Severe Necrotizing infection of the Perineum: Beyond Necrosectomy

Author Information

Abdihakin M.1, Saidi H1,2

  1. Aga Khan University Hospital

  2. University of Nairobi

Corresponding author:

Dr. Abdihakin M., P.O. Box 30270, 00-100, Nairobi, Kenya.


The evolution of systemic inflammatory response syndrome (SIRS) to septic shock is a continuum that can be stemmed using dedicated and early goal directed interventions. In the setting of necrotizing soft tissue infection, mortality approaches 100% when debridement is delayed or altogether omitted. Volume depletion, vasodilatation, myocardial depression, high metabolism and attendant global hypoxia that precede multi- organ dysfunction syndrome (MODS) and mortality need to be addressed early, avoiding delays in the emergency department, hospital ward, or the intensive care unit. Early goal -directed therapy denotes the use of interventions such as administration of crystalloid solutions, vaso-active agents, blood transfusion and inotropic agents to achieve specific targets, namely, a central venous pressure of 8 – 12 mmHg, a mean arterial pressure of 65 – 90 mmHg, a urine output of > 0.5mls/kg/hr, a hematocrit of >30% and a central venous oxygen saturation of > 70% in a patient who is intubated, sedated and paralysed.We present an illustrative case of the management of severe Fournier’s gangrene and how a series of misadventures at home, the A & E and the wards contributed to the inevitable demise.


Fournier’s Gangrene is a fulminant necrotizing fascitis of the penis and scrotum (1) with reported mortality rate of 20% which peaks to 39% when debridement is delayed (2). Upon diagnosis, the disease also warrants an aggressive multimodal approach, which includes hemodynamic stabilization and broad spectrum antibiotics (3). This management strategy may assist to stem the transition to multiple organ dysfunction and mortality. Indeed, initiation of fluid resuscitation, transfusion, and vasoactive support at the A & E reduces mortality significantly (4 ). This advantage is lost when the interventions are intiatied at the intensive care unit.


MX was a 53 year old male who presented with five days history of pain, swelling and foul discharge of the scrotum. He had fever, nausea and anorexia but reported no history of cough, night sweats, weight loss or contact with a person with TB. His past medical history was not significant. Two weeks earlier, he used herbal medications to treat a painful leg swelling. He had a history of heavy alcohol use.

On examination, he was wasted, dehydrated and had generalized lymphadenopathy but was not pale, or jaundiced. He was hypotensive (BP 90/50 mmHg), tachycardic (pulse 137/min) and febrile (temperature 38.50C). The respiratory rate was 16/min and saturations were 98% on room air. Perineal findings included bilateral ischiorectal abscesses and a swollen, erythematous, crepitant scrotum with a discharging blister (Fig 1).


The lower limb was excoriated, hyper-pigmented with nonpitting edema, but no signs of inflammation. Respiratory system exam revealed vesicular breath sounds bilaterally with no crepitations. The abdomen was moving with respiration and was soft and non-tender on palpation and bowel sounds were heard and normal.

MX was subsequently admitted with a diagnosis of sepsis secondary to Fournier’s gangrene, resuscitated with crystalloid fluids, catheterized for output monitoring and started on ceftriaxone 1gr twice daily, metronidazole 500mg three times daily and morphine infusion titrated to the pain experienced. The response to resuscitation was a blood pressure of 95/60mmHg, pulse of 90/min and SPO2 of 98%. Initial investigations showed leucocytosis (WBC-12.78 x 109(N-92% L-4%) and a low platelet count (84 x109/l ), hyponatraemia (Na+-127 mmol/l) and elevated urea (15.7mmol/l). The rest were normal (haemoglobin 14.5g/dl, K+-3.5mmol/l, Cr-101mmol/l, blood sugar 4.7 mmol/l, urinalysis ( 2-4 WBC/HPF, no bacteria, blood+). He was HIV negative.

A scrotal ultrasound revealed a viable left testis with the right obscured by surrounding air. Early on the second day, he was alert but clinically dehydrated. Urine output ranged between 80 and 100mls/hr. He was still tachycardic and hypotensive (table 1) with a respiratory rate of 24/min and saturation 100% on 3L of oxygen. Arterial blood gas analysis showed a PH of 7.3 and base excess of -12.2 (table 1)


He was taken to the operating room, induced with ketamine/midazolam and debrided under face-mask. Necrotic tissues involving the ischioanal fossae, the right and left groins, scrota and base of the penis were excised to bleeding surfaces (Figures 1 and 2) and thoroughly irrigated.


Both testes were healthy. He had a nadir blood pressure of 73/39mmHg and urine output > 30mls/hr during the operation. He was adequately reversed, and was breathing spontaneously. A re-look surgery was planned for two days later. Post-operatively, he was nursed in the high dependency unit.

At admission to this unit, his blood pressure was 88/40 mmHg, RR 18/min and saturations 92% on 5L of oxygen. Shortly after, the systolic blood pressure fell to 73 mmHg. This was attributed to the morphine infusion. One hour later however, he became unresponsive (GCS of 5/15) and developed deep sighing respirations. The CVP was 9cmH2O, output 30mls/hour despite an input of 200mls/hr. The arterial blood gases showed worsening acidosis (table 1). He was commenced on Norepinephrine 4mcg/ min, Naloxone 0.2 mg, fluid boluses of haesteril and transferred to the ICU. During the initial stay in ICU he was rousable (GCS 10/15) but remained hypotensive (BP 87/68mmHg) with a pulse rate of 105/ min, respiratory rate of 15/min and saturations of 100% on 4L of oxygen. The groin wound discharged pus. Dopamine was added to the Norepinephrine and enteral feeding considered. Several hours later however, he desaturated to SPO2 88% and was tachypnoiec with grossly reduced air entry bilaterally. He was then intubated and mechanically ventilated on SIMV mode, PS of 16, TV of 450, PEEP of 5, FiO2 of 60% and Rate of 18. He had a low urine output of 15-20 mls/hr. His arterial blood gases were pH-6.69 pCO2-29.8 pO2- 141 HCO3-3.4 BE -30.4. He developed hypoglycemia of 2.1mmols/L and his WBCs were 32.7 x 109(N 92%). His haemoglobin was 9.0g/dl and platelets of 42 x 109/L. Inotropic support was maximized and he received a stat dose of Sodium Bicarbonate. The antibiotics were changed to Imipenem 2gr twice daily for a broader coverage as culture results were awaited and a renal review was requested for dialysis due to the severe metabolic acidosis. He was commenced on intermittent haemodialysis. Dialysis was stopped 3hrs after commencement due to a further drop in the blood pressure (30/12 mmHg). He became hypothermic (temperature 340C).There was a mild improvement in the blood gasses after dialysis (table 1).

MX remained hypotensive on the second postoperative day and developed generalized edema with cold and cyanosed peripheries. CVP remained 13cmH2O with urine output of 4mls/hr. His pupils were dilated and non-reactive to light. The chest x-ray findings were consistent with ARDS. Several hours later, he went into bradycardia and did not respond to resuscitation.


The causes of death in Fournier’s gangrene include severe sepsis, coagulopathy, acute renal failure, diabetic ketoacidosis, and multiple organ failure (3). Diabetes mellitus, alcoholism, neurological deficits, malignancy, advanced age and immunosuppresion are well-known predisposing factors for Fournier’s gangrene (6).

The diagnosis is mainly clinical and the application of investigations such as ultrasonography in its diagnosis is complicated (5,7). Upon diagnosis, the disease warrants an aggressive multimodal approach, which includes hemodynamic stabilisation, broad spectrum antibiotics, and emergency surgical debridement (3). This article highlights the management of the case presented in the context of critical care. MX presented five days after the onset of perineal symptoms. By the time of presentation his disease had evolved from SIRS to severe sepsis. The events after admission illustrate how quickly the continuum moved to MODS and death. Several poor prognostic factors were already at play on admission. His advanced age, heavy alcohol use and extent of the severe necrosis