BAAPS

(BUDDING AND ADMIRING PLASTIC SURGEONS)

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BAAPS

BED SORE
Name:
Age:
Sex:
Occupation:
Resident of:
Comes with complaints of a wound over lower back / buttock / heel / ankle / back of head / elbow of this
duration, weakness of lower limbs of this duration & loss of sensation over the limbs of this duration.
On enquiry patient gives a history of fall / road traffic accident after which he was unable to stand or
walk (or history of progressive weakness: multiple sclerosis, fever followed by weakness: Acute transverse
myelitis, symptoms suggestive of tuberculosis with weakness: Acute tubercular meningitis, history suggestive
of syphilis with weakness: tabes dorsalis)

History of incontinence. Dribbling or overflow, sensation of urine in bladder present / absent. How
is the patient managing the problem? : Foley / condom catheter or clean intermittent
catheterization. Any history suggestive of UTI / calculi.
History of constipation / fecal incontinence. How is the patient managing the problem? Use of
laxatives / Finger evacuation / reflex stimulation
History of progression or regression of weakness from time of initial event to present.
Any history of use of physiotherapy / splints
History of progression / regression of areas of anesthesia from time of initial event to the
present.
History of appearance of tightness in the movement of any joints (Spasticity). When appeared,
progression & treatment history of the same.
History of the development of any deformity of the joints (contractures)
History of wound: when appeared, progression, initial and present site & size. Pain in the wound.
History of any surgeries for the previous mentioned problems.
History of Diabetes / hypertension / smoking / alcoholism

General examination: ATTITUDE IN THE BED

Nutritional assessment by measurement of MAC indicates protein loss (males 23cm and females 22 cm)
Triceps skin fold thickness indicates lipids loss (males 12mm and females 23mm) and evaluation of any
vitamin deficiencies.
Vital signs
Systemic examination
RS
CVS
CNS
1. Atrophy of muscles: circumference measured from fixed bony points
2. Tone of muscles
3. Power
Hip Flexion
L 1, L 2
Knee extension
L 3, L 4
Ankle dorsiflexion
L5
Ankle plantar flexion S1, S2
Knee flexion
L 5, S 1
Hip extension
L 5, S 1
4. Sensory examination of the dermatomes (start from T10 level)
Anterior thigh
L 1, L 2
Knee
L3
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Medial leg
Lateral leg

L4
L5

Plantar foot & posterior leg

Posterior thigh

S1
S2

5. Reflexes Deep Tendon reflexes

Knee jerk:
L 3, L 4
Ankle jerk:
S1
Superficial abdominal reflexes
Plantar response
6. Spasms (which joints)
7. Contractures (which joints, active & passive ROMs, structures contracted clinically)
8. Trophic changes (Thin dry skin, sparse hairs, brittle nails)
Local examination
Inspection of decubitus ulcer
Number, situation, size, position, extent, shape, margin, edge, floor discharge, surrounding skin
Palpation
1. Warmth/Tenderness (??????)
2. Size of full extent of the undermined ulcer examined with a gloved finger and marked (This
is the usual extent of debridement required)
3. Base of the ulcer
4. Fixity of the ulcer to the underlying tissues
5. Distal vascularity
6. Any limb length discrepancies
7. Enlarged lymph nodes
DIAGNOSIS
UMN or LMN type of paraplegia / Paraparesis which is recovering / nonrecovering type with decubitus ulcer
of X grade with / without complications secondary to trauma / myelopathy.

APPROACH
All preventive measures put in place like weight redistribution for at least 5 mins every 2 hours, keeping part
away from moisture, physiotherapy, nutritional improvement (correct Anemia / Hypoproteinemia). Measures
to rehabilitate Urinary / fecal incontinence. Measures to rehabilitate sexually / socially. Treat spasm. Correct
contractures.
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Evaluation of wound: wound C/S,
X-ray / CT scan.
Investigations to assess fitness for GA:
Routine blood tests / ECG / CXR.
When patient is fit debridement of wound (necrotic & scarred soft tissue / bursa / ostectomy) followed
by cover.

Doses of antispasmodics.

In order to achieve proper positioning of the patient, spasticity must be relieved. This can be achieved
pharmacologically or surgically.
a. Diazepam, (benzodiazepine and GABA agonist) 10 to 40 mg, maybe given every 8 hours or in
combination with Baclofen.
b. Baclofen _-(aminobutyric acid B (GABA-B) agonist) is usually started at 10 mg every 6 hours and may be
increased to as much as 25 mg every 6 hours.
c. Dantrolene, (direct muscle inhibitor) 50 to 800 mg every 12 hours. Some caution should be used
because hepatotoxicity has been reported. Serum transaminases should be monitored.
Why GA? --- to tackle the flexor spasms, adequate control over blood loss..

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bladder innervation
parasympathetic S2-4 : contracts the detrusor for emptying
relaxes sphincter
sympathetic T10-L2 : contracts the sphincter
and inhibits the detrusor
rectum innervation:
parasympathetic: S234 -modulates the left colon function and relaxes sphincter
sympathetic : L1-2 opposite of the sympathetic
reproduction organs : nerva erigentes
parasympathetic S2-4 : erection due vasodilatation
sympathetic : ejaculation due to contraction of the vas deference and pelvic floor
spinal cord ends at L1 so any injury below it would only injure the cord hence its lower motor neuron type
injuty any thing above would be upper motor neuron

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UNILATERAL CLEFT LIP & PALATE.

Name:
Age:
Sex:
Occupation:
Resident of:
Came with:

C/O cleft of lip/palate/nose by birth, (speech (nasal twang), hearing c/o in case of
operated child)

1st / 2nd / 3rd Issue, out of a nonconsanguineous marriage, as a FULL TERM HOSP. DELIVERY. Age
of mother at the time of birth was years and that of father was years.
Antenatal history: Rubella, Radiation, drug consumption (phenytoin, retinoids, steroids)
History of any other congenital anomalies
Developmental milestone if adequate:
Head lift 3 months
Sit 6 months
Crawl 9 months
Stand 1 year
Walk 15 months
Immunization history if adequate:
At birth: BCG, OPV
6 weeks: DPT, OPV
10 weeks: DPT, OPV
14 weeks: DPT, OPV
9 months: measles
18 months: DPT, OPV
5 years: DT
10 years; TT
History of

associated ear discharge,

Repeated URTI,
Feeding problems,
Speech problems,
Nasal regurgitation

Family history
General examination: If other congenital anomalies are present (Vander woude, VACTERAL, Anorectal,
Genitourinary, Downs, Craniofacial microsomia, Pierre robin syndrome)
Vital signs:
Systemic examination:
Local examination:
There is discontinuity of lip / nasal floor / alveolus / palate
Lip
1. There is discontinuity of lip
2. There is discontinuity of white roll
3. Apex of cupids bow is raised on CS
4. Lip height is reduced on the CS
5. Vermilion tubercle is deficient
6. The premaxilla is anterior and rotated to the non CS
7. There is bunching up of muscles on the lateral element.
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Nose
1. Nasal sill is intact or discontinuous
2. There is discontinuity of nasal floor (or depression)
3. Nasal floor appears wider
4. Columella base is shifted to non CS
5. Columella is short on the CS
6. Nasal tip is deviated to CS
7. Nasal septum is slanting over the cleft
8. Ala is flattened
9. Alar facial grove is obtuse
10. Alar base is shifted out and down
11. Angle between medial and lateral crura is obtuse
12. There is maxillary hypoplasia on the CS
Alveolus
1. There is discontinuity of alveolus
2. The gap between the segments is so many cm
3. Arches are aligned / collapsed
4. If collapsed, direction of collapse of medial and lateral arches (In / Out)
5. Number of teeth on medial element and that on the lateral element.
Palate
1. The cleft in palate is complete / incomplete.
2. The gap is approximately X cms
3. Palatal shelves are horizontal and of adequate / inadequate width
4. Palatal length is adequate /inadequate
5. Vomer is in the midline / attached to right / left side
6. Soft palate movements can / cannot be seen when the baby cries
7. Movement of Pharyngeal muscles is seen / not seen
Lower jaw is normal: r/o Pierre robin sequence.
If there is fistula, comment as: there is a communication between.
DIAGNOSIS
Right /Left sided Complete /Incomplete cleft of the Primary / or & Secondary palate with / without nasal
deformity with / without syndromic associations in a baby aged X months.
APPROACH
Lip is operated between 3 to 6 months (Tennison / Millard and Macomb primary nasal repair),
Palate at one year (VWK for incomplete & 2 flap Palatoplasty for complete with intravelar
veloplasty).
Rhinoplasty at 5 years prior to school.
At 8 to 9 years after orthodontic therapy alveolar bone grafting.
After orthodontic therapy Lefort I advancement for maxillary retrusion at 18 years.
Followed by definitive Rhinoplasty.
ADVICE AT BIRTH
1. Explain nature of Illness, the schedule of surgeries usually required
2. Examination for concomitant congenital anomalies by pediatrician
3. Genetic counseling: incidence of cleft palate 1: 1200, cleft lip palate 1:750

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One sibling
One parent
One sibling one parent
Two siblings

CL/P
4.4%
3.2%
15.8%
9%

CP
2.5%
6.8%
14.9%
8%

4. Feeding advice:
Feed Slowly These babies have faulty lip seal due to cleft, Inability to suck due to loss of negative
suction due to cleft in palate
Smaller feed at more frequent intervals
If unable to breast feed give in pallada / spoon
Hold the baby keeping head up in a sitting position and pour milk with a spoon at the back of
tongue
Burp babies more frequently
Mead Johnson bottles/Hebberman (longer teats, larger holes)

Secondary deformities (c/o):

Lip scar
Hearing problems
Speech (nasal twang)
Misalignment of dental arches
Cosmetic deformity
Steroids consumption cleft palate only
Testing hypernasality: with spatula in front of nares, test the frosting on it, which indicates nasal emission.
Prealveolar fistula: best treatment is to do a complete lip revision. (provides excellent access to nose)
Indication of ABG in B/L CL: to stabilize mobile premaxilla.
Genu of soft palate: Levator eminence (located anterior to uvula) makes contact with pharyngeal wall.
Examination of the patient with cleft palate only should assess the following:
1. Size of the cleft (e.g., partial cleft of the soft palate).
2. Complete cleft of the soft palate and partial extension into the hard palate.
3. Complete cleft of the soft and hard palate.
4. Width of the cleft.
5. Shape of the cleft (U-shaped clefts of the hard and soft palate are extremely rare and present a
difficult surgical problem).
6. Position of the lower ridge of the vomer.
7. Inclination of the palatal shelves.
8. Length, symmetry, and mobility of the soft palate.
9. Degree of motion of the lateral pharyngeal walls.
10. Distance between the posterior edge of the soft palate and the posterior pharyngeal walls.
11. Presence of Passavant's pad.
12. Amount of adenoid tissue.
13. Size and status of the tonsils.
Preoperative evaluation of patients with complete unilateral and bilateral cleft of the lip, alveolus, and
palate should include assessment of the following to determine readiness for operation:
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1. Width of the cleft.
2. Position of the maxillary segments.
3. Attachment of the lower edge of the vomer to the palatal shelf on the nonCS.
4. Distance between the alveolar ridges.
5. Inclination of the palatal shelves.
6. Length, symmetry, and mobility of the soft palate.
7. Presence and quality of dentition.
8. Distance between the posterior edge of the soft palate and the posterior pharyngeal wall.
9. Mobility of the lateral pharyngeal walls.
10. Presence of Passavant's pad.
11. Presence and amount of adenoid tissue on the posterior pharyngeal wall.
12. Size and status of the tonsils

According to the present notion of the influence of palatoplasty on speech development and maxillofacial
growth, various trends have appeared in the surgical techniques for cleft palate. With respect to speech,
two major trends are apparent: one focuses on achieving complete closure of the cleft; the other is
designed to achieve maximum retropositioning of the soft palate to obtain the best possible
velopharyngeal closure.
In regard to maxillofacial growth also, two major trends are apparent: one focuses on complete
closure of the palatal cleft in one surgical procedure, while the other is designed for early closure of the
soft palate, and delayed closure of the hard palate.
With respect to speech, the first trend is represented by an operation designed by von Langenbeck.
who initially intended to close the cleft of the hard palate only, using two parallel incisions: one on the
medial edge of the cleft and the other a lateral incision parallel to the alveolar ridge. Mucoperiosteal flaps
on the hard palate were undermined from the bone and sutured at midline. In this operation, the
mucoperiosteal flaps from the hard palate were always maintained by a narrow pedicle in the anterior
portion of the palate, never being totally elevated from the bone. Further development of the von
Langenbeck procedure involved complete closure of the hard and soft palate. Relaxing procedures were
designed to facilitate closure with less tension and to avoid postoperative complications, especially
oronasal fistulas. To improve results, other procedures were added to the original technique. These
procedures included:
1. Extension of the lateral incision into the space of Ernst.
2. Fracturing of the hamulus, or dislocation of the tendon of the tensor muscle.
3. Fracturing of the entire medial plate of the pterygoid process.
4. Removal of the posterior wall of the major palatine foramen.
5. Extension of the neurovascular bundle by pulling or dissecting it from the mucoperiosteal flap.
6. Severing of the neurovascular bundle.
7. Closure of the nasal layer using MP flaps from the nasal surface of the palatal shelves.
8. Use of mucoperiosteal vomerine flaps.
9. Lengthening of the soft palate.
10. Use of transverse incisions on the nasal MP along the posterior edge of the bony palate.
11. Detachment of muscles from the posterior edge of the bony palate.
12. Creation of a muscle sling.
VEAU:
Single, unipedicled, mucoperioteal advancement flap
Advocated Ganzer V incision
Vomerine flaps for nasal layer closure
Released abnormal insertion of musculature, reoriented and suture them with a metallic suture.
WARDILL:
Perfected V-Y retropositioning
Dissection of nasal mucosa from edges of hard palate

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Fractured hammulus
Divided Greater Palatine vessels
Modified V-Y by transecting the MP flaps in the midline
3 flap method for incomplete palate,
Superior pharyngeal flap based PHARYNGOPLASTY

10

KILNER:
Refused to divide greater palatine vessels
Did not consider pharyngoplasty in all cases.
CHARLES PINTO modification: converted 4 flaps of VWK into 2 large flaps.
Hole in one procedure ( as in golf)
OPERATIVE STEPS IN UNILATERAL CLEFT PALATE:
1.
2.
3.
4.
5.

GA with oral intubation using RAE tube in the center of lower lip & fixed in midline.
Position: max possible neck extension
Neosporin eye oint. In eyes, covered with wet gauze pieces. P & D
Tongue stitch in midline (deep bite)
Dingmann mouth gag is applied taking care to avoid undue compression of ET tube (1. Check nail
& mucosa colour 2. Ask anaesthetist for any increased resistance in ventilation). Tube should be in
the fenestration of tongue blade of retractor.
6. Oral cavity is cleansed with betadine/saline, any secretions in the oropharynx sucked & oral pack
introduced on both sides of tube (again avoid compressing tube!)
a. Packing prevents peritubal leak of air (froathing)
b. Prevents aspiration of blood
c. Secures tube in midline
7. Infiltration: 1:2 lacs of ADR (not to exceed 0.3 ml/kg) with 2cc syringe and 26 G needle at 4
sites: given deep to MP.
a. Medial margin of the cleft
b. At maxillary tuberosity
c. Uvula &
d. Junction of hard & soft palate
The end point: BLANCHING of mucoperiosteum & hydrodissection, wait for 7 minutes.
8. Cleft pairing incisions: with no 15 blade for whole extent of cleft B/L (at the junction of PINK
oral mucosa & PALE nasal mucosa). It should be placed more on the oral side so as to facilitate
the elevation of MP flaps (as the incision is constantly under vision) & to facilitate dissection of
nasal layer. It also gives more tissue for nasal layer closure.
9. S shaped incision around maxillary tuberosity: starting along pterygomandibular raphe , curving
it around the maxillary tuberosity posteriorly, then bringing it forward & medial to alveolus.
Wound margins are distracted down to the hamulus, which is fractured medially. The wound is
packed temp. with moist gauze.
10. Lateral incisions: for development of MP flaps, started from the anterior end of S shaped incision
& carried anteriorly upto the canine tooth (medial to alveolar ridge). From this point, the incision
continues at right angles to the apex of cleft, to meet the anterior most part of the pairing incision.
All incisions should reach the bone in first go.
11. MP flaps are elevated with ROSE RASPARATORY starting from few mm behind the anterior end
of the flap with gentle shaking movements of wrist, avoiding any button holes.
12. Flaps are elevated ant post & medial lateral. Progressing posteriorly, greater palatine vessels
are visualized. Careful gentle dissection on both sides of vessels. (it will mobilize flap for 6-10
mm)
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13. Posterior nasal spine & post border of hard palate are identified, abnormal insertions11of the
muscles from post border of hard palate & cleft margins are separated.
14. Nasal layer is identified & dissection is started from junction of soft & hard palate remaining
towards bone, avoiding perforation of nasal mucosa (using hockey stick elevator). Oral & nasal
layers are dissected & muscle freed from both layers
15. Suturing:
a. Closure of nasal layer post ant with interrupted 5-0 vicryl on a 5/8 circle needle, keeping
knots on nasal side (leaving uvula)
b. Muscles are overlapped & sutured in midline with 4-0 vicryl horizontal mattress sutures.
c. Oral layer: post ant with interrupted 4-0 vicryl on a 5/8 circle needle, keeping knots on
oral side (leaving uvula), vertical mattress. (2-3 sutures of this layer are passed through
repaired nasal layer to approximate oral & nasal layers , this eliminates dead space)
d. Uvula is sutured in the last.

16. Lateral raw areas: either sutured loosely or packed

17. Wet saline gauze is pressed firmly over the suture line & lateral raw areas x 10 minutes mouth
gag is released completely after removing the pack gently & patient is observed for any bleeding
no bleeding oral pack is removed & secretions are sucked head is flexed to deliver any
clot /blood from nasopharynx to oropharynx sucked
18. Anaesthetist is asked to make the patient light check for bleeding clear extubated pt
placed in lateral decubitus position tongue stitch is secured to cheek with tape elbow
restraints are applied pt shifted to recovery.
19. Postop: IV fluids, IV antibiotics X 3 days oral, daily intraoral inspection, feeding: liquid diet
and mother is instructed to give clear water after feeding. The packs in the lateral areas are
removed after a week.
Goals of palatoplasty:
1. Construction of air & water tight velopharyngeal valve
2. Preservation of hearing
3. Preservation of facial growth
4. Functional occlusion & esthetic dentition.
Deciduous dentition: starts at 6 months & all are appeared at the end of 2nd year.
6 months:
lower central incisor
7 months:
upper central incisor
8-9 months: upper & lower lateral incisor
12 months:
upper & lower 1st molar
18 months:
lower canine
24 months:
second molars
Permanent dentition:
First molar:
Medial incisiors:
Lateral incisiors:
First premolar:
Second premolar:
CANINE:
Second molar:
Third molar:

6 years
7 years
8 years
9 years
10 years
11 YEARS
12 years
17-25 years.
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teeth are numbered as follows: the maxillary dental arch, right to left, 1 to 16; the mandibular12dental
arch, left to right, 17 to 32. The deciduous teeth are numbered 1 to 8 in the maxillary arch, right to left,
and 9 to 16 in the mandibular arch, left to right.
Steffensen in 1953 listed five criteria for satisfactory lip repair:
1. Accurate skin, muscle, and mucous membrane union;
2. Symmetrical nostril floors;
3. Symmetrical vermilion border;
4. Slight eversion of the lip; and
5. A minimal scar which by its contraction will not interfere with the accomplishment of the other stated
requirements. One of the authors (Musgrave, 1963) has called attention to two additional criteria, which
can properly be added to this list:
6. Preservation of the Cupids bow and the vermilion-cutaneous ridge;
7. Production of symmetrical nostrils as well as symmetrical nostril floors.
OPERATIVE STEPS IN UNILATERAL CLEFT LIP: (from PRACTICAL PLASTIC SURGERY)
General endotracheal anesthesia with an oral RAE (= Reversed Angle Endotracheal) tube is used for all
stages of cleft lip repair. A cursory description of a modified Millard operative technique is as follows:
Presurgical Marking
The key points that are identified and marked are as follows:
Midline and bases of the Columella (1, 6)
Alar base
Peak and midpoint of Cupids bow on the NCS (2, 3)
Proposed point of Cupids bow on the CS (4)

Two key elements are involved in the markings:

the placement of the final position of the new Cupids bow peak and
the vertical length of the philtral column to be created on the CS.
Referring to the diagram, Point 3 is determined as the mirror image of Point 2 based on the distance from
the midpoint to the peak of the Cupids bow on the NCS.
The peak on the CS, Point 4, is not determined as easily but typically is placed level with Point 2, where
the dry vermilion is widest and the white roll above is well developed. The white roll and the dry
vermilion taper off medial to this point. It is unreliable to determine the peak on the CS, using the distance
between the peaks of the Cupids bow from the commissure on the NCS because of unequal tension of the
underlying orbicularis muscle.
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Once the anatomic points are marked, draw incision lines that define the five flaps involved
in the
lip reconstruction. These are the inferior rotation flap (R) of the medial lip element, the medial
advancement flap (A) of the lateral lip element, the columellar base flap (C) of the medial lip element, and
the two pared mucosal flaps of the medial and lateral lip elements. An additional flap that refines the
repair is the vermilion triangular flap to allow for a smoother transition at the VC junction and at the
vermilion contour.
The essential marking is the line that determines the border between the R and C flaps. This line
becomes the new philtral column on the CS. For the vertical lengths of the philtrum on the CS and NCS to
be symmetric, the length of the RA FLAP (y) should equal the vertical length of the philtral column (x) on
the NCS (distance between alar base and Cupids bow peak). For the two lengths, x and y, to be equal, the
path of y must be curved as illustrated. In marking the curve, take care to avoid a high arching curve that
comes too high at the columellar base to create a generous philtrum, as this significantly diminishes the
size of the C flap.

Description of the Repair

After markings, 0.5% lidocaine with epinephrine (1:200,000) is injected into the lip and the nose. In the
region of the VC junction, incise the muscle for approximately 2-3 mm on either side of the cleft
paralleling the vermilion border to allow development of VC muscular flaps for final alignment.
Develop the R and C flaps by incising the line (x) between the flaps to allow inferior rotation of
the R flap so that it lies horizontally tension free with Point 3, level with Point 2. For this to occur, release
must be at all levels (skin, subcutaneous tissue, muscle, fibrous attachments to the anterior nasal spine,
labial mucosa). Correspondingly free the C flap with the medial crus of the alar cartilage and allow it to be
repositioned, creating a large gap to be filled by the A flap.
Develop the A flap from the lateral lip element for advancement into the gap between the R and C
flaps. In developing the A flap, keep the incision along the alar base at a minimum; it rarely is required to
extend much beyond the medial-most aspect of the alar base. A lateral labial mucosal vestibular release is
also required to mobilize the A flap medially and to avoid a tight-appearing postoperative upper lip
deformity.
As part of the mobilization of the ala, make an incision along the nasal skin-mucosal vestibular
junction (infracartilaginous) where the previously developed L flap may be interposed if needed. Widely
undermine the nasal tip between the cartilage and the overlying skin approaching laterally from the alar
base and medially from the columellar base. While the A flap can be inserted as a mucocutaneous flap
incorporating the orbicularis, the author repairs the muscle separately to allow for differential reorientation
of its vectors. Dissect the muscle from the overlying skin and the underlying mucosa to accomplish this
and divide it into bundles that can be repositioned and interposed appropriately.
Once all the flaps are developed and the medial and lateral lip elements are well mobilized, begin
reconstruction. Typically, this begins with creating the labial vestibular lining from superior to inferior
and then proceeding to the junction of the wet-dry vermilion with completion of the remainder of the
vermilion after the cutaneous portion of the lip is completed. At this point, the labial mucosa can be
advanced as needed, with additional lengthening and a back cut to allow for adequate eversion of the lip
and to avoid a tight-appearing lip postoperatively. Approximation of the muscle bundles must be
complete. Appropriately reorient the nasolabial group of muscles toward the nasal spine. Follow this by
approximating the orbicularis, interdigitated with its opposing element along the full length of the vertical
lip.
Inset the C flap to create a symmetric columellar length and flare at its base. Millard originally
described the C flap to cross the nasal sill to insert into the lateral lip element as a lateral rotationadvancement flap. Millard later refined the C flap as a medial superior rotation flap to insert into the
medial lip element, augmenting the columellar height and creating a more natural flare at the base of the
medial footplate.
The latter method occasionally results in a nexus of scars at the base of the columellar with
unfavorable healing if the flaps are not well planned. However, the author continues to use the C flap in
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either
position as needed. Set the ala base in place. As the C and A flaps and the ala are inset, take14care to
leave an appropriate width to the nasal sill to avoid a constricted-appearing nostril, which is nearly
impossible to correct as a secondary deformity.
Approximate the vermilion-cutaneous junction and inset the vermilion mucocutaneous triangular
flap. Use dermal sutures to approximate the skin edges. Final approximation is with nylon sutures, ideally
removed at 5 days. If the cutaneous edges are well approximated with dermal sutures alone, one may
occasionally use a cyanoacrylate-type adhesive. Reposition the cleft alar cartilage with
suspension/transfixion sutures and a stent. Further shape the ala with through-and-through absorbable
sutures as needed.

Repair of Bilateral Cleft Lip

Originating on either side of the columellar base, vertical lines are marked ending in a triangular base such
that Cupids bow is 6 to 8 mm wide. Lateral forked flaps are also outlined prior to making the skin
incisions. All philtral-based flaps are elevated from the surrounding vermilion. The prolabial mucosal
vermilion complex is thinned before being sutured together, creating the midline posterior labial sulcus.
The lateral lip segments are incised vertically down from the medial alar base, analogous to the originally
made prolabial incisions. Medially-based buccal mucosal flaps are rotated from the alar base horizontally.
The alar cartilages are freed via an intercartilaginous incision, originating from the piriform aperture, and
secured together at the domes and to the upper lateral cartilages. The buccal mucosal flaps are then
sutured into the inferior intercartilaginous incision to increase length for the nasal floor reconstruction.
The mucosal orbicularis flaps are sutured together to create the anterior labial sulcus, with the most
superior suture secured to the nasal spine to prevent inferior displacement. Finally, the inferior white rollvermilion-mucosal flaps are apposed to create Cupids bow and tubercle complex.
Postoperative Considerations
For the child who is breastfed, the author encourages uninterrupted breastfeeding after surgery. Some
centers will allow bottle-fed children to resume feedings immediately following surgery with the same
crosscut nipple used before surgery, while others have the child use a soft catheter-tip syringe for 10 days
and then resume normal nipple bottle feeding.
The author uses Velcro elbow immobilizers on the patient for 10 days to minimize the risk of the
child inadvertently injuring the lip repair. The parents are instructed to remove the immobilizers from
alternate arms several times a day in a supervised setting. For the child with sutures, lip care consists of
gently cleansing suture lines using cotton swabs with diluted hydrogen peroxide and liberal application of
topical antibiotic ointment several times a day. This is continued for 10 days. If cyanoacrylate adhesive is
used, no additional care is required in the immediate postoperative period until the adhesive film comes
off. The parents are told to expect scar contracture, erythema and firmness for the first 4-6 weeks
postoperatively, and that this gradually begins to improve 3 months after the procedure. Typically, parents
are also instructed to massage the upper lip during this phase and to avoid placing the child in direct
sunlight until the scar matures.

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15

BILATERAL CLEFT LIP & PALATE.

Name:
Age:
Sex:
Occupation:
Resident of:
Came with:

C/O cleft of lip/palate/nose by birth, (speech (nasal twang), hearing c/o in case of
operated child)

1st / 2nd / 3rd Issue, out of a nonconsanguineous marriage, as a FULL TERM HOSP. DELIVERY. Age
of mother at the time of birth was years and that of father was years.
Antenatal history: Rubella, Radiation, drug consumption (phenytoin, retinoids, steroids)
History of any other congenital anomalies
Developmental milestone if adequate:
Head lift 3 months
Sit 6 months
Crawl 9 months
Stand 1 year
Walk 15 months
Immunization history if adequate:
At birth: BCG, OPV
6 weeks: DPT, OPV
10 weeks: DPT, OPV
14 weeks: DPT, OPV
9 months: measles
18 months: DPT, OPV
5 years: DT
10 years; TT
History of

associated ear discharge,

Repeated URTI,
Feeding problems,
Speech problems,
Nasal regurgitation

Family history
General examination: If other congenital anomalies are present (Vander woude, VACTERAL, Anorectal,
Genitourinary, Downs, Craniofacial microsomia, Pierre robin syndrome)
Vital signs:
Systemic examination:
Local examination:
LIP
1. There is discontinuity of lip on the right and left side
2. There is discontinuity of white roll on both sides
3. The central segment between the clefts is formed by the prolabium
4. There is no well formed cupids bow / philtral columns / philtral grove / wet vermilion. Prolabial
vermilion is deficient.
5. Prolabial gingivobuccal sulcus is shallow
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6. The vermilion and white roll of the lateral lip element show obliquity with gradual thinning
and
eventual disappearance at the cleft edge.
7. There is bunching up of muscles in the lateral lip
8. The prolabium is narrow / wide.

NOSE
1. Nasal sill discontinuous on right / left side
2. There is discontinuity of nasal floor on right / left side
3. Nasal floor appears wider on right / left side
4. Columella is short
5. Nasal tip is depressed
6. Nasal septum appears in the center / deviated to one side
7. Ala is flattened with flaring on right / left side
8. Alar facial grove is obtuse on right / left side
9. Alar base is shifted out and down on right / left side
10. Angle between medial and lateral crura is obtuse on right / left side
11. There is maxillary hypoplasia on right / left side
12. There is excessively obtuse Nasolabial angle
ALVEOLUS
1. There is discontinuity of alveolus on right / left side
2. The gap between the segments is so many cms on right side, so many cms on left side
3. The premaxilla is protruding and carries so many teeth
4. The lateral alveolar segments are aligned / collapsed
5. If collapsed, direction of collapse of right and left segments (In / Out)
6. There are so many teeth on right alveolus and so many on the left alveolus.
7. There is enough or not enough space between the alveolar segments for the premaxilla
PALATE
1. The cleft in palate is complete / Incomplete
2. The gap is approximately so many cms
3. Palatal shelves are horizontal and of adequate / inadequate width
4. Palatal length is adequate /inadequate
5. Vomer is in the midline / attached to right / left side
6. Soft palate movements can be seen when the baby cries
DIAGNOSIS
Bilateral Complete /Incomplete cleft of the Primary / or & Secondary palate with / without nasal
deformity with / without syndromic associations in a baby aged X months.
APPROACH
Lip operated between 3 to 6 months (straight line repair, millard repair), palate at one year (VWK for
incomplete & 2 flap palatoplasty for complete with intravelar veloplasty). Rhinoplasty at 5 years prior to
school. At 8 to 9 years after orthodontic therapy alveolar bone grafting. After orthodontic therapy lefort I
advancement for maxillary retrusion at 18 years. Followed by definitive rhinoplasty.
ADVICE AT BIRTH
1. Explain nature of Illness, the schedule of surgeries usually required
2. Examination for concomitant congenital anomalies by pediatrician
3. Genetic counseling ( Single dose : 1 in 20 i.e. either one parent or one previous child, Double dose : 1 in
4 i.e. both parents or one parent one previous child or 2 previous children (Simplified from Dr karoon
Aggarwal))
4. Feeding advice: Similar to unilateral lip.

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After palate repair: orthodontic treatment avoids collapse of lateral maxillary segment , expansion
Premaxillary setback at 4-5 years
Break segment of vomer and push back premaxilla, fix with K wire.
Soft tissue / nose correction before 6 years ???

PALATAL FISTULA
History:
Hearing problems, any ear discharge
Swallowing difficulty
Speech difficulty
Breathing difficulty
Intraoral examination:
Oral hygiene
Maxillary arch
Prealveolar fistula
E/O scars of previous surgeries
Palatal fistula
Dentition / occlusion
Uvula (bifid/ hypoplastic)
Passavants ridge (upper part of superior pharyngeal constrictors)
Tongue
Serous otitis media destruction of ossicular chain conductive deafness
Single layer nasal closure, leaving oral layer to mucosalise
Tongue flap: intraop IMF release postop liquids after 48 hours
While drawing cleft palate, draw pharynx also.
Boundaries of space of earnst:
Anteriorly maxillary tuberosity
Medially levator palatine
Laterally pterygoid plate
Muscle suturing: if edge to edge simple interrupted sutures with delayed absorbable material
Overlapping: horizontal mattress sutures.
Revision for intravelar veloplasty:
1. Furlows double opposing Z-plasty / mirror image Z-plasty
2. Pharyngeal flap (superiorly based) base is at the anterior arch of the ATLAS.
Normann Dotts modifications of Boyle Davis gag:
Groove in the tongue blade to accommodate the ET.
Port for introducing suction catheter
Dingmann added the cheek retractors.
Pharyngoplasty is indicated when speech is perceived to be hypernasal as a result of VPI.

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In the normal individual, the velopharyngeal sphincter separates the oropharynx from
the
nasopharynx. During continuous speech, the sphincter closes for oral speech production, shutting off the
nasal cavity, and opens for nasal speech production, opening the passage between the oral and nasal
cavities.
The velopharyngeal sphincter is formed by the muscles of the soft palate and by the superior
constrictor muscle of the pharynx. The function of these muscles determines the effect of the sphincter
motion. Additionally, the presence of adenoid tissue and/or of Passavant's pad may influence the degree of
closure of the sphincter. The synchronous action of the soft palate and pharyngeal muscles results in
closure of the velopharyngeal sphincter and separation of the oropharynx from the nasopharynx. In some
instances, compensatory movements develop to facilitate closure. For example, when the palate is short, increased
mobility of the lateral and posterior pharyngeal walls, such as that seen in Passavant's pad, may compensate for the
inadequacies of the soft palate length and/or movement.
The quality of speech with respect to nasalization is the primary indicator for pharyngoplasty. A
short palate may be accompanied by perceptually good speech due to the compensatory function of the
other elements of the sphincter. Several factors that should be considered when one analyzes the function
of the velopharyngeal sphincter and speech quality include:
the length and mobility of the soft palate,
the medial movement of the lateral pharyngeal walls,
the anterior movement of the posterior pharyngeal wall,
the presence or absence of Passavant's pad and/or adenoid tissue, and
nasal airway obstruction, such as hypertrophy of the lower turbinates, septal deviation, or choanal
atresia.

Following palatoplasty, good speech may develop, although hypernasality may recur after some time,
indicating that changes have occurred that influence speech production. Typically, this happens following
spontaneous atrophy of the adenoid tissue, resulting in a velopharyngeal port that cannot be sufficiently
occluded. In most cases adenoidectomy is contraindicated in patients with a repaired cleft palate or
submucous cleft palate. Adenoidectomy often creates an enlarged velopharynx, causing VPI in these
patients. This can be prevented by performing a selective adenoidectomy. Tonsillectomy in carefully
selected patients may be performed when necessary.
Changes in speech production may also occur after intranasal surgery. For some patients,
hypertrophy of the lower turbinate or airway obstruction due to deviation of the septum may be beneficial
in terms of speech production, although the obstruction is detrimental for nasal breathing. Conversely,
improving the nasal airway by straightening the septum or by excising part of the lower turbinate may
impair speech production.
Hypernasality and nasal air emission during articulation are the most typical characteristics of cleft
palate speech
ASSESSMENT OF VPI: Diagnostic evaluation may include
an intraoral examination of the speech mechanism,
articulation testing,
videofluoroscopy,
nasoendoscopy,
lateral still cephalometric x-ray studies, and
aerodynamic measurements.
The earlier the flap treatment is performed, the better the resulting speech production will be. Perhaps at
younger ages the speech production mechanism is better able to adapt to the structural changes of
pharyngeal flap surgery.
A number of speech symptoms are associated VPI. These include hypernasality, nasal air
emission, weak pressure consonants, and compensatory articulation.
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All four speech symptoms need not be present for VPI to be suspected. Hypernasality, nasal
air
emission, and weak pressure sounds are the result of excessive oral nasal coupling. Compensatory
articulation is the result of an attempt to counterbalance the inadequate velopharyngeal function, and is
associated with maladaptive articulatory placements which are used as substitutes for pressure phonemes.
These maladaptive articulatory placements may persist following physical management of the VPI

1. Articulation. The term is used by speech-language pathologists to refer to movements of the vocal tract
that produce the sounds of speech. Speech articulators include the lips, mandible, palate, tongue, and the
pharynx.
2. Phonation. The sounds of speech may be dichotomized into two groups. Voiced or phonated sounds,
such as vowels and voiced consonants (b, d, and g), are produced as a result of the vibration of the vocal
chords of the larynx. This vibration is initiated as a result of the build-up and the pulselike release of
subglottal air.
Unvoiced sounds (p, t, and k) are not, by their nature, characterized by vocal chord vibration.
Instead, air from the lungs passes through the open, nonvibrating larynx and is modified by articulatory
movements of the tongue, lips, jaw, and pharynx.
3. Resonance. Both voiced and unvoiced sounds are modified by the resonance characteristics of the vocal
tract. Resonance refers to the vibratory response of the vocal tract to sound.
4. Compensatory articulations. Compensatory articulations are believed to be the cleft palate speaker's
attempt to achieve oral-nasal valving. The speaker employs the correct "manner" of articulation (plosive,
affricate, glide, etc.) but shifts the "place" of articulation from the expected site. In general, cleft palate
speakers tend to shift the place of articulation in a backward direction. Compensatory articulations, like
the glottal stop and pharyngeal fricative, reflect the speaker's attempt to create as successful a valve as
possible, at a site other than the velopharyngeal portal. The most common types of compensatory
articulations are:
a. Nasal snort. The nasal, or nasopharyngeal snort is often associated with the /s/ phoneme and other
fricatives. The auditory perception is that of excessive force of production, and represents the introduction
of air through an initially closed velopharyngeal valve. Intraoral pressure mounts until the velopharyngeal
valve is forced open, culminating in a brief but noisy escape of air into the nasal airways.
b. Posterior nasal fricative in phoneme-specific velopharyngeal incompetence. The posterior nasal
fricative is characterized by audible nasal emission accompanied by audible frication, which is created by
"velar flutter" activity. The posterior nasal fricative is notably present in non-cleft palate patients with
velopharyngeal incompetence, specifically in phoneme-specific velopharyngeal incompetence which is
seen after a pharyngeal flap procedure. Biofeedback training will help many patients overcome this
problem.
c. Pharyngeal stop. The pharyngeal stop is a compensatory substitution for /k/ or /g/. This involves tongue
positioning that is posterior and inferior to that required for /k/ or /g/ production. These stops can occur as
high as the level of the greatest velopharyngeal constriction or as low as the area slightly superior to the
glottis.
d. Pharyngeal fricative. The pharyngeal fricative is compensatory frication between the dorsum of the
tongue and pharyngeal wall.
e. Middorsum palatal stop. Middorsum palatal stops are substitutions for the /t/, /d/, /k/, or /g/ sounds.
Each substitution occurs in the place of production for the /j/ sound (as in young). With the middorsum
palatal stop, voiced equally and unvoiced sound substitutions, like /t/ or /k/, sound similar. This is because
the phoneme boundaries are lost between the /t/ and /k/, and /d/ and /g/.
f. Velar fricative. The velar fricative involves the replacement of back velar stops /k/ and /g/ with a
linguavelar articulation. This is seen often in dysarthric speakers who have neuromotor involvement of the
posterior portion of the tongue. The sound produced has a fricative quality.
Common Error Types and Speech Patterns in Cleft Palate Patients
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1. Speakers
may evidence sound distortions (phoneme nasalization), substitutions (substitutions20of one
/f/ phoneme for another), or omissions (failure to articulate a phoneme).
2. Speakers with cleft palate are more likely to articulate plosives correctly, followed by nonsibilant
fricatives and sibilants. Fricatives and affricates have the highest rate of misarticulation. The /s/ sound is
the phoneme that cleft palate speakers most frequently and consistently misarticulate.
3. In cleft palate speakers, sounds that require lingual contacts (/s/), are more often defective than sounds
requiring lip movement (/w/). Sounds made with posterior lingual activity (/k/) are more often disordered
than those made with the tongue.
4. Voiceless sounds are more likely to be misarticulated than their cognates. (Cognates are sounds that
only differ in the presence of voicing, such as the unvoiced /p/ and voiced /b/).
5. Unless nasalization is a problem, speakers with cleft palate generally articulate vowels correctly.
However, when compared with noncleft speakers, they are more likely to have problems producing
intelligible vowels and have more errors in vowel production.
6. There is a relationship between the vowel sound and perceived nasality. High vowels (/i/ as in beat) are
perceived as more nasal than low vowels (/ae/) as in battle), and front vowels (/i/ as in beat) are more
nasal than back vowels (/u/ as in boot).
7. Cleft palate speakers are more likely to misarticulate sounds in blends (two sounds together, as in bl)
than a single sound (one sound, as in b).
8. Speakers with cleft palate tend to misarticulate sounds inconsistently.
9. Children with cleft palate have slower articulatory development than noncleft speakers and are at
greater risk for disordered articulation. However, the articulation of cleft speakers does tend to improve
with age.
10. Speakers with cleft palate may have weak consonant production because of reduced intraoral air
pressure.

During the perceptual evaluation, the speech pathologist looks for a number of variables. These include:
1. Articulation.
a. Compensatory articulation - often used to compensate for inadequate velopharyngeal function.
b. Distortions (oral)-due to dental anomalies or orthognathic or occlusal deficits.
c. Nasal emission.
2. Aesthetic abnormalities.
a. Due to occlusion, dentition.
b. Facial nasal grimace- used to compensate for an inability to obtain velopharyngeal closure.
3. Resonance.
a. Hypernasality.
b. Hyponasality.
c. Mixed.
4. Phonation.
a. Quality-hoarseness, due to laryngeal hyperfunction resulting from an attempt to compensate for
velopharyngeal valving difficulties.
b. Intensity-reduced, due to loss of air through the velopharyngeal mechanism.
c. Frequency-monopitch often accompanies reduced intensity.
Articulation is influenced by a number of factors including structural and functional anomalies of the oral
mechanism. Thus it is important to assess:
1. Occlusion and dentition-the relationship of the teeth, missing dentition, supernumerary teeth.
2. Maxillary arch-maxillary collapse, orthodontic expansion device.
3. Palatal vault-fistula.
4. Lips- poor lip movement, due to inappropriate surgical correction of muscles.
Clinical examination is of limited value but nonetheless is important.
1.The degree of hypernasality is judged subjectively. For most examiners, evaluation is still rather
imprecise, and the most common classifications are mild, moderate, and severe.
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2.The
facial movements are noted, and the type and degree of grimacing are recorded.
3.Lip movement is observed to detect any muscular dysfunction that may be responsible for articulation
defects.
4.Dental occlusion is inspected and the condition of the teeth is noted. Any dental gaps or fistulas are
recorded. Poor occlusion and missing teeth contribute to articulation defects; fistulas may be responsible
entirely or in part for nasal emission as well as articulation defects.
5.The soft palate is inspected for scarring, motion, and length. Scarring indicates poor primary surgery and
difficulty during the healing process. Scarring may result in reduced palatal movement and AP palatal
shortening. The motion of the soft palate is very carefully observed. Palatal movement may be absent,
poor, or adequate. The position of the movement may be satisfactory, or movement may occur too far
anteriorly; it may be symmetric or asymmetric.
6.The length of the palate can be examined, but it is often difficult to assess palate length accurately unless
it is extremely short. The shortness may be anatomic or functional. Functional shortness occurs in a palate
that is of good length but does not move sufficiently to effect velopharyngeal closure. During clinical
examination, nasal emission of air can be demonstrated by the fogging of a cool dental mirror held at the
nostrils during the production of plosives.

ADDITIONAL ASSESSMENT TECHNIQUES

1. Videofluroscopy:
Lateral View
The lateral view shows five features: length, thickness, and movement of the palate; posterior pharyngeal
wall movement; and tongue movement. Examination is facilitated by barium coating, and the length of the
palate is easily assessed using a series of test words and phrases. The distance from the palate to the
posterior pharyngeal wall is noted, especially in the production of nonnasal sounds, for which there should
be complete closure of the velopharyngeal area.
The thickness of the palate is of interest since a thin palate suggests absence of muscular bulk.
Variations in thickness, particularly anterior thickening and posterior thinning, indicate faulty positioning
of the palatal musculature.
Perhaps the most useful information supplied by lateral Videofluroscopy concerns the extent and
position of movement and the level of maximal closure.
The presence or absence of Passavant's ridge is noted. This seems to be more prominent in
association with velopharyngeal incompetence. Abnormal tongue movement may be noted also. This is
generated by an effort to elevate the tongue to close off the velopharyngeal region.
Frontal View
The frontal view gives information on the level and extent of movement of the lateral walls. Again,
barium coating enhances viewing and facilitates interpretation.
Basal View
The basal view is the most useful view but also the most difficult to obtain. With barium coating, the
velopharyngeal aperture can be readily viewed. Sphincteric action is normally symmetric with closure on
nonnasal sounds. In individuals with incompetence, it can be determined whether the incompetence is due
to symmetric or asymmetric palate malfunction. The lateral walls may or may not demonstrate good
movement.
Videofluoroscopy can be performed in young children when the surroundings and personnel create an
atmosphere that has a calming effect on the child. Useful information can be gained even if only a lateral
view is obtained.
2. Nasopharyngoscopy
Nasoendoscopy provides information related to the amount, symmetry, and consistency of velopharyngeal
movement, as well as information regarding velopharyngeal gap size, shape, and location. This study is
important for assessing velopharyngeal closure, as well as conditions following pharyngoplasty. In
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velopharyngeal
incompetence, a definite gap is observed, or bubbles of mucus may be seen 22coming
through a small aperture that does not close properly.
3. Airflow studies.

Disadvantages of the pharyngeal flap procedure:

Mouth breathing, particularly after physical exertion or secondary to nasal congestion;
snoring (sometimes very severe);
partial or total nasal airway obstruction; and
collection of mucus above the flap in the nasopharynx, which may be difficult to evacuate.
In some cases, sleep apnea may occur.
Relevance to facial growth and development: AP dimension of the midface is affected, as
indicated by retrusion of the maxillary complex.
There is no defensible rationale for the routine use of the pharyngeal flap at the time of primary palate
repair since only 20% to 30% of cleft palate patients are expected to show velopharyngeal dysfunction
after primary palatoplasty.
Given all these considerations, and when indicated, pharyngoplasty is usually performed at our
centers between 4 and 6 years of age, We feel that the reliability of the diagnosis is adequate by this age,
and that the child adjusts to the operation much better than when it is performed later, in adolescence or
adulthood.
There have been those who have advocated the use of a palatal lift or obturator as a means of
improving articulation in the patient with borderline closure, or intermittent closure, and in the presence of
a surgical risk.
Inferiorly Based Pharyngeal Flap
The pharyngeal flap operation, initiated by Schoenborn was refined and popularized by Rosenthal. The
Schoenborn-Rosenthal: a mouth gag was inserted and the tongue was retracted to expose the posterior
pharyngeal wall. The pharyngeal flap was raised from the posterior pharyngeal wall as far cranially as
possible at the level of the cervical fascia. The level of the base of the flap was chosen so that the flap
reached the posterior edge of the soft palate. The soft palate was incised transversely and the nasal and
oral layers were dissected, creating a fishmouthlike defect. The free edge of the pharyngeal flap was
inserted into this defect and the oral surface of the soft palate was sutured on the raw undersurface of the
pharyngeal flap. The major portion of the flap had a raw area of tissue exposed which subsequently
contracted during the healing process, decreasing the width of the flap and increasing the size of the lateral
ports.
The inferiorly based pharyngeal flap pulls the soft palate inferiorly and posteriorly, decreasing
its mobility.
Presently, the inferiorly based pharyngeal flap is used only occasionally, and the vast majority of
surgeons use the superiorly based pharyngeal flap.
Superiorly Based Pharyngeal Flap (Sanvanero-Rosselli,1935)
Another design for the suyeriorly based pharyngeal flap was provided by Meissner. This design seemed
more logical, as longer flaps could be raised and inserted into the soft palate with less tension.The
decision as to the required width of the flap is related to the degree of velopharyngeal incompetence.
In this operation, the soft palate is split transversely or longitudinally and a superiorly based
pharyngeal flap is inserted into the soft palate. The raw area left on the pharyngeal flap creates a problem
since postoperative healing is associated with unpredictable scarring and contracture.
The surgical procedure is performed using a mouth gag that exposes the pharyngeal wall. The
posterior pharyngeal wall and palate are infiltrated with 1% lidocaine (Xylocaine) and 1:200,000
epinephrine. Use of local anesthesia is helpful for dissection of the pharyngeal flap from the prevertebral
fascia. A flap of predetermined width, up to the full extent of the posterior pharyngeal wall, is elevated.
The base is at the upper part of the tonsillar fascia, and the flap is made as long as necessary.
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The flap may be inserted into the palate in various ways. The free posterior margin of the23 palate
may be incised transversely and the flap inserted into a fishmouth like defect similar to that used for the
inferiorly based pharyngeal flap. Another method of insertion is to split the soft palate longitudinally at
midline and create two flaps, which are then elevated from the nasal aspect of the soft palate and sutured
together at midline, creating the lining for the pedicle of the pharyngeal flap. In this technique the entire
flap is covered, which decreases the possibility of postoperative changes, especially flap contracture. Flap
contracture decreases the width of the flap and increases the size of the ports.
Another way to insert the flap was first described by Meissner: A transverse incision is made just
behind the hard palate opening a gap between the hard and soft palate With long sutures used on the
pharyngeal flap, it is pulled through the defect and anchored to the muscles of the soft palate. The oral
layer is then closed.
Hogan Modification of the Pharyngeal Flap
Hogan described a procedure to line the raw surface so that there would be less change postoperatively in
the size of the pharyngeal flap and hence the size of the lateral ports. The entire raw surface of the
pharyngeal flap was covered with mucosal flaps from the nasal surface on the soft palate. Hogan et al.
introduced this concept of lateral port control. The technique was based on the premise that insertion of a
10-12F catheter would facilitate establishment of the size of the ports with more precision than any other
surgical method.

Lateral Pharyngoplasty : Hynes was the first to introduce the concept of lateral pharyngoplasty. He
believed it would be more functional since the nerve supply to the lateral pharyngeal muscles comes from
a superior origin. Any flap lifted laterally would contain neuromuscular elements and would contract.
Hynes lifted small faucial flaps and sutured these onto the posterior wall of the palate. Moore raised the
salpingopharyngeus muscle and used it to augment the posterior margin of the soft palate.
Orticochea Pharyngoplasty
An inferiorly based pharyngeal flap is elevated in standard fashion. Bilateral posterior tonsillar pillar flaps
are raised that are superiorly based and contain the palatopharyngeus muscle. These flaps are sutured to
the superior end of the pharyngeal flap and to themselves so that there is a midline opening between the
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mouth
and the nose. A careful muscle suture is carefully placed in the palatopharyngeus muscle. As
these
flaps heal, the central opening becomes narrower.

Sphincter Pharyngoplasty (Jackson and Silverton)

Difficulties were encountered using the inferiorly based flap in adults, and because too many raw areas
were left, a superior flap was used instead. The lateral flaps were sutured to the superior flap and all areas
were covered except the posterior pharyngeal wall. This technique subsequently has been modified to
eliminate raw areas, simplify the procedure, and place the pharyngoplasty in a more superior and
functional position.

PHARYNGEAL FLAP AND MAXILLARY ADVANCEMENT

Cleft patients with borderline velopharyngeal closure who require maxillary advancement may be at risk
for development of VPI. Nasopharyngoscopy and videofluoroscopy are good tools for assessment of these
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patients.
The possibility of postoperative VPI is discussed with patients who are determined to be25at risk.
In some cases, a pharyngeal flap procedure is performed at the time of the maxillary advancement. In
others, when airway problems exist at the time of surgery, the flap is delayed for at least 6 months after
advancement.
Relapse of the maxilla was highly possible if a pharyngeal flap procedure was performed soon
after taking the patient out of intermaxillary fixation. If intermaxillary fixation is present at the same time
that the flap is healing, then relapse is less likely. In patients who have a pharyngeal flap and require
maxillary advancement, it is necessary to simultaneously advance the pharyngeal flap. This incision
extends to the prevertebral fascia. The mucosa and muscle are rotated superiorly, allowing release and
lengthening of the base of the pharyngeal flap. The raw surface remains exposed. This simple procedure
facilitates effective lengthening of the pharyngeal flap in patients undergoing maxillary advancement.
There have been no problems in patients who have undergone maxillary advancement procedures after
sphincter pharyngoplasty.

What is the concentration of adrenaline in Mcg when used in palate surgery

Explanation :
1 ampule of adrenaline
1:1000 ml dilution
1gm : 1000ml
1000mg : 1000ml
1mg: 1ml
what we want is 1 : 200000 ml of dilution
1000mg : 200000
1mg: 200ml
1000mcg:200ml
10ug: 2ml
now in a palate case child is 10kg and max dose of adrenaline permissible is 6.7Mcg = 7Mcg
70Mcg can be given for 10kg
1ml contains 5Mcg
thus we can give 14ml of the diluted saline containing adrenaline
CHOPS (Childrens hospital of Philadelphia) modifications
1. Relaxing incision from posterior tonsillar pillar to incisor foramen
2. Space of Ernst dissection
3. unhooking of the Tensor palatani muscle from hammulus
4. cutting the levator aponeurosis

Space of Ernst:

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the muscle of the soft palate are supplied by the vagus except tensor palatani which is supplied26by the
mandibular nerve branch of trigeminal nerve
All the muscles of the pharynx are supplioed by vagus except stylopharyngeus which is supplied by
glossopharyngeal
All the muscles of the tongue are suppled by hypoglossal except palatoglossus which is supplied by vagus
Anterior palate repair

markings are made by dotted line:

consider the cleft in the alveolus as the box having four side, posteriorly it extends into the pyriform
aperture upto the nasal floor as an extension of cone from this box. As shown in the diagram below.

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27

the nasal floor is closed by two flaps based on the septal and lateral turbinate,
then the cleft is closed by gingivoperiosteal flaps on either side, on cleft you cut upto the first premolar if
required give a back cut. This would cover the alveolus anteriorly.
Finally the oral and posterior surface will be covered with mucopericosteal flaps on the palatal surface
After closure the final picture would be as shown below

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29

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30

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31

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CRANIOFACIAL MICROSOMIA
C/O: hearing
Facial deformity
IQ: ? Mental retardation.
Intraoral:

parotid duct
Alveolus
Cleft palate
Interincisor distance
Tongue movements

Feel for both condyles with bimanual examination

Examine facial nerve
Low set hairline
Ear: developed / not developed /hypoplastic /smaller
Extraocular movements
Intranasal examination
Hearing function
Palpate zygomatic arch & body
W/f any e/o torticollis
diagnosis: CRANIOFACIAL MICROSOMIA

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MICROTIA / Prominent ear / Lop ear / cryptotia.

Name:
Age:
Sex:
Occupation:
Resident of:
Came with:

deformity of left / right ear by birth

Loss of hearing of right / left ear by birth

1st / 2nd / 3rd Issue, born FTND to parents aged X / Y years married non / consanguineously
Antenatal history: Radiation, drug consumption
History of any other congenital anomalies
Developmental milestone if adequate:
Head lift 3 months
Sit 6 months
Crawl 9 months
Stand 1 year
Walk 15 months
Immunization history if adequate:
At birth: BCG, OPV
6 weeks: DPT, OPV
10 weeks: DPT, OPV
14 weeks: DPT, OPV
9 months: measles
18 months: DPT, OPV
5 years: DT
10 years; TT
Family history
History of previous surgery no, timing, nature
General examination: Associated with urogenital anomalies in 5 %, Cleft lip & palate in 5%,
Macrostomia in 2.5%, CVS anomalies in 2.5%, vertebral anomalies. Look for features of craniofacial
microsomia / Trecher Collins syndrome
Vital Signs
Local examination
1. Deformed ear which is small / large, describe helix, antihelix, lobule, concha.
2. Describe position and orientation of the remnant
3. Examine External auditory canal
4. Examine facial asymmetry : Hypo plastic mandible maxilla
5. Chin is deviated to same side
6. Examine occlusion
7. Cant of dentition / oral commisure
8. Masticatory muscles
9. Epibulbar dermoids ( Goldenhar syndrome)
10. Preauricular pits
11. Evaluate facial nerve
12. Classify Microtia as per NAGATA classification:

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Lobule type:
Concha type:
Small concha type:
Anotia:
Atypical:

No concha / tragus / EAC

small malpositioned deformed lobule and concha present
lobule present with a small indentation instead of concha
Absent ear
Combinations of above

13. Root of helix is attached to temporal skin without a grove in cryptotia

14. Prominent ear is characterized by deep conchal cup, underdeveloped antihelix, widened ear /
mastoid angle.
15. Cup ear is characterized by inadequate helical rim causing the concha to cup forward and a
floppy upper helix which is bent forward.
Cup ears are classified as per the TANZER classification
Grade I
GradeII
Grade III
16. Assess tissues around the ear for scarring
17. Assess the level of hair line
18. Assess for presence / absence of pulsations of superficial temporal artery
19. Assess donor site for CCG.
DIAGNOSIS
Microtia Grade / Lop ear grade / Cryptotia / Prominent ear in a patient aged .
APPROACH
Congenital anomalies of ear are managed usually at 4 to 5 years. Microtia at about 8 years. Microtia can
be managed either by Brent method or Nagata Method.
Proportions of the aesthetic ear

The long axis of the ear inclines posteriorly at approximately a 20 angle from the vertical
The ear axis does not normally parallel the bridge of the nose (the angle differential is
approximately 15)
The ear is positioned at approximately one ear length (5.57 cm) posterior to the lateral orbital rim
between horizontal planes that intersect the eyebrow and columella
The width is approximately 5060% of the length (width 34.5 cm, length 5.57 cm)
The anterolateral aspect of the helix protrudes at a 2130 angle from the scalp
The anterolateral aspect of the helix measures approximately 1.52 cm from the scalp (although
there is a large amount of racial and gender variation)
The lobule and antihelical folds lie in a parallel plane at an acute angle to the mastoid process
The helix should project 25 mm more laterally than the antihelix on frontal view

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McDowell's goals of otoplasty:

1. All upper third ear protrusion must be corrected
2. The helix of both ears should be seen beyond the antihelix from the front view
3. The helix should have a smooth and regular line throughout
4. The post-auricular sulcus should not be markedly decreased or distorted
5. The helix-to-mastoid distance should fall in the normal range of 1012 mm in the upper third, 1618
mm in the middle third, and 2022 mm in the lower third
6. The position of the lateral ear border to the head should match within 3 mm at any point between the
two ears.
CLINICAL CLASSIFICATION OF AURICULAR DEFECTS (TANZER)
Anotia
Complete hypoplasia (microtia)
With atresia of external auditory canal
Without atresia of external auditory canal
Hypoplasia of middle third of auricle
Hypoplasia of superior third of auricle
Constricted (cup and lop) ear
Cryptotia
Hypoplasia of entire superior third
Prominent ear

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Converse: The tunnel procedure is an effective technique for moderate-sized defects of the auricle and in major
defects it has the advantage of preserving the retroauricular sulcus .In employing this technique, one presses the
auricle against the mastoid area and draws an ink line on the skin in this area, keeping the line parallel and adjacent
to the edge of the auricular defect . Incisions are made through the skin along the ink line and also through the edge
of the auricular defect . The medial edge of the auricular incision is sutured to the anterior edge of the mastoid skin
incision . A cartilage graft is then placed in the soft tissue bed and is joined to the edges of the auricular cartilage
defect . The mastoid skin, which has been undermined, is advanced to cover the cartilage graft, and the edge of this
skin flap is sutured to the lateral edge of the auricular skin. A healing and vascularization period of 2 or 3 months is
permitted; during this period, the cutaneous tunnel behind the auricle must be cleaned with cotton-tipped
applicators. The auricle is detached in a second stage, and the resulting elliptical raw areas on the ear and mastoid
region are grafted .

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FACIAL PALSY
Name:
Age:
Sex:
Occupation:
Resident of:
Comes with C/O: inability to move forehead / eyelid (O.Oculi) / lips by birth / acquired
Duration
Onset: Insidious (Bells), Acute (Trauma / Surgery)
Progression
History of obstruction to upward gaze
History of absent tears
History of Epiphora
History of nasal obstruction
History of drooling of saliva
History of Collection of food in the mouth
History of difficulty in speech
History of inability to smile
History of Hyperacusis
History of trauma on the face
History of surgery on the face
History of any infections on the face / ear
History of any brain tumors
History of Herpes attacks
Family history (In Mobius syndrome, craniofacial microsomia)
General examination
Vital Signs
Local Examination
Inspection
1. Expressionless face
2. Loss of forehead wrinkles
3. Brow ptosis
4. Dry eye or Excessive tears with epiphora
5. Increased size of palpabral fissure (> 10 mm)
6. Scleral show
7. Lower eyelid ectropion (Paralytic)
8. Lacrimal punctum not in contact with the conjunctiva
9. Decreased visual fields
10. Ask Patient to close eyes & check for if bells reflex:(Indicates protection afforded during sleep)
11. Corneal / Conjunctival exposure with Inflammation / Ulcer
12. Absence / Presence of nasolabial folds
13. Flow of air in the nasal airway
14. Asymmetry of the oral commissure in repose and in smile
15. Incisor show (depressor anguli oris, supplied by marginal mandibular N)
16. Speech assessments (Bilabials & Labiodentals)
17. Any evidence of cheek bite
18. Oral Hygiene
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19. Any synkinesis (Example: Eye closure with smile)

20. Assessment of cranial nerves (Multiple CN involved in Mobius syndrome)
21. Tongue symmetry: XII nerve (possible donor)

38

Palpation
1. Test forehead
2. Snap test for the lower eyelid
3. Shirmirs test I & II
4. Blow test for tone of buccal muscles
5. Evaluation of taste sensation
6. Evaluation of corneal reflex
DIAGNOSIS
Congenital / Idiopathic / Post-traumatic left / right facial nerve palsy at X level with / without
complications of X duration.
INVESTIGATIONS
1. X-rays
2. ENMG in post-traumatic cases
3. CT /MRI
4. Impedance audiometry for checking presence of stapedial reflex.
APPROACH
Initiate Conservative measures including Night taping, Eye patches Eye glass with shield, blinking
exercises, artificial tears, Ointments at night. In acute cases surgical repair if indicated. In post-traumatic
cases if there is likelihood of improvement, electrical stimulation of facial muscles while awaiting
regeneration of nerve fibers. If repair is a possibility (no improvement after 15 to 18 months) then
reconstruction either Static / Dynamic (Pedicled or free).

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FLAP DISSECTION
1. Radial artery forearm flap
2. Posterior Interosseous artery flap
3. Lateral arm flap
4. Pectoralis major MC flap
5. Deltopectoral flap
6. Groin flap
7. Latissimus dorsi flap
8. Trapezius flap
9. Scapular & Parascapular flaps
10. TRAM flap
11. Gracilis flap
12. Tensor fascia latae flap
13. Reverse sural artery flap
14. Gastonemius / Soleus flaps
15. Free ALT flap
16. Free Fibula flap
APPROACH:
v Mention the Vascular basis, type (Muscle: 1 5, Fasciocutaneous- A C)
v Indications
v Relevant anatomy
v modifications,
v markings,
v arc of rotation,
v how the flap can be extended,
v steps, (Use loupe for dissection)
v Uses for coverage, uses for functional reconstruction.

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Forehead flap

40

Historic / salvage
Type A (M&N) facsiocutaneous flap. (Type B C&L)
Based on superficial temporal vessels
22 x 7 cms.
May harvest forehead as an esthetic unit
Transposed over/under zygomatic arch.
Must delay or else tip necrosis (10-15%)
For tongue, oral cavity and oropharyngeal recon.
Historically, the forehead flap is one of the first axial flaps described.
INDICATIONS
A forehead flap is long enough to reach any part of the ipsilateral face and will provide cover to the
carotid artery in the upper neck. It also can be used to reconstruct the cervical esophagus, provided that it
is passed under the malar region and that the body of the mandible is removed. The elderly patient is not
confined to bed with a limitation of neck movements with the use of a forehead flap.
Skin taken from other regions for facial reconstruction does not provide a good color and texture
match and does not supply the deep support necessary, as in the reconstruction of a nose. The difference in
color and texture is difficult to disguise.
APPLICATIONS
Coverage
Middle and Inferior Thirds of Face
Lateral Face
Oral Cavity
Frontal and Maxillary Sinus

Reconstruction
Eyelids
Nose
Tongue

Dominant pedicle: Frontal branch of superficial temporal artery

Minor pedicles: Supratrochlear artery ;supraorbital artery
The flap is based laterally on one side of the forehead and extends across the forehead to the edge of the
hair-bearing temporal scalp on the contralateral side.
NERVE SUPPLY
MOTOR: Tmporal branch of facial nerve
SENSORY Supratrochlear, supraorbital,lacrimal, and auriculotemporal nerves
Brow function is completely lost with use of the standard forehead flap. As a result, there is no animation
of the upper third of the face, requiring skin graft coverage after flap transposition.
Modifications:
1. Extended scalp flap
2. Islanded flap
3. Reverse Flow Island Flap: This flap design will reach defects on the ipsilateral forehead and
superior orbit.
4. Tissue Expanded flap
5. Sensate flap: The supraorbital nerve opposite the base of the flap may be included in the flap.
6. Lined flap (Prelaminated).
7. Delayed forehead flap.
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In patients with frontal alopecia the flap may be designed over the frontal skull or may include hairbearing scalp if required for lower face reconstruction.
PEDICLE LOCATION: The pedicle, the superficial temporal artery and vein, is palpable anterior to the
tragus of the ear beneath the preauricular skin. A Doppler probe is used to trace the pedicle along the
zygomatic arch to the level of its bifurcation into the frontal and parietal branches. This bifurcation occurs
2 to 4 cm superior to the zygomatic arch. At this level the frontal branch is traced until the territory of the
supraorbital and supratrochlear vessels is reached in the midline of the forehead.
POSITION: The patient is kept in the supine position during flap elevation and inset.
INCISIONS: Outlines of the flap are incised with the skin beveled toward the flap to minimize the
contour deformity of the flap donor site after subsequent skin graft Closure. The incision is then carried
through the frontalis muscle on the contralateral forehead.
The flap is generally elevated at the level of the periosteum. It is also possible to elevate the flap
superficial to the frontalis and corrugator muscles to preserve facial expression. At the lateral one third of
the forehead dissection is deep to the temporoparietal fascia. The superficial temporal artery and vein are
visualized or palpated through the thin fascia and carefully preserved at the level of the zygomatic arch.
The frontal branch of the facial nerve crosses the medial zygomattc arch and passes in close
proximity to the lateral eyebrow into the frontal musculature. If a dissection is performed superficial to the
frontal muscles, loupe magnification is required to avoid injury to the frontal branch of the facial nerve in
the plane beneath the superficial fascia. The medial sensory nerves (supraorbital) are divided during flap
elevation.
The superficial temporal artery and vein are traced inferior to the zygomtic arch where the vessels
pass beneath the parotid gland. If a skin island is formed by dividing the skin superficial to this pedicle,
the arc of rotation is extended.
FLAP ELEVATION: The perimeter of the forehead flap is incised either to the surface of the frontalis
muscle or to the periosteum of the frontal bone. Flap elevation begins at the distal flap margin located on
the forehead contralateral to the base of the flap. As flap elevation proceeds across the orbital rim the
supraorbital and supratrochlear vessels are divided. The dissection reaches the ipsilateral orbit. At this
point dissection proceeds from the superior aspect of the flap edge at the hairline toward the ipsilateral
zygomatic arch. The parietal branch of the superficial temporal artery and associated vein are divided and
dissection proceeds deep to the temporoparietal fascia inferiorly. At the level of the zygomanc arch the
dissection proceeds toward the tragus of the ear only as required to increase the flap arc of rotation. In the
standard forehead flap design, particularly for intraoral defect coverage, the flap elevation is completed
1.5 cm inferior to the zygomatic arch. At this level a tunnel is formed to transpose the flap into the oral
cavity.
EXTENSION OF PEDICLE LENGTH: When the standard, island, or extended scalp flap requires a
greater arc of rotation, it is possible to elevate the vascular pedicle to the flap, the superficial temporal
artery and vein, to the level of the external meatus of the ear at the midtragal region. At this level the
vessel progresses deep in the parotid gland and further dissection may result in vascular injury. This
extension of the vascular pedicle length below the zygomatic arch generally provides an arc of rotation to
cover middle and inferior defects of the face and defects within the oral cavity and lateral pharymgeal
wall.
BILOBAR & TRILOBAR FOREHEAD FLAPS (NARAYANAN M)
The branches of the superficial temporal artery are identified by palpation or with a Doppler
device. The lines of incision start as with the standard forehead flap, but at a point about 5 cm above the
bifurcation of the anterior and posterior branches of the temporal artery, the incision deviates
posteriorly to enclose a wide parietal scalp flap that has the exact dimensions of the skin defect. The flaps
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canBAAPS
be measured accurately by cutting out patterns of the mucosal and skin defects on sterile gauze.
The
frontalis muscle and the parietal scalp flap are raised at this same loose areolar tissue level.
The single bilobar flap narrows to a small pedicle 2.5 cm wide just above the zygomatic arch . The
whole flap is everted and turned down .The forehead flap at this stage fits snugly into the mucosal defect,
where it is sutured. The parietal scalp flap then is folded forward across the face to fit exactly into the skin
defect of the cheek, chin, and lips. It is sutured there except for the fold at the posterior border. To cover
the raw area of the forehead, a split-thickness skin graft from the clavicular area is applied. The scalp
defect is covered with a split-thickness skin graft from the trunk.

ISLANDED BILOBAR FLAP

TRILOBAR FLAP: Where the skin loss is below and posterior to the ear, this area cannot be covered by
the bilobar forehead and scalp flap. A trilobar flap is designed consisting of the usual forehead and parietal
flap with an added vertical flap from the frontal area of scalp on the end of the forehead flap. This whole
flap is turned down so that the transverse portion of the forehead flap covers the mucosal defect. When the
scalp flap is folded forward, the portion of flap from the frontal scalp (the third lobe) everts posteriorly to
cover the defect on the surface of the neck. The parietal scalp covers the cheek

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DELTOPECTORAL FLAP

Type C facsiocutaneous flap.
10X20 cm standard, 10X27 cm delayed.
Based on 1-3 anterior perforators of IMA: 2nd (dominant), 3rd, and 4th
These vessels pass through the pectoralis major, then travel to the skin
Delay must interrupt perforators from thoraco-acromial a. & deltoid m.
Delay by raising a bi-pedicled flap or by raising flap lateral to DP groove.
Can be tubed for tongue and esophageal recon
Tip necrosis 5-15%
Overall complication rate 40-50%
Often used as a salvage flap.
ARC OF ROTATION
Standard Flap: The flap will reach the neck, lower face, and oral cavity.
Delayed Flap: This flap has a longer reach and may be folded for intraoral reconstruction or for an
extended arc of rotation to the midface.
SENSORY SUPPLY: second through the fourth intercostals nerves provide segmental sensory
innervation.
DOMINANT PEDICLE: 1-3 anterior perforators of IMA: 2nd (dominant), 3rd, and 4th. These vessels
pass through the pectoralis major, then travel to the skin.
REGIONAL SOURCE: Internal mammary artery
LENGTH: 1 to 2 cm
DIAMETER: 1 to 2 mm
LOCATION: Within 3 to 4 cm of the midsternal line
APPLICATIONS:
COVERAGE
Middle and Lower Thirds of Face
Intraoral Cavity
Neck

RECONSTRUCTION
Esophagus

MICROVASCULAR TRANSPLANTATION
Distant Coverage of Head and Neck
SKIN TERRITORY
DESIGN: For the standard flap the skin territory is located between the sternum and anterior axillary line
and extends from the clavicle to the fourth or fifth intercostals space.
For the extended flap the skin territory is extended over the deltoid muscle. A preliminary flap
delay is required to extend the flap length.
MODIFICATIONS
1. Expanded
2. Delayed
3. Twin flaps

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GUIDELINES
FOR FLAP ELEVATION
LANDMARKS: The sternal edge, infraclavicular line, deltopectoral groove, and nipple
FLAP DIMENSIONS: Standard flap, 10 X 20 cm; delayed flap, 10 X 27 cm
FLAP DESIGN: The flap is designed diagonally upward across the upper chest and shoulder. The base lies
over the second, third, and fourth costal cartilages; the upper border follows the infraclavicular line
beyond the deltopectoral groove onto the anterior shoulder. A delayed flap can be extended safely to the
tip of the shoulder. The lower border runs parallel to the upper border and usually lies a few centimeters
above the position of the undisplaced nipple.
Patient Positioning: The patient is supine. The ipsilateral arm may be abducted or adducted according to
the surgeon's preference.

FLAP ELEVATION TECHNIQUES

Standard Flap: Flap elevation proceeds from distal to proximal. The distal end is incised through skin
and subcutaneous tissues down to and including the fascia over the deltoid (subfascial). The dissection
then proceeds rapidly through a relatively bloodless plane across the deltoid, across the deltopectoral
groove, and onto th pectoralis major. The axially oriented vessels can sometimes be seen within 5 to 6
cm of the midline just above the fascia. The dissection is continued until the perforators are seen emerging
through the pectoralis major muscle.
Delayed Flap: The delayed flap is outlined beyond the deltopectoral groove and onto the anterior border
of the shoulder almost to the tip. That portion of the flap extending beyond the deltopectoral groove is
then elevated and resutured into the donor site. A Silastic sheet or tissue expander may be placed beneath
rhe area of flap delay. It may be accomplished by ligation of the cutaneous branch of thoracoacromial
artery.
TRANSPOSITION
Face and Neck Coverage: The flap is usually transposed to the head and neck .The arc of rotation is based
on the upper border of the flap, the upper border being shorter in length than the lower border. As the flap
is transposed, the lower portions are easily tubed. Raw surfaces at the proximal flap may be skin grafted or
covered with temporary dressings.
Intraoral Coverage: For intraoral reconstruction the flap is tubed with the cutaneous surface directed
inside the tubed flap to establish a temporary controlled salivary fistula.
Esophageal Reconstruction: For staged reconstruction of the esophagus with a tubed deltopectoral flap,
the flap is tubed with the cutaneous surface directed inside to provide lining for the neoesophagus The
upper border of the tubed flap is then approximated to the esophagus and the lower border remains open
as a temporary controlled salivary fistula. At the second stage (usuaIIy 2 to 3 weeks later) the attached
base of the deltopectoral flap is divided, the tubing completed, and the distal esophageal anastomosis
completed.
FLAP INSET: The flap is inset according to the reconstructive requirements. For intraoral reconstruction
the tubed flap is approximated to the mucosal and muscular edges of the extirpative defect. The
reconstruction is then completed at a second stage where the tube is divided and the proximal divided
portions of the flap are then definitively inset. The second stage is usually performed 2 to 3 weeks
following the initial reconstruction. In the meantime the tubed DP flap serves as a controlled salivary
fistula.
PRECAUTIONS
v For transposition to the head and neck, skeletonization of the perforating vessels should be
avoided.
v A preliminary delay is necessary for flaps extending beyond the deltopectoral groove.
v The donor site in females will result in distortion of the ipsilateral breast.
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FOOT DEFECTS
Name:
Age:
Sex:
Occupation:
Resident of:
Comes with C/O: Injury to the right / left foot with wound since this duration
Patient was walking / traveling when he /she was hit by a 2 wheeler / 4 wheeler resulting in a fall and
patient had injury to left / right leg with severe pain
Progression
History of any other injuries in the accident
History of smoking / alcoholism
History of diabetes / hypertension
History of any previous surgeries or treatments for the wound
History of having developed deformities in the foot / loss of sensation
General examination
Vital signs
Attitude of patient (Resting position of the foot)
Local examination
Inspection
1. Any obvious limb length discrepancies
2. Single raw area is seen on right / left foot in the dorsal / plantar surface area, -----x----- cms,
extending ---- cms from the medial / lateral malleoli. The margin of the raw area shows healing
epithelium / none healing indurated. Edge is sloping / punched out. The periphery of the raw
area is covered with healing type of granulation tissue. In the centre of the wound the bone is
exposed, measures -----x----- cms in size and is dull yellow color without any periosteum.
3. The surrounding skin appears / does not appear inflamed / any hypertrophy
4. There is edema / atrophy of the limb
5. Any varicose veins in the leg.
Palpation
1. Tenderness around the raw area
2. Increased warmth
3. Base of the non healing ulcer
4. Distal sensations in tibial and peroneal nerve areas.
5. Distal pulsations (capillary refill) feel ATA, PTA both legs.
6. Any restriction in the range of motion
7. Power of various muscle groups
8. Evaluate for presence of Charcots joints
Eichenholtz Grading
Grade 0:
Autonomic Neuropathy
Grade I:
Fracture / Dislocation of tarsal / metatarsal skeleton
Grade II:
Stage of coalescence
Grade III:
Stage of resolution
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9. Evaluate for altered biomechanical forces in the foot resulting in deformities like hammer toes /
hallux valgus
10. Look for prominent metatarsal heads in the bed of the wounds
11. Look for tendoachilis shortening, (If tightness in dorsiflexion is present irrespective of
keeping the knee in flexion or extension then the shortening is at TA region: TA release required, If
tightness in dorsiflexion is present only with knee in extension and absent with knee in flexion then
the shortening is in the region of the gastrocnemius portion of TA: Gastrocnemius recession
required in tongue in groove fashion)
12. If deformity is present measure true and apparent defects
13. If an amputation stump is present describe the level:
Transmetatarsal / Choparts (leaves intact talus, calcaneus)
Lisfrancs: proximal to all metatarsals
Symes: (Talus calcaneus removed).
Choparts & Lisfranc levels need proximal transfer of the tibialis muscle to balance TA)
14. Any atrophy / limb length discrepancy in long standing cases as measured from fixed bony
points.
15. Lymph nodes draining the region.
Donor sites examined and found adequate
DIAGNOSIS
Post traumatic composite defect / non healing ulcer over plantar / dorsum of the foot with / without
exposed bone with / without distal neurovascular deficit in a patient with Diabetes / peripheral vascular
disease.
INVESTIGATION
1. X-ray
2. Wound C/s
APPROACH
Optimize the condition of the wound. When patient is fit wound is debrided and covered with Pedicled /
free flap / SSG

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Hand Assessment
1. History
Name:
Age:
Sex:
Handedness:
Occupation:
Hobbies:
Complaint stiffness, pain, deformity, decreased power, decreased sensation, inability to use hand for
daily activities
Trauma:
History/mechanism of injury or disease
When, (Time elapsed since injury)
Where (work, home or play) Clean/ dirty environment
Mechanism, Exact posture of the hand at the time of injury.
(dates injury, investigation(s), & treatment(s))
Previous hand injuries, surgeries, therapy etc.
Non-trauma:
When did pain, sensory change, swelling, contracture begin?
Sequence
Progressive?
Any impairment in ADL
Are other joints or tendons in involved or other extremity painful in similar way?
If painful, what are aggravating / relieving factors?
Family history of hand problems (e.g. RA etc.)
2. Physical Examination
a) Inspection
Hand in space: posture, cascade
Posture, contractures, signs of arthritis
Color, temperature, atrophy, swelling, bruising, skin/nail changes
FDS/FDP laceration, Malrotation
b) ROM
Active & passive ROM (start from shoulder!)
Measurements with goniometer
c) Neurological Examination
Sensory
Dynamic 2 PD most reliable (normal is < 3-4 mm at distal phalanx)
Static 2 point, light touch, pressure (Semmes-Weinstein), vibration are other modalities
1000 F and 450 F are temperatures for warm & cold testing
Motor
Median
proximal - PT, FCR, PL, FDS
distal APB, OP, FPB(superf), lumbricals (index & long)
AIN - PQ, FPL, profundus to index (& long) (O fish-eye sign)
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Ulnar
proximal - FCU, FDP to ring or small
distal interossei (1st DI), hypothenars, FPB (deep), AP
Radial
proximal triceps, BR, ECRL, ECRB, supinator, anconeus
distal (PIN) EPL, EPB, APL, wrist and finger extensors
The classic order of innervation for PIN, distal to the leading edge of the supinator:
EDC-ECU-EDM -APL-EPL-EPB-EIP

Sweating nerve injuries result in dry skin 2 SNS interruption

Muscle Grading (MRC)
0 - no contraction
1 - trace or flicker of contraction
2 - poor active motion, gravity eliminated
3 - fair active motion, against gravity
4 - good active motion against some resistance
5 - normal
d) Musculotendinous function
Individually test all wrist and finger flexors and extensors
Remember to flex D3/D4 and extend D2/D5 to test EIP & EDM
Remember other thenar muscles can extend the IPJ
EPL is the only one that can lift thumb off table
Remember to separate testing of FDP (one muscle belly) & FDS
If FDP to index is independent, it can flex the PIPJ so, the only test to assess if FDS is injured is to
make the fish eye sign and
Assess FDS strength by pulling your finger or paper out - similar to Fromments
Other tests in uncooperative patients (drunks, kids) or comatose patients:
Tenodesis effect
Squeeze proximal forearm muscle bellies and look for wrist/finger flexion
Reflexes Biceps (C5 (6)) BR (C6 (5)) Triceps (C7 (8))
Pinch and grip strength
e) Other Specific Tests in the Hand
(1) ORL Tightness Test
Decreased DIPJ flexion when PIPJ extended
(2) Intrinsic Tightness Test
Decreased PIPJ flexion when MPJ hyperextended, can flex PIPJ when MCPJ flexed
(3) Extrinsic Tightness Test
Unable to flex PIP & MP simultaneously, decreased PIPJ flexion when MPJ flexed, can flex PIP with MP
extended
(4) Tinel's
Regenerating/growing axons no indication of eventual quality or quantity of return
Good prognostic sign reducing Tinel at injury site & increasing Tinel distally
(5) Sweating
Sympathetic disruption & nerve loss results in sweat loss. Returns late & closely parallels return of 2PD
(6) Wrinkle (Prune) Test
Occurs only in skin that is normally innervated (ie. no nerve injury) immerse in warm water for 5 minutes
(7) Finkelstein's
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Traction
& stretching over 1st dorsal compartment reproduces pain (indicating de Quervain's)
(8) Grind Test
Axial load and rotate base of 1st MC to reproduce pain of OA
(9) Allen's Test
Compress the radial and ulnar arteries and have the patient make a fist several times, then release one of
the arteries and look for arterial return (normal is < 5 secs) assesses the competence of major arterial
contributions to blood supply in hand & the functional efficiency of the vascular arches in the hand can
also do a digital Allens test.
(10) Capillary Refill
Too fast (= venous insufficiency) & too slow (> 2 secs) or absent (= arterial insufficiency) can also put an
O2 sat monitors on the digit to assess arterial perfusion

SIMPLIFICATION:
Intrinsic plus is contracture
Intrinsic minus is nerve injury
AT THE END OF EXAMINATION, COMMENT ABOUT FUNCTIONAL EVALUATION OF THE
PATIENT AND ALSO ABOUT THE ACTVITIES OF DAILY LIVING WHICH HE IS NOT ABLE
TO PERFORM.
3. Investigations and Imaging
Growth centers in upper limb: away from elbow
Growth centers in lower limb: towards the knee
While taking measurements, take for arm also (length & girth).

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DUPUYTRENS DEFORMITY
Name
Age
Sex
Occupation
Resident of
Right or left handed
Comes with complaints of deformity of right / left hand resulting in day to day, problems like not being able to
put hands in the pocket. (exactly what activities he is not able to do??)
Duration
Onset
Which hand first, which finger first?
Progression
History of any nodule or pit
History of similar problem in the sole / Penis
History of trauma
History of smoking
History of alcoholism
History of diabetes
History of epilepsy, phenytoin
History of treatment / surgery for same
Family history
General examination
Vital Signs
Local examination
Inspection
1. Pits: No, Position, Size
2. Nodule: No, Position, Size
3. Contracture band: No, Which finger, Extent, Does it blanch on finger extension
4. Scars from previous surgery or trauma
5. Penile / plantar pathology if any Palpation
1. Local warmth
2. Tenderness
3. Is skin involved or not
4. Measure skin shortening (True defect)
5. Contracture band: Does it blanch on finger extension
6. Tubiana Grade of the deformity (Mathes)
7. Range of movements at DIP / PIP / MP
8. Distal sensation
9. Distal Pulsations / Capillary refill / Digital Allen in an operated case
10. Power of individual Musculotendinous units
DIAGNOSIS
Dupuytrens contracture deformity involving the following finger of the right / left hand of X Grade.

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APPROACH
Table top test (Hueston TEST) and degree of contractures of PIP and MP decide the indication for surgery. If
fit procedures vary with 3 issues:
1.Access:
Closed: Access with tip of 11 no blade or needle
Open: Brunners or mid Volar straight line with Z plasties at Joint crease or dermafasciectomy.
2. Management of Fascia: Radical, Regional / Partial, Segmental
3. Closure: Closure with or without Z plasties at joint crease or SSG or Leaving wound open
(McCash)
Mention post op protocol.

GRADING: (Tubiana and Michon )

0
N
1
2
3
4

NO LESION
PALMAR/DIGITAL NODULE WITHOUT FLEXION DEFORMITY
0-450 TOTAL FLEXION DEFORMITY
45-900 TOTAL FLEXION DEFORMITY
90-1350 TOTAL FLEXION DEFORMITY
> 1350 TOTAL FLEXION DEFORMITY

Fate of Normal Fascia Bands in Dupuytrens Disease:

Normal Fascia
Pretendinous band
Pretendinous band
Spiral band
Lateral digital sheet
Graysons ligament
Lateral digital Sheet
None
Natatory ligament

Diseased Cords
Pretendinous cords

Contracture
MP flexion

Spiral cord

PIP flexion

Lateral cord
Central cord
Natatory cord

PIP flexion
PIP flexion
MP Adduction (webspace contracture)

LIGAMENTS NOT INVOLVED IN DUPUYTRENS DISEASE

Superficial TRANSVERSE Ligament
Deep TRANSVERSE Ligament
CleLANDS Ligament
LANDsmeers Ligament
Diathesis:
Commonly bilateral (65%), more severe, more radial involvement
Plantar Fibromatosis (Ledderhosens)
Knuckle Pads (Heloderma or Garrods) (dorsum of PIP)
Penile Fibromatosis (Peyronies) (dorsum of penis) see also Peyronies disease
Commonly: radial disease, bilateral disease, and high rate of recurrence
Indications for Surgery
A contracture of either IP joint or MP joint which is producing a functional disability
MPJ contracture greater than 30 degrees (failure of table top test)
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Any PIP flexion contracture

Significant web contracture, especially of the thumb
Disturbed neurovascular function
Articular cartilage loss
Concomitant trigger finger

Medical management
Splints, skeletal traction
Ultrasound, laser, radiation
Allopurinol, colchicine, calcium-channel blockers, -interferon, vitamin E, dimethyl sulfoxide
Steroid injection of early nodules less beneficial
Salvage Procedures
Dorsal wedge osteotomy
Arthrodesis
Silastic Implant
Amputation
All may lead to shortening of the digit

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NERVE PALSY
Name
Age
Sex
Occupation
Handedness:
Resident of
Comes with complaints of:
Inability to move thumb / finger / wrist of Right / left hand
Deformity of hand / fingers
Loss of sensation over forearm / hand
Patient is a known case of leprosy / sustained injury to arm /forearm / hand on right / left side while at home
/ workplace when he was doing this (describe in detail the event).And sustained injury with pain. Was then
treated at a hospital where dressings / suturing of the wound was done. The wound then healed.
Then patient noticed inability / weakness to move these fingers / wrist / elbow and loss of sensation in
these areas. The weakness improved / remained same from the time of original incident. Loss of sensation
has improved / remained same since the original incident. Any deformities the patient has since developed.
History of physiotherapy / use of splints
History of any surgery for the present disease
History of treatment for leprosy in a case of leprosy. How many types of tablets and for
What duration? Is the patient on steroids?
History of facial / foot deformities secondary to leprosy
History of Diabetes / hypertension
History of smoking / alcoholism
History of lead / arsenic exposure
General examination: Look for stigmata of leprosy (Facial deformities / foot deformities, examine the whole
body for hypo pigmented anesthetic patches, Examine for enlarged tender nerves)
Attitude: Patient is supine / sitting with forearm, elbow in neutral position the wrist shows wrist drop (in radial
palsy), fingers show clawing (median / ulnar palsy)
Vital signs:
Systemic examination:
Inspection
ALWAYS DEMONSTRATE CASCADE WITH FOREARM SUPINATED!
1. Note atrophy in thenar / hypotheanar eminences / dorsal intermetacarpal spaces
2. Note trophic changes of denervation: Skin is dry / shiny / sparse hair / brittle nails
3. Describe the scar if any in terms of no, site, size, shape, hypo / hyper pigmented, hypertrophic /
keloid changes, tender, itchy, blanching / not blanching on touch, indurated / supple on palpation of
centre / edges.
4. Deformities: Clawing of fingers / wrist drop
Palpation
1. Denervated extremity is less warmer
2. Assess distal sensation (AUTONOMOUS ZONES OF ALL 3 NERVES)
3. Assess distal vascularity
4. Assess for level of Tinels sign
5. Assess Power of all extrinsic & intrinsic. Grade from 1 5.

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(Will identify paralyzed motors & motors available for transfer)

6. Specific signs:
Froments sign (Ulnar N)
Finger crossing test (Ulnar N)
Pen test (Median N)
Holding cylindrical objects (To test integration of MP with IP flexion)
7. Range of Motion Passive & active (Calculate TAM & TPM)
8. Assess Triceps / Biceps / Brachioradialis reflexes
9. Donor sites for Nerve grafts assessed in appropriate cases
10. Specific test for claw deformity

54

I. Deformity angle: Forearm rested vertically on a table top in mid prone position with wrist in
neutral position ask patient to straighten the fingers: Measure PIP angle on dorsal side.
Normally is zero degree.
II. Disability (unassisted) angle: Ask patient to attempt lumbrical position with MP at 90 deg.
The PIP angle is now measure on dorsal side. Normally is zero degree.
We measure the extent of soft tissue adaptation of finger to paralysis. Inversely
proportional to prognosis.
III. Assisted angle: MP is flexed to 90 degree by examiner ask patient to extend PIP now
measure PIP angle on dorsal side. Normally is zero degree.
In the absence of contracture or if the assisted angle falls short of the contracture
angle, it reveals defects in the line of the tendon forces such as a lack of continuity of dorsal
expansion beyond PIP joint, or an anterior displacement of lateral bands around head of PPx
(hooding / boutonniere deformity).
IV. Contracture angle: Try to passively extend the PIP. If PIP angle on dorsal side is now
zero then it means the extensor mechanism is attenuated or damaged. If PIP cannot be fully
extended then there is contracture of skin / flexor sheath / flexor tendon / volar plate. This angle
is then called the Contracture angle
This angle represents gross limitation of full extension of joint. May be due to:
Skin contracture (good prognosis for skin alone)
Capsular contracture (prognosis not so good)
Long flexor contracture
PIP joint is the KEY JOINT of the finger. Capsular contracture Treatment: sectioning of both
collateral ligaments. This does not result in permanent instability as the ligaments reunite
during 3 weeks of immobilization in extension.
V. Angle of Adaptive shortening: If the contracture angle can be reduced to zero by flexion at
wrist then it is due to shortening of flexor tendon. (Volkmanns test) should be corrected by
physiotherapy before tendon transfers.
Supination: by Biceps in when elbow is flexed, by Supinator with elbow extended.
Pronation: by PQ in elbow flexion, by PT in elbow extension
DIAGNOSIS
High / Low Radial / Median / Ulnar nerve palsy secondary to trauma / leprosy of this duration with tinels sign
at this point (with other stigmata of leprosy in a case of leprosy).
INVESTIGATION:
ENMG
NCS
X-ray
MR Neurography
APPROACH
Open Injury if clean cut repair primarily. In open injury of crush / avulsion type tag the ends wait 3
weeks to allow demarcation of ischemic segments then repair if gap is less than 2 cms or else consider nerve
grafting.
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In closed wait for a period equal to lag period plus time taken for tinels / recovery to progress55distally
at 2.5 cms per month to sensory receptors / motor units (ENMG & NCS also help). If no progression,
operate. Repair if gap less than 2 cms or else consider nerve grafting. While awaiting recovery physiotherapy
is initiated to prevent shortening of muscle tendon units & splinting to prevent stiffness of the joints. Consider
electric stimulation of paralyzed muscles to prevent their atrophy.
In late presentation usually beyond 2 years or when motor recovery is not anticipated tendon
transfers / pedicled or free muscle transfers are considered strategic re-deployment of available motors.
Boyes classification sets the prerequisites for a tendon transfer. In cases where a choice of donor motors are
not available a simplification of functional reconstruction is attempted by appropriate arthrodesis / tenodesis.
Sensory reconstruction is then attempted with Littler's neurovascular island transfer / nerve
transfer from available non critical nerve branches / end to side nerve captions.
Rehabilitation is begun with motor and sensory re-education.

Tactile Adherence Test:

Wrinkle /prune test.
Reversal of donor nerve is done to avoid AXONAL WASTAGE (funneling distally in its normal
location).
Post injection radial palsy: oily injection causes more extensive damage. Palsy immediately after
injection indicates INTRANEURAL INJECTION.
INTRAOPERATIVE IDENTIFICATION OF HEALTHY NERVE ENDS:
1. Chemical tests: Ach for Motor nerve ends, Carbonic anhydrase for Sensory ends
2. Frozen section
Uses of nerve conduction study:
1. Diagnosis of level / type of nerve injury
2. For assessing nerve growth after repair/grafting.
Techniques for Electrical Stimulation: The techniques are generally divided into three:
Faradic Electrical Stimulation: Faradic stimulation is used for innervated muscle, ie when the lower
motor neurons are intact. Stimulation is applied via the nerves often at the muscle motor points. The
nerves depolarisation leads onto muscular contraction.
Faradic stimulation can be considered to be AC with pulse widths <1ms (typically around 0.3ms
with a frequency <100 Hz (due to the absolute refractory period of normal muscle).
The contractions produced can be:
approaching near normal voluntary levels of muscle force
sustained
tetanic
It is for these reasons that the majority of functional electrical stimulation techniques require intact lower
motor neurons, and use faradic stimulation techniques to achieve the desired muscle contraction.
Galvanic Electrical Stimulation: This is often known as interrupted DC as it conventionally requires pulse
widths of about 100 ms. It is used to stimulate denervated muscle directly, but at best produces weak
tetanic forces.
Interferential Electrical Stimulation: This is used for deep tissues where with faradic type pulses a high,
and consequently often painful, stimulation intensity is needed to reach the desired muscles, eg pelvic
floor muscles. Interferential stimulation is not often used for functional neuromotor stimulation as
compared with faradic type stimulation, it requires greater energy consumption and often a greater number
of electrodes.
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Trophic
ulcers in leprosy: most commonly on ball of metacarpals, fingertips, proximal part of the
palm,
due to pressure effects. Tendon transfers decrease the number of these ulcers despite insensate hand!

Ulnar nerve paralysis: Normal finger flexion is initiated at the MP joint by the intrinsic and then all three
joints flex simultaneously to grasp objects. With paralysis of intrinsic, flexion at MP joint does not start
until the IPs are flexed, which tends to push objects away from the palm.
Loss of ulnar nerve function in the hand causes:
loss of power pinch (Jeanne and Froment signs),
digital clawing, asynchronous digital flexion, and
persistent abduction of the small finger at the MCP joint (Wartenberg sign).
(High ulnar nerve palsy)
+
weakened wrist flexion (loss of FCU) and
power grip (loss of FDP ring, little)
Intrinsic plus deformity: MP flexion, often fixed extension of PIP and flexion of DIP. It is d/t
contracture either of the muscle belly of lumbrical or interosseous muscle as a result of resolved leprous
myositis, or it may be d/t fibrous contracture of the infiltrated dorsal expansion. Can be seen as a primary
deformity in lepromatous leprosy. May also be seen as secondary deformity in postop hand in which FDS
transposition has been carried out in a hypermobile finger.
Deficits and their Eponyms in Ulnar Nerve Palsy (ASSH, 2003)
Eponym
Duchennes Sign
Bouviers Manoeuvre
Pitres-Testut Sign

Wartenbergs Sign
Jeannes Sign
Froments Sign
Masses Sign
Pollocks Sign

Deficit
Clawing of ring & small fingers
If when MP hyperextension passively corrected by applying
dorsal pressure the IPs extend, IP extension can occur via EDC
Inability to move the extended long finger in radial & ulnar deviation
Mechanism: paralyzed interossei
Related test: inability to cross the index & long fingers when fingers
placed on flat surface.
Inability to adduct the extended small finger
Mechanism: tendency of EDM to abduct the small finger is
unopposed due to paralyzed 3rd PI muscle
Thumb MP hyperextension with key pinch or gross grip
Mechanism: adductor pollicis paralysis. It adducts the thumb but
also contributes to MP flexion and IP extension
Hyperflexion of thumb IP joint with key pinch.
Mechanism: denervation of AdP and 1st DI leads to weak pinch. To
compensate, patients use FPL to flex & stabilize the thumb
Flattening of palmar metacarpal arch and loss of hypothenar
elevation
Mechanism: hypothenar muscle paralysis
Weakness of DIP flexion of ring & small finger

Functional Reconstruction:
1.
2.
3.
4.
5.

Co-ordination of MP & IP Flexion

Thumb adduction & key pinch
Index abduction & stabilization
MC arch restoration
Little finger abduction
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CLASSIFICATION OF PARALYTIC CLAW HANDS:

Based on the physiologic characteristics of hypermobility

and other features and on the chronicity and etiology of the deformity, Anderson developed a simple
classification of claw hand. By understanding the type of claw hand, the selection of the appropriate
corrective procedure is more straightforward.
Type I:
Type II:
Type III:
Type IV:
Type V:

Supple claw hands with no hypermobile joints and no contractures at the IP joints
Hypermobile joints as demonstrated by 20 degrees or more of painless passive
hyperextension, measured at the PIP joints
Mobile joints in association with adaptive shortening of the long flexors, usually the
superficialis tendons (myostatic contractures), with no IP joint contracture
Contracted claw hands demonstrating PIP joint flexion contracture of 15 degrees
or more, related either to the volar skin, joint capsule, or volar plate contracture
and with or without adaptive shortening of long flexors
Claw hands with attrition of the dorsal extensor apparatus at the PIP joint with
hooding deformity, fibrous or bony ankylosis of the PIP joint, and MP joint
extension contracture

RADIAL NERVE PALSY:

Sensory branches:
Lower lateral cutaneous nerve of arm
Posterior cutaneous nerve of arm
Posterior cutaneous nerve of forearm
Superficial sensory branch of radial nerve
PT inserts on most convex surface of the radius. Dissect upto midpoint of muscle belly.
Single curvilinear incision on dorsoradial aspect.
Tension:
Wrist in 300 extension
Fingers with wrist & MP neutral, ? IP flexed
Thumb extended and maximum radial abducted

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standard

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SYNDACTYLY
Name
Age
Sex
Resident of
Brought by mother/father with Chief Complaints of fusion of this and this finger of right / left hand by
birth.
1st / 2nd / 3rd Issue, born FTND to parents aged X / Y years married non / consanguineously
Antenatal history: Radiation, drug consumption
History of other congenital anomalies
Developmental milestone if adequate:
Head lift 3 months
Sit 6 months
Crawl 9 months
Stand 1 year
Walk 15 months
Immunization history if adequate:
At birth: BCG, OPV
6 weeks: DPT, OPV
10 weeks: DPT, OPV
14 weeks: DPT, OPV
9 months: measles
18 months: DPT, OPV
5 years: DT
10 years; TT
Family history,
Parents give history that the child is / is not using the affected hand in day to day activities
Right / left handed if in adult
General examination: Look for features of Poland syndrome / Apert Syndrome. (Comment as: no visible
deformities in the craniofacial region)
Vital signs:
Systemic examination: CVS / RS / PA to be assessed for abnormalities.
Local examination
1. Fusion of this & this finger of right / left hand extending from the web space till this point
proximal to fingertip.
2. Nails fused / not fused (fused nails indicate complex Syndactaly!!)
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3. There is absence/presence of movements between the two affected fingers (absence is suggestive
of complex type)
4. Abnormal deviation of finger from this side to this side if present.
5. Length discrepancy between fingers
6. Palmar surface shows / does not show creases at this and this joints
7. ROM at MCP / PIP /DIP joints
8. Power: Flexors / extensors
9. Distal sensation
10. Distal vascularity
11. Any scars of previous surgery are described
12. Any syndactyly in the foot is noted.
DIAGNOSIS: Complete / Incomplete, Simple / Complex. Complicated / uncomplicated syndactyly
between this and this finger of the right / left hand in a child aged this.

APPROACH
Complex & syndactylies of unequal fingers are delt with early otherwise syndactylies are treated
by the age of two years. Adjacent sides of any given finger is NOT released in one setting to prevent a
vascular compromise. Most common method is dorsal rectangular flap (width is the distance between the
MPJ and length is 2/3rd of distance between MPJ and PIP) with volar triangular flap with Zig-zag
incisions made in such a way as to cover the IP joints. If nail is fused it is separated by the Buck-gramcko
method. Raw areas are ideally covered with FTSG.
Finger involvement upto 2/3rd length: web space contracture
> 2/3rd: syndactyly

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POLYDACTYLY
Name
Age
Sex
Resident of
Brought by mother/father with Chief Complaints extra thumb / finger in right / left hand by birth.
1st / 2nd / 3rd Issue, born FTND to parents aged X / Y years married non / consanguineously
Antenatal history: Radiation, drug consumption
History of other congenital anomalies
Developmental milestone if adequate:
Immunization history if adequate:
Family history,
Parents give history that the child is / is not using the affected hand in day to day activities
Right / left handed if in adult
General examination: Look for features of Poland syndrome / Apert Syndrome. (Comment as: no visible
deformities in the craniofacial region)
Vital signs:
Systemic examination: CVS / RS / PA to be assessed for abnormalities.
Local examination
1. Extra digit is present at the level of proximal / middle / distal phalanx of this finger of the right /
left hand.
2. Extra digit is present on the radial / ulnar side of the finger and consists of 1 / 2 / 3 phalanges
3. Extra digit is shorter / thinner than its counter part
4. In the duplicated finger the radial / ulnar digit appears dominant
5. Joint creases are present / absent in the duplicated fingers
6. MP / PIP / DIP joint movements are present / absent in the duplicated fingers and ROM
7. Distal sensation
8. Distal vasularity
9. Any abnormality in the remaining fingers
10. Any abnormality in the toes

DIAGNOSIS
Preaxial / postaxial type of polydactyly of this finger in right / left hand in a child aged this.
APPROACH
Ideally operated by 2 years. Radial duplication is classified as per Wassals classification.

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MACRODACTYLY
Name
Age
Sex
Resident of
Brought by mother/father with Chief Complaints increase in size of thumb / this finger in right / left hand
by birth
1st / 2nd / 3rd Issue, born FTND to parents aged X / Y years married non / consanguineously
Antenatal history: Radiation, drug consumption
History of other congenital anomalies
Developmental milestone if adequate:
Immunization history if adequate:
Family history,
Parents give history that the child is / is not using the affected hand in day to day activities
Right / left handed if in adult
Is the deformity static or progressive?
General examination: Look for features of Poland syndrome / Apert Syndrome. (Comment as: no visible
deformities in the craniofacial region), look for stigmata of generalized neurofibromatosis (Caf au lit
spots, nodules, pigmentation)
Vital signs:
Systemic examination: CVS / RS / PA to be assessed for abnormalities.
Local examination
1. There is an increase in the size of this finger as compare to its counterpart in the opposite hand
2. Length of affected finger is increased compared to its counterpart (measure from bony point)
3. Circumference of affected finger is more compared to its counterpart (as measured at a fixed
distance from a bony point.
4. Nails appears larger
5. Measure active and passive ROM of all the finger joints
6. Distal sensation
7. Distal vascularity: Digital Allens test.
8. Assess for other congenital anomalies

DIAGNOSIS
Congenital gigantism of this finger/ toe of right / left hand / foot in a child aged this of this type (as per the
flatt classification)
APPROACH
Mild cases may be left alone, severe cases may require amputations. Other cases are treated by soft tissue
reduction and skeletal reduction (Tsuge / Barsky) in some cases stapling of epiphysis to reduce growth.

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Flatts
classification:

63

Grade I: Associated with Lipofibromatosis

Grade II: Associated with Neurofibromatosis
Grade III: Associated with Hyperostosis
Grade IV: Associated with Hemihypertrophy
Growth stops with epiphyseal closure.
Treatment goals:
Decrease length
Decrease circumferential bulk
Maintain sensation, circulation
Preserve as much motion as possible
Treatment options:

Bulk reduction procedures (Stripping excess digital nerves???)

Epiphysiodesis
Ray amputation
Digit shortening
Angulation osteotomies

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BRACHIAL PLEXUS INJURY

Name
Age
Sex
Occupation
Handedness
Resident of
Comes with complaints of weakness / inability to move left / right upper limb and loss of sensation over
right / left upper limb since this duration.
Onset: After fall from height / assault / accident (if RTA was high velocity / low velocity) with injury in
the region of neck / axilla / arm or by birth (OBP). In post traumatic enquire about the position of head in
relation to that of the body at the time of the accident
traction-adduction: C5, C6 injury,
traction abduction: C8, T1 injury &
traction @ 90 degree: C7 injury
Ask for deformity of the arm at the time of the accident (To rule out # humerus)
Progression
History of pain: Duration, onset, progression, type, frequency, radiation, response to treatment
(severe persistent pain immediately after initial injury is suggestive of root lesion)
History of diabetes / hypertension
History of smoking / alcoholism
History of treatment, surgeries taken for the present disease
History of deformities.
History of having received physiotherapy, electrical stimulation of paralyzed muscles, splints, and
massage from time of injury to present date.
General examination
Vital signs
Attitude
Local examination
Inspection
1. Wasting of paraspinal muscles (root level injury), head will be deviated to normal side!
2. Neck shoulder asymmetry (SAN), comment about trapezius.
3. Winging of scapula (long thoracic nerve lesion: root level lesion)
4. Signs of Horners syndrome (T1 root / sympathetic chain lesion)
5. Wasting of pectoral region / arm / forearm
6. Bone deformity (# humerus / clavicle / scapula)
7. Describe external scar if any
8. Distal trophic changes due to denervation
9. Look for any deformities due to joint contractures.
Opposite extremity is NORMAL!
Palpation
1. Tenderness
2. Test muscle power of all muscle groups from shoulder girdle muscles proximally to intrinsic
distally
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Shoulder muscles:
Arm muscles:
Long extensors:
Long flexors:
Intrinsic:

C5 (except: Serratus anterior-C5C6C7, Latissimus dorsi-C6C7C8)

C6
C7
C8 (except PT, PQ, Supinator and FCR: C6)
T1

(PT pronates in Extension PQ in flexion, Supinator supinates in Extension and Biceps

supinates in flexion)
(Teres minor is supplied by axillary nerve and teres major by lower subscapular nerve)
3. Check ROM active & passive
4. Sensory evaluation
Lateral arm:
C5
Lateral forearm, thumb, and index: C6
Middle finger:
C7
Ring, little finger, and ulnar hand: C8
Medial forearm, arm:
T1
Objective tests:
1. Tactile adherence test
2. Look for presence of sweat beads using a magnifying glass
3. Starch Iodine test
4. Ninhydrin-sweat test
5. Bromophenol blue test
6. Cobalt chloride test
Subjective tests:
1. Pin prick for pain
2. Semmes Weinstein monofilaments (threshold)
3. Two point discrimination with Diskcriminator (Innervation density)
4. Vibration sense with 256 tuning fork (threshold)
5. Moving 2PD using Disckriminator (Innervation desnsity)
S0: is absent sensation,
S1: is return of pinprick sensation,
S2: is return of moving touch,
S3: is return of moving 2PD, and
S4: is return of static touch & static 2PD
When to see what?
Wait for return of the tinels at fingertips. If tinels is positive proceed to check for pinprick
sensation if pinprick is positive check for moving touch. If positive check moving 2PD with
Diskriminator. If positive check static touch with Semmes Weinstein monofilament. If positive
check static 2PD. Return of moving touch signals the time to start sensory reeducation.
5. Reflexes: Biceps C5, Triceps C6, Brachioradialis C7
6. Tinels sign (distal to proximal, infraclavicular, supraclavicular along posterior border of
SCM)
Activities of daily living affected & Functional Evaluation of the patient.
DIAGNOSIS
Obstetric / Post traumatic brachial plexus palsy of this type of this duration, recovering / not recovering
with / without complications
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MILLESI CLASSIFICATION
Type I: Supraganglionic
Type II: Infraganglionic
Type III: Trunk
Type IV: Cord
LEFFERTS CLASSIFICATION
Type I: Open Injury
Type II: Closed tractional injury
INVESTIGATIONS
1. X-ray cervical spine: # Transverse process cervical vertebra with root injury
2. X-ray Clavicle: # with Trunk injury
3. X-ray Scapula: # with Suprascapular nerve injury
4. X-ray Humerus: # with radial nerve palsy / shoulder dislocation with axillary N Injury
5. X-ray forearm bones: # with median / ulnar nerve injury
6. X-ray Chest in full inspiration:
Diaphragmatic paralysis with Phrenic nerve injury &
# Ribs with ICN injury (implies loss of a donor nerve)
Shoulder dislocation
# Clavicle
7. ENMG: (Locates the site of lesion / SNAP / CMAP)
8. NCS: (locates site by inching)
9. CT Myleogram (To identify nerve root avulsion)
10. MRI (To identify root avulsion)
11. Vascular studies when vascular injury is suspected.
APPROACH FOR DIAGNOSIS
Level of injury can be established by evaluation of the following points listed below
1. Presence / absence of axon reflex
2. Presence / absence of SNAP in EMG
3. Clinical examination of Rhomboid muscles
4. EMG of paraspinal muscles
5. Presence / absence of sweating
6. Presence / absence of Horners
7. Motor paralysis
8. Anesthesia
There are 3 levels of Injury
LEVEL I: Distal to Sympathetic ganglia: paralysis of limb muscles, anesthesia in the affected
dermatome, absent sweating in the affected dermatomes, Horners syndrome if T1 root is involved, absent
axon reflex, absent SNAP, and normal paraspinal muscles.
LEVEL II: Between the dorsal root sensory ganglion and the point of attachment of the sympathetic
ganglion to the ventral ramus: Paralysis of limb muscles, anesthesia in the affected dermatome,
NORMAL sweating in the affected dermatomes, Horners if T1 root is involved, absent axon reflex,
absent SNAP, paralyzed paraspinal muscles.
LEVELIII: Proximal to the dorsal root ganglia: Paralysis of the limb muscles supplied by that root,
anesthesia of the affected dermatome, NORMAL sweating, Horners if T1 root is involved, NORMAL
axon reflex, NORMAL SNAP, paralyzed Para spinal muscles. CT, MRI Myleogram will demonstrate
Myleoceles suggestive of root avulsion.
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APPROACH FOR TREATMENT

In an open injury it is generally agreed that at the time of exploration any vascular injury is
repaired & brachial plexus is explored to determine level / extent of the injury. Repair is done secondarily
after 3 weeks to allow for exact level of ischemia to demarcate and to precisely identify the level of
proximal neuroma. In a closed injury wait for spontaneous recovery for a period upto 9 months when
recovery is monitored clinically with improvement in weakness and anesthesia and electrophysiological
with EMG, NCS. While waiting for improvement patient is started on physiotherapy and splints to prevent
stiffness of joints and shortening of Musculotendinous units, electrical stimulation of paralyzed muscles to
minimize atrophy & compression garments, massage for scars if any. If no improvement occurs, surgery is
undertaken in the form of nerve grafting (when proximal ends are available) or with nerve transfers (in
root lesions) in early lesions when the motors have not atrophied. In late cases tendon transfers or muscle
transfers (pedicled or free) are undertaken.

Nerve transfers:
Oberlin 1: fascicle from ulnar N to motor branch to BICEPS
Oberlin 2: fascicle from median N to motor branch to BRACHIALIS
Mackinnon?
Somsacks: MOTOR BRANCH OF LONG HEAD OF TRICEPS TO ANTERIOR DIVISION OF
AXILLARY NERVE.
Bertilli: MOTOR BRANCH OF LONG HEAD OF TRICEPS TO POSTERIOR DIVISION OF AXILLARY
NERVE.
MOTOR DONORS:

Extraplexus donors:
Spinal accessory nerve
Intercostals C3-C6
most commonly used sources
+ Segmental nerve to rectus
Phrenic
Motor branches of the cervical rami
Hypoglossal (split)
Intraplexus Donors:
Medial Pectoral
Thoracodorsal
Ipsilateral C7
Cross-chest grafts - branches of the contralateral brachial plexus C7 and the lateral pectoral
C5-C6 avulsion: Part of the normal functioning ulnar nerve, redundant FCU fascicle in the arm to
the motor nerve of the biceps Oberlins procedure
Distal anterior interosseous nerve to deep branch of the ulnar nerve
Radial branch to long head of triceps to axillary
Testing for preganglionic lesion:
1. Gray rami communicans of T1 : Horners Syndrome
2. Dorsal rami of C3,4,5 : paraspinal muscles (look tangentially along posterior cervical prominence
while patient is flexing the neck)
3. Phrenic nerve (LITTON SIGN: paradoxical hollowing in the hypochondrium on involved side
while breathing )
4. Dorsal scapular nerve (Rhomboids , exaggerated military position)
5. N to serratus anterior (winging of scapula)
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Rule of 10 for diagnosing neuropraxia on NCS: in comparison to normal side, the involved side will show:
1. 10% in latency
2. 10% in amplitude
3. 10 m/s in conduction velocity of sensory nerve

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VOLKMANS ISCHEMIC CONTRACTURE

Name:
Age:
Sex:
Occupation:
Resident of:
Comes with chief complaints of:
deformity of right / left hand since duration
Loss of sensation over the hand
Inability to move the fingers
Onset: Acute / Insidious
Progression
Right or left handed
History of Trauma
History of tight bandages
History of burns
History of snakebite
History of IV extravasations
History of vascular trauma
History of surgery to arm or forearm
History of loss of sensation
Any history of treatment taken for the present disease
History of smoking & alcoholism
General examination
Vital signs
Attitude of the patient: Patient is lying supine in bed with shoulder and elbow joints in neutral position.
Local examination
Inspection
1. Flexion / Extension deformity of wrist, MP, PIP & DIP joints
2. Atrophy of arm / forearm / interosseous / Theanar & Hypotheanar areas
3. Trophic skin changes: Dry shiny skin, Sparse hairs & brittle nails
4. Scars of previous surgery, trauma & burns
Palpation
1. Tenderness
2. Local rise in temperature
3. Limb girth measurements
4. Limb length measurements
5. Volkmann sign for tendon shortening
6. Test for intrinsic contracture( Inability to flex the PIP joint with MP in extension as much as
when MP is in flexion)
7. Power of all muscles in the upper limb
8. Range of motion of all joints
9. Distal pulsations / Capillary refill
10. Distal sensations
Functional evaluation: what functions patient can do and what not??
DIAGNOSIS
Volkmann ischemic contracture Of Zancolli Type I / II / III secondary to X cause of -- DURATION
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INVESTIGATION
1. X-rays
2. ENMG
3. NCS
4. CT Scan may help delineate Live Vs. Dead Tissues
Intraoperative tissue biopsies.
APPROACH
Splinting & Physiotherapy. Surgery is usually in 2 stages. 1st stage is Excision of fibrotic tissue, Z
lengthening of FCR & FCU and neurolysis. 2nd stage is Tendon transfers, usually BR to FPL & ECRL to
FDP & EIP to APB. Intrinsic contracture requires release which may be proximal (zancolli) or distal
(Littler)

Management:
TIMING: Controversial
Safe answer is to do delayed excision.
- Tsuge: advocates waiting 6-12 months for exploration & infarct excision;
- can take >2-3 months for hand sensation & movement to return.
- earlier exploration may inflict more muscle injury
- give extensors time to recover completely
- zuker: difficult to isolate critical nerves and arteries amongst the ischemic tissue great risk of injury
which jeopardizes future reconstruction
Non-operative : Splinting, physiotherapy
Management based on Severity
(i) Mild contracture
Delayed faciatomy (>48h)
Controversial - neurologic benefit of delayed decompression vs. risk of infection
If pain still present, some living muscle still present, thus do faciatomy
Dynamic splinting once edema resolves to prevent wrist contracture
Active use of muscles, aggressive physiotherapy
if not improved >3 months, consider: tendon lengthening OR muscle sliding procedure
(ii) Moderate contracture
excision of dead (early) or fibrotic (late) muscle mass
neurolysis of median & ulnar nerves
options for surgical correction of contracture:
Muscle sliding procedure
Tendon transfers:
EIP/EDM/BR to FPL
FDS/FCU/FCR/ECRL to FDP
Free functioning muscle transfer
(iii) Severe contracture
Staged approach required
Initial procedures:
excision of all necrotic muscles
median & ulnar neurolysis and/or nerve grafts - restore sensibility & intrinsic function
treat joint contractures (wrist, hand)
interim: aggressive physio to improve/prevent joint contractures; allow healing
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Delayed procedures:
Restoration of mobility
Tendon transfer - not an option if extensors injured
Free innervated muscle transfer: gracilis, Latissimus, pec major
Soft tissue coverage:
gracilis - can be transferred as musculocutaneous flap bulky
distant flap - groin, chest
free tissue transfer
(skin graft - poor distal tendon coverage)
(local flap - not available)
MUSCLE SLIDING PROCEDURE ( Maxphage)
Difficult technically
Indications: mild or moderate injury
Technique:
zigzag incision from supracondylar region down forearm
superficial then deep muscles elevated off medial epicondyle and ulna
for moderate injury, also need to detach radial flexor muscles from the radius
median & ulnar n, brachial A & V - all identified and protected
muscles elevated distally until it is possible to extend fingers fully (2-3 cm)
Nerve stretching is a LIMITING FACTOR in muscle sliding operation.
muscles tacked down to periosteum in new position
Postoperative: splint with elbow 90, wrist & fingers in extension, active ROM & dynamic splinting after
2 weeks
Complications:
neurovascular injury
contracture recurrence
poor flexion
+/- pronator release
Differential tenotomy of FCU & FCR & suturing distal edge of one to proximal edge of other (similar
to what is done in torticolis release)
FREE FUNCTIONING MUSCLE TRANSFER:
Pre-requisites:
Good passive ROM
Finger sensibility
Mechanism for finger/thumb extension to provide useful grip function
Intrinsic muscle function present
Compliant patient (very long rehab)
Good skin coverage for distal tendons
Available motor nerve (preferably AIN)
Proximal end of muscle sutured to medial epicondyle of humerus. FPL & four profundus tendons attached
to distal end of muscle under appropriate tension.
Postoperative: splint in flexion 5 wks - passive ROM > 3 wks - active ROM > 6 monthss (muscle
becomes innervated) - heavy resisted exercises. Slight contraction at 3 months; finger flexion at 6 months;
gradual strength increase thereafter.

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AMPUTATED THUMB
Name:
Age:
Sex:
Occupation (In detail with reference to type of grip/ grasp employed)
Right / Left handed
Resident of:
Comes with complaints of a short thumb of this duration
Onset: Nature of injury, level of injury, injury to other finger / other hand, injury anywhere else in the
body.
History of pain, type, intermittent / continuous, radiation, region of pain
History of loss of sensation any where in the affected upper limb.
History of stiffness in the movement of the thumb
History of use of affected thumb (to see if patient has already developed substitution patterns)
History of diabetes/hypertension
History of smoking / alcoholism
History of treatments, surgeries for the present disease.
General examination
Vital signs
Attitude of the limb
Local examination
Inspection
1. Level of the thumb amputation
2. Describe the scar
3. Atrophy of the thenar eminence.
Palpation
1. Increased warmth
2. Tenderness
3. Level of amputation as related to the opposite normal thumb (measure the true defect and mark
on an aluminium finger splint, fix the splint to thumb and check if opposition can be achieved with
that length)
4. Distal sensation (See the discussion in brachial plexus chapter)
5. Distal vascularity (capillary refill), Radial / Ulnar artery pulsations in the affected hand, Allens
test, (digital Allens when pollicization is a possibility)
6. Active /Passive ROM at IP, MP & CMC joints.
7. Power of all intrinsics and extrinsics (flexor & extensors) graded 1 5 to assess paralyzed
muscles and available motors.
8. Stability of the thumb skeleton is assessed.
9. Assess the depth and adduction contracture of the first web
10. If toe transfer is an option examine the toe, foot circulation, Allens test.
DIAGNOSIS
Post traumatic amputation of the thumb at this level with / without complications of -- DURATION

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Classification
Type I:
Type II:
Type III:
Type IV:

73

Partial amputation: distal to middle of proximal phalanx

Subtotal amputation: Around the MP Joint with sparing of thenar muscles
Near total: through proximal shaft of Ist MC bone with loss of thenar
Total: Loss of thumb through the CMC joint

APPROACH
Type I has a functional length options include no intervention to prosthesis to all other options of
thumb reconstruction.
Type II requires intervention. Is too short for phalangisation / prosthesis, other options can be
considered.
TypeIII: Options include Pollicisation / toe transfer.
Type IV is the ideal indication for pollicisation.
Mark the Incision used for surgery on the thumb. Mark the dorsal flap if pollicisation is planned. Mark &
plan the flap for osteoplastic thumb reconstruction. Mark the incisions on the foot if a toe transfer is
planned by using the planned aluminium finger splint.

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DELAYED RECONSTRUCTION OF FLEXOR TENDON INJURY

Name:
Age:
Sex:
Occupation:
Resident of:
Comes with inability to bend this and this finger since this duration
Right / left handed
History of Injury to forearm / hand / finger so many months back when patient was doing this resulting in
a wound in this region which was treated at a hospital where suturing of the wounds was done. The
sutured wound healed without any complications. Subsequently patient noticed an inability to bend this
and this finger.
History of pain
History of loss of sensation
History of physiotherapy / splinting / compression garments / massage for the scar
History of diabetes / hypertension
History of smoking / alcoholism
General examination
Vital signs
Attitude of the limb
Local examination
Inspection
1. Finger cascade. The affected finger is out of cascade
2. Describe the scar in detail
3. Distal Trophic changes of denervation if any
4. Any evident atrophy in the forearm / hand.
5. Deviation of the finger
Palpation
1. Tenderness
2. Increase in warmth
3. Determine if scar is immature (blanching / hypertrophy / itchy) or if any raw areas are present.
4. Determine if any atrophy as measured by circumference from fixed bony points.
5. Determine if any limb length discrepancies
6. Feel for tendon movement
7. Distal vascularity: Pulsations / capillary refill
8. Distal sensation in median / ulnar / radial nerve territories
9. Passive & Active ROM is measured. (Passive ROM > Active ROM is tenodesis)
10. Power of all extrinsics & intrinsics are determined, graded 0 5.
11. Evaluate for any persisting fractures / dislocation / subluxation
DIAGNOSIS
Injury / rupture of repair / tenodesis involving these & these tendons in the region of forearm / hand /
finger on the right / left side of this duration with / without complications
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APPROACH
Prerequisites for a late flexor tendon repair are supple joints, good vascularity and preferable preserved
distal sensation. Fractures and dislocations are addressed. Tissue equilibrium must have been achieved wit
coverage of all raw areas and supple scars. In cases of tenodesis an attempt for improvement with
physiotherapy should be made for at least 6 months and surgery considered only after the benefits have
platued. Patient must be explained about the possible need for a 2-staged tendon grafting. If gap between
the cut ends is not significant, repair is done. If gap is significant to cause tension on the repair a tendon
grafting is done. If bed is scarred / pulleys are disrupted / nerve is injured / joint needs to be released & 2
Stage tendon repair is done.

In case there is contracture across the volar aspect, release and resurface it first tendon reconstruction.
Isolated FDP injury with intact FDS: either arthrodesis or tenodesis.
Single stage treatment / pt not willing for follow up: go for arthrodesis.
Multiple stages in stiff joints: arthrolysis collateral ligament reconstruction.
BOYES PREOPERATIVE CLASSIFICATION:
Grade 1
Grade 2
Grade 3
Grade 4
Grade 5

Good: minimal scar, mobile joints, no contractures, no trophic changes secondary to nerve
damage
Cicatrix: scarring from injury or previous incisions; contractures as a result of scar tissue
rather than joints; may need preliminary Z-plasty or flap coverage to compensate for soft tissue
damage
Joint damage: restricted range of motion
Nerve damage: trophic skin and joint changes from nerve injury
Multiple damage: multiple digits injured with tendon damage in more than one digit

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HYPOSPADIAS

Name:
Age:
Sex:
Occupation:
Resident of:
Came with:

C/O Passing urine from undersurface of the penis.

1st / 2nd / 3rd Issue, out of a nonconsanguineous marriage, as a FULL TERM HOSP. DELIVERY. Age
of mother at the time of birth was years and that of father was years.
Antenatal history: Rubella, Radiation, drug consumption (phenytoin, retinoids, steroids)
Urinary stream is thin/adequate and is directed towards floor/ thigh. Patient passes urine with/without
difficulty (or takes time: it indicates meatal stenosis).
History of erections in sleep: any obvious bending at that time.
History of any other congenital anomalies
Any urinary tract infections (which may be manifested as FTT) or known abnormalities of the
upper genitourinary tract.
Developmental milestone if adequate:
Immunization history if adequate:
Local examination:
1. Penis is.....cm in length (Normal: 3-4cm at age of 2 years). Strectched penile length & girth should
be measured. If the penis in a term infant is > 1.9 cm , micropenis should be suspected.
2. Meatus is present on the ventral aspect of penis at ------ location with or without meatal stenosis.
3. Shape of glans is conical /flat with flaring of glanular wings. (Conical glans is good for tubed flap
and flat glans for onlay procedure).
4. Prepuce is hooded.
5. Urethral plate is present on ventral aspect of penis extending from ectopic meatus up to the glans.
6. Urethral plate is splayed/broad/thin and shallow/deep.
7. Presence of curvature (Ventral chordee (mild/severe).
8. Dorsal penile skin is unscarred.
9. Testes and scrotum are normal.
10. Rest of genitourinary examination is normal.
11. Inspect groin to r/o any inguinal hernia.
Diagnosis: Midpenile Hypospadias with minimal chordee without meatal stenosis in........... old child.
Operative steps:
1. GA with ET, Supine position, cleaned with savlon (smegma), P & D, SUPPLEMENTARY
CAUDAL/PENILE BLOCK for postop analgesia.
2. Surgery is done using magnification with operating loupes.
3. Stay suture at glans tip with 4-0 prolene
4. Inspection under GA, look for meatus, location/condition of urethral plate, assess chordee.
5. 1:200000 ADR infiltration, wait x 7 minutes
6. Try to pass IFT/Foleys through the meatus.
7. Circumferential penile degloving incision sparing 1mm rim on the glanular side.
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8. Degloving on dorsal side, on ventral side urethral plate is preserved by taking a U shaped 77
incision
(in case of midshaft/distal HPS , in proximal HPS, the fibrotic tissue distal to the meatus is incised
so that meatus receeds proximally).
9. Gitte & Mclaughlins artificial erection test: after degloving penis held straight holding stay
suture tourniquet at the base of penis (with IV line or IFT) NS is injected using a butterfly
needle either on horizontal aspect of corpora or through the glans tip (avoids injury to the NV
bundle) check for chordee release tourniquet.
10. Orthoplasty/dorsal placation: Nesbits method , use of skin graft / skin substitutes
11. New meatus location is defined Further plan executed / modified
12. Glanular wings created and excess tissue underneath is excised to accommodate the neourethra.
13. Snodgrass: urethral catheterization (IFT/Foleys) urethral plate is defined 2 edges held with
plain forceps plate is incised in the midline (vertical fashion) check for adequacy over the
IFT. not adequate deepened further recheck neourethra is created by suturing the 2
edges of plate over IFT with 6-0 vicryl interrupted sutures (subcuticular inverting ?????)
If the edges are not getting approximated convert procedure into SNODGRAFT use an inlay
patch over dorsal aspect to create neourethra. the dorsal area is left to heal spontaneously
14. Second layer coverage: inner prepuce / Tunica Vaginalis. Inner prepuce is dissected from the
hooded prepuce upto the base of the penis. First while doing neourethra creation, the last stitch is
kept long covered by approximation of glanular wings (either 2 layered closure or mattress
sutures) remaining neourethra is covered by transposing and suturing the inner preputial flap.
With 5-0 vicryl (avoid obvious twisting of the penile shaft)
15. Meatoplasty: distal end of meatus is sutured with the glanular wings in a slit like manner, to avoid
futute stenosis.
16. Ventral Skin coverage: the hooded prepuce remaining on dorsal aspect is used.
Button hole glans is passed through it used to close ventral aspect.
Central slit unfirled suture is taken at the proximal end of the slit to centralize it brought
around on ventral aspect any obvious excess is excised sutured loosely with 5-0 vicryl
longitudinally circumcoronal closure.
17. The IFT/Foleys is secured to the glans tip with 4-0 prolene
18. Cleaning with savlon Sofratulle gauge piece loose sticking plaster application.
19. Postop: IV antibiotics for 5 days, in younger children Smooth muscle relaxants are given ti avoid
bladder spasms, in older children, Diazepam is given to avoid penile erections.
20. Dressing and catheter removal done on 8th POD. Check for urinary stream discharge Pt.

In 2 stage repairs: the width of urethral plate: 14-15mm

Oxybutynin is an anticholinergic medication used to relieve urinary and bladder difficulties, including
frequent urination and inability to control urination (urge incontinence), by decreasing muscle spasms of
the bladder. It competitively antagonizes the M1, M2, and M3 subtypes of the muscarinic acetylcholine
receptor. It also has direct spasmolytic effects on bladder smooth muscle as a calcium antagonist and local
anesthetic,
but
at
concentrations
far
above
those
used
clinically.
Oxybutynin is also a possible treatment of hyperhidrosis, or hyper-active sweating.
Embryological development of the penis and urethra:
During the 3rd week of development, primitive streak mesenchymal cells migrate around the
cloacal membrane to form the cloacal folds which fuse cranial to the membrane to form the genital
tubercle.
The fetus is sexually indeterminate until the 6th week of gestation when the cloacal membrane
divides into urogenital and anal membranes whilst the cloacal folds also divide into urethral folds
anteriorly and anal folds posteriorly with genital swellings lateral to them (these form the scrotal
swellings in the male and labia majora in the female).
During the 6th to 11th weeks, the genital tubercle elongates to form the phallus under the influence
of androgens. As the phallus develops, it pulls the urethral folds forwards to form the
lateral walls
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of the urethral groove which extends only up to the distal part of the phallus here the epithelial
lining is of endodermal origin and is known as the urethral plate (glandular urethra).
During the 12th week, the urethral folds come together and close over to form the penile urethra
(the glandular part of the urethra is not canalized at this stage).
During the 13th week, the glandular urethra becomes canalized by the inward migration of
ectodermal cells to form the external urethral meatus and the genital swellings enlarge to form
each half of the scrotum.

Hypospadias results from incomplete closure of the urethral folds during the 12th week of development
and may represent abnormal fusion between endodermal and ectodermal processes.
Incidence: 1 in every 300 live male births.
There is a link with cleft palate and hypertelorism i.e.SchilbachRott syndrome, which is very rare.
Aims of correction of hypospadias:
Allow micturition while standing with a nonturbulent stream.
Achieve a natural appearance with slit-like meatus located at the distal extent of the glans.
Allow normal sexual function.

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LEG DEFECTS
Name:
Age:
Sex:
Occupation:
Resident of:
Comes with complaints of Injury to the right / left leg since this duration
Patient was walking / traveling when he /she was hit by a 2 wheeler / 4 wheeler resulting in a fall and patient
had injury to left / right leg with severe pair. Patient was unable to stand / walk. Was shifted to a local hospital
where he was told he had broken a bone in his leg for which some orthopedic procedure was done. Now
complains of wound on the right / left leg with pain and discharge.
History of any other injuries in the accident
History of smoking / alcoholism
History of diabetes / hypertension
History of any previous surgeries
General examination:
Vital signs:
Attitude of patient:
Local examination
Inspection
1. Single WOUND is seen on right / left leg in the upper / middle / lower one third of leg over the
anterior / medial / posterior / lateral area, A x B cms, extending so many cms above the lateral malleoli.
The margin of the raw area shows healing epithelium. The periphery of the raw area is covered with
healing type of granulation tissue. In the centre of the wound the tibia / fibula is exposed measure so
many cms by so many cms in size and is dull yellow colour without any periosteum. The fracture site
is exposed / not exposed in the base of the raw area. There is an external fixator spanning the wound
with so many pins above and so many pins below the raw area, so many pins in the raw area.
2. The surrounding skin appears / does not appear inflamed
3. There is oedema / atrophy of the limb
4. Any obvious limb length discrepancies
5. GAIT: walking /not walking/ not allowed/advised??
Palpation
1. Tenderness around the raw area
2. Increased warmth
3. Limb girth and length discrepancies
4. Distal sensations
5. Distal pulsations
6. Any restriction in the range of motion: Knee / Ankle /subtalar joint/ midtarsal joint/ Toes
7. Power of various muscle groups. Comment about strength of QUADRICEPS
8. Lymph nodes draining the region
Donor sites examined and found adequate.

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DIAGNOSIS
Post traumatic composite defect over upper / middle / lower third of the leg with / without exposed fracture
tibia / fibula stabilized with external fixator / plate / screws with / without neurovascular deficit.
INVESTIGATION
1. X-ray
2. Wound C/s
3. Angiogram(for vascular status)
4. Doppler study (for vascular status)
5. General anaesthetic fitness.
APPROACH
Optimize the condition of the wound. When patient is fit wound is debrided and covered with Pedicled / free
flap.

Justification for fasciocutaneous flaps: subsequent surgeries may need re-opening.. so would like to
provide a supple skin cover.
Alternate treatment plan: the FIRST plan should not have violated the skin / vascular territory of the
proposed second plan!! Like distally based reverse Sural Artery flap as a first option and supramalleolar
as second does not suit!!
Limb length discrepancy > 2.5 cm is considered as significant.
Cross leg flap: cover donor site and bridging pedicle with SSG before insetting the flap as it would be
difficult to do so after flap is inset.
Gustillo & Andersons classification for open # is for ACUTE injuries. So better not to mention it in
diagnosis.

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LYMPHOEDEMA
Name:
Age:
Sex:
Occupation:
Resident of:
Comes with complaints of swelling over the right / left leg of duration / by birth,
Onset is acute / insidious. Patient noticed the swelling to begin in the distal / proximal region.
Progression
History of trauma
History of swelling over the region of groin prior to the complaints
History of Irradiation
History of periodic fevers
History of surgery
History of lump in the abdomen
Does the swelling reduce with elevation of the limb?
Does it increase with work over the course of the day?
History of pain in the limb
History of any secondary skin change: Pigmentation / Ulceration
History of complications:
Red streaks Lymphangitics
Tender enlarged lymph nodes: Lymphadenitis
Past history of periodic fevers
History of similar illness in the locality
General examination
Vital Signs
Local examination
Inspection
1. Unilateral / Bilateral
2. Extent from distal to proximal
3. Increase in girth
4. Prominent skin creases
5. Hump on the dorsum of foot
6. Obliteration of normal indentation above and below the malleoli
7. Squaring of the toes
8. Dry skin
9. Sparse hairs
10. Hyper pigmentation
11. Ulceration
12. Purplish papules (Of Stewart Treaves syndrome)
13. Any Scars (from Injury / Surgery / Radiation)
14. Obvious abdominal lumps
15. Enlargement of lymph nodes in the drainage area
Palpation
1. Increased warmth
2. Tenderness
3. Dry skin
4. Limb Girth in relation to bony points
5. Stemmers sing ( pinchability over toe dorsum) :lipoedema

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6. Pitting / Non pitting

7. Distal Sensation
8. Distal pulsation
9. Range of movement of joints
10. Enlargement of draining lymph nodes
11. Abdominal lumps / organomegaly

DIAGNOSIS
Primary / Secondary lymph edema of right / left leg of Grade I, II, III (Brunner) with / without secondary
changes
INVESTIGATIONS
CBC: eosinophilia
1. X-rays
2. Ps for MP
3. LFT
4. USG abdomen
5. Visual / Indirect Lymphangiography
6. Lymphoscintigraphy
7. MRI evaluation
APPROACH
Mention that you would like to see if swelling reduces with elevation over a period of time. Educate the
patient that there in no cure BUT, the disease can be kept under control, Conservative management of
limb elevation, complex lymph edema therapy, heat therapy (Chinese method). If investigations show
proximal obliteration with normal distal lymphatics then physiologic procedures can be attempted.
Otherwise in patients with severe restriction of day to day life due to elephantiasis reduction procedure
most commonly Homans procedure. (staged surgical debulking)
Classification: based on aetiology (primary / secondary)
Primary: congenital (<2 years, Milroys, AD), precox (2-35 years Meigs AR), tarda (>35 Yrs)
Clinical grading of commonly followed for filarial lymphoedema in india :
Grade I:
Grade II:
Grade III:
Grade IV:

pitting oedema relieved completely on overnight limb elevation.

pitting oedema relieved only partially on overnight limb elevation.
mostly non-pitting without skin complications
mostly non-pitting with skin complications (ulceration, nodules, etc)

Aim of surgery:
1. To reduce size of limb & MAINTAIN it
2. To treat complications
3. To reduce attacks of ADL (adenolymphangitis)
Indications of Sx:
1. Grossly swollen/heavy limb interfering with daily activities
2. When ADL attacks cant be treated by conservative Rx.
3. Treatment of skin complications.

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EXCISIONAL OPERATIONS:
Sistrunk: wedge of skin & subcut excised & wound closed primarily. MC used to reduce thigh
girth.
Homans operation (Hemicircumference operated initially other after 6 months)
Charles operation: full circumference in single stage
Suction lipectomy
Femoral artery ligation
PHYSIOLOGIC PROCEDURES:
Nodovenous shunts
Lymphovenous anastomosis
Bridging by lymphatic transplant
Drainage through omental flap
Mesenteric bridge operation (submucosa of isolated segment of ilium is transposed over transected
iliac nodes. Drainage mesenteric lymphatics
Thompsons (swiss roll /buried dermal flaps) operation
Kondoleons operation: a strip of seep fascia is removed presuming that sup & deep lymphatics
will communicate reducing lymphoedema.
Drainage thru strips of fascia/ fascia lata
Drainage thru skin flaps
Creation of new lymphatics (capillary action)
Combination of surgeries.
Embryology: Develops from 4 primitive cystic spaces, 2 in the neck and 2 in groin. Cisterns elongate &
develop communications. Condensations along the connections are lymph nodes.
Persistence of primitive cisterns are cystic hygromas.
Allows macromolecules (upto 1000KDa ) to pass thru capillaries.
Brunners classification:
0:
I:
II:
III:

histological abnormalities, not clinically evident

pitting edema , subsides with elevation
non-pitting edema, not relieved with elevation
irreversible skin changes, fibrosis, pappilae

Treatment:
Complex lymphoedema therapy: (CLT)
Manual lymphatic drainage
Low stretch bandaging
Skin care (examine, dry: moisturisation)
Exercises
Weight reduction
Psychological support and occupational therapy
Medications:
DEC 6mg/kg single dose (or 3 weeks)
Doxycycline 100 mg/day for 6 weeks

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INVESTIGATIONS: (Infrequently required to establish the diagnosis!)

To determine residual lymphatic function
To establish treatment preferences
To evaluate therapy
Isotopic lymphoscintigraphy:
A reliable and reproducible method for confirming the diagnosis. The radiolabelled macromolecular tracer
(99mTc-antimony sulfide colloid or 99mTc-rhenium sulfate, among others) is injected intra- or
subdermally within one of the interdigital spaces of the affected limb. The lymphatic transport of
themacromolecule is tracked with a gamma camera. The rate of tracer disappearance from the injection
site and the accumulation of counts within the lymph node are both quantifiable.
Although various routes of administration may be utilized, subdermal injection has been
recommended for optimal evaluation of the epifascial lymphatic transport. Lymphoscintigraphy enables
the adequate assessment of lymphatic function and the visualization of major lymphatic trunks and lymph
nodes.
Typical abnormalities observed in lymphedema include:
Dermal backflow,
Absent or delayed transport of tracer,
Cross-over filling with retrograde backflow, and
Either absent or delayed visualization of the lymph nodes

MRI is also helpful in the identification of lymph nodes, enlarged lymphatic trunks, and in the
differentiation of the various causes of lymphatic obstruction in secondary lymphedema.
The CT technique provides an anatomic definition of edema localization (subfascial versus epifascial),
and can identify skin thickening as well as the characteristic honeycomb pattern of the subcutaneous tissue
in lymphedema. It is used also to monitor responses to therapy in lymphedema through serial
measurements of the crosssectional area and tissue density in the tissue compartments of interest.
USG: thickening of the cutaneous, epifascial and subfascial compartments has been ultrasonographically
observed. High frequency ultrasound (20 MHz) reveals characteristic patterns of cutaneous fluid
localization in various types of edema. In lymphedema, there is a distinctively uniform pattern of
distribution.
Indirect lymphangiography
Contrast lymphography.
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RADIOLOGY

1. Hand fractures
2. Leg Fractures
3. Facial Series (Read Rowe Williams)
4. Waters View
5. Towne View
6. Caldwell View
7. Lateral View
8. Submentovertical View
9. TMJ Oblique anterior View
10. TMJ Oblique lateral View
11. Orthopantomogram (OPG)
12. CT Midface, Mandible Axial / Coronal cuts
13. CT / X-ray of Mandibular tumors

APPROACH:
When asked about management, enquire about clinical findings, whether open or closed before planning
treatment. Mention you would like to do x-rays of other possible fracture sites before planning treatment (For
example: In a X-ray of Mandible fractures do mention you would like to get the maxillary views before planning
treatment).

DIAGNOSIS FORMAT:
Plain / Contrast
X-ray / CT / OPG
View
Showing Fracture / Dislocation / Lesion: Site, Size, Sclerotic / Lytic
Mention any evidence of surgery done as seen in the x ray (K wire / mini plate)

5 things to see in OPG of SCC in Oral cavity
1. Presence of Invasion
2. Extent of invasion
3. Condition of dentition (to decide on RT)
4. Position of Mental foramen (To decide Osteotomy cuts)
5. Size of mental foramen (enlarged mental nerve due to invasion)

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Oblique Lateral View (Lateral Jaw)

Film Placement
1. The film is placed against the side of the patient's face so that the cheek and body of mandible are
contacting film.
2. The x-ray beam is directed posteroanteriorly from the opposite side with the center of the beam entering
slightly posteroinferiorly to the angle of the mandible. The center of the x-ray beam is perpendicular to
the film in the horizontal plane and is aimed at the mandibular first molar region.

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Lateral Head Plate

Film Placement
1. The midsagittal plane of the patient's head is parallel to the film.
2. The side of the patient's head to be radiographed touches the film.
3. The x-ray beam is directed perpendicularly to the film, entering the opposite side of the patient's head

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Postero-anterior (PA) View

Film Placement
1. The midsagittal plane of the patient's head is perpendicular to the film which touches the anterior aspect
of the patient's head.
2. Forehead and the tip of the nose contact the film.
3. The x-ray beam is directed perpendicular to the film entering the posterior aspect of the patient's head.

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Antero-posterior (AP) View
1.

Film Placement
1. The midsagittal plane of the patient's head is perpendicular to the film which touches the posterior aspect
of the patient's head.
2. The posterior aspect of the patient's head touches the film in such a way that a line from the external
auditory meatus to nasion is perpendicular to the film.
3. The x-ray beam is directed perpendicular to the film, entering the anterior aspect of the patient's head

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Water's (PA Oblique) View

Film Placement
1. The midsagittal plane of the patients head is perpendicular to the film which touches the anterior aspect
of the patients head.
2. The patients chin touches the film in such a way that a line from external auditory meatus to nasion forms
an angle of 37 degrees with the film.
3. The x-ray beam is directed perpendicular to the film, entering the posterior aspect of the patients head.

Lines of Dolan
Line 1 (orbital line, from lateral to medial) fractures of lateral orbit or diastasis of frontozygomatic suture,
fracture of orbital floor.
Line 2 (zygomatic line) fractures of lateral orbit and zygomatic arch.
Line 3 (maxillary line) fractures of lateral wall of maxillary sinus and zygomatic arch.




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Lateral Transcranial View of TMJ

Film Placement
1. The midsagittal plane of the patients head is parallel to the film which touches the side of the
patients head to be radiographed.
2. The center of the x-ray beam enters the opposite side from a point approximately two inches
superior and one inch posterior to the superior border of the external auditory meatus and is
directed posteroanteriorly through the condyle to be radiographed.

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Submentovertex (SMV) View

Film Placement
1. The midsagittal plane of the patient's head is parallel to the film which touches the side of the patients
head to be radiographed.
2. The center of the x-ray beam enters the opposite side from a point approximately two inches superior and
one inch posterior to the superior border of the external auditory meatus and is directed
posteroanteriorly through the condyle to be radiographed.

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OPG

100

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Film
sharpness: the definition of facial bones is much better with a PA projection than AP since
object
film distance is shorter with PA projection. AP projections are inadequate for diagnosis, particularly
undisplaced #, & have very little place in rad. Assessment of facial trauma.
Patients unable to sit up should be radiographed while lying PRONE not supine.

Exposure times:
Plain X-ray: 0.1-0.2 seconds
CT: 2-3 seconds
Radiation dose:
Basic unit: gray (Gy)
SI unit: defines gray as the dose of ionizing radiation which results in absorption of 1 J/Kg material.
1centigray (cGy) = 1 rad
Sievert (Sv) is the unit used in radiological protection & is a measure of the absorbed dose (in grays) & a
biological quality factor Q which depends upon the nature of the radiation & tissue damage it produces.
Sv = Gy x Q
Most radiosensitive parts: cornea, lens, pituitary gland. PA PROJECTIONS RESULTS IN LOWER
DOSE TO THESE than AP.
Few high quality, well positioned films are much better than a large no. of poorly positioned , badly
exposed & blurred films!
Radiographic reference lines:
1. Orbitomeatal (OM) line / baseline joins the outer canthus of the eye with centre of the EAM.
ADV: readily identified by radiographer without touching the patient & it can be seen on a lateral
radiograph of the facial bones.
D/ADV: it may be displaced by an orbital # or by soft tissue swelling d/t oedema or hematoma.
2. Interpupillary (IP) line: joins the 2 pupils, may be distorted by facial injury.
These 2 lines define a two dimensional spatial plane & it is in relation to this plane that all descriptions of
standard radiographic projections refer.
MAXILLA & ORBITS:
1. Standard projections:
2. Extra projections
& techniques :

MANDIBLE:
1. Standard projections:

OM
300 OM
Lateral facial bones
occipitofrontal 250
Frontooccipital 25 0
Submentovertical (SMV)
Intraoral occlusal views
Lateral nasal bones
Radiographric tomography
CT
Cephalometric radiography
CSF scintigraphy
CT cisternography.
PA 100
Townes view (AP 300)
Posterior lateral oblique view (right or left)
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2. Extra projections
& techniques:

Structure to be
viewed or investigated
1. Maxillary sinus
2. All other sinus
3. Mandibular fracture
i. condyle
ii. angle
iii. body
iv. canine region
v. ramus
vi. coronoid
4. Zygomatic fracture
5. Tempromandibular joint

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anterior lateral oblique

Intraoral occlusal views
Panoramic radiography
TMJ views
Radiographic tomography
Cephalometric radiography
Bone scintigraphy
Radiographic technique
or projection used
Waters view
Standard occlusal posterior
maxillary cross sectional projection
Waters or paranasal sinus view
Reverse townes projection
Mandibular lateral oblique projection (body and
ramus)
Mandibular lateral oblique projection (body)
Mandibular lateral oblique projection (body)
Mandibular lateral oblique projection (ramus)
Mandibular lateral oblique projection (ramus)
Waters view
Waters view
Submentovertex projection
Transcranial view
Transorbital view
Transpharyngeal view
Reverse townes view

TEMPOROMANDIBULAR JOINTS
1. Oblique AP View: Oblique, anteroposterior, frontal occipital view of the temporomandibular joints
provides an oblique, posterior view of the condyloid processes of the mandible, mandibular fossa,
temporal bones, petrous bones, internal auditory canals, occipital bone, posterocranial fossa, and foramen
magnum. Fractures in the region of the temporomandibular joints, with displacement medially or laterally,
can be detected in these views
2. Oblique Lateral Views : The views are taken by the lateral, transcranial projection and demonstrate
the temporomandibular joints in opened and closed mouth positions. The closed mouth view demonstrates
the temporomandibular joint, the relation of the mandibular condyle to the condylar fossa, and the width
of the joint cartilage. The open mouth view demonstrates the excursion of the head of the condyle
downward and forward in relation to the glenoid fossa and tubercle. This projection is useful in
demonstrating fractures and dislocations of the mandibular condyle and the condylar process. The external
auditory meatus and the mastoid process are also shown
3. Mayer View : The temporomandibular joint, external auditory canal, mastoid process, and petrous
pyramid are shown in the unilateral, superoinferior view (Fig. 66-37). Medial or lateral displacement of
the bone fragments of the mandibular condyle can be shown by this projection. Fracture-dislocation of the
bony portion of the external auditory canal may also be demonstrated by this technique.
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4. Panoramic Films: Panoramic films are helpful in defining location and displacement of mandibular
fractures. A study by Chayra et al reported that it is the most accurate plain view, from which
approximately 92% of mandibular fractures were diagnosed. A diagnostic accuracy rate of 92% for the
panoramic radiograph and 67% for the traditional mandibular series was reported. CT scans have accuracy
rates better than or similar to those of panoramic films. The sites in which mandibular fractures are most
commonly underdiagnosed on the panoramic view are the condylar, angle, and symphyseal regions,
especially if there is some blurring by the patient's movement or hardware. In the traditional mandibular
series, fractures were missed in every site except the ramus..
INTRAORAL OCCLUSAL VIEWS: Intraoral non-screen films provide clear definition of the
trabecular pattern of maxilla & mandible & will sometimes demo. An undisplaced crack # (not apparent
on standard extraoral projections). Best for showing injuries to teeth & demo. Small FB in soft tissues.
Occlusal views of maxilla: anterior projection is particularly useful for detecting midline separation of
maxilla. The film is placed between the upper & lower teeth as far posteriorly as possible, the cone of
dental X ray machine is placed over bridge of nose, angled 750 to the occlusal plane & aimed at the
centre of the palate.
The lateral occlusal view of the maxilla is taken with film in same position but tube is angled 450
to the occlusal plane with central ray directed through the canine fossa at the premolar region of opposite
side.
Occlusal views of mandible: taken with an intraoral film between teeth, the neck extended & the cone of
dental X ray machine is aimed at a point midway between the molar teeth & at right angles to the film.
Otherwise, the angle can be reduced to 450 to produce an oblique occlusal view of the anterior part of the
mandible.
PANORAMIC RADIOGRAPHY: (OPG / orthopentomograms) are tomographic images in which the
slice of tissue image is curved to conform with the shape of the dental arches. This is usually achieved
with a narrow X ray beam which rotates around the patients head opposite a special cassette which
moves at the same time. The shape of the curve is fixed & this can result in poor definition, particularly in
the anterior region if the dental arches are unusual in shape.
The aim of the technique is to project the whole mandible, dental arches, the maxillary sinuses, &
the orbits on a single film.
It is a good screening procedure for patients with suspected mandibular # but most equipment
requires a substantial degree of pt co-operation as the film is taken with the pt sitting up & keeping quite
still during exposure (2-3 seconds). Not possible with uncooperative & confused pts & satisfactory
positioning is sometimes impossible in recently injured pts. d/t gross swelling of soft tissues.
Some modern equipment can carry out exam with pt in supine position. The technique is excellent
for F/u treated mandibular # as the whole mandible, including the TMJ & the occlusion, is shown on just
one film.
Artefacts by: poor positioning, pt movement, metallic dental restorations, FB & jewellary.
Mandibular fracture.
(a) Unfavourable fracture. Displacement is likely. Upward arrow represents pull of the temporalis,
masseter and medial pterygoid muscles whilst the downward arrow represents the digastric and mylohyoid
muscles.
(b) Favourable fracture. Displacement is unlikely as muscle forces tend to compress fragments together.

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Indications for ORIF of condylar fractures

* Failure of IMF to correct occlusion after 2 weeks.
* Bilateral fractures fix one side.
* Foreign bodies.
* Head-injured patients/mental retardation and unable to tolerate IMF.
* Significant displacement especially laterally or into middle cranial fossa intracapsular fractures are
usually stable.
Surgery can be difficult access is difficult, there is a risk of facial nerve injury and the small fracture
fragments make standard ORIF techniques a problem.
In general:
* No malocclusion soft diet and observe for developing malocclusion which then requires IMF with
elastics.
* Malocclusion closed reduction (IMF with elastics) except for lateral anterior open bite which
probably requires ORIF, especially if displaced, if bilateral or if there are panfacial fractures. High
fractures of the condyle or ramus are approached via a Risdon incision combined with a pre-auricular
incision. Early active ROM exercises are needed to rehabilitate the TMJ.

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NOSE DEFECT
v Local examination of any defect can be described by observing the anatomical land marks.
v Composite tissue defect is present on the left ala of nose.
v Size of defect is ......cm ......
v Horizontally defect extends from left alar base up to the soft triangle region. Vertically it extends for about
2cm over the lateral wall of nose.
v Defect involves skin, cartilage and mucosa. Mucosal defect is more than the skin defect.
v Tissue at the margin of defect is scarred and is pulling the tip of nose, lateral wall of nose and cheek skin.
Left nasal sill is normal.
v Tip definition points are well defined except for slight distortion at the left side.
v Length of columella is equal bilaterally.
v Right ala and nostril sill are normal.
v Dorsum of nose and right lateral wall of nose are normal.
v No other feature suggesting distortion of nasal anatomy is observed.
v Nasal septum is in midline.
v No turbinate hypertrophy present.
v Donor sites for flaps and graft at forehead, bilateral post auricular region, scalp, left arm, and thigh are
unscarred.

SCALP DEFECT
v Skin grafted alopecia patch present on the right parietal region.
v Size of patch is 5cm x 5cm. Graft is soft and covered with oil.
v No raw area present over the graft.
v Rest of scalp is normal with adequate density of hairs without evidence of any scar.
v My diagnosis is post traumatic grafted alopecia patch over right parietal region of ............ duration.

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1. ORAL MALIGNANCY
Name :
Age :
Sex:
Occupation: (In particular SUN EXPOSURE)
Resident of:
Comes with complaints of ulcer/lesion in the mouth of this duration. Onset Insidious.
Progression: Initially was of this size and has rapidly / gradually progressed to the present size.
History of pain, nature, continuous / intermittent, any radiation of pain, does it disturb the sleep (Pain only
while at rest or on movement, painful lesion often imply malignant invasion into nearby peripheral nerve/s)
Any history of bleeding from the ulcer
History of smoking
6 S:
History of alcoholism
Spirits
Smoking
History of tobacco use, areca nut use. Frequency. Duration.
Spices
History of caries tooth, sharp teeth
Sharp tooth
History of trismus
Syphilis
History of loose teeth
Sepsis
History of difficulty in chewing
History of difficulty in swallowing / pain during swallowing
History of drooling of saliva / excessive salivation
History of halitosis
History of change in speech or hoarseness of voice
History of any white / red patches in the mouth antedating the ulcer (Leuko/erythro/melanoplakia)
History of cough, wheeze, hemoptysis, chest pain
History of Lump / pain in the abdomen
History of bone pains
History of weight loss
History of enlarged swellings in the neck
History of any treatment taken for the present disease.
History of diabetes / hypertension
An occupational exposure to heavy metals such as nickel, and previous radiation exposure to head and neck
are other important risk factors
Personal history: Married, how many children
Socioeconomic History

General examination: Conscious, Co-operative, oriented in time, place & person. Pallor, Icterus, Cyanosis,
Oedema, Nutrition (Lipids: Triceps skin fold thickness male > 11, female > 13cms; Proteins: MAC male > 25,
female >23 cms; Also look for signs of vitamin deficiencies)
Vital signs: Pulse : regular, force (S), volume (PP), tension (D) , RR, Temperature, BP

Systemic Examination
1. RS: (Lung Metastasis)
2. Abdomen (Metastasis, Organomegaly)
3. CVS

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LOCAL EXAMINATION
Inspection (use tongue blade): there is an ulceroproliferative growth
1. Extra oral examination: fullness in the region adjacent to ulcer in mouth
2. No, size, shape, position, edge, floor, surrounding skin of the ulcer infiltrating the skin, exact extent
of lesion and whether it is crossing / encroaching GB sulcus
3. Restriction in mouth opening (Trismus suggests ominous pterygoid and masticator space
involvement)
4. Any patches of leucoplakia / erythroplakia / melanoplakia. Clinical characteristics of lesions
suggesting the presence of dysplasia include:
large size,
tongue or floor of the mouth location,
red color,
friability, and
the patients prior history of oral cancer or dysplasia.
5. Occlusion / Dentition : No of absent teeth, caries, oral hygiene (complete or partial if edentulous)
tumors may, as the first sign, displace or loosen teeth.
6. No, size, shape, position, extent, edge, floor of the ulcer
7. Any Synchronous lesion: floor / palate / retro molar trigone / pharynx
8. Put tongue out and demonstrate mobility
9. Any fullness in the neck for lymph nodes
10. Inspect possible flap donor sites. (Comment as possible flap donor sites inspected & found
adequate)
A complete examination of the cranial nerves is performed, emphasizing
sensation over the chin for mandibular nerve deficit,
tongue mobility for hypoglossal nerve deficit,
facial nerve function,
palatal elevation and gag reflex and
function of the accessory nerve.
Palpation
1. Increased warmth
2. Tenderness
3. Anesthesia in Infraorbital and Inferior alveolar Nerve territories
4. Measure mouth opening (IID)
5. Ulcer: Surface, consistency, tenderness, extent of skin involved (mark), extent of bone involved
(mark on skin of same or opposite side if skin ulcerated), and extent of mucosal involvement (mark on
skin of same side or opposite side if skin is ulcerated). Method of palpation of bone: Use thumb and
index of right hand to feel lingual and buccal cortex of the mandible. (+/- Thickening)
6. Test Lingual Nerve, chorda tympani nerve
7. Check for loose tooth
8. Palpate neck systematically for neck nodes (stand behind the patient, flex his neck & then examine)
9. Palpate for possible face / neck vessels for microvascular anastomosis
10. Palpate the abdomen for organomegaly / any mass.
Normal neck structures commonly mistaken for metastatic masses include:
the transverse process of C2 in the jugulodigastric region of thin patients,
the scalene muscles,
a tortuous carotid artery,
a carotid aneurysm,
a prominent carotid bulb,
a cervical rib, and
ptotic submandibular glands.
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DIAGNOSIS
Malignancy / ulceroproliferative growth of this region of the oral cavity, probably SCC of this T N M
grade of this Stage with / without complications.
INVESTIGATIONS
1. Edge / Punch Biopsy of the Ulcer to confirm the diagnosis
2. FNAC of the Lymph nodes to confirm neck metastasis
3. Indirect Laryngoscopy to rule of synchronous malignancies (5% Incidence)
4. OPG to evaluate
a. Involvement of mandible, (loss of cortical outlines & irregular areas of radiolucency)
b. Status of dentition (e/o caries & periodontal disease, resorption of dental roots
c. Site & size of mental foramen, (enlarged mental nerve d/t invasion) and
d. To determine site of cuts for mandibular resections or access osteotomies
e. To confirm adequacy of reduction and fixation of access osteotomies.
5. CT plain & contrast to evaluate precise extent of involvement.
Advantages of CT include
good soft-tissue discrimination and vessel identification and
excellent definition of bone soft-tissue interfaces.
readily available and affordable.
Cortical destruction and tumor in the alveolar canal and the bone marrow can be seen on CT. Special
coronal reconstructions of dedicated mandible CT scans (Dentascan) is particularly helpful in imaging
the mandible. CT scans of the oral cavity should be combined with neck CT to assess for suspicious
subclinical metastatic nodes. Axial and coronal views with bone and soft-tissue windows with contrast
from the orbital floor to the base of the tongue as well as axial views of the neck are obtained.
Disadvantages: include
radiation exposure,
possible contrast dye sensitivity,
dental amalgam interference,
difficult positioning for coronal views, and
no direct sagittal views.
6. MRI plain & contrast
CRITERIA FOR +VE NECK NODES ON CT/MRI
Increase in size (short axis >8-10 mm)
Central necrosis & rim contrast enhancement
Extra-capsular extension
Obliteration of surrounding fat planes
Advatages:
enhanced soft-tissue discrimination,
excellent skull base and CNS assessment,
sagittal views, and
no radiation exposure
Disadvantages:
examination takes longer,
is more expensive,
is poorly tolerated by some, and
the black signal of bone makes cortical bone abnormalities difficult to see
7. CXR to rule out lung metastasis,
8. USG abdomen to rule out liver mets.
9. Routine blood investigations, ECG for fitness for surgery.
10. Bone scan for possible bony involvement of mandible or other bone mets.
11. Barium Swallow to r/o tongue base lesions.
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indications for examination under anesthesia include: an inadequate assessment of the extent
of the
disease by history and physical examination and imaging, or the presence of symptoms referable to the trachea,
larynx, hypopharynx and esophagus that need endoscopic assessment.

Symptoms suggesting lesions of the trachea, larynx, hypopharynx, or esophagus include:

o dysphagia,
o odynophagia,
o pain,
o hoarseness,
o hemoptysis or
o stridor.
APPROACH

The biopsy confirms the diagnosis as SCC & CXR / USG stage the disease. Explain nature of illness,
natural history, prognosis, need for surgery & alternatives to patient. If patient consents plan is Dental
evaluation for caries tooth and treatment for it followed by wide excision ( Mark on skin) of the
malignancy : skin / bone / mucosa ( 1 cm and proceed when frozen section facility is available or else 2
cms margin) after the completion of Neck dissection ( either staging Supraomohyoid neck dissection
for N zero neck with T3 / T4 lesion or RND for N1 N2N3 disease) with the RND incision connected to
the full thickness excision of the lesion ( avoiding lip split to prevent necrosis of the ipsilateral lower
lip). The excision defect is reconstructed usually with Deltopectoral flap for cover & pectoralis major
flap for lining. Stage I, II need either Surgery OR radiotherapy & Stage III, IV require both surgery
AND radiotherapy.
Commisuroplasty
PL Sling

Preop considerations:
1. General physical health & functional status
a. Comorbidities
b. Nutrition: hyperalimentation may be required as tumor prevents adequate oral intake +
cachexia of malignancy.
2. Cardiovascular fitness (prolonged surgery)
3. Preop dental evaluation:
a. Management of postsurgical defect
b. Extraction or restoration of tooth for radiation
4. SALT, medical oncologist
5. Social counseling
Airway: Patients may be difficult to orally intubate due to trismus, hemorrhage, or tumor bulk, and the
presence of the oral endotracheal tube may interfere with the resection. The appropriate solution is
nasal intubation with or without flexible fiberoptic nasopharyngoscopic guidance. Another option for
airway management is preoperative tracheostomy under local anesthetic.

Indications for tracheostomy after oral cancer surgery include:
(1) The anticipation of significant postop edema of the pharynx, FOM or the base of the tongue,
(2) A significant risk of postoperative hemorrhage,
(3) The presence of any bolster or other inspirable dressing material,
(4) Pre-existing pulmonary disease or obstructive sleep apnea, or the simultaneous operation or
compromise of the nasal airway, and
(5) The need for frequent endotracheal suctioning or ventilation support.
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Approach
to buccal mucosa:
Transoral / cheek flap / access osteotomies of mandible / partial mandibulectomy or maxillectomy in recurrent
cases

Approach to FOM: (early regional mets)

1. Transoral excision of T1-2 lesions with primary closure/ SSG
2. Extensive: midline or paramedian (preferable) mandibular osteotomy with mandibular swing
3. Larger lesion: marginal mandibulectomy of only superficial or periosteal bone involvement OR
segmental if bony invasion.
4. Marginal mandibulectomy:
a. Sagittal (inner table only)
b. Horizontal (upper portion only) OR COMBINATION THEREOF.
c. At least 1 cm of mandible height should remain for future osseointegrated implants.
Routes of spread to mandible:
1. Direct cortical destruction
2. Along alveolar sockets (in edentulous patients)
3. Along mental nerve.
First, the proximity of the tumor is assessed by observation, palpation, and by CT scan, if the lesion is
fixed to the bone.
If the tumor is > 1 cm away from the bone: no resection.
If the tumor is < 1 cm from the mandible: a marginal resection of the mandible will ensure 1 cm
margins.
If the tumor involves the gingival mucosa and the periosteum without clinical or radiologic evidence
of cortical or cancellous bone involvement, then a marginal resection of the mandible is
satisfactory, because any subclinical bone involvement is likely to be localized to the alveolar
process.
If the tumor is fixed to the occlusal surface with clinical or radiologic evidence of cortical or
cancellous bone involvement, then a segmental resection is performed because, once the occlusal
cortex is breached, there is no barrier to the vertical spread of tumor through cancellous bone to the
alveolar canal.

Retromolar lesions are relatively difficult to treat because they spread early to deep structures such as
the ascending ramus of the mandible, pterygoid muscles, the masticator space, and the skull base.
Another avenue of local spread is the foramen of the inferior alveolar nerve into the ramus of the
mandible. Tumor may also spread proximally along the perineurium or within the nerve to the
trigeminal ganglion and the CNS. Surgical access to this region is challenging. Bone resection is nearly
always indicated, and recurrence is difficult to diagnose.
Indications for mandibular reconstruction:
Anterior mandible: cosmesis, tongue fall --------- reconstruct (or else ANDY GUMP deformity)
Lateral mandible: Dentate , young patient: reconstruct. Edentulous: PMMC, Forehead, DP
Indications of adjuvant radiotherapy:
1.
2.
3.
4.
5.
6.

Close (<5mm) / involved margins & further excision is impracticable

Perineural spread
Perivascular spread
Large tumors
Poorly differentiated tumors
>1 LN involved
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7. Extracapsular spread in LNs

SCC originates in spindle cell layer.

A depth of invasion by tongue cancer of greater than 5 mm is associated with an increased incidence of occult
metastasis. Except for oral cancers < 2 mm thick, all early staged oral cancer patients should receive elective
supraomohyoid neck dissection (SOHND).
Keratoacanthoma has similar presentation to verrucous Ca (treatment is curettage).
The more keratinizing, well differentiated histology of SCC is asso with less reliable RT & CT
Choice of treatment depends on:

Site,
location,
stage ,
histology,
nodal status

& also

Competence
Convenience
Cost
Compliance
complications

Perimeter tongue flap (bipedicled from ventral surface): for vermilion reconstruction

GOALS OF TREATMENT:
Oncologic
Staging
Local control
Regional control
Use of Adjuvant treatment
Recontructive
General : rapidly as possible, preferably in one stage
Functional [Some are currently un-attainable (e.g. taste, velum & tongue movements, coordinated
peristalsis etc.)]
Watertight internal lining: mucosa, dura.
Oral continence.
Facilitated deglutition / swallowing.
Mastication.
Comprehensible speech.
Prevent aspiration.
Protect vital structures.
Protective sensation
Anatomic
Cover, structure, lining
Protect vital structures
Cosmetic
Color, contour
Facial landmarks hair, nose, eyes
Appropriate use of prosthesis
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Recipient vessels in the H&N

Arteries
Transverse cervical
Superior thyroid
Facial
Superficial temporal
External carotid artery**
AV loop ***
Vessels from previous flap

Veins
IJV (end to side)
Tributaries of EJV
Cephalic vein " turnover "
* Vessels from previous flap

*: For skull base

**: Above level of digastric muscle if the arteries above are previously taken
***: If ipsilateral vessels are affected.

Mandible Reconstruction
The Role of the Mandible:
Functional
Support for tongue & muscles of floor of mouth
Mastication
Articulation
Deglutition
Respiration
Aesthetic
Determines shape of the lower face (height & projection)
Goals of Mandibular Reconstruction
1.
2.
3.
4.
5.
6.
7.
8.
9.

restore oropharyngeal function

restore a solid mandibular arch
maintain oral continence
facilitate swallowing
allow mastication: dental restoration, pre-op occlusion, jaw mechanics, incisal opening
preserve speech
restore sensation
achieve primary wound healing
restore facial aesthetics

Classification of Defects
A. HCL Classification. 1992 (Boyd et al PRS 1992 (7)
Bone defect:
H: lateral defect of any length including condyle- not crossing the midline
L: lateral defect not involving condyle, up to midline not crossing the midline
C: central segment crosses the midline (23-33, all 4 incisors and 2 canines)
Soft tissue defect:
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o: osseous - neither skin nor mucosal component

s: skin
m: mucosal
sm: skin + mucosa

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Surgical Planning
tracheostomy, feeding tube, patient positioning, two team approach for synchronous resection and flap
elevation, Assess defect & recon requirements (skin / bone / mucosa)
Graft shaping
May be done while ablation is in progress
Measurements of total flap dimensions & locations where osteotomies are required
Shaping:
1. External fixator
2. IMF
3. Dental splint
4. 3D modeling (use mirror image from contralateral.) and pre-bend plate
Lateral Defects
Angle of mandible usually planned where vascular pedicle enters bone
Ramus height determined from resections specimen
Dont necessarily need rigid reconstruction, can use soft tissue only (Lipa)
For L defects mandibular condyle can be mounted directly onto flap
Anterior Defects
These are difficult to inset correctlylateral segments are difficult to stabilize
Use maxillary arch for visual guide
Consider interarch distance (dental recon), facial height, pro/retrognathia
Plan location of central segment so as to maximize flap pedicle length place it as
posteriorly as possible
Bony fixation
molding recon plate to mandible prior to resection
CT generated mandibular model for recon plate modeling
if edentulous, can apply plate to fix mandible to maxilla prior to resection
TYPES OF MAXILLECTOMY:
Type I (limited maxillectomy) defects, which involve two walls of the maxilla excluding the palate,
require reconstruction with a large-surface area/low-volume flap such as the radial forearm
fasciocutaneous (RFF) flap.
Type II (subtotal maxillectomy) defects involve the lower five walls of the maxilla, but spare the orbital
floor, and are best reconstructed with a large-surface area/medium-volume flap such as the radial forearm
osteocutaneous (RFO) sandwich flap.
Type IIIa (total maxillectomy with orbital preservation) defects include all six walls of the maxilla,
and should be reconstructed with a mediumlarge-surface area/mediumlarge-volume flap such as the
rectus abdominis myocutaneous (RAM) flap combined with calvarial bone or rib grafts for orbital floor
reconstruction.

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Type
IIIb (total maxillectomy with orbital exenteration) defects require reconstruction with114
a largesurface area/large-volume flap, such as the RAM flap.

Type IV (orbitomaxillectomy) defects include the orbit and upper five walls of the maxilla, sparing the
palate, and are best reconstructed with a large-surface area/large-volume flap such as the RAM flap.
Masticator space: space containing the masticatory muscles (medial and lateral pterygoid muscle,
masseter muscle, temporal muscle); these muscles attach to the ascending ramus and angle of
the mandible. The nerve of the masticator space is the mandibular nerve (third branch of the trigeminal
nerve); it supplies the motor innervation of the masticatory muscles and provides via the inferior alveolar
nerve sensation to the mandibular teeth, gums and lower lip/chin region. The part of the masticator space
below the level of the zygomatic arch is sometimes called the infratemporal fossa, and the part above it
the temporal fossa. Trismus (masticatory muscle spasm causing inability to open the mouth) is a common
symptom in masticator space pathology, restricting the clinician's examination of this area.
Contains:
-masseter muscle
-the external and internal pterygoid muscles
-the posterior body and the ramus of the mandible
-the inferior alveolar vessels and nerves
-the insertion of the temporalis muscles
The blood supply of the buccal mucosa originates primarily from:
1) The buccal artery---a branch of the maxillary artery
2) The anterior superior alveolar artery of the infraorbital artery---a branch of the third part of the
maxillary artery
3) The middle and posterior superior alveolar arteries---branches of the maxillary artery
4) Accessory vessels from the transverse facial artery---a branch of the superficial temporal artery
Rehabilitation of swallowing after oral cavity surgery is important. Swallowing can be divided into the
preparation phase, the oral phase and the pharyngeal phase. Oral cavity surgery impacts most on the
preparatory phase and the oral phase. The preparatory phase of swallowing begins with lubrication of the
food bolus by saliva. This is impaired when pre- or postoperative radiation therapy is employed.
Significant xerostomia results in the majority of irradiated patients. The xerostomia significantly limits
the types and consistencies of food that can be swallowed. Most patients with oral cavity radiation require
frequent sips of water to maintain moisture and liquid to wash down the food at mealtimes.
Give allowance of 2cm for mouth opening (in cases with trismus) while planing flap dimensions.
Reconstruction: staged recconstruction with lining and cover.
Always comment on nodes bilaterally.
ORN: more damage on mucosal side.
Post-RT recurrence: hemimandibulectomy, neck dissection with macfee bipedicled incision (skin flap
viability with any other method is doubtful)
Role of tracheostomy in extensive defects: good for maintaining oral hygeine, flap care.
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Internal maxillary artery branches

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POST BURN CONTRACTURE DEFORMITY

Name:
Age:
Sex:
Occupation:
Resident of:
Comes with complaints of inability to look up / tightness in the neck / other joints / deformity since this
duration.
On enquiry patient sustained thermal burns / scalds so many years / months ago when patient was
cooking / working when the cotton / nylon garment patient was wearing caught fire. Fire was doused / not
doused immediately. Any history suggestive of inhalation. Patient sustained burn on these regions. How was
the fire doused? Was taken to the hospital and treated with IV fluids and regular dressings. These wounds
healed with dressings. These wounds were grafted in so many operations. At the time of discharge all wounds
had healed except these. After discharge patient was / was not treated with massage / compression garment /
splint / physiotherapy (give details).
So many months after discharge patient developed tightness over these joint regions, and the deformity
progressively increased and the patient is presently unable to do this and this.
History of blood transfusion / allergies
History of diabetes / hypertension
History of smoking / alcoholism
History of any surgeries other than above.
History of fall / head injury in case of electric burns.
Personal history: Married / unmarried, if married how many children, if any sustained burns in the same
episode?
General examination: including nutritional assessment by measurement of MAC (proteins), Triceps skin fold
thickness (Lipids) and evaluation of any vitamin deficiencies.
Pallor / Icterus / Cyanosis / Oedema
Describe area of burn scars all over the body (in terms of size, shape, whether it is a healed burn scar or a
healed SSG scar, hyper or hypo pigmented, hypertrophy or keloid changes, indurated / supple in the
centre and edges, blanching /not blanching on touch, tenderness, any itching in the scar.) other than the
principle scar being examined for the examination.
Vital Signs
Describe the attitude of the patient: Patient is supine / sitting with these & these joints in neutral position and
these & these joints in flexion / extension deformity.
Local examination (AFTER THE SCAR, ALWAYS EXAMINE DONOR SITES!!)
1. SCALP: Describe the scar (in above terms)
Classify the post burn wound as (Harrisons classification)
Class I:
Periosteum is present
Class II:
Periosteum is absent / outer table present
Class III:
Outer table absent / inner table present
Class IV:
Inner table is absent
2. FOREHEAD: Describe the scar
Total / Partial loss of eyebrow, distortion of eyebrows.

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3. CHEEK: Describe the scar

Distortion of near by landmarks like eyelid, ala, commisure.
4. EAR: Describe the scar
Mention any loss of pinna (partial / total), lobule.
Describe anatomical units burnt.
Any exposed cartilage.
Examine EAC.
If hearing appears impaired weber, rinne test.
5. NOSE: Usually described as a thin shiny nose
Eversion of nares
Alar retraction, Lower lateral cartilages form leading edge of nostril.
Nostril stenosis
Columellar contracture
Loss of partial nasal units or total nasal loss.
Check air flow during regular breathing (Ideally by frosting of tongue depressor)
Intranasal examination.
6. EYES Describe the scar
Ectropion / Scleral show (Mark the incision for release)
Epiphora
Canthal web
Stenosis of palpabral fissure
Corneal ulcer
Symblepharon
Eyelashes
Check vision
7. MOUTH: Describe the scar
Microstomia, assess mouth opening
Ectropion: Incisor / canine show
Effacemet of mentolabial sulcus
Changes in cupids bow, white roll, dry wet vermillion
Blunting of comissures
Assess lip seal
Assess speech
Assess lower sulcus depth
Mark the incision for release / excision

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8. NECK: Describe the scar,

Classification:
Class I:
Class II:
Class III:
Class IV:

Normal ROM but tightness present

Restriction in ROM but Straight forward gaze is spared
Straight forward gaze not possible
Mentosternal adhesion

Assess lip seal / salivary drool

Assess oral Hygiene
Assess state of dentition and if normal occlusion is possible
Assess for airway problems /any mandibular growth restriction in children
Mark the scar. Assess distances from bony landmarks (Mentum, angle of mandible & Sternoclavicular joint,
midpoint of clavicle and acromioclavicular joint) to measure the TRUE DEFECT after mentosternal
contracture release.
Assess if the breast is pulled up when patient extends the neck
Assess range of motion at the neck
Cervicomental angle is between 105 & 1200,
Flexion 800,
Extension is 450,
Lateral flexion is 450 &
Rotation 800
Mark the lines on incision (usually from mastoid to mastoid at the region of Hyoid bone / point of maximum
contracture) Fish tail the end of the incision.
Plan for local/ regional / distant flaps if exposure of deeper structures is anticipated.
Aims of neck release:
1. Improve alimentation
2. Improve vision and satisfactory forward gaze
3. Assist further intubation.
Anaesthesia:
Try endotracheal intubation
Fiberoptic assisted intubation
Local anaesthesia + Ketamine (Conscious Sedation) incise the scar intubate
(Ketamine does not cause bronchoconstriction)
1.
2.
3.
4.
5.
6.
7.
8.
9.
10.
11.
12.
13.
14.

Position: supine with bolster under shoulder (Maximum neck extension), arms by side.
Pass Ryles tube under vision (preferably by anesthetist), pass Foleys catheter
I will start with incisional release followed by excision of the hypertrophic scar.
Adequate release upto neutral line. (anterior border of trapezius) Depth of release?? Usually platysma
is also excised with scar.
Prepare for flap if vital structures are exposed.
Hemostasis
Application of medium thickness, sheet grafts (preferably unmeshed) with few fenestrations. Grafts are
applied in horizontal direction so that juncture comes along RSTL
Secure the graft to bed, paraffin gauge
Application of the tie over/bolster dressing.
POP application (contoured to the dressing, keeping neck fully extended)
Postop position: neck maximally extended with pillow under the shoulders.
RT feeding continued till 7 to 10 days, IV fluids, IV Antibiotics for 5 days
Graft inspection on 5th postop day.
Repeat dressing on 7th postop day.
Changeover to custom-made thermoplastic splint (hard collar) with soft lining. (+/- Silicone sheet)
+/- chin strap
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15. Flaps are indicated only for recurrent contractures

16. Use of tissue expansion.

9. AXILLA: Describe the scar

Classification
Class I:
Class II:
ClassIII:
Class IV:

Anterior or posterior axillary fold

Both the folds
Entire axilla
III + Periaxillary

Pattern of hair loss due to burns

Apparent size of scar & Assessed true defect as measured from bony landmarks
Assess distal sensation, vascularity, distal limb length discrepancies
Assess Range of motion
Normal Shoulder ROM:
Flexion 1800,
Extension 450,
Abduction 1800,
Adduction 450,
External rotation 900,
Internal rotation 450
Mark the Incision / Excision lines at the point of maximum contracture
Plan for local/ regional / distant flaps if exposure of deeper structures is anticipated
10. CUBITAL FOSSA: Describe the scar
Apparent size of the scar & assessed true defect as measured from fixed bony land marks
Assess distal sensation, vascularity, limb length discrepancies.
Measure any atrophy as assessed by circumference from fixed bony points.
Assess ROM, Normal:
Flexion 1450
Extension 00
Pronation 700
Supination 850
Mark the line of incision / excision at point of maximum contracture.
Plan for local/ regional / distant flaps if exposure of deeper structures is anticipated

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11. HAND: Describe the scar

Classification:
Class I:
Class II:
Class III:
Class IV:

Full ROM but tightness is present

Decreased ROM but does not affect ADL
Is restricting ADL
Severe contracture with complete loss of hand functions.

Attitude of the limb.

WRIST deformity:
Flexion / Extension,
Fixed / Mobile,
Apparent /True defects,
Passive / Active ROM,
Assess what structures may be contracted (Skin / Tendons). Mark the Incision / Excision lines.
Normal ROM:
Flexion 750,
Extension 700,
Radial deviation 200,
Ulnar deviation 350
MP Joint Deformity:
Flexion / Extension,
Fixed / Mobile,
Apparent /True defects,
Passive / Active ROM,
Assess what structures may be contracted (Skin / Tendons). Mark the Incision / Excision lines.
PIP & DIP Joint Deformity:
Flexion / Extension,
Fixed / Mobile,
Apparent /True defects,
Passive / Active ROM,
Assess what structures may be contracted (Skin / Tendons). Mark the Incision / Excision lines.
Assess Web contractures / burn syndactylies
Assessment for reversal of arches of the hand
Assess distal sensation / vascularity (Pulsations / capillary refill)
Fingers
DIP
PIP
MCP

Flexion
800
1000
900

Extension
00
00
450

Thumb
IP
MCP
CMC

Flexion
800
550
450

Extension
150
100
?

Motor examination of all muscles (Tone / Power).

Assess Tinels sign in case of post burn Nerve injury.
Mention the presence / level of any amputated digits due to burns.
Plan for local/ regional / distant flaps if exposure of deeper structures is anticipated.
Electric burns: examine all 4 extremities!!

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11. POPLITEAL FOSSA: Describe the scar

Classification:
Grade I:
symptomatic tightness Normal ROM, Normal Ambulation
Grade II:
mild decreased extension, contraction bands +, Ambulation +
Grade III:
moderate to severe decrease in flexion/extension, Ambulates with LIMP.
Grade IV:
fixed flexion contracture, Ambulation
Apparent size of the scar & assessed true defect as measured from fixed bony land marks
Assess distal sensation, vascularity, limb length discrepancies.
Measure any atrophy as assessed by circumference from fixed bony points.
Assess ROM
Mark the line of incision / excision at point of maximum contracture.
Plan for local/ regional / distant flaps if exposure of deeper structures is anticipated
12. FOOT: Describe the scar
Attitude of the limb, is opposite limb normal?
Plantar (Is weight bearing involved) / dorsal
Any limping in the gait.
Flexion / Extension,
Fixed / Mobile,
Apparent / True defects,
Passive / Active ROM,
Normal ROM:
Dorsiflexion 200
Plantar flexion 900
Inversion 300
Eversion 150
Assess what structures may be contracted.
Mark the Incision / Excision lines.
Web contracture / burn syndactyly
Distal sensation / vascularity (capillary refill) / limb length discrepancies
Assess for reversal of arches of the foot due to burns
Mark the Incision / excision lines
Plan for local/ regional / distant flaps if exposure of deeper structures is anticipated
DIAGNOSIS: Post Burn Contracture deformity of diffuse / band like nature over these and these regions of
this duration with / without complications. Patient wants the correction of these deformities.
APPROACH: Wait for the complete contracture to evolve i.e. till scar matures (Should not blanch) unless the
contractures cause exposure of cornea/ conjunctiva or is causing airway problems or is causing difficulty in
feeding or is restricting the growth of bones/ causing joint deformities as in children. While waiting for the scar
to mature regular physiotherapy, massage, compression garments are implemented.
After scar matures and patient is fit Z plasty for linear bands or contracture release with STSG or
serial excision or tissue expansion and rotation advancement flap for different regions is prioritized in order of
more useful function in consultation with the patient. Usually treated with excision / incision release followed
by STSG. If exposure of deeper structures is anticipated during release 2 options are full release and flap
cover or STSG at that point with fixation of distractors and distraction after the STSG takes at 2 weeks.

Supraclavicular Flaps: 10 cm in width and 20 cm in length, anterior edge to reach the inferior border of
the clavicle, the posterior edge to reach the upper area of the trapezius, and the distal edge to reach the
upper arm.
The supraclavicular artery is a perforator that arises from the transverse cervical artery in 93 % of
cases or from the suprascapular artery in 7 %. It divides into one or two arteries before reaching the deep
fascia of the deltoid muscle in the third medial clavicle. These one or two arteries then run toward the
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acromioclavicular
joint, where they further divide into small branches to reach the superior part
of the
deltoid muscle. At this level, they become interfused with the cutaneous branches of the posterior
circumflex humeral artery. The supraclavicular artery is also interfused with the vascular network of the
musculocutaneous perforator of the trapezius muscle in the dorsal region, and with the vascular network
of the cutaneous branches of the thoracoacromial artery in the anterior chest.
On the body surface, the transverse cervical artery can be identified under the skin as being on
average 34.5 cm from the sternoclavicular joint.

A D Dias: bipedicled flap from raised from the scar itself and rest of the raw area is grafted.

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HISTORY OF PLASTIC SURGERY IN INDIA

Lives of great men all remind us,
We can make our lives sublime;
And departing leave behind us,
Footprints on the sands of time.
-H.W.Longfellow.
The earliest replantations were done by Lord Shiva by attaching an elephants head on his sons body and by
Ashwini Kumars who successfully replanted the severed head of Yagna. Thus the history of plastic surgery in India
dates as far back or before the Vedic times nearly 4000 years ago.
Brahma, the creator of the universe evolved, Ayurveda (the science of life) by meditation and imparted it to Daksha
Prajapati, who in turn taught the Ashwini Kumars (twin gods). Lord Indra, the celestial ruler, learnt it from Ashwini
Kumars and in turn passed on the knowledge to many rishis, namely, Sage Bharadwaja (Guru of Atreya), and King
Divadaasa of Banaras (Lord Dhanvantri). Sushruta, who was Vishwamitras son, along with others approached
Dhanvantri and requested him to accept them as his shishyas and teach them the science of Ayurveda.
Sushruta Samhita is believed to be part of one of the four Vedas (part of Atharva-veda) and was written by Sushruta
in approximately 600 BC compiling what he had learnt from his Guru Dhanwantri and his predecessors. It is said
that Sushruta taught surgery at the Banaras University.[2] He has very succinctly described the reconstruction of the
nose by cheek flap, repair of cut earlobe, piercing of earlobe, repair of cut lip, skin grafting, classification of burns,
wound care and wound healing. Sushruta has been rightly called the Father of Plastic Surgery and Hippocrates
of the 6th or 7th century BC. He described rhinoplasty for a cut nose as follows: [1],[2]
1) The leaf of a creeper, long and broad enough to fully cover the whole of the severed or clipped off part, should be
gathered,
2) A patch of living flesh, equal in dimension to the preceding leaf should be sliced off from the region of the cheek.
3) After scarifying the severed nose with a knife, the flesh is swiftly adhered to it.
4) Insert two small pipes in the nostrils to facilitate respiration and to prevent flesh from hanging down.
5) The adhesioned part is dusted with the powders of Pattanga, Yashtimadhukam and Rasanjana pulverized
together.
6) The nose should be enveloped in Karpasa cotton and several times sprinkled over with the refined oil of pure
sesamum.
7) When the healing is complete and parts have united, remove the excess skin.
Even in those days he had emphasised the accurate cutting of the pattern to the size of the defect, the accurate
cutting and suturing of the flap to the nose and maintaince of airway with tubes.[3] Frank McDowell has very aptly
described Sushruta in the book The source book of plastic surgery[2] as follows:
Through all of Sushrutas flowery language, incantations and irrelevancies, there shines the unmistakable picture
of a great surgeon. Undaunted by his failures, unimpressed by his successes, he sought the truth unceasingly and
passed it on to those who followed. He attacked disease and deformity definitively, with reasoned and logical
methods. When the path did not exist, he made one.
There was a second method of rhinoplasty in India as practiced by Tilemakers. This involved using a free graft from
the buttock. The skin and the underlying tissue of the shape of the defect on the nose was beaten with wooden
slippers and applied on the defect with some cement
In the 4th century, another scholar named Vaghbat wrote Ashtanga Sangraha and Ashtanga Hridyans. In Ashtanga
Hridyans, he described rhinoplasty as done by Maharishi Atreya and emphasized the need for the provision of an
inner lining by turning down the nasal skin.
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The classical cheek flap rhinoplasty of Sushruta and Vaghbat was later modified by using a rotation flap from the
adjacent forehead, The Traditional Indian Method of Rhinoplasty. This was kept a secret for centuries in India, and
practiced by Marattas of Kumar near Poona, certain Nepaly families and Kanghairas of Kangra (Himachal Pradesh).
Dr. S. C. Almast personally met the last Hakim of Kangra, Mr. Dinanath Kanghaira whose family was practicing
the art of rhinoplasty since the war of Kurukshetra and at Kangra since 1440 AD. Those with cut noses and
deformed noses due to leprosy and syphilis were operated by them. The patient was given wine to drink to put him
to sleep (since anesthesia did not exist in those days). A pattern of the defect was made on a paper. A handkerchief
was tied around the neck to make the veins of the forehead prominent, and the flap was marked including the vein
on the forehead (in the pedicle between the eyebrows). The forehead flap was folded in itself to form the inner
lining.
The knowledge of rhinoplasty spread from India to Arabia and Persia and from there to Egypt and Italy in the 15th
century. The first translation of Sushruta Samhita was in Latin by Hessler in 1844 and in Arabic by Ibn Abi Usaybia
(1203-1269 AD) and later into German by Vellurs. Bhishagratna translated it in English in 1907. [2]
Although Britishers lived in India for a long time, they were not aware of Indian Rhinoplasty till 1793. Mr. James
Findlay and Mr. Thomas Crusoe who were surgeons at the British Residency in Poona in 1793 witnessed the
operation on Cowasjee and reported the details of the operation in the Madras Gazette. The same operation on
Cowasjee was later published in Gentlemans magazine, London, Oct. 1794 by a letter from Mr. Lucas[2] as
follows: Cowasjee, a Mahratta of the caste of the husbandmen, he was a bullock driver with the English Army in
the war of 1792, and was made prisoner by Tipu Sultan, who cut off his nose and one of his hands. He joined the
Bombay Army near Seringapatam. For about 1 year he remained without a nose, when he had a new one put on by a
man of the Brickmaker (potters) caste near Poona.
Towards the end of the 19th century, two important works were published in India. One was titled Rhinoplasty by
Tribhovandas Motichand Shah in 1889, who was then the Chief Medical Officer of Junagadh.[6] He described over
a hundred cases treated by him in 4 years and gave minute operative details and discussed the advantages of
forehead rhinoplasty. He used paper to make a pattern and used anesthesia. (Till now there was no mention of
anaesthesia. Patients were just given wine to drink before surgery.) His name became a legend and it was said that
Kalu cuts the nose and Tribhovan reconstructs it. Kalu was a local dacoit of that time who used to cut off peoples
noses. The other book was Rhinoplasty operations, with a description of recent improvements in the Indian
method by Keegan in 1900.[7] Even today, the western world gives credit to India for rhinoplasty called as the
Indian Rhinoplasty. This of course, later received a few modifications, but the basic principles as laid down by
Sushruta remain the same.
Plastic Surgery in modem India owes a great deal to Sir Harold Gillies, Eric Peet and B.K. Rank for developing this
speciality. In 1945, two Indian maxillofacial surgical units were established. No.l unit at Kirkee under Fitzgibbon
and later under Gibson. No. 2 unit was at Secunderabad under Eric Peet. In 1946, Dr. C. Balakrishnan was posted at
the No. 1 unit. The two units later merged to form a maxillofacial center for the Indian Army at Bangalore.
In 1950, the first two Plastic Surgery departments were established in India. One at Patna under Dr. R. N. Sinha and
the other at Nagpur under Dr. C. Balakrishnan. Sir Harold Gillies paid a visit to India and he was pleased with the
work being done by Indian surgeons, especially Major Sukh, at the Armed Forces Medical College, Pune.[8]
In 1955, the Govt. of India invited Mr. B. K. Rank, from Australia, to advise on the development of Plastic Surgery
in India. He welcomed the idea of forming a plastic surgery section of Association of Surgeons of India. In 1957 Sir
Harold Gillies visited India again. During his visit to Pune, he demonstrated various operations and techniques. He
visited and lectured at several centres in various parts of the country, namely, Calcutta, Delhi, Patna, Jaipur and
lastly Nagpur where he formally inaugurated the Plastic Surgery section of Association of Surgeons of India. The
members were Dr. R. N. Cooper, Dr. C. Balakrishnan, Dr. M. Mukerjee, Dr. R. N. Sharma, Dr. N. H. Antia, and Dr.
Hiveda.[8] The late Dr. C. Balkrishnan, was a devoted and dynamic plastic surgeon. He succeeded in establishing
the first Department of Plastic and Maxillofacial surgery at the Govt. Medical College and Hospital, Nagpur. M. S.
degree in Plastic Surgery was started in 1960, for the first time in India. Dr. Balkrishnan described Z-plasty for the
nasal lining in cleft palate, classification of cleft lip and palate called as the Nagpur Classification and skin
grafting in total avulsion of testes. In the same year, another department of Plastic Surgery was established at Patna
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under
Dr. R. N. Sinha. Later, two more departments were started at Calcutta under Dr. M. Mukerjee
and at
Lucknow under Dr. R. N. Sharma.

Dr. Antia, the 3rd generation trained Plastic Surgeon under Sir Harold Gillies worked at the Leprosy home in
Khandala (near Pune) in 1958. He was the first surgeon to succeed in the integration of leprosy in general hospital
practice. The unit at Sir. J. J. Hospital, Mumbai, was started in 1959 under Dr. N. H. Antia. In 1964, Tata Trusts
provided a substantial grant to carry out two projects - one on Leprosy and other on Burns. The worlds first
microvascular surgery on humans, a free flap transfer using microvascular anastomosis was done in 1966 by Dr.
Antia and Dr. Buch (Scandinavian journal of Plastic surgery 1977).
In 1961, another plastic surgery unit in Mumbai was established at K. E. M. Hospital, under Dr. Charles Pinto. Eric
Peet from Oxford was a regular visitor to this department for the first 3 months. Dr. Pinto advocated one stage
repair of cleft lip and palate, called as the Hole-in-one procedure. In 1964 one more department was started in
Mumbai at G. T. Hospital, under Dr. R. J. Manekshaw.
In 1963, Safdarjung Hospital, Delhi started a department of Burns, Plastic and maxillofacial surgery, with Dr. J. L.
Gupta, as its head. Gradually, multiple centers in Plastic Surgery were established all over the country and various
associations were formed.
In 1971, Burns Association of India was formed during the 1st Congress of Burns at the J. J. Hospital. Dr. M. H.
Keswani was the Secretary. Later under his leadership, the Burns Association flourished with contributions like
potato peel dressings, prevention campaigns by way of radio and TV talks, small documentary ads, etc. Pour water
on Bums has received worldwide popularity.
In 1974, Indian society of surgery of the hand was formed with Dr. Ashok Sen Gupta as the president. A hand
surgery unit was started at the Stanley Medical College at Madras under Dr. R. Venkataswami. Today it is one of
the biggest and best hand surgery units in the world. Indian Society for Reconstructive Microsurgery was also
formed at Madras in 1992 with Dr. R. Venkataswamy as the president.
The contributions made by various Plastic Surgeons in India are numerous by way of devising new instruments,
research and publications (papers and books). To mention all is beyond the scope of this paper. Today every state in
India has multiple plastic surgery training centres. Each centre trains a number of postgraduate students every year
who have spread all over India and abroad serving the community to their fullest. The specialty continues to grow
and advance in all the fields of Plastic Surgery.

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PTOSIS
Name:
Age:
Sex:
Occupation:
Resident of:
Comes with complaints of
History Onset, by birth / aquired (Congenital / aquired) INDEFINITE ONSET / GRADUAL P.
History of Injury to the eye in the past (Traumatic)
History of any swelling / lumps over the eye lid (Mechanical)
History of fatigability / variability / weakness in eye ball movement / weakness of other muscles in
the body (Myasthenia Gravis)
History of previous surgery on the eyelid (Iatrogenic)
History of association with jaw motion (Marcus gunn), CHIN LIFT
History of ability close the eyes (to rule out lagophthalmos which may C/I ptosis correction)
History of double vision (diplopia)
History of headache/browache (frontalis overactivity)
History of treatment taken for the same
History of itching / foreign body sensations (dry eye)
H/o facial N palsy: poor blinking & lagopthalmos postop.
Past medical and surgical history
History of smoking, alcoholism
Family history if significant
General Examination:
Vital Signs
Systemic examination
Local examination
Action of frontalis muscle should be blocked with thumb when making measurements of the eyelids!
1. Degree of ptosis: Good / Moderate / Poor (MRD)
2. Levator function: Good / moderate / poor (speed of retraction, slow: MG)
3. Presence of lid lag
Chin lift & frontalis overaction indicates severe
4. Position of Supra Tarsal Fold (MCD)
ptosis and its presence also predicts possible
5. Jaw winking phenomenon
success of frontalis sling surgery
6. Fatigability /variability
7. Pupillary Reflexes
8. EOMs , association with lid closure.
9. Visual Fields
10. Horners (Upper lid ptosis, lower lid elevation, miosis, anhidrosis on ipsilateral side of face)
11. Lid swellings/ Scar
12. FACIAL Nerve
13. CORNEAL REFLEX , BELLS PHENOMENON
14. SCHMIRS TEST I, II
15. Tarsal height: (if F.S. is being planned, minimum of 8mm is essential)
Pseudoptosis: hemifacial spasm & essential blepharospasm.

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DIAGNOSIS
Congenital / Acquired ptosis of Right / Left Upper eyelid of mild / moderate / severe grade with good /
moderate / poor function secondary to X cause.
INVESTIGATIONS
1. Tensilon test (MG)
2. EMG (MG)
APPROACH
In Traumatic wait for at least 6 months if reinnervation is anticipated. If patient is not fit for
surgery a ptosis crutch is useful. If levator function is good tarsoconjuctiva - mullerectomy, levator
Plication, Levator resections are options. If levator function is poor: Frontalis sling operation.

Surgery often causes some lid stiffness & lagophthalmos; corneal protective mechanisms should be intact
prior to surgery:
1. Bells phenomenon present
Normal MRD1: 4-5mm
2. No keratitis
Normal MRD2: 5mm
3. Corneal sensation present
Palpebral fissure height: 9mm
4. No Lagopthalmos
MCD: 8-10 mm in females, 6-8 mm in males
The weaker the LPS, weaker is the crease!
By defn pts with involutional ptosis have N LPS
function, and all can be treated with aponeurosis
advancement operation
Triad: N LPS function
High skin crease
Lid drop on downgaze
Brow elevation, deep forehead wrinkles
Chin up position


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SCHIRMERS TEST
Schirmer's test I measures both basic and reflex secretion by the amount of wetting that occurs on a
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535
mm filter paper placed on the lower conjunctiva for 5 minutes; less than 10 mm of wetting
is
considered abnormal. Schirmer's test II is similar to the first test, except that a local anesthetic is used to
block reflex secretions.

Blepharochalasis:
Excess eyelid skin particularly evident in older individuals.
Poor lid crease precludes a conjunctival approach ptosis surgery.
Preexisting lagopthalmos is likely to worsen postop.
Bells phenomenon: ask the patient to tightly close the eye while examiner lifts the upper eyelid.
> 2/3 rd of cornea disappears under lid:
1/3rd to 2/3rd:
< 1/3rd:
Cornea moves upwards & inwards:
Cornea moves downwards:
Cornea moves in any other direction:

GOOD Bells phenomenon

FAIR
POOR
INVERSE
REVERSE
PERVERSE

POOR Bells deliberate undercorrection may be planned to avoid corneal exposure

Marcus Gunn Phenomenon:
Lid retraction (on jaw movt)
2 mm
2-5 mm
>5 mm

degree of severity
mild
moderate
severe

In an eye with squint, measure ptosis with eye concentrating on an object in order to eliminate component
of pseudoptosis.
1. FASANELLA SERVAT PROCEDURE:
Indications
Mild ptosis: 2 mm
Good levator function: 10mm or more
Tarsal height: 8mm or more

Contraindications
Moderate to severe Ptosis
Poor LPS Action
Inadequate tarsal Height
Poor lid crease
Lax upper lid skin
Tendency to entropion
Lash ptosis

Steps:
Frontal block
Infiltration ?????
Lid eversion
Traction sutures on tarsoconjunctiva
Traction sutures passed through superior fornix coming out at the lid margin
Excision line marked at least 2mm away from the lid margin.
Excision hemostasis closure with continuous catgut, knot brought on skin.
Frost suture.
2. LPS Rescetion:
Indications

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Moderate to severe ptosis:

Moderate to good LPS action:

132

3-4mm
5mm or more

Steps:
1.
2.
3.
4.
5.
6.
7.
8.
9.

Upper lid incision line is marked at the MCD of the opposite eye
Marginal sutures (one in centre and 2 on both sides)
Skin, orbicularis incised, exposing orbital septum
Tarsal plate is exposed for 4-5 mm
Infiltration on conjunctival surface with 2% xylocaine with adr inflating it and dissecting it
off the LPS-Muller muscle complex.
Stay sutures at LPS aponeurosis tented up disinserted, dissected off the deeper str.
Separation of orbital septum till orbital fat is prolapsing.
Lateral & medial horns of LPS A are cut to separate it completely
Sutures passed thru upper tarsus (4mm below upper edge) and passed just anterior/ thru
/post to Whitnalls ligament tied (Berkes rule) cornea is centred redundant LPS
excised orbicularis is closed taking cut end of LPS to form the lid crease skin closure.

DETERMINATION OF LENGTH OF LEVATOR TO BE RESECTED:

Levator action
2-3 mm
4-5 mm
6-7 mm
8-9 mm
10-11 mm

Lid position
upper limbus
1-2 mm below limbus
2-3 mm below limbus
3-4 mm below limbus
6 mm below limbus

3. TARSO-FRONTAL SLING SURGERY:

Indications:
Severe ptosis:
4mm or more
Poor LPS action:
4mm or less
1. Lid incisions: 3mm above the lid margin, 8mm apart, (deepened upto tarsal plate)
2. Brow incisions: medial & lateral 1mm above the margins, central, (deepened upto frontalis
muscle)
3. Stay sutures: 3 (one in centre)
4. Passage of sling: thru middle eyebrow incision, medial (thru frontalis) passed towards
eyelid, deep to orbital septum superficial entering medial lid incision supratarsal
plane lateral lid incision deep to orbital septum lateral brow incision middle brow
incision, thus forming a PENTAGON .
5. 2 ends of sling passed thru a silicone sleeve tightened to get lid position at the level of
limbus differential adjustments of 2 ends to get desired lid contour sleeve is anchored
to frontalis (6-0 prolene)
Postop care: (All surgeries)
Frost suture in lower eyelid, anchored to forehead with tape.
Topical antibiotic drops
Systemic antibiotics, analgesics
Topical lubricants
Daily inspection
Watch for: lagopthalmos / corneal exposure.

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24/03/2012 17:13

TMJ ANKYLOSIS
Name:
Age:
Sex:
Occupation:
Resident of:
Comes with C/O: Inability to open the jaws of so much duration / present since birth
History of ear infection
History of trauma with a jaw fracture
History of wound with pus discharge around the region of the ear
History of deformities in fingers (Juvenile rheumatoid arthritis)
History of facial deformities
History of dental caries
History of forceps delivery
Pain is totally absent!
General examination
Vital signs
Local examination
Inspection
1. Facial asymmetry with rounding on one side and flattening on the other side
2. Cant of the oral commisure with one angle at a higher level than the other
3. Incisor show present / absent, if present is so many mms
4. Lip seal present / absent
5. Presence of retrognathia / Micrognathia
6. Occlusion is Class II (??????)
7. Mouth opening if present express in Cms (In children: 3 finger breadth of patient)
8. Cant of dentition: One side dentition is higher than the other
9. Oral Hygiene, Dental caries
10. Any scars in the preauricular area suggestive of previous surgery / injury
Palpation
1. Anthropometry to quantify the facial asymmetry from fixed bony points
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2. Condylar movement assessment (One finger in the EAC one in the preauricular area)
3. Assessment of Hearing (Rinne / Weber Test)
4. Assessment of the facial nerve
5. Palpate for superficial temporal artery pulsations
6. Length & Height of the mandible on both sides.
7. Antegonial notch is prominent / deep on involved side
Donor site for CCG examined and found adequate.

DIAGNOSIS
Right / Left / Bilateral TMJ ankylosis Fibrous / bony secondary to Infection / Trauma with /
without complications

INVESTIGATION
1. X-rays: TMJ views
2. CT with contrast and plain
3. MRI
Dr Sawhney Classification of TMJ Ankylosis
Type I:
Fibrous ankylosis, minimal condylar distortion
TypeII:
Bony ankylosis, misshaped head, No involvement of sigmoid notch and coronoid
process
TypeIII:
A bony block between the ramus & zygomatic arch, medially an atrophic and
dislocated fragment of condyle can still be found & elongation of coronoid process seen
Type IV:
Bony block between ramus & skull base with total distortion of normal anatomy
APPROACH
Interposition gap arthroplasty with costochondral graft by Preauricular approach. Mark the
incisions. Describe the steps.
Clinical Manifestations
Clinical manifestations vary according to:
(a) severity of ankylosis,
(b) time of onset of ankylosis, and
(c) duration.
1. Early joint involvementless than 15 years: Severe facial deformity and loss of function.
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2. Later joint involvement after the age of 15 years: Facial deformity marginal or nil. But,
functional loss severe. Those patients in whom the ankylosis develops after full growth
completion have no facial deformity.
Unilateral Ankylosis
Seen in a child or in a person where the onset was usually in the childhood.
1. Obvious facial asymmetry.
2. Deviation of the mandible and chin on the affected side.
3. The chin is receded with hypoplastic mandible on the affected side.
4. Roundness and fullness of the face on the affected side.
5. The appearance of the flatness and elongation on the unaffected side.
6. The lower border of the mandible on the affected side has a concavity that ends in a welldefined antegonial notch.
7. In unilateral ankylosis some amount of oral opening may be possible. Interincisor opening will
vary depending on whether it is fibrous or bony ankylosis.
8. Cross bite may be seen.
9. Class II angles malocclusion on the affected side plus unilateral posterior cross bite on the
ipsilateral side seen.
10. Condylar movements are absent on the affected side.
Bilateral Ankylosis
1. Inability to open the mouth progresses by gradual decrease in Interincisor opening. The
mandible is symmetrical but micrognathic. The patient develops typical bird face deformity
with receding chin.
2. The neck chin angle may be reduced or almost completely absent.
3. Antegonial notch is well-defined bilaterally.
4. Class II malocclusion can be noticed.
5. Upper incisors are often protrusive with anterior open bite. Maxilla may be narrow.
6. Oral opening will be less than 5 mm or many times there is nil oral opening.
7. Multiple carious teeth with bad periodontal health can be seen.
8. Severe malocclusion, crowding can be seen and many impacted teeth may be found on the Xrays.
Diagnosis
Diagnosis is based on the following:
1. History of trauma, infection, etc.
2. Clinical findings.
3. Radiographic findingsare important in arriving at a final diagnosis.
a. Orthopantomographwill show both the joints picture which can be compared in unilateral
cases. Presence of Antegonial notch can be appreciated which develops secondary to the
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contraction of the depressor muscles and their action against elevator group of muscles. The
antegonial notch becomes more pronounced in severe cases.
b. Lateral oblique viewwill give anteroposterior dimension of the condylar mass. Elongation of
coronoid process can be seen.
c. Cephalometric radiographis taken to evaluate the associated skeletal deformities.
d. Posteroanterior radiographwill reveal the mediolateral extent of the bony mass. It will also
highlight the asymmetry in unilateral cases.
e.CT scanvery helpful guide for surgery. Relation to the medial cranial fossa, the
anteroposterior width, mediolateral depth can be assessed. Any presence of fractured condylar
head on the medial aspect of ramus can be located. In cases of reankylosis, the bony fusion can
be seen. 3-D CT scan will give life-size picture of all aspects of the deformity.
Radiographic Findings
Fibrous Ankylosis: reduced joint space and hazy appearance can be seen. But, still the normal
anatomy of the head and glenoid fossa can be appreciated.
Bony Ankylosis: Complete obliteration of joint space. Normal TMJ anatomy is distorted.
Deformed condylar head or complete bony consolidation replacing the joint space can be seen.
Elongation of the coronoid process on the side of hypomobility will be seen.
-Antegonial notch.
Sequelae of Untreated Ankylosis
1. Normal facial growth and development affected.
2. Speech impairment.
3. Nutritional impairment.
4. Respiratory distress (tongue fall in sleep), especially, in bilateral involvement with severe
micrognathia.
5. Malocclusion.
6. Poor oral hygiene.
7. Multiple carious and impacted teeth.
Aims and Objectives of Surgery
1. Release of ankylosed mass and creation of a gap to mobilize the joint.
2. Creation of a functional joint.
a. To improve patients nutrition.
b. To improve patients oral hygiene.
c. To carry out necessary dental treatment.
3. To reconstruct the joint and restore the vertical height of the ramus.
4. To prevent recurrence.
5. To restore normal facial growth pattern (based on functional matrix theory).
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6. To improve esthetics and rehabilitate the patient (cosmetic surgery may be carried out at a
later date or at second phase).

The Internationally Accepted Protocols (Kaban, Perrot and Fisher in 1990)

1. Early surgical intervention.
2. Aggressive resection: A gap of at least 1 to 1.5 cm should be created. Special attention should
be given to the fusion on the medial aspect of the ramus. Old malunited condylar fractured piece
can be seen attached on the medial side.
3. Ipsilateral coronoidectomy and temporalis myotomy: In most of these cases there is always
association of elongated coronoid process. After carrying out gap arthroplasty, the
coronoidectomy on the same side should be carried out either separately or in combination with
the gap arthroplasty cut from the same extraoral incision. The coronoid process is cut from the
level of sigmoid notch till the anterior border of the ramus. The temporalis muscle attachments
are severed by carrying out temporalis myotomy. The oral opening is checked after this
procedure by the assistant. If maximum interincisal opening > 35 mm is obtained no need to
carry out contralateral coronoidectomy
4. Contralateral coronoidectomy and temporalis myotomy is necessary: If maximum incisal
opening is < 35 mm uninvolved side coronoidectomy and temporalis myotomy can be
carried out through intraoral incision
5. Lining of the glenoid fossa region with temporalis fascia.
6. Reconstruction of the ramus with a costochondral graft.
7. Early mobilization and aggressive physiotherapy for the period of at least six months
postoperatively.
8. Regular long-term follow-up.
9. To carry out cosmetic surgery at the later date when the growth of the patient is completed.
Bilateral ankylosis: aggressive resection will result in anterior open bite.
SURGICAL APPROACHES:
The various approaches are listed,
(1) Pre-auricular (Risdon, 1934; Blair & Ivy, 1936; quoted by Bellinger, 1940; Milch, 1938;
McCann, 1965; Rowe & Killey, 1968; Giles, 1969; Thoma, 1969; Rowe, 1972).
(2) Submandibular (Risdon, 1934; Sleeper, 1952; Ward, 1961).
(3) Post-auricular (Bockenheimer, 1920; Axhausen, 1931 ; Alexander, 1975).
(4) Closed condylotomy (Ward, 1961).
(5) Endaural (Rongetti, 1954; Davidson, 1956; Hosxe, 1972).
(6) Intra-oral (Keen, 1909; Silverman, 1925; Wielage, 1928; Lewis, 1953; Dingman & Natvig,
1964; Sear, 1972; Quinn, 1977).
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(7) Horizontal incision along the lower border of the malar arch (Balyeat, 1933; Dingman &
Harding, 1951; Riessner, 1952; Hueston, 1959).
(8) Temporal (Gillies et al., 1927).
(9) Through soft tissue laceration or scars (Gillies et al., 1927; Bingham, 1955; Rowe & Killey,
1968).
AL KAYAT BRAMLEY MODIFIED PREAURICULAR APPROACH:
The incision is question mark-shaped and begins about a pinna's length away from the ear,
antero-superiorly just within the hair line and curves backwards and downwards well posterior of
the main branches of the temporal vessels till it meets the upper attachment of the ear. The
incision then follows the attachment of the ear and just endaurally as described by Rowe (1972).
The temporal incision must be carried through the skin and superficial fascia to the level of the
temporal fascia. The nerve filaments run in the superficial fascia and it is very important that the
full depth of this fascia is reflected with the skin flap. Blunt dissection in this plane is carried
downwards to a point about 2 cm above the malar arch where the temporal fascia splits. The
pocket formed by the division contains fatty tissue which is easily visible through the thin lateral
layer. Beyond this point there should be no attempt at further dissection of the superficial fascia
from the temporal fascia.
Starting at the root of the malar arch, an incision running at 45 upwards and forwards is made
through the superficial layer of the temporal fascia. Once inside this pocket, the periosteum of
the malar arch can be safely incised and turned forward as one flap with the outer layer of
temporal fascia, superficial fascia containing the nerves and skin.

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The pocket can be developed anteriorly as far as the posterior border of the frontal process of the
malar bone and posteriorly joined to the preauricular dissection which follows closely the
cartilagenous external auditory canal beneath the glenoid lobe of the parotid gland and the
superficial temporal vessels. A small tortuous branch, the auricular artery, runs backwards from
the superficial temporal artery to the ear. The middle temporal artery which comes off the
superficial temporal artery perforates the temporal fascia to supply temporalis muscle. These
should be divided and ligated.
Proceeding downwards from the lower border of the arch and articular fossa, the tissues lateral to
the joint capsule are dissected and retracted. The base of the neck of the condyle can be exposed.
The bifurcation of the facial nerve is not nearer than 2.4 cm in an infero-posterior direction from
the post-glenoid tubercle. Care is needed not to extend deep dissection below the lower
attachment of the ear.
Advantages:
(1) There is minimal bleeding and less sensory loss. The posterior placement of the skin incision
and its wide backwards and upwards sweep spares the main branches of vessels and nerves.
(2) Fascial places are easily identified.
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(3) There is excellent visibility. This is partly due to the large flap and partly because the
unyielding temporal fascia is not reflected with the skin as in the approach described by Rowe
and Killey (1968).
(4) The potential complications of muscle herniation and fibrosis are avoided. The muscle is
never exposed and the superficial layer of temporal fascia can be closed without tension.
(5) There is remarkably little post-operative discomfort or swelling.
(6) A good cosmetic result is achieved except in the very bald.
(7) The technique is easily teachable and speedily executed.

Complications:
1. Difficult intubation
2. During Surgery
a. Haemorrhage due to damage to any of the superficial temporal vessels, transverse facial artery,
inferior alveolar vessel and internal maxillary vessels, pterygoid plexus of veins.
b. Damage to external auditory meatus.
c. Damage to zygomatic and temporal branch of facial nerve.
d. Damage to glenoid fossa and thus leading entry into middle cranial fossa.
e. Damage to auriculotemporal nerve.
f. Damage to parotid gland.
g. Damage to the teeth during opening of the jaws with jaw stretcher.
3. During Postoperative Follow-up
a. Infection
b. Open bite
c. Recurrence of ankylosis.
d. Freys syndrome
Surgical steps (Exposure)
Step 1. Preparation of the Surgical Site
P & D should expose the entire ear and lateral canthus of the eye. Shaving the preauricular hair is
optional. A sterile plastic drape can be used to keep the hair out of the surgical field. Cotton
soaked in mineral oil or antibiotic ointment may be placed in the external auditory canal.
Step 2. Marking the Incision
The incision is outlined at the junction of the facial skin with the helix of the ear. A natural skin
fold along the entire length of the ear can be used for incision. If none is present, posterior digital
pressure applied on the preauricular skin usually creates a skin fold that can be marked . The
incision extends superiorly to the top of the helix and may include an anterior (hockey-stick)
extension
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Step 3. Infiltration of Vasoconstrictor

The preauricular area is quite vascular. A vasoconstrictor can be injected subcutaneously in the
area of the incision to decrease incisional bleeding. However, if local anesthesia is also being
injected, it should not be injected deeply because it may be necessary to use a nerve stimulator
on exposed facial nerve branches.
Step 4. Skin Incision
The incision is made through skin and subcutaneous connective tissues (including TP fascia) to
the depth of the temporalis fascia (superficial layer). Any bleeding skin vessels are cauterized
before proceeding with deeper dissection.
Step 5. Dissection to the TMJ Capsule
Blunt dissection with periosteal elevators and/or scissors undermines the superior portion of the
incision (that the part above the zygomatic arch) such that a flap can be retracted anteriorly for
approximately 1.5 to 2 cm .This flap is dissected anteriorly at the level of the superficial (outer)
layer of temporalis fascia. This layer is usually hypovascular. The superficial temporal vessels
and auriculotemporal nerve may be retracted anteriorly in the flap. Failure to develop the flap
close to the cartilaginous external auditory canal increases the risk of damage to these structures.
Below the zygomatic arch, dissection proceeds bluntly, adjacent to the external auditory
cartilage. Scissor dissection proceeds along the EAM in an avascular plane between it and the
glenoid lobe of the parotid gland. The EAM runs anteromedially, and the dissection is parallel to
the cartilage. The depth of the dissection at this point should be similar to that above the
zygomatic arch.
Attention is again focussed on the portion of the incision above the zygomatic arch. With the flap
retracted anteriorly, an incision is made through the superficial (outer) layer of temporalis fascia,
beginning at the root of the zygomatic arch just in front of the tragus, anterosuperiorly toward the
upper corner of the retracted flap. The fat globules contained between the superficial and deep
layers of the temporalis fascia are then exposed. At the root of the zygoma, the incision can be
made through both the superficial layer of temporalis fascia and the periosteum of the zygomatic
arch. The sharp end of a periosteal elevator is inserted in the fascial incision, deep to the
superficial layer of the temporalis fascia, and swept back and forth to dissect this tissue from the
underlying areolar and adipose tissues. The undermining proceeds inferiorly toward the
zygomatic arch, where the sharp end of the periosteal elevator cleaves the attachment of the
periosteum at the junction of the lateral and superior surfaces of the zygomatic arch, freeing the
periosteum from its lateral surface. The periosteal elevator can then be used to continue
dissecting bluntly inferiorly with a back and forth motion, taking care not to dissect medially into
the TMJ capsule. Blunt scissors can also be used to dissect inferiorly to the zygomatic arch. Once
the dissection is approximately 1 cm below the arch, the intervening tissue is sharply released
posteriorly along the plane of the initial incision.
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The entire flap is then retracted anteriorly, and blunt dissection at this depth (just superficial to
the capsule of the TMJ) proceeds anteriorly until the articular eminence is exposed. The entire
TMJ capsule should then be revealed. Because of subperiosteal dissection along the lateral
surface of the zygomatic arch, the temporal branches of the facial nerve are located within the
substance of the retracted flap. To help determine the location of the articular space, the
mandible can be manipulated open and closed.
Step 6. Exposing the Interarticular Spaces
With retraction of the developed flap, the joint spaces can be entered. To facilitate the surgery, a
vasoconstrictor-containing solution can be injected into the superior joint space . With the
condyle distracted inferiorly, pointed scissors or a scalpel is used to enter the upper joint space
anteriorly along the posterior slope of the eminence. The opening is extended anteroposteriorly
by cutting along the lateral aspect of the eminence and fossa. The incision is continued inferiorly
along the posterior portion of the capsule until the capsule blends with the posterior attachment
of the disk. Lateral retraction of the capsule allows entrance into the superior joint space.
The inferior joint space is opened by making an incision in the disk along its lateral attachment
to the condyle within the lateral recess of the upper joint space. The incision may be extended
posteriorly into the posterior attachment tissues. The inferior joint space is then entered. The
articular disk can be lifted superiorly or inferiorly, exposing either joint space
Step 7. Closure
The joint spaces are irrigated thoroughly, and any hemorrhage is controlled before closure. The
inferior joint space is closed with permanent or slowly resorbing suture by suturing the disk back
to its lateral condylar attachment. The superior joint space is closed by suturing the incised edge
with the remaining capsular attachments on the temporal component of the TMJ. If no such
attachments are left attached to bone, the capsule can be suspended over the zygomatic arch to
the temporalis fascia.

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TUMOURS ON THE FACE

Name:
Age:
Sex:
Occupation:
Resident of:
Comes with C/O: swelling on this region of the face of this duration (Usually a SCC / BCC / Melanoma)
Onset: Insidious
Progression: Rapid / slow
History of exposure to sunlight
History of exposure to radiation
History suggestive of Immunocompromised status
History of the swelling developing in a chronic wound
History of exposure to Chemicals (Aromatic hydrocarbons / chromates)
History suggestive of existence of any premalignant lesion before the swelling was seen.
History of smoking / alcoholism
History of Diabetes / Hypertension
History of all previous treatments for the present illness
Significant family history (Xeroderma pigmentosa)
General examination: Generalized lesions in Xeroderma pigmentosa, for metastasis
Vital Signs
Local Examination
Inspection
1. No, size, shape, position, extent, surface, borders, surrounding areas.
2. Enlargement of draining lymph node areas
Palpation
1. Increased warmth
2. Tenderness
3. Solid / Cystic
4. Fixity
5. Plane of swelling
6. Consistency
7. Enlarged draining lymohnodes: No, size, shape, consistency, fixity.
Donor sites were examined and found adequate
DIAGNOSIS
Malignancy of----- region of the face probably SCC / BCC / Melanoma of this TNM and of--- STAGE.
APPROACH
Biopsy to confirm the diagnosis of tumor, FNAC for confirming the diagnosis of the nodes. CXR, CT
scan, USG abdomen to Stage the malignancy. When patient is fit, wide excision (with 2cm margin for
SCC, 0.5 cm margin for BCC and as per the T stage for Melanoma)
Reconstruction as per the algorithms.

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VASCULAR MALFORMATION / HEMANGIOMA

Name
Age
Sex
Occupation
Resident of
C/O Swelling over this region of this duration
History of pain
History of deformity
Onset: Present at birth / acquired
Progression: Started at this point when it was of this size. Now it is in this region and of this size. Is
the progression commensurate with child growth?
Any history of regression in size
Colour of the swelling
Is it expansible?
Does it increase in size when the child cries?
Developmental milestone if adequate
Immunization history if adequate
History of bleeding
History of ulceration
History of previous surgeries / Injections
History of similar swellings elsewhere
Obstructive symptoms (in case it is obstructing visual axis, vocal cords)
There are / no FUNCTIONAL DEFICITS.
Family history
History of any other congenital anomalies
General examination:
Vital Signs
Local Examination
Inspection
1. No, site, size, extent, shape, color, surface, surrounding skin, soft tissue deformity, bony deformity,
Limb atrophy / gigantism, limb length discrepancies
2. Post involution skin changes of Hemangioma: Creepy laxity, telangiectasia, Yellow discoloration,
and fibro fatty residuum
3. Is the swelling Pulsatile
4. Deformity / Distortion, obstruction to visual axis
5. Intraoral examination in cases involving face
6. Any pattern of distribution related to nerve territory (particularly V nerve)
Palpation
1. Tenderness
2. Increased warmth
3. Consistency
4. Borders well / not well defined
5. Thrill / expansible
6. Compressible
7. Palpate for feeders demonstrate decrease in thrill with occlusion of feeders
8. Nicoladoni / Branhams sign (sudden bradycardia on compression of feeding vessel)
9. Any underlying bony erosion
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10. Distal pulsation

11. Distal sensation
12. Motor examination of distal musculature
13. Note atrophy as measured from circumference from fixed bony points
14. Note limb length discrepancies as measured from fixed bony points
15. Mark the line of incision

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DIAGNOSIS: CM / VM / AVM / Hemangioma (Which phase: Proliferating, Involuting, Involuted) of this

region of this duration, congenital / acquired with / without complications (DDO: Destruction / Distortion /
Obstruction). If arterial malformation mention the Schobinger grade of the lesion.
INVESTIGATIONS
1. X-ray will show soft tissue shadow, plebholith in VM, soft tissue and bony hypertrophy in a vascular
malformation
2. USG: Well defined borders with Hemangioma (fast flow), Ill defined borders in Vasc. Malformation (Fast
AVM / slow flow CM / VM)
3. MRI: Well defined borders with parenchymal staining in a Hemangioma. Diffuse in vascular malformation
4. DSA in AVM to study feeders
APPROACH
Hemangioma generally treated if causing DDO otherwise allowed to disappear under watchful eyes.
Post Involutional changes of hemangioma may require excision with primary closure / SSG / Tissue
expansion / Serial excision. If causing DDO are managed with Steroids / Interferon therapy / FDP
Laser / Excision.
CM are managed with camouflage / Excision with SSG or Tissue expansion / Lasers.
VM are managed with Sclerotherapy / Excision of lesion (complete or in stages) / Soft tissue and
Osseous contouring.
Arterial malformations are shrunken in size with embolization 72 hours prior to therapy and excised
COMPLETELY.
Mark & cut pattern of the flaps.
------------------------------------------------------------------------------------------------------------------------------------Local complications:
Ulceration +/- infection of skin
Bleeding
Anatomic destruction & Deformation
Hypo / hyperpigmentation
Obstruction: airway, vision, ear.
Schobinger grade of AV malformations:

Stage I (Quiescence): Pink-blush stain, warmth, and AV shunting by continuous Doppler or 20MHz color Doppler
Stage II (Expansion): Same as stage I, plus enlargement, pulsations, thrill, bruit, and
tortuous/tense veins
Stage III (Destruction): Same as above, plus dystrophic changes, ulceration, bleeding persistent
pain, and expansion/destruction
Stage IV (Decompensation): Same as stage II, plus cardiac failure

There are curious instances in which a facial hemangioma occurs with malformative anomalies. The
acronym for these associations is PHACES
P = Dandy-Walker or other cystic malformations in the posterior cranial fossa;
H = large, often plaquelike, facial hemangioma;
C = Cardiac defects;
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Eye anomalies;
S = Sternal cleft.

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Lumbosacral hemangioma also presents in association with occult spinal dysraphism (lipomeningocele,
tethered cord, and diastematomyelia). Diffuse hemangioma of the perineum and lower limb is also seen
with urogenital and anorectal anomalies.
Sturge-Weber syndrome comprises facial CM in association with ipsilateral leptomeningeal and ocular
vascular anomalies. The capillary stain involves the ophthalmic (V1) trigeminal dermatome, whereas
patients with either maxillary (V2) or mandibular (V3) involvement are at low risk for having the
disorder.
Sclerotherapy: ??
Distinguishing features of hemangioma of infancy and vascular malformations
Hemangiomas
Neoplasm
30% visible at birth, seen as red macule; 70%
become apparent during first few weeks of life
Females:male = 3:1
Rapid postnatal growth followed by slow involution
Endothelial cell hyperplasia
Increased mast cells
Multilaminated basement membrane
No coagulation defects
Angiographic findings: well-circumscribed, intense
lobular-parenchymal staining with equatorial
vessels
Infrequent "mass
hypertrophy rare

effect"

on

adjacent

bone;

30% respond dramatically to corticosteroid

treatment in 2 to 3 weeks
Immunopositive for biologic markers GLUT1, Fc
RII, merosin, and Lewis Y antigen.

Vascular Malformations
Congenital abnormality
Present at birth, but may not be evident until
months or even years later
No gender predilection
Slow steady growth, with no involution; may
expand secondary to sepsis, trauma, or hormonal
changes
Normal endothelial cell turnover
Normal mast cell count
Normal thin basement membrane
Primary stasis (venous); localized consumptive
coagulopathy
Angiographic findings: diffuse, no parenchyma
Low-flow: phleboliths, ectatic channels
High-flow: enlarged, tortuous arteries with
arteriovenous shunting
Low-flow: distortion, hypertrophy, or hypoplasia
High-flow: bone destruction, distortion, or
hypertrophy
No response to corticosteroids or antiangiogenic
agents
Immunonegative for these biologic markers

Klippel-Trenaunay syndrome: is a complex congenital malformation that may affect the upper or lower
extremities, and less commonly the trunk, head or neck.The three main components are
Varicosities and venous malformations,
port wine stains, &
hypertrophy of the bone and soft tissue
Treatment of VM: Unlike hemangiomas, the endothelium of VM is not hyperplastic and exhibits normal
turnover and is not susceptible to anti-proliferative treatments like steroids, interferon, or radiation/
chemotherapy. Prior to surgical management of AVM any underlying consumptive coagulopathy should
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be BAAPS
treated. The treatment of venous malformations includes elastic compression garments for
lower
extremity lesions with analgesia for pain control.

Facial VM:
Comment about mandible
Occlusion: cant/crossbite
Check for tongue. Intraoral examination
Compressibility
Discoloration, flat/raised /indurated.
Dont say DEBULKING! Instead say: reduction Chelioplasty or ------ (mark vermillion-cutaneous
junction, grasp with thumb forceps and pull it inside mark desired width to be cut GO ACROSS
THE COMMISSURE IN THE CHEEK, this only give desirable effect!)
Nonsurgical Treatment: camouflage.

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