Fournier’s Gangrene

Fournier’s Gangrene

This paper is dedicated to my mentor Dr. P. Rajan, Associate Professor of General Surgery at Calicut Medical College. An excellent teacher, a great surgeon, an astute clinician and above all a wonderful human being, he was instrumental in my taking up general surgery as my post graduation subject. This paper is a humble tribute of a grateful student to his teacher who taught him the principles in the management of this life threatening condition.

Fournier’s Gangrene Fournier’s gangrene has remained an enigma to surgeons and urologists alike. Controversies do exist regarding its aetiology, definition and even its management. But nobody can dispute the fact that it remains a true surgical emergency with a high mortality rate. Previously termed as idiopathic scrotal gangrene, it was first reported by Baurienne in 1764. In 1884, Jean Alfred Fournier, a Parisian dermatovenereologist described fulminant gangrene’ with these features. Sudden onset in a hitherto, healthy young man, rapid progression to gangrene, absence of a definite cause Fournier’s gangrene is a synergistic, necrotising fasciitis which has been defined as a suppurative bacterial infection of the perineal, rectal or genital area which leads to thrombosis of small subcutaneous vessels and with infection, results in the development of gangrene of the overlying skin.

An Etiology: Anorectal – haemorrhoids, fistula in ano, rectal perforation , tumours, Urological – catheterisation, circumcision, paraphimosis, post coital, post TURP, urethral stricture, vasectomy, Dermatological – furuncles, scabies, Gynaecological – bartholin’s abscess, septic abortion, hysterectomy, episiotomy… (There is an entity called female fournier’s gangrene!) The usual causative organisms isolated are e.coli, klebsiella, pseudomonas, micro aerophilic streptococci,staphylococci, clostridia, bacteroides etc Liberation of toxins R Perifascial spread Aerobic-Anaerobic Synergism Obliterative endarteritis R Gangrene

Predisposing factors: Diabetes mellitus, HIV infection, Inflammatory bowel disease, Alcoholism, Trauma, Intravenous drug abuse, Poor hygiene, low socioeconomic status.

Clinical Features: Patient usually complains of fever, scrotal pain and swelling. On examination, there will be scrotal erythema (fig.1), oedema, tenderness, fetid odour, crepitus etc followed by sloughing away of the scrotal skin (fig.2) and shameful’ exposure of the testis. Occasionally, there may be features of gram negative sepsis and the patient might be in shock. fig.1

Investigations: Routine ones including renal function tests and liver function tests, pus culture and sensitivity, proctoscopy and urethrogram (whenever necessary). Skin biopsy, X-ray and USG of the scrotum etc are of academic interest only. In other words, the diagnosis of Fournier’s Gangrene is purely a clinical one.

Principles of Treatment: Haemodynamic stabilization – including correction of shock and adequate hydration. Control of sepsis – usually achieved with parenteral broad spectrum antibiotics pending pus c and s reports. Liberal drainage of the affected area and adjuvant measures – Radical debridement (fig.3) including fasciotomy (fig.4) whenever necessary, catheterisation, urinary and faecal diversion procedures like suprapubic cystostomy or colostomy (wherever appropriate) etc. Very recently, pure , unadulterated honey has been tried because of its bacteriostatic properties. Construction of testicular thigh pouches may be necessary when extensive debridement of the scrotal skin has been done.

Reconstructive procedures – like skin grafting – at a later date. Role of hyperbaric oxygen in the management of this condition is controversial. Poor prognosis is seen in those with advancing age, abdominal wall/thigh involvement, anorectal source, shock/sepsis at presentation, > 5% body surface area involvement, positive blood culture, lack of colostomy, blood urea nitrogen > 50 mg%, Se.albumin < 3.0 mg % and prothrombin time prolonged by > 3 seconds.

Mortality usually results from multiple organ dysfunction syndrome, diabetic ketoacidosis, acute renal failure, severe sepsis, coagulopathy etc and is usually around 40%.

Changing Trends: The pattern of this condition has changed quite a lot since Fournier’s original description. It is no longer idiopathic – as a portal of entry can be identified in nearly 95% of cases. It has a less abrupt onset. It is often seen in the elderly. It can occur in females also. It has a polymicrobial aetiology. Diabetes mellitus is a major predisposing factor.

Address for correspondence:
Dr.Vijay R
PG Trainee in general surgery
C/o Mr.S.V.Venkataraman,
19/1931, Bhajana Kovil Lane,
Chalappuram. Calicut, Kerala. PIN – 673002.
e-mail: [email protected]

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