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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

Dupuytrens’s Contracture


Also called as the benign fibromatosis of the palmar and digital fascia, Dupuytrens’s disease develops in the palmar ligaments causing pathological changes in them.

It is considered to be a genetic disorder with autosomal dominance (Variable penetrance). An altered beta catenin pathway has been implicated in the pathogenesis of the disease.  Common in the 6th decade with males affected more than the females 3:1. The digits more commonly includes the 4th and the 5th.

  • Early presentation associated with high recurrence rates.
  • More prevalent in Diabetics with more complication rates after surgery for dupuytrens.
  • Also associated with smoking, chronic alcoholism, AIDS and vascular diseases.
  • It is a pathologic fibroproliferative disorder.

Diathesis Group by Hueston ( Associated with multiple surgeries and significant hand impairment)

  • Positive history of 1st and 2nd degree relatives.
  • ectopic deposits beyond the palmar surface (knuckle pads, plantar surface, penile tissue like peyronies disease)
  • Early Age younger than 50 years (some say 40 )
  • Bilateral severe radial disease

Relevant Anatomy

Palmar skin is attached to the skeleton by the retention ligaments which keep the Skin in place during processes like gripping and pinch. This connective tissue can be divided into:

  • Digital fascia
  • Palmar fascia
  • Palmar-digital junction fascia

Digital fascia

  • Lateral digital sheath.
  • Superficial fibrofatty palmar/dorsal fascia.
  • Cleland’s ligament (dorsal to neurovascular bundle).
  • Grayson ligament (volar to the neurovascular bundle).
  • **Cleland ligament not involved in the disease process.

Palmar fascia

  • Pretendinous bands.
  • Superficial transverse bands.
  • Vertical septa (these structures are mentioned superficial to deep)

Palmar digital fascia

  • Spiral band.
  • Natatory ligament.
  • Vertical fibre of Legueu and Juvara.
  • ** In digit these attach to proximal portion of Grayson ligament and lateral digital sheath
  • ** In palm they connect the pretendinous bands with the superficial transverse ligaments.

Pathological anatomy

Dupuytrens’s results from deformation of normal anatomic structures (ligaments or bands) to abnormal structures (cords).

  1. Pretendinous aponeurosis changes to pretendinous cords.
  2. Natatory ligament changes to natatory cords (natatory cords contract the web space from side to side and prevents fingers from separating)
  3. Central cord originates from the pretendinous bands and the palmar superficial fibrofatty fascia. This cord causes combined MP and PIP joint contractures.
  4. Similarly lateral cords, retrovascular cords are also formed.
  5. Spiral cords form by 5 separate structures namely pretendinous bands, spiral band of gosset, lateral digital sheath, vertical band and grayson ligament. Natatory ligament not involved with the spiral band.
    • spiral cords pass deep to the neurovascular bundle to reach the side of the finger . Then it passes superficial to the bundle to reach its attachment at the base of the middle phalynx.
    • As it shortens it pulls the neurovascular bundle to midline and in a more superficial position prone to damage during surgery.
  6. Retrovascular ligament itself does not cause a PIP contracture but with lateral cord it can hyperextend the DIP contracture.
  7. Lateral sheath proximally coalesce to form natatory ligaments and the spiral ligaments. They are deficient on the ulnar side of little fingers. But the tendon of ADM can be found pathological in 25% of affected cases. it does not displace neurovascular bundle.
  8. Histology: clinical nodule has a lot of smaller nodules that are non-encapsulated but surrounded by connective tissue and collagen bundles. Predominant cell in early disease is fibroblast making collagen (type 3 instead of type 1). Diseased state one finds  myofibroblasts with smooth muscle actin production.

MP joints usually affected by the pretendinous cords. MP joint of thumb never crosses 30 degrees due to weak pretendinous cord.

PIP joint affected by the following cords in the order as central cord (maximum) followed by spiral and lateral cords (minimum)

DIP joint is rarely involved ( if it gets involved retrovascular and lateral bands are to blame)


Difference between MP and PIP joint contracture

MP joint has a cam like effect with its eccentric centre of orientation relative to the collateral ligaments which are stretched when the joint is flexed. Thus after the release of the contracting cords don’t tether the joints and MP joint easily returns to extension. MP joint contracture more than 30 degrees is an indication for surgery.

PIP joint contractures when present lead to collateral ligament and volar plate shortening leading to some intrinsic contracture even after release of cords. PIP contracture of 20 degrees or progressing is indication for surgery (some say any PIP contracture should be intervened)


  • Functional limitations
  • Measure the angles of each contracture ( especially Dynamic contractures). MP if held in neutral extension maximises the PIP contracture. if MP joint is flexed the recordable PIP contracture is reduced significantly.
  • Quality of overlying skin with nodules in palmar, plantar and penile areas
  • History of Carpal tunnel syndrome.
  • clinical diagnosis only: no biopsy needed, no imaging needed until arthritis present.
  • joint movements in sequence from thumb to little, deviation of fingers from axis.
  • Kaplan line


There is no surgical cure for Dupuytrens’s disease. Surgical goal is to improve the hand function. Surgery does not eliminate the disease. Options include

  • Needle fasciotomy
  • closed fasciotomy
  • open fasciectomy
  • enzymatic fasciectomy (experimental)

Scenario 1: No contracture, no pain : tightness only no contractures. These patients are treated with reassurance and follow up at regular interval for progression of the disease.

Scenario 2: Painful Palmar nodules: Don’t excise, put steroids. excision only if it is associated with trigger finger or causing unrelenting pain.

Scenario 3: Dorsal Dupuytrens’s disease: Diathesis Group by Hueston, monitoring or excision as per patients choice.

Scenario 4: Established contractures

  1. Needle aponeurectomy: cord weakened by percutaneous needle insertion and broken by finger manipulation. It is more effective for MCP than PIP.
    • may cause some neuropraxia, tendon rupture and frequent recurrences.
    • recurrence rate expected high as diseased tissue not removed.
    • Put local Anesthetic only superficially so that the digital nerve is spared and patient can warn paresthesia indicating needle is close to the nerve.
    • 25 gauge needle used to perforate the cord in multiple region along the area of 5 square mm up and down motion not sawing action.
    • After multiple passes finger manipulates and ruptures cord.
    • Release any residual cords if any.
    • useful when skin is not involved.
  2. Limited fasciectomy: standard treatment.
    • Removal of diseased cord.
    • Amount of tissue removed is individualised.
    • splintage till suture removal (10-14 days) followed by active physiotherapy several times a day.
    • Night splintage continued later on 3-4 months.
    • reduces recurrence rates, more durable
    • May cause nerve or vessel injury (level of palmar digital nerve and vessel should be identified), hand stiffness
    • long rehabilitation time.
  3. Dermatofasciectomy and SSG:
    • More aggressive procedure.
    • especially for PIP
    • Skin involved, Residual disease or young patients.
    • FTG applied.
  4. Distraction : for PIP contracture where distractor used for stretching the soft tissue. After adequate stretching limited fasciectomy is done and distractor removed.
  5. Collagenase (clostridium histolyticum)
    • effective for MCP joint
    • hand injected with medicated injection as per label.
    • hand manipulated after 24 hours to rupture the coed
    • bruising and swelling are expected
  6. McCash technique: open fasciectomy without skin closure.
  7. Segmental open fasciectomy.

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