FDMA flap

First described by – Kuhn & Holvetich

Neurovascular pedicle was described by – Foucher and Brown ( a/k/a- Foucher flap)

Lister described  axial flap on 2nd DMA

Earley  described – 2nd DMA flap

Maruyama & Quaba – Reverse 2nd DMA flap

Anatomy –

FDMA based on branch to dorso-radial aspect of index proximal phalanx

FDMA courses – within the fascial layer overlying the FDI. Runs parallel to index metacarpal

Anomaly –

in ~10% cases runs deep within the substance of FDI index head.

In some cases it becomes deep at head of 2nd metacarpal

Both these anomaly precludes raising the FDMA flap

Second DMA-

More consistent anatomy than FDMA

Also generally larger than FDMA

Passes below extensor tendon and then runs in fascia over 2nd dorsal interosseoi muscle.

Approx 1cm proximal to head of 2nd metacarpal it gives off branch to skin and then ramify at the web.

FDMA flap –

Skin territory – dorsum of proximal phalanx. Proximal limit is – MP joint. Distal limit is – PIP joint. Laterally – mid-lateral lines

Blood supply – type A, fasciocutaneous

Nerve supply – dorsal sensory branch of radial and ulnar nerve

Dominant pedicle – FDMA. Regional sourse – dorsal carpal arch and radial a

Raising the flap –

Mark the course of FDMA using hand help pencil Doppler.

Mark the flap over dorsum of proximal phalanx – tailor made to defect or full size within the limits

Mark the proximal incision over 1st web space – either S-shaped or tear drop

Dissection proceeds from distal to proximal and ulnar to radial side.

Flap is elevated in the loose areolar plane above the extensor paratenon.

FDMA enters the flap at the radial border of MP joint – extreme care must be taken while elevating the flap here.

Proximal dissection over 1st web space –

After skin incision, skin flap is elevated in plane superficial to the adipose tissue.

After completely raising the skin flap, the pedicle is dissected by incising the fascia overlying the FDI (first dorsal interosseoi). The fascia is incised at radial edge of muscle and over 2nd metacarpal periosteum at the ulnar edge (so as to include all of the fascia overlying the FDI, and hence elevating all of the structures passing through it – vein, artery, nerve)

Periosteum over 2nd metacarpal is elevated and dissection proceeds radially and deep to muscle fascia.

Dorsal vein and superficial branch of radial sensory nerve enter the flap at ulnar border of MP joint and is included in the pedicle.

The pedicle is dissected proximally till the pivot point, which is juncture of 1st and 2nd metacarpal.

Tourniquet is then released and vascularity of the flap is assessed.

Flap can then be tunneled through subcutaneous tunnel to the defect or through open incision.

Donor site over index finger dorsum is covered with FTG.

Motion of thumb is permitted on day 10.

Fully dissected FDMA flap

Second DMA flap –

Skin flap can be raised in two ways –

Second web space raised with skin extension over index and middle finger proximal phalanx or

Skin on the dorsum of index or middle finger proximal phalanx with adjacent web skin.

Pedicle is dissected to the point where it arises deep to extensor tendon

Fascia overlying the dorsum of 2nd interosseoi is included in the pedicle.

Second DMA with retrograde flow (Maruyama pattern) –

Skin island is elevated over the intermetacarpal space and is elevated in continuity with the underlying SDMA. SDMA is divided at its proximal end beneath the index tendon.

Dissection of vascular pedicle is continued distally to the web space. Connections between the SDMA and digital arteries are preserved

Distally based dorsal hand flap (Quaba pattern) –

Skin over the dorsum of hand is elevated without the dorsal metacarpal artery.

Flap is based distally on the branches given to skin approximately 1 cm proximal to the metacarpal head.

Skin is supplied by the anastomosing branches of adjacent metacarpal arteries.

Venous drainage of the flap is ensured by preserving cuff of tissue around the arterial pedicle.

Proximal limit of the flap is – wrist joint.

Flap can reach – just distal to PIP joint.


Disproportionately large digit noted at birth or that develops within 1st year of life.

Both soft tissue and skeletal elements are enlarged

(Other descriptive terms that are used – megalodactyly, gigantism, macrodystrophia, lipomatosa, macrodactylia fibrolipomatosis)


It is uncommon – incidence – 0.9%

Most cases are sporadic. No evidence of inheritance.

Most common form – isolated anomaly with lipofibromatosis of proximal nerve.

It can occur in association with other anomalies


Flatt’s classification

Type 1 – gigantism and lipofibromatosis

Type 2 – gigantism and neurofibromatosis

Type 3 – gigantism and digital hyperostosis

Type 4 – gigantism and hemihypertrophy


Most common is- Type 1.


Type 1 –

Macrodactyly a/w enlarged nerve infiltrated with fat within digits and extending proximally through carpal tunnel

Type 2 –

  1. Macrodactyly with plexiform form of NF and is often bilateral
  2. There may be osteochondral mass a/w skeletal enlargement

Type 3 –

  1. Osteocondral periarticular masses developing in infancy.
  2. No significant nerve involvement.
  3. Digits are nodular and stiff and other skeletal anomalies can be seen.
  4. Rare type

Type 4 –

  1. Rare
  2. All digit involved but less severe than type 1 & 2
  3. Intrinsic muscle hypertrophy or abnormal intrinsic anatomy
  4. Deformity present with flexion contracture, ulnar deviation and adducted thumb deformity.


[Bilateral involvement – type 2]

[No nerve involvement – type 3]

[Intrinsic muscle involvement – type 4]

[Contracture – type 4]


Macrodactyly a/w lipofibromatosis –

Noted at birth or within 3 yrs

Growth of affected digits is disproportionate – progressive macrodactyly

Growth may be in consistent proportion with rest of hand – static macrodactyly

Usually unilateral

May affect more than one digit

Multiple digit involvement is 2-3 times more common than single digit involvement.

Most common affected finger – Index (a/w long finger or thumb)

Radial digits deviated radially

Ulnar digits deviates ulnarly

If two digits involved then they deviate divergent.

Enlarged thumb are typically – abducted and extended.

Osseous growth and deviation stops after physeal closure, but soft tissue continues to enlarge.

Radiograph – enlarged skeleton with

  1. Advanced bone age
  2. Abnormal digits and deviation
  3. Osteoarthritic changes

Soft tissue swelling may be present – signifying underling nerve fatty infiltration.

Compression neuropathy may result

Thickening of flexor sheath – may result in trigger finger

Syndactyly seen in – 10% cases.


Macrodactyly a/w neurofibromatosis –

Shows typical skin features of NF 1 (Café-au-lit spots, multiple neurofibroma, peducalated skin tumors and ocular lesions)


Hyperosteotic macrodactyly –


Nodular enlargement of digit and profound loss of motion secondary to periarticular osteochondral mass formation

Radiology confirms diagnosis – showing periarticular osteochondral masses.


Macrodactyly can be part of a broader gigantism –

Segmental gigantism – affecting only a part of one limb

Hemihypertrophy – affecting one side of body (a/w NF or KTS)


Other syndromes a/w digital enlargement –

  1. Ollier disease
  2. Maffuci syndrome
  3. KTW syndrome
  4. Proteus syndrome



Not known

Possible explanation – nerve territory oriented macrodactyly

Abnormal nerve supply leading to unimpeded growth (most cases occur in single digit or in a region supplied by a single nerve)

Other theories – an increase in blood supply and/or an abnormal humoral mechanism stimulating growth.


Macroscopic finding –

  1. Increased subcutaneous fat
  2. Enlarged tortuous digital nerve
  3. Skeletal overgrowth in all direction
  4. Palmar aspect is more affected than dorsal
  5. Distal finger is more affected than proximal
  6. Flexor sheath may be thickened
  7. Tendons are normal


Histology –

  1. Thickening of skin with decreased sweat gland density
  2. Abundant subcutaneous fat with increased fibrous stroma
  3. Fatty infiltration of the digital nerve with endoneural and perineural fibrosis and enlarged digital artery
  4. Bone – wide medullary canal, irregular trabeculae and thickening of periosteum



Aim – functional and aesthetic improvement

Counseling –

Inability to establish normal digit

Need for multiple surgeries


Surgical procedure aimed at –

  1. Limiting ongoing growth
  2. Reduce size of digit
  3. Correct deviation
  4. Amputation


Limiting digital growth –

Most reliable method is – Epiphysiodesis

(Other options includes – digital nerve stripping, digital nerve resection, digital artery ligation, compression bandage)


Epiphysiodesis –

Can be achieved by –

  • Burring or drilling
  • Resection of epiphyseal plate
  • Physeal stapling in larger bones

Timing of epiphysiodesis –

It is done when the digit reaches the length of the corresponding digit in parent of same gender.

Digital deviation may be corrected in the same setting by a closed wedge resection.

(Hemiepiphysiodesis is another way to manage progressive deviation, but it is not as reliable as corrective osteotomy)

Percutaneous K-wire is required for post-op stabilization following physeal resection, more so if corrective osteotomy was also done.

Complications –

Joint stiffness

Excessive bone formation at the site of physis

Secondary angulation, in case of incomplete phseal destruction

Physeal arrest do not reduces – soft tissue growth and transverse (appositional) growth of the bone.


Reducing the digits/ soft tissue debulking –

Usually one side of the digits is debulked at a time (with 3 month interval)

Approach through – midlateral incision or Brunner’s incision

Skin flaps are elevated –> neurovascular bundle is isolated –> excess fat and skin is resected.


Skeletal reduction –

Can be achieved by either –

  • Narrowing or
  • Shortening

Narrowing –

Burring the side of bone or

Performing longitudinal osteotomy. (longitudinal osteotomy is limited by the attachment of flexor sheath)


Shortening –

  1. Terminalization
  2. Excision of middle phalanx
  3. Corrective osteotomy (in case of deviated digit – trapezoid osteotmy rather than wedge osteotomy)



It is the simplest procedure.

Many procedures aims at preserving nail while shortening the digit.

  1. Barksy procedure – nail on palmar pedicle

Modified by Flatt – to include distal part of distal phalanx and shortened middle phalanx

  1. Tsuge procedure

Nail on dorsal pedicle including dorsal cortex of distal phalnx (although dorsal pedicle is unreliable)

  1. Nail island flap – by Rosennberg

Nail raised as islanded flap based on digital neurovascular pedicle – achieved greater transposition proximally and hence greater shortening can be achieved

  1. Segmental osteotomies along the length of digit
  2. Excision/arthrodesis of MCP joint
  3. DIPJ arthrodesis
  4. Fujita described radial and ulnar neurovascular pedicle and excising each other to match other
  5. Thumb reduction –
    1. MCPJ arthrodesis
    2. Millesi procedure



Amputation –

It is the ultimate reduction procedure

Option for single digit or showing progressive uncontrollable growth

Ray amputation/transmetacarpal amputation with digit transposition

Digit transfer from foot or pollicization to create thumb

Amputation is a difficult decision to make for parents, but can save multiple stage surgery to save a deformed digit with limited function


Summary of treatment of macrodactyly –

Limitation of growth

  1. Digital nerve stripping
  2. Epiphysiodesis

Digit reduction –

Soft tissue reduction – debulking

Skeletal reduction – terminalization

Methods of terminalization –

Repositioning of the nail unit on a shortened skeleton

      • Palmar pedicle (Barsky procedure)
      • Dorsal pedicle (Tsuge procedure)
      • Nail island flap

Resection of the distal portion of the nail and pulp (Tsuge, Hoshi, Fujita, Bartelli)

Correction of deviation – Closing wedge osteotomy (combined with epiphysiodesis as required)

Thumb macrodactyly

Metacarpophalangeal arthrodesis

Millesi procedure

Amputation – Ray amputation (with transposition of the digit for central ray amputation)







Skin Banking – short notes

Need for skin banking –

Large burn areas.

Donor sites not available.

Homografts can work as temporary dressing.


Methods of skin storage –

  1. Refrigeration
  2. Deep freezing or cryopreservation


Refrigeration –

Most common method of storage.

Skin kept at 4 ° C.

Preservation maximum up to 3 weeks.

But, best used within 1 week.

Cryoprotective medium can prolong life of the grafts. Eg. –

Dilute homologus serum,

Tissue culture medium,

Balanced salt solution

Grafts is kept in a sterile bottle after wrapping in a Vaseline gauze (epidermal side on the gauze) followed by saline soaked gauze.


Deep freezing or cryopreservation

Cooling of tissue to ultra-low temperature.

Cryoprotective agents are used.

Storage temperature can be -80°C to -196°C

Stored in deep freezer or liquid nitrogen

Liquid nitrogen is used for cooling.

Cryoprotective agents are used to protect cells from disintegrating.

Cryoprotective agents used are –

  1. Glycerol,
  2. Ethylene glycol,
  3. Dimethylsulfoxide (DMS)

Grafts stored at -80°C can be stored – for up to 6 months

Grafts stored at -196°C can be stored – for indefinite period.


Freeze drying or lyophilization

Grafts is rapidly cooled and then

Water is removed by sublimation

Tissue is then vacuum sealed

Sterilized by gamma radiation

Stored at room temperature

Tissue is non-viable and used as biological dressing


Cadaveric skin banking

SSG harvested from refrigerated cadavers within 24 hours of death.

Consent is taken

Age limit – 12-60 yrs

No h/o – malignancy, hepatitis, jaundice, skin disease or veneral disease

Following markers should be negative – HIV, HBsAg, HCV, VDRL

Skin harvested using dermatome

Strips between 0.25mm – 0.35mm is harvested.

Skin tissue sample sent for streptococcus, pseudomonas, staphylococcus culture

Graft with more than 10 organism is discarded.


Cryo-preservation :

Harvested grafts is spread on meshed Vaseline gauze with epidermal side on gauze.

Rolled up and then immediately immersed in sterile solution of 15% glycerol and RL at 4°C for 2-4 hours

(Other cryopreservative used are – dimethylsulphoxide, ethanediol, propane-diol)

After 4 hours – solution is poured off and skin graft strips transferred to heat stable polyester plastic envelope.

It is then properly labelled with patient name and size of grafts.

If grafts are planned to be used within days then its stored @ 4°C in refrigerator.

Otherwise, it is deep freezed.

Freezing can be –

Controlled – with gradual cooling 1°C/ min to reach  -80°C to -100°C

Direct – where grafts is directly kept in liquid nitrogen vapor (with temperature reaching -100°C) or directly to refrigerator @ -70°C

Controlled cooling is better than direct cooling, with better skin cell viability.


Increasing the cell viability –

After harvest, skin cell viability decreases due to –

  1. Lack of nitrogen and oxygen
  2. Build of toxic material
  3. Generation of free radicals causing lipid peroxidation
  4. Osmotic changes
  5. Uncoupling of biological pathways


    1. Addition of 10-35% concentration of homologus serum –
      1. Provides nutrition
      2. Dilutes and buffers acid produced during metabolism
    2. Tissue culture medium –
      1. Provides nutrition
      2. Neutralizes harmful metabolites
    3. Reducing temperature –
      1. At 0°C oxygen requirement is zero.
    4. Balanced salt solution
    5. University of Wisconsin solution



For use of stored grafts, it is rewarmed

Rewarming is done @ 50-70°C per minute

Microwave @ lowest setting

Hot saline bath @ 42°C

After rewarming – graft is to be used within 2 hours

Skin stored in flat pockets are rewarmed faster than ones stored in cylinder.

Faster rewarming is better.


[During preservation slower cooling is better]

[During rewarming faster is better]


Future –

Improving the homograft “take”

  1. Removing the epidermis and covering with keratinocyte culture
  2. Immunosuppression – cyclosporin A has good safety profile (Given for 120 days can keep grafts alive for 2 yrs)





Keratinocyte culture – short notes

Types of keratinocyte culture –

  1. Autologous
  2. Allografts


Autologous keratinocyte culture –

Patient selection –

Usually patient with >50% TBSA burn with most being 3rd degree

Contraindications – Cutaneous tuberculosis, AIDS, Hepatitis B

Age and inhalational injury are not contraindications.

Biopsy –

Minimum delay from biopsy to culture plating.

Less than 48 hours.

If >48 hours, antibiotics needs to be added to culture medium.

Biopsy – A SSG of 1-5 cm2 is harvested.


Keratinocytes isolation –

Sample is washed

Differential trypsinization is done

Separated epidermal component is centrifuged and cell suspension obtained


Technique of culture –

Described by Green

Keratinocytes are now routinely cultured on feeder layers

Feeder layer consists of fibroblasts (locally irradiated or treated with mitomycin)

Murine fibroblast line or human fibroblasts are used.

Isolated keratinocytes are seeded on petridish/culture flask containing mitomycin C treated mouse fibroblast 3T3 cells.

Keratinocytes are cultured in 3:1 mixture of Dulbeco’s modified Eagle’s medium supplemented with –

Hams F12 medium

Hydrocortisone (0.4 mg/ml)


Transferrin (5mg/ml)

Adenine (8 x 10-4 mmol/l)

Triiodothyronine (2 x 10-2 mmol/l)

Cholera toxin (10-10 mmol/l)

Fetal calf serum (10%)


Culture is incubated @ 37°C in humidified atmosphere with 5% CO2

After 3 days, 10 ng/ml of human epidermal growth factor  is added.

Primary culture is now established and can be passed ‘n’ number of times depending on requirement.

Keratinocytes adhere to matrix synthesized by fibroblasts and produce 3 types of clones –




Basal cell produce holoclone (with maximum growth potential allowing 5-6 subculture)

Suprabasal cell produce paraclones (with least growth potential).

Holoclones gradually develop into meroclones during culture.

So, only 2nd and 3rd passage are used for grafting.

Each colony grows from periphery and become confluent by 8-10 days.

Cultures are seeded/reseeded with attenuated 3T3 cells.

Once a confluent and multicellular epithelium is obtained, it is detached enzymatic from culture disk/flask by dispose and rinsed in PBS.

Epidermis is then taken on paraffin gauze.

Cultured epithelial autografts usually takes 2-3 weeks.

Detached epithelium is assessed for viability.

The cultured graft is transported in aseptic conditions in petri-dishes containing DMEM under 5% CO2 to OT.


Patient preparation –

Meanwhile patient burn wounds in serially debrided.

Patient condition in stabilized.

Excision is done as required.



Grafting is done as soon as cultured graft arrives in OT

Carrier gauze is directly applied to the prepared bed.

Carrier gauze is then covered with saline gauze f/b thick dry dressing.

1st dressing is done after 5 days.

Then alternate day.

Carrier gauze is removed at 6-8 days.


Drawbacks of cultured keratinocytes –

(Most of the drawback is due to absence of dermal layer.)

Healed wound are thin and stiff

Lacks durability

Scarring and wound contraction are often

Keratinocytes also lack a well formed BM (or forms gradually) making grafts to shear off easily.

Fragile graft – leads to ‘delayed losses’.


Future –

Lack of dermal component makes cultured keratinocytes less than desirable – using dermal equivalent is a option to increase uptake (but, makes it costly.)

Using acellular fibrin gel as biological support media – does not require enzymatic detachment –

Improves adhesion potential of cells – increases attachment to the bed.

Also reduces culture time to 15 days to produce sheet graft.


Epidermal allograft culture –

Easily available

But, only a temporary measure (it gets rejected after some time).










Leg defect

History –

Particular of patient-

Name, age, sex, r/o, occupation, SES

Chief complain-


Past history

Personal history

Family history


Physical examination-

CCO well oriented to TPP

Attitude of the patient-

Pulse- rate rhythm volume character compared to other site


BP- mmHg arm supine/sitting

CVS- S1S2 heard no murmur

Resp- b/l AE present, no crepts or added sound

PA- soft non-tender, no organomegaly, bowel sounds normally present


Peripheral edema/Lymphadenopathy/Pallor/Cyanosis/clubbing/icterus


LOCAL examination-

Examination of ulcer-

There is a wound of approx size…………… on the …………..aspect of ………leg approximately in the ……third of the leg

Wound has well defined margin with sloping edges having granulation tissue in the floor and ?exposed bone around …….x…….cm .

Wound is having serous/purulent/seropurulent/bloody/serosanguinous foul-smelling discharge from the wound which is scanty/moderate/large in quantity.

Skin around the wound is normal for his skin color/reddish/dark red.

There is granulation tissue present/ or not. Healthy granulation tissue- healthy when bright, beefy red, shiny and granular with a velvety appearance. Unhealthy- pale pink or blanched to dull, dusky red color.

Bone- The exposed bone is lusterless, dry, and yellow in color.

Fixator- There is uiplanar, unidirectional /uniplanar,birectional/ biplanar,unidirectional/ biplanar,bidirectional/ circular fixator present, having …….number of pins above and …..numbers of pins below .


Attitude of the limb-

Patient is lying in supine position/ sitting with

Hip flexed/extended, knee flexed, ankle joint flexed.

Limb externally / internally rotated. Apparent limb shortening.



Findings of inspection confirmed on palpation.

Wound is …………X ………..in maximum dimension. ………cm  from tibial tuberosity and …….cm from medial malleolus. ?Medial and lateral margins of the wound.

The wound is tender/ nontender on palpation.

There is no bleeding on touch.

Wound is around …….mm in depth.

Base is formed by ……bone/ muscle.

Wound is not fixed to underlying structures.

There is/no surrounding tissue edema or regional lymphadenopathy.

There fixator has …….number of pins above and …..numbers of pins below Approximately …..cm from tibial tuberosity (each pin distance).


Limb length measurements-

Greater trochanter to medial condyle-   right……. Left…….cm

Tibial tuberosity to medial malleoulus- right………left………cm.

Girth of leg at 15 cm from tibial tuberosity is ………….cm on right side and …………cm on left side.

Girth of thigh 20cm above medial femoral condyle is ………….cm on right side and ……..cm on the left side.

Range of active motion at knee joint is ……….degree flexion……….degree extension on right side and …….on left side.

Range of active motion at ankle joint is …………..degree of plantar flexion…………..degree of dorsal flexion on right side and ……………..on left side.

Range of passive motion at knee joint is …… degree flexion……….degree extension on right side and …….……….degree flexion……….degree extension on left side.

Range of passive motion at ankle joint is …………..degree of plantar flexion…………..degree of dorsal flexion on right side and ……………..degree of plantar flexion…………..degree of dorsal flexion on left side.

There is no sensory loss.

Peripheral pulses palpable-

Femoral/ popliteal/ anterior tibial/posterior tibial/ dorsalis pedis.



Diagnosis– post traumatic soft tissue defect over upper/middle/lower third with exposed bone without neurovascular deficit with secondary diagnosis (chronic osteomyelitis) with limb shortening.


Plan –


Routine investigation

PAC fitness

Investigations specific to diagnosis-

Wounds c/s


Muscle charting

USG Doppler

CT angiography



Till the investigations are done, I would do regular dressing of the wound with betadiene or saline.

Once the patient is fit for surgery, I would like to debride the wound with around 0.5 cm margin and underlying bone till healthy normally bleeding bone is found and then cover the defect with muscle flap.



  1. What are the site of perforators?
  2. medially- from below upwards. With reference point – lower border of medial malleolus






Laterally-from below upwards

4-10 from lateral malleolus tip



5-6cm from fibular head


  1. What is the axis of the vessels in leg along which perforators are found?

Ans . Axis of perforator on medial side from post. tibial artery- 4.5 cm medial and parallel to the line joining tibial tuberosity and midmalleolar point.

Axis of perforator on lateral side from anterior tibial artery- 2.5 cm anterior and parallel to the line joining head of fibula and tip of lateral malleolus.

Axis of perforator on lateral side from peroneal artery- 2.5 cm posterior and parallel to the line joining head of fibula and tip of lateral malleolus.










  1. What is the difference in quality and quantity of perforators in leg?
  2. How many compartments are there in the legs?

4- Anterior, lateral and superficial posterior, deep posterior

  1. What is the different vessels that supply each compartment?

Anterior – anterior tibial artery

Lateral – peroneal artery

Posterior – posterior tibial artery


  1. What is the Ponten flap?

Superiomedial based fasciocutaneous flap in leg is called Ponten flap. Also called superflaps of legs because the length to breadth ratio can be extended beyond the usual 1:1 to up to 3:1

  1. Ponten described its flap in which specific area of the leg?
  2. superomedial aspect of the leg
  3. What is the classification for fasciocutaneous flap?

Cormack & Lamberty classification

Type A- pedicled fasciocutaneous flap dependent on multiple fascio-cutaneous perforators at the base and oriented along long axis of the flap (in prominent direction of the arterial plexus at the level of deep fascia)

Eg- Super flaps of Ponten, Sartorius flap without muscle, upper arm flap

Type B – single sizable and consistent fasciocutaneous perforator feeding a plexus at the level of the deep fascia.

Eg – supraclavicular

Median arm flap

Saphaneous artery flap

Parascapular flap

Type C – ladder type. Skin is supported by fascial plexus which is supplied by multiple small perforators along its length, which passes along septum b/w muscle.

Eg. – Radial forearm flap (Chinese forearm flap)

Type D – osteo-myo-fascio-cutaneous flap

An extension of type C – which takes muscle and bone supplied by the same artery.

Eg. – Radial forearm flap with radius


Mathes Nahai classification –

Type A – direct cutaneous àpedicle travels deep to fascia for a variable distance and then pierces fascia to supply skin à Eg. Groin flap, Temporoparietal fascia flap

Type B – septocutaneous à pedicle courses within intermuscular septum. à Eg. Lateral forearm flap, Radial forearm flap

Type C – musculocutaneous à vascular pedicle runs within the muscle substance and then supply skin à Eg. DIEP flap



  1. what’s the blood supply of skin?

Ans: Blood supply of skin is through various plexus –

  1. Subepidermal plexus
  2. Subdermal plexus
  3. Subcutaneous plexus
  4. Suprafascial plexus
  5. Subfascial plexus

These plexus can be supplied by various types of perforators –

  1. Direct cutaneous
  2. Septo-cutaneous
  3. Musculo-cutaneous
  4. what is the characteristics of artery and perforator through length of leg?

Ans: The size of the peroneal artery decreases as we go from proximal to distal but posterior tibial artery diameter remains almost the same as since it continues as the main vessel of the foot.

The perforators can be classified based on their internal diameter into three groups:

Small= 0.8-1.2 mm;

Intermediate= 1.3-2.0 mm;

Large= more than 2.0mm

The sizeable Perforators to sustain a flap are the intermediate or large ones.


  1. Whats are the limits of fasciocutaneous flap dissection in lower leg?

Ans: for retrograde flaps the lower limit of dissection decides the reach of the flap. Since lower two perforators are approximately within 8 cm from malleoli, that is taken as the safe limit of dissection inferiorly.

The safe upper limit of a retrograde flap is about 10 cm from the joint level in an adult.


  1. What is the Open fracture classification?

Gustilo-Anderson classification-

Type I = an open fracture with a wound < 1 cm long and clean

Type II = an open fracture with a laceration > 1 cm long without extensive soft tissue damage, flaps, or avulsions.

Type IIIA = open fractures with adequate soft tissue coverage of a fractured bone despite extensive soft tissue laceration or flaps, or high-energy trauma regardless of the size of the wound

Type IIIB = open fractures with extensive soft tissue injury loss with periosteal stripping and bone exposure, usually associated with massive contamination

Type IIIC = open fractures associated with arterial injury requiring repair


Classification is limited- almost limitless variety of injury patterns, mechanisms, and severities with a small number of discrete categories.

Limited interobserver reliability

Surface injury does not always reflect the amount of deeper tissue damage

Does not account for tissue viability and tissue necrosis


OTA Open Fracture Classification (OTA-OFC)


  1. Laceration with edges that approximate.
  2. Laceration with edges that do not approximate.
  3. Laceration associated with extensive degloving.


  1. No appreciable muscle necrosis, some muscle injury with intact muscle function.
  2. Loss of muscle but the muscle remains functional, some localized necrosis in the zone of injury that requires excision, intact muscle-tendon unit.
  3. Dead muscle, loss of muscle function, partial or complete compartment excision, complete disruption of a muscle-tendon unit, muscle defect does not reapproximate.


  1. No major vessel disruption.
  2. Vessel injury without distal ischemia.
  3. Vessel injury with distal ischemia


  1. None or minimal contamination.
  2. Surface contamination (not ground in).
  3. Contaminant embedded in bone or deep soft tissues or high-risk environmental conditions (eg, barnyard, fecal, dirty water).

Bone loss

  1. None.
  2. Bone missing or devascularized bone fragments, but still some contact between proximal and distal fragments.
  3. Segmental bone loss.



Advantages of External Fixation-

Provides rigid fixation when other forms of immobilization are not feasible. For example, severe open fractures cannot be managed by plaster casts or internal fixation due to risk involved.


Allows compression, neutralization, or fixed distraction of the fracture fragments.

Allows surveillance of the limb and wound status.

Allows other treatments like dressing changes, skin grafting, bone grafting, and irrigation, is possible without disturbing the fracture alignment or fixation.

Allows immediate motion of the proximal and distal joints This aids in reduction of edema and nutrition of articular surfaces and retards capsular fibrosis, joint stiffening, muscle atrophy, and osteoporosis.

Allows limb elevation by suspending frame from overhead frames

Allows early patient ambulation.

Can be done with the patient under local anesthesia, if necessary

External fixators cause less disruption of the soft tissues, osseous blood supply, and periosteum. This makes external fixation excellent choice in

Acute trauma with skin contusions and open wounds

In chronic trauma where the extremity is covered in thin skin grafts and muscle flaps,

Patients with poor skin healing

Ability to fix the bone avoid fixation at the site of fracture or lesion, and still obtained the rigid fixation


Disadvantages of external fixation

Pins inserted in the bones are exposed to internal environment and risk of pin tract infection is always there

Fracture may occur through pin tracts after frame removal. Extended protection may be required.

Assembly of the fixator lies outside the limb, is cumbersome and needs meticulous care.

High degree of compliance and motivation is required

Not suitable for non-cooperative patients

In fixators with pins near the joint or fixators that span joint, joint stiffness can occur.


Types of External Fixators

In strictest sense there are two types of fixators –

Unilateral and


A combination of two is called hybrid fixators.


Uniplanar- fixation in single plane

Biplanar- fixation in two planes

Unilateral-fixation on only one side

Bilateral- fixation on both sides


Parts of fixator-

Pins (Schanz screw)




Safe corridors in external fixation in lower leg –

The tibia can conveniently be divided into three segments –

  1. Knee joint line to the neck of fibula
  2. The neck of fibula to the distal metaphyseal flare
  3. The distal metaphyseal flare to the ankle joint line

Pins or wire can be used for fixation – Half pins (shown as bold arrows), and wire.


At the most proximal level of segment 1, approximately two fingers’ breadth below the knee joint line –

There are two main wire corridors –

  1. The coronal plane wire
  2. The medial face (so called as it parallels the medial subcutaneous face) wire

Half pins (bold arrows) have a wide corridor in this segment – inserted across the palpable anterior surface of the tibial plateau




Segment 2 –

Mid-shaft –

Plane of insertion of half-pins –

Sagittal plane medial to the tibial crest

Perpendicular to the anteromedial surface of the tibia.

Plane of wire insertion –

Medial face wire (from a posteromedial to anterolateral direction) – it goes slightly through gastrosoleus complex – stretch the muscles before inserting the wire.

Coronal plane wire –

Palpate the anterior and posteromedial limits of the subcutaneous surface of the tibia and determine the midpoint—a transverse trajectory from this point in the coronal plane is the position for this wire.

Segment 2 – At the beginning of the metaphyseal flare

Here posterior tibial neurovascular bundle moves from a midline location to posteromedial.

The medial face wire placed a little more anteriorly.


Segment 3 – between the widened metaphysis to the ankle joint –

Two additional wire can be placed other than medial face and coronal plane wire – transfibular and another behind the peroneal tendons but anterior to the lateral edge of the tendo Achilles.

Pins are similar in location, except that the sagittal pin is placed medial to tibialis anterior to avoid injury to ATA.


The hindfoot –

Wire –

One medial wire is placed across the calcaneum posterolaterally just posterior to posterior tibial neurovascular bundle.

Another complementary wire is placed at 45–60°, passing from anterolateral (behind and a little distal to the peroneal tendons) to posteromedial.

Half pins are inserted from lateral to medial in two areas:

  1. The posterior third of the body of the calcaneum (the pin can be inserted from posterior to anterior as an alternative direction)
  2. The neck of the talus




MC causative agent- staph aureus. Others staphylococcus epidermidis and Enterobacter species.

MC causative agent in Sickle cell anemia- Salmonella

MC causative agent in IV drug abuser- Pseudomonas or klebsiella.

Three main routes for spread of osteomyelitis have been described; these are

  1. Haematogenous,
  2. Contiguous and
  3. Direct inoculation.

Haematogenous spread-

Blood-borne organisms, usually bacteria, are deposited in the medullary cavity and form a nidus of infection.

In long bones, the region which is most predisposed to infection is the metaphysis, because it has a large supply of slow-flowing blood.

The metaphysis is also prone to infection because there is discontinuity in the endothelial lining of the metaphyseal vessel walls.

The gaps in the metaphyseal vessels allow bacteria to escape from the bloodstream into the medullary cavity.

In flat bones, the equivalent regions where infection tends to originate are the bony-cartilaginous junctions

Contiguous spread-

Infections originating from soft tissues and joints can spread contiguously to bone.

Direct inoculation-

Direct seeding of bacteria into bone can occur as a result of open fractures, insertion of metallic implants or joint prostheses, human or animal bites and puncture wounds.


Cierny-Mader Staging System of osteomyelitis-

Anatomic type    

Stage 1: Medullary osteomyelitis- involves only medullary cavity

Stage 2: Superficial osteomyelitis- involves only cortex

Stage 3: Localized osteomyelitis- involves both cortical and medullary bone, but not the full thickness

Stage 4: Diffuse osteomyelitis- involves the entire thickness of the bone, with loss of stability, as in infected nonunion.

The Cierny-Mader system adds a second dimension, characterizing the host as either A, B, or C.

A hosts- patients without systemic or local compromising factors.

B hosts- affected by one or more compromising factors.

C hosts – patients so severely compromised that the radical treatment necessary would have an unacceptable risk-benefit ratio.


Osteomyelitis can be divided into acute and chronic stages.

Acute osteomyelitis-

Bacterial proliferation within the bone induces an acute suppurative responseàaccumulation of pus within the medullary cavity leading to raised intramedullary pressure and vascular congestionàdisrupt the intraosseous blood supply.

Reactive bone and hypervascular granulation tissue may form around the intramedullary pus, giving rise to a well-circumscribed intraosseous abscess, also known as a Brodie’s abscess.

The rise in intramedullary pressure may eventually lead to rupture of the bony cortex, producing a cortical defect known as a cloaca.

Intramedullary pus can spread outward through the cloaca and form a subperiosteal abscess. This causes elevation of the periosteum and disrupts the periosteal blood supply to the bone.

Continual accumulation of pus in the subperiosteal space leads to rupture of the periosteum and spread of infection to soft tissues through a channel between the bone and skin surface known as a sinus tract.


Chronic osteomyelitis-

Pathological features of chronic osteomyelitis are a result of osteonecrosis, caused by disruption of the intraosseous and periosteal blood supply during the acute stage of disease.

A fragment of dead infected bone becomes separated from viable bone and is known as a sequestrum.

In an attempt to wall off the sequestrum, an inflammatory reaction characterised by osteoclastic resorption and periosteal new bone formation occurs. The sequestrum becomes surrounded by pus, granulation tissue and a reactive shell of new bone known as an involucrum.


Age-dependent differences-

Mechanism of infection-

Haematogenous spread is the predominant mechanism of infection in children.

Adult osteomyelitis is most commonly caused by contiguous spread from soft tissue infections or direct inoculation.

In adults, haematogenous spread is less common and when it does occur, usually leads to vertebral osteomyelitis.


Intraosseous vascular anatomy-

Below 18 months of age, growth plate is not ossified. Metaphyseal and epiphyseal vessels anastomose via transphyseal vessels that perforate the growth plate. So, osteomyelitis originating in metaphyses can migrate to epiphysis. This may result in slipped epiphyses, growth impairment and joint destruction.


In children older than 18 months of age (18m-16yrs), the growth plate ossifies and forms a barrier between the metaphysis and epiphysis, limiting the spread of infection from the metaphysis.

In adulthood (16yrs), the growth plate is reabsorbed, removing the barrier between the metaphyseal and epiphyseal vessels. These vessels reanastomose, once again allowing spread of infection into the epiphysis and joint space.


Subperiosteal abscess formation-

Subperiosteal abscesses are more common in children than in adults for two main reasons-

In children, the cortical bone is thinner and more easily ruptured, leading to spread of infection from the medullary cavity to the subperiosteal space.

The periosteum in children is also more loosely attached to the surface of the cortex and is easily separated.


Plain radiography-

Low sensitivity and specificity for detecting acute osteomyelitis.

Bone marrow edema, which is the earliest pathological feature, is not visible on plain films.

The features of acute osteomyelitis that may be visible include

A periosteal reaction secondary to elevation of the periosteum

A well-circumscribed bony lucency representing an intraosseous abscess and

Soft tissue swelling.

Regional osteopaenia

Periosteal reaction/thickening (periostitis): variable, and may appear aggressive including formation of a Codman’s triangle

Focal bony lysis or cortical loss

Endosteal scalloping

Loss of bony trabecular architecture

New bone apposition

Eventual peripheral sclerosis

Brodies abscess.

In chronic osteomyelitis, a sequestrum may be visible on plain radiographs as a focal sclerotic lesion with a lucent rim.


Codman triangle– it is a triangular area of new subperiosteal bone that is created when a lesion, often a tumour, raises the periosteum away from the bone.



Other investigations-

CT scan


Bone scintigraphy- 99mTc-MDP (methylene diphosphonate)- delayed bone scan shows increased uptake in affected bone.


  1. what is definition of a propeller flap?

Ans. It’s an islanded flap that reaches its recipient site through axial rotation.

It is different from other pedicled flap as the rotation is Axial around its pedicle.

  1. what is the classification of propeller flap?

Ans . They can be classified according to the type of nourishing pedicle- Tokyo consensus, 2009.

  1. Subcutaneous pedicled propeller flap is based on a random subcutaneous pedicle and allows for rotations up to 90°
  2. Perforator pedicled propeller flap is based on a skeletonized perforator pedicle. This is the most commonly used type of propeller flap and can be rotated up to 180°.
  3. Supercharged propeller flap is modification of the perforator pedicled propeller flap- a superficial or perforating vein of the flap is anastomosed to a recipient vein or an extra artery is anastomosed to a second arterial pedicle of the flap, to increase venous outflow or arterial inflow.

Recently, the “axial propeller flap” has been described that includes propeller flaps based on known vessels (e.g., suprathrochlear artery and lingual artery) and not on a perforator.


  1. Advantages of perforator propeller flaps?


  1. They allow for a great freedom in design and choice of the donor site, based on the quality and volume of soft tissue required and on scar orientation.
  2. They represent a simpler and faster alternative to free flaps and expand the possibilities of reconstructing difficult wounds with local tissues.
  3. Their harvest is easy and fast, provided that appropriate dissection technique is applied.
  4. Donor site morbidity is kept very low, avoiding the sacrifice of any unnecessary tissue.



  1. How to choose best perforator if more than one can be identified?

Ans: Best perforators is identified based on –

  1. Caliber,
  2. Pulsatility,
  3. Course and orientation,
  4. Number and caliber of accompanying veins, and
  5. Proximity to the defect and to a sensory nerve


  1. what is the course of posterior tibial artery?

Ans: The posterior tibial artery (Fig. 551) begins at the lower border of the Popliteus, opposite the interval between the tibia and fibula; it extends obliquely downward, and, as it descends, it approaches the tibial side of the leg, lying behind the tibia, and in the lower part of its course is situated midway between the medial malleolus and the medial process of the calcaneal tuberosity. Here it divides beneath the origin of the Adductor hallucis into the medial and lateral plantar arteries.

Relations.—The posterior tibial artery lies successively upon the Tibialis posterior, the Flexor digitorum longus, the tibia, and the back of the ankle-joint. It is covered by the deep transverse fascia of the leg, which separates it above from the Gastrocnemius and Soleus; at its termination it is covered by the Abductor hallucis. In the lower third of the leg, where it is more superficial, it is covered only by the integument and fascia, and runs parallel with the medial border of the tendo calcaneus. It is accompanied by two veins, and by the tibial nerve, which lies at first to the medial side of the artery, but soon crosses it posteriorly, and is in the greater part of its course on its lateral side.

Branches.—The branches of the posterior tibial artery ar


Posterior Medial Malleolar.




Medial Calcaneal

The peroneal artery -is deeply seated on the back of the fibular side of the leg. It arises from the posterior tibial, about 2.5 cm. below the lower border of the Popliteus, passes obliquely toward the fibula, and then descends along the medial side of that bone, contained in a fibrous canal between the Tibialis posterior and the Flexor hallucis longus, or in the substance of the latter muscle. It then runs behind the tibiofibular syndesmosis and divides into lateral calcaneal branches which ramify on the lateral and posterior surfaces of the calcaneus.

It is covered, in the upper part of its course, by the Soleus and deep transverse fascia of the leg; below, by the Flexor hallucis longus.


  1. what is the course of anterior tibial artery ?

Ans: The anterior tibial artery commences at the bifurcation of the popliteal, at the lower border of the Popliteus, passes forward between the two heads of the Tibialis posterior, and through the aperture above the upper border of the interosseous membrane, to the deep part of the front of the leg: it here lies close to the medial side of the neck of the fibula. It then descends on the anterior surface of the interosseous membrane, gradually approaching the tibia; at the lower part of the leg it lies on this bone, and then on the front of the ankle-joint, where it is more superficial, and becomes the dorsalis pedis.

Relations.—In the upper two-thirds of its extent, the anterior tibial artery rests upon the interosseous membrane; in the lower third, upon the front of the tibia, and the anterior ligament of the ankle-joint. In the upper third of its course, it lies between the Tibialis anterior and Extensor digitorum longus; in the middle third between the Tibialis anterior and Extensor hallucis longus. At the ankle it is crossed from the lateral to the medial side by the tendon of the Extensor hallucis longus, and lies between it and the first tendon of the Extensor digitorum longus. It is covered in the upper two-thirds of its course, by the muscles which lie on either side of it, and by the deep fascia; in the lower third, by the integument and fascia, and the transverse and cruciate crural ligaments.                  2

The anterior tibial artery is accompanied by a pair of venæ comitantes which lie one on either side of the artery; the deep peroneal nerve, coursing around the lateral side of the neck of the fibula, comes into relation with the lateral side of the artery shortly after it has reached the front of the leg; about the middle of the leg the nerve is in front of the artery; at the lower part it is generally again on the lateral side.

Branches.—The branches of the anterior tibial artery are:            6

Posterior Tibial Recurrent.



Anterior Medial Malleolar.

Anterior Tibial Recurrent.

Anterior Lateral Malleolar.



Median Nerve Palsy


  • Contains fibers from C6,7,8 & T1
  • Composed of lateral and medial roots from lateral and medical cords respectively

In axilla and arm –

  • Medial and lateral roots join to form Median nerve on the anterolateral side of 3rd portion of axillary artery
  • Courses distally in the medial intermuscular septum on anterior surface of brachial artery at middle level of arm
  • It then lies medial to brachial artery at level of elbow – here it is below the bicipital aponeurosis and superficial to brachialis muscle
  • (NO branches in arm)

In cubital fossa –

  • Nerve passes below bicipital aponeurosis and then continues to pass between two heads of Pronator Teres (Here it is separated by ulnar artery by deep (ulnar) head of PT.
  • Here it gives off muscular branches and AIN
  • After which it cross ulnar artery and passes beneath the tendinous band between two head of FDS- to enter the septum between FDS and FDP.
  • From here it continues in midline of forearm.
  • About 5cms from flexor retinaculum the nerve appears to lateral edge of FDS
  • It then lies between tendons of FDS & FCR and beneath tendon of PL before entering carpal tunnel

In the Carpal Tunnel

  • Nerve becomes palmar to tendons of FDS and lies immediately deep to flexor retinaculum
  • During travel in tunnel for about 2.5-3.0cm the median nerve becomes large and flattened
  • At distal edge of retinaculum, nerve divides into ulnar and radial terminal trunks
  • Radial trunk divides into thenar motor branch and 1st common digital nerve
  • Ulnar trunk divides into 2nd, 3rd and common digital nerve

Anterior Interosseous Nerve (AIN)

  • Originates from median nerve 5cm distal to medial epicondyle
  • Passes between FDP & FPL on interosseous membrane and supplies these two muscles
  • Further it courses between Pronator Quadratus and interosseous membrane and supplies PQ
  • It ends in articular branches of wrist
  • (AIN supplies radial side of FDP used for flexion of index and middle fingers]


Surface marking

In arm

  • with arm abducted, a line can be drawn from a point on the lateral wall of axilla, just posterior to the eminence of coracobrachialis and passing along medial bicipital groove to a point in the distal portion of cubital fossa

In forearm

  • With elbow extended, a line drawn from distal end of cubital fossa to point between the tendon of FCR and PL at wrist.
  • Nerve is found along this line



Motor supply of Median Nerve








Abductor Pollicis Brevis (APB)

FPB (Superficial head)


Lumbrical – 1st and 2nd


AIN – Motor supply to FPL and FDS to index and middle

sensory distribution

MCNF – Medial cutaneous Nerve of forearm

LCNF- lateral cutaneous nerve of forearm

RN – Radial nerve sensory branch

MN- median nerve sensory branch

PCNF- posterior cutaneous nerve of forearm (Radial nerve)



Palmar cutaneous branch of median nerve –

– given off from radial side of median nerve

– 8.5cm proximal to the wrist crease

– Courses between FCR and PL

– pierces fascia (antebrachial fascia) 4.5cm proximal to wrist crease

– Reaches the wrist- superficial to flexor retinaculum and divides into several branches to supply thenar eminence and palm- central part


Ques-Low vs High Median nerve palsy?

Ans – Median nerve injury is classified into high or low depending on whether injury is proximal or distal to innervation of forearm muscles.


Function lost:

Low median nerve injury:

  • Loss of thenar function and opposition

High median nerve injury:    

  • Loss of thenar function and opposition
  • Loss of FDS to all fingers
  • Loss of FPL
  • Loss of index FDP

Functional loss

  • Loss of oppositional and oppositional pinch
  • Diminished grip strength
  • Loss of PT and PQ is compensated by shoulder rotation.
  • FCR is lost, but wrist function maintained by FCU
  • Loss of fine motor control and prehension
  • Sensory loss- is in critical area of hand and palm. For this reason, even if motor recovery is not possible and tendon transfers are required, median nerve should be repaired or reconstructed or sensory transfer in hand considered to restore this critical area of sensibility.


Causes of median nerve palsy

Above elbow:   

  1. Brachial plexus injury –  Trauma,   SOL
  2. Humerus Fracture
  3. Ligament of Struthers compression
  4. Crutch Compression
  5. Sleep palsy
  6. Anterior dislocation of humerus

At elbow:

  1. Compression due to joint effusion
  2. Pronator Teres syndrome
  3. Ventral dislocation of radial head

At forearm:

  1. AIN syndrome
  2. Deep laceration

At Wrist:

  1. Carpal tunnel syndrome
  2. Laceration

Other causes:

  1. Aneurysm
  2. Gout
  3. Diabetes
  4. Thyroid disorder
  5. Pregnancy
  6. Genetics


Median nerve injury Signs

  • Ape-hand deformity: hyperextended and adducted thumb
  • Thenar hypotrophy
  • Pointing index finger: inability to flex index on making fist
  • Inability to make “OK” sign
  • Pain, paresthesia, numbness in sensory distribution of median nerve
  • Loss of opposition
  • Phallen test and Reverse Phallen test: Patient holds wrist in maximum palmar flexion for up to 2 minutes- this increases pressure on carpal tunnel and provokes paresthesia in the area of median nerve
  • Maximum extension of wrist provokes similar provocation – Reverse Phallen.


Goal of tendon transfer in median nerve injury

  • Low median nerve injury- Restoration of thumb opposition
  • High median nerve injury- above + restoration of FPL and index FDP


Biomechanics of thumb opposition

  • Trapezio-metacarpal joint- Abduction + Flexion + Pronation [AFP]
  • (Palmar abduction+ Flexion + Pronation)
  • Prime muscle of Opposition – Abductor Pollicis Brevis
  • Aided by FPB and OP


History of Opponensplasty

  • Steindler – 1st Opponensplasty (radial slip of FPL)
  • Cook – used EDM
  • Ney – FCR or PL to EPB
  • Huber (1921)- ADM
  • (Nicolayson- 1922)
  • Bunnell (1924), Camitz (1929) used PL
  • Royal and Thomson – Superficialis transfer
  • Caplan and Aguirre (1956) –EIP


Critical points for tendon transfer

  • Tendon transfer not to be done in unhealed wound
  • Tendon transfer not to be done in joint function limitation
  • Tendon transfer should not pass through scarred tissue, and skin graft or skin incision
  • Other principles of Tendon transfer should be followed


Prevention and preoperative treatment of contracture:

In median nerve palsy and complete thumb intrinsic paralysis- thumb may adopt supinated and adducted position. Thus 1st web space contracture can occur.



Physiotherapy – passive thumb abduction and opposition

Splint – Abduction splint


Treatment of established first web space contracture:

Two possible causes

  • Contracture of skin and deep fascia on its exterior surface
  • Contracture of dorsal capsule of CMCJ (resists opposition but permits abduction)


  • Physiotherapy
  • Splint
  • Surgical release

Surgical release:

  • Dorsal web space incision
  • Fascia over Adductor pollicis and FDI released
  • Skin is widened with SSG or Flap
  • Capsule contracture of CMCJ- incision over base of joint
  • Severe contracture- rotational osteotomy at base of 1st metacarpal and trapezoidectomy



Pulley formation –

  • Line of lull of transfer should pass parallel to APB muscle
  • So, all extrinsic opponensplasties should pass around a stout, fixed pulley in the region of pisiform on ulnar border of wrist
  • Forearm extensor can pass over ulna or through interosseous membrane
  • Forearm flexor- pulley created on ulnar border of wrist


Insertion for opponensplasty

  • Single insertion
  • Double insertion – one for opposition and other for MP joint stabilization or preventing IPJ flexion

Single insertion is better, following single function principles.

Single insertion

  • into APB
  • used in isolated median nerve palsy

Dual insertion

  • APB insertion + Dorsal MP capsule or thumb extensor expansion
  • Useful in completely intrinsic minus thumb


Four standard opponensplasty

  • Superficialis ooponensplasty- Royle Thomson technique or Bunnell technique
  • EIP (Burkhaulter)
  • Huber transfer (ADM)
  • Camitz procedure (PL)


Assessment of outcome of opponensplasty

Sundararaj and Mani –

Excellent – Opposition to ring or little finger with IPJ extended

Good – Opposition to middle or index finger with IPJ extended

Fair – IPJ flexes during opposition

Poor – No opposition restored


Superficialis Opponensplasty

Ring finger FDS is widely used.

Ring FDS harvest:

  • Royle & Thomson divided FDS tendon at its insertion into middle phalanx
  • North & Littler- suggested division of FDS through a window between A1 and A2 pulley (before its bifurcation)

Drawback of Royle & Thomson method – dividing FDS at its insertion

  • Involves lot of dissection in flexor sheath – fibrosis
  • Destroys vincula – disrupts blood supply to FDP
  • PIP joint capsule may be damaged – contracture

Benefits of North & Littler method

  • Avoid injury to flexor sheath and PIPJ capsule
  • Leaves 3cm of FDS tendon that glides freely within the flexor sheath

Complication of donor digit

  • DIPJ extension lag
  • PIPJ fixed flexion deformity
  • Swan neck deformity

These complications are avoided if FDS is harvested through incision in distal palm


Pulley formation –


  • Passing FDS around FCU- problem of proximal migration
  • Distally based strip of FCU (based on its attachment to pisiform)
    • Problems
      • Raw surface over FCU- will cause adhesion
      • Radial migration can occur (FCU strip can be attached to ECU tendon to prevent radial migration)
    • Angle between distal edge of flexor retinaculum and ulnar border of palmar aponeurosis
    • Window in flexor retinaculum



Choosing a site of pulley formation-


Transfer’s line of action passes through –

Pisiform – maximum abduction and opposition but small amount of MCPJ flexion

Distal to pisiform – More thumb flexion, less abduction

Proximal to pisiform – more palmar abduction


Superficialis transfer (Royle & Thompson)

Incision 1: 3cm longitudinal incision at the base of the palm on the medial border of hypothenar eminence.

Ulnar border of palmar aponeurosis exposed and retracted radially.

FDS of ring finger identified, as it emerges from carpal tunnel proximal to superficial palmar arch

FDS of ring finger is then divided through a separate transverse incision (2nd incision) at base of digit.

FDS then delivered into palmar wound, keeping it ulnar to palmar aponeurosis.


Third incision at dorsum of thumb MP joint.

Subcutaneous tunnel created between this and palmar incision

FDS then passed through this tunnel superficial to palmar aponeurosis and carpal tunnel (and hence acting as a pulley for FDS)

This is then inserted into APB.


Tension of suture –

Should be maximum with thumb in full opposition and wrist in neutral

Postop-Immobilization for 4-6 weeks with thumb in full opposition


Bunnell’s technique

Ring FDS harvested as described above.

Distally based FCU pulley is made- distal portion of FCU exposed and split into 2 – for 4 cm proximal to its insertion at pisiform

One part cut and sutured back onto its base at pisiform- forming a loop

Ring FDS is delivered via the wrist incision and passed through FCU pulley and subcutaneous tunnel into insertion to dorsal thumb

FDS passes over EPL over dorsum of thumb and then passes through a drill hole in the base of PP of thumb in ulnar to radio palmar dissection

Transfers’ tension if set with thumb in full opposition and wrist is neutral.

Bunnels superficialis transfer


EIP Opponensplasty

Favored by Burkhaulter

Preferred to superficialis transfer as it does not weaken grip

  • First Incision: Short incision over dorsum of index MP joint. EIP is divided immediately proximal to extensor hood. (EIP is ulnar to EDC)
  • Second incision: On the ulnar side of distal forearm on the dorsum. EIP is delivered into this incision (EIP tendon is retrieved out of extensor retinaculum)
  • Third incision: Over dorsoradial aspect of thumb MPJ
  • Subcutaneous tunnel then created passing from extensor surface of forearm, passing around ulnar border of wrist, across the palm to reach the incision of thumb
  • EIP then passed through the tunnel and attached to APB tendon (in case of isolated Median nerve palsy)
  • Suturing done with thumb in maximum opposition and wrist in 30deg flexion.
  • In combined median and ulnar nerve palsy, transfer is attached sequentially to APB tendon, MPJ capsule, EPL tendon over proximal phalanx (Riordan).
  • This attachment restricts IPJ flexion and thus helps FPL flex MPJ more effectively substituting FPB function


  • Post op: Immobilization in wrist in flexion and thumb in full opposition for 3-4 weeks.

EIP transfer


ADM opponensplasty (Huber)

This transfer also improves hands appearance by increasing the bulk of thenar eminence.

  • Incision: Mid-lateral incision over ulnar border of little finger
  • Incision extended proximally and radially to distal palmar crease and then incision turns ulnarly across as it crosses the distal palmar crease
  • ADM divided from its insertion (It has 2 insertions- one at base of Proximal phalanx and second into extensor apparatus)
  • ADM freed of soft tissue attachments by retrograde dissection towards its origin at pisiform
  • Pitfall- great care must be taken not to damage this neurovascular pedicle which is on its dorso-radial aspect.
  • Once neurovascular pedicle is isolated ADM is freed up more proximally elevating its origin from pisiform. While retaining an attachment on the FCU tendon by dissecting a slip of FCU proximally
  • Next incision- over thumb MPJ dorsoradially
  • Subcutaneous tunnel created to this area immediately proximal to pisiform
  • This dissection is easier if done through another incision made in the thenar crease at base of thenar eminence
  • ADM is then turned 180° on its long axis to reduce tension on its neurovascular pedicle (as if turning page of a book)
  • ADM passed through subcutaneous tunnel and then attached to APB insertion.
  • Postop immobilization: Thumb in full opposition for 4 weeks
  • The position of wrist is not critical as transfer does not cross this joint
  • Difficult transfer
  • ADM barely reached APB insertion risk of damage to neurovascular bundle
  • This is to be done when other opponensplasties are not possible.
  • Origin of ADM at pisiform may be preserved, but then it will require short tendon graft

Huber transfer


Palmaris longus opponensplasty –

  • Described by Camitz
  • Simple procedure
  • Done usually in severe carpal tunnel syndrome – leading to loss of abduction and opposition
  • Procedure can be performed in regional anesthesia
  • It restores palmar abduction rather than opposition
  • Not recommended in traumatic median nerve palsy, as PL may be injured as well.
  • Transfer usually performed with carpal tunnel release- Abduction is restores till the median nerve recovers



  • PL is confirmed (by opposing the thumb to little finger and flexing the wrist)
  • Incision – longitudinal incision starting 2cm proximal to distal wrist crease and progressing till proximal palmar crease in line of ring finger
  • Identify and avoid injury to palmar cutaneous branch of median nerve
  • PL tendon is freed in forearm- into the palm with 1cm wide strip of palmar aponeurosis
  • 2nd incision over dorsoradial aspect of MP joint
  • PL is tunneled into the incision and attached to APB tendon insertion
  • Suturing done with thumb in full opposition, MP joint extended and wrist in neutral

Post-op immobilization:

  • Light cast holding wrist in neutral and thumb opposed for 4 weeks.
  • Followed by night splint for 1 week


Other Opponensplasties

  • ECU
  • ECRL
  • EDM
  • EPL
  • FPL


Postop management –

  • Thumb immobilized in opposition for 3 weeks
  • For EIP transfer – additional wrist flexion is required in immobilization
  • For FDS- wrist is kept in neutral
  • If transfer’s tendon is inserted to APB or extensor mechanism then IPJ is kept in full extension
  • Splint discontinued after 3 weeks
  • Splint can be continued for longer period if more complex nerve injury.
  • Combined high median and ulnar nerve injury, Charcot Marie Tooth disease and Leprosy- Splint for 3 months

Preferred Opponensplasties –

PL for CTS (Carpal Tunnel Syndrome)

EIP for other

ADM when others cannot be done



  • Outcome depends on whether
  • underlying neurologic pathology is progressive or static
  • Disability attributable to the isolated loss of opposition
  • Disability attributable to other problems such as sensory loss or other motor loss (More sensory deficit means less likely benefit from reconstructive surgery)


High median nerve palsy –

Aims of tendon transfer –

  • Restoration of opposition
  • Restoration of index finger flexion
  • Restoration of thumb flexion


Extrinsic donor available

  • ECRL
  • ECU
  • BR


Usual transfer

  • BR to FPL
  • ECRL to Index FDP (or side to side suturing to other FDP)
  • ECU to Opponensplasty


Restoration of Opposition

In high median nerve palsy – EPL, EIP, EDM are more readily available


Restoration of index flexion

  • Side to side suturing of index FDP and conjoint middle, ring and little finger FDP in distal forearm- this restores index finger flexion but does not restore strength
  • ECRL to index finger FDP- if independent index flexion is wanted and strength is required on radial side of hand
  • ECRL to index finger FDP should not be too tight- flexion contracture will occur
  • Tension should be just adequate that tenodesis effect is not restricted


Restoration of thumb flexion

BR to FPL transfer –

  • BR needs to be extensively released of soft tissue attachments to achieve good excursion
  • The tension should not be tight- it should be possible to passively extend all three joints of thumb with wrist flexed
  • BR transfer warrants 45deg elbow flexion during adjustment of tension
  • Since BR is an elbow flexor primarily, following the transfer to FPL the thumb flexion is maximally achieved when elbow is extended


Postoperative Splintage

  • For high median nerve palsy-
    • wrist 20° flexion
    • Thumb palmar abduction and flexion
    • Index in intrinsic plus position (Alone if ECRL to FDP transfer, or all fingers in intrinsic plus position if side to side suturing of FDP tendons done)




(Credits : Dr Anoop S (SR, MCh plastic Surgery, VMMC & SJH, New Delhi). Dr. Rohit M (SR, MCh plastic Surgery, VMMC & SJH, New Delhi)- Illustrations)

Developmental milestones

Developmental milestones


Periods of growth

Prenatal period –

Ovum – 0-14 days

Embryo – 14 days to 9 weeks

Fetus – 9 weeks to birth

Perinatal period – 22 weeks to 7 days after birth

Postnatal period –

Newborn – first 4 week after birth

Infancy – first year

Toddler – 1-3 yr

Preschool – 3-6 yr

School age – 6-12 yr

Adolescence –

Early – 10-13 yr

Middle – 14-16 yr

Late – 17-20 yr



Approximate anthropometric values by age

Age Weight (kg) Length or height (cm) Head circumference (cm)
Birth 3 50 34
6 m 6 (doubles) 65 43
1 year 9 (triples) 75 46
2 yr 12 (quadruples) 90 48
3 yr 15 95 49
4 years 16 100 50


Key Gross Motor developmental milestone

Age Milestones
3 m Neck holding
5 m Rolls over
6 m Sits in tripod fashion (sitting with own support)
8 m Sitting without support
9 m Stands holding on (with support)
12 m Creeps well; walks but fails; stands without support
15 m Walks alone; creeps upstairs
18 m Runs; explores drawers
2 yr Walks up and downstairs (2 feet/step); jumps
3 yr Rides tricycle; alternate feet going upstairs
4 yr Holds on one foot; alternate feet going downstairs



Key Fine Motor developmental milestone

Age Milestones
4 month Bidextrous reach (reaching out for objects with both hands)
6 month Unidextrous reach (reaching out for objects with one hand); transfers objects
9 month Immature pincer grasp, probes with forefinger
12 m Pincer grasp mature
15 m Imitates scribbling, makes tower of 2 blocks
18 m Scribbles, makes tower of 3 blocks
2 yr Tower of 6 blocks, vertical and circular strokes
3 yr Tower of 9 blocks, copies circle
4 yr Copies cross, bridge with blocks
5 yr Copies triangle, gate with blocks




Key Social and Adaptive Milestones

Age Milestone
2 m Social smile (smile after being talked to)
3 m Recongnizes mother; anticipates feeds
6 m Recognizes strangers; stranger anxiety
9 m Waves “bye-bye”
12 m Comes when called, plays simple ball game
15 m Jargon
18 m Copies parents in task (eg sweeping)
2 yr Asks for food, drink, toilet, pulls people to show toys
3 yr Shares toys, knows full name and gender
4 yr Plays co-operatively in a group; goes to toilet alone
5 yr Helps in household tasks, dresses and undresses




Key Language milestones

Age Milestone
1 m Alert to sound
3 m Cooing (musical vowel sounds)
4 m Laughs loud
6 m Monosyllables (ba, da, pa); ah-goo sounds
9 m Bisyllables (mama, baba, dada)
12 m 1-2 words with meaning
18 m 8-10 word vocabulary
2 yr 2-3 word sentences, uses pronous (I, me , you)
3 yr Asks questions, knows full name and gender
4 yr Says song or poem; tells stories
5 yr Asks meaning of words



Upper age limit for attainment of milestone

Milestone Age
Visual fixation or following 2 m
Vocalization 6 m
Sitting without support 10 m
Standing with assistance 12 m
Hands and knee crawling 14 m
Standing alone 17 m
Walking alone 18 m
Single word 18 m
Imaginative play 3 yr



Timing of Dentition

Primary dentition Time of eruption , months Time of fall, years
  Upper Lower Upper Lower
Central incisors 8-12 m 6-10 m 6-7 yr 6-7 yr
Lateral incisors 9-13 m 10-16 m 7-8 yr 7-8 yr
First molar 13-19 m 14-18 m 9-11 yr 9-11 yr
Canine 16-22 m 17-23 m 10-12 yr 9-12 yr
Second molar 25-33 m 23-31 m 10-12 yr 10-12 yr
Permanent teeth Time of eruption (in years)
  Upper Lower  
First molar 6-7 6-7  
Central incisor 7-8 6-7  
Lateral incisor 8-9 7-8  
Canine 11-12 10-12  
First premolar 10-11 10-12  
Second premolar 10-12 10-12  
Second molar 12-13 11-13  
Third molar 17-21 17-21  


Further reading – Essential pediatrics, 8th edition


Q .What is craniofacial distraction or distraction osteogenesis?

A. It is a technique that applies gradual and incremental traction force onto surgically separated bony segments to produce additional bone

(Distraction Histiogenesis – distraction of skeleton also causes enlargement of overlying and surrounding soft tissues)



Codivilla – 20th Century – Femur elongation following osteotomy

Abbot – 1927- Femur elongation following osteotomy

Ilizarov – popularized the distraction osteogenesis in long (endochondral) bone of extremities for limb lengthening and closure of bony defects

McCarthy – 1989 – Craniofacial distraction



Terminology – 

Distraction Zone: The location of bony separation

Latency period: Duration of reparative callus formation in distraction zone

Activation period: Duration during which distraction forces are applied to callus (for elongation)

Distraction degenerate: The newly formed bone following activation

Consolidation period: Period for which external fixation is maintained in position to allow newly formed bone to consolidate

Rhythm: The rate of activation

0.25 mm four times a day or   0.5 mm two times a day

i.e. Total 1 mm /day

Vector: Direction along which forces are applied



  1. Bony separation in two segments (osteotomy or corticotomy)
  2. Latency period (5-7 days)
  3. Activation period
  4. Consolidation period (8 weeks)

Process of distraction starts with –

Performing osteotomy or corticotomy.

After which the distraction device will be applied depending on which direction the bone lengthening is desired (vector of distraction).

Following osteotomy a latency period (usually of 5-7 days) is given for callus formation, before activation of the device.

Following latency period, gradual distraction force is applied to separate the segments and thus elongate the intersegmentary callus – this is the activation period.

After, the desired length of bone has been achieved, the activation is stopped and the distraction device in maintained in position to allow consolidation of the newly formed bone- the consolidation period.


Osteotomy – Full thickness bony separation

Corticotomy – Spares the endosteum or marrow space

The most usually done distraction is  – transosteotomy (or transcorticotomy) distraction.

Distraction can be done across a open suture (such as in young patient) – trans-sutural distraction.


Three types of Distraction

  • Unifocal
  • Bifocal
  • Trifocal

Bifocal and Trifocal is across a skeletal defect

Unifocal: Single osteotomy

Distraction forces on either side of osteotomy

Bifocal: Single osteotomy

Transport segment (of bone) spanned across the defect using single distraction device

Trifocal: Two osteotomies used to fill skeletal defect in bidirectional manner


When distracting across a skeletal defect the transport segment has a fibro-cartilagenous

cap which needs to be removed after final “docking” and replaced with bone graft.


Histological Analysis

  • Latency period: Hematoma formation

Migration of inflammatory cells into osseous gaps (PMNs)

  • Activation Period: Presence of tapered cells similar to fibroblasts

New blood vessels (endothelial cells)

New fibrovascular matrix (Type 1 collagen)

At Day 14 –      Osteoid synthesis and mineralization

At day 21 –       Calcification of linearly oriented collagen bundle

Appearance of osteoblasts

Formation of bony spicules

(Linear orientation is parallel to distraction vector)

Four Temporal Zones –

  1. Fibrous central zone – mesenchymal proliferation
  2. Transition zone – osteoid formation
  3. Remodeling zone – osteoclasts
  4. Mature bone zone


Biomolecular analysis

Marked increase in TGF-B1 level

TGF-B1:         Activates VEGF & bFGF

Increase collagen deposition and non-collagen ECM proteins

Leading to mineralization and remodeling of bone

Osteoclast migration, differentiation and bone remodeling



Tensile force applied to developing callus causes elongation of callus.

The mechanical forces are converted to cellular signals – termed as mechanical transduction.

This mechanical transduction is mediated by – Integrin mediated signal transduction


Tensile strain: Defined as amount of elongation as a fraction of original bone length

Eg.     1mm elongation in 1mm osteotomy defect- tensile strain 1/1 = 100%

By day 10 the bone gap will be 10mm

So, tensile strain will be 1/10 = 10%

Maximum tensile strain for bone is 1-2%

So, bone formation does not occur in distraction zone until approx. 4 weeks of activation

i.e. 1/30 = 3%


Mechanical environment in distraction zone depends upon –

  1. Stability of distraction device
  2. Applied distraction force
  3. Inherent physiological loading (muscle action)
  4. Properties of all the local soft tissue


For formation of successful (stable) regenerate –

  1. The distraction device must be stable
  2. Latency period should be adequate (not too short or too long)
  3. Distraction should be gradual
  4. Sufficient time should be given for consolidation


Patient factors that can affect regenerate formation –

Age –

In younger patient – better and faster distraction can be achieved. Latency period in children can be as low as 2-3 day (due to rapid callus formation).

Blood supply – adequate neovascularization should occur to support newly forming bone.

Radiation or chemotherapy – patient receiving RT or CT has poor blood supply and impairs osteogenesis.


[Credits : Dr. Anoop S. (Mch, department of burn and plastic surgery, VMMC & Safdarjung Hospital New Delhi)]

Reconstruction of acquired lip defects


Philtral column

Philtral groove/dimple

Cupids bow

White roll- junction of vermillion and cutaneous surface



Vermillion – the red/pink dry part of lip seen outside


Vermillion is widest in central lip

Philtrum columns are formed by C/L orbicularis oris fibers.

Philtrum columns slightly diverge as then come down.

White roll created by pars marginalis fibers of orbicularis oris.


Upper lip elevators-

  1. Z. major
  2. Z. minor
  3. LLS AN
  4. LLS
  5. LAO

[levator labii superioris anguli nasalis, levator labii superioris anguli, levator  anguli oris]

Retractors and depressor of lower lip-

  1. Platysma
  2. Depressor labii
  3. Depressor anguli oris

Lower lip elevator– Mentalis (makes pout)

Nasolabial crease formed by-

  1. Z. major
  2. LLS
  3. LAO


Orbicularis oris-

Two components-

  1. Pars marginalis
  2. Pars peripherlais

Marginalis anterior to peripherialis [Peripheralis- Posterior]

Marginalis mostly deep to vermillion area

Peripheralis mostly deep to cutaneous portion of lip


Muscular sling that presses lip against gingiva and teeth is formed by-

  1. Orbicularis
  2. Risorius
  3. Buccinator
  4. Pharyngeal constrictor


Blood supply-

Facial artery courses through a plane which between two muscle layers.

Muscles anterior/superficial to artery are-

  1. Risorius,
  2. Z major,
  3. Superficial lamina of orbicularis oris (OO)

Muscles that are deep to the artery are-

  1. Buccinator,
  2. LAO,
  3. Deep lamina of OO

Facial artery branches approx- 1.5cm lateral to oral commissure

Into – superior labial and inferior labial a.

Superior labial- found within 10mm of lip margin

Inferior labial- found within 4-13 mm of lip margin


Labial artery lies within or posterior to orbicularis oris muscle but Never anterior to it.


Nerve supply-


Zygomatic and buccal branch – lip elevators and retractors

Marginal mandibular- lip depressor


V2 –infraorbital & V3 mental branch of trigeminal nerve


Etiology of lip defect –

Most common cause is – Carcinoma lip. MC type of cancer is Squamous cell ca.

96% lip cancer occur in lower lip

96% is SCC type.

96% of patients are male.


Reconstruction – defect wise


Defect by definition does not crosses white roll.

So, reconstruction should – Avoid crossing white roll.

Simplest method—undermining of adjacent oral mucosa with defect closure by advancement.

Wilson & Walker – laterally based bipedical mucosal flap

For Full-thickness defect of vermillion –

-lateral vermillion musculomucosal advancement flap (based on labial artery)

-musculocutaneous flap composed of intraoral mucosa and orbicularis advanced from sulcus in V-Y fashion

Other regional flaps-

Unipedicle vermillion lip switch flap from opposite lip -divided after 10-14 days

Random musculomucosal flap

FAMM flap (facial artery myomucosal flap) – buccinators muscle based on facial artery

Tongue flap (from lateral/lower surface) – two stage procedure cumbersome.


Partial thickness defect-

Primary closure

Advancement flap

Transposition flap

Skin graft not routinely used/required

Except, central philtral defect- full thickness graft used instead of STSG.


Small full thickness defect-

Primary closure-

Lower lip- up to 40% defect

Upper lip- up to 25 % defect


Large full thickness defect-

Two resources to recruit extra tissue to fill the defect – opposite lip & adjacent cheek.

Orbicularis oris- better competent stoma. Microstomia a risk.

Cheek- microstomia less common, functionally and aesthetically inferior outcome


Large central upper lip defect-

Abbe flap (based on inferior labial artery)  –> flap division after 2-3 weeks

Abbe flap with perioral crescent


Large central lower lip defect-

B/L Karapandzic

Modified Bernard (Webster- Bernard)

Nasolabial flap


Karapandzic Bernard
Musculocutaneous rotation advancement flap

Neurovascular flap

First 1cm incision full thickness- after that only skin and muscle divided, mucosa is intact

Burrow’s triangle excised

Lateral advancement flap

First 1cm full thickness incision after that only skin and mucosa intraorally

Burrow’s triangle excised


Interdigitating nasolabial flap

Partial thickness random flap

Full-thickness “Gate-flap”- based on facial a

Full thickness flap denervates upper lip.


Large lateral and commissure defect-


Medially based rotation advancement flap from upper lip to lower lip

Reverse Estlander- from lower lip to upper lip

Gillies-fan flap- rotational advancement flap. A quadrilateral flap

McGregor & Nakajima modified fan flap –

  1. Pivotal flap
  2. Stoma size unchanged
  3. Need for vermillion reconstruction

Abbe-Estlander flap-

Preserves commissure

Need second stage of flap division

Temporary microstomia

U/L Karapandzic

U/L Bernard

U/L Nasolabial flap


Total lip reconstruction-

>80% defect-

B/L Bernard or Nasolabial flap

Submental flap (flap based on submental branch of facial artery)

Radial forearm free flap (RAFF)

Karapandzic – will cause microstomia, so not preferred.

RAFF is the best choice for total lip reconstruction.

Palmaris longus tendon can be harvested along with the flap to be weaved into remaining OO muscle or into modulus.


Lip replantation –


Most commonly – by traumatic amputation by dog bite.

Every attempt should be made for reimplant as the aesthetic and functional outcome is better than free tissue transfer.

Main obstacle in reimplant of lip is – poorly formed labial vein.




Algorithm –

Defect size Defect location Reconstructive option
Up to 25% – upper lip

Up to 40% – lower lip

  Primary closure
25-80 % Upper lateral lip or lower lateral lip Lip switch (Estlander/Abbe) or

Unilateral Karapandzic/ Bernard/ Nasolabial flap

  Central lower lip Bilateral Karapandzic/ Bernard
  Central upper lip Abbe flap +/- perioral crescent
>80%   Bilateral Bernard/ Nasolabial flap or

Free tissue transfer – RAFF

(further reading – Grabb and Smith Plastic surgery 7th Ed. chapter 34)

Radial nerve palsy

Course of radial nerve?

Radial nerve is terminal branch of posterior cord, a continuation of it. It receives supply from C5-T1.

It then descends in front of subscapularis and latissimus dorsi and posterior to axillary artery.

At the level of lower border of teres major it courses posterolaterally and passes through triangular interval (between long head of triceps, teres major and humerus).

It then courses in shallow groove on posterior surface of the humerus – between lateral and medial head of triceps where it gives off branches- muscular and cutaneous.

At level of middle and lower 1/3rd of arm it penetrates lateral intermuscular septum to enter anterior compartment.

It travels between brachialis (medially) and brachioradialis & ECRL (laterally).

At the level of capitulum of humerus it divides into superficial and deep branches.

Deep branch (PIN) passes between two heads of supinator à wraps around lateral aspect of radius to reach back of forearm. [PIN emerges from supinator approx. 8cm distal to elbow joint]

After emerging from supinator it travels between superficial and deep layer of muscles of extensor compartment i.e. it passes/travels over APL & EPB and under the EDC.

It then courses on the dorsal surface of interosseous membrane underneath the EPL and EIP.

At wrist joint it is almost flattened giving sensory fibers to wrist joint and DRUJ.

Superficial branch –

Courses underneath the brachioradialis.

In the proximal third of foreram – it lies on the supinator

In the distal part it travels sequentially over pronator teres àFDS (radial side) à FPL

In the distal forearm – Approx. 7-8cm proximal to the wrist it emerges between BR & ECRL – pierces the deep fascia.

After emerging from BR it winds around radius. Travels over (crosses) the tendons of APL & EPB.

Passes through anatomical snuff box, over the extensor retinaculum and then divides into four or five dorsal digital nerves.


The branches of radial nerve?

Near axilla –

Medial muscular branches – medial and long head of triceps

Cutaneous branches -Posterior cutaneous n of arm (arises in axilla)

In the groove –

Posterior muscular branches – medial and lateral head of triceps

Cutaneous branches – @ the start of groove (originating almost just after first muscular branches) a branch of radial n penetrates lateral head of triceps and overlying fascia and then splits into these two nerves –

Posterior cutaneous n of forearm

Lateral cutaneous n of arm

Lateral muscular branches – branches given after radial nerve, penetrates lateral I/M septum – BR & ECRL

Branches before entering supinator –

  1. ECRB & Supinator

After emerging from supinator –

  1. Short muscular branches – EDC, ECU, EDM

Two long muscular branches –

  1. Medial – EPL & EIP
  2. Lateral – APL & EPB


Sequence of innervation of muscle by radial nerve?

In order of innervation from proximal to distal (helps in guiding the recovery process) –

  1. BR
  2. ECRL
  3. ECRB ↔ supinator
  4. EDC
  5. ECU
  6. EDM
  7. APL
  8. EPL
  9. EPB
  10. EIP

High or low radial nerve injury?

When injury occur above the elbow there is loss of almost all the function of radial n – this is called high radial nerve injury.

When the injury is distal to the elbow, so that only PIN is injured. In this case innervation to BR, ECRL, ECRB (variable) is preserved and hence wrist extension is preserved. When wrist extension is preserved its called Low radial nerve injury.


The sensory distribution of radial nerve?

In the arm – posteriorly and inferior lateral

In the forearm – posterior

In the hand – radial aspect of half of dorsum of hand, proximal portion of dorsum of radial 3 and ½ finger (excluding the tip)


The deficit that you will notice in radial nerve injury?

In motor loss there will be –

  1. Loss of finger extension at MCPJ
  2. Loss of wrist extension
  3. Loss of thumb extension and abduction
  4. Loss of elbow extension if nerve to triceps if also injured

In sensory, there will be loss noted in –

  1. 1st dorsal web space- also known as the autonomous zone of radial sensory nerve.
  2. Lateral 3 & ½ fingers (except distal phalanx)
  3. Posterior aspect of forearm

Surface marking of radial nerve ?

Mark points –

First point – lateral wall of axilla – lower limit

Second point – junction of upper 1/3rd and lower 2/3rd of line joining lateral epicondyle and insertion of deltoid

Third point – in front of elbow joint below level of LE approx 1 cm lateral to insertion of biceps brachii.

1st point to 2nd point – oblique course in radial groove.

2nd point to 3rd point – anterior compartment course.

In forearm –

4th point – junction of upper 2/3rd and lower 1/3rd of line along lateral border of forearm lateral to radial artery.

5th point – anatomical snuff box

3rd point to 4th point – radial nerve is straight

4th point to 5th point – radial nerve curves backwards.


Planning for nerve injury – nerve exploration vs nerve repair vs tendon transfer?

Nerve grows @ 1mm/day with 30 days of latency period.

In case of closed fracture its prudent to wait till the expected(calculated) time of recovery. Nerve exploration to be done if no recovery seen. if more than 3-6 months has passed from expected time of recovery without any recovery.

If more than 16-18 months has elapsed since time of injury then directly planned for tendon transfer.


When do you time the tendon transfer?

There are two approach for tendon transfer-

“Early” tendon transfer – tendon transfer done simultaneously with nerve repair or before the expected time of reinnervation of muscle.

“Conventional” or late tendon transfer – when reinnervation of most proximal paralysed muscles (BR & ECRL) fails to occur by three months after the expected time of reinnervation.

In early tendon transfer there can be –

“Limited” transfer – which is PT –> ECRB only

  1. Provides for internal splintage (eliminates need for external splintage) while the nerve is recovering,
  2. Provides immediate restoration of power grip (by stabilizing the wrist)
  3. If the nerve recovers it works as a helper by adding power of a normal muscle to innervated muscle.

Complete set of transfer (advocated by Brown) –

This is reasonable approach in case where prognosis of nerve repair is poor –

  1. Nerve gap >4cm
  2. There is large wound or extensive scarring or skin loss over the nerve.

Bevin advocated directly proceeding to tendon transfer without attempting nerve repair – benefit of reduced time of disability. This has not been well accepted.


Historical perspective of development of tendon transfer in radial nerve palsy?

First transfer was described by Franke – FCU to EDC.

Followed by Capellen – FCR to EPL

First complete set of transfer was given by Sir Robert Jones (1906)

  1. PT  –> ECRB & ECRL
  2. FCU –> EDC III-V
  3. FCR –> EPL, EIP, EDC II

He subsequently modified it in 1921 (Jones II)

And used FCR to additionally to EPB & APL

  1.  PT –> ECRB & ECRL
  2. FCU –> EDC III-V

Starr was firs to use PL to EPL transfer and left one wrist flexor intact.

Zachary convincingly proved that it’s desirable to leave at least one wrist flexor intact.

In 1949, Scuderi refined PL to rerouted EPL transfer.

These studies resulted in what is called “Standard” set of transfer –

  1. PT to ECRB
  2. FCU to EDC II-V
  3. PL to rerouted EPL

Brand proved that FCU should not be used as it is too strong, too short excursion and is prime ulnar stabilizer of wrist. He then, along with Starr described FCR transfer (which was used instead of FCU) –

  1. PT to ECRB
  2. FCR to EDC II-V
  3. PL to rerouted EPL

Boyes reasoned that FCU is a more important wrist flexor to preserve than FCR because the normal axis of movement of wrist movement is dorso-radial to volar-ulnar (a dart-throwing type of movement).

Boyes also reasoned that wrist flexors (FCU & FCR) (33mm) has inadequate excursion compared to finger extensors (50mm), and it’s better to use FDS which has better excursion (70mm).

Boyes described Superficialis transfer

  1. PT to ECRB & ECRL
  2. FDS IV to EDC
  3. FDS III to EIP & EPL
  4. FCR to APL & EPB.


Aims to achieve by tendon transfer in radial nerve palsy?

Aim is to achieve –

  1. Wrist extension
  2. MCPJ extension
  3. Thumb abduction and extension


The principles of tendon transfer?

  1. One tendon , one transfer
  2. Straight line of pull
  3. Similar amplitude of excursion
  4. Adequate strength (muscle to be transferred should be atleast >85% of its normal strength)
  5. Supple joint
  6. Synergistic muscle
  7. Expendable donor

Example of synergistic muscle – wrist flexor with finger extensor & wrist extensor with finger flexors.


Describe the incision and procedure of FCU set of transfer.

Incision –

First incision – directly over the FCU in distal half of forearm longitudinally. Distal end in J-shaped extension to reach PL.

FCU is transected just proximal to pisiform and freed up as far as possible through that incision.

Second incision – begins 2 cm below the medial epicondyle and angles across the dorsum of proximal forearm directed towards Lister tubercle.

Deep fascia overlying the FCU muscle is incised. Fascial attachments of FCU is completely freed up .

Upper limit of dissection of FCU muscle is 2 inches from its proximal origin where its nerve supply enters.

Third incision – begins on the volar-radial aspect of mid-forearm, passes dorsally around the radial border of forearm in the region of insertion of PT and then angles back on the dorsum.

Tendon of PT is identified in the volar aspect – followed to its insertion on the radius –tendon insertion is freed with a cuff of periosteum around 2-3 cm – muscle tendon unit freed up proximally – PT then transferred around the radius, superficial to BR and ECRL to be inserted to ECRB just distal to musculocutaneous junction .

Through dorsal incision – Kelly’s clamp is passed around the ulnar border to grab FCU and pulled into dorsal wound. (FCU muscle belly may be required to be trimmed if too bulky)

EPL is identified àdivided at its musculotendinous junction à rerouted out of Lister’s canal towards the volar aspect of wrist across anatomical snuffbox à PL transected at the wrist –muscle-tendon unit freed up proximally to allow for straight line of pull.

FCU can alternatively be passed through a window in interosseous membrane.

FCU is sutured to EDC tendons by weaving through all four EDC tendons in end to side fashion at an angle of 45° just proximal to retinaculum.


How will be the tension in tendons adjusted?

1st suture will be PT to ECRB – to be sutured with wrist in 45° extension with PT in maximum tension.

2nd suture is FCU to EDC – to be sutured with wrist in neutral position, with FCU in maximum tension with full extension at MCPJ.

After these two sutures – there should be full flexion of fingers with wrist extended and – full extension of digits with wrist flexed.

Final suture is PL to EPL. Both tendons are sutured under resting tension with wrist in neutral position.

Reconstruction is checked again for full movements – finger flexion with wrist extension & finger extension with wrist flexion.


Post-op care following tendon transfer?

Long term splint for immobilization –

  1. Forearm in – 15-30° pronation
  2. Wrist – 45° extension
  3. MCPJ – slight flexion – 10-15°

Thumb in – maximum abduction and extension

Remove sutures after around 6-7 days

Remove cast at 4 weeks – start physiotherapy.


Potential problems after FCU repair?

Excess radial deviation – removing the only remaining ulnar deviator can lead to radial deviation of hand, especially if ECRL is functioning well (PIN only palsy.). this is also more aggravated if PT to ECRL transfer has been done, less so if PT to ECRB transfer.

Solution –

Avoidance – if preoperatively there is already radial deviation present (PIN only palsy) – avoid FCU transfer.

After transfer – reposition ECRL insertion – i) into ECRB; ii) attach PT to ECRB & ECRL and then detach ECRL; iii) detach from 2nd metacarpal- reroute and inset into 3rd and 4th  metacarpal bone (Tubiana).

Absence of PL –

Solution – i) Use superficialis transfer; ii) include EPL into FCU to EDC transfer ; iii) include EPL, EPB, APL into FCU to EDC transfer; iv) Use BR (if low radial n palsy) to EPL; v) Use FDS III or IV.


Highlights of Superficialis transfer?

Incision –

Long incision on volar side of the radial aspect of mid-forearm.

Expose PT and ECRB

Remove PT with 2-3 cm of periosteum and interwoven into ECRB.

Exposure of FDS (ring and middle) –

Through transverse incision in distal palm or at base of each finger.

Tendon divided proximal to chiasma- freed up and delivered into forearm.

@ Level just proximal to pronator quadratus, two incision made of size 1 x 2 cm in I/O membrane.

“J-shaped” incision in dorsum of distal forearm –

Transverse limb from radial styloid to ulnar styloid. Vertical limb extends proximally along ulna.

Bring out FDS through I/O membrane. FDS of long finger passed radial to profundus mass and FDS of ring finger passed on ulnar side of profundus mass.

FDS III – attached to EIP & EPL

FDS IV – attached to EDC.

Setting of tension – an assistant holds wrist in 20° extension with fingers and thumb held in a fist, until all transfers are done with reasonable tension.

Transverse incision at base of thumb – free FCR tendon –-> pass it dorsally –-> attach to APL (preferably only to APL or with APL & EPB both).


FCR transfer highlights?

Incision –

Straight longitudinal incision in volar forearm on radial side in distal half b/w FCR & PL.

Both tendons identified, transected near their insertion, freed up to middle of the forearm.

Longitudinal incision on dorsum – extending just distal to retinaculum to mid forearm.

FCR passed around radial border of forearm through subcutaneous tunnel.

EDC tendons are identified and divided at musculotendinous junction – withdrawn distally superficial to intact extensor retinaculum to a point over distal radius and sutured to FCR

Adjusting the tension – wrist and MCPJ in neutral position – FCR sutured in maximum tension.

PT to ECRB & PL to rerouted EPL as described for others.


Nerve transfer option for radial nerve injury.

Median nerve to radial nerve

Fascicles of FDS or FCR to PIN & ECRB.

  1. FDS to ECRB
  2. FCR to PIN

Indications –

  1. Very proximal nerve injury – where proximal stump is not available for repair, or even if available regeneration will take a very long time.
  2. Avoiding an area of scarring
  3. Nerve injury presenting in delayed fashion
  4. Partial nerve injury – presenting with well defined motor function deficit.
  5. Level of injury is unclear (idiopathic, radiation induced injury)



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