Case #023

Pain grossly out of proportion to visible skin changes, in a septic diabetic patient with a rapidly advancing margin, is necrotizing fasciitis until surgically disproven. Several features separate it from simple cellulitis: the woody induration extending past the erythema, patchy anaesthesia from destruction of cutaneous nerves as infection tracks along the fascial plane, crepitus, haemorrhagic bullae, and systemic toxicity out of keeping with the visible lesion. The laboratory picture is captured by the LRINEC score (leukocytosis, high CRP, hyponatremia, raised creatinine and hyperglycemia) though a low score never excludes the diagnosis and should not reassure. Soft tissue gas on plain film is highly suggestive but present in only a minority. The single most important point is that this is a clinical diagnosis requiring immediate exploration: CT or MRI may support it, but arranging them delays the only intervention that alters outcome. Diabetes is the commonest predisposing condition, and infection is usually polymicrobial, though group A Streptococcus causes the fulminant monomicrobial form. Treatment is the operation and everything else is adjunct: radical debridement back to bleeding, healthy tissue is at once the diagnostic test and the cure, and a creatine kinase of 1860 U/L says the necrosis already involves muscle, so the exploration must go deeper than fascia. Broad-spectrum cover for Gram-positives, Gram-negatives and anaerobes runs alongside, with clindamycin added specifically because it suppresses streptococcal exotoxin production rather than merely killing the organism. Repeat debridement at 24 hours is the rule rather than the exception. The urgency is quantifiable: mortality roughly doubles for every 12 hours surgery is delayed, and with a blood pressure of 94/56 and a margin moving 4 cm in three hours, those hours are already being spent.