neck usually short and may be webbed, cervical mobility restricted
o Usually left untreated.
- Winged Scapula
o Due to weakness of serratus anterior---which stabilizes the scapula on the
thoracic cage. Usually not apparent unless contracting the serratus anterior
against resistance. Ie push against a wall.
o Causes: Damage to Long thoracic nerve, injury or viral infxn to 5th, 6th and
7th cervical roots, certain types of muscular dystrophy
- Acromioclavicular Instability
o Common condition resulting from dislocation of AC joint and rupture of
ligaments which tether the outer end of the clavicle. \
o Fairly obvious bump/step over the AC joint. If X-ray not obvious, ask
patient to carry weight on the affected arm and re-shoot the X-ray.
- OA of AC joint
o Common in old people.
o Relieved by H&L injections or excision of the lateral end of the clavicle.
FRACTURES OF THE CLAVICLE
- [MCQ] Embryology of clavicle: membranous ossification
- Mechanism of injury: fall on the shoulder or outstretched hand (FOOSH)
- May have a subcutaneous lump
- Note: in children, clavicle fractures easily but unites rapidly w/o complications too.
- X-ray features:
27
  Most commonly involve the middle 1/3 of the clavicle, outer fragment will - X-ray:
be pulled down by the weight of the arm while inner half held up by SCM  Stress view may be needed to differentiate AC subluxation from dislocation
 Displacement may be severe in outer 1/3 fractures when the coracoclavicular (patient is standing and holding a 5kg wt on each hand; diff in the distance
ligaments are torn btw the coracoid process and inf border of the clavicle >50% diagnostic of
- Complications: AC dislocation)
 Early
1. Pneumothorax
2. Damage to subclavian vessels
3. Brachial plexus injury
 Late
1. Non-union, esp displaced outer 1/3 fractures
2. Malunion (healed #leaves a lump, most common Cx)
3. Shoulder stiffness
- Treatment:
 Middle 1/3#:Support arm in a sling for 2-3wks followed by physio; internal
fixation rarely required - Complications:
 Displaced outer 1/3 #: ORIF (i) Supraspinatus tendinitis
(ii) Unreduced dislocation
(iii) Ossification of the ligaments
FRACTURES OF THE SCAPULA (iv) secondary OA
- Mechanism of injury: body is fractured by a crushing force, a/w rib fractures, lung - Treatment:
contusion and haemo/pneumothorax, neck is fractured due to a blow or a fall on the  AC subluxation- Rest arm in a sling+physio
shoulder  AC dislocation: fixation with a screw for 8wks, rest the arm for 2 wks
- Fractures of the scapula (high energy fracture) can be a/w injuries to the chest, followed by physio; considered only for young and active patients
brachial plexus, spine, abdomen and head
- Treatment:
 Sling and physio for body and neck# STERNOCLAVICULAR DISLOCATIONS
 ORIF for fracture-dislocation(glenoid #) - Mechanism of injury: lateral compression of the shoulders
- Complications: - Anterior(prominent lump over SC jt) more common than posterior dislocation
- Posterior dislocation more serious as there can be pressure on the trachea and large
 Malunion (+ crepitus)
vessels, causing venous congestion of the neck and arm
- Treatment:
 Anterior dislocations: Conservative mx ( IF dangerous as large vessels are
ACROMIOCLAVICULAR SUBLUXATION/DISLOCATIONS behind the sternum)
- Definitions  Posterior dislocations
 AC subluxation- acromioclavicular ligaments are torn with upwards 1. Closed reduction (sedate patient first, then pull at the shoulder)
subluxation of clavicle 2. If unreduced  ORIF or acceptance of some degree of permanent
 AC dislocation- both the acromioclavicular ligaments and coracoclavicular instability (depending on patient characteristics and functionality)
ligaments may be torn, clavicle is elevated, causing a visible and palpable step
- Mechanism of injury: fall on point of shoulder with arm adducted (sports injury)
- Clinical manifestations: pain & swelling over AC joint; inability to ab/adduct arm

28
IMPORTANT ORTHOPAEDIC CONDITIONS IN THE ARM  4 major segments involved: head of humerus, lesser tuberosity, greater
tuberosity, shaft
One part No matter how many
fracture lines there are,
as long as they are
undisplaced, considered
as one part
Two part 1fragment is displaced
FRACTURES OF THE PROXIMAL HUMERUS
- Epidemiology: occurs after middle age. Most common in osteoporotic post-
menopausal women
- Mechanism of injury: fall on the outstretched arm (causes # in older patients, Three 2 fragments are
dislocation in younger patients) part displaced, usu head (#
- Clinical features: large bruise on upper part of arm, may have associated axillary n. along surgical neck) and
and brachial plexus injury greater tuberosity
- X- ray: Four part All the major parts are
displaced
 single impacted fracture extending across surgical neck
in elderly, fragments more clearly separated in younger
patients
 Obtain axillary and scapular lateral views to exclude
shoulder dislocation
 Inf subluxation of the humeral head as fracture heals
Collar & cuff for 1-2 wks
Active exercises once fracture unites (usu aft
6wks)
Cause few problems
Closed reduction, collar & cuff for 4wks
IF if reduction fails or fracture unstable after
reduction
For fractures of the anatomical neck in elderly
may need prosthesis due to high risk of AVN of
humeral head(rare); fixation in younger patients
For 2-part fracture dislocations, closed reduction
usu possible
Fracture of the greater tuberosity may be a/w ant
dislocation of shoulder while fracture of the
lesser tuberosity a/w post dislocation
ORIF
3 part fracture dislocation requires ORIF, at risk
of brachial plexus injury
A/w poor outcome, high risk of vascular injury,
brachial plexus damage, injuries of chest wall
and AVN of humeral head
Usu needs prosthetic replacement (reserved for
the elderly)

- Complications: One part fracture involving surgical neck

1. Vascular and nerve injuries esp axillary nerve
2. Stiffness of the shoulder maximal at the outset
3. Malunion with loss of rotation
4. Avascular necrosis of the head of humerus: 10% of 3-part fractures, 20% of 4-part
fractures

- Treatment Proximal humerus fractures in children

 Neer’s classification: distinguishes btw no of displaced fragments(defined as - In children, the physis can separate or there can be metaphyseal fractures,
>45o angulation or >1cm separation) considerable displacement and angulation is acceptable

29
- Fractures may be pathological as proximal humerus is a common site of bone cysts
and tumors in children
- Fractures due to bone cyst: rest the arm in a sling for 4-6 wks
FRACTURES OF THE SHAFT OF HUMERUS
Mechanism of injury:
 RTA / FOOSH (fall on oustretched hand)
 Fall on the hand causes a spiral fracture.
 Fall on the elbow with the arm abducted causes a oblique or transverse #
 Direct blow to the arm causes a transverse or comminuted fracture
 Note: In the elderly, fracture may be due to mets
Clinical features:
o Painful, bruised and swollen arm
o Displacement of fragments depends on relation of the site of fracture to
the insertion of the deltoid.
- If fracture line proximal to deltoid insertion, proximal fragment adducted by
pectoralis major, lat dorsi and teres major while distal fragment abducted by deltoid
- When fracture is distal to delotoid insertion, proximal fragment is abducted by
deltoid and distal fragment pulled proximally by biceps and triceps
- May have radial n. injury (radial nerve lies in the spiral
grove on the posterior surface of the humerus under to
cover of the triceps). Test radial n. function before and
after treatment by assessing active extension at MCP jt
- X-ray: Look for tumors in elderly as fracture may be
pathological
Complications:
Early
1. Brachial artery injury (dx with arteriography)
2. Radial nerve injury- patient presents with wrist drop and
paralysis of the MCP extensors; common with oblique #s
at the junction of the middle and distal 1/3 of bones
Late
1. Delayed union, malunion and non-union (common in
conservatively managed patients)
2. Joint stiffness
Treatment:
- U slab  Cast  Brace, or
- ORIF
- Most heal readily; weight of arm with external cast enough to pull fragments
together. Hanging cast is applied from shoulder to wrist with elbow flexed and
forearm is suspended by a sling around patient’s neck
- Spiral fractures unite in about 6wks while other fractures take 4-6wks longer
- Cx rate after IF of humerus high (compression plate, screws, intramedullary nail,
external fixation)

Indications for surgery:

 Radial n palsy
 Segmental #
 Open #
 Pathological #
 Intra-articular extension
 Floating elbow (humeral + forearm #)
 Non-union

30
ANATOMY OF THE ELBOW JOINT

Type of jt: Hinge jt, Stability due to the shape and fit of the bones that make up the jt
and the capsular and collateral ligaments
Articulation: Btw the trochlea and capitulum of the humerus and the trochlea notch of
the ulna and head of the radius

Ligaments:
Lateral collateral lig attached by apex to the lateral epicondyle and base to annular
ligament of radius
Medial collateral lig attached to the medial epicondyle to medial margins of olecranon
and coronoid process

Nerve supply: branch from median, ulnar, musculocutaneous, radial n.

Movements:
Flexionbrachialis, biceps brachii,, brachioradialis, pronator teres; in flexion, the bony
points form the boundaries of an equilateral triangle
Extension triceps, anconeus; in extension, the med and lat epicodyles and top of the
olecranon are in a straight line

Relations: FRACTURES AROUND THE ELBOW IN CHILDREN

Ant brachialis, biceps tendon, median n., brachial artery
1. SUPRACONDYLAR FRACTURES
Post triceps, small bursa One of the commonest # in children
Medulnar n. passes behind the med epicondyle and crosses medial ligament of the jt
Lat common extensor tendon, supinator Mechanism of injury: Posterior displacement due to fall on outstretched hand
(hyperextension injury), distal fragment pushed backwards and twisted inwards while
Forearm normally slightly in valgus in relation to the upper arm, average carrying angle
proximal fragment can poke into the soft tissue anteriorly, injuring the brachial artery or
in children being abt 15 degrees.
median nerve.
In children, the secondary ossification centres can be seen on x-rays. The average ages
Anterior displacement use due to direct trauma (rare) with jt in flexion
at which the ossific centres appear are ‘CRITOE’
C apitulum-2yrs
Clinical features: ‘S’ deformity in posteriorly displaced #. Examine for vascular (check
R adial head- 4yrs
pulse and capillary return) and nerve injury.
I nternal (medial) epicondyle-6yrs
Trochlea-8yrs
X-ray:
O lecranon-10yrs
Fracture best seen on lat view
E xternal (lateral) epicondyle-12yrs Fat pad sign in undisplaced # : triangular lucency in front of distal humerus due to fat
pad being pushed forwards by a haematoma

31
 cortex still in continuity length of the arm with counter-traction
above elbow correct lateral shift and
Type IIa Less severe and merely angulated tilt correct rotationcorrect
backwards shift and tilt. Check pulse!
Type IIb More severe, both angulated and Collar and cuff x 3wks
malrotated Reduce under GA, hold with wires
Increased risk of neurovascular
injury or circulatory compromise due
to swelling
Type III #, distal fragment tilted Type III Completely displaced fracture Reduce under GA, hold with wires
Increased risk of neurovascular Open reduction if
injury or circulatory compromise due (i) closed reduction fails
Both anterior and posterior fat pads
to swelling (ii) open fracture
backwards visible, sail sign configuration
(iii) vascular damage present
Continuous traction through a screw in
the olecranon or skin traction with the
Baumann’s angle: assess degree of medial angulation (angle is elbow almost straight and the arm in a
subtended by longitudinal axis of humeral shaft and a line small Thomas splint (Dunlop traction)
through coronal axis of capitellar physis; usually <80 degrees)
Increase in Baumann’s angle occur in residual varus and internal 2. FRACTURES OF THE LATERAL CONDYLE
rotation deformities Mechanism of injury: Fall on outstretched hand with elbow extended and forced into
varus. Fragment “capsized” by extensor tendons. Fracture always involves joint;
Complications: fracture line usu runs along the physis and into the trochlea; fracture may damage the
Early growth plate
1. Brachial artery injury, can cause Volkman’s ischaemia
2. Compartment syndrome pain + 1 positive sign [pain on passive extension of the Clinical features: swollen and deformed elbow, passive flexion of the wrist (pulling on
fingers, tnese and tender forearn, pulseness, blunted sensation, increased capillary refill the extensors) may be painful.
time], KIV angiography, vessel graft, forearm fasciotomy
3. Median n., esp anterior interosseous branch, recovery usu in 6-8wks X-ray: Oblique view should be taken
4. Ulnar n. damaged by careless pinning Usu there is a fracture through the middle of the trochlea and the elbow is unstable and
Late may dislocate (Salter Harris Type II)
Less commonly, the fracture runs through lateral condyle into the trochlea, stable
1. Malunion, causing varus deformity of the elbow（gunstock deformity,） rarely
fracture with no involvement of the humero-ulnar jt (Salter Harris Type IV)
valgus(may cause late ulnar n. palsy), may need correction by supracondylar osteotomy
2. Elbow stiffness
Complications:
3. Myositis ossificans
1. Non-union and malunion, causing cubitus valgus and tardy ulnar n. palsy
2. Recurrent posterolateral dislocation of elbow
Treatment
Type I Undisplaced fracture Immobilize in 90o, sling x 3wks
Check x-ray 5-7days later to ensure no Treatment:
displacement  Minimal displacement – backslab
Type II Angulated fracture with the posterior Reduce under GAtraction in the with elbow flexed & wrist extended

32
 (relaxes extensor mechanism) for 2/52 Treatment:
 Displaced # (gap of >2mm) – ORIF, immobilize arm in a cast for 3-4/52  Displacement <30deg- collar and cuff
 Displacement>30 deg- closed or open reduction. IF not necessary
3. FRACTURES OF THE MEDIAL CONDYLE  Never remove radial head as it interferes with growth of the radius
Mechanism of injury: Fall on outstretched hand, elbow forced into valgus or fall from
ht with direct blow to the elbow, medial fragment may be displaced by pull of the flexor
muscles FRACTURES AND DISLOCATIONS AROUND THE ELBOW IN ADULTS
Clinical features: pain and swelling 1. FRACTURES OF THE DISTAL HUMERUS
Type A Type B Type C
X-ray: intra-articular #; in younger children, much of the medial condylar epiphysis is Extra-articular Intra-articular bicondylar# with
cartilaginous and may not be visible on x-ray, an arthrogram may be useful in some Intra-articular unicondylar #
supracondylar # varying degrees of comminution
cases - rare in adults - high energy # with soft tissue damage
- usu displaced - examine for vascular or nerve injury
Complications: and unstable
Early Late ORIF Undisplaced #
1. Ulnar n. damage 1. Stiffness of the elbow  Posterior slab with elbow flexed almost 90 deg
2. Late ulnar n. palsy due to friction in roughened bony  Check x-rays 1/52 after injury
groove Displaced#
 ORIF, elbow held at 90 deg with arm in a sling, healing occurs
Treatment: by 12wks
Undisplaced-splint and repeat x-ray
 Skeletal traction may be considered for severely comminuted #
Displaced- closed reduction with percutaneous pinning or ORIF
 Elbow replacement in the elderly
Complications
4. PULLED ELBOW Early
Mechanism of injury: pull on the arm with forearm pronated, causing subluxation of 1.Vascular injury
annular ligament over head of radius into radiocapitellar joint. 2.Median n. or ulnar n. damage
- Usually affects a child between 2-3yo Late
1. Elbow stiffness
No x-ray findings 2. Heterotopic ossification

Treatment: Supinate then flex the elbow, ligament pops back in place

5. FRACTURED NECK OF RADIUS 2. FRACTURED HEAD OF RADIUS

Mechanism of injury: Fall on outstretched hand, forcing elbow into valgus and
pushing radial head against capitulum; same injury in adult usu causes radial head #
Clinical features: pain on rotating forearm
X-ray: may have a Salter Harris II injury; proximal fragment is tilted distally, forwards
and outwards
Common in adults but rare in children
Mechanism of injury: Fall on outstretched hand with elbow extended and forearm
pronated articular cartilage of the capitulum may be bruised or chipped
Clinical features: tenderness over radial head, pain on pronation and supination
X-ray: to exclude concomitant injury of distal RUJ i.e. damage to interosseous memb.

33
Complications:
1. Joint stiffness of the elbow and radioulnar jt X-ray: lateral view needed, check position of radial head as it may be dislocated
2. Myositis ossificans
3. Recurrent instability of the elbow if injury to the medial collateral lig and if there Complications:
is excision of the radial head 1. Stiffness 3. Transient ulnar n. palsy
2. Non-union 4. OA
Mason classification
Treatment:
- Comminuted # with triceps intacttreat as a bruise and rest in sling for 1/52 as
immobilization can lead to stiffness in the elderly; obtain check x-ray
- Undisplaced transverse#  immoblise at 60 deg in a cast for 2-3/52
- Displaced transverse # ORIF with tension band wiring

Type I Type II Type III

Vertical split in the Single fragment of lateral Head is comminuted 4. DISLOCATION OF THE ELBOW
radial head portion of the head broken off - Posterior or posterolateral dislocation in 90% of cases; lateral shift may occur
and usu displaced distally - Reduction usu stable and recurrent dislocation unlikely if there are no associated #
LA injection and Reduction and fixation with a Excision of radial head - If there is # of the radial head, coronoid process or olecranon process, joint is more
aspiration of small screw unstable and more prone to redislocation unless # are fixed
haematoma Reconstruction of radial head if - Considerable soft tissue disruption and possible vascular and nerve injuries
there are forearm injuries,
Collar and cuff for disruption of the distal RUJ Mechanism of injury:
3/52 which increases risk of - FOOSH with elbow in extension causes posterior dislocation
proximal migration of the - Side swipe injury (driver with elbow out of the window) causes forward
radius and instability dislocations usu a/w # and severe soft tissue damage
Fracture dislocation: reduction Clinical features: obvious deformity, patient supports forearm with elbow
and fixation, need to restore
- Examine for vascular or nerve damage
radial pillar
**TERRIBLE TRIAD = Radial head # + coronoid process # + MCL injury ** X-ray: confirms dislocation and identify associated #

3. FRACTURES OF THE OLECRANON

Mechanism of injury:
- Direct blow or fall on the elbow causing a comminuted #
- Traction when patient falls on hand with triceps contracted, causing a clean
transverse break

Clinical features:
- Bruise over the elbow in comminuted #, intact triceps
- Palpable gap and patient unable to extend elbow against resistance in transverse #

34
Complications:
Early
1. Brachial artery injury
2. Median or ulnar n. injury

Late
1. Stiffness
2. Heterotopic ossification, myositis ossificans; if bone mass restricts elbow function,
excise when mature
3. Unreduced dislocation
4. Recurrent dislocation if there is a large coronoid# or radial head #
5. Secondary OA Line drawn down the long axis of the radius does not intersect the capitulum,
indicating radial head dislocation
Treatment:
Uncomplicated dislocation: reduce under anaesthesia
Slight flexion of elbow and traction on forearm correct lateral displacement further
flexion of elbow while pushing olecranon forwards check nerves and circulation +
check x-raycollar and cuff for 3/52 with elbow flexed>90deg

Dislocation with associated #: fix the #

Side swipe injuries — repair vascular damage, skeletal stabilization
Persistent instability — temporary external fixation

5. RADIAL HEAD DISLOCATION

- Isolated dislocation are rare
- Usually a/w ulna # (Monteggia injury)
- Common in children; rule out NAI
 Another mechanism of injury: parents pulling kids by the hands (yanking)
- Important to identify ulnar # in children as if a minor deformity allowed to persist,
may prevent full reduction of dislocation
- Look for posterior interosseous nerve injury
- Treatment: manipulation under anaesthesia (supination, direct pressure), cast 6/52

35
IMPORTANT ORTHOPAEDIC CONDITIONS IN ELBOWS & FOREARMS TENNIS ELBOW (LATERAL EPICONDYLITIS)
CUBITUS VARUS (GUNSTALK DEFORMITY) Cause: minor trauma to origin of wrist extensors / fibrosis of extensor carpi radialis
Cause: Malunion of supracondylar # brevis (ECRB) e.g. painting, carpenter
Rx: wedge osteotomy of lower humerus Features:
o Lateral epicondylar pain, aggravated by shaking hands & opening doors.
Cx: median nerve palsy
o Pain on active wrist extension with a straight elbow. Normal ROM.
o Pain reproduced by extending wrist against resistance or by passively flexing in
thus extending the tendons
CUBITUS VALGUS
Rx: rest, lifestyle modification, H&L injection, extra-corporal shockwave, excision of
Cause: non-union of # lateral condyle (a/w bony knob on medial elbow)
fibrous mass, lengthen tendon (ECRB)
Mx:
 Undisplaced – backslab
 Moderate displacement – closed reduction and backslab GOLFER’S ELBOW (MEDIAL EPICONDYLITIS)
 Unstable – K-wire and cast Similar to tennis elbow, but affecting flexor origin at medial epicondyle
 Rotated – Open reduction and K-wire Memory aid: Golfer’s already has ‘L’ hence Medial Epicondylitis
 X-ray weekly to detect slipping
Cx: Tardy ulnar nerve palsy – manage by transposing ulnar nerve anterior to elbow
CUBITAL TUNNEL SYNDROME
Compressive ulnar neuropathy at the elbow, in the retrocondylar groove or as ulnar
RHEUMATOID ARTHRITIS nerve passes between the 2 heads of the flexor carpi ulnaris
 Caused by constriction of fascial bands, subluxation of ulnar nerve over medial
Features: pain, tenderness, swelling, stiffness, usually bilateral epicondyle, cubitus valgus, bony spurs, tumours, ganglions, repetitive elbow
X-ray: bone erosion, radial head destruction, widened trochlear notch of the ulna flexion & extension
Rx: splint, radial head resection, partial synovectomy, arthroplasty Features: paraesthesia along ulnar 1.5 fingers; weak grip strength especially when
patient rest upon or flexes the elbow; +/- nocturnal symptoms; loss of fine dexterity;
rarely, wasting of intrinsic muscles & clawing/abduction of little finger. Male> Female.
OSTEOARTHRITIS DDx: cervical spondylosis, ulnar tunnel syndrome (compression at canal of Guyon at
Cause: intraarticular #s, loose bodies, crystal deposition dz the wrist) – preserved strength of wrist and 4th & 5th digit flexors
Features: pain, stiffness, ROM,  ulnar n palsy
McGowan Grading system
X-ray:  Jt space, bone sclerosis, osteophytes, loose bodies 1) Parasthesia in distribution, clumsiness in hand,
2) Weak interossei & muscle wasting,
3) Paralysis of interossei, marked weakeness.
OLECRANON BURSITIS Rx: Simple decompression, medial epicondylectomy if a/w non-union of epicondyle #,
Causes: pressure, friction, infxn, gout (a/w tophi), RA (a/w polyarthritis & subcutaneous anterior transposition of the ulnar nerve, injection of steroids in the cubital tunnel
nodules over the olecranon)

36
SUPRACONDYLAR FRACTURES Support  Collar & cuff for 3 wks
Fractures in distal 1/3 of humerus proximal to the trochlea & capitulum  Sling for another 3 wks to avoid extension, but flexion is
allowed.
Epidemiology: common childhood #. Adults: More proximal, commonly with
comminution, spiraling & angulation
Cx:
Mechanism of injury: FOOSH 1. Arterial obstruction: Brachial arterial kinking by proximal fragment. Arterial wall
Features: pain over elbow, swelling, deformity damage results in Volkmann’s ischaemic contracture. Symptoms = Pain, Pallor,
Paraesthesia, Paralysis, Perishing cold, swelling & bruising)
Important complication: Volkmann’s ischaemic contracture – df: irreversible
contracture of flexor muscles of the hand due to ischaemic processes in the forearm 2. Median nerve injury
3. Malunion – cubitus varus (may cause ulnar tunnel syndrome)
DDx: dislocation of elbow (equilateral Δ by epicondyles & olecranon is disrupted)
X-ray: # line across distal humerus, posterior tilt/displacement of distal fragment, 
medial or lateral displacement. ELBOW DISLOCATIONS
Mechanism: fall on outstretched hand
Mx:  Assoc injuries routinely checked for: #s of epicondyles (usually medial), lateral
Indications for  Arterial obstruction condyle, coronoid & radial head & neck
reduction  # displacement &/or angulation X-ray: posterolateral dislocation of elbow
 <50% bony contact
Rx:
 Backward tilt 15% o Apply strong traction in the line of the limb under GA. Slight flexion might be
 Medial or lat tilting of 10% (may cause tardy ulnar n palsy) required.
 Severe torsional deformity o Alternative: clasp humerus from behind & push olecranon fwd & medially while
Manipulation Manipulation under GA asstant applies traction in moderate flexion
technique 1. Disimpaction: Traction applied at 20o flexion with o Support with sling for 3 wks.
countertraction applied to arm Cx: exclude ulnar n, median n & brachial arterial injuries; elbow stiffness, myositis
2. Reduce post tilt/displacement: Flex elbow to 80o while ossificans.
maintaining traction
3. Correct lat displacement/torsional deformity: manipulate
epiphyseal complex
MEDIAL CONDYLAR INJURY
Fixation  Fix with elbow at greatest angle of flexion possible w/o Mechanism: direct violence or avulsion by ulnar collateral ligament on forceful
compromising circulation (check radial pulse) abduction
 Never apply a complete plaster due to risk of swelling Mx: immobilize in plaster cast for 2-3 wks
X-rays AP & lateral Cx:
Remanipulation  No more than 2 remanipulations due to risk of swelling. 1. Tardy ulnar n. palsy
if reduction is Employ continuous traction instead (e.g. Dunlop traction) 2. Trapping of medial epicondyle in the elbow joint
poor
 K-wires & plaster backslab may be used for unstable #
Observation  Overnight, esp for complications of vascular compromise

37
RADIAL HEAD FRACTURE Monteggia  Fracture of upper ulnar (shortening & angulation) + radial head
dislocation (MUF: Monteggia Ulnar Fracture)
Mechanism: direct violence, or FOOSH  Mechanism: direct violence on forearm or forced pronation (eg fall
Features: elbow pain, swelling, bruising, restricted elbow extension on outstretched hand with trunk rotation)
Galeazzi  Fracture lower radius + inferior radioulnar joint dislocation with
X-ray: # radial head,  subluxation of distal end of ulna. ulnar displacement (GUD: Galeazzi Ulnar Dislocation)
(+) AP projections in mid-prone & full pronation required. Assess type of #.
 More common than Monteggia.
Mx:
Mx:
Fracture Rx o Principle: Restore length of fractured bone, then reduce dislocation
Hairline Light compression bandage & sling for 3 wks, + o Children: manipulation + plaster fixation <good remodeling potential>
Undisplaced (marginal backslab if pain is severe. Excellent outcome o Adults or children w displaced #s: ORIF (plate & screw), plaster fixation in 90
or segmental) degrees flexion with supination
Displaced (marginal or Conservative Rx, r/v in 3 mths. Late excision of radial Cx:
segmental) head if movts are severely restricted o Cross union – radius malunites with ulnar
Comminuted Radial head excision w/in 48hrs  silastic prosthetic o Loss of pronation/supination
replacement, splint for 3 wks o Loss of extension of elbow
o Difficult to reduce and maintain closed. Usually requires ORIF
o Shoulder to hand syndrome (frozen shoulder)
o If due to persistent unreduced dislocation or late Dx:
RADIAL NECK FRACTURE
Monteggia  Anterior protrusion of radial head :.  elbow ROM
Mechanism & Dx: Similar to radial head # – Rx: excise radial head
Mx:  Tardy ulnar n palsy – Rx: transposition of ulnar nerve
Minimal tilting Conservative Galeazzi  Prominent ulna & chronic wrist pain – Rx: excise distal ulna
 Ligaments potentially torn :. Instability at DRUJ – Rx: put in
Marked tilting (>20o Manipulate – apply traction, pronate & supinate, cast, arm in supination OR use K-wires
adults, >30o children) apply pressure when prominent part of radial head
presents, + K-wire if unstable
NIGHTSTICK INJURY
 Isolated fracture of the ulnar with minimal displacement.
FOREARM FRACTURE-DISLOCATIONS  MOI: Holding up arm to protect face from blow
 More commonly fracture of both bones of the forearam, usually displaced.  Rule out fracture clinically and radiographically
 If only one bone fractured, look for dislocation of the other.  Rx: Below elbow cast for 6 wks for distal one-third #. If angulation of proximal
 Displaced fractures of the forearm usually treated by ORIF as non-surgical means two-thirds severe, consider ORIF.
often result in limitation of pronation/supination.
CAUSES OF TARDY ULNAR NERVE PALSY
Types: Remember, “Big bone #s, small bone dislocates”  Medial / Lateral condylar fracture
 Monteggia fracture

38
IMPORTANT ORTHOPAEDIC CONDITIONS IN THE HANDS & WRISTS DDX OF PAINFUL WRIST & HAND
TYPES OF CASES Painful Wrist Painful Hand
Lumps  Ganglion  Haemangiomas Referred Cervical spondylosis Neck
 Pigmented villonodular synovitis (PVNS)  Pseudoaneurysms Shoulder
 Implantation dermoid cyst  SCC Mediastinum
 OA – Heberden’s & Bouchard’s nodes  Glomus tumours Joint RA RA
OA OA
Joint  RA hands  OA hands Infection
Vascular  Haemangiomas Periarticular De Quervain Carpal tunnel
Nerve  Ulnar n palsy  Radiculopathies Tenosynovitis Tenosynovitis
 Median n palsy  Erb’s palsy (C5-6) Instability Infection
 Radial n palsy  Klumpke palsy (C8-T1)
 Carpal tunnel syndrome NB. CTS, De Quervain’s disease and trigger finger are all tenosynovitis (i.e. same Mx)
Muscle /  de Quervain’s dz  Trigger finger
tendon  Tenosynovitis  Dupuytren’s contracture I. HANDS
 RA – Swan neck & Boutonniere  Mallet finger ACUTE INFECTIONS
deformities, tendon rupture
GENERAL
Bones  Colles’ #  Boxer’s #
 Smith’s #  Gamekeeper’s thumb - Frequently limited to 1) Nail Fold, 2) Pulp space, 3) Subcutaneous tissues, 4)
 Scaphoid #  Scaphoid dislocation Tendon sheath, 5) Deep Fascial spaces or joint
 Bennett’s #  Lunate dislocation - Cause: Almost invariably implanted Staphylococcus
- Pathophysiology: Acute inflammation and suppuration in a small compartment will
result in increase in pressure leading to threatened local blood supply tissue
necrosis or a stiff and useless hand
- Clinical features: Usually a hx of trauma, may be unnoticed. Painful and swollen
hand. Throbbing pain. May be a/w with fever. Exquisite tenderness, red and tense
PATHOLOGIES
tissues with decreased ROM.
1. Trauma
2. Tumour - Principals of Rx: 1) Antibiotics—usually flucloxacillin, and in severe cases, fusidic
3. Infection acid or a cephalosporin as well. 2) Rest and elevation. 3) Analgesics 4) Drainage
4. Inflammation only if there’s sign(s) of abscess (throbbing pain, marked tenderness and toxaemia.
5. Degeneration 5) Splintage in a the position of safe immobilisation (wrist slightly extended, MCP
in full flexion, IP joints extended and thumb abducted—ligaments are at greatest
length. 6) Physiotherapy

SPECIFIC TYPES
PARONYCHIA
Infection under nailfold.

39
PULP SPACE INFECTION MUSCLE / TENDON DISORDERS
Usually prick or splinter of the finger tip
DUPUYTREN’S CONTRACTURE
TENDON SHEATH INFECTIONS  Definition: nodular hypertrophy & contracture of palmar aponeurosis.
 Uncommon but dangerous. Risk of tendon necrosis and pt may end up with useless  Pathogenesis: local microvessel ischaemia  increased xanthine oxidase activity
hand. Present with painful, tender swollen hand with zero ROM (active and passive  superoxide free radical production  stimulate myofibroblast proliferation &
not permitted) type III collagen formation. Specific platelet-derived and fibroblast growth factors
 Rx: As above. May require surgical drainage if no improvement over 24 hrs. also play a role in the aetiology.
o Allopurinol may help to reduce symptoms (XO inhibitor)
DEEP FASCIAL SPACE INFECTION o The process of chronic inflammation is thought to be essential to the
 Usually infection from a web space or tendon sheath. The palm is ballooned. Loss subsequent fibrosis
of normal concavity, with whole hand held still.  Features: Middle-aged man.
 Rx: Incision and drainage. LOOK o Appearance of any visible cords, any pitting/tethering of skin on
palmar aspect of hand
JOINT INFECTION o Scars from previous surgery
 Can be infected directly or indirectly. Clinically hard to distinguish from acute gout. o Flexion deformities at MCPJ and PIPJ of the involved fingers
So aspirate joint. o Involvement of thumb & 1st web space (a sign of more aggressive dz)
o Garrod’s pads at PIPJs on dorsum of hand (thickening of s/c tissues)
 Rx: IV antibiotics and splint. If no improvement in 24 hrs  open drainage.
FEEL o Palpate swelling, note fixation to skin
o Compare with other palm!
BITES
MOVE o ROM of involved fingers
 Animal Bites: Usual organisms — Staph and strep
o Passively move the joints with fixed deformities
Human Bites: Organisms more varied and includes Anaerobes.
OFFER o To enquire about causes & associations
 X-ray done to exclude fracture or foreign body.
o Assess patient’s function, e.g. writing & dressing
 Mx:
o Look for other features of diffuse fibromatosis
o Fresh wound: Examined in OT. Swab for c/s. Explore for foreign bodies such
as tooth. Splint elevate and start prophylactic antibiotics  DDx:
o Infected Bites: debridement and washout. Start IV antibiotics—Broad o Skin contracture (look for scar from previous wound)
sprectrum penicillin and cephalosporin. Consider Rabies. o Tendon contracture (thickened area or ‘cord’ moves on passive flexion of
o Post op: Physiotherapy. Deal with tendon lacerations when tissues are involved finger)
completely healed. o Congenital contracture of little finger (affects PIPJ)
o Ulnar nerve palsy (claw hand deformity)
 Conditions associated with Dupuytren’s contracture (DEAFEST PAIL)
SKIN
o DM
SKIN CONTRACTURES o Epilepsy
- Cuts and burns are liable to heal with contractures, causing puckering of the palm o Age
or fixed flexion deformities. Surgery incisions should never cross flexor creases. o Family history (AD) / fibromatoses
- Rx: Established contractures may require excision of the scar and Z–plasty of the o Epileptic medication (e.g. phenobarbitone)
overlying skin. o Smoking
o Trauma & heavy manual labour

40
 o Peyronie’s disease (fibrosis of the corpus cavernosum – seen in 3% of Bone (avulsion #) Muscle (imbalance)
patients with Dupuytren’s contracture) Extra-articular or involving <2/3 of joint Treat with mallet splint (conservative)
o AIDS  conservative Rx
o Idiopathic Intra-articular or involving ≥2/3 of joint
o Liver disease (secondary to alcohol)  surgical reduction
 Treatment: Indicated when deformity is progressive and interferes with function
(i.e. when MCPJ or PIPJ contracture exceeds 30deg).
RUPTURED EXTENSOR POLICIS LONGUS
o Fasciotomy – for prominent bands
o Partial fasciectomy (with Z-plasty to lengthen wound) – in conjunction with  Injury to long thumb extensor after fraying
post-op physiotherapy (early active flexion ROM exercises for grip strength)  Secondary to colle’s fracture, rheumatoid arthritis
and night-time splintage in extension  Rx: Tendon transfer usually required
o Dermofasciectomy (with full-thickness skin grafting) – a/w lowest risk of
recurrence DROPPED FINGER
o Arthrodesis/amputation – for late presentations & repeated recurrences
 Rupture of extensor tendon
 Patient unable to hold finger at extension at MCP joint
MUSCLE CONTRACTURE  Rx:
Forearm  Ischaemic contracture of forearm muscles, commonly caused by: (1) direct repair
o Volkmann’s ischaemic contracture: # causing compartment (2) distal portion of the tendon attached to adjacent finger extensor
syndrome resulting in muscle ischaemia & necrosis. Infarcted
muscles replaced by fibrous tissues. Usually follows circulatory BOUTONNIERE
insufficiency due to injuries at or below the elbow.
 Flexion deformity of PIP joint due to interruption of central slip of extensor tendon
o Tight plaster cast & limb swelling
 Lateral slips separate and head of proximal phalanx pops up in between
 Shortening of long flexors causing flexion deformity of fingers which
 Rx: post traumatic usually repairable. Chronic deformity (in RA) usually cannot be
is only correctable on wrist flexion (tendodesis effect)
repaired
 May be a/w ulnar and/or median nerve palsies
 Treatment: If marked disability: muscle release, Excise dead muscle or
tendon transfer SWAN NECK DEFORMITY
Intrinsic  MCPJ flexion, IPJ extension & thumb adduction  Reverse of Boutonniere – PIP hyperextended, DIP flexed
muscles  Causes: spasticity (eg CP), scarring (trauma and infection)  Due to imbalance of extensor vs flexor action in finger (commonly in RA)
 Treatment: muscle release  Rx: tendon rebalancing and joint stabilisation
 Aka intrinsic plus. Intinsic minus is used to describe Ulnar claw due to
paralysis of the intrinsic muscles.
TRIGGER FINGER (STENOSING TENOVAGINITIS)
 Epidemiology: 55- 60 years old, women > men
MALLET FINGER
 Causes:
 Injury to extensor tendon of terminal phalanx o Idiopathic
 Clinical features: loss of active DIPJ extension, normal o Congenital
passive DIPJ extension o Overuse / Local trauma causing sheath thickening
 Types & Rx o RA
 Clinical features:

41
 LOOK Flexion of ≥1 finger; commonly affecting middle & ring fingers of o Divide entire A1 pulley (tendon sheath) in the midline under vision, then
dominant hand (NB. finger doesn’t need to be in fixed flexion the whole ask patient to actively move the digit to confirm full release (motion
time for it to be triggering) encouraged immediately following the procedure)
FEEL Ask if there’s any pain. o Complications: incising too distally  cut the A2 pulley  bowstringing
Palpate for small nodule overlying the tendon sheath (usually approx. at
the level of proximal transverse palmar crease).
MOVE Triggering on extension, snapping sensation, tenderness over A1 pulley LUMPS
PIGMENTED VILLONODULAR SYNOVITIS (PVNS)
 Pathology:  Definition: benign proliferative disorder of synovial lining of joint, bursa & tendon
» Most often due to formation of nodule in FDS tendon where it glides under the sheaths. Produces localised/diffused nodular thickening of the synovial membrane.
A1 pulley in the region of the metacarpal head.
» Flexor tendon trapped at entrance of tendon sheath; forced extension causes  Epidemiology: commonest hand lump disorder, occurs in patients 20-50yo
opening snap. Tender nodule may be felt in front of sheath at the MCPJ  2 types (+ sites)
i) Diffuse form
 DDx: o Affects entire synovial lining of a joint, bursa or tendon sheath; affects
» RA large joints
» Septic arthritis o More commonly in the knee, followed by the hip; ankle; shoulder joints
» Suppurative tenosynovitis ii) Localized/nodular form
» Tumour of tendon sheath o Appears in the form of a localized nodule or mass in a synovium, and the
» Dislocation surrounding synovium is generally normal
» Dupuytren’s contracture o Affects tendon sheaths around small jts of hands & feet (termed nodular
tenosynovitis)
 Staging & Mx (Green’s Classification):
 Presentation: solitary, well circumscribed, tan colored, and sometimes has pale
Stage Features
yellow regions of lipid deposition. Insidious onset, dull aching jt pain, nodular or
Pre-triggering Hx of triggering not demonstratable on PE; tenderness
diffused jt swelling, ROM, locking of joint.
Triggering Demonstrable catching, but patient can actively extend the digit
Triggering & Demonstrable locking, requiring passive extension (IIIa) or inability  X-ray: joint swelling, periarticular erosions, joint space narrowing, sub chondral
cyst, osteophytes formation (secondary OA changes)
Locking to actively flex (IIIb)
Contracture Fixed flexion contracture of PIP joint  Treatment: Surgical Excision. However, diffuse lesions have a high rate of
recurrence (>50%) If refractory to repeated surgery, may be managed with low-
 Mx: dose radiotherapy
» Splinting (MCP joint flexed 15˚; not that efficacious)
» Activity modification (i.e. reduce local trauma) IMPLANTATION DERMOID CYSTS
» H&L into tendon sheath: high rate of success in female patients, with short  Usually sited along the volar surfaces of the fingers & palms
duration of symptoms (<4mths), for discrete palpable nodule, single digit  Associated with trauma to the overlying skin – look for scars
involvement, no associated conditions (e.g. RA, DM)
» Surgical release
o If injection therapy failed or if patient has other pathologies (e.g. RA) GOUTY TOPHI
which is suspected to cause triggering & cannot be treated conservatively  Relatively mobile, stuck to tendon/joint, firm, can be soft, whitish, not
transillumnant, tender in acute cases
 Where: ear, ankle, elbow, finger

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 Complications: skin ulceration ENCHONDROMA
 DDx: PVNS  Commonest primary bone tumor of hand
 Hard, irregular, fixed swelling
SQUAMOUS CELL CARCINOMAS
 Due to burns, sunburn, Arsenic MALIGNANT MELANOMA
 Spread by lymphatics
NEUROMA
NEUROFIBROMA
 Localised to digit and part of hand GIANT CELL TUMOUR
 4-5cm, irregular and wrinkled skin, soft, mobile with skin, a/w cafe au lait spots
LIPOMA
GLOMUS TUMOURS
 AKA glomangioma, or nonchromaffin paraganglioma): a rare benign neoplasm, OSTEOCHONDROMA
specialized arteriovenous anastamosis and usually found in the skin of the
extremities. It arises from the glomus body (Component of the dermis layer of skin, II. WRISTS
involved in body temperature regulation. The glomus body consists of an AV shunt
surrounded by a capsule of connective tissue. Glomus bodies are most numerous in Carpal Bones (lateral to medial):
the fingers and toes. The role of the glomus body is to shunt blood away from skin “Some Lovers Try Positions That They Cannot Handle”
surface when exposed to cold temperature, thus preventing heat loss, and allowing Scaphoid, Lunate, Triquetrium, Pisiform, Trapezium,
maximum heat flow to the skin in warm weather to allow heat to dissipate.) Trapezoid, Capitate and Hamate
 Small, vascular & tender swelling, usually occuring at the region of the nail beds.
 Treatment: Radiotherapy and surgery Alignment in Gilula’s Arc (Carpal Arc)

VASCULAR TUMOURS
May have thrills and bruits
JOINT DISORDERS
PYOGENIC GRANULOMA CHRONIC CARPAL INSTABILITY
 Relatively common benign vascular lesion of skin and mucosa. Exact cause Causes:
unknown  Injury
 Usually occurs in children and young adults as a solitary, glistening, friable,  Arthritis
polypoid bright red papule or nodule. Prone to bleeding and ulceration.  Kienböck’s disease (patchy lunate AVN after trauma)
 Ranges from few mm to several cm in size.
 Regressing lesions: Appear as soft fibroma. Normally occurs at head & neck, and Features:
distal extremities.  Pain
 Typically evolves rapidly over a period of a few weeks.  Weakness
 Usually Hx of trauma preceding the onset of lesion may be elicited  Clicking on movement
 Untreated lesions eventually atrophy, fibrose and slowly regress.  Commonest type: Scapholunate dissociation – X-ray shows
Terry Thomas sign (abnormal gap between scaphoid & lunate)

43
Rx: 3. Occult
 Acute: reduction & fixation with plaster or K-wires 4. Interosseous
 Chronic: splintage, analgesics, H&L injections, arthrodesis
Treatment:
KIENBOCK’S DISEASE  Usually disappears after some months. So there’s no haste to Rx
 Aspiration (recurs 6-12 mths later)
 Patchy AVN secondary to post-stress/injury of the lunate.  Excision if recurrence: Cosmesis or if ganglion is causing pain (recurs in 20-30%)
 Predisposing factor: relative shortening of ulna  excessive stress on lunate
 Presentation: ache and stiffness, localised to centre of dorsal wrist. Possible
limitation of wrist extension MUSCLE / TENDON
 Imaging: Earliest signs of osteonecrosis only detected by MRI. X-ray: increased TENOSYNOVITIS/TENOVAGINITIS
density, later irregularity and flattening of bone. Eventually OA features. - Extensor retinaculum contains 6 compartments which transmit tendons lined with
 Treatment: (1) Osteotomy of distal end of radius (reduce pressure on lunate) synovium
(2) Microrevascularisation of bone if expertise available. (3) Partial arthodesis in - Causes: Unaccustomed movement, overuse, repetitive minor trauma. Sometimes
late cases. spontaneous occurrence.
- Pathophysiology: resulting synovial inflammation  secondary thickening of the
TEARS OF TRIANGULAR FIBROCARTILAGE COMPLEX (TFCC) sheath & stenosis of compartment  further compresses the tendon
 TFCC fans out from the base of ulnar styloid - 1st dorsal compartment (APL and EPB), and 2nd dorsal compartment (ECRL, ECRB)
process to medial edge of distal radius. most commonly affected.
 S/S: chronic pain, clicking on supination and - 3rd compartment: extensor pollicis longus
loss of grip strength - 4th compartment: extensor digitorum comunis (four tendons) and extensor indicis
 Dx: Arthroscopy - 5th compartment: extensor digiti minimi
 Rx: Arthroscopy—repair and remove fragments - 6th compartment: extensor carpi ulnaris

LUMPS DE QUERVAIN’S DISEASE (STENOSING TENOSYNOVITIS)

Definition:
GANGLION
Entrapment tendinitis of the tendons contained within the first dorsal compartment at
 Cystic degeneration of joint capsule or tendon sheath. the wrist (MCQs: APL & EPB); causing pain with tendon movement
 Locations (from most to least common):
o Dorsum of wrist (at scapholunate joint) Pathology
o Volar aspect of wrist  Inflammation causes thickening & stenosis of synovial sheath of the 1st dorsal
o Volar aspect of MCP joint compartment containing the EPB & APL
o Dorsal aspect of DIPJs (termed mucous cysts)  Cause: wringing out clothes, pruning roses, cutting with scissors
 Well defined, cystic, non-tender, positive transillumination. Contains glairy fluid Features:
(i.e. uncooked egg-white colour & consistency). May be attached to tendon.  Women 30-50 YO
 Pain over radial styloid process, swelling & palpable thickening of fibrous sheath
Types: along course of tendons
1. Simple  Finkelstein’s test +ve (exquisite pain in region of radial styloid on forced ulnar
2. Compound – chronic inflammation distends tendon sheath above & below the deviation of wrist with thumb in fist); NB. This test may also be positive in CMC
flexor retinaculum ( a/w TB, RA) degenerative joint disease, e.g. OA

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DDx: Aetiology
Arthritis thumb MCP jt, scaphoid fracture, scapholunate instability o Most common cause is IDIOPATHIC! Others include
o Anatomical abnormalities
Radiograph:  Bone: previous wrist #s (e.g. Colles’ #), acromegaly
If diagnosis is still in doubt, obtain Robert’s view in order to profile CMC joint  Soft tissues: lipomas, ganglia
Treatment o Physiological abnormalities
Conservative Surgical  Fluid balance alterations: pregnancy, menopause, hypothyroidism, obesity,
 NSAIDs Decompression of 1st compartment sheath amyloidosis, cardiac/renal failure
 Cold compression (tendon sheath release)  Inflammatory conditions: RA, GA
 H&L injection: inject in sheath - Determine if there is any instability of  Neuropathic conditions: DM, alcoholism
AND/OR the wrist joint & correct it if present
Thumb spica splint for 1 month Pathophysiology
o Pressure on nerve  blood flow obstruction in vasa nervorum  venous
Complications of surgical release: congestion & oedema
 Infection o With time, fibroblast proliferation occurs in the nerve  inefficiency of cell
 Radial n palsy (+ve Tinel’s) transport mechanisms and the sodium pump  n. conduction impairment
 Snapping of extensor tendon (due to extreme radial release of extensor retinaculum)
 APL & EPB tendon adherence (will limit thumb movements) Features
 Symptoms may present at night or with certain activities e.g. driving, reading
newspaper. Pain, paraesthesia numbness over lateral 3.5 fingers. Burning pain &
OTHER SITES OF EXTENSOR TENOSYNOVITIS paraesthesia over median n distribution. Usually occurs at night, waking the patient
- Extensor Carpi Radialis Brevis (most power extensor of the wrist— up, relieved by shaking arm and/or hanging arm over side of bed.
Second Compartment  Late symptoms: Wasting of thenar eminence, weak thumb abduction (autonomic
o Pain and point of tenderness just medial to anatomical snuff box innervations by median n.), decreased sensation of lateral 3.5 fingers
- Extensor Carpi Ulnaris – 6th compartment  Tinel’s & Phalen’s tests positive
o Pain and point of tenderness immediately distal to head of ulnar  DDx:
- Treatment: Splintage and H&L injections usually effective. o Cervical n. root lesions (e.g. cervical spondylosis of C6-7 level, or secondary
to a cervical disc herniation)
NERVES o Thoracic outlet syndrome
o AIN syndrome: entrapment usually at the origin of the deep head of pronator
CARPAL TUNNEL SYNDROME teres; supplies FPL, pronator quadratus and radial side of FDP  inability to
Definition make OK sign but sensory INTACT
Compression ischaemia of median nerve o Pronator syndrome: compression of median n. by ligament of Struthers
(fibrous band arising from medial epicondyle of humerus, attaches to
Epidemiology supratrochlear spur on the lower anterior humerus), pronator teres muscle or
 40-50YO proximal arch of FDS
 Women > men
Investigations
Anatomical boundaries Nerve conduction studies (to rule out other differentials)
 Radial side: scaphoid & trapezium
 Ulnar side: pisiform & hook of hamate
 Volar aspect: trasverse carpal ligament

45
Treatment
Non-surgical
 NSAIDs
 Splinting of wrist in a neutral position (especially at night)
 H&L injections just proximal to the carpal tunnel
Surgical
 Carpal tunnel decompression (division of flexor retinaculum under tourniquet
control) – either as open or endoscopic procedure
 Potential complications to be explained to patient
o Scar formation (keloid/hypertrophic scars)
o Scar tenderness post-op
o Failure to relieve symptoms due to incomplete division of flexor retinaculum
o Nerve injury – palmar cutaneous n. (lies supf to flexor retinaculum) and
motor branch of thenar muscles (usually leaves the radial side of median n.
towards distal extent of the standard incision) – risk of n. injury can be
decreased by making the skin incision on the ulnar side of the palmar crease
ULNAR TUNNEL SYNDROME
 Compression of ulnar n. as it passes between pisiform & hook of hamate (Guyon’s
canal)
 Clinical features: small muscle wasting, weakness of hand, sensory disturbance on
volar aspect of little finger.
 Causes: ganglions, trauma, ulnar artery disease, old carpal or metacarpal #s
 DDx: Cubital tunnel syndrome, cervical spondylosis
III. JOINT DISORDERS OF WRIST & HANDS
RHEUMATOID ARTHRITIS
OSTEOARTHRITIS
 Primary OA: usually in DIPJ (most common) and Carpometacarpal joint of the
thumb in postmenopausal women. Usually a presentation of polyarticular disease.
 Secondary OA: history of trauma or # e.g. scaphoid #, Kienbock’s disease
 Features: bilateral pain, swelling & tenderness. Usually starts with 1 or 2 fingers,
which usually spreads to all fingers and both hands. Bony thickening around the
DIPJ (Heberden’s nodes), PIPJ (Bouchard’s nodes) & carpometacarpal joint of
thumb. Square hand.  ROM & crepitus. In CMCJ OA, tenderness localised to 1
cm distal to radial styloid.
 X-ray: Narrowing of joint spaces, osteophytes, bone sclerosis, irregularity of carpal
bones, signs of old injuries.
 Management: For CMC joint: Corticosteroid injection may help to relieve the
pain and ↓ ROM. Everything: Rest, splint, surgery if fracture or if necessary (e.g.
arthrodesis)
o TRUE [MCQ]
 OA of CMC joint of thumb can be treated conservatively / by excision
arthroplasty / by replacement arthroplasty
 OA of DIPJ can be treated by arthrodesis
IV. BONE DISORDERS OF WRIST & HANDS
MCQ
Commonest complication of injury in hand fractures is tendon adhesion
But deformity in hand fractures is due to malunion!
COLLES’ FRACTURE
 Fracture of radius within 2.5 cm of wrist (deformity) – extra-articular #!
 ‘Dinner-fork’ deformity: palmar & ulnar angulation (AUA), dorsal & radial
displacement (DRD) of distal fragment, torsional deformity, DRUJ disruption
(ulnar styloid avulsion or tearing of fibrocartilage)
 Mechanism: FOOSH, commonly in elderly osteoporotic women
 S/S: wrist pain & tenderness over distal radius, characteristic deformity
 X-ray: distal fragment is
o Dorsally displaced with dorsal comminution
o Dorsally tilted fragment with apex of fracture volar
o Supinated
o Radially deviated
o Shortened
o Extra-articular features:
46
 Radial height from scaphoid Radial Inclination Volar tilt sweaty skin
From head of ulna to tip of Seen on lateral view  Mx: physioRx, rest & splintage for pain,
radial styloid chemical sympathetic blockade if severe
Carpal tunnel syndrome Most common complication
Delayed rupture  Of the extensor pollicis longus.
 Mx: tendon transfer
Radioulnar joint subluxation TFCC tear
Associated scaphoid #
Comminution of radial fragment
Normal: 11mm Normal: 22˚ Normal: 11˚ Persisting stiffness Shoulders & fingers
If #: <11mm If #: <20˚ If #: <11˚
 Management: SMITH’S FRACTURE (AKA REVERSED COLLES’ #)
Manipulation Indicated if displaced, deformity or angulation present, joint line in  Ant displacement & post angulation of distal fragments due to fall on back of hand
lateral X-ray tilted 10o posteriorly  Mx: M&R, splintage with wrist extended, above elbow cast for 6 wks
Reduction 1. Bier’s block (IV lignocaine), haematoma block (intraosseous) or GA BARTON’S FRACTURE
method 2. Disimpaction (distraction): apply traction in line of forearm with  Distal radial # with fracture line running into the wrist joint; anterior displacement
countertraction applied by assistant to flexed elbow of distal fragment carrying the carpus with it; a/w joint subluxation (volar/dorsal)
3. Maintain traction with elbow extended  Mx: inherently unstable, therefore require ORIF
4. Correct anterior angulation & post displacement: apply pressure
anteriorly
5. Correct radial displacement: push distal fragment ulnarwards SCAPHOID FRACTURE
6. Correct ulnar angulation by putting wrist in full ulnar deviation  Accounts for 75% of wrist #
Backslab  Apply backslab w wrist in full pronation, full ulnar deviation &  Mechanism of injury: FOOSH with wrist extended. Combination of dorsiflexion &
slight palmar flexion radial deviation
 Plaster should extend from olecranon to metacarpal heads  Blood supply of scaphoid diminishes proximally [supply by dorsal and volar
 Final moulding with pressure over post-lat aspect of distal fragment branches of radial artery]
External If # is unstable  NB. Rare in the elderly osteoporotic patient [MCQ]
fixation
Post X-ray: Repeat to ensure adequate reduction
reduction F/U: check circulation & assess swelling, complete plaster if swelling
is minimal
Finger, elbow & shoulder exercises
 Complications
Malunion / persistent deformity Radial drift of distal fragment
Sudeck’s atrophy  Pain, trophic skin changes, vasomotor
instability & osteoporosis due to sympathetic
overactivity - swelling, erythema, warmth,
changing to cyanosis with blotchy, cold &  Clinical Features:
o Pain in anatomical snuffbox***

47
 o Pain over scaphoid tubercle (following course of FCR)
o Restriction of thumb movement (not so much the wrist movement)
o Axial loading along 1st metacarpal bone also increases the pain
 X-ray: often hard to see, 4 views required (AP, lat & 2 oblique), repeat in 14 days if
unsure (# may not be seen in first few days). Usually # is through narrowest part of
bone (i.e. waist); other potential # sites include tubercle and proximal pole #.
Type a
Type b Type c
 Mx:
Initial Mx Scaphoid plaster & sling, repeat X-rays in 2 wks
Undisplaced # »Scaphoid plaster for 6 wks: Fix hand in full pronation, radial
deviation & moderate dorsiflexion. “Glass holding position”
Plaster to extend from below elbow to just below MCP & IPJ
of thumb. Incorporate proximal phalanx of thumb.
» 90% should heal.
» If still tender and X Ray shows no healing at 6 wks, continue
plaster cast for another 6 wks
» Consider internal fixation and bone graft if non-union found
at f/u at 12 wks
Displaced # ORIF (with compression screw)
Scaphoid tubercle # needs no splintage; treat it as wrist sprain.
 Cx:
o AVN of proximal pole causing secondary radiocarpal OA (X Ray at 2-3
months shows density of proximal fragment) – excise scaphoid, consider
arthrodesis of carpal bones
o Non-union – plaster fixation, internal fixation & bone grafting. Excise radial
styloid if OA threatens
 Poor blood supply at proximal part of scaphoid, hence union may take
several months.
o Osteoarthritis
COMPLICATIONS OF WRIST FRACTURES
 Most common complications are poor grip strength, stiffness and radial shortening
 80% have normal function in 6-12 months
 Early Cx:
O Difficult reduction +/- Loss of reduction
O Compartment syndrome
O EPL tendon rupture
O Acute carpal tunnel syndrome
O Finger swelling with venous or lymphatic block
 Late Cx:
O Malunion, radial shortening
O Painful wrist secondary to ulnar prominence
O Frozen shoulder (shoulder-hand syndrome; aetiology unknown)
O Post-traumatic arthritis
O Carpal Tunnel Syndrome
O Reflex sympathetic dystrophy
LUNATE DISLOCATION
 Rotation & anterior displacement of lunate
 X-ray: crescent moon shape of bone becomes obvious on AP view
 Cx: median n. palsy, Sudeck’s atrophy, AVN (& secondary OA)
 Rx: closed reduction under GA + plaster fixation, open reduction if closed
reduction fails
PERILUNATE DISLOCATION
 More common than Lunate dislocation
 Rest of Carpus displaced backwards
Lunate vs. perilunate dislocation
The key to differentiation between both is what is
centered over the radius. If the capitate is centered over
the radius and the lunate is tilted out, it is a lunate
dislocation (left). If however the lunate centers over
the distal radius and the capitate is dorsal, we are
dealing with a perilunate dislocation (right).
Radiology Assistant, Wrist – Carpal Instability

48
SCAPHOID DISLOCATION
 Displacement is usually anterior
 Rx: closed reduction + plaster fixation in stable position. If instability is present, fix
with K-wires
BENNETT’S FRACTURE
 Fracture of 1st metacarpal bone with fracture line
extending to the CMC joint
 Small medial fragment of bone seen on X-ray. Proximal
& lateral subluxation of 1st metacarpal present.
 Rx: closed reduction & plaster fixation
GAMEKEEPER’S THUMB
 Rupture of ulnar collateral ligament. Also equals to skiier’s thumb
 Mechanism: forced abduction of thumb (FOOSH, killing of game animals by
breaking their neck in between thumb and finger)
 Progressive MCPJ subluxation and impaired grasp results, with tenderness over
medial side of MCPJ. May be a/w avulsion fracture
 Rx: Scaphoid cast for 6 wks if minimally displaced. Internal fixation, Sx repair,
MCPJ fusion depending on severity of displacement / tear.
BOXER’S FRACTURE
 At 5th metacarpal (picture on the right)
 60 degree flexion at fracture site acceptable. Dropped
knuckle deformity permanent.
METACARPAL SHAFT FRACTURE
 Mostly stable and undisplaced.
 If displaced, need ORIF with plates or K-wire. Make sure
that there is no rotational deformity. Otherwise will have
scissoring of fingers on flexion.
RUGGER JERSEY FINGER
Results from forceful hyperextension of DIPJ with FDP in
maximal contraction (e.g. player grasping the jersey of his
opponent during tackling) – opposite MOI from mallet finger
 Tendon may rupture directly from its insertion into the
bone, or it may avulse bone fragment from the base of
distal phalanx
 Patient usually presents late
 Ring finger most often involved (75%)
 Pain & tenderness over volar distal finger, finger lies in slight extension relative to
other fingers in resting position
Acronym: ReaCTeD
H & L INJECTIONS
 Common hand indications: Trigger finger, De Quervain’s tendosynovitis, CTS, RA
 Up to 2 injections on the same digit (interval of at least 3 months)
 Complications: tendon rupture
BRACHIAL PLEXUS LESIONS
Types
 Lesions in continuity – more than half of plexus injuries. Traction commonest
cause. Nerve roots affected postganglionic. Treatment is expectant.
 Lesions with ruptured nerve roots – only surgical intervention can offer any hope of
recovery
 Complete avulsion lesions – nerve avulsed from cord (both dorsal n ventral roots
ruptured) as opposed to brachial plexus injuries where dorsal roots are spared.
 Partial avulsion – dorsal roots spared thus muscle paralysis with preservation of
sensation
Long standing plexus lesions
 Erbs’s palsy (C5 C6, sometimes c7) – overweight babies with shoulder dystocia at
delivery (upper obstetrical palsy); waiter’s tip deformity – shoulder internally
rotated, elbow extended, wrist flexed n pronated. N to rhomboids and long thoracic
N spared.
 Klumpke’s palsy (C8, T1) – lower obstetrical palsy; intrinsic muscles wasted,
clawhand, sensory loss on medial side of forearm n wrist, commonly a/w Horner’s
syndrome because T1 is affected.
 T1 root only – wasted intrinsic muscles, sensory loss on medial side of hand,
(incomplete lower obstetrical palsy, cervical spondylosis, neurofibromatosis, CA)
 Acute traumatic lesions – commonest mechanisms - depression of shoulder with lat
flexion of the neck to opposite side or traction of arm will find bruise on lateral
jaw, inferior jaw and on shoulder.
o Might have subclavian artery trauma
49
SEDDON’S CLASSIFICATION SUNDERLAND SYSTEM Wallerian Degeneration: degeneration
1. Neuropraxia: mildest for nerve injury. an interruption in conduction of the impulse 1. First-degree: "Seddon’s neuropraxia" of axons distal to sight of transection
down the nerve fiber with axonal continuity conserved 2. Second-degree: "Seddon’s axonotmesis" (resorbed by phagocytes)
 Likely a biochemical lesion caused by concussion /shock-like injuries to the fibres. 3. Third-degree: endoneurium disruptured, epineurium & perineurium intact
 Recovery takes place without wallerian degeneration.  Thus, when the axons regenerate, they may enter an incorrect nerve sheath,
 Temporary loss of function reversible within hours to months of the injury (the resulting in abnormal regeneration.
average is 6-8 weeks). (not the ‘1mm/day’ rule).
Nerve Site of Entrapment Provocative Test
 Frequently greater involvement of motor than sensory function with
autonomic function being retained. Brachial plexus Supra/infraclavicular Arm elevation
2. Axonotmesis: loss of the relative continuity of the axon and its covering of
Pressure between the scalene muscles
myelin, but preservation of the connective tissue framework of the nerve
 Distal wallerian degeneration occurs. Radial nerve Distal forearm Forearm pronation + wrist ulnar deviation
 Loss in both motor and sensory fnx is more complete with axonotmesis
Pressure over tendinous junction of ECR and brachioradialis
than with neuropraxia,
 Usually the result of a more severe crush or contusion than neuropraxia. Ulnar nerve Cubital tunnel Elbow flexion + pressure on cubital tunnel region
 Regeneration requires a number of weeks.
Guyon's canal Pressure at Guyon's canal
3. Neurotmesis:
Median nerve Proximal forearm Forearm supination + pressure on pronator teres
 Occurs on severe contusion, stretch, lacerations.
 Surgical repair essential and quality of recovery always imperfect. For Carpal tunnel Wrist flexion and/or extension with pressure proximal to carpal tunnel
neurotmesis is better to use a new, more complete classification, , called  Accompanying the loss of the nerve sheath is intraneural scarring, which further
Sunderland System obstructs axonal regrowth through the site of injury.
 Recovery may range from poor to complete and depends on degree of
MCQ: Worst nerve injury (after surgical intervention) – traction injury
intrafascicular fibrosis;
4. Fourth-degree: interruption of all neural and supporting elements; epineurium intact; the
nerve is usually enlarged.
5. Fifth-degree: complete transection with loss of continuity. Grade V corresponds to
Seddon's classification of a neurotmesis lesion

ZONES OF THE HAND

Zone 2 is no man’s land.
Return of function is difficult in Zone I because of short stump of FDP

50
IMPORTANT ORTHOPAEDIC CONDITIONS IN THE HIP Treatment
PELVIC FRACTURES • ABCs
Most common fracture involves pubic rami, followed by ilial, ischial, acetabular, • Assess genitourinary injury (rectal
coccygeal and sacral bones exam/vaginal exam mandatory)
• Type A - bedrest and mobilization
Tile Classification w walking aids
• Type B/C - external or internal
fixation

Complications
• Hemorrhage - life threatening
• Fat embolism
• Bladder/bowel injuries
Type A Type B • Neurological damage
Type C
• Obstetrical difficulties
• Type A: stable, minimally displaced, includes avulsion fractures and fractures not • Persistent sacro-iliac (SI) joint pain
involving pelvic ring, e.g. rami fracture • Post-traumatic arthritis of the hip with acetabular fractures
• Type B: partially unstable, rotationally unstable, but vertically stable, e.g. “open
book” fracture from external rotational force to pelvis [MCQ] Trendelenburg test is a test of stability of pelvis on femur
• Type C: unstable, rotationally and vertically unstable, associated with rupture of
ipsilateral ligaments, e.g. vertical shear fracture APPROACH TO HIP PAIN
Diagnosis CAUSES OF PAINFUL HIP
 History of injury, high energy trauma Referred pain  Discogenic dz
 Examination reveals local swelling, tenderness; if Joint disorders  Infection  Perthes’ dz  Slipped capital femoral epiphysis
unstable, may have  OA  Osteonecrosis
 Deformity of the hips and instability of pelvis with  RA
palpation Periarticular  Hernia  Tendinitis  Bursitis / synovitis
disorders
 X-rays (i.e. AP, inlet, and outlet views) judet view
for acetabular fractures HISTORY AND PHYSICAL EXAMINATION:
6 lines to look for in a pelvic X-ray specifically 1. Site of pathology
looking for acetabular fracture - Hip pain (anterior) — usually at groin
1. Iliopectineal line – anterior column of pelvis - Pain at gluteal region (posterior) — usually lumbar pathology
2. Ilioischial line – posterior column 2. Cause of pathology
3. Acetabular teardrop – should in line with - Vascular: Perthes’ disease, AVN
ilioischial line - Infection: OM, TB, Transient synovitis
4. Dome – superior weight bearing area costing - Trauma: OA, dislocation, fracture
of both ant and post column - Autoimmune: RA
5. Ant wall of acetabulum - M
6. Post wall of acetabulum - I

51
 - N » Medial gap – the greater the gap, the greater the possibility of dislocation
- Congenital: SCFE, CDH » Neck/shaft angle (normal 120-135˚; <120˚ coxa varus, >135˚ coxa valgus)
4. Other neighbouring structures
3. Look for predisposing factors e.g. Osteoporosis and fall risk
» Acetabular margins
4. Look for complications of pathology » Sacroiliac joint
» Joint space
5. Assess premorbid status (goal for mgmt is to regain premorbid status) » Ischium
6. Assess carer support

COMMON HIP DISORDERS BY AGE

<1YO CDH
1-5YO Transient synovitis (commonest cause of hip pain in child)
Septic arthritis
5-10YO Perthes’ disease
Juvenile Chronic Arthritis
10-20YO SCFE
Adults OA, AVN, RA
GAIT ANALYSIS
FEATURES OF AP HIP X-RAY TO NOTE
Normal Gait
1. Any fractures 1. Stance phase = heel strike + mid stance + push off
» Neck of femur (subcapital, transcervical, base of neck) 2. Swing phase = acceleration + initial swing + midswing + deceleration
» Intertrochanteric
» Subtrochanteric Type of gait Notes Causes
2. Quality of bone Antalgic Short stance phase Pain (infxn, inflammation, transient synovitis)
» Bone texture Trendelenburg ‘Sound side sags’ Contralateral abductor weakness, hip
» Density of femoral head dislocation/ subluxation, short NOF, hip pain
3. Lines Short leg Ipsilateral hip Previous # or congenital shortening
» Shenton’s line – broken in drops when weight
 Congenital dislocation of hip is on short leg
 Posterior dislocation of hip Adductor lurch Hip dysplasia, CP
 Pathological dislocation of hip Toe to heel CP, club foot, idiopathic
 Tom-Smith arthritis (septic arthritis of the hip in infants which destroys High steppage Foot lands flat or Proprioception loss, foot drop (damage to L5;
the whole head of femur) on ball instead common peroneal n. palsy)
Not broken in impacted NOF # Broad based Ataxia (cerebellar lesions)
» Perkin’s line (line drawn along lateralmost aspect of acetabular roof) & Parkinsonian / Small shuffling Parkinson’s disease
Hilgrenreihner’s line (line drawn horizontally through superior aspect of the festinant steps
triradiate cartilages) – both lines are perpendicular to one another. Femoral Spastic Jerky, feet in UMN lesion e.g. cord compression, multiple
(scissoring) quinus, hips sclerosis or CP
head should be in the inner lower quadrant of both these lines.
adducted
» Acetabular index – should be low (want acetabulum to hug femoral head)

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CONGENITAL DISLOCATION OF THE HIP (CDH) / DEVELOPMENTAL – U/S not done at birth because laxity of hip joint, may get spurious reading
DYSPLASIA OF THE HIP (DDH) at birth (in order for baby to come out of birth canal) – hence earliest U/S
is at 6 weeks
Features • When to do U/S
 Easily dislocatable hip secondary to shallow acetabulum – usually posterior & – For high-risk cases (e.g. positive family history / extended breech delivery)
superior dislocation / hip laxity / hip clicks
 1 per 1000 live births (common enough for it to be screened by neonatologists) – To ensure concentric stable reduction after treatment
 Girls > boys » Weekly after with splint to ensure reduction and correct
 Bilateral in 30% application of splints
 Risk factors » Every 6 weeks after once hip reduced
o 1st female child » Most effective <3 months old (3 months onwards: X-rays; must
o Family history ensure concentric reduction with good acetabular cover, if not
o Breech delivery mechanical forces of hip not evenly distributed  may get OA)
o Condition predisposing to crowding of uterus (multiple pregnancies, Mx
oligohydramnios, fibroids, baby too big, mother too small) 1. Watch Observe if
– Hip laxity only
Possible causes: – Hip clicks
 Intrauterine malposition  Postnatal posture (hip  Shallow acetabulum
(a/w breech presentatn) extension) (acetabular dysplasia) Repeat U/S at 4-6 weeks
 Tight iliopsoas  Hypertrophic lig teres  Fibrous tissue in – If hips reduced and stable, no further Rx
 Hourglass capsule acetabulum – Otherwise treat as DDH
When to watch instead of intervening for DDH?
Physical examination: When you are not sure of the diagnosis.
 Assymetrical skin creases, short limb, internally rotated,  hip abduction ROM 2. Abduction 0 to 6 months
 Ortolani’s test (tests reducibility) – impeded hip abduction + clunk as dislocation splint / – Abduction splint (old mtd) or Pavlik Harness
reduces Pavlik – Repeat U/S in harness after 1/52 and out of harness at 6/52
 Barlow’s test (tests dislocatability) – dislocate the hip by flexing the hip joint and harness – Worn for at least 3 months until 1st X-rays
adducting it followed by posterior force in the line of the shaft of femur. – If X-rays show concentric hips with good acetabular cover,
 Trendelenburg’s test – positive then wean off splints
Ix
U/S Hip Abnormal acetabular shape and femoral head position
X-ray Abnormal sloping of acetabular roof
shallow acetabulum
small underdevted femoral head
femoral head displaced upwards & outwards
For Pavlik harness:
- Human position: 50deg of abduction of each side and 100deg of
• Diagnosis is CLINICAL flexion (preferred position)
• U/S or X-rays can be used but both are NOT used to diagnose at birth - Frog position: entire hip down at 90deg, can cause AVN (femoral
– X-ray: radiation + hip is not ossified head very sensitive to tension)

53
3. Close 0 to 6 months Acetabular surgery (Salter osteotomy)
reduction – If unable to achieve stable reduction with splints then closed - Done at 2yo
& hip reduction and hip spica attempted - In Salter’s osteotomy the entire acetabulum, together with the pubis and ischium, is
spica rotated anteriorly and laterally as a unit, with the symphysis pubis acting as a hinge.
The osteotomy is held open anterolaterally by a wedge of full thickness bone graft,
usually taken from the anterior part of the iliac crest
- Osteotomy redirects entire acetabulum so that its roof covers femoral head both
anteriorly and superiorly
- In young children, the acetabular deficiency is usually anterior, and therfore the
Salter Osteotomy is designed to provide coverage anteriorly at the expense of
posterior coverage;
- Success of procedure depends to some extent on the flexibility of the symphysis
pubis (which decreases w/ age)
- Importance of screening so as to intervene earlier
BEFORE AFTER

Decreased joint space after reduction

4. Open 6 to 12 months
reduction – Closed reduction can still be attempted but more difficult to Prognosis
& hip achieve stability  Good results if treated <6yo
spica – Open reduction then done  For chronic neglected dislocations: reductions usually not attempted if
o >8yo for unilateral (no more remodelling past 8yo :. reduction may cause OA)
12 to 18 months o >5yo for bilateral
– Child is already weight bearing  Consequences of not reducing
– Open reduction usually involves femoral derotation and o Partially dislocated (formation of false joint) – progressive deformity,
shortening disability & secondary OA hip
– Acceptable is thought to remodel accordingly o Completely dislocated – will have Trendelenburg gait, cost of energy to walk
will be high hence not ideal (have to sit on side  back pain, will get
Above 18 months
scoliosis
– Potential for acetabular remodeling is less
o Bilateral: waddling gait, hips dislocated behind so nothing to hold pelvis in
– Both acetabular and proximal femoral surgery will be required.
between, would get lordosis
o ALL will walk assuming muscles and nerves are functional

54
DISLOCATION OF THE HIP  Myositis ossificans
 Knee injury
Mainly seen in artificial hips
 Coxa magna (occurs in up to 50% of children after a hip dislocation)
Cause X-ray Management
Pyogenic arthritis Absent femoral head Traction, open reduction, varus
PERTHES’ DISEASE (COXA PLANA)
osteotomy of femur
Features
Muscle imbalance Valgus femoral head As for CDH + muscle rebalancing  Femoral head necrosis secondary to disturbance in blood supply
operation  4-8YO, boys:girls = 4:1, 5-10% bilat
Trauma Look for associated Reduction, ORIF if rim # present  DDx: non-specific transient synovitis
acetabular rim #  Precipitant: effusion, trauma or synovitis occluding blood supply to femoral head

Dislocation after Total Hip Arthroplasty (THA) Stages (similar to AVN classification)
 Occurs in 1-4% of primary THA and 16% in revision cases  Stage 1: ischaemia causing femoral head bone death. Normal X-ray
 About 74% are posterior dislocations, 16% anterior and 8% central  Stage 2: revascularisation & repair. X-ray shows  bone density
 THA are unstable in the position of flexion and internal rotation
 Stage 3: distortion & remodelling. Epiphyseal collapse, flattening or enlargement
Posture may result.
 Anterior dislocation: hip flexion, abduction and external rotation [MCQ]
Clinical features:
 Posterior dislocation: hip flexion, abduction & internal rotation, shortened leg. X-ray  Hip pain & irritation
shows smaller femoral head and less prominent trochanter because leg adducted and  Limp, shortened leg
internally rotated. [MCQ: AVN is a distinct possibility]  Decreased abduction & internal rotation

Treatment X-ray:
1. Muscle relaxtion is key—conscious sedation (IV fentanyl) or spinal or GA  Apparent widening of joint space
2. Assistant applies downward pressure to pelvis   epiphyseal density – healing & reossification Small dense
 capital epiphysis
3. Reduction for posterior dislocation — Fully flex hip, abduct and externally rotate Flattening, fragmentation & lat displacement of epiphysis
hip, apply upward traction on femur  Subchondral fracture
(i) Known as Bigelow’s manoeuvre  Metaphyseal rarefaction & broadening
(ii) Maintained until patient is pain-free (approx. 2 weeks)
Catterall grading
4. Reduction for anterior dislocation – Fully flex hip, adduct and internally rotate hip,
According to degree of femoral head involvement
apply downward pressure on femur (Barlow’s equivalent)
Grade Severity Prognosis
Complications 1 Involves anterior portion of epiphysis only. Revascularisation may be
 Post-traumatic arthritis due to cartilage injury or intra-articular loose bodies No collapse or sequestrum complete w/o bone collapse
 # femoral head, NOF, femoral shaft
 Slipped upper femoral epiphysis
2  50 % involvement with a sequestrum Bony collapse inevitable
 AVN femoral head 3 ~75% involved, with collapse & sequestrum Bony collapse inevitable.
 Sciatic nerve palsy (esp when rim # is present) whole epiphysis involved Poor prognosis
4
 Femoral vein compression – causing thrombosis & embolism
 Secondary OA hip
 Recurrent dislocation

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Mx:
Initial Skin traction until pain resolves
Definitive Good prognosis:
 Onset <6YO
 Partial fem head involvement
 No metaphyseal rarefaction
 Normal fem head shape
Poor prognosis:
 Onset >6YO
 Complete fem head involvement
 Severe metaphyseal rarefaction
 Lateral fem head displacement
SLIPPED CAPITAL FEMORAL EPIPHYSIS (SCFE)
Epidemiology:
 Usually occurs in very tall, fat pubertal (11-15yo)
boys with delayed gonadal development.
 Boys > girls
No Rx needed
Containment of femoral head
 Abduction splint OR
 varus osteotomy of femur OR
 innominate osteotomy of
pelvis
 AVN
 Coxa vara – Rx: osteotomy to prevent secondary OA
 Secondary OA
 Bilat SCFE: 1/3 of cases
Mx
Manipulation is contraindicated!!!
Displacement <1/3 of Accept position
epiphyseal width Epiphyseal fixation with pins
Displacement 1/3 to half  Epiphyseal fixation with pins
of epiphyseal width  Osteotomy: if residual deformity is present even
after remodelling
Displacement >half of  Epiphyseal fixation with pins +/- osteotomy
epiphyseal width  OR Epiphyseal replacement & fixation with pins
PYOGENIC/SEPTIC ARTHRITIS
Epidemiology:
Children <2yo, usually Staph by haematogenous or local spread (from femoral OM)

History: *** True clinical emergency; if undiagnosed, may result in complications such as
 Pain in groin  radiation to anterior thigh or knee complete destruction of the articular cartilage and the underlying epiphysis, loss of the
(referred) adjacent growth plate, and dislocation of the joint ***
 Limp Investigations:
 Hx of trauma » Culture blood & joint aspirates
» Choice of ABx depending on Gram stain results & culture sensitivities
Physical Examination:
 Coxa vara deformity Management:
 Externally rotated short leg  Medical
 Decreased abduction & internal rotation o IV antibiotics (penicillin – for strep; and cloxacillin – for staph)
 Pain on movement o ESR and CRP levels are valuable indicators of clinical response. The CRP is
generally more sensitive than the ESR, and antibiotics should be continued at
X-ray: least until this measure has normalized.
 Wide & “woolly” epiphyseal plate o Switching to oral antibiotics is also acceptable, provided that adequate blood
 Trethowan’s sign: femoral head falls below line levels of the antibiotic are demonstrated, the patient’s parents are reliable, and
drawn along superior surface of femoral neck the antibiotic does not cause a gastrointestinal disturbance that would interfere
(normally cuts through fem head) – “ice-cream with its absorption.
falling off cone”  Surgical
Complications
o Consider septic joint to be a closed abscess :. Don’t expect ABx alone to work

56
 o Perform repeated percutaneous joint aspirations in cases of involvement of an
easily accessible peripheral joint; a clinical course shorter than 6 days; and no
evidence of an associated OM, immune deficiency, or other chronic illness TB HIP
o If the patient's condition fails to improve, perform open drainage in OT Groin / thigh pain, limp, muscle wasting, limb shortening, hip deformity, ROM
 Definitely indicated in the hip and the shoulder and in peripheral joints
that do not respond to percutaneous aspiration. X-ray:
 Indicated in patients who are systemically ill, and it should be given  General rarefaction
greater consideration when the suspected organism is S aureus or a  Femoral epiphyseal enlargement
gram-negative bacterium that produces cartilage-damaging enzymes.  Bone abscess
(Gonococcal arthritis less likely to rapidly damage a joint :. may be  Articular destruction
managed with repeated aspirations if the joints involved are peripheral.  Healing by fibrous ankylosis
Open drainage should still be performed in cases of gonococcal Management:
arthritis of the hip.)  Anti-TB drugs
o If treatment was significantly delayed, substantial capsular damage may have  Skin traction
occurred. If instability is suspected, immobilize the patient for a longer period.  Evacuate abscess, joint debridement
A neglected septic hip with radiographic instability requires a spica cast, and an  Arthrodesis or joint replacement if joint is destroyed
unstable shoulder requires a sling and swathe.
 Follow-up (at least up to 1 year after surgery)
o Whether joint function has returned to normal RA HIP
o No radiographic evidence suggestive of loss of joint space, AVN of the
epiphysis, joint instability, or damage to the growth plate  Multiple joint involvement, groin pain, limp,  & painful movement
X-ray:
 Osteoporosis
TRANSIENT SYNOVITIS  Decreased joint space
 Epidemiology: boys 2x more than girls, 3-10yo; commonest cause of irritable hip  Periarticular erosion and bone destruction
 History
Management:
o Unilateral groin/hip pain
 Total hip replacement
o Very young children: no other symptoms except crying at night
o Recent Hx of URTI, pharyngitis, bronchitis or otitis media (in >50% of cases)
o No definitive cause known OA HIP
 Physical examination
Causes:
o Antalgic gait
o Tenderness during palpation even during passive movement Young adults Congenital subluxation
o Mild restriction of motion (in 2/3 of patients) Perthes’ disease
o Log roll (most sensitive test): detect involuntary muscle guarding of one side SCFE  Coxa vara,
compared to the other Acetabular deformities / injury
 Treatment Older adults RA,
o Apply heat & massage AVN,
o Bed rest for 7-10 days in a position of comfort Paget’s dz,
o Medications: NSAIDs (naproxen/ibuprofen) Primary OA

57
Clinical features:  Transplant surgery
 More common in Caucasians (in Caucasians, OA hip > OA knee; in Asians, OA knee
> OA hip) Others
 Antiphospholipid antibodies
 Groin pain  radiation to knee
 Joint stiffness due to synovial hypertrophy & capsular fibrosis  Gaucher disease (hereditary, autosomal recessive disease of
 Limp, Trendelenburg positive glucocerebroside metabolism, results in accumulation of cerebroside-
 Fixed flexion deformity filled cells in bone marrow)
 Leg in ext rotation & adduction posture  Decompression disease (Caisson disease)  nitrogen bubbles
 Decreased ROM  Sickle cell disease

X-ray: PATHOGENESIS
 Decreased joint space
 Multifactorial, involving
 Subarticular sclerosis
(a) Metabolic factors
 Cyst formation
(b) Local factors affecting blood supply to bone
 Osteophytes (‘elephant trunk’ osteophytes)
- Vascular damage
Management: - Increased intraosseous pressure
 Analgesics - Mechanical stresses
 Physiotherapy  Summary of various pathogenetic mechanisms
 Walking aids 1) Arterial supply interruption:
 Surgery: Osteotomy, arthroplasty - Fracture
- Dislocation
- Infection
AVASCULAR NECROSIS OF THE HIP 2) Arterial occlusion:
AETIOLOGY / PREDISPOSING FACTORS: (intra-vascular occlusion / venous stasis & regrograde arteriolar stoppage)
Traumatic  Neck of femur fracture - Sickle cell disease
 Fracture-dislocation or dislocation of the hip joint - Vasculitis
Atraumatic Iatrogenic - Caisson disease
 Glucocorticoid use, including TCM (causes two things: 1) changes in 3) Capillary compression: (by marrow swelling)
circulating lipids  microemboli; 2) changes in venous endothelium  - Steroids
stasis  increased intraosseous pressure  necrosis) - Gaucher’s disease
 Alcohol
 Begins with interruption of blood supply  hyperaemia of surrounding area 
Congenital demineralisation, trabecular thinning  collapse of bone with mild stress
 Perthes’ disease
 SCFE-associated AVN
CLINICAL FEATURES
 Usually affects anterolateral femoral head
 Inherited thrombophilia e.g. Factor V Leiden
 Other bones that can be affected: humeral head, femoral condyles, proximal tibia,
Immunocompromised states vertebrae, small bones of hands and feet – scaphoid, talus
 Systemic lupus erythematosus (3-30% of SLE patients get AVN;  Commonly presents with pain
SLE+steroids  highest risk) - Weight-bearing and motion-induced pain in most cases
 HIV - Rest pain occurs in two-thirds of patients, and night pain in one-third

58
 Surgery
IMAGING (a) Core decompression with or without bone grafting
(a) Plain films  Centre of head of femur is excavated
 Earliest findings are mild density changes (plain XR may be normal for months  Fibular graft or other formed graft is used to fill up the cavity
after symptoms begin)  Used in stage 0 to 2 disease in young and active patients – best chance of
 Sclerosis, cysts in subsequent part of disease preserving femoral head
 Pathognomonic crescent sign – subchondral lucency (evidence of subchondral
collapse) (b) Osteotomy
 Later stages: Loss of sphericity or collapse of femoral head  Joint-sparing – redistributes weight-bearing forces to articular cartilage which is
 Ultimately joint space narrowing, degenerative changes in the acetabulum result supported by healthy bone
 For late stage 2 disease with cyst formation, and stage 3 disease
(b) MRI
 98% sensitivity for diagnosis (c) Resurfacing arthroplasty
 Changes can be seen early in the disease when other investigations are negative (d) Total hip replacement
 Earliest finding is a single low-density line on T1 weighted scan that represents  For stage 4 disease and in older sedentary patients with not so severe disease
the separation between normal and ischaemic bone
 A high-intensity line on T2 weighted images represents hypervascular
granulation tissue  pathognomonic double-line sign (low-density line plus PROXIMAL FEMORAL FRACTURES SUMMARY
high-density line) DDX OF HIP FRACTURES:
DIAGNOSIS  Pubic ramus fracture
 Clinical, based on typical symptoms with compatible findings on imaging  Acetabular fracture
 Rule out other causes of pain and bony abnormalities  Isolated fracture of greater trochanter
 Trochanteric bursitis/ contusion
FICAT-ARLET STAGING
Stage 0 Hip-at-risk BLOOD SUPPLY OF FEMORAL NECK***
Stage 1 CT scan and XR normal
Extent of dz:  Nutrient artery of femur
Positive findings on MRI or biopsy
A: <15%  Retinacular Arteries (from medial and lateral circumflex arteries)
Stage 2 XR changes seen but no collapse
B: 15-30%  Artery through ligamentum teres (from obturator artery)
Stage 3 Early flattening of dome – crescent sign C: >30%  In NOF fracture
Stage 4 - Nutrient artery severed
Flattening of femoral head with joint space narrowing
- If significant displacement, retinacular vessels severed  AVN
Signs of early OA
- Only ligamentum teres vessels remain
TREATMENT
PREDISPOSING FACTORS
Conservative (ineffective at halting progression)
Non-  Old Age
 Bed rest modifiable  Early menopause
 Partial weightbearing with crutches
 Female Sex
 NSAIDs or other analgesics
 Nulliparity
 Bisphosphanates – slows resorption of necrotic bone
 Caucasian
 Family/Personal History of fractures

59
 Modifiable Anything that causes increased risk of falls, e.g. Radiological  AP Pelvis (not hip)
 Poor vision, vestibular dysfunction  Lateral XR of affected hip joint
 LL weakness Preop  FBC
 Hazards at home  U/E/Cr
 Significant co-morbitidies e.g. CCF, CVA  PT/aPTT
Reduction of bone strength  urinalysis
 Osteoporosis, low Ca intake  GXM
 Steroids, alcohol, smoking, thyroxine, increased/decreased T4  CXR
 Physical immobility  ECG
 Pathological bone conditions
 Chronic liver and renal failure INITIAL MANAGEMENT
 Analgesia
HISTORY  Antibiotics if infection suspected
 Pre-op traction for pain relief and to ensure union takes place in a good position
Fall  How pt fell – e.g. landed on bum  Thromboembolism prophylaxis (SC heparin 5000 units BD)
 Pain, tenderness, deformity
 Can walk? (If yes  impacted [Garden 1] fracture, which TYPES OF FRACTURES ACCORDING TO SITE
is undisplaced  need to admit to prevent progression to
displaced fracture which has poorer prognosis) NOF Intracapsular Subcapital
Transcervical
What happened [hazards at home] Extracapsular Basal
before fall
Other Intertrochanteric
Predisposing  Modifiable Pertrochanteric
factors to fracture  Non-modifiable  Involves the trochanter(s) which are themselves
 Comorbidities fractured
 Premorbid functional status
 Osetoporotic Risk Factors GARDEN CLASSIFICATION OF NOF FRACTURES
1 Undisplaced Inferior cortex not completely broken
PHYSICAL EXAMINATION Fracture line not complete
May have some angulation of trabeculae
 Shortened 2 Inferior cortex completely broken
 Externally rotated Fracture line complete
 [MCQ] # of proximal half: flexion & abduction Minimal displacement
 Bruising (suggest extra capsular #) 3 Displaced Inferior cortex completely broken
 Tenderness over femoral neck Fracture line complete
 Painful limited hip movements Significant displacement
Head internally rotated, abducted (distal fragment externally rotated)
INVESTIGATIONS 4 Inferior cortex completely broken
 Confirm diagnosis, determine severity Fracture line complete
 Pre-operative investigations Complete displacement
Head retains neutral position in acetabulum

60
WHO FRACTURE RISK ASSESSMENT TOOL (FRAX)
- Developed by WHO to evaluate fracture risk for patients
- Gives 10-year probability of hip fracture and the 10-year probability of a major
osteoporotic fracture (clinical spine, forearm, hip or shoulder fracture).
o For local Chinese: use Hong Kong Chinese
o For local Indians: use US (Asian)
- Disadvantages
o Cannot calculate for patients <40yo
o Does not take into account type of fractures, number of fractures
o Does not tell you who to treat – still rely on clinical judgement
- Website: http://www.shef.ac.uk/FRAX/faq.jsp
- Risk factors used:

MANAGEMENT
- Conservative: if undisplaced, clinically stable & ROM is full and painless
- Total hip replacement: for OA hips, pathological #, acetabular involvement, or
revision hip
For NOF #:
Gardens 1, 2 Gardens 3, 4
<60yo Cancellous bone screw [PRESERVE HEAD]
>60yo Cancellous bone screw (~65yo) Hemiarthroplasty
Hemiarthroplasty (uni/bipolar) (~90yo) Total hip replacement
Ultimately depends on patient’s pre-morbid ADL status & his/her aims, probability of
successful op & risks of requiring a 2nd operation
- Sample of questionnaire:
For Intertrochanteric / Pertrochanteric
 Internal fixation with a dynamic hip screw will suffice usually. Unless it is a
reverse oblique fracture.
 [MCQ] If treated conservatively, will result in MALUNION

61
NOTE: Total Hip Replacement involves replacement of the acetabulum also, usually Physiotherapy Preserve joint movement
reserved for patients with OA, pathological fracture, revision of implant – will see on Restore muscle power
X-ray that acetabulum is metal as well, with screws going into hip bone Assess what type of mobility aids needed
Treat osteoporosis and comorbidities
Thompson DHS Plate
(has neck, no holes, and Screw COMPLICATIONS OF FEMORAL FRACTURES
needs cement)  Non-union in 30%
 Redisplacement
Austin Moore  AVN in intracapsular NOF #, rarely occurs in intertrochanteric
(has 2 holes, no neck, - Undisplaced – 10-30%
doesn’t need cement)
- Displaced – 50-80%
- Rx: total hip replacement
Moore’s has a short neck, thus used for subcapital and mid-neck fractures; Thompson  Erosion of femoral head in unstable IT fractures causing coxa vara
has longer neck, used for fractures near base of NOF
 Complications: delayed union, non-union, malunion (coxa vara), OA
Thompson better for osteoporotic patients
COMPLICATIONS OF TOTAL HIP REPLACEMENT
Lifespan: about 10 yrs [must explain to patients before and after op that lifespan varies
between patients – if you have no symptoms past 10 years, you need not replace it Intraoperative Perforation/# of the acetabulum or femur
immediately] Immediate Dislocation (due to incorrect placement of the prosthetic
Material: ultra high molecular wt polyethylene and surgical grade stainless steel (within 24h) components)
Early (within Infection
30 days) DVT (most common complication) / PE
HIP ARTHROPLASTY Fat embolism
Bipolar arthroplasty Sciatic n. palsy (more common in the posterior surgical approach
Hip Arthoplasty Hemi arthroplasty to the hip joint)
(Only femoral component) Unipolar arthroplasty Late Infection
(Moore’s & Thompson) (>30 days) Heterotopic ossification
Total Hip replacement (THR) Disuse osteoporosis
(Femoral & acetabular component) Tissue atrophy
Implant failure
 Wearing of articular surfaces (esp acetabulum for unipolar’s)
AFTER-CARE:
 Loosening
Weight Implant  Erosion, cut-out etc
bearing  Try and get pt to sit up by 24h, walk by 72h  Peri-prosthetic #
Internal fixation
 Sit up by 24h POST-OP MANAGEMENT
 Encourage mobility with non-wtbearing (wheelchair)by 72h  Use GS principles
 Do not weight bear until healing of # occurs, if not high risk of  Ask about relevant social history & family support
cutout  Management of post-op DVT

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 o Pre-op: thromboembolic deterrent (TED) stockings fitted pre-op o Immobilize leg with Thomas Splint
o Peri-op: TED stockings, minimize duration of surgery, use compression boots o Adequate analgesia
& foot pumps o Surgical fixation (intramedullary nail) within 24 hours
o Post-op: low dose of LMWH, early mobilization of patients with the help of  high rate of surgical union after 6 to 12 weeks
physiotherapists o Early mobilization of hip and knee

OUTCOME OF NOF FRACTURES SUPRACONDYLAR FEMORAL FRACTURE

 25% mortality at one year
 high energy, multiple trauma
 10% bedbound
 knee joint is disrupted severely with bicondylar fracture
 33% wheelchair bound
 33% ambulating + walking aid
 distal fragment moves posteriorly due to pull of gastrocnemius
 poor prognosis with comminuted fractures
Union takes about 3 months  can be intra or extra articular
 high incidence of post-traumatic arthritis
 Treatment
o internal fixation and early knee ROM
SUBTRONCHANTERIC FRACTURES o if conservative treatment need pearson knee piece to allow flexion and
 least common hip fracture, seen in younger population with high energy injuries thus decrease pull and prevent flexion deformity.
 highly unstable o quadriceps strengthening
 transverse, spiral or oblique fracture passes below lesser trochanter
 x-rays show flexed and abducted proximal fragment, from pull of iliopsoas on lesser INTERTROCHANTERIC FRACTURE OF THE FEMUR
trochanter, gluteus medius and minimus on greater trochanter Evans- Jensen Classification
 Treatment I 2 fragments, undisplaced
a. obtain a good closed reduction under fluoroscopy on the fracture table II 2 fragments, displaced
b. internal fixation with intramedullary nail III 3 fragments w/o posterolateral support (ie # of the greater trochanters)
IV 3 fragments w/o medial support (ie # of the lesser trochanter)
FEMORAL DIAPHYSIS FRACTURES V 4 fragments
 high energy (MVA, fall from height, gunshot wounds) R Reversed oblique # (prone to displacement)
 low energy (spiral fracture in children) *Alternative classification: according to number of fragments + reversed oblique #
 high morbidity/mortality (hemorrhage, fat embolism, ARDS, MODS)
 blood replacement often required
 frequently comminuted with soft tissue trauma
 Clinical
a. leg is shortened, externally rotated
b. unable to weight bear
c. assess neurovascular status
d. r/o: open fracture, soft tissue compromise
e. r/o: child abuse with spiral fractures in children
 Treatment
o ABCs of trauma are essential

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IMPORTANT ORTHOPAEDIC CONDITIONS IN THE KNEE Vein Saphena varix (@ Gaiter area: look for complications of varicose v.
KNEE – DDX saphenopopliteal - Venous eczema
Anterior Posterior Lateral junction) - Lipodermatosclerosis
- Ulceration: active & healed (latter causes
Lump  Osgood-Schlatter dz  Baker’s cyst  Meniscal cyst
white patch called atrophie blanche)
 Housemaid’s knee  Popliteal cyst
- Peripheral oedema
 Clergyman’s knee  Popliteal aneurysm
Look for varicosities along long saphenous v.
Pain  Chondromalacia  Meniscal tear
Tourniquet test, Trendelenburg test, Perthes test
Generalised patellae (CMP) (med & lat)
DVT
 OA  Patellofemoral OA
 RA  Osteochondritis Nerve Neuroma E.g. tibial n.
dissecans (OCD) Enlarged bursae - Above the joint line
 Meniscal disorders - a/w semimembranosus and medial head of
 Tendinitis gastrocnemius medially & with popliteus and
 Bursitis lateral head of gastrocnemius laterally
 Osgood-Schlatter’s dz Cysts Baker’s cyst - Below the joint line & deep to gastrocnemius
Deformity  RA - a/w degenerative changes in knee joint
 TB Popliteal cyst Enlargement of popliteal bursa
 Recurrent dislocation of patella Knee joint is normal
 Genu varum / valgum
 Charcot jt: DM, perineuropathy, tertiary syphilis, tabes dorsalis,
syringomyelia, myelomeningocele COMMON KNEE SYMPTOMS
Instability  Ligamentous instability (ACL, PCL, med & lat collateral ligs) - locking = spontaneous block to extension
 Recurrent dislocation of patella • torn meniscus, loose body
 Osteochondritis dissecans - pseudo-locking = restricted ROM without mechanical block
 RA • arthritis (effusion, pain), muscle spasm following injury
- instability = “giving out”
DIFFERENTIALS FOR POPLITEAL FOSSA SWELLINGS (OSCES) • torn ACL, patellar subluxation, torn meniscus, loose body
Tissue type Pathology PE & Comments - traumatic knee swelling
Skin & Lipoma - Soft to firm; smooth/lobulated surface • effusion, usually represents hemarthrosis
subcutaneous - If large & soft  elicit fluctuation • ligamentous injury with hemarthrosis
tissues - ‘slip sign’ • meniscal injury
- Elicit which layer lipoma is in e.g. S/C or I/M • traumatic synovitis
(in the latter, the lipoma disappears on m. - non-traumatic knee swelling without trauma
contraction) • septic or crystal-induced arthritis
Sebaceous cyst - Soft to firm; smooth surface • seronegative arthritis (P-A-I-R: Psoriatic, AS, IBD, Reiter's)
- +/- punctum (present in 50%) • seropositive arthritis (RA, SLE)
- Attached to the skin, hence does not move • avascular necrosis (rare)
independently from the skin • sickle cell disease
Artery Popliteal artery - 50% bilateral; expansile pulsation
aneurysm - Comment on diameter (≥2cm diameter) History
- Palpate all LL pulses (distal pulses may not be - ligamentous injuries require high energy force
palpable if aneurysm is thrombosed) - meniscal injury in young & old person requires moderate & mild force respectively

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 Cx:
X-Rays of the Knee Recurrent synovial effusion & articular cartilage damage due to loose meniscal tag 
AP, lateral weight-bearing swelling, OA
Skyline view • with knees in flexion, beam is aimed from anterior tibia to
anterior femur MENISCAL CYSTS
• allows for view of patellofemoral joint
 Tender & tense swelling arising from outer part of meniscus along the joint line
(usu lateral)
Tunnel view Knee bent, can see the hollow between 2 articular surfaces
 Hx of joint injury may be present
Oblique For intra-articular fractures
 Rx: if symptomatic, arthroscopic decompression or removal
Erect-leg full- • radiograph from hip to foot with patient in standing position
length view • useful in evaluating limb length discrepancies and genu varus /
valgus CHRONIC LIGAMENTOUS INSTABILITY
Rosemberg • 30-40 deg flexed weight bearing view with the x-ray beam  Chronic instability – sense of joint wanting to or actually giving way
view tilted caudal to profile the joint line   pain & recurrent swelling
• Best view to visualise loss of medial joint space  O’Donahue’s triad (aka unhappy triad): ACL tear + med meniscus tear + med
collateral lig tear
MENISCAL TEARS  ACL injury more common than PCL injury
History & PE: ACL Tear PCL Tear
 Mechanism: twisting injury, usually during sports (esp football) History o indirect varus blow to knee o fall onto flexed knee
 Locking of knee in partial flexion: torn portion of menisci jammed between femur o hyperextended knee + internal rotation with plantar flexed foot
& tibia, blocking extension. Unlocks with flexion. Suggestive of bucket-handle type o audible pop, knee instability o hit anterior tibia on
meniscal tear. o “giving way” dashboard in MVA
 Pain, swelling, effusion. o immediate swelling (dashboard injury)
 Tenderness: medial meniscal tear (well localized med joint line tenderness); lateral o inability to continue activity o hyperflexion or
meniscal tear (ill-defined joint line tenderness) o patients with greater Q-angle got hyperextension with
 Course: Symptoms resolves, recurs periodically w twists/strains. Sometimes, knee greater chance of ACL tear anterior tibial force
gives way spontaneously. Anterior drawer + Sag sign +
PE
 McMurray’s & Apley’s grinding test positive Lachman’s + (falsely +ve in PCL tears) Posterior drawer +
Ix: Apley’s distraction test + Apley’s distraction test +
 Arthrography Rx  Conservative – hamstring & quadriceps ex., physio, external brace
 MRI  Stabilization / Reconstruction –
o Reattachment (tightening of loose lig / capsule),
Prognosis & Mx: o Reinforcement (diversion of healthy muscles or tendons to
Outer 1/3 Good vascular supply, good healing. strengthen weak structures), using hamstrings, patellar,
Attempt operative repair Post-op physio quadriceps
Mid 1/3 Intermediate vascular supply & healing impt in all cases o Replacement (rerouting living structures or inserting synthetic
Inner 1/3 Avascular, poor healing. Excision required material)

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 MCL Tear LCL Tear  Intermittent ache or swelling, locking, giving way, effusion
History o valgus force to knee o varus force to knee  15-20yo, Bilateral in 50%, male > female
o +/– "pop" heard o similar history to MCL  X-ray – tunnel view: Loose fragment in joint, crater on the medial femoral condyle
o severe pain with partial tears o rule out common peroneal n.  Rx: removal of small fragments, fixation of larger fragments, cast for 6 wks.
o complete tear may be painless injury (difficult dorsiflexion
and decreased sensation at the PATELLAR FRACTURE
top of the foot) History
PE  swelling  Direct - blow to patella (Usually comminuted)
 tender above and below medial joint line  Indirect - sudden strong contraction of the quadriceps femoris against resistance
 Medial & Lateral collateral ligament tears: Valgus & Varus stress (Usually a transverse #)
tests + respectively  Immediate pain
 assess joint space opening with valgus force
o pain Physical
o Laxity with end point - partial tear  Swelling & bruising of knee joint +/- abrasions
o absence of end point - complete tear  Marked tenderness at knee joint
o rule out ACL and medial meniscus tear  Patellar deformity (+/- palpable gap)
Rx  minor  Inability to extend knee
o immobilize briefly, early ROM and strengthening  Proximal displacement of patella
 moderate
X-Ray
o knee immobilizer or cast (NB. Ligaments take 3/52 to heal)
 AP, lateral (need to exclude bipartite patella - common congenital fragmentation of
o early physiotherapy with ROM and strengthening
the patella)
 severe or combined
o surgical repair of associated injuries Treatment
o surgical repair of isolated MCL/LCL tear is controversial  Isolated vertical fractures - non-operative treatment - plaster cast 6/52, early ROM
 Transverse displaced fracture – ORIF with wires.
OSGOOD-SCHLATTER DISEASE  Comminuted fracture - ORIF; may require complete or partial patellectomy
 Traction injury of apophysis which patellar ligament inserts into (partial avulsion of  Indications for surgical tx
tibial tuberosity cos of unequal growth rate between patellar ligament and bone) o sig articular step-off > 2mm
 Tender lump over tibial tuberosity o loss of extensor mechanism with displacement > 3mm
 Pain after activity, usually on active knee extension o open #
 Usually young adolescent
 X-ray: fragmentation/displacement of tibial apophysis RECURRENT DISLOCATION OF THE PATELLA
 Rx: Restrict activities especially sports. Spontaneous recovery.  Girls > Boys
 [MCQ] patient doesn’t present with loose bodies in knee joint because it is extra-  Usually bilateral
articular!  Apprehension test +: Lateral dislocation of patella if quadriceps contract when knee
is in flexion. Results in pain and inability to extend knee.
OSTEOCHONDRITIS DESSECANS  Predisposing factors: lax ligaments, abnormalities of patella (high, low or lateral) or
 Separation of small osteocartilaginous fragment of condyle articular surface, lat fem condyle, genu valgus, tibial tubercle mal-alignment
usually a/w hx of trauma

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Mx CHONDROMALACIA PATELLAE
 Reduction & backslab  Anterior knee pain in adolescent girls – worse on climbing stairs
 Quadriceps strengthening exercise  Retropatellar tenderness, friction test +, effusion
 Operation: repair of torn medial structures / soft-tissue realignment / transposing  Chronic / recurrent overload of patellar articular surface due to malcongruence of
patellar ligament medially (realignment procedure) patellofemoral surfaces OR abnormal tracking of patella during flexion/extension.
 A/w development of OA
PATELLAR/QUADRICEPS TENDON RUPTURE
Ix: skyline views of patella, CT, arthroscopy
 Low energy injury, sudden forceful contraction during attempt to stop fall
 Partial or complete Rx:
 More common in patients with DM, SLE, RA, steroid use  Conservative: analgesics, reduce activities, physioRx, quadriceps-strengthening
 History exercises
o fall onto flexed knee  Operative: shaving of articular cartilage, arthroscopy lavage, realignment of patella,
o inability to extend knee patellectomy
 Physical
o palpable gap between patella and quadriceps RHEUMATOID ARTHRITIS
o may have hemarthrosis / effusion of knee  Stage 1 (synovitis) – pain, chronic swelling, large effusion, thickened synovium
 Investigations  Stage 2 (articular erosion) – joint instability, ROM. X-ray: loss of jt space &
o knee radiographs to rule out patellar fracture marginal erosion, but lack of osteophytes c.f. OA
o joint aspirate may show hemarthrosis  Stage 3 (deformity) – pain, deformity, instability & disability. X-ray: bone
 Treatment destruction
o surgical repair of tendon
Rx:
DISLOCATED KNEE  Conservative – splintage, intraarticular steroid injection
 Operative – osteotomy, TKR
 Bad high energy injury
 Can be anterior (most common), posterior, rotatory or lateral
 Associated injuries BAKER’S CYST
o popliteal artery (immobile due to geniculate arteries and the anterior tibial - Definition
artery going thru hiatus in interosseous membrane) intimal tear or disruption o Posterior herniation of knee joint capsule
in 35-50% o Leading to escape of synovial fluid into the posterior bursae, stiffness &
o capsular, ligamentous and common peroneal nerve injury knee swelling (fluid distention of the gastrocnemio-semimembranous bursa)
 Investigations o Common in children, occurring more often in boys
o Angiogram, doppler o Often a/w OA and Charcot’s joints
 Treatment o Important to rule out DVT, but the two can co-exist
o closed reduction, above knee cast x 4 weeks - Diagnosis
o alternately, external fixation especially if vascular repair o PE: swelling usually below the joint
o surgical repair of all ligaments if high demand patient  Fluctuant
 Cx : ischemia, peroneal nerve injury, compartment syndrome, reperfusion injury,  Transillumination possible
stiffness  Non-tender
 Positive slip sign – it is a deep structure.

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  Reducible only if connected to knee joints which not all baker’s cysts
are – especially in children. CLERGYMAN’S KNEE (INFRAPATELLAR BURSITIS)
o U/S: fluid between semimenbranosus & medial gastronemius tendons in Swelling superficial to patellar ligament & distal to the patella
communication with posterior knee cyst (100% accuracy) Rx: firm bandaging, avoid kneeling, aspiration, excision if chronic
- Because of their anatomic location, Baker’s cysts can increase risk of DVT
o Most commonly, the Baker cyst is located between tendons of the medial
head of the gastrocnemius and the semimembranous bursa. Occasionally, SEMIMEMBRANOUSUS BURSA
the Baker cyst can be found between the heads of the gastrocnemius Painless fluctuant swelling in medial part of popliteal fossa
muscles. This can result in a lateral deviation of the popliteal vein, and a Enlargement of bursa between semimembranousus & medial head of gastrocnemius
compression of the popliteal vein-predisposing to venous stasis and DVT Rx: excision if symptomatic (pain)
- Treatment
o In children, surgical excision of popliteal cysts is rarely indicated CHARCOT’S JOINT
 Usually spontaneous resolution of cysts in 10-20 months;
Causes:
 A prolonged period of observation is strongly recommended before
- Peripheral neuropathy
surgical excision is considered.
- DM
 In protracted cases, cysts may respond to aspiration and steroid
- Tertiary syphilis
injection, (note that unlike adults, the cyst may not be intra-articular
- Tabes dorsalis
and therefore may respond to aspiration
- Syringomyelia
o In adults: reoccurrence is common, even following surgical removal, and
- Myelomeningocele
therefore treatment is directed toward intra-articular pathology;
- Cauda equina lesion

POPLITEAL CYST Rapidly progressive OA

- Definition Gross jt deformity, but painless
o Cyst located on the medial side of popliteal fossa, just distal to flexion Unstable jt, effusion, no warmth
crease of the knee, under medial head of gastrocnemius
- Epidemiology Mx: Rest, immobilize
o Found in children & young adults Stabilize with cast/ calipers
o 2x more common in boys Surgical arthrodesis
o Usually unilateral Popliteal Fossa Boundaries (right)
- roof: fascia lata
- Diagnosis
- floor: (prox to distal) popliteal
o More prominent during knee extension & vice versa
o If cyst is not found in medial part of popliteal fossa or has a solid surface of femur, capsule of
component (on U/S), rule out tumour with CT/MRI scan knee joint, popliteus m. covered
- Treatment by its fascia
o Asymptomatic ones can be treated non-surgically with good results
o Though spontaneous remission is not to be expected in all cases

HOUSEMAID’S KNEE (PREPATELLAR BURSITIS)

Swelling over patella due to friction between skin & patella
Rx: firm bandaging; avoid kneeling; aspiration; excision if chronic

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Osteoarthritis (Knees)
Most common joint disease in the world
Degenerative joint disease

Morphological changes
 Cartilage degeneration
o Fissuring
o Pitting
o Eburnation as joint motion polishes surface
 Bone Hypertrophy
o Osteophyte formation
 Mild synovitis

Two types
Primary Secondary
- Senile (old-age)  Trauma – acute or chronic
- Post-menopausal  Rheumato – RA
 Infections – Syphilis
Joints affected:  Metabolic – Hyper PTH
 PIPJs of hands (Bouchard’s nodes)
 DIPJs of hands (Heberden’s nodes)
 Thumb joints
 MTPJ of big toe
 Cervical and lumbar spine
 Hip
 Knee
* frequency of OA: Asians: knees > hips; Caucasians: hip > kness
OA of knees and hands – F>M ; OA hip- M> F

Other risk factors

 Hereditary
 Obesity
 Competitive contact sport
 Deformities – e..g genu valgus/varum
 Recreational running is NOT a risk factor

Differentials – need to exclude other DDx of hip/knee pain from history

 Referred pain from hip, back
 VITAMIN
» Vascular – AVN
» Infections – warmth, fever, inoculation e.g. intra-articular injection by GP
» Traumatic
» Autoimmune/ inflammatory – PMHx
» Metabolic – Gout, tophi
» Neoplastic – LOW/LOA, SOB, goiter, urinary, GIT

History
 NO systemic involvement
 Joint pain
o The usual 6 points about pain
o Which joints?
o Insidious onset
o Morning stiffness not prominent (<30mins)
o Worsened by activity
o Alleviated by rest
 ASK ABOUT BACK PAIN, HIP PAIN WHICH CAN BE REFERRED TO THE KNEE
 Precipitating causes
o Trauma
o History of contact sports / occupation
o Associated conditions – RA, syphilis
o BMI of patient
 Functional Loss
o Job scope
o Recreational activity restriction
o Premorbid status: function & mobility
 Social hx – ask about housing (floor, lift landing)
 Treatments tried (TCM?)
 GI bleed risk
o History of ulcer disease and/or GI bleeding

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 o High dose or multiple NSAIDs
o Concomitant use of corticosteroids and/or warfarin
o Age >60 yrs

Physical Examination
 Genu varum/valgus predisposes to OA – usually genu varum
 Fixed flexion deformity
 Externally rotated
 If joint swelling, is MILD
 Joint line tenderness
 Crepitus
 Decreased ROM
 Patellofemoral OA (5%)
 Examine other joints as well
 Note absence of rheumatoid nodules / tophi / rashes / Sjogren’s
 Examine HIP, BACK
 Neuro exam – SMART – sensory, motor, autonomic, reflexes, trophic changes

Investigations
 To confirm diagnosis and exclude differentials
 To look for causes (not applicable usually)
 To look for complications (not applicable usually)
Radiological AP weight bearing (so that even small degrees of articular cartilage thinning can be seen) L-O-S-S findings
Lateral Loss of joint space
Skyline (tangential) view Loose bodies
Long film (to see degree of varus/valgus) Osteophytes
Subchondral sclerosis
To view all 3 compartments – medial, lateral, patellofemoral compartment Subchondral cyst
Mechanical axis – centre of hip to centre of ankle
Anatomical axis – line of femur to line of tibia (normally 4-6 valgus)

Management
Nonpharmacological
Physiotherapy Preservation and improvement of joint mobility
Exercise Range of motion and muscle strengthening exercises
Load reduction Body weight reduction if obese
Use of walking aids
Avoid kneeling and squatting.

Pharmacological
Paracetamol Should be first line drug; effective in a proportion of patients
NSAIDs Must be used with special care in
 >60y
 previous history of GI bleed
 concurrent warfarin/ steroid medications
 renal dysfunction
Prescribe with PPI/H2RA in patients with increased likelihood of GI bleeding
COX-2 inhibitors Vioxx a/w increased risk of stroke and cardiac events.
Glucosamine with Glucosamine has anti-inflammatory properties
chondroitin Chondroitin inhibits cartilage breakdown and stimulate cartilage repair
Have been found to be at least as effective as NSAIDS, with the added advantage of fewer side effects
Tramadol Consider in patients with highly-resistant pain
Intraarticular injections of Consider is patients with highly resistant pain. It is recommended that no more than 4 glucocorticoid
corticosteroids injections be administered to a single joint per year because of the concerns with long-term damage to
cartilage
Intraarticular hyaluronic acid Marketed as ‘joint replacement’ substances; expensive, no evidence to support its efficacy
injections (e.g. Synvisc)

Surgical
Minimally For early degenerative arthritis
invasive Alternative to osteotomy and TKR if the patient is reluctant to have more aggressive surgery
(Arthroscopic) Techniques include
 Washout and debridement
 Cartilage regeneration procedures
o Chondrocyte transplant
o Microfracture of subchondral bone
o Mosaicplasty
Arthroscopic surgery may defer definitive operation by up to 5 years

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High tibial Only in certain cases e.g. unicompartmental involvement. Osteotomy permits redistribution of weight
osteotomy Contraindications
 Inflammatory arthritis
 Severe flexion deformity >15o
 Varus/ valgus >15o
 >5mm loss of subchondral bone
 lateral thrust while walking
Knee replacement When symptoms are severe
Try to avoid doing in patients <60 as TKRs usu last only ~10y
Types
o Unicompartmental
o Total +/- preservation of PCL; PCL preservation preserves proprioception function but  wear of prosthesis
Complications
Intraop – GA, # of tibia or femur
Immediate – vascular injury to superficial femoral, popliteal and genicular vessel
Early – DVT/PE, fat embolism, infection, peroneal nerve palsy (1%)
Late –loosening, patellar instability, #, disruptn of extensor mechanism, periprosthetic #, wear of polythene surfaces
For PFOA Arthroscopy to confirm diagnosis
Rx
- Realignment procedures
- Cartilage transplantation (still under research)
- Patellectomy (problems a/w it include loss of normal knee power and function, quadriceps weakness, and failure to
resolve anterior knee pain, may eventually require total knee arthroplasty for knee arthritis)
- Patellofemoral arthroplasty
- Total knee arthroplasty

Cartilage regeneration procedures

Chondrocyte transplant Harvest condrocytes from non weight-bearing sites, e.g. patellofemoral surface, culture, reimplant
Microfracture Subchondral penetration of bone, inducing regrowth of fibrocartilage
Mosaicplasty Cylindrical cartilage taken from non-weight bearing areas, implanted on knee joint surface to form a
new layer of cartilage, comprised of the intact original cartilage and the transplanted grafts

Post-surgical
Physiotherapy To maintain joint ROM & muscle power
Continuous Passive Movement (CPM)

Approach to OA knee
1) Confirm Dx of OA knee: pain and its characteristics
2) Exclude other sites of pathology
a) back – pain, PU claudication
b) hip
c) ischaemic pain or neuropathic pain
Ischaemic pain Neuropathic pain
 Fixed claudication distance  Variable claudication distance
 Better walking downslope  Better walking upslope
 Recovers quickly with rest  Recovers slowly with rest
 Pain present at night  Pt usu sleep in kyphosed
position with no pain
3) Exclude DDx
a) malignancy – other bone pain, LOW, LOA etc.
b) septic arthritis – fever, tenderness, swelling, trauma, intraarticular injectn
c) RA – other jts, morning stiffness, pain
d) gout – precipitant, inflammation

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IMPORTANT ORTHOPAEDIC CONDITIONS IN TIBIA 2. Fractures that do not result in joint instability or deformity and can therefore be
TIBIAL PLATEAU FRACTURE treated with nonoperative modalities.
 Results from femoral condyle(s) being driven into the proximal tibia often due to a
valgus (eg. Bumper # from getting hit by a car from the side) or varus force TIBIAL DIAPHYSIS FRACTURE
 Lateral > medial  Most common long bone #.
 Associated injuries / complications: popliteal artery injury, compartment syndrome,  Commonly open #
ligament tear, meniscal tear, malunion  High intensity injury
o associated with crush injuries and MVAs
Schatzker classification
 Soft tissue, nerve and vessel injury common
 I – lateral split o assess neurovascular status
 II – lateral split with depression (the force o rule out open fracture
may have been greater or underlying bone  Displacement is difficult to control
may be osteoporotic & unable to resist
 Good reduction is required
depression)
o minimal shortening and angulation
 III – pure lateral depression
 Healing time: 16 weeks on average
 IV – pure medial depression
 V – bicondylar Treatment
 VI – split extends to metadiaphysis  ATLS principles first
 Conservative managemenet
Treatment o For closed injuries (= closed reduction)
Fracture displacement ranging from 4-10 mm can be o Long leg cast x 4-6/52
treated nonoperatively o Followed by below-knee cast until healed
 if depression is < 3 mm  Surgical management
o Sarmiento program of functional cast o For open injuries
bracing, NWB x 2 months • ORIF with external fixator
 if depression > 3 mm, displaced or comminuted • wounds on anterior surface heal poorly and may necrose
o ORIF +/- bone graft to elevate fragment o For unstable injuries or failed closed reduction  require IM nail
o For patients with high risk of compartment syndrome
Absolute indications for surgery:
 Closed reduction and cast; admit and observe for compartment
 Open plateau fractures syndrome; prophylactic fasciotomy if operating on tibia fracture
 Fractures with an associated compartment syndrome
 Fractures associated with a vascular injury
Indications for surgery
Definitive indications Associated intra-articular and shaft fractures, open fractures,
Relative indications for surgery: major bone loss, neurovascular injury, limb reimplantation,
 Most displaced bicondylar fractures compartment syndrome, and a floating knee.
 Displaced medial condylar fractures Relative indications Associated intra-articular and shaft fractures, unstable fractures,
an inability to maintain reduction, relative shortening of
 Lateral plateau fractures that result in joint instability segmental fractures, a tibial fracture with an intact fibula, a
Contraindications for surgery transition zone fracture, and polytrauma.
1. Presence of a compromised soft-tissue envelope (for immediate open reduction) Delayed indications Failure to maintain reduction, unacceptable reduction,
complications

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PILON FRACTURE OF DISTAL TIBIA
 Combination of talar # & distal tibial metaphyseal #, usually with intra-articular
comminution
 Vertical loading drives talus into tibial plafond. The cortical bone shatters; the
softer metaphyseal bone can also be affected.
 20-25% of these will be open #
 Associated injuries / complications:
30% will have ipsilateral injuries and 5-10% will have bilateral injuries;
- compartment syndrome
- compression # of vertebral column, particularly L1;
- contralateral # of: os calcis, tibial plateau, pelvis, or acetabulum (vertical
shear injuries)
- vascular injuries
 Treatment
o Conservative
 Pain relief
 Antibiotic prophylaxis (open # / internal fixations)
 Splint  cast immobilisation if # is undisplaced
o Surgical
 Preliminary stabilisation with external fixator +/- fibular # fixation
 Definitive surgery after condition of soft tissues is optimised (blisters
have epithelised, skin is wrinkled)
 Types: ORIF, external fixation, limited internal fixation with external
fixation, percutaneous pinning
 Indications for surgery include the following:
o Open fracture
o Displaced fracture
 Articular fragments with a gap of >2 mm or step of >1 mm
 Rotational malalignment
o Vascular compromise
o Compartment syndrome

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IMPORTANT ORTHOPAEDIC CONDITIONS IN THE ANKLE • avulsion fractures are transverse
EVALUATION OF ANKLE COMPLAINTS • shear fractures are oblique if pure inversion / eversion
• shear fractures are spiral if rotational force
Most common dislocation of ankle joint is subtalar joint – must reduce before X-ray!
History
DANIS WEBER CLASSIFICATION
Ask about pain, swelling, mechanism of injury, effect on standing/walking
Based on level of fibular fracture relative to syndesmosis
PE
 neurovascular status
 look, feel, move (dorsiflexion, plantarflexion)
 assess for tenderness at knee (Maisonneuve), lateral and medial malleoli
 special test: anterior draw (for ankle), talar tilt, squeeze test, Thompson test

X-ray
 views
o AP, Lateral and Mortise (15 degrees internal rotation)
o Mortise gives true view of talus in tibiotalar joint
o space between talus ––> tibia and talus ––> fibula
o space should be symmetric and < 4 mm with no talar tilt
o disrupted space signifies ligamentous or bony injury
 When to x-ray - Ottawa ankle rules
• Ankle x-ray is only required with
o pain in malleolar zone AND
o bony tenderness over posterior aspect of the distal 6 cm of medial or lateral
malleolus OR inability to weight bear both immediately and in E.R.
• Foot x-ray series is only required with
o pain in midfoot zone AND
o bony tenderness over navicular or base of fifth metatarsal OR inability to
weight bear both immediately and in E.R.
(Types A  C = increased risk of syndesmotic injury)
Type A (infra-syndesmotic)
• avulsion of lateral malleolus below plafond or torn calcaneofibular ligament
• +/– shear fracture of medial malleolus
Type B (trans-syndesmotic)
• avulsion of medial malleolus or rupture of deltoid ligament
• spiral fracture of lateral malleolus starting at plafond
Type C (supra-syndesmotic)
• avulsion of medial malleolus or torn deltoid ligament
• fibular fracture is above plafond
• frequently tears syndesmosis
• Maisonneuve fracture if at proximal fibula
• posterior malleolus avulsed with posterior tibio-fibular ligament

Ring Principle of the Ankle LAUGE HANSEN CLASSIFICATION

The ankle can be thought of as a ring comprising of Based on mechanism of injury;
• a: lateral malleolus • d: deltoid ligament First word= position of foot,
• b: medial malleolus • e: syndesmotic ligament Second word = direction of movement of the talus in relation to the leg
• c: posterior (medial) malleolus (syndesmosis) NB. supination = inversion, pronation = eversion of the foot
• f: calcaneofibular ligament
Fractures of the ankle involve Supination-External Rotation (Weber B)
• ipsilateral ligamentous tears or bony avulsion • most common (45-65%)
• contralateral shear fractures • supination and external rotation  oblique fracture at level of the sydesmosis
Pattern of fracture
• determined by mechanism of injury

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Pronation-Abduction (Weber B/C) In Summary...
• sequence of injury: Lauge Hansen classification Corresponds to Danis Weber type...
1) avulsion fracture of medial malleolus or rupture of deltoid ligament; SA A
2) abduction force then either ruptures the syndesmosis or avulses its bony SE B
attachment sites; PA
3) lateral force from talus impacts and fractures fibula at or above level of PE C
syndesmosis and ruptures interosseous membrane

Pronation-External Rotation (Weber C)

• sequence of injury:
1. transverse fracture of the medial malleolus or disruption of deltoid ligament;
2. external rotation then results in rupture of the anterior tibiofibular ligament or its
bony insertion;
3. oblique or spiral fracture of fibula above the level of the joint;
4. posterior injury with tibiofibular ligament rupture or avulsion of posterior
malleolus
• fibular fracture may be proximal (i.e., Maisonneuve fracture2)

Supination-Adduction (Weber A)
• sequence of injury:
1. supination force may rupture portions of lateral collateral ligaments or may
avulse distal fibula, resulting in transverse fracture below the level of intact
syndesmosis;
2. adduction forces talus against the medial side of the joint, resulting in vertical
fracture of the medial malleolus

Treatment
 Undisplaced fractures: NWB BK cast
 Displaced fractures: reduce ASAP
 Indications for ORlF
• all fracture-dislocations
• all type C fractures
• trimalleolar (lateral, medial, posterior) fractures
• talar shift or tilt
• failure to achieve or maintain closed reduction
 Prognosis dependent upon anatomic reduction
• high incidence of post-traumatic arthritis

2
Maisonneuve fracture: spiral fracture of the proximal third of the fibula associated with a tear of the
distal tibiofibular syndesmosis and the interosseous membrane

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LIGAMENTOUS INJURIES - Crutches are only necessary for a few days.
- Physiotherapy
Medial Ligament Complex (deltoid ligament) - Usually return to play within 2-3 weeks
 Responsible for medial stability
 Usually avulses medial or posterior malleolus
Grade III sprains are treated non-operatively nowadays
 usually a/w syndesmotic or lateral ankle sprain
- Bracing with a hinged knee orthosis (in the past: BK walking cast for 3 weeks)
Lateral Ligament Complex (ATFL, CFL, PTFL) - Crutches for 1-2 weeks
 Responsible for lateral stability - Physiotherapy
 Makes up for >90% of ankle ligament injuries - Usually return to play after ≥6 weeks
 Clinical: swelling and discoloration, ‘pop’ sound,
giving way Focus of rehabilitation (NB. Allow sufficient healing of ligament first = 3wks)
 Diagnosis: stress x-rays and mortise view » Restore full ROM at the knee
o talar inversion produces joint separation exceeding the unaffected side by » Controlled strengthening. Often in the knee, the functional strength of the
six degrees (talar tilt test) quadriceps muscle, especially the medial VMO muscle, is weak and atrophied.
 Frequncy of injury: ATFL > CFL > PTFL » Sport-specific or function-based training. Upon achieving full strength and
pain-free ROM in the lower extremity, the athlete can be cleared to return to
Anterior Talofibular Ligament (ATFL)
their sport, most often without any brace or external support.
 Most common ligamentous ankle injury
 Sprained by inversion and while ankle is in plantar flexion
 Swelling and tenderness anterior to lateral malleolus, ++ ecchymoses RECURRENT ANKLE SUBLUXATION
 Anterior draw test for ankle positive with Grade III ATFL injury  Aetiology
• attempt to sublux talus anteriorly • ligamentous laxity
• if positive then stress other lateral ligaments  Joint (loss of normal proprioception)
 Talar tilt test for integrity of other ligaments • internal derangement of anatomy
• intra-articular loose body
Grading and Treatment of Ligamentous Ankle Injuries  Treatment depends on cause
Initial treatment of all sprains follows the RICE protocol (Rest, Ice, Compression,  Strengthening and balance training for neuropathic joint
Elevation). Protective weight-bearing is instituted with crutches. This is continued until • ligament reconstruction for lateral laxity and talar tilt
normal gait is restored. • arthroscopy / arthrotomy for internal derangement

Goal of therapy: decrease pain, restore ROM & regain strength

Grade I – microscopic stretch/tear (pain)

Grade II – macroscopic tear (pain on motion)
Grade III – complete tear (unstable ankle, talar tilt apparent on mortise view)

Grade I and II sprains are routinely treated nonoperatively.

- Ankle brace, usually in dorsiflexion & eversion (individualized to the patient's
discomfort).

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IMPORTANT ORTHOPAEDIC CONDITIONS IN THE FOOT Painful callosities: phalanx (to contractures
EVALUATION OF FOOT COMPLAINTS Terminal include nail &  Resection of
phalangectomy matrix) metatarsal heads
History • pain, swelling, loss of function, sensory changes, deformity, of the lesser toes
mechanism of injury, activity level of patient
Physical • inspection, palpation, active and passive ROM, weight bearing status
• neurovascular status Hammer toe
X-rays • AP, lateral, oblique (as a minimum)

HAMMER/MALLET/CLAW TOE Mallet toe Claw toe

Hammer toe Mallet toe Claw toe
Epidemiology More common in Females, Elderly, with RA
Aetiology Imbalance between intrinsic (lumbricals & interossei) and extrinsic (long
flexors & extensors) muscles of the lesser toes
For claw toe: may be 2˚ to neurological disorders e.g. peripheral
neuropathy (Charcot-Marie-Tooth disease, DM), LMN disease (polio),
UMN disease (CP, stroke, multiple sclerosis)
LOOK Affects lesser toes, most commonly 2nd toe Usu all 4 lesser toes
involved; may be B/L
 Flexion deformity at  Flexion deformity  Flexion deformity HALLUX VALGUS
PIPJ at DIPJ at PIPJ and DIPJ  Definition: valgus angulation of 1st metatarsal (i.e. lateral angulation of big toe)
 +/- DIPJ extension  NO MTPJ/PIPJ  + hyperextension of  Epidemiology: most common disorder involving the 1st MTP joint
+/- MTPJ extension involvement MTPJ  Causes: idiopathic; hereditary, loss of muscle tone, RA; increased incidence in those
Any callosities who wear enclosed footwear
FEEL Any tenderness  Associated deformities: inflamed bunion, hammer toe, metatarsalgia, secondary OA
MOVE Is the deformity fixed or mobile of 1st MTP jt
OFFER Watch the patient walk  Ix: do a plain weight-bearing X-ray to assess
Examine patient’s shoes 1) degree of valgus deformity
Ask questions to assess effect of the condition on his/her life 2) presence of OA of the first MTPJ
Non-surg Rx Appropriate footwear (usually unhelpful for mallet toe)  Rx:
Surgical Rx Mobile deformity Mobile deformity Mobile deformity - Non-surgical: appropriate footwear & physiotherapy
Flexor-to-extensor Flexor digitorum Flexor-to-extensor - Surgical: depending on patient’s wishes, level of activity & state of peripheral
tendon transfer longus tenotomy tendon transfer vascular system
Fixed deformity Fixed deformity Fixed deformity  Bunionectomy
 Resection of  Resection of  Resection of  1st metatarsal realignment osteotomy
proximal phalangeal middle phalangeal proximal  Excision arthroplasty (Keller’s procedure) – essentially a proximal
H&N +/- flexor & H&N +/- flexor phalangeal H&N hemiphalangectomy
extensor release tenotomy +/- flexor &  Fusion – for degenerative joint disease
 Proximal  DIPJ arthrodesis extensor release
phalangectomy  Amputation of  Extensor tenotomy
 PIPJ arthrodesis distal ½ of distal for MTPJ

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HALLUX RIDGDUS  Unable to tip toe
 Definition: literally means “stiff great toe”; however, limited ROM is only one of  Gap felt 5cm above insertion of tendon
the symptoms that constitute this diagnosis  Weak plantar flexion, not a/w tautening of tendon
 Epidemiology: second most common disorder involving the 1st MTP joint (the first  Thompson aka Simmond’s test: lack of plantar flexion on squeezing calf
being hallux valgus). Seen in adolescents & in adults.  Mx: Acute – plaster cast with foot in equines to approximate tendon ends + shoes
with raised heels for 6 wks
 Causes: Primary OA of MPJ of great toe.
Operative – repair to equinus, plaster and raised heels for 8 wks
 Diagnosis
• Symptoms: pain on top of great toe +/- diffuse, lateral forefoot pain
resulting from increased weight-bearing on lateral foot to offload the hallux. PES PLANUS (AKA FLATFOOT)
Pain is worse with certain activities and with certain footwear.
• Signs: tender dorsal osteophyte at 1st MTP joint (usually confirms this dx); Definition: = flat foot
Condition whereby the arch of the foot collapses with the entire sole of
slightly antalgic gait; limited plantarflexion & dorsiflexion a/w pain
the foot coming into complete / near complete contact with the ground.
especially at the end of ROM
 Treatment Epidemiology: very common
• Conservative
- Activity modification: use of in-sole orthotics, avoid extreme DF of
great toe (e.g. kneeling/squatting with toes in great extension)
- Pharmacological: paracetamol, NSAIDs
• Surgical
- Cheilectomy: excision of all irregular bony spurs that limit motion
- MT osteotomy: based on the premise that metatarsus elevatus or a
long first MT are the underlying causes of hallux rigidus Aetiology:
- Joint arthroplasty (commonly known as Keller technique): involves Young Adult
the excision of the base of the proximal phalanx; indicated in Flexible Rigid Acquired
moderate to severe cases of hallux rigidus in individuals with low  Functional  Tarsal coalition
functional demands who desire the maintenance of joint motion;  Hypermobile – lig laxity  Inflammatory jt dz
however, complications are common such as hallux weakness,  Tibialis post tendon dysfunction  Neurogenic disorders
elevation, floppiness, a short hallux, and development of transfer Diagnosis:
lesions under the second MTP joint
 Physical Examination (see picture)
- Arthrodesis: salvage procedure should other surgical interventions fail
o Abducted forefoot
& hallux rigidius is severe enough
o Valgus hindfoot
o Flexible flatfoot: arch appears when patient dorsiflexes (not a true
RUPTURED TENDO ARCHILLES collapsed arch because medial longitudinal arch is still present)
 Degenerate tendon ruptures during pushing off (jumping/ running) Treatment:
 >40 years old (i.e. middle-aged), a/w long term steroid use  When to treat: (1) if patient has rigid flatfeet, (2) if there is associated foot or
 Rupture at musculous tendinous junction occurs most often in young people, but lower leg pain, or if the condition affects the knees or the lower back
ruptures near the calcaneus also occur
 Use of orthotics (arch support – to be used for the rest of patient’s life;
 Mechanism usually involves eccentric loading on a dorsiflexed ankle with the knee
exercises recommended by podiatrist)
extended (soleus and gastroc on maximal stretch)
 Surgery as last resort (usually time-consuming & costly)

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  Mechanism: MVA or fall from height
FOOTBALLER’S ANKLE • axial loading or hyper-plantar flexion injury
• talar neck driven into tibial margin
Anterior ankle impingement syndrome  Rule out potential associated injuries
- Definition of ankle impingement syndrome: painful mechanical limitation of full • spinal injuries, femoral neck fractures, tibial plateau fractures
ankle ROM secondary to an osseous or soft-tissue abnormality
 X-Rays
• AP/lateral films with CT scan of talus
Repeated forced dorsiflexion  tearing of anterior capsule of ankle joint  subsequent
 Treatment (aims: revsacularisation & fracture healing)
bone spur formation (osteophytes) aka anterior exostoses of the tibia  subsequent pain
• BK cast, NWB x 6 months
+ limited ROM
• ORIF: to reduce displacement and prevent AVN or non-union
Treatment:  Complications
Acute phase • undisplaced: 0-10% risk of AVN
 Conservative: NSAIDs, physiotherapy, orthotics, bracing • displaced: 100% risk of AVN
 Surgical: arthroscopic excision & debridement
Recovery phase CALCANEAL FRACTURE
 Posterior splinting for 1/52 with supportive brace & compression stocking  Mechanism: axial loading (fall from a height onto heels)
 Physiotherapy for 2/52 for strengthening, ROM, proprioception and sports-  Rule out potential associated injuries
specific rehabilitation • Spinal injuries (10%)
• Femoral neck fractures
ACHILLES TENDONITIS • Tibial plateau fractures
- Chronic inflammation from running and shoe-wear (high heels) • Knee ligamentous injuries
- May develop heel bumps (Haglund’s deformity: prominence of the posterior  Physical
superior calcaneus where the Achilles tendon laterally inserts into calcaneus) • Heel viewed from behind is wider, shorter, flatter,
varus tilt
Diagnosis • May be swollen, with bruising on soles
 pain, aggravated by passive stretching  X-Rays
 tenderness, swelling • Broden’s views (oblique views of subtalar joint)
 crepitus on plantar flexion • Bohler's Angle decreased (normal: 20 - 40 degrees) Bohler's Angle
 Treatment
Treatment • Goal is to prevent widened heel and maintain subtalar joint congruency
 rest, gentle stretching, NSAIDs • NWB, early ROM
 proper footwear +/- orthotics • ORIF if depressed centrally or tongue-type fracture
 do NOT inject steroids (prone to rupture) • Closed vs. open treatment is controversial (open: potential vascular
complications)
TALAR FRACTURE (RARE) • Primary arthrodesis if severe
 60% of talus covered by articular surface (7 articular facets!)  Cx : malunion, subtalar arthritis, chronic heel pad pain, calcaneal widening (
• Decreased surface area for vascular perforation increase in shoe size)
• Blood supply to talus: distal to proximal
• Fractures of the neck at risk of AVN

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PLANTAR FASCIITIS intrinsics
• secondary exostosis forms with bursa and thick skin creating the bunion
 Repetitive strain injury of plantar fascia
 Treatment: (1) cosmetic reasons, (2) for pain with shoes
 Most common cause of heel pain [MCQ]
• Conservative: properly fitted shoes and toe spacer
 Epidemiology: common in runners, jumpers, ballet dancers, obese individuals
• Surgical: removal of bunion with realignment of 1st MTP joint
 Pathogenesis: chronic inflammation due to microtears of plantar fascia
 History
• Intense pain on waking or after rest METATARSAL FRACTURE
• Subsides as patient walks As with the hand, 1st, 4th, 5th metatarsals (MT) are relatively mobile, while the 2nd and
• May be associated with systemic diseases 3rd are fixed
 Diabetes mellitus
 Enthesopathies including seronegative and seropositive arthritis Types of Metatarsal #s
 Physical
• Swelling, local tenderness over plantar fascia
 mostly at medial calcaneal tubercle
• Pain with toe dorsiflexion (stretches plantar fascia)
 X-Ray
• Sometimes show heel spur at insertion of fascia into medial calcaneal
tubercle
• Note: spur is reactive, not the cause of pain
 Treatment
• Non-operative (90% resolve)
 Rest and NSAIDs x 4-6 months
 Stretching exercises
 Supportive shoes with heel cup
 Steroid injection
• Surgical in refractory cases (rule out nerve entrapment as cause of pain first)
 Release of plantar fascia--50% effective at pain relief
 Spur removal not required
 Can be done endoscopically
Fracture Mechanism Clinical Treatment
BUNIONS Avulsion of base of Sudden inversion Tenderness at base of Requires ORIF if
5th MT followed by 5th MT displaced
 Definition: localised painful swelling at the base of the big toe contraction of peroneus X-ray foot
• Joint is enlarged, toe is often malaligned brevis
• Frequenly associated with inflammation Jones Fracture - Stress injury Tenderness along shaft NWB BK cast x 6/52
midshaft 5th MT of 5th MT ORIF if athlete
• Can be a/w degenerative joint disease (OA) or bursitis
Tends to displace b/c
 Epidemiology: 10x more frequent in women of peroneus brevis and
 Two primary causes: heriditary, shoewear tilting
 Diagnosis & pathogenesis: a/w hallux valgus deformity March Fracture - Stress injury Painful shaft of 2nd or Symptomatic
• valgus alignment of MTP joint is aggravated by eccentric pull of EHL and shaft 2nd, 3rd MT 3rd MT

80
1st MT Fracture Trauma Painful 1st MT ORIF if displaced
otherwise NWB BK
cast x 3 weeks then
walking cast x 2 weeks
Lisfranc Fracture Fall onto plantar flexed Shortened forefoot ORIF
2nd Tarso-MT foot or direct crush prominent base
fracture- dislocation injury

Kohler’s disease – AVN of navicular bone

MCQ --- Stress fractures: common sites

a. head of femur
b. 2nd metatarsal
c. distal end of femur
d. tibia

81
IMPORTANT ORTHOPAEDIC CONDITIONS IN THE SPINE
APPROACH TO LOWER BACK PAIN

LOWER BACK PAIN

Axial Leg Pain
Facet Discogenic Radicular Claudication
Diagnosis Spondylosis (OA) Degenerative PID (commonly L5, S1  S1 Spinal stenosis
disc disease affected)
Epidemiology Old Young Old
Pain Back Back Leg Leg
dominance
Worse with Extension Flexion Flexion Extension
Onset Gradual Congenital/acquired
Hx
Duration Short (days to weeks) Long (weeks to Short episode attacks (minutes) Acute or
months) chronic (weeks to months)
Other aspects NB. Patient is usually Symptoms of radiculopathy Neurogenic claudication
of history asymptomatic. Lumbar  Sciatica (+/- cross sciatica)  Pain, weakness and/or
spondylosis is hence  Shooting pain down calf numbness in the legs
not found unless a  a/w m. weakness, tingling / while walking (ask for
complication ensues, numbness segmental sensory
e.g. nerve root  Cough impulse positive deficits)
compression from Rule out cauda equina syndrome  Variable claudication
posterior osteophytes (impt complication) distance
with superimposed  Urinary retention  Pain even on standing
spinal stenosis  Saddle anaesthesia (loss of  ‘Park bench to park
sensation over the buttocks bench’ – relieved with
& the perineum) flexion
 LL weakness  No pain at night (patient
sleeps on lateral
decubitus foetal
position)
Rule out vascular claudn
PE Normal 1. Listing (to relieve n. root Same as radicular
compression), paravertebral (+) 4. Pulses
m. spasm, restricted ROM
2. SLR, Bowstringing,
Laseague tests +ve
3. Tone, Reflex, Power
4. Sensation
Ix MRI X-ray (to exclude bone disease) & MRI
Conservative NSAIDs NSAIDs Back care education
Activity modification Bed rest
Exercise/physiotherapy Epidural steroid injection
Lumbar corset Physiotherapy
Tx Back care education
Surgical Fuse Discectomy Nerve decompression
(all under GA) - Indication: failure of 3
months of conservative mx,
cauda equina syndrome
- Usually only alleviate
symptoms of radiculopathy,
not of LBP
& fuse
(Transforaminal Lumbar Interbody Fusion, or TLIF)

Caveats
 Sciatica (df): leg pain localised in the distribution of one/more lumbosacral nerve roots, typically L4-S2, with or
without neurological deficit. [when the dermatomal distribution is unclear, please describe it as ‘non-specific
radicular pattern’]
 Both spondylosis and degenerative disc disease may occur at the same time (chicken & egg phenomenon)
 Can have 2 or more concurrent pathologies, e.g. lumbar spondylosis with spinal stenosis (spinal stenosis increases
with age but the symptoms may be exacerbated by further compression due to spondylosis)
 Causes of spinal stenosis can also cause radiculopathy as well
 Give the other as differential, e.g. PID – ddx spinal stenosis

82
Other differentials
- Cauda Equina syndrome
- Neoplastic (primary, metastatic)
- Trauma - fracture (compression, distraction, translation, rotation)
- Spondyloarthropathies (e.g. ankylosing spondylitis)
- Referred pain - aorta, renal, ureter, pancreas

Important Red flags (rule out malignancy, infection, trauma)

- Age (<20 or >50  increased risk of conditions listed above)
- LOW, LOA
- Hx of malignancy
- Night pain
- Fever, chills, rigors
- Hx of trauma
- Any bladder/bowel symptoms

How to read Spine X-rays

Lateral view Lateral view of spine

1) anterior vertebral line
2) posterior vertebral line
3) spinolaminar line
4) interspinous line
• Also look out for soft tissue
(prevertebral fat stripe)
should be
– <6mm at C2
– <2mm at C6

X-Ray
Oblique views: look for "Scottie Dog" sign (= spondylolysis)
S – superior facet
N – transverse process
I – inferior facet
P – pars interarticularis

83
PROLAPSED INTERVERTEBRAL DISC (USUALLY YOUNGER PTS) Surgical - Fenestration & discectomy OR microdiscectomy
- Usually only alleviate symptoms of radiculopathy, but not of LBP
- Acute posterior or post-lateral herniation of nucleus pulposus causing pressure on
nerve root (traversing nerve root, not exiting nerve root) - Indications: failure of 3 months of conservative management (i.e.
- Young adult progressive neurological deficit, persistent pain), cauda equina
- DDx: AS, TB spine, vertebral tumours, nerve tumours syndrome
- L4/5 commonest (a/w L5 radiculopathy) followed by L5/S1(a/w S1 radiculopathy)
Symptoms SCOLIOSIS
- Backache (pressure on post longitudinal ligaments) Causes
- Sciatica (pressure on dural envelope or nerve root)
Non- - Limb length discrepancy (apparent or true shortening of one leg)
- Radiculopathy (usu L5 or S1): Numbness, paraesthesia & muscle weakness in leg or
structural - Hip contracture
foot (compression of nerve root)  relieved by flexion to 1 side (listing)
- Aggravated by coughing, straining, lifting, flexion of spine - Muscle spasm – eg 2o to PID
Structural - Adolescent idiopathic (commonest, 80%)
Signs
- Listing (to relieve compression on nerve root), paravertebral muscle spasm, - Infantile idiopathic – may resolve or progress
protective scoliosis, loss of lumbar lordosis - Osteopathic – due to congenital vertebral anomalies
- Restricted ROM - Neuropathic – eg 2o to polio or CP. Causing asymmetrical muscle
- SLR limited, + bowstringing / sciatic nerve stretch test weakness
- Cross sciatic tension + - Myopathic – due to muscular dystrophies
- Neurofibromatosis
- Segmental myotomal/ dermatomal deficits – sensory deficits, power, reflexes

Lumbar Radiculopathy/Neuropathy
Root L4 L5 S1 ADOLESCENT IDIOPATHIC SCOLIOSIS
motor Quadriceps, tibialis anterior ankle dorsiflexion, great toe ankle plantar flexion
extensor, hip abductor - Progression: greatest during pubertal growth spurt, minimal progress post-puberty.
sensory posteromedial lateral calf or 1st web space lateral aspect of foot - Deformity:
reflex knee reflex hamstring reflex ankle reflex  Fixed 1o curve may be in thoracic or lumbar spine.
test limitation of femoral stretch limitation of SLR limitation bowstring  Vertebrae are rotated w spinous processes pointing to the concavity of the curve.
 Ribs on the convex side are carried around to form a prominent hump
Complications:
 Shoulder is elevated on side of convexity, hip sticks out on side of concavity
- Cauda equina syndrome – urinary retention, saddle anaesthesia, lower limb weakness
 Mobile 2o curves may develop above &/or below 1o
Investigations: curve to maintain normal head & pelvic position
- X-rays: AP, lat, oblique to exclude bone disease
- CT/MRI/myelogram X-ray:
- full length AP spine X-ray (measure Cobb’s angle – sup & inf
Management extent of scoliosis is where both sides of the intervertebral
Conservative - Bed rest space is of equal height)
- NSAID - lateral flexion X-rays,
- Epidural steroid injection - X-ray pelvis (look for Risser sign)
- Physiotherapy
- Back care education

84
 Definition: Risser sign is defined by the
amount of calcification present in the iliac S/S
apophysis and measures the progressive - Backache – intermittent; aggravated by standing, walking & prolonged sitting;
ossification from anterolaterally to relieved by lying down
posteromedially. Measure of skeletal maturity - Pain referred to buttocks and sometimes extends down leg
(Risser III  patient has past peak of growth - Acute incidents of pain, locking or giving way
spurt, a period of rapid spinal growth during - Reduced lumbar ROM
which scoliosis curvatures can increase
X-rays – narrowed disc space, osteophytes
rapidly)
Grade I: 25% ossification action of the iliac Mx:
apophysis - Conservative – modify activities, exercise, manipulation, NSAIDs, lumbar corset
Grade II: 50% - Surgical – spinal fusion
Grade III: 75%
Grade IV: 100% SPINAL STENOSIS (USU OLDER PTS)
Grade V: means the iliac apophysis has fused
to the iliac crest after 100% ossification - Causes: disc degeneration, OA & hypertrophy of post disc margin & facet joint,
degenerative spondylolisthesis (usually L4/5 level), spondylolytic spondylolisthesis
Complications: (usually L4/5 or L5/S1)
- Pulmonary – TLC & FVC due to thoracic lordosis deformity (Cobb’s angle >70o) - Causes of spinal stenosis can cause radiculopathy as well
- Cardiac – Right heart dz causing pulm HPT. ( Cobb’s angle >80o)
- Listing S/S:
- Limb length discrepancy - Neurogenic claudication: Thigh aches, numbness, paraesthesia after standing upright
- Backache / walking. Claudication distance is variable
- Radiculopathies - Relieved by spine flexion / sitting Patient stands in slight flexion
- Limited spinal extension
Mx: - Segmental sensory deficits, power, reflexes
Age Cobb’s Mx
Angle Neurogenic claudication Vascular claudication
Pre- <20o 4mthly F/U & full length spine X-ray to check for - Variable claudication distance - Constant claudication distance
pubertal/ progression of scoliosis - Better walking uphill due to spine - Better walking downhill as effort is
Pubertal 20-40o Supports (e.g. Milwaukee brace) flexion. Worse on walking downhill less. Worse on walking uphill
>40o Spinal fusion + supports post-op to prevent recurrence - Pain even on standing - ‘Shop window to shop window’ – pain
Post- >50o Spinal fusion - ‘park bench to park bench’ – pain relieve simply by resting, even if
pubertal requires spine flexion to be relieved. standing up
- No pain at night – PT sleeps on lateral - Pain at night
decubitus fetal position Also ask for PMHx of peripheral
LUMBAR SPONDYLOSIS vascular disease, hx of smoking...
Definition:
Flattening of disc & displacement of posterior facet joints, due to 2o OA facet joint Invx: lat X-ray, CT myelogram (waisting of dye column, posterior indentation, partial
or complete block)
Epidemiology:
Usually >40YO, males > females

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Mx: CAUDA EQUINA SYNDROME
Conservative Education on spinal posture
Definition
Surgical Nerve root compression Decompression Cauda equina syndrome (CES) has been defined as low back pain, unilateral or usually
Nerve root compression & spinal Decompression & spinal fusion bilateral sciatica, saddle sensory disturbances, bladder and bowel dysfunction, and
instability variable lower extremity motor and sensory loss usually due to mechanical compression
of the cauda equina.
SPONDYLOLISTHESIS Aetiology
Forward translation of upper vertebral body over the lower vertebral body, usually at V Spinal epidural hematoma
L4/5 or L5/S1 level Spinal anaesthesia
IVC thrombosis
Causes I Abscess
1. Dysplasia – congenital lumbosacral facet jt dysplasia Spondylolytic T Traumatic injury
2. Isthmic (spondylolytic) – break in the pars interarticularis Pathological A -
3. Elderly (degenerative) – OA degeneration of facet joints Operative M -
4. Trauma Trauma I Idiopathic
5. Suspicious (pathological) – neoplasm Elderly N Tumour (primary/metastatic)
6. Post-op – due to laminectomy for decompression Dysplastic Lymphoma
S/S Others  Spinal anaesthesia
- Backache – intermittent, worse on exercise or straining  Lumbar disk herniation
- ‘Stepping’ of spine  Late-stage ankylosing spondylitis
- Stiffness (for degenerative type)
History
X-ray:  Low back pain - This pain may have some characteristic that suggests something
- Fwd shift of upper spinal column
different from the far more common lumbar strain. Patients may report severity or a
- Elongation of the archs / defective facets
- Gap in the pars interarticularis on oblique view (Scotty dog sign) trigger, such as head turning that seem unusual.
 Radiating pain
Meyerding classification o Acute or chronic
Grade % translation of VB  Unilateral or bilateral lower extremity motor and/or sensory abnormality
I 0-25  Bowel and/or bladder dysfunction
II 25-50 o Initial presentation may be of difficulty starting or stopping a stream of
III 50-75 urine that may be followed by frank incontinence first of urine then of
IV 75-100 stool. Urinary incontinence is on the basis of overflow.
Mx o Usually with associated saddle (perineal) anaesthesia (Examiner can ask if
Conservative – bed rest & supporting corset Old patients, non-disabling symptoms toilet paper feels different when wiping.)
Operative – spinal fusion Disabling symptoms, young adult,
neurological compression

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Physical Examination
 Local tenderness to palpation over the lower back
 Pain radiating to the legs
 Loss or decreased reflexes
o Hyperactive reflexes may signal cord involvement, hence ruling out CES
o Similarly, Babinski sign / other signs of UMN involvement rule out CES
 Sensory loss/abnormality in perineal area or lower extremities
o Test light touch
o Anaesthetic areas may show skin breakdown
 Muscle weakness
o +/- muscle wasting (if chronic)
 Alteration in bladder function may be assessed empirically by obtaining urine via
catheterization. A significant volume with little or no urge to void, or as a post-void
residual, may indicate bladder dysfunction. Bedside ultrasonography may be also
used to estimate or measure post-void residual bladder volume.
Management
- Prehospital care should focus on associated symptoms related to the pain (ie, what
besides the pain is different).
 Stabilize acute life-threatening conditions.
 Immobilize the spine if traumatic.
- Emergency Department Care
 No proven medical treatment exists, and therapy generally is directed at the
underlying cause of cauda equina syndrome (CES).
 For mechanical compression of the cauda due to disk herniation, surgical
intervention may be indicated.
- Admit patients to appropriate service (usually neurology, neurosurgery, or
orthopedic surgery) with frequent neurologic checks.
- Complications: Residual weakness, incontinence, impotence, and/or sensory
abnormalities are potential problems if therapy is delayed

Other Problems to Be Considered Remember, it is a SURGICAL EMERGENCY! It will cause permanent urinary/bowel
 Conus medullaris syndrome incontinence if untreated. Must operate on patient within 48h.
 Spinal cord compression
LUMBAR SPINE FRACTURES
 Lumbosacral plexopathy
Elements of 3 Column Spine***
 Peripheral nerve disorder
Anterior Column Middle Column Posterior Column
Ant longitudinal ligament Post longitudinal ligament Post body elements
Investigations Ant annulus fibrosis Post annulus fibrosis Supra- & intraspinous lig.
 Imaging Ant 1/2 of vertebral body Post 1/2 of vertebral body Facet joints
o Plain radiography - Unlikely to be helpful in cauda equina syndrome but Ligamentum flavum
may be performed in cases of traumatic injury or in search of destructive
changes, disk-space narrowing, or spondylolysis
o CT with and/or without contrast - Lumbar myelogram followed by CT
o MRI - Superiority of MRI over CT only suggested by case reports (Early
consultation with the appropriate subspecialty is encouraged to guide
imaging studies.)7
o Ultrasonography may be used to estimate or measure post-void residual
volume.
 Other Tests
o Catheterization for residual urine volume may reveal urinary retention
suggesting a neurogenic bladder.

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Basic Types of Spine Fractures and their Mechanisms variable depending on severity
Type Mechanism of stenosis)
Compression Flexion - Radiculopathy(if n. root is
• Anterior Anterior flexion compressed by underlying
• Lateral Lateral flexion spinal stenosis)
Burst Axial load +/- flexion/rotation
Flexion - Flexion, distraction, common in lap-belted motor vehicle
CERVICAL MYELOPATHY
Distraction collision (Chance)
(NEUROLOGICAL DISEASE WITH POSSIBLE ORTHO CAUSE)
Fracture Flexion-Rotation, Shear, Flexion Distraction
dislocation Site
- C5-6 > C4-5 > C3-4 > C6-7
Chance Fracture of the Spine
- Hyperflexion injury Causes of cervical myelopathy
- Fracture extends through all 3 columns! - Cervical spondylosis – due to bony spurs & thickened ligament
- Most commonly seen in MVC lap-belted passenger - Infection
- CT scan to assist with diagnosis - Vascular disease
- Trauma
Insert notes from Spine Trauma slides from CGH - Degenerative conditions
- Demyelinating disorders
PID VS SPINAL STENOSIS*** - Tumours

PID Spinal stenosis Causes of compression

Patient age Younger Older (unless cause is PID) - Anterior: protruding disc or posterior osteophytes
LBP - Increase in abdominal pressure Neurogenic claudication - Anterolateral: jts of Luschka (uncovertebral jt)
aggravating (laughing, coughing, lifting, symptoms - Lateral: cervical facets (thickening / bony spurs)
factors straining) - Posterior: ligamentum flavum
- Spine flexion, prolonged sitting
Symptoms
Relieved by Listing to 1 side Spine flexion
- Weakness and clumsiness of the hands, paraesthesias in the hand
Neuro Pain, numbness, paraesthesia, Pain, numbness, paraesthesia, - Tightness, hot or cold sensations in the trunk
symptoms weakness weakness - Tingling in the legs
Inspection Listing, scoliosis, loss of lumbar Pt stands in flexion - Gait disturbances (ataxic, broad based, clumsy, shuffling)
lordosis, paravertebral spasm - May have symptoms associated with malignancy – LOA, LOW, malaise, etc.
Straight leg - SLR elicits nerve root SLR, SNST, Bowstring and cross
raise compression (i.e. SLR may or may not be positive Signs
radiculopathy) (depending on whether nerve root - Lower motor neuron findings at the level of the lesion
- SLR, SNST, Bowstring and is compressed by underlying - Upper motor neuron findings below the level of the lesion/cord compression
cross SLR positive cause of spinal stenosis) - Upper limbs usually show a mix of UMN & LMN signs, while lower limbs usually
Neurological Radiculopathy (usu L5 &/or S1) - Spinal stenosis: LMN signs at show UMN signs only
signs level of compression, UMN - Skipping of the face & head
signs downwards (but signs are -  Clonus, Lhermitte's sign (electric shock-like, radiating down body on neck flexion),
Babinski and Hoffman's pathologic reflexes

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-  "Finger escape sign" (the patient is asked to hold out their hand with fingers - Radiation: occiput (‘headache’), scapular muscles, down one or both arms.
extended and the medial fingers drift into flexion) - Paraesthesia, weakness, clumsiness
-  Urinary retention (rare) - Periods of exacerbation & quiescence
- Posterior neck & scapular tenderness
Investigations -  neck ROM throughout with pain
- Exclude tumour! - Limb numbness, weakness,  reflexes
- Plain X-rays
- CT (bony spurs & ligament ossification) Investigations
- MRI (disc prolapse & cord compression) - X-ray: narrowed IV disc space, bony spurs (‘osteophytes’), encroachment of IV
- Pavlov's Ratio: ratio of the distance from the foramina in oblique view
posterior aspect of the vertebral body to the
anterior aspect of the lamina (i.e. space allowed Management
for the cord at the same level) to the AP width of Conservative:
the vertebral body. Normal:  1 Abnormal: - Heat & massage, NSAIDs, cervical collar, physioRx
0.85 Surgical:
Management - Discectomy  anterior fusion
- As for cervical spondylosis - Corpectomy (removing part of vertebral body; latin corpus vertebrae)
- Laminoplasty
- Laminectomy  foraminectomy.
- Indications: progressive neurological deficits, multiple levels of cord compression
CERVICAL SPONDYLOSIS
(ORTHOPAEDIC DEGENERATIVE DISEASE OF THE C-SPINE)
CERVICAL LESIONS
Features
TORTICOLLIS
- IV disc degenerate & flatten + bony spurs on ant & post margins of vertebral bodies
- Posterior spurs may encroach upon the IV foramina compressing nerve roots Causes
- >40YO, male > female, usually C5/6 Acquired
DDx  Acute - muscular damage caused by inflammatory diseases, such as myositis,
- Thoracic outlet syndrome (look for signs of limb ischaemia; perform Roos test and lymphadenitis, or tuberculosis (TB); from cervical spinal injuries that produce scar
Adson’s manoeuvre) (a/w ulnar n. palsy) tissue contracture; and, less commonly, from tumor or medication
- Carpal tunnel syndrome  Spasmodic - organic central nervous system disorder, probably due to irritation of
- Rotator cuff lesions (abnormal shoulder movements, no neurological signs) the nerve root by arthritis or osteomyelitis. Benign paroxysmal torticollis – might
- Cervical tumour (symptoms are constant)
be migraine variant.
Risk factors  Ocular torticollis - compensatory mechanism enacted by patients with trochlear
- Smoking nerve palsy or superior oblique muscle weakness
- Drinking  Hysterical
- Excessive driving
Presentation
- Neck pain & stiffness, worse in the morning

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Congenital
 Traumatic – infants after difficult delivery - breech presentation (delivery buttocks
first instead of heads first)
 Skeletal anomalies, atlantoaxial instability
 Klippel-Feil syndrome
The presence of craniofacial asymmetry (e.g. hypoplasia of the face including the small
left eye) indicates congenital or long-standing torticollis.
Management
- Pre-hospital care: ensure patent airway, perform C-spine immobilisation / precaution
for patients with history of trauma
- A&E: ABCDEs, give antibiotics if infection suspected
- Definitive treatment
» Generally supportive; includes analgesics, benzodiazepines, anti-cholinergics,
heat, massage, stretching exercises
» Drug-induced torticollis: treated with diphenhyrdramine, benztropine, or
benzodiazepines
» Surgical Rx: SCM release (>1yo: don’t need to wait or try conservative Rx)
o N root – pain, paraesthesia in one / both (rare) arms. Radiating to outer elbow,
dorsum of wrist, middle n index finger. Weakness is rare. Prolapse usually
above/below C6 vertebrae so C6 & C7 N roots commonly affected
 Acute torticollis may be present
 X-ray shows  disc space. MRI to confirm.
 Ddx
o Soft tissue sprain – neurological S&S absent.
o Neurological amyotrophy (acute brachial neuritis) – sudden, severe pain @
back or shoulder. Multiple neurological sites affected & might have winging
of scapula. Pain followed by flaccid paralysis a few days later.
o Cervical spine infection – unrelenting & local spasm with severe pain. X-ray:
erosion of bone
o Cervical tumors – neurological signs progressive. X-ray/MRI shows bone
destruction. Primary tumors rare, secondary more common. Of primary,
sarcoma & multiple myeloma most common.
 Treatment
o Heat, analgesics
o Rest with collar (in 75% of patients symptoms will resolve with non-operative
measures)
o Reduce: traction intermittently placed for 30 mins @ a time. Up to 8kg
o Remove: anterior approach discectomy – fuse affected area / maintain height
using bone grafts.

THORACIC OUTLET SYNDROME CERVICAL SPINE TRAUMA

1. Lower trunk of brachial plexus n subclavian artery pass btw the ant n middle
scalene muscles and over the 1st rib. Neuro examination by levels (check dermatome for each of them)
2. Compression maybe due to cervical rib (rare), fibrous bands or abnormalities of  C4 – spontaneous respiration
scalene attachments, or by a pancoast tumour  C5 – biceps reflex, deltoid strength
3. Symptoms increase with increasing age as shoulders sag  C6 – wrist extension, brachioradialis reflex
4. Typically woman in her 30s complains of pain n paraesthesia extending down from  C7 - wrist flexion, triceps reflex
her shoulder down the ulnar aspect of her arm to the medial two fingers  C8 – finger flexion
5. Worse at night, agg by bracing shoulders or raising arms above shoulder height  T1 – interossei
 L1, L2 – hip flexion (femoral n.)
ACUTE PROLAPSED INTERVETEBRAL DISC (PID)  L2, L3 – hip adduction (obturator n.)
 Precipitated by local sprain or injury, usually underlying pathology already present  L3, L4 – knee extension (femoral n.) – knee jerk
e.g.  intervertebral disc pressure  L4 – dorsiflexion (deep peroneal n.)
 Leads to compression of  L4, L5 – hip abduction (superior gluteal n.)
o Post intervertebral lig – pain, stiffness, from back of neck to scapula, occiput  L5, S1 – hip extension (inferior gluteal n.)
 S1 – knee flexion (sciatic n.)
 S1, S2 – plantarflexion (tibial n.) – ankle jerk (S1)

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Pathologic reflexes (UMNL) – Hoffman’s sign, Babinski’s reflex, Oppenheim’s sign 1) Anterior vertebral line
(dorsiflexion of big toe elicited by downward irritation of medial side of tibia) 2) Posterior vertebral line
3) Spinolaminal line
Sacral sparing: incomplete injury - perianal sensation, rectal motor function, great toe 4) Interspinous line
flexor activity
 Frankel Score Also look for soft tissue swelling
(prevertebral fat stripe) which should be
A Complete Motor / Sensory
- <6mm at C2 level
B Complete Motor / Incomplete Sensory
C Incomplete Motor < 3 / Incomplete Sensory - <2mm at C6 level
D Incomplete Motor > 3 / Incomplete Sensory
E Normal

Spinal shock - state of complete spinal areflexia.

 over in 24-48 hours - Bulbocavernosus reflex signifies the end of spinal shock
 Treatment of Spinal Cord Injury
o attributed to contusion and/or compression - Microvasculature disruption
o Treatment: Methylprednisolone- bolus 30mg/kg followed by 5.4 mg/kg/hr
over 23 hours. Patients treated within 8 hours respond best.
TRAUMA C-SPINE SERIES – AP, lateral, open mouth odontoid
Who needs C-spine X-ray?
 Midline cervical tenderness
 History of neck/distracting injury
 Have focal neurological deficits
 Intoxicated / not response to person, time, place and event
NB. Pure dislocation of the spine is commonest in the cervical region
Lateral
 adequate exposure - must see occiput to T1, need to be able to see soft tissue
shadows, Swimmers view or CT if unable to see to T1
 Specific things to look for
1. anatomic lines -> 4 parallel lines
2. Step deformity of >3.5mm anywhere
 Anterior subluxation of 1 vertebra on another indicates facet dislocation
 Less than 50% of the width of a vertebral body implies unifacet
dislocation
 Greater than 50% implies bilateral facet dislocation
 This is usually accompanied by widening of the interspinous and
interlaminar spaces
3. Atlantodens interval (ADI) – distance between odontoid process and posterior
border of arch anterior of atlas – atlantoaxial instability (AAI) present if
 >3mm in adults
 >5mm in children
4. Uniformity of shape & height of IV disc (all the same except C1 & C2)
 Compression #: anterior wedging of vertebral body or teardrop fractures
of antero-inferior portion of body
 Burst #: anterior compression of greater than 40% of normal vertebral
body height (with retropulsion of fragments of the vertebral body into
the spinal canal)
 Loss of height  disc herniation
5. Angulation 11° greater than contiguous segments (Disruption of the PLL,
Subluxation of C3 on C4)
6. Anterior Occipitoatlantal Dislocation (Powers Ratio)

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Odontoid view Complete the exam –
 Shows C1 burst fractures, C1-2 alignment, Dens fractures If films negative remove collar and complete exam.
 C1 Ring Fracture Classification - Posterior Arch - 28%, Jefferson Burst Fx,
Anterior Arch “Blow Out”, Lateral Mass Fx, Transverse Process Fx Palpation- one person supports the head with axial traction while the other palpates
 Jefferson Fracture - Axial loading. Open Mouth View - Lateral Mass Spreading, > from occiput to T1. Check for tenderness, swelling, stepoff. cannot rely on clinical
6.9 mm = Transverse Lig Avulsion. exam if decreased mental status or distracting injury.
 C1 Burst Fracture Treatment If symptomatic replace collar.
1. Stable (Intact Transverse Ligament) - Rx - Halo 10 - 12 wks. If negative then proceed to ROM.
2. Unstable - Traction Reduction, Halo 12 - 16 wks,
Late Instability: C1-2 Fusion Active ROM only. Should be full and pain free.
 Odontoid Fracture Classification If exam completely negative and films negative at this point may remove collar. Write
1. Type 1 - Tip Avulsion, Type 2 – Waist (worst), order that C-spine is clear
Type 3 – Body If unable to perform ROM but the rest of exam is negative: replace collar and have
2. Type 2 – Unstable, Easily Missed, 10% Spinal patient return in 10-14 days for flexion and extension views. If done acutely muscle
Cord Injury due to translation, Poor Prognosis, spasm or guarding may hide a ligamentous injury.
Assoc Fx 20 - 30%
3. Type 3 - Good prognosis, Reduction, Brace (halo Obtunded patient with normal films - Leave the collar on. Dynamic Fluoroscopy.
device) vs fixation, heals easily MRI
AP view  Hangman’s Fracture of C2
 Spinous processes should line up and have equal gaps  Flexion Tear drop fracture of ant-inf part of vertebral body. Unstable fracture.
 sagital plane fractures
 lateral mass fractures Treatment – gardner-wells traction tongs, halo device
 facet fractures / dislocations (below)

LEFT: Unilateral facet dislocation. (A) Lateral view

of this fracture caused by a flexion-rotation
mechanism shows that it is stable. Anterior
displacement of spine is less than one half of the
diameter of a vertebral body. (B) Anteroposterior
view shows disruption of a line connecting spinous
processes at the level of the dislocation. (C) Oblique
view shows that the expected tiling of the laminae is
disrupted, and the dislocated superior articulating
facet of the lower vertebra is seen projecting within
the neural foramina.
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DM FOOT (ORTHO)  Osteomyelitis / septic arthritis
EPIDEMIOLOGY  Gangrene (dry/wet)
- Prevalence of DM is 8.2% (28.4% in 60-69 age group)  Charcot’s osteoarthropathy
- 5% of all Diabetics develop foot ulcers  Necrotising fasciitis
- In S’pore, 2 amputations done daily
o Foot ulcers commonly become infected  gangrene  result in Major Lower
HISTORY:
Limb Amputation
- Mortality: 10% at time of amputation, 30% within a year, 70% within 5 years PATIENT PROFILE (include OCCUPATION! – nature of job)

PATHOGENESIS OF DM FOOT PRESENTING COMPLAINT: ulcer/abscess/gangrene, pain/swollen/infection

 When did you sustain the injury? How was it sustained? What were you doing at
1. NEUROPATHY (20-40% of all diabetics) that time?
o Sensory  Footwear at point of injury?
o Motor  When did you discover it? How did you realize it?
o Autonomic
 If not discovered at point of injury  reason? Numbness/weakness
2. VASCULOPATHY:  Precipitating injuries: trauma, rusty nails, pressure
o Microangiopathy:  Type of wound: open/closed, bleeding?
 terminal arterioles  Progression of injury: grew bigger, more painful, discharge, gangrene
 thickening of basement membrance of endothelium  1st episode? Any previous injuries of similar nature?
o Atherosclerosis: middle-sized and large arteries  Ask for poor wound healing

3. IMMUNOPATHY PAIN:
 SOCRATES
o Defects in leukocyte function (phagocytosis, chemotaxis, adherence,
neutrophil dysfxn)  Localised to toe/heel?
o Inherent susceptibility to infections  Vascular claudication
 Mild – monomicrobial 1) Pain in muscle (usu described as cramp)
 Severe – polymicrobial, a/w ostemyelitis 2) Only on exercise (ask abt claudication distance: quantify in eg. no. of bus stops)
 Prior use of ABx predisposes to MRSA & Pseudomonas 3) Disappears on rest

o Predominantly Gm positive cocci (Staph aureus, coagulase –ve staph eg.
epidermidis, Group B Strep, Enterococci, Corynebacterium)
 All forms of Staphylocci a/w increased risk of mortality
o Followed by Gram negative rods (eg. Pseudomonas (rotten fruit smell, green
discharge), Proteus, E. coli) and anaerobes eg. Bacteroides (faecal smell)
MODES OF PRESENTATION:
 Cellulitis
 Abscess (supf/deep)
 Ulcer (decubitus / vascular / neuropathic)
 Rest pain (present at rest throughout day and night) –
o Continuous severe aching pain bad enough to stop sleep and use of limb;
o Usu in most distal part of limb (toes and forefoot)
o A/w gangrene pain at border of living and dead tissue
o Relieved by hanging leg over side of bed; prefer to sleep sitting in chair
o May be so bad (unremitting, progressively worse) that beg for amputation
 NB: Critical limb ischaemia (rest pain and ulceration/gangrene)
o ? Night pain

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ULCER:  Monitoring of DM: hypocount, HbA1c; what are the usual values? How often
 Site: follow-up? Did doctor say good control?
 Plantar (sole) – neuropathic  Previous hospitalizations for DM, any surgery done? – DKA, HHNK, abscess, ulcer,
 Heel/toes – vascular (ischaemic) gangrene etc
 Complications:
 Size
o Microvascular
 Any discharge? Colour? (green – Pseudomonas)
 Retinopathy – blurring of vision, cataracts, previous laser PRP
 Foul-smelling? (eg. fish, rotten fruit smell)  Nephropathy – bubbly urine (?microalbuminuria), 24hr urine test CCT,
 Pain? UTP
 Recent trauma / foreign body penetration eg. rusty nail (even seemingly  Neuropathy – Sensory: numbness, paraesthesia, loss of proprioception
insignificant) Motor: weakness
 Footwear (ill-fitting shoes, slippers, barefeet) Autonomic: postural hypotension, gastroparesis,
diarrhoea, impotence
SWELLING: o Macrovascular
 Acute onset  CAD – IHD (CP, SOB), h/o AMI, cardiomyopathy
 Pain  CVA – TIA, major stroke
 Erythematous, warmth  PVD – paraesthesia, intermittent claudication, pallor, poor wound healing
 Discharge? – colour, odour, pus
 Fever chills rigors  Co-morbidities – HTN, IHD, CVA, CRF (worst combination with DM),
 Other risk factors – smoking, HTN, HCL (aggravates atherosclerosis)
SWOLLEN JOINT  Functional status – community walker / housebound / unable to walk (stroke), can
 Symptoms of inflammation – red, hot, swollen, pain, loss of function  think do household chores? ADL independent? How does the current orthopaedic
septic arthritis problem affect the pt’s function in general?
 Weakness, difficulty walking, deformity  think Charcot’s arthropathy  Care-giver?
 Family history of DM
GANGRENE:
 Toe/ heel/ foot Determine if Foot ulcer is: Vascular Neurogenic
 Dry/ wet? - punched out - painless
 Other symptoms of ischaemia – claudication, rest pain, cold extremities, - gangrene - deformed joints
discolouration - ischemic limb sympts - loss of sensation (vibration,
proprioception)
HISTORY OF SELF-MEDICATION
 Seek medical help from doctors?
 Sinseh : skin burns  ulceration  sepsis PHYSICAL EXAMINATION:
 Self-medicate : nail digging, self cutting callosity GENERAL:
 Well / ill / toxic
DIABETES HISTORY (DETERMINE TYPE 1 OR 2):  Acidotic breathing (Kussmaul)
 How long? How was it diagnosed?  Alert, oriented / drowsy (hypoglycaemia)
 Treatment: Diet/OHGAs/Insulin/Combination? Dosage/med changes, compliance  Pallor / sallow appearance (renal failure)
 Control: Symptoms of poor control to ask: 1) polyuria, 2) polydipsia, 3) polyphagia  Dehydration: furred tongue, dry mucosa, sunken eyes
 Fundoscopy – diabetic retinopathy

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 Popliteal pulse
VITALS Femoral pulse
 BP (both sides, postural) o NB: Vasculopathy assessment: (prognostic significance for distal amputation)
 Palpate ALL pulses – carotids (thrill, bruit), UL, LL  2 pulses palpable – v good chance of success
 1 pulse – fairly good
SYSTEMIC REVIEW: Heart, lungs, abdomen
 0 pulses – NO chance
LOCAL EXAMINATION:  Ulcer:
Inspection: o Tenderness, bogginess around ulcer
 Skin: o Squeeze surrounding skin for discharge – quantity, colour, odour
o Scars, Sinus, Healed wounds  Tenderness of each individual metatarsal bone / joint (OM, SA):
o dorsal surface
o Signs of PVD (chronic ischaemia): o deep palpation of SOLE (pus tends to be dependent)
 Shiny  Sensation:
 Loss of hair o Semmes-Weinstein monofilament (5.07 gauge applies 10g of force – test 9
 Dusky discolouration, pale points on sole and 1 point in 1st web space – if pt cannot feel means high risk!!!
 Trophic nail changes
o Vibration
 Pigmented skin
o Propioception
 NO varicose veins (good negative to mention) o Pin prick
o Signs of DM neuropathy o Light touch
 Sensory: Joint deformity (charcot’s jt, claw toe, hammer toe)  Motor (usually not required): test ankle reflexes.
 Motor: Muscle wasting  Test upper limb for glove and stocking distribution too!
 Autonomic: Dry skin, Fissuring, Callosity
 Ulcer: Move:
o Site – interdigital web space, dorsum, sole, heel
o Size
o Shape
o Floor: pus, slough, necrotic tissue, granulation tissue
o Edge: punched-out  vascular; irregular
o Any foreign body in ulcer?
o Surrounding skin : erythematous, necrotic, warm, tender
 Swelling
 Cellulitis
 Gangrene – dry / wet?

Palpation:
 Temp – warm (normal?) / hot (infected) / cold (ischaemia)
 Capillary refill time (<2sec)
 Pulses – DP (midpt of 2 malleoli, 1/3 way down to 1st digital cleft)
PT (hip in ER, knee flexed, foot dorsiflexed, 1/3 way down line from med
malleolus to TA)

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 Buerger’s test (2 components): CULTURES
o Pt supine, raise LL, look for pallor of sole and toes, record vascular angle  Wound swab of ulcer – take pus and from deepest possible part to increase yield
 Normal: 90deg pink o Gram stain
 Ischaemia: 15-30deg pallor o C/s (aerobic and anaerobic)
 Critical Ischemia: <20deg
IMAGING
o Pt sitting with legs hanging over side of bed, note time of reactive hyperemia
 ECG – cardiac status
 Normal: remain pink
 Ischaemia: white to pink  CXR – anaesthesia fitness
 CAPILLARY FILLING TIME >15-30 secs = severe ischaemia  X-ray foot (AP, Lat):
 ABI: 1. Osteomyelitis – rarefaction / osteopaenic, erosions, periosteal reaction (early),
o Doppler ultrasound probe used to measure ankle systolic pressure (should have cortical sclerosis (chronic)
3 waveforms – systolic, diastolic, recoil. If only 2 means already partial 2. Septic arthritis – widening of jt space, periarticular osteoporosis (early), jt
obstruction.) space narrowed (+/- erosions) (late)
o ABI = Ankle systolic press/Brachial systolic press 3. GAS gangrene – Clostridium, Strep. Microaerophiles – excl NECROTISING
 Normal > 1.0 FASCIITIS if there’s gas present
 Ischaemia <0.8 4. Bony destruction (Charcot’s/ LisFranc jt) – neuropathic changes
 Min to mod dz 0.5 – 0.9 5. Calcification of vessels
 Severe dz <0.5 6. Foreign body
 Critical ischemia <0.3  Duplex scan – arterial insufficiency
o Digital pressure index
 Angiogram, femoral (if vascular reconstruction needed) – localize areas of
 Normal >0.7
occlusion amenable to bypass Sx or angioplasty
 Abnormal <0.7
MANAGEMENT:
INVESTIGATIONS:
WAGNER CLASSIFICATION of DM foot ulcers: This determines management. In
BLOODS general, lower grades respond to ABs and debridement. Higher grades (2-5) require
 FBC – anaemia, TWC with differential count for infx ( leukocytosis, ↑ polymorphic amputation.
neutrophils) Grade Description Treatment
 ESR, CRP (acute phase reactants) 0 Foot at risk, No open wound Patient education
 U/E/Cr – nephropathy Accommodative footwear
 Venous bld glucose (fasting >8mmol/l, random> 11mmol/L) Regular clinical, podiatry exam
1 Superficial ulcer, no penetration Offloading with total contact cast
 Hypocount (TDS including 10pm)
into deeper tissue, no infection Walking brace/special footwear
 HBA1c – normal 4-7% 2 Deep ulcer extending to muscle, Surgical debridement
 Urinalysis – glycosuria, ketonuria (DKA), proteinuria (nephropathy) tendon, bone, ligament Wound care
 Blood c/s if septic Offloading
 (For medical case, please include urine dipstix, lipid profile) Culture-specific Antibiotics
3 Infection of deep tissue with pus, Debridement or partial amputation

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 gangrene (e.g. tendinitis,
osteomyelitis, deep abscess)
4 Forefoot gangrene
5 Whole foot gangrene
Offloading
Culture-specific antibiotics
Lower extremity amputation
Vascular consultation
Major extremity amputation
Vascular consultation
 Ray amputation (open/closed)
 Amputation of digit through metatarsal removing large part of 1 ray
 Open ray – for adequate drainage of pus involving 1 ray, upon healing
with health granulation tissue, split skin graft is used
 Closed ray – if after debridement all infectious tissue has been removed,
close wound by tagging

KING’S CLASSIFICATION o Dry gangrene:

 Pulses usually v bad
Stage Clinical Condition  Gangrene – dry / wet determines  Clean with ethanol, splint and dressing
1 Normal management options
 Prophylactic antibiotics (sides usually get infected)
2 High-risk  If vascular cause consider whether
 Toe may auto-amputate
3 Ulcerated amenable to bypass or not
 Ray amputation can be considered in young pt (in older pts better to leave it
4 Cellulitic
alone after all it’s quite easy to care for dry gangrene)
5 Necrotic
 +/- Hyperbaric Oxygen Therapy (HBOT)
6 Major Amputation
o Wet gangrene: AMPUTATE
o General measures:  Disarticulation at joint (PIP, DIP)
 IV Line for DS/NS at least 1.5L/day to prevent DEHYDRATION  Ray amputation (through metatarsal)
 Intake/output charts – urine output monitoring  Forefoot
 Diabetic chart – Hypocount TDS including 10pm (watch out for  Lisfranc (Tarsometatarsal)
HYPOGLYCAEMIA)  Chopard’s (Midtarsal)
 IV antibiotics (broad spectrum: Augmentin (Gm positive cocci, Gm negative  Syme’s (through ankle) – rare, requires good PT pulse [MCQ]
rods, anaerobes) or Clindamycin (Gm positive, anaerobes, esp for necrotising  BKA – require 30% more energy to walk; bilateral BKA – 40%
fasciitis) + Ciprofloxacin (Gm negative), ONCE c/s results obtained change to  Through knee (Stokes-Gritti)
culture-specific antibiotics  AKA – require 40% more energy to walk
 Daily wound dressing – Chlorhexidine, flush with H202, saline then  Hip disarticulation
Chlorhexidine dressing  Hindquarter amputation (hemipelvectomy)
 Elevate leg if swollen
 Topical antibiotics: o Multidisciplinary approach
 BNP (bacitracin, neomycin, polymycin) powder for Pseudomonas  Orthopaedic surgeon, vascular surgeon
 Bactroban cream for MRSA  Endocrinologist
 Infectious Disease Specialist
o Surgery:  Podiatrist
 I&D for ABSCESS  Diabetic Nurses, Wound-Care Nurses
 Dietician
 Radical debridement for ULCER – all slough excised, exposed tendons  PT/OT
excised (or else become necrotic), in heel whole part of TA exposed must be
 MSW
excised (desloughing)
 Amputation support group
 Heel ulcer / gangrene unless successfully resurfaced = BKA

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POLYTRAUMA
Motor Response (6)
Definition of polytrauma
Obeys commands – 6
 Injury to several (>1) physical regions or organ systems where at least 1 injury or a
Localising to pain – 5
combination of several injuries is life threatening
Withdrawing from pain – 4
 Different from multiple injuries – not life threatening – or a severe life-threatening
Flexion to pain – 3
single injury (barytrauma)
Extension to pain – 2
Trimodal peak of trauma mortality: No motor response – 1
- 1st hour after injury: most patients die
- 1-4 hours after injury: “golden hour” Death usually caused by hypovolemic shock Important to break the figure down into its components, such as E3V3M5 = GCS 11.
- Several weeks later: late complications & multiple organ failure A Coma Score of 13 or higher correlates with a mild brain injury, 9 to 12 is a moderate
injury and 8 or less a severe brain injury.
Mechanism of accident
Deceleration trauma Abbreviated Injury Scale
Fall trauma  An anatomical scoring system.
Trauma resulting from being run over  Injuries are ranked on a scale of 1 to 6, with 1 being minor, 5 severe and 6 an
Crush trauma unsurvivable injury.
Avulsion trauma
Penetrating injury Injury Severity Score AIS Score Injury
Explosion injury  Each injury is assigned an AIS score and is 1 Minor
Thermal injury allocated to one of six body regions (Head, 2 Moderate
Chemical injury Face, Chest, Abdomen, Extremities (including
Radiation injury 3 Serious
Pelvis), External). Only the highest AIS score
in each body region is used. The 3 most 4 Severe
Suspect Polytrauma when: severely injured body regions have their score 5 Critical
- Fall from height > 3m squared and added together to produce the ISS 6 Unsurvivable
- Ejection from vehicle score.
- Death of fellow passenger  The ISS score takes values from 0 to 75. If an injury is assigned an AIS of 6
- Pedestrian/Motorcyclist and car (unsurvivable injury), the ISS score is automatically assigned to 75.
- High speed accident  The only anatomical scoring system in use and correlates slinearly with
- Entrapment, Pinning or Burial mortality, morbidity, hospital stay and other measures of severity.
- Explosion  weaknesses
o any error in AIS scoring increases the ISS error,
Glasgow Coma Scale o many different injury patterns can yield the same ISS score and
injuries to different body regions are not weighted.
Eye Response (4) Verbal Response (5) o the ISS (along with other anatomical scoring systems) is not useful as a
Eyes open spontaneously – 4 Oriented – 5 triage tool.
Eyes open on verbal command – 3 Confused – 4
Eyes open to pain – 2 Inappropriate words – 3
No eye opening – 1 Incomprehensible sounds – 2
No verbal response – 1

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Example o Less inhibitory stimulation of baroceptors in aortic arch & carotid sinus →
Region Injury Description AIS Square Top Three reflex inhibition of vagal activity + ↑sympathetic stimulation to heart & vessels
→ ↑ CO & SVR
Chest Cerebral Contusion 3 9 o (cerebral & myocardial vessels not involved; peripheral
vasoconstriction in cutaneous, skeletal & visceral tissue, preserving
Head & Neck No Injury 0 circulation to important organs (brain, heart & kidneys)
Face Flail Chest 4 16 o Further intravascular loss → distortion of incompletely filled chambers
stimulates cardiac C fibres → reflex vagal slowing of heart rate + vasodilation
Abdomen Minor Contusion of Liver 2 25
→ circulatory collapse
Complex Rupture Spleen 5
o Chemoceptors of carotid sinus & aortic arch becomes more sensitive to ↓PaO2
Extremity Fractured femur 3 at ↑PaCO2 (↓pH) → tachypnea, vagal slowing of HR, sympathetic
External No Injury 0 vasoconstriction in skeletal muscles
o High sympathetic drive causes catecholamine release from adrenals →
Injury severity 50 activation of renin-angiotensin-aldosterone system → further release of
corticosteriod, antidiuretic hormone, glucagon, insulin & human growth
hormone → Na & water retention to incr circulating blood volume & maintain
Physiological response to polytrauma BP
 Cellular compensation by anaerobic respiration
Mediated mainly by: o compensatory anaerobic metabolism → lactic acidosis
Tissue damage
Hypovolaemia Classification of shock
(% of blood Class I Class II Class III Class IV
Manifested by loss) <15% 15-30% 30-40% >40%
Changes in cardiovascular system Pulse pressure ↑ ↓ ↓(SPB↓) ↓
Inflammatory reaction Resp Rate 14-20 20-30 30-35 >35
→ SIRS → ARDS → MOF Urine outpt >30 20-30 5-15 Neg
→ immune suppresion Mental status - Mild anxiety Confused Lethargic/
Changes in metabolic status obtunded
Closely interlinked by the neuroendocrine system.
Inflammatory response 1,2
Hypovolaemia 1
 Any tissue injury generates a local inflammatory response
Systemic compensation by (with/without pre-existing infection) → directed at elimination of dead
 sympathetic activation tissue, foreign invaders & healing
 Renin-angiotensin-aldosterone activation  Greater trauma causes more inflammatory reaction
 Anti-diuretic hormone secretion
o Reduced right heart filling pressure → reduced oxygen uptake  Cellular mediators: PMNs, macrophages & fibroblasts
o Reduced left heart filling pressure 2° reduced pulmonary venous return →  Cytokines: esp IL-1 & TNF-α
reduced cardiac output  Complement system: esp C3 (anaphylactoid reaction) & C5 (PMN
stimulator)
 Prostaglandins: thromboxane, prostacyclins etc

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  Acute-phase reactants Liver synthesis of acute phase reactants such as  Liver → Glycogenolysis & gluconeogenesis
opsonins (CRP), protease inhibitor, haemostatic agents (fibrinogen) &  Anaerobic metabolism → lactic acidosis
transporters (transferin) Skeletal muscle catabolism (-ve nitrogen balance) substrate for liver
 Stress hormones: adrenaline, cortisol release Insulin secretion gluconeogenesis (negative nitrogen balance)
suppressed, glucagon enhances glycogenolysis → overall hyperglycaemia Lipolysis → release of FFA & glycerol (↑TG & LDL)
High resting energy expenditure - General catabolic state
↑ body temperature
Overwhelming inflammatory response
 Both pro-inflammatory + anti-inflammatory cytokines are generated in an
inflammatory response Convalescent state
Major trauma causes systemic release of inflammatory agents Insulin secretion resumes, insulin resistance decreases
Spillover of such inflammatory agents systemically can occur with major trauma Aerobic respiration reestablished
→ Systemic inflammatory response syndrome (SIRS)
→ ARDS /MOF
 In severe states, SIRS can evolve into acute respiratory distress syndrome
(ARDS) or multi-organ failure (MOF)
 SIRS can occur in a non-septic state
 ARDS or lung failure is usually the first to occur followed by other organ
systems damage with hypoxia(MOF).
 MOF can occur in without SIRS
 SIRS can be precipitated by a 2nd time injurious event (eg: surgery or secondary
infection) after the initial trauma → “2-hit” theory of SIRS

Clinical manifestation of SIRS

Defined as presence of ≥2 of the following signs:
 Hyperthermia >38C or hypothermia <36C
 Tachycardia >90bpm
 Tachypnea >20breaths/min or PaCO2<32mmHg
 Elevated/depressed white cell count [>12,000/uL or <4000/uL] or 10%
immature band forms

Initial hypermetabolism
Early hyperglycaemia
 Plasma cortisol increases in proportion to injury with corresponding sympatho-
adrenal response (until adrenal perfusion fails)
 Early hyperglycaemia occurs with increased sympatho-adrenal activity
 Peripheral insulin resistance & depressed insulin secretion with high circulating
catecholamines & glucagon release
 Skeletal glycogenolysis

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 Life and Limb Threatening Conditions  Risk is higher w/ non-operative therapy but is also higher w/ over-
zealous reaming of femoral canal
Life Threatening Conditions:  Multiple trauma w/ major visceral injuries and blood loss (incidence may
Airway be as high as 5-10%)
1. Facial fractures - Cause of death on 3rd day after pelvic fracture is due to fat embolism
a. major fractures of maxilla and mandible - NB. Complications of skeletal traction do not include fat embolism
b. nasal intubation not recommended - Clinical manifestations
2. Larynx injuries  Symptoms usually begin 24-48 hours after injury
a. presents with stridor, hoarseness, crepitus in the neck and rapid respiratory  Major criteria
obstruction  Hypoxia
b. do tracheostomy to secure airway  Altered mental status
 Petechial rash
Breathing  Minor criteria
1. Spinal injury  Tachycardia (>110/min)
a) always assume cervical injury until proven otherwise  Tachypnoea
b) high cervical cord transection paralyses intercostal muscles and diaphragm,  Hypotention
c) resulting in apnoea in minutes to hours  Fever (>38.5 º C)
d) steroids useful if administered within first 8 hrs
 Retinal changes of fat globules or petechiae
2. Chest injuries
 Renal dysfunction
a) Rib fracture: presents with tenderness and crepitus
b) Tension pneumothorax: accumulation of air under pressure in the pleural  Jaundice
space. This develops when the injured tissue forms a one-way valve,  Acute drop in hemoglobin and/or platelets
allowing air to enter the pleural space & preventing the air from escaping  Elevated ESR
naturally.  1 major and 4 minor criteria, plus fat microglobulinemia, must be
i. Air trapped pushes heart and mediastinal structures to the present to formally diagnose fat embolism syndrome
contralateral side, impinging on the contralateral lung. - Treat the hypoxaemia
ii. Hypoxia decreases venous return and cardiac output, causing 4. Thromboembolism (DVT)
hypotension. - develops 5-7 days later, worried about pulmonary embolism
iii. Haemodynamic collapse leads to death. 5. Tetanus
c) Haemothorax - develops 7 days later
d) Pulmonary contusion: parenchymal damage leads to impaired gaseous - administer tetanus toxoid as prophylaxis, especially with lacerations, abrasions,
exchange. dirty wounds and open fractures
e) Flail chest: paradoxical movement of a segment of chest wall, usually
caused by fracture of 3 or more ribs, resulting in injury to heart and lungs, Circulation
leading to pulmonary contusion, VQ mismatch and respiratory distress. 1. Posterior dislocation of sternoclavicular joint
3. Fat embolism 2. Abdominal injuries: liver injuries and splenic rupture
- Results when embolic marrow fat macroglobules damage small vessel 3. Pelvic ring fracture
perfusion leading to endothelial damage in pulmonary capillary beds 4. Hip injuries: may sustain internal bleeding and neuropathies as well. Usually
- Risk factors caused by dislocations and fractures.
 Long bone # [note that the risk is especially high with femoral shaft 5. Femoral shaft fractures: femoral artery involved
fracture and concomitant head injury]

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Limb Threatening Conditions: - lack of oxygenated blood and lack of waste product removal results in pain
 Vascular Impairment and decreased peripheral sensation secondary to nerve irritation
- Haemorrahge: visible or occult - caused by either external restriction of compartment (eg. tight splints, casts,
- Ischaemia: acute interruption of flow of blood to a limb or organ. dressings) or internal increase in compartment volume (eg. haemorrhage,
Anaerobic respiration predominates, leading to lactic acidosis and post-ischaemic swelling)
eventually cell death. - 5Ps: Pain, paresthesia, pallor, paralysis, pulselessness
- Causes: Dislocations or fractures - Complications: muscle necrosis, Volkmann contracture
- Arteries involved: Axillary, brachial, femoral, popliteal - Treatment: Fasciotomy

 Mangled Extremity  Necrotizing Fasciitis

- High energy transfer or crush resulting in some combination of injuries to - insidious soft tissue infection characterized by tissue necrosis
arteries, bones, tendons, nerves and/or soft tissue - organisms spread from subcutaneous tissue along superficial and deep
- Scored using MESS (Mangled Extremity Severity Score) tissue planes, of which the latter causes vascular occlusion, ischaemia and
tissue necrosis.
A) Skeletal/ Soft Tissue Injury - less seen in multiple trauma
 Low energy (stab: simple fracture; pistol/ gunshot wound) 1 - 3 types of NF: Type 1 – Polymicrobial NF
 Medium energy (open or multiple fractures; dislocation) 2 Type 2 – Grp A Strep NF (Flesh-eating bacterial infection)
 High energy (high speed MVA or rifle GSW) 3 Type 3 – Gas gangrene
- presents with fever, chills, erythema and painless bullae formation
 Very high energy (high speed trauma + gross contamination) 4
- treatment: antibiotics and surgical debridement
B) Limb Ischemia
 Pulse reduced or absent but perfusion normal 1*
 Gas Gangrene
 Pulseless; paresthesia, diminished capillary refill 2 - onset: 12-24hrs after injury
 Cool, paralysed, insensate, numb 3* - commonly Clostridial infection, but may be caused by other organisms
C) Shock - decreased oxidation reduction potential promotes advance of a highly
 Systolic BP always > 90mmHg 0 lethal condition
 Hypotensive transiently 1 - less seen in multiple trauma
 Persistent hypotension 2 - present with intense pain and swelling around the wound
D) Age (years) - associated with a brownish discharge and bronze discolouration of wound
 <30 0 - gas (with a musty odour) formation usually not marked
 30-50 1 - important to distinguish from anaerobic cellulitis, which presents with
abundant gas formation that is foul smelling in nature
 >50 2
- distinction between the 2 made by doing a Gram stain of the exudate
* Score doubled for ischaemia > 6hrs - management: fluid & electrolyte replacement, antibiotics, multiple
- Acutely differentiates salvageable and unsalvageable limbs
incisions & fasciotomy, hyperbaric oxygen
- MESS  7 carries a 100% predictive value for amputation
 Osteomyelitis
 Acute Compartment Syndrome - infection of bone and bone marrow
- pressure within a closed muscle compartment exceeds the perfusion - difficult to treat, can be life threatening as well due to septicaemia
pressure - routes of spread: haematogenous, contiguous from a focus of infection
- tissue pressure exceeds venous pressure and impairs blood outflow - bacteria can be inoculated at the time of trauma

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 - present with fever, headache, vomiting, severe bone pain Secondary period (3-8 days)
- treatment: antibiotics and extensive debridement of necrotic tissue
• Continued haemodynamic and resp stability
• Debridement of soft tissue necrosis
Principles in management of orthopaedic injuries in polytrauma
• Eliminate septic foci
Polytrauma is defined as the presence of 2 long bones# plus 1 visceral injury OR 2
visceral injuries OR  3 # • Wound closure
• Joint reconstruction
In polytrauma patients, limb injuries are the commonest and this can take the form of
long bone # or soft tissue injuries. However it is the head and visceral injuries that are Tertiary period
most lethal.
• Patient weaned off intensive care
Management • Physiotherapy initiated
• Primary survey • If patient has developed multiple organ failure, no further operative procedures
• Secondary survey
can be considered at this stage.

Optimal timing of long bone # stabilization in trauma patients in the primary period –
divided into 3 groups of patients:
4 different periods in orthopaedic management of trauma injuries
Polytrauma * Early stabilisation (within 48h) does not improve
• Acute or resuscitation period (1-3 hrs after trauma) without brain survival but it will benefit some patients, e.g. reduces
• Primary or stabilization period (<24hrs) and chest injury the number of days of mechanical ventilation
(? Improves morbidity)
• Secondary or re generation period (3-8 days) * Hence it is preferable to perform long bone
• Tertiary or rehabilitation period (>8 days) stabilisation in polytrauma patients
Brain injury * No evidence that early stabilisation (within 48h)
Acute period Chest injury improves survival compared to late stabilisation

• Decompression of organ cavities (tension pnemothorax, cardiac tamponade)

• Haemorrhage control In definitive treatment of #, in order to preserve normal function, there should be
• If pelvis is fractured, early stabilisation with pelvic clamp is crucial – articular congruity
– stable fixation
Primary period(<24 hrs): stabilization of fractures
– axial alignment with the rest of the extremity
• Decision on temporary and definitive fixation of fractures – restoration of full range of motion
• Limb salvage v.s. amputation (many scoring systems i.e. mangled extremity
Special considerations
scores/Hannover fracture scale)
• Pelvis
• Spine

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• Long bones FRACTURES

Pelvic # General Mx of #
ABCDE
 Ensure that there’s no need for general surgical intervention e.g. intra-abdominal - Assess neurovascular status, beware of compartment syndrome
or retroperitoneal haemorrhage - If hypovolaemic  IV fluids, packed cells, whole blood
 Haemorrhage control with pelvic packing and temporary stabilisation with external Analgesics
fixators and pelvic clamps Preliminary skin traction  to relieve pain, minimize further displacement
How to determine if # is displaced or not: compare continuity of trabeculae lines
Spine #

Urgent spinal stabilisation required (urgent = within 24h of injury) Traction: things to note
Traction can be skin or skeletal
Long bones # Skeletal traction can be with Thomas’s splint or pulley frame or both
 Traction care
Pts with # shaft of femur can lose up to 1L of blood. Femoral shaft fractures
should undergo immediate stabilization of the fracture within 24h of injury Ring pressure (Thomas’s splint)

Immediate stabilization of long bone fractures has many advantages in the Pressure sores: Buttocks, Tendo Achilles, under heel
multiply injured patient, such as improved long-term function, prevention of Common peroneal palsy  weakness of dorsi flexion
deep venous thrombosis and decubitus ulcer, decreased need for analgesia, and Loosening of Steinmann pin
reduction in the incidence of adult respiratory distress syndrome and fat
emboli19
Upper limb fractures dislocations by Lee Yizhi
Recommendations for staged treatment of femoral shaft fractures Fracture Method Remarks
Clavicle Malunion in adults
Sling 3/52 Excellent remodeling in
children
Physio
Scapula body: Associated with 1)rib #
Scapula neck: Sling & physio 2)lung contusion
3)hemo/pneumothorax
ORIF if # dislocatn
Body # by crushing force
AC subluxatn: Partial dislocatn: AC
AC dislocatn: Sling ~1/52 & physio ligaments torn
Complete dislocation: CC
young and active : Arthrodesis, 3/52
ligaments torn (conoid &
rest, physio
trapezoid)
Inactive: Sling & physio
Tenting of skin may cause
Late OA: excision outer 1/3 clavicle
necrosis
Sternoclavicular Anterior: conservative Post dislocatn: Tracheal and
dislocatn Posterior: ORIF vascular compressn
Anterior dislocatn: Reduction under GA X-ray to exclude #
Hippocrates/Kocher’s Axillary n often damaged
95% of shoulder dislocatns

104
 dislocation pressure), cast 6/52
Sling 3/52 Pulled elbow Sling 3/7 or Pain, lateral tenderness,
Supinate + flex elbow refusal to move arm
Physio 9m-6yrs
No X-ray findings
# prox humerus: ORIF Radial head slips out of
Recurrent: Surgery annular lig
Posterior GA Reductn Commonly missed! Radius and ulnar ORIF (plates/screws/rods) Compartment sx, PIN/ AIN
dislocatn: 4% of shoulder dislocatns in adults: Long arm cast 6/52, check x-ray at 2/52 inj, delayed/non/mal-union,
Same as ant dislocatn in PIN
Prox humerus: Neers 1: Sling 6/52 Usually seen in osteoporotic children:
Neers 2: Collar cuff 6/52 pple >50yrs Single forearm ORIF or long arm cast 12/52 Non-union!
Neers 3: ORIF/HemiA Try to conserve head in bone Cross-union
Neers 4: HemiA young pts even with Neers Monteggia’s: ORIF (ulnar plating, reduce radial head), Radial/ PIN palsy (Mont),
All followed by physio 3/4 long arm cast 90o flexion, partial supinatn ECU & EDM inj (Gal)
Shaft of humerus Suspect mets in elderly! ORIF (radial plating, reduce ulnar head), myositis Ossificans, non-
U-slab 3-6/52 + sling Galeazzi’s: long arm cast in supination 6-8/52 union, missed dislocation
Reduction under GA, immobilisatn 6/52
If very unstable, plate/nail
Supracondylar Closed reductn ASAP Cx: Shortening, angular Both in children:
C&C 3/52 then sling 3/52 deformity (gunstock),
Colles’ Undisplaced: Splintage in plaster slab EPL rupture, malunion,
ORIF (dbl plating) in adult for early f(x) decreased ROM
Displaced: MUA (Bier’s/ hematoma median n compression,
Acute: Brachial A inj,
block), below elbow backslab 6/52 in Sudeck’s atrophy, DRUJ
GENTLE physio compartment sx, volkmann’s
neutral or slight flexion, xray @ 2/52 subluxatn, hand shoulder
ischaemia
stiffness
Myositis ossificans
Smith’s (reverse As for Colles’ but with wrist extension
Lateral condyle Undisplaced: C&C 3/52 Cubitus valgus, tardy ulnar
Colles’)
Displaced: ORIF (Kwire) palsy: corrective osteotomy
Barton’s ORIF with buttress plate
Proximal radius Mason 1: C&C 3/52, gentle physio
Radial styloid/ Percut K-wire/ lag screw A/w lunate dislocatn
in adults: Mason 2: ORIF plate & screw
Chauffeur’s
Mason 3: Excision in 48hrs
Undisplaced Below elbow cast (exclude PIPJ) 10/52 AVN, non-union, scaphoid
Mason 3 with Essex L: Prosthesis, splint
scaphoid collapse, OA
2/52, physio
<20o: C&C 2/52 Displaced ORIF, cast 3/52
>20o: MUA, if fail OR. If unstable, IF (K- scaphoid Chronic carpal instability
In children: wire) Trans-scaphoid
perilunate
Olecranon Stable & undisplaced (<2mm + no
dislocation
change in flexion + extend against grav):
C&C 3/52
Displaced: tension band wiring Peri-lunate Closed reduction, cast 6/52 Median n compression
Displaced + comminuted: plate & screw dislocation If irreducible, OR with IF of scaphoid # if Lunate AVN leading to OA
present, CTR and ligamental + capsular
Elbow dislocation MUA (tractn, flexion, push olecranon) Posterolateral most common
repair
then C&C 3/52 or above elbow backslab Cx= brachial A, median
(AIN)/ulnar, stiffness, Metacarpal Undisplaced: Crepe bandage 3/52 and Rotational malunion,
myositis ossificans, finger exercises stiffness
associated #s Displaced: Closed reduction, plaster
slab 3/52, finger exercises
Radial head trauma: MUA (supination, direct Monteggia #, PI Nerve inj
Displaced + unstable: ORIF with K-wire

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Bennet’s (intra- CRIF with precut kwires displc
art # dislocation o Typ 4: complete #, totally
@ base of CMCJ displc
of thumb) Neck of fem, basal (extracap) # o Displc/ Undisplc --> ORIF w
Cxs
Phalangeal Undisplaced: buddy splintage 3/52 Treat open wounds first!! -- shortened, ext rot DHS or Gamma Nail, fixation
o AVN & non-union NOT
Displaced: MUA, plasterslab 3/52 or IF not removed unless pat < 45 y.o
common
with Kwires or pain
Mallet finger Splinting in extension 6/52 Intertroch # o Stable, little frag  DHS w
Game-keeper’s Partial tear: short arm cast w thumb -- shortened, ext rot long plate
thumb spica Types: o Unstable  DHS w long plate Cxs
Gross instability: ligamental repair 1) # line thru mass of Great or Gamma Nail, then non- o Failure of fixation (cutting
Troch, weight bear crutches after 48 hrs out of fixation device) 
2) (1) + separation of Less to 16 weeks coxa vara*
Impt Hip & Lower Limb #s and Ds (plus impt tendon ruptures) Troch, o Alt -->Traction +/- Thomas’s
Type Treatment Remarks & specific Cxs 3) separation of Great & Less splint *if early, bedrest & skeletal
Acetabulum, # o minimal displc/ highly frag  Troch, traction
Cxs 4) 4. w a spiral # down prox
Traction, Hamilton-Russell
o Hemorrhage > 5L fem shaft
o main part intact, fem head displc
o Ruptured urethra, bladder
 ORIF w cancellous screws & Fem shaft # o Traction to overcome pull of
o Bowel injury
plates -- leg is shortened, ext rot, abd  quads & hams
Hip, post. D o Muscle relaxant + Reduce, flex Cxs due to pull of quds & hams o Intramed Nail
-- Hip is flexed, add & int rot knee, hip 900, correct add & int o Irreducible due to in-turned o Alt --> Traction, EF (Ilizarov),
rot, lift fem head into labrum or bony frags in Plating
acetabulum acetabulum
o OR if irreducible o # (fem head, NOF, patellar, o Fem & Tib #  Cx rate high,
o ORIF if a/w #s elsewhere fem shaft) early mobilisation by Intramed Cxs
Hip, ant. D o Sciatic nerve palsy Nail o Hypovolemic shock
-- Hip is abd, ext rot o AVN due to tearing of o Metastatic #  Intramed Nail o Fat embolism
o Muscle relaxant + Reduce, flex capsule + packed cement to relieve pain o Delayed Union, Non-union
knee, hip 900, correct abd & ext o 20 OA & give support  esp. conservative
rot, push down, convert to post. o Recurrent D o Fem shaft # w nerve palsy  o Mal-union lat. Angulation
D, lift fem head into acetabulum o Myositis Ossifcans (post exploration w repair + IF  Tx = osteotomy
exploration or D a/w head o Fem neck & prox shaft # o Limb Shortening
injury) DHS + long Plate o Knee stiffness  due to
Fem epiphysis, slipped o IF w screws + Manipulate if slip o Fem shaft & patellar #  close quads tethering, knee jt
-- fem shaft move up & ext rot on > 30% + epiphyseal closure o AVN nailing for both, mobilise knee invovlement or prolonged
epiphysis o Subtroch Osteotomy if o Involvement of Other Hip early immobilisation
epiphysis closed (chronic) o Open # deribement + IF o Infection
o Open #, IIIB,C conservative
Neck of Fem (intracap) # or EF
Tx principles
-- shortened, ext rot
o Undisplc --> CRIF o Young (< 50 y.o.)  CRIF Fem Supra, Uni, T & Y o Child supracondylar  plaster
-- 1. subcapital, 2. transcervical
o Displc --> Arthroplasty o Elderly --> arthroplasty condylar # o Others  IF for good reduction
-- osteoporosis impt factor
o unfit for multiple Sx or badly & permit early mobilisation
Garden Classification
o Typ 1: incomplete #,
displc, typ 4, avn & non-union Cxs o If displc, grossly comminuted 
likely --> Hemiarthroplasty/ o AVN  disruption of conservative w traction
trabeculae angulated
Total hip replacement w/o arterial ring @ base of neck
o Typ 2: complete #, trabeculae
tryring CRIF o Non-union  typ 3 & 4,
disrupted but NOT angulated
bone graft (young), Patellar D o CR, plaster backslab x 3/52,
o Typ 3: complete #, fem head knee exercise Remarks
arthroplasty (elderly)
rotated, trabeculae disturbed,

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Patellar #
Tibial tubercle, avulsion
Quads tendon, rupture
Patellar ligament, rupture
Tibial plateau, #
o all involve articular surface
o key is to get knee f(x) vs pretty
x-ray
o knee exercises ASAP
o “bumper #”
o commonly lat. tibial condyle
Tibia & Fibula, #
o Usu. # both, esp. adult
o commonly open
o usu. spiral #
o vertical # --> cylinder cast 6/52
w crutches during first 2/52,
physio after cast removal
o horizontal, undisplc # --> as of
above
o horizontal, displc # --> 1. sight
communition: ORIF, 2. limited
damage to patellar: partial
patellectomy, 3. major damage:
patellectomy, repair quads
insertion & lateral expansions
o CRIF (w screw)
o ORIF (risk of premature
epiphyseal fusion in child)
o Tendon reattachment, plaster
cast, quads exercises at 2nd
week, weight bear at 4th week,
felxion at 6th week
o As of above
o minimally displc --> aspirate
hemarthrosis, compression
bandage, CPM & active
exercise, weight bear after 6/52
o comminuted--> aspirate,
compression bandage, sk
traction, CPM & exercise
crutches after 6/52
o depressed # --> CR or ORIF,
active exercises ASAP, cast-
brace after 2/52
o closed, minimally displc --> full
cast x 12/52 (upper thigh to MT
necks, knee slight flexion, ankle
at 900), exercise foot, ankle,
knee ASAP
o closed, displc --> MUA (IF
when CR fails), full cast x
12/52, exercise ASAP
o comminuted --> EF x 6/52 +
partial weight-bear, then f(x)al
brace
o open --> Ab ASAP, debride,
clean, leave open (above grd II),
EF to stabilise, WI, suture or
graft when granulate
Injuries to patellar & extensor
apparatus of knee
(patellar #, rupture of quads
tendon, rupture of patellar
ligament, avulsion of tibial
tubercle) due to:
1) direct force on knee
2) violent contraction of quads
Every knee injury, exclude:
o damage to extensor
apparatus
o lateral D of patellar w
spontaneous reduction
o torn ligaments
o torn mensici
Cxs
o Compartment syndrome
o Valgus deformity
o Joint stiffness
Cxs
o Infection
o Vascular injury (prox #
damage pop artery)
o Compartment Syndrome
o Delayed, Non-union -->
Intramed Nail + bone graft
indicated
o Malunion --> angulated -->
osteotomy
Ankle, ligament injury
o partial/ complete tear of lateral
ligament
o bruising, swelling, tenderness
o painful passive inversion
o complete tear --> excessive
movement
Ankle #
o normally talus seated in
mortise
o one or both mall can be #
o eversion + ext rot = oblique #
of lat mall (pushed off),
transverse # of med mall
(pulled off); vice-versa for
inversion
Distal tibial & fibular
epiphyses, #-separation
o physeal injury
Calcaneum #
o fall from height
o calcaneum driven up against
talus
o flattened Bohler’s angle
o check hip, pelvis, spine for #
o extra-art --> involve posterior
part, calcaneal processes
o intra-art --> oblique # line, run
to superior articular surface
o partial --> crepe bandage,
activity ASAP
o complete --> plaster Cxs
immobilisation or operative o Adhesions
repair o Recurrent subluxation
o 1 mall # --> reduce, cast x 6/52
Tx principles
(below knee), IF with screw if
o reduce to restore shape of
frag large
mortise
o 2 mall #, below tibiofibular jt --
o plaster x 8/52
> CR, +/- IF ,cast
o 2 mall #, above tibiofibular jt -->
Cxs
unstable, IF with screw for frag
o Joint stiffness
& plate for fibula, +/- transverse
o OA (not common)
screws between tibia & fibula
o Salter-Harris 1,2 --> MUA, full
cast x 3/52, below knee cast x Cxs
next 3/52 o Mal-union (valgus)
o Salter-Harris 3,4 (undisplc) --> o Asymmetrical growth (# thru
as above, re x-ray 5d after to epiphysis may cause fusion
ensure good reduction of physis)
o Salter-Harris 3,4 (displc) --> o Shortening of leg
ORIF, below knee cast x 6/52
o undisplc --> exercise ASAP, Tx principles
bandage after swell subside, o elevate leg + ice packs -->
nwb crutches x 6/52 decrease swelling
o displc, avulsed tuberosity --> o x-rays, CT scans (better
CRIF, immobilise in equinus views)
(relieve tension of tendon Ach),
wb after 6/52 Cxs
o displc, intra-art --> ORIF + o Broadening of foot
bone grafts, splint & elevate, o Talocalcaneal stiffness -->
exercises ASAP, nwb crutches subtalar arthrodesis or triple
after 3/52, wb after 12/52 arthrodesis
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BONE & JOINT INFECTIONS  Chronic OM: pus discharges through cloacae (perforations) in the involucrum

Types: Clinical features

1. Acute haematogenous osteomyelitis  Pain, malaise, fever, toxaemia
2. Subacute haematogenous osteomyelitis  Cellulitis, swelling, oedema, erythema, warmth, tenderness, ROM
3. Post-traumatic/operative osteomyelitis
4. Chronic osteomyelitis Investigations
5. Acute suppurative arthritis  X-ray: normal in first 10 days. Later, rarefaction of metaphysis & periosteal new
6. TB infxns of bone & joints bone formation. Sclerosis when healing occurs
 FBC: leukocytosis
Waldvagel Classification:  ESR 
A – haematological spread  Blood C/S
B – a/w wound  Bone scan (usu. technetium or gallium radioisotopes used): turns + before x-ray
C – contiguous spread from local infection changes appear. For doubtful cases.
Complications
3 things to consider:
 Spread – septic arthritis, metastatic OM (i.e. to other bones)
1) type of organism A = sound bone  Growth disturbance – shortening / deformity if physis is damaged
2) site of infection B = new bone  Chronic OM
3) host response (immunocompromised?) C = involucrum
D = cloaca Management
Principles of treatment E = sequestrum
 Empirical antibiotics first, changing when C/S returns
5. Rest affected part - Adults/older children – flucloxacillin & fusidic acid (IV 3/7, PO 3-6/52)
6. Provide analgesia & general supportive measures - Children <4YO or G negative organisms cultured – Cephalosporin
7. Initiate antibiotic treatment  Analgesia
8. Surgical debridement (of pus & necrotic tissue)  CRIB & splintage (+ traction in upper femur OM to prevent hip dislocation)
 Drainage for subperiosteal abscess or persistent pyrexia & local tenderness of >24h
ACUTE HAEMATOGENOUS OSTEOMYELITIS
Common organisms: SUBACUTE HAEMATOGENOUS OSTEOMYELITIS
 Adults: Staph. Aureus <1YO: GBS, Staph A, E Coli  Milder form of acute OM – less virulent organism or better patient resistance
 Children <4YO: H. influenzae 1-16YO: Hib, Staph A, Strep, Enterobacter
 Common sites: distal femur, prox & distal tibia
 Hx of sickle cell anaemia: salm onella Adults: Staph, Strep, Pseudomonas, E Coli
 PT: child/adolescent
Site:  X-ray: Brodie’s abscess (small oval cavity surrounded by sclerotic bone) (DDx:
 Adults: anywhere, esp thoracolumbar spine. Adults are usu immunocompromised osteoid osteoma)
 Management: drainage & ABx cover
 Children: usu. metaphysis of growing long bone. Growth plate limits spread
towards epiphysis.
 Infants: risk of epiphyseal extension, jt involvement & growth disturbance.
Pathology
 Infection spreads to form subperiosteal abscess
 Bone dies, forming a sequestra encased by the involucrum (periosteal new bone)

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POST-TRAUMATIC / OPERATIVE OSTEOMYELITIS
Investigations
 Risk factors: DM, old age, immunosuppressed, steroid Rx, chronic disease, obese,  Blood C/S
multiple ops at same site, difficult / long ops, haematoma formation, tight dressings,  Joint aspiration, pus microscopy & C/S
wound tension  X-ray: widened joint space & soft tissue swelling; subarticular bone destruction if
late stage
 Organism: Staph. Aureus
 U/S: joint effusion
 Opley classification:
Complications:
A Early – 1 mth
 Dislocation
B Intermediate – 1mth to 1 yr
 Epiphyseal destruction & pseudoarthrosis
C Late – >1 yr
 Growth disturbance – shortening or deformity if physis is damaged
 Management:  Ankylosis – if articular cartilage is eroded
 Clean surgical technique  Sepsis – 25% if untreated
 Thorough debridement
 Drainage Management:
 Antibiotic cover  Joint aspiration
 External fixation of unstable/unfixed #  Systemic antibiotics
 Splintage
 Drainage and joint washout
CHRONIC OSTEOMYELITIS  Rehab: increasing movement when joint is not inflamed. If cartilage has been
 Sequelae of acute haematogenous, post-traumatic & post-op OM destroyed, keep immobile to allow ankylosis to occur
 Recurrent flares of acute infxns – pain, pyrexia, erythema, tenderness, discharging
sinus, non-healing ulcer TUBERCULOSIS
Investigations: Main TB entities in orthopaedics Common sites (wt bearing joints)
 X-ray: bone rarefaction surrounded by sclerosis  sequestra  TB spondylitis  Spine (50%)
 Bone scan: to reveal hidden foci of infxn  TB osteomyelitis  Hip
 TB arthritis  Knees
Management:  TB tenosynovitis
 Incise abscess, remove necrotic bone, fill with bone chips  TB myositis
 Antibiotics – fusidic acid or cephalosporins
 Sequestrectomy Pathology
 Spreads to skeleton by haematogenous seeding
ACUTE SUPPURATIVE ARTHRITIS  May spread to articular surfaces causing jt destruction and fibrosing ankylosis
Common organisms:  May spread to soft tissue to form subacute abscess, which may form a chronic
 Adults: Staph. Aureus discharging sinus
 Children <4YO: H. influenzae Clinical features
 TB symptoms: fever, wt loss, night sweats etc
Clinical features
 Acute monoarthropathy – usu. hip in children & knee in adults  Joint symptoms: chronic course, pain, swelling, wasting, synovial thickening,
ROM, joint stiffness and deformity
 Swelling, erythema, warmth, tenderness, fluctuation, ROM, pain, spasm

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 Spine: vertebrae may collapse causing a Pott’s gibbus (usu. thoracic)
Investigations:
 X-ray: soft tissue swelling, rarefaction of bone, joint space narrowing &
irregularities w bone erosion on both sides of joint, periarticular osteoperosis
 Synovial biopsy
 ESR , Mantoux test +
Management:
 Anti-TB drugs – as for pulmonary TB (isoniazid, rifampicin, pyrazinamide - RHZ)
 Rest, traction, splintage, operation
 If articular surfaces are destroyed – Immobilize joint
 Long term – Joint arthrodesis or replacement

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OSTEOPOROSIS  If both Z & T-scores are abnormal, it means patient has secondary osteoporosis
DEFINITION
 A bone disease characterized by INDICATIONS FOR BMD SCREENING OF OSTEOPOROSIS:
o Decreased bone mass  Previous fragility fracture
o Weakening of microarchitectural structure of bone  Patients with strong risk factors
 Leading to  High risk postmenopausal women as categorized by OSTA
o Increase in bone fragility and hence fractures, commonly at  Radiological evidence of osteopaenia / vertebral deformity
1. Distal radius (Colles’)  Women who are considering prevention therapy for osteoporosis
2. Spine (compression fracture)  Monitoring of treatment
3. Hip fracture (NOF or intertrochanteric)
4. Head of humerus
RISK FACTORS
5. Pubic rami
 “Little of normal bone” – Prof S Das De Osteoporosis Self-  Use age – weight = x
assessment Tool  If x >20, measure BMD
for Asians (OSTA)  If x = 0-20, measure if other risk factors present
PATHOGENESIS
 If x <-20, low risk, no need to measure unless positive
 Loss of balance between bone resorption and bone formation. history of fragility fracture
 Bone matrix manufactured by osteoblasts. Bone resorption by osteoclasts. Nonmodifiable  Previous adult fracture history
 Each cyle of remodelling takes abt 4-6 months. Annual rate of turnover is abt 4% for  Previous family history fracture
cortical and 25% for trabecular bone. [bone loss occurs within 2wks; bone formation Modifiable  Weight (lean people predisposed to osteoporosis)
takes 3 mths]  Drugs – smoking, alcohol (both a/w nutritional def),
 Bone size increases from childhood to adolescence and peaks at ard 35 yrs. From then steroids, thyroxine, anticonvulsts
on, decrease at 0.3%/yr for men and 0.5%/yr for women till 50 yrs old. Menopause  Early menopause (<45YO)
for women (50-60 yr old) causes decrease at 3%/year due to decrease in oestrogen; it  Comorbidities – hyperthyroidism, hyperPTHism, Cushing
subsequently normalises again at 0.5%/yr. syndrome, liver disease, COPD, CRF, RA, organ
 Wolff’s law - Bone is deposited and resorbed in accordance with the stresses placed transplant etc.
upon it.  Immobilization
 Lack of physical exercise
LAB DEFINITION, BY BONE MARROW DENSITY AT THE HIP
BMD T-score Definition INVESTIGATIONS
>-1 Normal  X-Ray if applicable
-1 to -2.5 Osteopaenia o Vertical trabeculae bears the most weight of stress hence disappear last.
<-2.5 Osteoporosis Osteoporosis got prominent vertical trabeculae but no horizontal.
<-2.5 + fragility fracture Severe osteoporosis o Picture-framing of vertebrae – accentuation of cortical outline
 T-score is the number of s.d. below the average for a young adult at peak bone o Codfish appearnace of vertebrae due to concave end-plates
density (based on BMD of 25yo Caucasian females) o Pathologic fractures –vertebral compression fracture (ant height of vertebrae is
 Z-score is the number of s.d. below an average person of the same age. 80% or less of the posterior height) if multiple of spine -> Dowager’s hump
 If Z-score is normal but T-score is not, it means patient has primary osteoporosis o Singh’s index for trabeculae at hip jnt – grade I (only one present) to grade VI
(i.e. senile or post-menopausal osteoporosis) (all present)
 Ca/ PO4 to exclude osteomalacia (normal in osteoporosis, low in osteomalacia)

111
 FBC, ESR, U/E/Cr, Vit D Selective Estrogen Raloxifene
 Others if suspect underlying associated disease Receptor (EVista)
o TFT; LFT; tumor markers and myeloma screen (FBC, ESR, bone marrow Modulators (SERMs)
aspiration, urine electrophoresis, skull X-ray)
oral
 Measurement of BMD
o Dual energy X Ray absorptiometry (DEXA) of hip for diagnosis, spine for Synthetic Steroid Tibolone
monitoring of treatment is the investigation of choice (Livial)
 Rationale for dual energy: to take X-ray of soft tissues and of bone at
different penetrance levels Others  Calcitonin
o Other rarely done investigations include U/S heel/ tibia, quantitative CT scan  Calcium & Vit D
Agonist in bone; antagonist in breast & uterine cells
Induces osteoclast apoptosis
Hot flushes, sweating, leg cramps
Increased risk of clots e.g. DVT, PE
Teratogenic
Has also been shown to be protective against breast ca
Has progestogenic and some androgenic properties as
well as oestrogenic effects
 Also has value in controlling hot flushes
 Intermittent PTH Rx
 Cyclical etidronate

MANAGEMENT:
BMD T-score Action
>+1 Re-BMD in 5y
1 to -1 Re-BMD in 2y
-1 to -2.5 Medical prevention, F/U BMD @ >1yr
< -2.5 + fragility fracture Medical treatment, F/U BMD @ >1yr
Lifestyle measures, to be encouraged in everyone
Nutrition Age Calcium Vitamin D
11-18 1000mg 400IU
18-65 800mg 400IU
>65 800mg 800IU
Exercise Weight bearing exercises (3x30min/wk)
Smoking, alcohol
cessation
Fall prevention Remove hazards (+ install bars, anti-slippery mats etc.)
Treat comorbidities predisposing to fall e.g. cataracts
Correct postural hypotension
Medications available
HRT Not to be used if osteoporosis is the only problem
Use only if other indications e.g. unbearable hot flushes
Switch to other treatments when symptoms abate
Bisphosphonates Aledronate  Similar in structure to pyrophosphate; osteoclasts
(Fosamax) ingest it  apoptosis
 Hypersensitivity
 Oesophageal reaction e.g. heartburn
 Take medicine sitting up, keep upright for 30min after
swallowing, wkly dosing
 Overuse will result in SSBT (severe suppression of
bone turnover) --- bone would hence be brittle

112
RHEUMATOID ARTHRITIS PATHOLOGY
DEFINITION
- 3 stages: Synovitis, Destruction, Deformity
Systemic chronic inflammatory disorder of unknown cause that affects the
peripheral joints in a symmetrical fashion
- Synovial cell hyperplasia - Erosion of articular - Deformity and loss of
& proliferation cartilage and function
EPIDEMIOLOGY
- Dense perivascular subarticular bone o Fibrosis/Ca2+ of pannus
- Prevalence: 0.8% of adult population inflammatory infiltrates o Direct invasion by o Fibrous/Bony Ankylosis
- Gender: 3x more common in females - ↑ vascularity pannus o Destruction of articular
(angiogenesis) o Degradative cartilage, subarticular
- Age of onset: 80% of patients develop it b/w 35 to 50 years old bone, tendon, ligaments,
- Neutrophils & enzymes secreted by
- Morbidity: High level of functional impairment neutrophils capsule
aggregates of organizing
If untreated, 20-30% will become permanently work-disabled fibrin on synovial surface o ↑ osteoclastic - P/E:
within 3 yrs activity in o Z-deformity of thumb
- P/E: Fusiform swelling @ o Swan-neck deformity
- Mortality: Related mainly to extra-articular manifestations underlying bone
PIP jts o Boutonneire’s deformity
- Tendons, ligaments, jt o Ulnar deviation @ MCP
PATHOGENESIS capsule also destroyed jts
- Cause unknown
- Postulated to be response of a genetically susceptible host to an infectious agent

CLINICAL PRESENTATION
SYMPTOMS / HISTORY TAKING
1. Joint involvement: typically affects PIP, MCP, wrist, elbow, shoulders, knees,
- HLA-DR4, HLA-DR1 - Persistent infection of articular ankles, feet
- Twin studies structures/retention of microbial
o Monozygotic twins: 30% pdts in synovial tissues
- Pain Insidious onset
concordance rate - Stiffness: Early morning stiffness at jt, last for >1hr before improvement
- Alterations of jt components by
o Dizygotic twins: 3% microorganism/response to - Swelling Symmetrical, Red inflamed, warm to touch
microorganism - Deformity Progressive in nature
- Molecular mimicry - ↓ ROM
 Usually periods of relative quiescence with periods of flare

2. Extra-articular manifestations (occurs later in the course of the disease)

3. Constitutional symptoms
- Fever
- Fatigue, malaise
- Weight Loss

113
4. Associated with Palm
- Sjogren’s Syndrome: Dry eyes, Dry mouth, Recurrent chest infection - Palmar erythema
- Felty’s Syndrome: Splenomegaly, Leg ulcers, Recurrent infections, LN, Dorsum
Wt loss - Wasting of the interossei, best
seen in 1st dorsal web space
5. Loss of function
- Class 1: Normal functional ability
- Class 2: Normal functional ability despite discomfort
- Class 3: can only perform a few tasks of work/self care
- Class 4: Complete/ Almost complete incapacity -
FEEL Palpate over swollen joints to detect warmth & tenderness of
acutely inflamed joints
6. Previous treatment history - Palpate the elbows for rheumatoid nodules (present in 25% of
- Medications: Anti-inflammatory drugs, Steroids (assess for adverse SEs) patients). You may also find rheumatoid nodules at other pressure
- Intraarticular injections areas, e.g. pulp of the fingers & radial side of index finger
- Previous operations MOVE Functional assessment
- Unbutton a shirt
7. Family history
- Write with a pen
8. Social History Hand exam (median n. for any carpal tunnel syndrome**)
- Occupation OFFER Examine other joints in the body that are affected by RA
- Family setup Examine the rest of the patient for extra-articular manifestations of RA
- Caregiver Ask patient how the condition affects his/her life

Extra-articular manifestations:
PHYSICAL EXAMINATION
Ophthalmic Sleritis
LOOK Wrist Episcleritis
- Volar subluxation Keroconjunctivitis sicca
- Radial deviation Respiratory Pulmonary effusion
- Piano key sign – subluxation of DRUJ causing head of ulna to Pulmonary fibrosis
pop up on dorsum of the wrist where it can be jogged up & down Cardiac Pericarditis
Thumb Vascular Vasculitis
- Z-thumb deformity (flexion of IPJ and hyperextension of MCPJ) Reticulo-endothelial Lymphadenopathy
Splenomegaly
Fingers Felty’s syndrome
- Ulnar deviation of the fingers, involving the more lateral digits in
Neurological Multifocal neuropathies
the more advanced cases
Carpal tunnel syndrome
- Volar subluxation at MCPJ, most commonly over index & middle
fingers
- Swelling of PIPJ
- Swan-neck deformity (flexion of DIPJ, hyperextension of PIPJ)
- Boutonniere deformity (hyperextension of DIPJ, flexion of PIPJ)

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American College of Rheumatology Diagnostic Criteria  C-spine: Atlanto-axial subluxation
(fulfill 5 out of 7 criteria)
1. Morning stiffness >1 hr MANAGEMENT
2. Affects at least 3 out of 14 joints with soft tissue swelling or First 4 must be
present  Goals: Control disease activity
fluid (PIP, MCP, Wrist, Elbow, Knees, ankles, MTP) continuously Prevent/ control joint damage
3. Arthritis of hand joints for 6 weeks Prevent Loss of function
4. Symmetrical joint swelling Control Pain
5. Subcutaneous nodules Maximise quality of life
6. Positive Rheumatoid factor test
CONSERVATIVE MANAGEMENT
7. Radiological changes consistent with RA
1. Non-pharmacological:
 Rest
INVESTIGATIONS  Patient education
BLOODS  Physiotherapy
1. FBC Anemia, Thrombocytosis, WBC & D/C: eosinophilia, exclude  Occupational therapy
infection 2. Pharmacological: (early aggressive treatment, Esp those w poor prognostic
2. U/E/Cr Assess renal function before starting treatment factors)
3. LFT Assess liver function before starting treatment  NSAIDs: Indomethacin, Diclofenac, Naproxen
4. ESR,CRP Inflammatory markers = indicate active disease o Symptomatic treatment: anti-inflammatory, analgesia
- Used for disease progression monitoring, treatment response o Does not alter disease progression
o ADRs: PUD
5. RF Anti-IgG autoantibodies (65-85% of patients) o Contraindication: Renal impairment
- Not diagnostic (present in healthy pple, SBE, TB, Viral infections)
- Prognostic: high titre = poor prognosis  Steroids: Prednisolone
o Symptomatic treatment: anti-inflammatory
6. ANA Positive in autoimmune disease o May help slow disease progression/joint damage
- Not diagnostic (present in SLE, Scleroderma, Sjogren’s,
 Disease modifying anti-rheumatic drugs (DMARDs): Methotrexate, Gold,
Raynaud’s disease)
Hydroxychloroquine (See Table)
JOINT ASPIRATION o Slow down disease progression of bone & cartilage destruction
o Take 1-6 months to be effective
1. Analysis of synovial fluid: Straw coloured, cloudy, flecks of fibrin
o Monotherapy/Combination
Large numbers of WBCs , esp neutrophils
 Anti-TNF α: Etanercept, Abcliximab, Infliximab
2. Biopsy: Histological features non-specific and not diagnostic
SURGICAL MANAGEMENT
IMAGING
1. Surgical Release for nerve entrapment syndromes (eg. Trigger finger, CTS, De
X-rays: disease monitoring, treatment response
Quervain’s)
 Early: Periarticular osteopenia
 Later: Marginal bone erosions 2. Synovectomy
 Advanced: Articular destruction, Joint deformities  For persistent synovitis > 6 mths

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  Symptomatic relief of pain and swelling
 Restore ROM
3. Arthroplasty
 Mainly for knees, can also be done for hip, shoulder, elbow
 Pain relief, correction of deformity, Stability and alignment, Preserve ROM
4. Others:
 Tendon repair
 Osteotomy: genu valgum
 Arthrodesis: mainly triple arthodesis of ankle
o surgical fusion of joint to give stability, pain relief, deformity correction

DMARDS SUMMARY TABLE

DMARDs Pharmacology Toxicity Investigations
Methotrexate - Recommended as initial - N+V - Baseline FBCs,
DMARD - Mucosal ulcers U/E/Cr
- Rapid onset of action (1- - Liver cirrhosis, ↑ LFTs - LFTs, Hep B/C
2mths) - Interstitial pneumonitis status
- Retards progression of - Severe BM suppression - CXR
radiological erosions
Hydroxy- - Rash - Eye
chloroquine - Abdominal cramps examination (6-
- Diarrhoea 12 mthly)
- Retinal pigmentation
Sulfasalazine - Faster onset (1-3 mths) - N+V - FBC, LFTs
- Retard Radiographic - Headache
progression - Rash
- BM suppression
Gold - Oral: Slow onset (6mths) - Rash - FBC
- IM: Faster onset (weekly - Ulceration, mucositis - UFEME,
injection of 22 wks) - Nephrotic syndrome U/E/Cr (at
- Pancytopenia every injection)
Leflunomide - Alternative to MTX - Diarrhoea - FBC, U/E/Cr
- Slows radiographic - Alopecia
progression - Headache
- Immunosuppression - LFTs, Hep B/C
- ↑ LFTs status
*Blue boxes: teratogenic

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ANKYLOSING SPONDYLITIS o a/w loss of spine extension
 Costovertebral & costotransverse joint involvement: difficulty breathing / chest
Definition: chronic, multi-systemic inflammatory disorder of the sacroiliac joints and
tightness
axial skeleton (characterised as a seronegative spondyloarthropathy)
 Predilection for SI joints & spine  progressive stiffening & fusion of axial skeleton
 Temporomandibular joint involvement: decreased ROM / jaw pain
 Extra-articular manifestations
EPIDEMIOLOGY Eye Acute anterior uveitis 2C Cauda equina syndrome
 15-25 YO Iritis Cardiac conduction defects
 Male : Female = 4:1 Spinal Myelopathy due to atlantoaxial 6A Anterior uveitis
Mnemonic: P-A-I-R
 HLA-B27 cord subluxation Atlantoaxial subluxation
 First degree relatives at risk of psoriatic arthritis, IBD & Reiter’s syndrome Cauda euina syndrome Aortic regurgitation
Heart Aortic regurgitation Apical lung fibrosis
PATHOLOGY Cardiac conduction defects Amyloidosis
 Enthesitis: subchondral granulation tissue that erodes the joint & is replaced Archilles tendonitis
Lung Apical pulmonary fibrosis
gradually by fibrocartilage and then ossification (occurs in ligamentous capsular
Systemic Amyloidosis
attachment sites to bone)
Osteoporosis
 In the spine, this occurs at junction between vertebral bodies and annulus fibrosus
of IV discs. Outer fibres of the discs eventually undergo ossification 
syndesmophyte is formed  progresses to the characteristic bamboo spine INVESTIGATIONS
ESR Raised
SIGNS Rh factor Negative
 Decreased lumbar lordosis FBC Normochromic anaemia
 Kyphosis ECG Conduction defects
 Restricted lumbar spine movement in all planes Synovial fluid Not depressed, decreased viscosity, leukocytosis
 Restricted chest expansion : <5cm at 4th intercostal space complement
 Extra-articular manifestations – Iritis, uveitis, myelopathy, AR, arrhythmia, X-ray  Squaring of vertebrae
pulmonary fibrosis  Vertebral fusion
 Romanus lesion: shiny corners of vertebrae due to sclerosis
 Bamboo spine – due to syndesmophyte formation
SYMPTOMS
 Erosion & sclerosis at anterior corners of vertebrae
 Recurrent lower back pain
 Facet joint fusion
o Insiduous onset
 Atlantoaxial dislocation
o For >3 months
 SI joint – bony erosion, marginal sclerosis, +/- fusion
o Often begins unilaterally & intermittently
 Whiskering – calcification of tendons attached to ischial tuberosity
 As the disease persists, it becomes more persistent & bilateral &
 Osteoporosis / OA changes ( jt space, sclerosis, ossified bone
progresses more proximally
cysts)
o Dull character
 Apical lung fibrosis
o Poorly localised to the buttock/thighs
 Costovertebral jt involvement
o Symptoms worse in the morning & after periods of inactivity, relieved with
Bone scan Sacroilitis & spinal involvement
exercise

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GRADES OF SACROILITIS GOUT
I Widening of joint Inflammatory arthritis caused by cellular reaction to uric acid crystal deposition
II Joint erosion (monosodium urate)
III Sclerosis on both sides Pathophysiology – accumulation of uric acid/urate in blood and tissues.
IV Ankylosis Supersaturation of tissues  urate crystals precipitate into crystals.
Rome criteria NY criteria  Causes – Hyperuricemia (incl renal impairment) Alcohol ingestion. Dietary excess
Bilateral sacrolitis > grade I + any of the Bilat Sacroilitis > grade I (especially sardines, kidney, liver, meat extracts). Thiazide diuretics. Salicylates.
following: OR Unilat Sacroilitis > grade II Lead poisoning.
 LBP + stiffness > 3 mths not AND any of the following:  Acute changes in the level of uric acid cause gout (not high levels)
relieved by rest  LBP of inflammatory nature  Hyperuricemia is found in 90% in individuals with gout, but also found in patients
 Thoracic pain or stiffness   lumbar spine movt in sagittal & taking diuretics and even in those taking low doses of aspirin
  lumbar spine ROM frontal planes  Most individuals with hyperuricemia do not have gout, but if high uric acid are not
  chest expansion treated, 90% develop gout in 30 yrs
  chest expansion
 Hx of uveitis Epidemiology – 90% male predominance; men > 20yo & post-menopausal women
Presentation –
MANAGEMENT  Redness, swelling, heat, tenderness and interference with range of movement
Aims: typically most intense in 24 hrs, tenderness exquisite.
 Relieve pain & stiffness  Monoarticular, 1st MTP jnt most commonly affected – podagra. Knee and ankle jnts
 Maximise skeletal mobility next most commonly affected.
 Avoid development of deformities  Tophus deposit may exist in the antihelix of the ear or subcut regions e.g.
olecranon, archilles tendon, fingertips, cornea
CONSERVATIVE  Other findings – fever, chills, carpal tunnel syndrome
Lifestyle modification Exercise, ensure good posture  May progress to chronic arthritis or even present as chronic arthritis
Pharmacotherapy DDx: septic arthritis, pseudogout (tends to affect larger jnts and women more), bursitis,
- NSAIDs (usually Pain relief (ask abt renal function, hx of GI bld,
RA if polyarticular gout affecting finger, haemarthrosis
indomethacin) coagulant Rx)
- Sulphasalazine For persistent peripheral arthritis. Not useful for Lab studies-
axial disease  Identification of causative crystals or classic radiographic findings
Radiotherapy If drug therapy is ineffective  Joint Aspiration: Negatively birefringent needle shaped urate crystals on polarising
Local corticosteroid injection For plantar fasciitis & enthesopathy examination. Synovial fluid WBC count usually elevated. (pseudogout – rhomboid
Systemic steroids For acute iritis shaped crystals)
SURGICAL  Blood Investigations:
Hip stiffness Total hip replacement o FBC: WCC often elevated, with left shift during acute attacks
Spine flexion deformity Vertebral osteotomy o ESR elevated during acute attacks.
o Hyperuricemia present in 95% of cases but not diagnostic.
 Once acute gout episode controlled, 24-hr urine uric acid lvl also assessed for
choosing medication to control the associated hyperuricemia

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 Imaging
o Punched out lesions / rat-bitten / lytic areas with overhanging edges(after 1st
year of disease)
o Erosion with joint space preservation is typical.
Treatment – to relieve pain, prevent disease progression and prevent tissue
deposition of uric acid
 Treatment of the acute attack
o NSAID (e.g. naproxen 500mg twice daily or indomethacin 50mg three times
daily) at full dosage (2-5 days), reduce to1/2 or 1/4 once attack controlled
o Low dose NSAIDs for the 1st 6-18 mnts Mx of underlying hyperuricemia - ppt
gouts in up to 50% of patients
o Avoid aspirin – paradoxical(increases urate absorption)
o Oral colchicine (anti-inflammatory) frequently causes unpleasant side-effects
 Treatment of underlying hyperuricemia – most untreated pts with gout will
experience a recurrent episode in 2 yrs
o Pharmacologial
Allopurinol (antihyperuricaemic) – once daily
- Frequent and disabling attacks,Signs of chronic gouty joint disease,
Tophi, Renal insufficiency, Recurrent nephrolithiasis, or Urinary uric
acid excretion > 1100 mg/day
Probenicid, Sulphinpyrazone (urocosuric) – multiple times daily
- Initial therapy < 60 who excrete <800 mg of uricacid perday, no renal
insufficiency, hx of urolithiasis or tophi
Colchicine
- Low dose prophylaxis during the initiation of anti hyperuricemic therapy.
NSAIDs if cannot tolerate colchicine.
o Non-pharmacological
Dietary:
- caloric restriction (↑ protein – low fat dairy not meat/fish, replace refined
with complex carbos, ↓saturated fat)
- Limit intake of alcohol.
Surgery:
- Complications of trophaceous disease – infection, nerve compression, jnt
deformity and intractable pain, cosmetic reasons

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BONE TUMOURS & CYSTS (OSCE ORIENTED) c. As little as possible of the tumour is exposed; block of tissue is removed –
DX OF BONE TUMOURS & CYSTS: ideally in the boundary zone, so as to include normal tissue, pseudocapsule
Impt differentiating features and abnormal tissue
 Site of lesion d. Frozen section examined; several samples taken if necessary
 Patient’s age e. If bone removed, the raw area is covered with bone wax or
 Special x-ray features methylmethacrylate cement
f. Drains should be avoided to minimise risk of tumour seeding
Diagnosis of Musculoskeletal Tumours
1. Imaging g. For tumours that are almost certainly benign: excisional biopsy can be
a. Plain X-rays done (remove entire lesion)
i. Site of lesion h. For cysts: careful curettage to remove representative tissue
ii. Solitary or multiple
Differential diagnoses for tumours
iii. Well-defined or ill-defined (i.e. narrow / widened zone of transition) 1. Chronic osteomyelitis
iv. Any cortical thickening a. Systemic features may have been suppressed by antibiotics
v. Any periosteal new bone formation & extension of tumour into b. Submit tissue for histological & bacteriological examination
soft tissues (malignant!) 2. Stress fracture (young adult with localised pain near a large joint)
- Periosteal hypertrophy may also mean infection, stress
fracture, soft tissue bruising Management
vi. NB. stippled calcification inside a vacant area is characteristic of Grade \ Compartment Intra-compartmental Extra-compartmental
cartilage tumours Low Wide excision - Radical incision
b. CT & MRI (w/o exposing tumour) - +/- bone graft OR prosthetic
i. Useful to assess true extent of tumour & its relationship to replacement
surrounding structures High - Radical incision and
prosthetic replacement OR
ii. Assuming that there are no metastases, the local extent of the amputation
tumour is the most important factor in deciding how much tissue - +/- chemo to ↓ risk of mets
has to be removed
c. Radionuclide scanning with technetium
i. Shows non-specific reactive changes in the bone
ii. Useful to reveal site of small tumour (e.g. osteoid osteoma) or the
presence of skip lesions / silent secondary deposits.
2. Biopsy --- essential for diagnosis & planning of treatment
a. Open Bx more reliable
b. Site is selected so that it can be included in any subsequent ablative
operation

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BONE TUMOUR CLASSIFICATIONS
Malignant Bone tumours by frequency Others Red marrow populated areas  Multiple myeloma
 Metastatic
1. Metastatic Common Pri site of metastatic tumours: Cartilage cap of osteochondroma OR  Chondrosarcoma
2. Multiple Myeloma  Thyroid  GI (except *Midline & paired Central medullary
3. Osteosarcoma  NPC rectum) structures Pelvis  Metastatic
4. Chondrosarcoma  Breasts  Renal *Most are osteolytic
5. Ewing’s sarcoma  Lungs  Prostate except prostatic (blastic) Bone tumours by Patient age
 Testes & breast (blastic & lytic)
Children/Adolescents (<20YO)  Chondroma (arise @ puberty, presents ~30YO)
Bone tumours by cell type  Osteochondroma
Cell type Benign Malignant  Osteosarcoma
Bone  Osteoid osteoma  Osteosarcoma  Osteoid osteoma (<30YO)
Cartilage  Chondroma  Chondrosarcoma  Non-ossifying fibroma
 Osteochondroma  Ewing’s tumour
Fibrous tissue  Fibroma  Fibrosarcoma  Simple bone cyst
Marrow  Eosinophilic granuloma  Ewing’s sarcoma
 Myeloma Young Adults (20-40YO)  Aneurysmal bone cyst
Vascular  Haemangioma  Angiosarcoma  Giant cell tumour
Uncertain  Giant-cell tumour  Malignant giant-cell tumour  Chondroma (arise @ puberty, presents ~30YO)
 Osteoid osteoma (<30YO)
Bone tumours by Site
Long bones Metaphysis  Osteochondroma Middle age / Elderly (>40YO)  Chondrosarcoma
 Simple bone cyst  Multiple myeloma
 Aneurysmal bone cyst  Osteosarcoma (~50YO)
 Giant cell tumour (proximal tibia, distal radius,  Metastatic tumours
distal femur)
 Non-ossifying fibroma (cortex)
 Osteosarcoma (esp knee & proximal humerus) [MCQ] Mets to spine: disc space not eroded!
 Chondrosarcoma
[MCQ] Ewing’s and osteomyelitis can be confused by all of the following:
Diaphysis  Ewing’s tumour 1. Swelling
Non-specific  Osteoid osteoma 2. Diaphyseal location
 Chondroma 3. Periosteal bone formation
 Metastatic 4. Exploration reveals liquefied material like pus
Spine  Aneurysmal bone cyst
 Giant cell tumours
 Multiple myeloma [MCQ] child with cystic lesion at epiphysis of lnog bone, most likely diagnosis:
 Metastatic osteoblastoma
Hands / feet  Chondroma
 Giant cell tumours (calcaneum)

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 FEATURES OF BONE TUMOURS & CYSTS
Bone tumour X-ray findings Site Age Others
Osteoid osteoma  Small round/oval radiolucent area surrounded by dense  Femur, tibia <30  Aspirin (pain relief)
sclerosis  Excision
 DDx: Brodie’s abscess
Osteochondroma  May be single or multiple  Edge of epiphyseal plate Adolescence  Bony hard lump  pain or disturbed tendon
o Multiple exostosis has AD inheritance & low rates of  Long bone metaphysis fxn
malignant change  Excise if symptomatic or growing (risk of
 2 main types: malign change)
i)conical (well defined)
ii)cauliflower with partial calcification of cartilage cap
Chondroma  Well defined rarefied area in medulla  Tubular bones of hands & Arises at puberty,  Excise / curette & replace w bone graft
(enchondroma)  Characteristic speckles of calcification w/in area of foot presents ~30YO.  Risk of malig change, esp if multiple
rarefaction  Long bones Need to rule out lesions are present
chondrosarc if >30y/o
Simple (solitary)  Translucent areas on shaft side of growth disc  Prox ends of humerus, Children up to puberty  Intralesional steroid injection
bone cyst  Bone expansion with cortical thinning femur, tibia.  Curette & filled w bone chips
 Fallen fragment sign  Usually in the metaphysis
Aneurysmal bone  Well defined margins around a rare area  Spine Young adults  Curette & filled w bone chips
cyst  Eccentrically placed  Metaphysis of long bones
 Bone expansion with cortical thinning
 Confined to metaphyseal side of growth plate (c.f. Giant cell
tumour which extends to articular surface)
 Diameter of cyst usu > diameter of bone
Non-ossifying  Cortex  Metaphysis of long bones Child  No Rx unless #ed.
fibroma (fibrous  Well defined sclerosed margins
cortical defect)
Giant cell tumour  Rarefied area situated asymmetrically  End of long bones (prox 20-40YO  Hx of patho #
 Extends to articular surface (MUST, otherwise excluded) tibia, distal radius, distal  High rate of recurrence if not completely
 Soap bubble appearance femur) excised
 Cortex is thinned, may be ballooned / perforated  Vertebral body  Curette & fill with bone chips
 Calcaneum  Excision & bone graft/ prosthetic
replacement
Osteosarcoma  Sunray appearance  Metaphysis of long bones Bimodal distribution:  Metastasize readily esp to lungs
 Bone areas of rarefaction in medulla  Knee & prox humerus 10-20YO; ~50YO  ALP  by 3-4X
 Subperiosteal new bone formation (a/w Paget’s dz)  Biopsy to confirm dx
 Codman’s triangle = lifting of periosteum prox to tumor @  ChemoRx  RT
the edge of the ‘sunray’  Resection / amputation
Chondrosarcoma  Central medullary type: initially appears like a chondroma.  Central medullary tumour >40YO  Tend to metastasize late
Destructive medullary tumour with flecks of calcification OR

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  Malig change in cartilage cap of osteochondroma type: large  malignant change in
exostosis surrounded by flecks of calcification in the cartilage cap of
cartilage cap osteochondroma
Ewing’s tumour  Bone destruction  Diaphysis of long bone 10-20YO  Rare, arise from vascular endothelium
(primitive neuro-  Overlying ‘onion-skin’ layers of periosteal new bone  Amputation, RT, adjuvant chemoRx
ectodermal
tumour, PNET)

Multiple  Overall reduction in bone density  Areas containing red 45-65YO  Osteoporosis + high ESR
myeloma (single  Multiple punched out defects (skull XR is often shown) marrow. Esp skull and  Urinalysis – Bence-Jones proteins
tumor = vertebrae  Serum/urine electrophoresis – monoclonal
plasmacytoma) Ig band
 ChemoRx & RT, int fixation of #, brace for
spinal #
 Other problems
o Nchormic Ncytic anaemia
o Hyperviscosity syndrome
o Renal stones
o Gout & hyperuricaemia
o Abnormal globulin: albumin ratio
Metastatic  Usually osteolytic EXCEPT prostatic CA mets which are  Areas containing red 50-70YO  Palliative ChemoRx & RT
tumours osteosclerotic marrow  Int fixation of #s
 Moth eaten appearance  Esp axial & long bones  Sx decompression & fusion of vertebrae to
 Generalised osteoporosis prevent neuro deficit
 Look for lung metastases

Enneking Classification
Grade G0 Benign Staging for Malignant Neoplasia Staging for Benign Neoplasia
(surgical) G1 Low grade malignant IA G1 T1 M0 1 Latent G0 T0 M0
G2 High grade malignant IB G1 T2 M0 2 Active G0 T0 M0
Site T0 Benign Intracapsular & IIA G2 T1 M0 3 Aggressive G0 T1 or 2 M0 or 1 (giant cell tumour)
intracompartmental IIB G2 T2 M0
T1 (A) Intracompartmental IIIA G1 or 2 T1 M1
T2 (B) Extracompartmental IIIB G1 or 2 T2 M1
Metastasis M0 No regional / distant mets
M1 Regional / distant mets

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ORTHOPAEDIATRICS Salter Harris Classification – examples
FRACTURES Type Example Basic Mx principles of physeal #s
Prevalence in Singapore I  11yo with ankle inversion injury
Extra articular #s usually treated
 Distal fibula #
 Bimodal distribution II  Distal radius #
with M&R
Modal peaks: 7 and 11 years old III  13yo with ankle injury • Intra articular extension
Median age: 7.64 ± 0.05 years old  Tillaux #
• Requires anatomical reduction
 By Gender IV  5yo with elbow injury
• Usually involves ORIF
Male modal peaks: 7 yrs & 11 yrs Male median: 8.18 ± 0.06 yrs  Lateral condylar # of humerus
Female modal peaks: 5 yrs & 10 yrs Female median: 6.66 ± 0.07 yrs » All dislocation must be stably reduced ASAP.
» Aim for acceptable alignment based on
Basic Principles o Age
• Presence of growth plate which gets injured before ligaments ( avulsion #s) o Potential for remodeling
• Presence of secondary ossification centers – CRITOE o Plane of motion
• Potential for remodeling in those less than 10 years of age o Fractured bone
• Less likely for joint stiffness due to casting o Fracture site – epiphysis, metaphysis and diaphysis
• Treatment is usually non surgical o Fracture personality – spiral, oblique, transverse, ,buckle, greenstick,
• Greenstick and Buckle #s Bayonet and Salter Harris
• Plastic deformation » Reduction maintained with plaster as children are less likely to get joint stiffness
• Pathological fractures
If surgery is required...
• Non-accidental Injuries
» Minimal dissection to ensure no damage to growth plate
» Usually smooth pins used instead of plate and screws as smooth pins produce
Growth plate
minimal growth plate damage and periosteum
» Usually combined with casting postoperative for added stability to fixation
» Pins inserted percutanoeusly where possible.
Remodelling
- Remodelling occurs 75% at the physis, 25% at the fracture site
- Physeal remodelling
» Once physis is aligned, it resumes symmetrical growth
- Diaphyseal remodelling
» Follows Wolff’s law – ‘form follows function’.
- The closer the fracture to an active physis, the greater the remodelling potential

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 iii. Grade IIB (with rotation component to the #) – closed reduction &
percutaneous pinning (CRPP)
iv. Grade III – M & R and CRPP
» Brachial artery & median nerve may kink (not rupture)
» Presents as pulseless hand
» Ulnar n. usually not affected (if affected, usually iatrogenic)
vi. Management – closed reduction (right)
vii. Complications
i. Cubitus varus (increased extension but reduced flexion)

Common types of #s in children

5. Clavicle #s
a. Very common amongst the very young after falling off the sofa at home.
b. Also as a result of birth trauma
c. Almost never treated with surgery
d. Arm sling will usually suffice
e. ONLY # ACCEPTABLE AS NON-NAI IN THE VERY YOUNG Axial force to correct varus alignment

6. Proximal humeral #s
i. Has great potential remodeling due to the fact that the shoulder is one most
mobile joint in the body.
ii. Usually treated with collar and cuff OR an O slab.
7. Supracondylar #s
iii. “In Singapore, the typical child who has a supracondylar fracture is a
7yo boy falling off a monkey bar with his non dominant hand”
iv. Most common fracture in KKH requiring surgery
v. Classification
i. Grade I (posterior fat pad sign seen) – Cast Immobilisation Flexion to correct the extension of fragment
ii. Grade IIA (Baumann angle = 75˚, anterior humeral line bisects
8. Lateral condylar #s
capitulum) – M & R
a. Important because it’s a SH IV fracture with joint extension
b. Displacements >2mm needs ORIF

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 c. Even if undisplaced, need close surveillance to intervene if there any c. Be aware of pathological fractures
further displacement (by muscles) d. Treatment
d. Can lead to non union, elbow deformity and instability if untreated o Gallows traction for those less than 2 years or 20 lbs
o Russell’s traction for others till next elective list
9. Radius/ulnar #s
o Early 1 leg hip spica. Allows for sitting. Better accepted.
a. Unlike in adults radius/ulna can usually be treated by M&R
o Immobilize with U Slab of sugar tong slab 12. Tibial #s
b. Surgery indicated if unable to achieve stable acceptable alignment e.g. a. Most common type of #s in children
o In older children/teenagers b. Aim is to achieve acceptable alignment
o Excessive rotation o No varus or recurvatum
o Excessive angulations (>200) o Angulation < 100.
c. Surgery if indicated done with minimal disturbance of growth plate and o No rotation
periosteum c. Above knee cast backslab.
d. Also think of Monteggia/Galeazzi #s d. Admit if
e. Radial neck MUST bisect the capitulum of humerus in all views o Concerns of Compartment syndrome
Flexor hallucis longus – pain on stretching of ischaemic muscle ---
10. Distal radius #s
extend the child’s toe (small movement but great pain)
a. Can be different varieties
o Good alignment cannot be achieved
b. Salter Harris II involving the distal radius epiphysis
o Open fracture.
o Below elbow cast after M&R
Tibia is superficial therefore predisposes to osteomyelitis and non-
c. Distal 1/3 fracture of the radius ulna which is the most unstable.
union (a/w poor blood supply for tibia unlike femur :. Vicious cycle)
o Above elbow cast after M &R
e. Beware of the Toddler’s fracture (Refuses to walk, keeps on falling)
o Bayonet acceptable for those < 10 years old if delayed presentation
d. Buckle fractures due to “buckling” of the periosteum Fractures in Adolescents
o Very stable 5. Tibial spine #s
o No M&R required a. In older children / adults, more likely ACL tear.
o May treat with Brace only b. But since ligament is stronger than bone, more likely avulsion # of tibial
spine (site of attachment still has cartilaginous contact, not bone)
11. Femur #s
c. Classification – Meyers & McKeever
a. General Concerns
i. Type I – minimal or no displacement
o Adequate pain relieve
ii. Type II – angular elevation of anterior portion with intact posterior
o ATLS for multiply Injured
hinge
b. Be aware of possible Non Accidental Injuries NAI
iii. Type III - complete displacement with or without rotation
o In those not ambulating
o Mentally retarded
o Non communicative yet

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  Refer early
- Brachial Plexus Injuries
- Clavicle fracture
 No intervention
 Reassure family
 Ensure no pressure on fracture site
 Exclude Brachial Plexus Injury
 If the infant initially demonstrates discomfort with the fracture, the long arm
sleeve of the infant's shirt can be pinned to the shirt for 7 to 10 days to provide
6. Tillaux #s
adequate immobilization.
a. Growth plate not completely closed yet and lig > bone :. Tillaux’s fracture
- Humerus fracture
 Mechanism of injury -- -- -- -- -- -- -->
- Femur Fracture
 Rx: pavlik harness

Specificity of Skeletal Trauma for Abuse

b. More growth plate = more # parts (e.g. triplane # in a 12yo girl) High Specificity Moderate Specificity
- Classic metaphyseal lesions - Multiple fractures, especially bilateral
- Posterior rib fracture - Fractures in various stages of healing
- Scapular fracture - Epiphyseal separation
- Spinous process fracture - Vertebral body fracture or subluxation
- Sternal fracture - Digital fracture
- Complex skull fractureLow specificity
- Clavicular fracture
- Long-bone shaft fracture
Imbalance of muscle and bone growth cause tension in unfused apophysis
- Linear skull fracture
7. Tibial tuberosity (Osgood Schlater Disease)
8. Inferior pole of patella (Sindig Johanssen Larsen)
9. Apophysis of calcaneum (Sever’s syndrome)
Tension can convert to fracture during sporting activity especially in those who are
heavy for their age
Traumatic Birth Injuries
- Osteogenesis imperfecta
 Life-threatening condition

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 Able to hyperextend the elbow (beyond 10 degrees)
- Left 1
- Right 1
Able to put hands flat on the floor with knees straight 1
Able to hyperextend knees (beyond 10 degrees)
- Left 1
- Right 1

CONGENITAL, DEVELOPMENTAL AND PHYSIOLOGICAL CONDITIONS

TORTICOLLIS (AKA WRY NECK)
Classification
• Primary/Muscular/idiopathic – tight SCM
• Secondary – always exclude & treat this first since this is the underlying cause
– Squint
– Hearing problems
– Flat head (plagiocephaly)
– Bony fusion of cervical spine (Klippel Feil)
– Tumours and infections in the neck
– Trauma
OSSIFICATION CENTRES
Clinical Features
CRITOE – ossification starts at  Childs tilts or looks to the sides opposite to the tight SCM
1. capitalium (1yo),
 Facial asymmetry on the side of the torticollis
2. internal/medial epicondyle (3yo),
3. trochlea (5yo),  Limited lateral rotation on the same side of torticollis
4. olecranon (7yo),  Limited lateral flexion on the opp side of torticollis
5. external/lateral epicondyle (9yo)
Management
• Exclude secondary causes
LIGAMENTOUS LAXITIES
• If under 1 year can be treated effectively with stretching (physio)
Assessed using Beighton scoring (out of 9) • Surgery usually needed for those above 1 year old.
Test Points • Release of the SCM is done with or without a reconstruction of the sternal head
Able to bend thumb backwards to touch volar forearm
• Post op aggressive physiotherapy with use of custom made cervical collar for
- Left 1
- Right 1 immediate post op period.
Able to bend little finger back (beyond 90 degrees)
- Left 1
- Right 1

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APPROACH TO LIMPING CHILD
Presentation: limping child / delayed walking / abnormal gait
Things to consider
1) Site/location
2) Painful versus painless
3) Age (NB. regardless of age, must always include trauma & infection [septic
arthritis, OM, synovitis] under painful causes)
Painful
<3yo Most commonly due to infection
Trauma (exclude NAI)
- Toddler’s # (1-4yo): distal tibial #
3yo to Transient synovitis
schoolgoing - DX OF EXCLUSION
- Inability to bear weight
- a/w excessive running
- May be related to upper respiratory
infection
- Gets better with rest
Growing pain
- Diagnosis of exclusion
- Usually between 4-5yo and during
puberty
- Bone growth rate faster than rate of
increase in length of muscle &
tendon
- Pain occurs usually at the end of the
day, often relieved with massage /
after a good night’s rest
Leukaemia (4-10yo)
Schoolgoing Perthe’s disease (4-8yo)
through - Loss of blood supply to the hip
adolescence - Unknown cause
- Can cause early degenerative disease
Painless
Limb length discrepancies
- Bone: femur versus tibia
Transient synovitis
shortening
 Commonest cause of irritable hip
- Joint: commonly DDH
 Epidemiology: boys 2x more than
- Generalised
girls, 3-10yo
o Muscle hypertrophy on
 History
one side; causes: nerves
o Unilateral groin/hip pain
(NF), vessels
o Antalgic limp
(haemangiomas)
o Very young children: no other
o Polio infection
symptoms except crying at
- Physiological
night
o Metatarsal adductors
o Recent Hx of URTI,
o Tibial torsion
pharyngitis, bronchitis or otitis
o Femoral anteversion
media (in >50% of cases)
o Flat foot
o No definitive cause known
Adolescents Slipped Upper Femoral Epiphysis
Biggest concern: undiagnosed
(~15yo)
dislocated hip ( DDH)
– Thought to be due to excessive
- Significant limb length
weight on a predisposed hip
discrepancy
– Maybe due to an endocrine
- Asymmetrical thigh crease
abnormalities (Pituitary, growth,
- Hip clicks
thyroid and parathyroids, gonadal
- Limited/asymmetrical
hormones)
abduction
– Diagnosis delayed because they can
present with knee pain
– Always need surgery to stop
progression
Growing pain (see above)
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DDH • Each Xray must show concentric reduction with good acetabular
• Incidence cover
– 1:1000 live births • Management
– Common enough for the condition to be screened by the neonatologists – Goals
• Risk factors • CONCENTRICALLY REDUCED AND STABLE HIPS WITH
– 1st female child GOOD ACETABULAR COVER
– Family history • To Avoid Early Degenerative Disease of the Hips
– Breech – Treatment
– Condition predisposing to crowding of uterus (multiple pregnancies, • WATCH – observe if
oligohydramnios, fibroids, baby too big, mother too small) • Hip laxity only
• Diagnosis: • Hip clicks
– Diagnosis is CLINICAL • Repeat U/S at 4-6 weeks
• Barlow maneuver – test of “dislocatability” • If hips reduced and stable, no further tx
• see if hip can come out or not, test positive when it goes • Otherwise treat as DDH
back in on the way • ABDUCTION SPLINT
• Ortolani maneuver – test of “reducibility” 0 to 6 months
• pushing a hip that is already out; clunk only when it • Abduction splint (old mtd) or Pavlik Harness
moves over labrum • Repeat U/S in harness after 1 week and out of harness at 6
– U/S or X-rays can be used but not to diagnose at birth weeks
• X-ray: radiation PLUS hip is not ossified • Worn for at least 3 months until 1st Xrays
• U/S not done at birth because laxity of hip joint, may get spurious • If Xrays show concentric hips with good acetabular cover,
reading at birth (in order for baby to come out of birth canal) – then wean off splints
hence earliest U/S is at 6 weeks In Human position: 50deg of abduction of each side and 100deg
– When to do U/S of flexion
• For high-risk cases (e.g. breech) / hip laxity / hip clicks
• To ensure concentric stable reduction after treatment
• Weekly after with splint to ensure reduction and correct
application of splints
• Every 6 weeks after once hip reduced
• Most effect <3 months old (3 months onwards :X-rays; must
ensure concentric reduction with good acetabular cover, if not
mechanical forces of hip not evenly distributed  may get OA)
– When to do X-rays
• 3 months onwards

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• CLOSED REDUCTION & HIP SPICA CLUBFOOT (CONGENITAL TALIPES EQUINOVARUS)
0 to 6 months Incidence
• If unable to achieve stable reduction with splints then  1:1000
closed reduction and hip spica attempted  2x more common in males, bilateral in 1/3 of patients
• OPEN REDUCTION & HIP SPICA
 a/w spina bifida & arthrogryposis (non-progressive condition characterized by
6 to 12 months
multiple joint contractures found throughout the body at birth)
• Closed reduction can still be attempted but more difficult
 Also screened at birth by neonatologist
to achieve stability
• Open reduction then done Types
12 to 18 months - Structural
• Child is already weight bearing o Something wrong with the structure, intervention required
• Open reduction usually involves femoral derotation and o Mainly Idiopathic
shortening o Neuromuscular [muscle imbalance – peroneals not working (S1)]
• Acceptable is thought to remodel accordingly o Syndromic – e.g.
Above 18 months - Positional (if able to dorsiflex foot then positional)
• Potential for acetabular remodeling is less o When you examine the feet  flexible, due to position in the womb
• Both acetabular and proximal femoral surgery will be
Clinical Features
required.
• Acetabular surgery (Salter osteotomy)
• FOR CHRONICALLY NEGLECTED CONDITIONS (RARE)
Reductions not usually attempted if
• > 8 years for unilateral (no more remodelling past 8yo, so
reduction would cause OA)
• > 5 years for bilateral
Consequences of not reducing
• Partially dislocated (formation of false joint) – Hindfoot equinovarus Forefoot supination
• Completely dislocated – will have Trendelenburg gait,
cost of energy to walk will be high hence not ideal (have
to sit on side  back pain, will get scoliosis
• Bilateral: waddling gait, hips dislocated behind so
nothing to hold pelvis in between, would get lordosis
• Will ALL will walk assuming muscles and nerves are
functional

Forefoot adduction Cavus

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Management #5 SUMMARY:
I) Ponseti casting • External rotation: tilt toe and turn out
- Serial casting and manipulations soon after birth. 60deg in relation to the knee
- Foot corrected distal to proximal • Principle: serial casting & manipulation
o Weekly for 4 weeks • FOREFOOT: casting (forefoot corrected
o Fortnightly for 4 weeks until external rotation of 60° achieved first then hindfoot!)
o Then assess need for TA tenotomy if hindfoot still uncorrected. • HINDFOOT: cut the tendon (if force into
#1 #2 casting, will cause vertical talus)
• Then BOOTS & BARS

II) Boots & Bars

- 23hrs/ day for 3 months
- Then wean till child being to cruise
- Then night and nap till 4 years old.
#3
FLATFEET (PES CAVUS)
Classification
Two diagnostic groups
• Dynamic
– Due to generalised ligamentous laxity
• All children have this till about 7yo
• Ask patient to tip toe – tightening of plantar fascia
arches  indicative of ligamental problems
#4 • Jack’s Test (reverse of tip-toe; pull toe up  arch appears)
– Due to tight TA
• Growth spurts creates muscle tightness esp TA due
to imbalance of muscle and bone growth
– Due to collagen tissue disorders, e.g. Marfan’s
• Fixed Flatfeet
– Neuromuscular e.g. CP
– Idiopathic
– Tarsal coalition with/without peroneal spasm

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 • Calcaneo Navicular Importance of aligning early:
• 9 to 12 years • Accept valgus till about 5-7yo
• Do an oblique x-ray • If valgus <7yo, mechanical axis will be lateral (i.e. pressure at lateral portion of
• Talo - calcaneum growth plate)  inhibition of lateral growth plate compared to medial 
• 12 to 15 years; 50% bilateral • OA of lateral compartment (about 30-40yo)
• Do a CT
Causes
Child HIP: Medial femoral torsion (femoral anteversion)
Management
- Usually bilateral
Dynamic with no tight TA Watch and Masterly Inactivity
Toddler LEG: Medial tibial torsion (commonest cause of bow-leggedness in 1yo’s)
Dynamic with tight TA Stretching, Good Shoeing and Medial Arch Support
Infant FOOT: Metatarsus adductus
Fixed Treat underlying problem - usually needs surgery
1. Metatarsus deviate medially
- Tarsal coalition - Treat if < 30% involved, with soft tissue interposition
2. Kidney-shaped sole
(fat & extensor digitorum brevis)
3. Splaying of first webbed space
4. Inverted sole

LOWER LIMB MALALIGNMENT SCOLIOSIS

Classification
- Idiopathic
- Neuromuscular
» CP
» SMA
» Myelomeningocoele
» Muscular dystrophies
- Congenital
» Hemivertebrae
» Block vertebrae
- Syndromic
• At birth: all children will have varus up to 2yo » Ehler-Danlos
• 4yo: maximal valgus occurs (reassure parents & monitor child’s inter-malleolar » Marfan’s
distance every 6 months to record progress) » Neurofibromatosis
• 7yo: resolves spontaneously; should a marked deformity persist past 10yo, » VACTERL
operative correction should be advised
• Normal adults/teens: Slight valgus, about 6deg or so

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Clinical Assessment
- General assessment + height
- Back examination
» Scoliometer (in clinic)
» Spinal balance: plumbline
» Screening test: Adam’s Forward Bending Test

Idiopathic scoliosis: important points in history-taking

Why positive? - Chronological age
- Menarche
- Family history
- Time of diagnosis
- Severity of first X-ray
- Any previous treatment
- Associated symptoms
» Back Pain
» Neurological: clumsiness/weakness, bowel/bladder function
Red flags that scoliosis may NOT be idiopathic
History
- Back pain that is well-localised and constant
- Pain that is becoming progressively worse over time
- Feelings of weakness or clumsiness
- Episodes of bowel or bladder incontinence
- Neurological examination
- Ejaculation problems
- Cobb’s angle (X-ray)

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Physical Examination CEREBRAL PALSY
- Foot deformity, particularly unilateral Definition
- A lack of rotational deformity on Adam’s forward bending test Non progressive insult on a developing brain
- Hyperkyphosis
• The brain lesion is permanent and non progressive, but the natural history of
- Tight hamstrings (popliteal angle > 50‐60 deg)
- Abnormal curve pattern : Not R thoracic and/or L lumbar cerebral palsy is not static.
- Unequal or abnormal reflexes • If non-progressive insult on a developed brain = stroke
X-rays
Aetiology
- Widened pedicles
- Kyphosis • About 10 to 15% of patients documented perinatal hypoxia.
- Atypical curve pattern • Cerebral palsy is not solely the result of prematurity because 60 to 65% of
- Lack of vertebral rotation afflicted children were born at full term
- Rapid curve progression (>1 degree / month) • Although only approximately 10% of cerebral palsy patients weigh less than
- Absent pedicles (`winking owl’) 1,500 grams at birth, in this low birth weight group the risk of having cerebral
- Limb length discrepancy palsy is 90 per 1,000, compared with 3 per 1,000 if weighing more than 2,500
MRI grams and appropriate for gestational age
When to order • Low birth weight for gestational age & prematurity are commonly
o Neurologic abnormalities on physical exam (don’t forget the feet) associated with the development of spastic diplegia
o Structural (congential) abnormalities on plain film
o Excessive kyphosis
o Apex left thoracic or thoracolumbar curves Types
o Early onset scoliosis Neuropathic Types*** Anatomic Patterns***
o Syndromic features present • Spastic • Hemiplegic
What to look for – Overactive Golgi • Diplegic
apparatus • Quadriplegic
- Syringomyelia
– The only one in which • Total body
- Chiari malformations Ortho team can intervene
- Tethered cord • Ataxic Others
- Diastematomyelia • Athetoid • Triplegic
• Hypotonic • Monoplegic
Treatment • Mixed

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Management is dependent on functional assessment of the child! (See right)
Type Functional Aim
Hemiplegic • Efficient Walking
– Supple Hamstrings
– Supple TA
• Upper Limb is the best position for function
Diplegic Walker
• Efficient walking
– No crouch/jump gait
– No tiptoeing
– Feet in neutral position
– No scissoring
• Consider need for assistance if power and control poor
• Dietary control (optimal BMI; too heavy, patient cannot bear weight)
• All should walk !! (if not, could be due to poor parental support, laziness
[rehab into society would be even more difficult])
Non Walker
• Investigate reason
• If reason for inability to walk is neurological then aims same as
quadriplegic sitter
Quadriplegic • Painless seating
– Seating Clinic
• Spine fairly straight and stable
• Hips painless and reduced
• No pelvic tilt
• Adequate abduction for hygiene care
• Adequate knee flexion

136
 • Done percutaneously in very young

• Hamstring release
• In those with very severe crouch gait and popliteal angles usually
exceeding 45o
Botulinum A Toxin
• Release of semitendinosus
• intramuscular injection of a neurotoxin produced by Clostridia bacteria.
• Fractional lengthening of semimembranosus and biceps femoris
• It is delivered into or near sites of nerve arborization, and blocks the release of
acetylcholine from presynaptic vesicles at the myoneural junction.
• Recovery of tone results from the sprouting of new nerve terminals, which
peaks at about 60 days
• The agent is injected using a 23- or 25-gauge needle, usually without local or
general anesthesia • Adductor release
• The muscles are located by palpation. • Done for significant scissoring in walker
• To reach muscles that are deep or difficult to localize, electromyographic • Uncorrectable tight adductor in non- walker such that perineal hygiene
guidance and electrical stimulation have been used is compromised
• BTX diffuses readily, so the injection should be placed in the muscle belly • Painful subluxed hips

Soft tissue surgery: basic principles

• Surgery only done when deformity progresses to contracture and is not
dynamic anymore (not dynamic = passive ROM still possible)
• Surgery is CONTRAINDICATED in joints with correctible deformity
• Surgery done with functional aim in view
• Cosmesis only a consideration in Upper Limb
• Tendo-Achilles Lengthening
• Indicated when ankle cannot be dorsiflexed to neutral in walker

137
Bony surgery: basic principles – Tendon Transfers
• Usually in older children • Split Posterior Tibialis Tendon Transfer
• When soft tissue surgery had failed with recurrence of deformity
[aka once joints are stuck/immobile]
• In areas where soft tissue surgery alone inadequate
– Spine
– Unstable hips
– Severely deformed feet due to uncorrected muscle imbalance.
• Spine
– Paralytic scoliosis due to muscle imbalance
– Not treatable with bracing
– Seating is difficult for Quadriplegics if uncorrected
• Unstable hips
– Hips need to be reduced because – Triple Arthrodesis
• Pain • Salvage procedure
• Severe pelvic tilt causing 2o scoliosis
• Pressure sores due to unequal pressure when sitting
– Not the same as DDH
– Usually needs Open Reduction
– With or without femoral and/or acetabular osteotomy
• Feet
– Usually done in older age group
– Many methods described
– Principle is to correct the foot alignment
– Indicated in walkers with passively uncorrectable deformities
– Valgus feet
• Calcaneal Shift, Grice Extra-articular Fusion

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IMPORTANT CLASSIFICATIONS FOR ORTHOPAEDICS  Gustilo Classification
 Open from within or without – latter has  risk of infxn,
FRACTURE TYPES
hemorrhage & injury to muscles, nerves or bld vessles. Also
Simple  Transverse (<30o)
usually comminuted & more difficult to manage.
 Oblique (>30o)
 Spiral
Comminuted  Spiral wedge – torsional forces OPEN FRACTURES: Gustilo Classification
 Bending wedge – characteristic butterfly fragment Type I  <1cm AND clean
 Comminuted wedge – bending wedge # with fragmented butterfly Type II  >1cm AND no extensive soft tissue damage, avulsions or flaps
fragment Type IIIA  Extensive soft tissue damage, avulsions or flaps but adequate soft tissue
 Complex spiral – >1 spiral fragments coverage of bone OR
 Complex segmental – double #  High-energy trauma cause irregardless of size of wound
 Complex irregular – bone lying btw main elements is fragmented Type IIIB  Extensive soft tissue loss + periosteal stripping + bone exposure
Hairline If not detected on XR initially:  Massive contamination common
 Do oblique XR Type IIIC  Arterial injury requiring repair
 Repeat film after 7-10 days
Greenstick  Children
HAEMORRHAGE IN FRACTURES
 Elastic spring of periosteum may cause recurrence of angulation, hence
Close # of femoral shaft 2-3L
plaster fixation must be well done.
 Rapid healing Haemothorax 3-5L
Compression Common sites Pelvic # 3-5L
 Vertebral bodies
 Heels EPIPHYSEAL PLATE INJURIES: Salter-Harris Classification
Avulsion Common sites Type 1  Whole epiphysis separated from shaft
 Base of 5th metatarsal (peroneus brevis) Type 2  Epiphysis is displaced together with a metaphyseal fragment
 Tibial tuberosity (quadriceps) (Osgood-Schlatter’s disease) Type 3  Separation of part of the epiphysis
 Lower pole of patella (Johansson-Larsen’s disease) Type 4  Separation of part of the epiphysis with a metaphyseal fragment
 Upper pole of patella (quadriceps) Type 5  Crushing of part or all of the epiphysis
 Lesser trochanters (iliopsoas) *Cxs: avascular necrosis, growth arrest
Impacted One fragment driven into another
UPPER LIMB
DESCRIBING FRACTURES Colles’ # # distal radius w/in 2.5 cm of wrist (aka dinner-fork #)
1. Level  Anatomical – epiphysis, epiphyseal plate, metaphysic, diaphysis Anterior & ulnar angulation
OR Dorsal & radial displacement of distal fragment
 Thirds – proximal, middle, distal Impaction of fragments.
2. Displacement  Direction of displacement in terms of movt of distal fragment Smith’s # # distal radius w posterior angulation  anterior displacement (aka
 Degree of displacement in % of # surfaces in contact reversed Colles’ #)
3. Angulation  Described in terms of the direction the point of # angulation is Galeazzi #- # of radius, inferior radioulnar joint dislocation (GUD)
pointing towards (eg anterior angulation in Colles’ #) dislocation
4. Axial rotation  Easily missed, examine the joints above & below the # Monteggia #- Ulna fracture + anterior dislocation of head of radius (MUF)
5. Open / Close Open dislocation

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TRIGGER FINGER FRACTURE OF NECK OF FEMUR:
Stage Features Mx (A) Gardens Classification
Pre-triggering Pain, no trigger NSAIDs Type Incomplete fracture (Inferior cortex 10
Triggering Correctable by active extension H&L 1 not broken)
Triggering & Correctable by passive extension H&L, Sx sheath No displacement
Lock incision Abduction # Fixation by:
Contracture Fixed flexion deformity Sx release Trabeculae are angulated  Cannulated screws /
Type Complete fracture line (inf. cortex pins 20
 DHS

Risk of AVN (%)

2 broken)
PELVIC FRACTURES: Tile classification No displacement
Type Stable #s A No involvement of pelvic ring Trabecular lines interrupted but not
A 1 angulated
A Stable, minimally displaced # of pelvic ring Type Complete fracture line  >65YO – 30
2 3 Slight-moderate displacement hemiarthroplasty.
Type B Rotationally B1 AP compression # (“open book” #) Rotation of femoral head – prox frag o Unipolar (Moore’s
unstable, B2 Lateral compression #, ipsilateral abducted & int. rotated or Thompson’s)
vertically stable B3 Lateral compression #, contralateral Type Severe displacement o Bipolar – for 40
Type C Rotationally & C1 Unilateral 4 younger PTs
vertically C2 Bilateral  <65YO – attempt joint
unstable C3 Associated acetabular # salvage

(B) Anatomical Classification

PERTHES’ DISEASE
A Subcapitate Intracapsular – risk of severing retinacular vessels
Catterall grading– according to degree of femoral head involvement
B Transcervical resulting in AVN (12-33% of all #NOF
Grade Severity Px
C Basilar Extracapsular
1 involve anterior portion of epiphysis Revascularisation may be
only. No collapse or sequestrum complete w/o bone collapse (C) Phases of AVN
2  50 % involvement with a sequestrum Bony collapse inevitable I Only head involvement
3 ~75% involved, with collapse & Bony collapse inevitable. Poor II Progress to secondary OA & acetabulum is affected as well
sequestrum Px
4 whole epiphysis involved
ANKLE FRACTURES
INTERTROCHANTERIC FRACTURE OF THE FEMUR Weber’s classification
Evans’ Classification Type Level of fibular #
I 2 fragments, undisplaced A Distal to syndesmosis
II 2 fragments, displaced B Involve the syndesmosis
III 3 fragments w/o posterolateral support (ie # of the greater trochanters) C Proximal to syndesmosis
IV 3 fragments w/o medial support (ie # of the lesser trochanter)
V 4 fragments
R Reversed oblique # - prone to displacement
*Alternative classification: according to number of fragments + reversed oblique #

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Pott’s Classification BONE TUMOURS
First degree # of a single malleolus (medial or lateral) Enneking’s Classification
Second degree # of both medial & lateral malleoli Grade G0 Benign
Third degree # of medial, lateral & posterior malleoli (surgical) G1 Low grade malignant
G2 High grade malignant
SCOLIOSIS Site T0 Benign Intracapsular & intracompartmental
List of Causes T1 (A) Intracompartmental
Non-  Limb length discrepancy (apparent or true shortening of one leg) T2 (B) Extracompartmental
structural  Hip contracture Metastasis M0 No regional / distant mets
 Muscle spasm – eg 2o to PID M1 Regional / distant mets
Structural  Adolescent idiopathic (commonest, 80%)
 Infantile idiopathic – may resolve or progress Staging for Malignant Neoplasia
 Osteopathic – due to congenital vertebral anomalies IA G1 T1 M0
 Neuropathic – eg 2o to polio or CP. Due to asymmetrical muscle IB G1 T2 M0
weakness IIA G2 T1 M0
 Myopathic – due to muscular dystrophies IIB G2 T2 M0
 Neurofibromatosis IIIA G1 or 2 T1 M1
IIIB G1 or 2 T2 M1
SPONDYLOLISTHESIS
 Causes Staging for Benign Neoplasia
1. Dysplasia – congenital lumbosacral facet jt dysplasia 1 Latent G0 T0 M0
2. Isthmic (spondylolytic) – break in the pars interarticularis 2 Active G0 T0 M0
3. Elderly (degenerative) – OA degeneration of facet joints 3 Aggressi G0 T1 or 2 M0 or 1 (giant cell
4. Trauma ve tumour)
5. Suspicious (pathological) – neoplasm
6. Post-op – due to laminectomy for decompression OSTEOPOROSIS
 Meyerding classification BMD T-score Definition
Grade % translation of >-1 Normal
VB -1 to -2.5 Oteopenia
I 0-25 <-2.5 Osteoporosis
II 25-50 <-2.5 + fragility Severe osteoporosis
III 50-75 fracture
IV 75-100

RHEUMATOID ARTHRITIS
 Stage 1 (synovitis) – pain, chronic swelling, large effusion, thickened synovium
 Stage 2 (articular erosion) – joint instability, ROM. X-ray: loss of jt space & marginal
erosion, but lack of osteophytes c.f. OA
 Stage 3 (deformity) – pain, deformity, instability & disability. X-ray: bone destruction

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DISEASES MNEOMONICS
9. Monoarthritis differential GHOST:
1. Osteosarcoma: risk factors PRIMARY:
Gout, Haemarthrosis, Osteoarthritis, Sepsis, Trauma
Paget's, Radiation, Infaction of bone, Male, Alcohol, poor diet, sedentary lifestyle
[adults only] Retinoblastoma, Li-Fraumeni syndrome, Young [10-20 yrs].
10. Can H&L (hydrocortisone and lignocaine) everything except plantar fascitis and
Osteosarcoma is the most common primary malignant tumor of bone.
archilles tendonitis
2. Osteosarcoma: features PEARL HARBOR:
Paget's disease (10-20%)*, Early age (10-20 yrs), Around knee, Raised periosteum
by expanding tumor: "sunburst pattern", Lace-like architecture, Hyaline
arteoriosclerosis, Alkaline phosphatase increased, Retinoblastoma*, Boys,
predominantly, Osteomyelitis DDx, Radiation*
· Sunburst pattern was Japanese Navy emblem during WWII.
*: Predisposing factors.

3. Sacroiliitis: causes PUB CAR: seronegative arthropathies + Bechet’s

Psoriasis, Ulcerative colitis, Behcet's disease, Crohn's disease, Ankylosing
spondylitis, Reiter's disease

4. Rheumatoid arthritis: features RHEUMATOID:

Ragocytes/ Rheumatoid factor (anti-IgG), HLA-DR4/ HLA-Dw4, ESR increase/
Extra-articular features (restrictive lung disease, subcutaneous nodules), Ulnar
deviation, Morning stiffness/ MCP joint, Ankylosis/ Atlantoaxial joint subluxation/
Autoimmune/ ANA, T-cells (CD4)/ TNF, Osteopenia
Inflammatory synovial tissue/ Idiopathic/ IL-1, Deformities (swan-neck,
boutonniere)

5. Seronegative spondyloarthopathy: diseases PAIR:

Psoriatic arthitis, Ankylosing spondylitis, IBD, Reiter's syndrome

6. Osteomalacia: features "Vit-D deficiency in ADULT":

Acetabuli protrusio, Decresed bone density, Under mineralization of osteoid,
Looser's zone (pseudofracture), Triradiate pelvis (females)

7. Osteomyelitis: complications FIBRES:

Fractures, Intraosseous (broidie) abscesses, Bacteremi/ Brodie abscess, Reactive
amyloidosis, Endocarditis, Sinus tracts/ Squamous cell CA

8. Deep tendon reflexes: root supply "1,2,3,4,5,6,7,8":

S1-2: ankle, L3-4: knee, C5-6: biceps, supinator, C7-8: triceps

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