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.

Platelet Rich Plasma ( PRP )- Short Note

PRP is an autologous biologically active product prepared from fresh blood of patients using one or two stage centrifugation. It is also called as platelet rich concentrate or platelet releasate or plasma gel. It has platelet concentration of around 1-1.5 million/microlitre which is 4-5 times the normal platelet concentration in blood.

PRP is a good source of growth factors such as IGF-1 , PDGF, VEGF, EGF, cytokines and plasma proteins. The alpha granules in platelet degranulate to release growth factors in high concentration on activation. The supra-physiological concentration of biologically active substances modulate inflammation and tissue repair. It stimulates cell survival, proliferation and differentiation. It promotes vascularisation and angiogenesis. It increases differentiation of fibroblasts promoting collagen synthesis and remodelling. It also increases myofibroblasts in wound promoting contraction. PRP with its regenerative and wound healing properties has wide application in plastic surgery. PRP being autologous carries decreased risk of hypersenstivity , immunogenic reaction and disease transmission.


  1. Hair Restoration in Androgenic Alopecia
  2. Facial and skin rejuvenation in patients with acne scars, atrophic scars, wrinkles, striae distensae
  3. With fat grafting to increase fat survival
  4. Chronic wounds like diabetic ulcers, venous ulcers to promote healing
  5. To promote flap survival
  6. To promote bone graft survival and healing

Preparation of PRP

Steps of PRP prepearation are as follows:

  1. Patient history: Platelet medications such as aspirin and statins affect platelet function. Any history of platelet function disorder, bleeding disorder, anticoagulation therapy, thrombocytopenia, hepatitis , local infection, hemodynamic instability and tendency for keloid formation are contra-indications for PRP therapy.
  2. Blood Collection: Around 20-60 ml of fresh blood sample is drawn preferably in single venepuncture using wide bore needle to avoid trauma to platelets, degranulation and loss of growth factors.
  3. Centrifugation: The force, time duration and number of cycles of centrifugation affect the concentration of PRP. Longer and more forceful centrifugation push platelets further down in sediment layer and potentially affect growth factors and cellular integrity. There is no standard method of centrifugation with some proposing single step centrifugation and others two step process i.e slow centrifugation followed by fast centrifugation. There is no protocol set for speed and duration of centrifugation and hence a lot of variation is seen with regard to this. This has led to lack of standardisation of PRP preparation and quality control.

The initial slow centrifugation at 1500 rpm for 15 min separates the erythrocytes at bottom, from lighter plasma with buffy coat at interface in middle and top layer of platelet poor plasma. Plasma and buffy coat are aspirated and centrifuged at high speed (3200 rpm for 10 min) when platelet separate as pellet with platelet poor plasma at top. Platelet pellet is resuspended in small volume of plasma for final product. In case of single step centrifugation at 3200 rpm for 15 min, out of the three layers the middle layer is used for PRP after removal of supernatant.

Commercial kits are also available for preparing PRP.

4. Anticogulation: Some may use the final product immediately. Others may add anticoagulants like sodium citrate, trisodium extract, acid citrate dextrose, heparin to prevent platelet activation and its conversion to fibrin matrix.

5. Activation: Calcium chloride or thrombin is added to reverse anticoagulation and activate platelets before use. 70% growth factors are released within 10 minutes and nearly all growth factors within 1 hour.

6. Injection: usually given in area of pathology in subcutaneous or intradermal plane using 26G to 30G needle.

Types of PRP

Based on platelet concentration and activation of platelets, it can be further classified as platelet rich plasma (PRP) and Platelet rich fibrin (PRF). PRP is liquid platelet suspension which needs activation step to release growth factors either by addition of exogenous factors or may be simply activated by trauma of injection. PRF is in the form of gel. It is activated fibrin matrix and has low platelet concentration. Further both can be subclassified based on leucocytes concentration as leucocyte rich or poor as follows:

  • P-PRP: It is leucocyte poor. It has small volume and minimal fibrin polymerisation.
  • L-PRP: It is leucocyte rich. It has small volume and minimal fibrin polymerisation.
  • P-PRF: It is leucocyte poor. It has larger volume and dense fibrin polymerisation.
  • L-PRF: It is leucocyte rich. It has larger volume and dense fibrin polymerisation.

Leucocytes in PRP are expected to help with their anti-infection properties which is beneficial. Practically we are unable to determine leucocyte content in routine and hence usually general term PRP is used. Usually we get L-PRP and cell separation is needed to process out leucocytes to form P-PRP.

Androgenic Alopecia

PRP enriched with leucocytes in addition to concentrated plasma proteins has shown good results in mild and moderate male as well as female patterned baldness. PRP promotes growth of hair follicles and significantly shortens time of hair formation. PRP promotes angiogenesis in scalp. PRP increases proliferation of dermal papilla cells and induces faster telogen to anagen transition. Bulge cells, inducible stem cells found along the shaft of hair follicle have been found to repopulate hair follicle epithelium and are fundamental to progression of hair cycling. It is these hair follicle stem cells that contain growth factor receptors responsible for hair growth manipulation and molecular pathway regulation. PRP when combined with CD34+ cells also shows good results. Only slight improvement is seen with non activated PRP.

Usually 3 sessions of PRP over 3 months, followed by two session over year has shown satisfactory results. If no improvement is seen in first three months, further attempts of injection are futile. PRP can be injected in areas of thinning i.e usually frontal, vertex and parietal areas. Interfollicular injections are given of about 2ml to 12ml volume i.e 0.1 to 0.2 ml/cm2 of scalp. It is usually given in intradermal plane but can be given in subcutaneous plane after topical local anaesthesia application on scalp for numbing.

Hair traction test, hair density index ,phototrichoscan and scalp biopsy are various methods of gauzing the improvements after PRP therapy. Increased hair density, number of hair follicles and decreased hair on traction test are seen. Increased thickness of epidermis of scalp, vascularisation of scalp between follicle and epidermis and increased ki-67 proliferation index of bulge stem cells and cells of basal layer of epidermis is seen on biopsy. Oil secretion is also improved post PRP treatment. Results are assessed 4 months after last session.

Facial and skin rejuvenation

PRP promotes collagen synthesis and remodelling improving skin elasticity. PRP alone or in combination with fat is injected intradermally in infra-orbital area, nasolabial folds, crow’s feet area, forehead/malar region and pre-auricular region. Also, dermaroller/microneedling/fractional laser followed by application of PRP is used, popular as vampire facials. The pores produced acts as route for penetration of PRP. It leads to improved collagen synthesis and hence skin texture with decreased erythema, edema and post-inflammatory hyperpigmentation. Improved results are seen in patients of acne scars and atrophic scars. Around 2ml of PRP is used at 2 – 4 weeks interval for 4 sessions.

PRF has postulated to yield better results than PRP as it releases growth factors over longer period of time. PRF has been used to treat crow’s feet, wrinkles, tear troughs, suborbital hollows, glabellar furrows, malar augmentation, zygomatic arch enhancement, correction of nasolabial folds and marionette folds as well as acne scars.

Fat Grafting

PRP with its pro-angiogenic, anti-apoptotic and anti-inflammatory properties has been seen to prevent fat atrophy after fat grafting in face. It also improves volume. PRP promotes proliferation and differentiation of stem cells and pre-adipocytes into mature adipocytes. PRP acts as scaffold for adipocytes and adipose derived stem cells(ADSC) retaining them at graft site for longer duration. Fibrin scaffold reduce apoptosis of differntiated adipocytes. When in fibrin clot, ADSC show higher secretion of VEGF and FGF. In vitro, when ADSCs were grown in scaffold of fibrin with adhesion molecules and growth factors, they differentiated into keratinocytes enhancing wound healing. Activated PRP is used for injection. 0.1 to 0.5 ml of PRP is used per ml of fat graft. The adequate concentration of PRP needed for optimal growth of ADSC is still uncertain with several studies stating 5-15% being optimal. Higher concentration of 40-50% PRP can have negative regulatory effect of platelets on fat. In breast fat grafting, no benefit of PRP is seen but higher rate of fat necrosis is seen.

Healing of Chronic Wounds

PRP encourages ADSC to differentiate into fibroblasts and keratinocytes that are crucial cells in wound healing process. PRP also encourages migration of fibroblasts to wound site. Direct infusion of PRP to wound bed and topical application of PDGF have shown positive results in diabetic foot ulcer healing.

Flap Survival

PRP enhances skin flap survival rate. It enhances angiogenesis and reduce the inflammation response to skin flap transplantation. Release of growth factors, platelets, immune activating factors and fibrin help in skin flap survival. Plateletsand fibrin accelerate coagulation and provide a scaffold for skin flap.

Bone grafting

PRP enriched bone grafts have higher bone augmentation, shorter time to bone regeneration, decreased post-operative pain, lower rates of haematoma and edema. An overall superior outcome is seen.

In conclusion, PRP with its wound healing properties, ease of preparation, great safety profile, being minimally invasive in application and showing satisfactory results, is becoming increasingly popular modality of treatment for improved outcomes in plastic surgery.


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).











Gynecomastia, or abnormal breast tissue enlargement in men. The aim of treatment is restoration of a normal male chest contour while minimizing the evidence of surgery and protecting the nipple areolar complex. Although excisional techniques have traditionally been the accepted standard, liposuction has now become established as the prime surgical modality either alone or in combination with more invasive methods. 

Basic science 

Gynecomastia is thought to primarily result from an increased estrogen to androgen ratio since estrogens stimulate breast tissue while androgens antagonize its effects. This hormonal imbalance may therefore arise from an absolute or relative excess of estrogens, or an absolute decrease of androgen levels or their action. 

Etiologically gynecomastia can be physiological or pathological in nature. The former may occur during three different age groups. 

A thorough history is important to determine the underlying cause of gynecomastia  and rule out breast cancer and other tumors. On the other hand, it should be noted that around 25% of gynecomastia cases may be idiopathic. Salient points include patient age, onset and duration of breast enlargement, symp-toms of associated pain, recent weight change, and a systems review with particular attention to possible endocrine and liver abnormalities. Medications and recreational drug use need to ascertained as they may cause 10–20% of gynecomastia cases. 

On physical examination, gynecomastia is usually bilateral and felt as glandular tissue under the nipple areolar complex and extends to a variable size in all directions. It needs to be differentiated from pseudogy-necomastia or lipomastia, which is adipose tissue hypertrophy without glandular proliferation. physical examination should include assessment of secondary sexual development and the thyroid, as well as looking for signs of chronic kidney or liver disease. When examining the genitalia, it is also important to look for any testicular masses or atrophy. Liver enlargement may sometimes be encountered. There  is  no  increased  risk  of  breast  cancer  in  patients with  gynecomastia  when  compared  with  the  unaffected male  population.s  The  exception  is  patients  with  Klinefelter syndrome.  These  patients  have  an  approximately  60  times increased  risk  of breast cancer 

Bio-chemical assessment includes tests for liver, kidney,  and thyroid function; and serum levels of testosterone, prolactin, follicle-stimulating hormone, and luteinizing hormone. Additional tests may be necessary in cases of recent or symptomatic gynecomastia to rule out tumors.2 For example, serum levels of estrogens, human chori-onic gonadotrophin (hCG), dehydroepiandrosterone (DHEA), and urinary 17-ketosteroids. 

Simon et al Classification

2b and 3 types need skin excision ( in same sitting or 4-6 months later). 

Letterman  and  Schuster‘  created  a  classification  system based  on  the type  of correction:  1:  intra-areolar  incision  with no  excess  skin;  2:  intra-areolar  incision  with  mild  redundancy corrected  with  excision  of skin  through  a  superior periareolar scar;  and  3:  excision  of  chest  skin  with  or  without  shifting the  nipple. 

Rohrich  et  al.  in  a  paper  discussing  the  utility  of  ultrasound-assisted  liposuction  in  the  treatment  of  gynecomastia,  developed  the  following  classification:  grade  I:  minimal hypertrophy  (<250  g  of  breast  tissue)  without  ptosis;  grade 2:  moderate  hypertrophy  (250  to  500  g  of breast tissue)  without ptosis;  grade  3:  severe  hypertrophy  (>500  g  breast tissue) with  grade  I  ptosis;  grade  IV:  severe  hypertrophy  with  grade 2 or3  ptosis. 

Types of gynecomastia  

Three  types  of  gynecomastia  have  been  described:  florid, fibrous,  and  intermediate. The  florid  type  is  characterized by  an  increase  in  ductal  tissue  and  vascularity.  A  minimal amount  of fat  is  mixed  with  the  ductal  tissue.  The  fibrous type  has  more  stromal  fibrosis  with  few  ducts.  The  intermediate  type  is  a  mixture  of  the  two.  The  type  of  gynecomatia  is  usually  related  to  the  duration  of  the  disorder.  Florid gynecomastia  is  usually  seen when  the  breast enlargement  is of new  onset  within  4  months.  The  fibrous  type  is  found  in cases  where  gynecomastia  has  been  present  for  more  than 1  year.  The  intermediate  type  is  thought  to  be  a  progression  from  florid  to  fibrous  and  is  usually  seen  from  4  to 12 months. 

Medical management  

Most cases of gynecomastia do not require treatment  as they are benign and self-limiting. Weight loss should be recommended for male patients with pseu-dogynecomastia in the first instance. Medical therapies essentially focus on correcting the imbalance of androgens and estrogens. furthermore, medications are probably most effective during the active, proliferative phase of gynecomastia. In patients with long-standing gynecomastia of over 1 year, medical treatment is often ineffective as the breast glandular tissue progresses to irreversible dense fibrosis and hya-linization. Such cases should be considered for surgical treatment. When treatment is indicated, most patients do not need a trial of medical therapies and are best managed with surgery, which is the mainstay modality. 

Surgical management  

Well-established  surgical  techniques  for  gynecomastia treatment  include  various  forms  of  liposuction,  open glandular  excision,  skin  reduction,  and  combinations  of these. 

General Anesthesia as day care except in patients where excision of skin is planned. All  patients  receive  perioperative  broad-spectrum  antibiotic  prophylaxis  at  general anesthetic  induction. Patients  are  marked  preoperatively  in  the  upright sitting  position  highlighting  the  inframammary  fold, breast  boundaries,  planned  stab-incision  sites,  and  concentric  topography-type  marks  centered  on  the  most prominent  portion  of  the  breast. Infiltration with superwet technique done (300 mg per litre lignocaine). 


Liposuction of Breast is done however residual  subareolar  tissue  is  a  frequently  encountered complication  with  this  technique. SAL  is  not  suitable  for severe  cases  or  in  breasts  with  primarily  fibrous  tissue. It  can  be  effective in  soft  breasts  even  if  large,  but  good  skin  quality  is important  for  later  contraction  and  avoiding  the  need for  skin  resection.  Liposuction  allows  the  achievement of  better  breast  contours  with  minimal  scarring. Cross-tunnel  suctioning  for  larger breasts,  ptotic  breasts,  and  those  with  excess  skin  or well-defined  inframammary  folds  makes  SAL  more effective. The  laterally  placed  incision  in  the  inframammary  fold allows  better  access  for  the  liposuction  to  the  whole breast  laterally  and  medially. Cross-tunnel  suctioning  for  larger breasts,  ptotic  breasts,  and  those  with  excess  skin  or well-defined  inframammary  folds  makes  SAL  more effective.  Such  extensive  cross-suctioning  enables  more consistent  contraction  of  the  skin  and  allows  it  to  redrape with  less  waviness  and  irregularity. A  4.6  mm  or  5.2  mm  Mercedes  cannula  is  used  for  the  initial  suction  employing the  palm  down  and  pinch  techniques. Finer refinement by 3 mm or 3.7 mm Mercedes cannula. Once a  satisfactory  contour  is  obtained,  the  surrounding  fat is  feathered  to  avoid  a  noticeable  saucer  deformity,  and any  well-defined  inframammary  fold  as  determined preoperatively  is  deliberately  disrupted  in  order  to avoid  the  gynecoid  (female)  contour  of  the  breast. When  liposuction  is  unsuccessful  at  removing  all  of  the tissue  required  to  achieve  a  good  result,  the  pull-through technique  is  added.  In  this  technique,  either  the  lateral  or periareolar  incision  is  opened  slightly  (about  1.5  em)  and  the residual  tissue  is  grasped.  The tissue  is  pulled  out through  the wound and removed  with scissors  or  electrocautery 

UAL is more effective for firmer Breast tissue . By  emulsifying  breast  fat,  it is  particularly  useful  for  addressing  dense,  fibrous gynecomastia.  It  has  also  been  suggested  that UAL  results  in  less  postoperative  bruising,  a  smoother breast  contour,  better  postoperative  skin  contraction, and  less  surgeon  fatigue. The  well  described  UAL  endpoints73  are determined  by  loss  of  tissue  resistance,  aspirate  volume, blood-tinged  appearance  of  the  aspirate,  and  planned treatment  time. UAL induces skin contraction also. 

Different Canula types

Open approach  

Liposuction  is frequently  not  effective  for  very  glandular  tissue,  small discrete  breast  buds,  and  body  builders  as  the  latter have  large  amounts  of  glandular  tissue  with  little  fat. Open  excision  via  an  inferior  periareolar  approach11 is  the  traditional  approach.  Various  other  incisions have  been  described  such  as  circumareolar,  periareolar, transareolar, circumepithelial. The  liposuction  serves  a number  of  purposes  such  as  pretunneling  to  facilitate resection,  reducing  bleeding  and  bruising,  and  partially  breaking  down  the  breast  tissue.  After  liposuction  the  tissue  can  be  resected  via  a  number  of  access  incisions. At  least  a  1  cm  disc  of  breast  tissue is  left  under  the  areola  to  prevent  a  depression  of  the nipple  areolar  complex. Excess skin may be reduced in same or different sitting according to the acceptance of scar by the patient. 

Skin  reduction There  are  a  number  of  procedures  used  to  reduce excess  skin  in  gynecomastia. In  patients  with  obvious  skin  excess  or  very  large breasts,  skin  reduction  techniques  should  also  be planned  usually  at  the  same  time  as  the  open  excision of  the  breast  tissue  or  as  a  second  stage,  a  minimum  of 4–6  months  later.  There  is,  however,  no  consensus  on when  and  how  to  undertake  skin  resection. 

Post operative  

Drains  are  not  routinely  used,  except  for  large  resections or  when  skin  reduction  is  performed,  such  as  in  post massive  weight  loss  patients. 

Possible Complications
Perioperative summary for patients

Craniofacial Microsomia

Craniofacial microsomia represents 2nd most common congenital anomalies after cleft lip and palate. It is seen as 1 in 3500 live births. Males are more affected than females (M:F = 63:39).


  1. Teratogens: Retinoic acid exposure is frequently associated with CFM.
  2. Stapedial artery haemorrhage.
  3. Genetic: CFM is also known to be transmitted as genetically as autosomal dominant and autosomal recessive trait both. Chromosome 10 deletion has been known to cause CFM. However even after genetic transmission as AD, the incidence is low possibly due to
    • maternal gene resistance
    • genomic imprinting
    • mosaicism

Face develops from first and second branchial arches. Several theories have been put to explain the development of face. Older ones by Dursy and His ( Failure of fusion), Stark ( Theory of mesodermal migration and penetration). latest being the neuromeric theory by Michael H Carstens. The timeline and sequence of of facial prominence coming together is given somewhere else.

Structures involved with CFM

  1. Ear.
  2. Mandible.
  3. Maxilla and rest of facial skeleton (zygoma, temporal bone, orbit, frontal bone.)
  4. Soft tissues.
  5. Facial Nerve.

There is Domino effect during development of face as explained by Pruzansky. Mal development is one area of face leads to involvement of other structures of the facial skeleton.

Mandible on the affected on the same side as the the rest of the structures. Condyle is hypoplastic or absent. Ramus is either hypoplastic or absent. The body curves upwards and joins the hypoplastic ramus. Chin is deviated to the same side.

Mandible on the normal side has increased gonial angle, increased horizontal dimensions and represents compensatory growth.

The posterior wall of glenoid fossa is partially formed by the tympanic portion of the temporal bone which also provides bony portion of EAC in normal developed ear. In CFM this posterior wall is deficient and cannot be identified. Ramus is hinged on a flat surface in such cases.

Occlusion cantt is deviated upwards on the affected side. Ramus and condyle are short as previously said.

Floor of the maxillary sinus and nose are higher on the affected side. Base of the skull may also be elevated. The styloid process is smaller. Mastoid process is flattened with reduced or absent pnematization. Zygoma is underdeveloped and malar eminence is flattened.

Soft tissue bulk is also reduced on the affected side as compared to the affected side. Lateral pterygoid is weakened on the affected side hence it shifts the mandible to the normal side. Hence on testing lateral pterigoid one finds inability to shift the jaw to the unaffected side or deviate the chin to affected side on forceful protrusion.

Facial nerve (Marginal mandibular being most commonly involved) involvement seen in many cases. Fourth, 5th, 6th cranial nerves may also be involved in CFM. Parotid hypoplasia is sometimes seen with patients having facial nerve involvement.

One of the contrasting feature of CFM from TMJ ankylosis is ability to open the mouth. In TMJ ankylosis the ability to open the mouth is greatly reduced.

Soft tissue, skeletal framework, ear and facial nerve involvement

Diagnostic criteria for Craniofacial microsomia (Cousley)

  1. Ipsilateral Mandible and Ear defects
  2. Asymmetrical mandibular or ear defects in association with either
    • positive family history of CFM ortwo or more indirectly associated anomalies. (anomalies not related either in terms of development, field or function to CFM).

Differential Diagnosis

  • TMJ ankylosis
  • Rombergs disease (click here)
  • Hemifacial Atrophy(Click here)
  • Condylar hyperplasia
  • Treacher collins syndrome.

Diagnosis is helped by clinical evaluation along with CT scans of facial skeleton. Nerve conduction studies may be needed in cases where cranial nerves are involved.

Classification systems

  • Pruzansky grading system
  • Modified Pruzansky system
  • Meurman system of auricle defects
  • Munro and Lauritzen Classification
  • SAT classification
  • OMENS Classification
  • OMENS plus classification

Pruzansky system:

Pruzansky subdivides the ear and the mandible deformities.


  • I a small ramus with identifiable anatomy
  • II a functioning TMJ but with an abnormal shape and glenoid fossa (IIa and IIb as modified by Kaban)
    • IIa  the glenoid fossa is in an acceptable functional position 
    • IIb  the TMJ is abnormally placed and cannot be incorporated in the surgical construction
  • III an absent ramus and nonexistent glenoid fossa

This system has two weaknesses.

• It is possible to have a Pruzansky II with a functioning TMJ but with or without a zygomatic arch and glenoid fossa.
• It is possible to have a Pruzansky III with no condyle and no functioning TMJ with or without a zygomatic arch and a glenoid fossa.

Modified pruzansky Classification (Kaban, Padwa, Mulliken)

  • I Small mandible.
  • IIa Short mandibular ramus of abnormal shape; glenoid fossa in satisfactory position.
  • IIb TMJ abnormally placed inferiorly, medially and anteriorly.
  • III Absent TMJ.

Meurman Classification of ear defects

  • E1 ear (mild hypoplasia and cupping with all structures present).
  • E2 ear (absence of the external auditory canal with variable hypoplasia of the concha)
  • E3 ear (malpositioned lobule with absent auricle).

OMENS classification

  • O- orbit defects (O0-O3)
  • M- mandible defects ( M0-M3)
  • E- Ear defects (E0-E3)
  • N- Nerve defects (N0-N3)
  • S- Soft tissue defects (S0-S3)

OMENS plus is an extension of existing OMENS classification. it includes extracranial manifestations.

SAT classification was put forward by David et al. It includes skeletal (S1-S5), auricle (A0-A3) and soft tissue (T1-T3) categories for classification.

Munro and lauritzen is a 5 part classification used for classification for CFM. OMENS is most frequently used classification system now a days.


There are two school of thoughts regarding pathogenesis of the CFM. The first school of thought believes it to be a progressive disorder where early intervention should be done to minimize the deformity. The second school of thought believes the disease is non progressive with age and the intervention can be delayed till CFM becomes stable. In second case the intervention will be minimal.

As the disease has several components a plethora of procedures are sometimes required in a single patient. Minimal deformity patients may get away with a simple fat grafting.

  • Tracheostomy if sleep apnea in infant.
  • Early Distraction osteogenesis if sleep apnea.
  • Distraction osteogenesis at any age before skeletal maturity achieved. (click here)
  • le fort Osteotomy if skeletal maturity achieved.
  • Fat grafting for soft tissue defects.
  • free flaps for soft tissue defect.
  • FFMT/ Static sling procedures for facial weakness.
  • Dental procedures for occlusion.
  • Ear reconstruction (click here)
Distraction osteogenesis

Algorithms for treatments 


  • Endoscopy (Feeding and respiratory problems) 
  • Mandible deficiency evaluation 
  • Mandible reconstruction (if respiratory deficiency)  
  • pulse oxymetry 
  • Sleep studies 
  • ET or tracheostomy if needed 
  • Gastrostomy if needed (resolves once sleep apnea is corrected) 
  • Removal of ear tags may be done 

Early childhood 

  • Mandible reconstruction (if respiratory deficiency)  
  • type III: Autogenous reconstruction. 
  • type IIA/IIB : Distraction osteogenesis 
  • No soft tissue augmentation. 
  • No orthodontic treatment. 
  • No ear reconstruction. 

Childhood (4-13 years) 

  • Mandible reconstruction (if respiratory deficiency of dysmorphogenesis)  
  • type III: Autogenous reconstruction. 
  • type IIA/IIB : Distraction osteogenesis. 
  • Ear reconstruction 
  • Fat injection 
  • Free flaps 
  • Orthodontic treatment starts at age of 4 years 
  • maxillary arch expansion 
  • mandibular space mantainence 
  • forced eruption of molar  


  • Orthodontic treatment. 
  • le fort osteotomy or BSSO. 
  • Genioplasty. 
Mandibular and maxillary osteotomy

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

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