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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.

Platelet Rich Plasma ( PRP )- Short Note

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

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


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

Preparation of PRP

Steps of PRP prepearation are as follows:

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

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

Commercial kits are also available for preparing PRP.

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

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

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

Types of PRP

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

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

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

Androgenic Alopecia

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

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

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

Facial and skin rejuvenation

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

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

Fat Grafting

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

Healing of Chronic Wounds

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

Flap Survival

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

Bone grafting

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

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


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

Both soft tissue and skeletal elements are enlarged

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


It is uncommon – incidence – 0.9%

Most cases are sporadic. No evidence of inheritance.

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

It can occur in association with other anomalies


Flatt’s classification

Type 1 – gigantism and lipofibromatosis

Type 2 – gigantism and neurofibromatosis

Type 3 – gigantism and digital hyperostosis

Type 4 – gigantism and hemihypertrophy


Most common is- Type 1.


Type 1 –

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

Type 2 –

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

Type 3 –

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

Type 4 –

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


[Bilateral involvement – type 2]

[No nerve involvement – type 3]

[Intrinsic muscle involvement – type 4]

[Contracture – type 4]


Macrodactyly a/w lipofibromatosis –

Noted at birth or within 3 yrs

Growth of affected digits is disproportionate – progressive macrodactyly

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

Usually unilateral

May affect more than one digit

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

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

Radial digits deviated radially

Ulnar digits deviates ulnarly

If two digits involved then they deviate divergent.

Enlarged thumb are typically – abducted and extended.

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

Radiograph – enlarged skeleton with

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

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

Compression neuropathy may result

Thickening of flexor sheath – may result in trigger finger

Syndactyly seen in – 10% cases.


Macrodactyly a/w neurofibromatosis –

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


Hyperosteotic macrodactyly –


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

Radiology confirms diagnosis – showing periarticular osteochondral masses.


Macrodactyly can be part of a broader gigantism –

Segmental gigantism – affecting only a part of one limb

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


Other syndromes a/w digital enlargement –

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



Not known

Possible explanation – nerve territory oriented macrodactyly

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

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


Macroscopic finding –

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


Histology –

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



Aim – functional and aesthetic improvement

Counseling –

Inability to establish normal digit

Need for multiple surgeries


Surgical procedure aimed at –

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


Limiting digital growth –

Most reliable method is – Epiphysiodesis

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


Epiphysiodesis –

Can be achieved by –

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

Timing of epiphysiodesis –

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

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

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

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

Complications –

Joint stiffness

Excessive bone formation at the site of physis

Secondary angulation, in case of incomplete phseal destruction

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


Reducing the digits/ soft tissue debulking –

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

Approach through – midlateral incision or Brunner’s incision

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


Skeletal reduction –

Can be achieved by either –

  • Narrowing or
  • Shortening

Narrowing –

Burring the side of bone or

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


Shortening –

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



It is the simplest procedure.

Many procedures aims at preserving nail while shortening the digit.

  1. Barksy procedure – nail on palmar pedicle

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

  1. Tsuge procedure

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

  1. Nail island flap – by Rosennberg

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

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



Amputation –

It is the ultimate reduction procedure

Option for single digit or showing progressive uncontrollable growth

Ray amputation/transmetacarpal amputation with digit transposition

Digit transfer from foot or pollicization to create thumb

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


Summary of treatment of macrodactyly –

Limitation of growth

  1. Digital nerve stripping
  2. Epiphysiodesis

Digit reduction –

Soft tissue reduction – debulking

Skeletal reduction – terminalization

Methods of terminalization –

Repositioning of the nail unit on a shortened skeleton

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

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

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

Thumb macrodactyly

Metacarpophalangeal arthrodesis

Millesi procedure

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







Skin Banking – short notes

Need for skin banking –

Large burn areas.

Donor sites not available.

Homografts can work as temporary dressing.


Methods of skin storage –

  1. Refrigeration
  2. Deep freezing or cryopreservation


Refrigeration –

Most common method of storage.

Skin kept at 4 ° C.

Preservation maximum up to 3 weeks.

But, best used within 1 week.

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

Dilute homologus serum,

Tissue culture medium,

Balanced salt solution

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


Deep freezing or cryopreservation

Cooling of tissue to ultra-low temperature.

Cryoprotective agents are used.

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

Stored in deep freezer or liquid nitrogen

Liquid nitrogen is used for cooling.

Cryoprotective agents are used to protect cells from disintegrating.

Cryoprotective agents used are –

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

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

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


Freeze drying or lyophilization

Grafts is rapidly cooled and then

Water is removed by sublimation

Tissue is then vacuum sealed

Sterilized by gamma radiation

Stored at room temperature

Tissue is non-viable and used as biological dressing


Cadaveric skin banking

SSG harvested from refrigerated cadavers within 24 hours of death.

Consent is taken

Age limit – 12-60 yrs

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

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

Skin harvested using dermatome

Strips between 0.25mm – 0.35mm is harvested.

Skin tissue sample sent for streptococcus, pseudomonas, staphylococcus culture

Graft with more than 10 organism is discarded.


Cryo-preservation :

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

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

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

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

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

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

Otherwise, it is deep freezed.

Freezing can be –

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

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

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


Increasing the cell viability –

After harvest, skin cell viability decreases due to –

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


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



For use of stored grafts, it is rewarmed

Rewarming is done @ 50-70°C per minute

Microwave @ lowest setting

Hot saline bath @ 42°C

After rewarming – graft is to be used within 2 hours

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

Faster rewarming is better.


[During preservation slower cooling is better]

[During rewarming faster is better]


Future –

Improving the homograft “take”

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





Keratinocyte culture – short notes

Types of keratinocyte culture –

  1. Autologous
  2. Allografts


Autologous keratinocyte culture –

Patient selection –

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

Contraindications – Cutaneous tuberculosis, AIDS, Hepatitis B

Age and inhalational injury are not contraindications.

Biopsy –

Minimum delay from biopsy to culture plating.

Less than 48 hours.

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

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


Keratinocytes isolation –

Sample is washed

Differential trypsinization is done

Separated epidermal component is centrifuged and cell suspension obtained


Technique of culture –

Described by Green

Keratinocytes are now routinely cultured on feeder layers

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

Murine fibroblast line or human fibroblasts are used.

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

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

Hams F12 medium

Hydrocortisone (0.4 mg/ml)


Transferrin (5mg/ml)

Adenine (8 x 10-4 mmol/l)

Triiodothyronine (2 x 10-2 mmol/l)

Cholera toxin (10-10 mmol/l)

Fetal calf serum (10%)


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

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

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

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




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

Suprabasal cell produce paraclones (with least growth potential).

Holoclones gradually develop into meroclones during culture.

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

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

Cultures are seeded/reseeded with attenuated 3T3 cells.

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

Epidermis is then taken on paraffin gauze.

Cultured epithelial autografts usually takes 2-3 weeks.

Detached epithelium is assessed for viability.

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


Patient preparation –

Meanwhile patient burn wounds in serially debrided.

Patient condition in stabilized.

Excision is done as required.



Grafting is done as soon as cultured graft arrives in OT

Carrier gauze is directly applied to the prepared bed.

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

1st dressing is done after 5 days.

Then alternate day.

Carrier gauze is removed at 6-8 days.


Drawbacks of cultured keratinocytes –

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

Healed wound are thin and stiff

Lacks durability

Scarring and wound contraction are often

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

Fragile graft – leads to ‘delayed losses’.


Future –

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

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

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

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


Epidermal allograft culture –

Easily available

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











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

Basic science 

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

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

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

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

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

Simon et al Classification

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

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

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

Types of gynecomastia  

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

Medical management  

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

Surgical management  

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

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


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

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

Different Canula types

Open approach  

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

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

Post operative  

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

Possible Complications
Perioperative summary for patients

Craniofacial Microsomia

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


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

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

Structures involved with CFM

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

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

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

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

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

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

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

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

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

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

Soft tissue, skeletal framework, ear and facial nerve involvement

Diagnostic criteria for Craniofacial microsomia (Cousley)

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

Differential Diagnosis

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

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

Classification systems

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

Pruzansky system:

Pruzansky subdivides the ear and the mandible deformities.


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

This system has two weaknesses.

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

Modified pruzansky Classification (Kaban, Padwa, Mulliken)

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

Meurman Classification of ear defects

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

OMENS classification

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

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

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

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


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

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

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

Algorithms for treatments 


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

Early childhood 

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

Childhood (4-13 years) 

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


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

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