Necrotising Fasciitis

Necrotising fasciitis is an insidiously advancing soft tissue infection characterized by widespread fascial necrosis. The condition was first described in the scrotum region by Fournier in 1883 (Fournier's gangrene) and as a more generalised condition by Meleney in 1924.

Although it is most often associated with S. pyogenes (group A beta-haemolytic streptococci) infection, this accounts for a minority of cases and most infections are polymicrobial, with both anaerobic and aerobic bacteria frequently present.^1,2 Organisms spread from the subcutaneous tissue along the superficial and deep fascial planes.

• Necrotising fasciitis is uncommon, but is a cause of severe morbidity and frequent mortality.
• The incidence in the United Kingdom is estimated at 500 new cases each year.³

Risk Factors

• In many cases, there is no association with any underlying factor.
• May develop after skin biopsy, needle puncture sites in intravenous drug abusers and associated with chronic venous leg ulcers, open bone fractures and surgical wounds.⁴
• Other predisposing factors include age over 60, malnutrition, penetrating wounds, diabetes mellitus, alcohol abuse, peripheral vascular disease, renal failure, underlying malignancy, obesity, intravenous drug misuse and immunosuppression.
• However, approximately 50% of cases of streptococcal necrotising fasciitis occur in young, previously healthy individuals.

• The diagnosis is clinical. Necrotising fasciitis can affect any part of the body but the extremities, the perineum, and the truncal areas are the most commonly involved.³
• Patients are very ill with disproportionate pain and only minor skin changes in the early phases.⁵
• Tends to begin with constitutional symptoms of fever and chills.
• Patients may present with some evidence of cellulitis, vesicles, bullae, oedema, crepitus, erythema, and fever.⁶
• The degree of pain may be out of proportion to the physical findings. As the infection progresses, their pain may decrease due to nerve damage.
• After 2-3 days, erythema and vesiculation or bullae develop.

Signs

• From a rapidly advancing erythema, painless ulcers may appear as the infection spreads along the fascial planes.
• A black necrotic eschar may be evident at the borders of the affected areas.
• Metastatic cutaneous plaques.
• In patients with diabetes, crepitus is often evident, as are non-clostridial anaerobic infections.
• Although the following features can occur with cellulitis, they may suggest necrotising fasciitis:
  • Rapid progression and poor therapeutic response.
  • Extreme local tenderness; blistering necrosis; cyanosis.
  • High temperature, tachycardia, hypotension, altered level of consciousness.

• Cellulitis
• Erysipelas
• Erythema Induratum
• Pyoderma gangrenosum

• Blood tests: leucocytosis acidosis, altered coagulation profile, hypoalbuminaemia, abnormal renal function.³
• X-ray: soft tissue gas.
• One study has shown that a white cell count greater than 15.4 x 10(9)/L and serum sodium less than 135mmol/L are useful parameters that may help to distinguish necrotising from non-necrotising infection.⁷
• New diagnostic techniques include rapid streptococcal diagnostic kits and a polymerase chain reaction involving SPE genes (eg, SPE-B).
• MRI or CT delineation of the extent of infection may be useful in directing rapid surgical debridement.
• Excisional deep skin biopsy may be helpful in diagnosing and identifying the causative organisms. Cultures of the affected tissue obtained at initial debridement may be helpful.

• Resuscitation as required, followed by aggressive early debridement of infected tissues is critical to management.³
• The role of hyperbaric oxygen is controversial but has been shown to improve survival and limb salvage.^3,8

Drugs

• Antimicrobial therapy is important but remains secondary to the removal of diseased and necrotic tissues.
• The choice of antibiotic(s) will depend on local guidelines and the individual situation of each patient. The choice should be discussed with the local consultant microbiologist.
• Empirical broad-spectrum antibiotics should be administered immediately. A foul smell in the lesion strongly suggests the presence of anaerobic organisms.
• Combination therapy: this approach involves the use of 2 or 3 antibiotics. To cover aerobes (usually gram-negative organisms), ampicillin and gentamicin are useful. For anaerobes, clindamycin or metronidazole has been used. In group A streptococcal infections, clindamycin has been used, specifically in combination with beta-lactam antibiotics.
• Single antibiotic: broad-spectrum beta-lactam drugs such as imipenem cover aerobes, including Pseudomonas species. Ampicillin also has broad-spectrum coverage, but it does not cover Pseudomonas species. The maximum doses of the antibiotics should be used. Once culture and sensitivity results are available, the antibiotic coverage should be reviewed.

• Deep infection causes vascular occlusion, ischaemia and tissue necrosis. Superficial nerves are damaged, causing local anaesthesia. Infection then spreads to septicaemia, which leads to severe systemic toxicity and rapid death unless appropriately treated.
• Streptococcal exotoxin production may lead to toxic shock with fever, rash, hypotension, multiorgan involvement (e.g. cardiomyopathy, renal failure, encephalopathy, hepatic necrosis) and desquamation of the skin of the palms and soles.
• Metastatic cutaneous plaques may occur.

• These infections must be detected and treated rapidly to prevent loss of limb or a fatal outcome.
• Estimates of mortality rate vary from 6-76% but recent studies suggest a mortality rate in the region of 25%.³⁹
• Increased mortality is associated with delays in diagnosis, poor surgical technique and diabetes.¹⁰