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Boutonneire Deformity

The deformity

  • Flexion at PIPJ
  • Extension at DIPJ
  • Extension at MCPJ

Pathology is at PIPJ alone.

It’s more of an aesthetic problem than functional – as the patient can still make fist and grasp objects

Deformity is characterized by –

Central slip dysfunction – either due to injury or attenuation secondary to synovitis (from inflammatory disorder such as RA)

Triangular ligament stretches over time – allowing the lateral bands to migrate volar to the PIPJ axis of rotation so that they become flexor of PIPJ and extension of DIPJ.

Ruptured central slip also allows the force from the lumbricals and interossei to be transmitted directly to distal phalanx resulting in DIPJ extension.

Classification –

Nalebuff’s classification –

Stage I – Mild – PIP extension lag that is passively correctable with some DIPJ flexion limitation.

Stage II – moderate – PIPJ flexion deformity >40 ° that may or may not be passively correctable

Stage III – Fixed – Fixed PIPJ flexion deformity with joint destruction

Burton’s classification –

Stage I – supple, passively correctable deformity

Stage II – fixed contracture with contracted lateral bands

Stage III – fixed contracture with joint fibrosis, collateral ligament and volar plate contracture

Stage IV – stage III plus PIPJ arthritis

Treatment –

Passively correctable deformity is managed by –

Splinting to achieve full PIP joint extension – by means of serial casting, splinting, or dynamic splinting. After full PIP joint extension is achieved it is maintained in this position for at least for 6 to 12 months.

During whole of this time DIP joint active and passive flexion exercise is done.

If full passive PIP joint extension is not achieved through non-operative means then – surgical release of contracted collateral bands or volar capsulotomy are done.

If full passive PIP joint extension is achieved but there is active extension lag then – there are multiple surgical procedure for correction.

Fixed deformities with joint destruction are managed by – PIP joint arthrodesis

Curtis staged reconstruction of boutonneire deformity –

These operation relies on full passive mobility of PIPJ preoperatively.

Surgery is performed under local anesthesia.

After release at each stage, PIPJ is actively extended by patient and surgery proceeds to next stage if full extension is not achieved.

Stage I –

Lazy “S” incision made centered over PIPJ laterally.

Transverse retinacular ligament is freed distally and proximally and

Tenolysis of extensor tendon performed.

If full extension is achieved then the operation stops

Stage II –

If full extension is not achieved then TRL is transected, allowing the lateral bands to swing dorsally.

If full extension is achieved after this then the MCPJ is splinted in 70° of flexion and PIPJ & DIPJ splinted in 0° for 1 week followed by dynamic PIPJ splinting.

Stage III –

If there is still 20-degrees or lesser extensor lag after stage II then – distal Fowler tenotomy is performed.

A “step-cut” lengthening of the lateral bands to prevent a mallet finger. Or the extensor mechanism can be obliquely transected just distal to the triangular ligament.

If full extension is present, then operation stops.

Stage IV –

If extensor lag after stage II is more than 20 degrees then step III can be skipped and operation proceeds directly to stage IV.

The central tendon is dissected free and advanced about 4 to 6 mm into a drill hole in the dorsal base of the middle phalanx. The lateral bands, now slack, are loosely sutured to central tendon.

After surgical correction –

PIPJ is stabilized in extension with K-wire.

DIPJ is kept free and active ROM exercises is ordered.

PIP joint ROM exercises begun after 3 weeks with intermittent splinting

Curtis stage reconstruction –

  • Stage I – Tenolysis of extensor mechanism
  • Stage II – Release of TRL
  • Stage III – Fowler tenotomy of distal extensors
  • Stage IV – Central slip reconstruction

Acute central slip injury –

Central slip rupture alone will not cause boutonneire deformity and hence acute central slip injury does not present as boutonneire deformity.

In acute stage, Elson test should be done to diagnose central slip injury in suspected cases.

If lateral bands are also cut over PIPJ or if triangular ligament is also injured allowing volar migration of lateral band then classical boutonneire deformity occurs with PIPJ extensor lag.

Untreated central slip disruption usually present after 2-3 weeks as triangular ligament stretches and lateral band migrate volarly.

Treatment of acute central slip injury –

Splinting or pinning PIPJ in full extension for 6 weeks with active DIPJ flexion exercise hourly

Central slip injury with avulsion of piece of bone.

Small piece of bone and minimally displaced – splinting for 6 weeks

Large piece of bone and displaced >2mm – K-wire fixation

Small or comminuted fragment – excision of fragment and tendon repaired directly to bone using pull-out suture or suture anchors.

“Pseudoboutonneire” deformity

PIPJ flexion contracture without DIPJ extension

Cause is usually due to collateral ligament injury typically following PIPJ hyperextension injury – resulting in collateral ligament and volar plate scarring.

Lateral bands and central slip remains competent.

Treatment – is aimed at decreasing PIPJ flexion contracture by dynamic splinting or serial static casting.

Terminal tendon tenotomy (Distal Fowler or Dolphin tenotomy) –

Surgery aims at operatively creating a “mallet finger” – this would decrease the extensor tone at the DIP joint thus allowing DIPJ flexion. This procedure will also result in proximal migration of extensor mechanism and hence increasing the extensor tension at PIP joint.

This procedure is designed for patient with – full passive PIPJ extension.

It is contraindicated in patient with a fixed PIP joint flexion deformity.

A dorsal incision is made over middle phalanx and the extensor mechanism is divided transversely over the junction of its middle and proximal thirds, distal to the triangular ligament.

Swan Neck Deformity (SND)

The deformity

Hyperextension at PIPJ

Flexion at DIPJ

Flexion at MCPJ


Possible causes of swan-neck deformity may involve any of the joints.

Site wise cause –


Synovitis of joint à leading to attenuation of volar plates and TRL (Transverse retinacular ligament) à allowing dorsal translocation of lateral bands & Destruction of FDS insertion àLeading to hyperextension of PIPJ

Hyperextension at PIPJ leads to tightening of FDP tendon and loss of tension in lateral bands à leading to DIPJ flexion

Over time adhesions develops leading to fixed deformity


Synovitis of MCPJ à causes weakening of insertion of long extension on proximal phalanx à causing force to be transmitted to base of proximal phalanx à leading to PIPJ hyperextension

Synovitis also leads to weakening of volar plates à cause subluxation of MCPJ – leading to adhesion and later shortening of intrinsic muscles – further contributing to PIPJ hyperextension.


Rupture of extensor tendon (due to trauma or synovitis) – leads to proximal migration and relaxation of lateral bands.

Extensor power is then concentrated on central slip à resulting in PIPJ hyperextension and SND

Wrist –

Synovitis causes – carpal collapse, carpal supination & ulnar tranlocation

Carpal collapse – leads to relative lengthening of long flexors and extensors à allowing intrinsics to overpower their action à leading to hyperextension at PIPJ and then to SND

Causes –

DIPJMallet finger (rupture of extensor tendon)
PIPJVolar plate laxity
Dorsal migration of TRL
FDS rupture
MCPJMP joint volar subluxation
Intrinsic muscle tightness
Weakening of insertion of long extensors on proximal phalanx
Wrist jointCarpal collapse

Classification –

Feldon et al

Type I – PIPJ – flexible in all position

Type II – PIPJ – flexion limited in certain position

Type III – limited flexion in all positions

Type IV – stiff joint with poor radiographic appearance

Nalebuff classification –

Type I – full PIPJ flexibility without intrinsic tightness

Type II – PIPJ flexible but with P joint volar subluxation and associated intrinsic tightness

Type III – motion of PIPJ limited by extensor mechanism but with radiographic preservation of joint surface

Type IV – stiff PIP joint with intrarticular joint destruction

Treatment –

Type I –

Can be managed non-operatively – by Splinting with Silver ring

Operative management –

If primary pathology at DIPJ – Mallet finger – DIPJ arthrodesis

If pathology at PIPJ level –

Flexor tenodesis @ PIPJ


Distally based slip of FDS

Littler’s ORL reconstruction

Free tendon graft (Spiral ORL reconstruction)

Type II –

In addition to above also require –

Intrinsic release

MCPJ reconstruction or MP implant arthroplasty

Type III –

In addition to above – PIPJ manipulation is required

Lateral band release

Central slip release or lengthening

PIPJ dorsal capsulotomy

Type IV –

PIPJ fusion or arthroplasty

Summary of treatment options for SND

TypeSite wise treatment required
I Dermodesis FDS sling (flexor tenodesis) Littler’s ORL reconstructionFusion
IIIntrinsic releaseAs for type IFusion
IIIAs for type I Plus MCPJ reconstruction as neededAs for type I Plus PIPJ manipulation(dorsal capsulotomy) Skin release Lateral band release Central slip release or lengthening Check flexor tendonsFusion
IVAs for type IIIAs for type III Plus Arthroplasty or fusionFusion

ORL (Oblique Retinacular ligament) –

ORL was described by Landsmeer hence a/k/a Landsmeer ligament

Originates – from flexor sheath at volar aspect of PIP joint and

Inserts – dorsally into terminal tendon

ORL thus connects flexor mechanism to extensor mechanism.

It tightens during PIPJ extension and results in DIPJ extension

ORL reconstruction –

Littler’s ORL reconstruction –

Ulnar lateral band is divided proximally and

Re-routed palmar to axis of PIPJ rotation using Cleland ligament as fulcrum and

Secured to flexor tendon sheath

Lateral band now act as ORL

Thompson’s Spiral ORL reconstruction –

Free tendon graft is used.

Tendon graft is placed through gauzed hole in distal phalanx and directed in spiral fashion over middle phalanx, deep to neurovascular bundle, over the flexor sheath and transversely through base of proximal phalanx

Graft tension is adjusted with PIPJ and DIPJ in neutral extension.

Proximal end is secured with button or hemoclips or both.

Active motion is allowed 3 weeks post-op.

Kleimen modification of Spiral ORL reconstruction –

Axial K-wire used to keep DIP in neutral and

Oblique K-wire to keep PIPJ in 10-15° of flexion.

Proximal pin removed at 3 weeks

DIP pin removed at 4.5 weeks

Followed by splinting of DIP for 1.5 weeks in extension

Secured the tendon graft to dorsal distal phalanx with 4-0 Bunnell steel pull-out wire

Proximal juncture was attached to palmar flexor sheath with non-absorbable suture.

FDS sling –

Distally based slip of FDS can be sutured to leading edge of A1 pulley or can be secured to bone at the base of proximal phalanx.

Lateral band release –

Lateral band release done through two parallel incision and released from central slip and now are slide volar to the condyle.

Central slip tenotomy or lengthening –

Relies on mature terminal tendon

Procedure is done usually 6-12 months after the injury.

The procedure results in proximal migration of extensor mechanism and thus correct “the slack” induced by elongation at the terminal tendon.

Finger is exposed by midlateral incision centered over PIPJ

Transverse retinacular ligament is incised

Freer elevator is inserted under the extensor mechanism proximal to the central slip and underneath the lateral bands distal to central slip.

The insertion of central slip is visualized under the extensor mechanism, the insertion is divided by sliding a scalpel from proximal to distal underneath the extensor mechanism and active extension of DIP joint attempted.

A dorsal view of extensor mechanism will not reveal any discontinuity.

This technique can correct extension lag of DIPJ up to 35°.

Triangular ligament is not damaged and hence boutonneire deformity will not occur.

Management of hand burn


Frequently involved in patient sustaining burn >50% TBSA

Frequently ignored as area seems less compared to total burn area.

Management –

Assess burn depth

1st degree – superficial

2nd degree superficial – pink, moist, painful and blanches on pressure and blistering

2nd degree deep – more whitish and dry appearance (waxy), does not blanches on pressure

3rd degree – full thickness – thick leathery skin, thrombosed vein

1st degree – heals within 2-3 days

2nd degree superficial – heals within 7 -10 days

2nd degree deep – heals within 14-21 days

3rd degree burn – does not heal by its own

Wounds that are unlikely to heal within 14 days should be managed by early excision and grafting.

1st degree and 2nd degree superficial burn – spontaneous healing

2nd degree deep and 3rd degree burn – excision and grafting

Initial management –

Gentle cleaning of the wound – of foreign material and loose skin.

Blisters are deflated with sterile needle.

Burn wound depth is assessed.

Wound is dressed with moist non-adherent dressing and topical antimicrobial.

Hand is immobilized with splint with –

Wrist in – mid dorsiflexion

MCPJ in 90° flexion

IPJ in full extension

Full range of movement is done between two dressings or splint be removed and fingers moved both actively and passively.

Alternatively, hand can be covered with antibiotic cream and placed in surgical gloves to allow continuous movements of hand.

Hand is kept in elevated position.

Acute hand burn – pathophysiology

Palmer skin – is thick, glaborous and attached to bone by fibrous septa

Dorsal skin – is thin and loosely attached to underlying structure.

Post burn edema cause –

Significant swelling on dorsum, leading to unphysiological joint positions.

Significant pressure on vessels on palmer side and median nerve in carpal tunnel.

Pressure in palm can cause arterial insufficiency and swelling in dorsum can compromise venous return – this combination causes compartment syndrome of intrinsic muscle.

In the stage of edema if hand is unsupported the wrist gets flexed, MCPJ hyperextended and PIPJ flexed.

Collateral ligaments are lax when MCPJ is hyperextended and if stiffness occurs in this position, then contracted ligaments resists correction.

Boutonneire deformity –

When the PIPJ is flexed and if central slip gets attenuated or if skin over PIPJ dorsum gets thin – boutonneire deformity occurs.

Swan-neck deformity –

If intrinsic muscle suffer compartment syndrome – swan-neck deformity and 1st web space contracture develops.

Early surgery for burn

Intermediate and full thickness burn require excision and grafting – it is done as early as possible.

Technique of “tangential excision” is useful. (Janzekovic, 1970)

Thin layers of tissue are excised sequentially until the all non-viable tissue is removed and underlying viable tissue is reached, evidenced by punctate bleeding.

This is done under tourniquet control using Humby knife.

Bleeding is confirmed after tourniquet release.

Hemostasis is achieved by cautery or wrapping the area.

The area is then skin grafted.

Palm – full thickness skin graft

Dorsum – split thickness skin graft (unmeshed)

Excision and grafting is done in PBD 4 (when patient has recovered from post burn shock)

Grafting is delayed in case of infected burn.

STSG is managed post operatively with closed dressing. (Open dressing is also efficacious in managing STSG in hand)

Hand is placed in splint.

Dressing is usually done within 48 hours – any subgraft collection is removed by rolling to the edge or by releasing the fluid using 18G needle.

Motion of hand can be started after 2-3 weeks when graft uptake is good.

Till then hand is kept in “functional position” – wrist in mid-extension, MCPJ in flexion, IPJ in extension.

Splint is continued even when movement is started and during period of inactivity and during night.

Excision of burn and flap cover –

Limited area can be covered

Definitely full thickness burn

Overlying critical areas, such as bone, joint, tendon etc.

Escharatomy in hand –

In full thickness circumferential burn or deep partial thickness burn causing circulatory compromise.

Significant increase in survival of finger have been found after escharatomy.

Escharatomy is started proximally in arm depending upon involvement.

If proximal escharatomy does not make the fingers warm then the escharatomy is continued to the hand and digits.

In the digits, escharatomy is done –

On ulnar side of index, middle, ring and little finger and

On radial side of thumb.

Escharatomy is extended proximally on dorsum of hand.

Aftercare of burned hand –

Hand physiotherapy

Daily supervised – aim to decrease edema, increase range of movement and prevent scar hypertrophy

Pressure garments –

Advocated by Park and Larson

Continuous controlled pressure of 25mm Hg above the capillary pressure

Custom made pressure garments are to be used

Pressure garments must be worn all the time except exercise

They must be worn for at least 6 months

Pressure garments are most effective in the early stage and hypertrophic scar is responsive to pressure in the first 3 – 6 month

Compliance for pressure garments is poor with active (even small) wound – so stable wound healing should be quickly achieved.

Silicon –

Perkins initiated its use

Mode of action is unclear, but it is effective in controlling HTS

Probably acts by decreasing evaporation from skin and maintaining optimum hydration

It is applied for few months

Silicon gel application allows early pain free movement of stiff joint

When applied over healed skin graft it prevents contraction of graft.

When applied over HTS, it softens it and makes them more amenable to pressure therapy

Post burn hand deformities

Hypopigmentation – treated by excision and skin grafting

Hypertrophic scar – pressure garments use. If a/w contracture, release of contracture relieves pressure in the scar and scar settle down.

Contracture –

Contracture release is done when the scar has reached equilibrium – evidenced by absence of scar tenderness and redness

This usually occurs by 3-6 months

Release and SSG of immature scar often leads to recurrence.

Matured scars are managed with incision release and grafting.

Incision release – eliminates tension in the scar and favourably influences the maturity of residual scar.

HTS – focal and linear – incisional release and SSG

HTS – large and diffuse – excision and SSG

Positions of hand

Position of comfort –

Wrist – volar flexion

MCPJ – hyperextended

IPJ – variable degree of flexion

Thumb – adducted and extended

Anticlaw or “safe” position –

Wrist – 35° extension

MCPJ – 40-70° flexion

IPJ – extension

Thumb – abducted and internally rotated (towards palm)

Contractures –




Dorsal contracture –

Most common

Due to scant tissue burn is usually deep

McCauley classification of burn contracture –

Grade I – symptomatic tightness. ROM – normal. Underlying architecture – normal

Grade II – ROM – mildly decreased. Architecture – normal. ADL – normal

Grade III – functional deficit present. Architecture early changes.

Grade IV – loss of hand function. Significant distortion of normal architecture.

[Tightness-Decreased ROM-function Deficit –function Loss]

Subset of grade III & IV

  1. Flexion contracture
  2. Extension contracture
  3. Both flexion and extension contracture

Treatment –

Grade I & II – conservative

Grade III & IV – surgical

Webspace contracture –

Depending on the contracture –

Z plasty

Double opposing Z plasty

Jumping man or five flap Z plasty

Intrinsic muscle release

Release and SSG

Joint deformities 

MCP joint –

Classification (Graham et al) –

Type 1 –

MCP flexion <30° with wrist flexion

MCP flexion >30° with wrist extension

Type 2 –

MCPJ flexion very limited with wrist flexion

MCPJ flexion <30° with wrist extension

Type 3 –

Fixed deformity

[Type I – >30 with WE; type II – <30 with WE; type III – Fixed]

Structures involved –

Type 1 – scarring limited to skin (also called dermodesis effect)

Type 2 – scarring involves – skin, dorsal capsule, dorsal apparatus, collateral ligament

Type 3 – extensive skin scarring, atrophy of intrinsic muscles, joint incongruity, dorsally subluxated or dislocated MCPJ

[SCJSkin – Capsule – Joint]

Surgery –

Type 1 – release and SSG

Type 2 – release of skin and deeper tissue capsulotomies with coverage with SSG or flap. Aims to achieve MCPJ flexion of 90° and maintained with K-wire or splint

Type 3 – arthrodesis of MCPJ with 10-45° of flexion

Recommended angle of arthrodesis –

Angle of arthrodesis at different joints

[PIPJ = MCP +5]

[2nd to 5th   + 5][2nd is 20]

PIP joint

PIPJ is the most frequent affected deep structure in burn hand

MC is flexion deformity

Classification (Stern et al) –

Type I – limited to skin

Type II – additional capsule contracture

Type III – joint involvement (decreased joint space, articular incongruity)

               [SCJSkin – Capsule – Joint]

Treatment –

Type 1 – skin release and SSG

Type 2 – additional capsulotomy and SSG or flap

Type 3 – joint arthrodesis

Boutoniere deformity

Thin overlying skin and scanty subcutaneous tissue over PIP joint – gives little protection to the structure of joint

Destruction of skin and extensor apparatus can result in Boutoneire deformity

Methods of correction of boutoneire deformity –

I – splinting

II – lateral band transposition

III – tendon graft

IV – arthrodesis

DIP joint

Rupture of weakening of the extensor tendon – results in Mallet finger.

If this a/w PIPJ hyper extension – Swan-neck deformity occurs.

Managed by wedge excision, arthrodesis or digital amputation

Amputation –

Vascular status of the digit should be assessed early in acute burn

Certain maneuvers can improve circulation in the early acute phase –

Elimination of edema



Digital amputation is managed as similar to other amputations.

For reconstruction –

Thumb and index are most important

Thumb reconstruction options –



Distraction lengthening

Toe to thumb transfer

Osteoplastic thumb reconstruction

Summary –

Management of burned hand starts with acute stage of injury –

Elimination of edema

Adequate positioning

Adequate early resurfacing and

Prompt physiotherapy

These are crucial in maintaining hand function

Post burn deformities require multidisciplinary approach and treatment based on functional assessment and the formulation of realistic goals.

FDMA flap

First described by – Kuhn & Holvetich

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

Lister described  axial flap on 2nd DMA

Earley  described – 2nd DMA flap

Maruyama & Quaba – Reverse 2nd DMA flap

Anatomy –

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

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

Anomaly –

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

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

Both these anomaly precludes raising the FDMA flap

Second DMA-

More consistent anatomy than FDMA

Also generally larger than FDMA

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

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

FDMA flap –

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

Blood supply – type A, fasciocutaneous

Nerve supply – dorsal sensory branch of radial and ulnar nerve

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

Raising the flap –

Mark the course of FDMA using hand help pencil Doppler.

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

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

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

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

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

Proximal dissection over 1st web space –

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

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

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

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

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

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

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

Donor site over index finger dorsum is covered with FTG.

Motion of thumb is permitted on day 10.

Fully dissected FDMA flap

Second DMA flap –

Skin flap can be raised in two ways –

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

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

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

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

Second DMA with retrograde flow (Maruyama pattern) –

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

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

Distally based dorsal hand flap (Quaba pattern) –

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

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

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

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

Proximal limit of the flap is – wrist joint.

Flap can reach – just distal to PIP joint.


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

Both soft tissue and skeletal elements are enlarged

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


It is uncommon – incidence – 0.9%

Most cases are sporadic. No evidence of inheritance.

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

It can occur in association with other anomalies


Flatt’s classification

Type 1 – gigantism and lipofibromatosis

Type 2 – gigantism and neurofibromatosis

Type 3 – gigantism and digital hyperostosis

Type 4 – gigantism and hemihypertrophy


Most common is- Type 1.


Type 1 –

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

Type 2 –

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

Type 3 –

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

Type 4 –

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


[Bilateral involvement – type 2]

[No nerve involvement – type 3]

[Intrinsic muscle involvement – type 4]

[Contracture – type 4]


Macrodactyly a/w lipofibromatosis –

Noted at birth or within 3 yrs

Growth of affected digits is disproportionate – progressive macrodactyly

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

Usually unilateral

May affect more than one digit

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

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

Radial digits deviated radially

Ulnar digits deviates ulnarly

If two digits involved then they deviate divergent.

Enlarged thumb are typically – abducted and extended.

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

Radiograph – enlarged skeleton with

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

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

Compression neuropathy may result

Thickening of flexor sheath – may result in trigger finger

Syndactyly seen in – 10% cases.


Macrodactyly a/w neurofibromatosis –

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


Hyperosteotic macrodactyly –


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

Radiology confirms diagnosis – showing periarticular osteochondral masses.


Macrodactyly can be part of a broader gigantism –

Segmental gigantism – affecting only a part of one limb

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


Other syndromes a/w digital enlargement –

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



Not known

Possible explanation – nerve territory oriented macrodactyly

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

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


Macroscopic finding –

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


Histology –

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



Aim – functional and aesthetic improvement

Counseling –

Inability to establish normal digit

Need for multiple surgeries


Surgical procedure aimed at –

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


Limiting digital growth –

Most reliable method is – Epiphysiodesis

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


Epiphysiodesis –

Can be achieved by –

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

Timing of epiphysiodesis –

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

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

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

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

Complications –

Joint stiffness

Excessive bone formation at the site of physis

Secondary angulation, in case of incomplete phseal destruction

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


Reducing the digits/ soft tissue debulking –

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

Approach through – midlateral incision or Brunner’s incision

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


Skeletal reduction –

Can be achieved by either –

  • Narrowing or
  • Shortening

Narrowing –

Burring the side of bone or

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


Shortening –

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



It is the simplest procedure.

Many procedures aims at preserving nail while shortening the digit.

  1. Barksy procedure – nail on palmar pedicle

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

  1. Tsuge procedure

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

  1. Nail island flap – by Rosennberg

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

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



Amputation –

It is the ultimate reduction procedure

Option for single digit or showing progressive uncontrollable growth

Ray amputation/transmetacarpal amputation with digit transposition

Digit transfer from foot or pollicization to create thumb

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


Summary of treatment of macrodactyly –

Limitation of growth

  1. Digital nerve stripping
  2. Epiphysiodesis

Digit reduction –

Soft tissue reduction – debulking

Skeletal reduction – terminalization

Methods of terminalization –

Repositioning of the nail unit on a shortened skeleton

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

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

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

Thumb macrodactyly

Metacarpophalangeal arthrodesis

Millesi procedure

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







Skin Banking – short notes

Need for skin banking –

Large burn areas.

Donor sites not available.

Homografts can work as temporary dressing.


Methods of skin storage –

  1. Refrigeration
  2. Deep freezing or cryopreservation


Refrigeration –

Most common method of storage.

Skin kept at 4 ° C.

Preservation maximum up to 3 weeks.

But, best used within 1 week.

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

Dilute homologus serum,

Tissue culture medium,

Balanced salt solution

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


Deep freezing or cryopreservation

Cooling of tissue to ultra-low temperature.

Cryoprotective agents are used.

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

Stored in deep freezer or liquid nitrogen

Liquid nitrogen is used for cooling.

Cryoprotective agents are used to protect cells from disintegrating.

Cryoprotective agents used are –

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

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

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


Freeze drying or lyophilization

Grafts is rapidly cooled and then

Water is removed by sublimation

Tissue is then vacuum sealed

Sterilized by gamma radiation

Stored at room temperature

Tissue is non-viable and used as biological dressing


Cadaveric skin banking

SSG harvested from refrigerated cadavers within 24 hours of death.

Consent is taken

Age limit – 12-60 yrs

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

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

Skin harvested using dermatome

Strips between 0.25mm – 0.35mm is harvested.

Skin tissue sample sent for streptococcus, pseudomonas, staphylococcus culture

Graft with more than 10 organism is discarded.


Cryo-preservation :

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

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

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

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

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

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

Otherwise, it is deep freezed.

Freezing can be –

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

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

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


Increasing the cell viability –

After harvest, skin cell viability decreases due to –

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


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



For use of stored grafts, it is rewarmed

Rewarming is done @ 50-70°C per minute

Microwave @ lowest setting

Hot saline bath @ 42°C

After rewarming – graft is to be used within 2 hours

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

Faster rewarming is better.


[During preservation slower cooling is better]

[During rewarming faster is better]


Future –

Improving the homograft “take”

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





Keratinocyte culture – short notes

Types of keratinocyte culture –

  1. Autologous
  2. Allografts


Autologous keratinocyte culture –

Patient selection –

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

Contraindications – Cutaneous tuberculosis, AIDS, Hepatitis B

Age and inhalational injury are not contraindications.

Biopsy –

Minimum delay from biopsy to culture plating.

Less than 48 hours.

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

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


Keratinocytes isolation –

Sample is washed

Differential trypsinization is done

Separated epidermal component is centrifuged and cell suspension obtained


Technique of culture –

Described by Green

Keratinocytes are now routinely cultured on feeder layers

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

Murine fibroblast line or human fibroblasts are used.

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

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

Hams F12 medium

Hydrocortisone (0.4 mg/ml)


Transferrin (5mg/ml)

Adenine (8 x 10-4 mmol/l)

Triiodothyronine (2 x 10-2 mmol/l)

Cholera toxin (10-10 mmol/l)

Fetal calf serum (10%)


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

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

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

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




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

Suprabasal cell produce paraclones (with least growth potential).

Holoclones gradually develop into meroclones during culture.

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

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

Cultures are seeded/reseeded with attenuated 3T3 cells.

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

Epidermis is then taken on paraffin gauze.

Cultured epithelial autografts usually takes 2-3 weeks.

Detached epithelium is assessed for viability.

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


Patient preparation –

Meanwhile patient burn wounds in serially debrided.

Patient condition in stabilized.

Excision is done as required.



Grafting is done as soon as cultured graft arrives in OT

Carrier gauze is directly applied to the prepared bed.

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

1st dressing is done after 5 days.

Then alternate day.

Carrier gauze is removed at 6-8 days.


Drawbacks of cultured keratinocytes –

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

Healed wound are thin and stiff

Lacks durability

Scarring and wound contraction are often

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

Fragile graft – leads to ‘delayed losses’.


Future –

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

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

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

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


Epidermal allograft culture –

Easily available

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










Leg defect

History –

Particular of patient-

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

Chief complain-


Past history

Personal history

Family history


Physical examination-

CCO well oriented to TPP

Attitude of the patient-

Pulse- rate rhythm volume character compared to other site


BP- mmHg arm supine/sitting

CVS- S1S2 heard no murmur

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

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


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


LOCAL examination-

Examination of ulcer-

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

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

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

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

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

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

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


Attitude of the limb-

Patient is lying in supine position/ sitting with

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

Limb externally / internally rotated. Apparent limb shortening.



Findings of inspection confirmed on palpation.

Wound is …………X ……… 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 … 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 …… 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 ………… of plantar flexion………… 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 ………… of plantar flexion………… of dorsal flexion on right side and …………… of plantar flexion………… 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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