Acute Hemolysis in the Emergency Department: Think about Clostridium perfringens!

Clostridium perfringens (CP) gives several clinical settings, from an asymptomatic to a massive intravascular hemolysis. We report a case of fatal intravascular hemolysis due to CP septicemia having a hepatic supposed starting point in the emergency department. Like in many cases, the diagnosis was made when patient had already gone into shock and died. The CP septicemia often complicated the course of the digestive or genital pathologies. The alpha toxin can damage the structural integrity of the red cell membrane by means of a phospholipase activity. Nevertheless, a massive intravascular hemolysis arises only rarely in this septicemia, only from 7 to 15% of the cases. The emergency physician has to think about this complication in case of hemoglobinuria and/or signs of hemolysis associated with a septic syndrome. An immediate antibiotic treatment adapted as well as the symptomatic treatment of the spread intravascular coagulation could improve the survival of these patients. 1. Clinical Case A 64-year-old man was brought to the emergency department by ambulance for faintness at home. He had history of diabetes, high blood pressure, and dyslipidemia. On arrival, the patient is alert but febrile (38.6°C/101.5？F). The initial vital signs showed tachycardia (109 per minute), blood pressure of 133/76？mmHg, a respiratory rate of 15 breaths/min, oxygen saturation 99% in room air and hyperglycemia of 2.70？g/L. The clinical examination was normal. The urinary tests find only a glycosuria without hemoglobin. The chest radiography and the ECG are without abnormalities. The entrance biological results focus on an inflammatory syndrome: leukocytes count of /μL and C-reactive protein: 95？mg/L. Complete blood count revealed a hemoglobin level of 15.4？g/dL, a hematocrit of 46, and 3？T/L and a platelet count of /μL. The total bilirubin is up to 40？μmol/L with hepatic cytolysis (serum aspartate transaminase ASAT: 114？U/L, serum alanine transaminase ALAT: 201？U/L, and a cholestasis γ-glutamyltransferase GGT: 253？U/L, alkaline phosphatase PAL: 146？U/L). The blood biochemistry analyses were normal. The physician suggested bed rest, analgesics, and intravenous antibiotherapy with ceftriaxone. Ten hours later, the patient experienced acute dyspnea with polypnea up to 46 per min and oxygen desaturation of 80%. He was admitted to intensive care unit. He presented a hyperthermia up to 39.5°C, and blood pressure dropped to 80/60？mm？Hg. He was resuscitated with 1？L of saline 9% through 2 peripheral lines. First blood gases showed metabolic acidosis. The focused chest sonography