Cutaneous vasculitis due to ciprofloxacin.

Drs IBRAHIMH FAHAL, DF SALLOMI, M YAQOOB, G M BELL (Royal Liverpool University Hospital, Liverpool L7 8XP) write: We report a case of acute renal failure secondary to ingestion of ecstasy (methylenedioxymethamphetamine, MDMA). On the night before admission a 23 year old man had attended an "all night rave" and taken three tablets of ecstasy. Six hours later he was admitted unconscious after a convulsion. On examination he was semiconscious with a temperature of40°C. He had a blood pressure of 120/60 mm Hg and a sinus tachycardia of 120 beats/min. Pupils were dilated and reacted sluggishly to light. Preliminary investigations revealed a haemoglobin concentration of 128 g/l, white cell count 8 8x 10'/1, platelet count 19x 109/, blood urea 9-1 mmol/l. Clotting screen showed: international normalised ratio (INR) 1-9, fibrinogen 1-8 g/l (normal 2-04-5), and activated partial thromboplastin time (APTT) 46 (25-33) s. Toxicology screen showed serum concentrationsofMDMA (ecstasy) of 0-2 mg/l and of amphetamine of 0-1 mg/l (values of 30-2 mg/l are associated with serious toxicity). MDMA was detected in the urine. His overall condition continued to deteriorate and 24 hours after admission investigations showed: haemoglobin 75 g/l, white cell count 7 7x 109/1, platelet count 9x 109/l, INR 3-6, fibrinogen 1-8 g/l, and APTT >115 s; peripheral blood picture showed fragmented red cells compatible with disseminated intravascular coagulation. Plasma urea concentration was 12-2 mmolll, serum creatinine 225 imol/l, serum albumin 49 g/l, serum calcium 1-95 mmol/l, serum unconjugated bilirubin 77 1lmol/l, alanine aminotransferase 289 U/1, aspartate aminotransferase 2659 U/l, lactate dehydrogenase 3510 U/1, and creatine kinase 5849 U/I (35-220). Infection screens and immunological tests showed no abnormality. Urine examination showed a pH of 9, red cells 50x I0'/1, white cells lOx 0I/l, haemoglobin +++, protein++, and no myoglobin. Renal ultrasound showed normal sized kidneys with no obstruction. The persistence of the coagulopathy prevented renal biopsy. He received blood, platelets, and fresh frozen plasma, but 36 hours after admission he developed oliguric renal failure. Serum creatinine rose to 727 ,umol/l with a blood urea of 27-7 mmol/l. After daily haemofiltration for 20 days he was managed conservatively with gradual resolution of his coagulopathy. During this period he underwent a polyuric phase and his renal failure resolved. There are three possible mechanisms of acute renal failure in this patient: a direct toxic effect ofecstasy, disseminated intravascular coagulation, and myoglobinuria. Amphetamine induced interstitial nephritis has been described.' A direct nephrotoxic effect of ecstasy may well have contributed to this patient's renal failure, but we could not perform renal biopsy. Disseminated intravascular coagulation results in varying degrees of microvascular obstruction due to fibrin-platelet desposition. This process may affect the kidney, resulting in sudden ischaemia and acute tubular necrosis, or it may cause a lesion resembling thrombotic thrombocytopenic purpura.2 Disseminated intravascular coagulation is well recognised in amphetamine related toxicity.3 Non-traumatic rhabdomyolysis, myoglobinuria, and renal failure are a recognised cLinical entity4; rhabdomyolysis with or without convulsions is also a recognised effect of amphetamine toxicity,'6 and may well have occurred in this patient, as suggested by the raised creatine kinase concentration. Myoglobinuria was absent but may only be transient. We believe that the cause of this patient's renal failure was multifactorial; ecstasy induced severe disseminated intravascular coagulation, rhabdomyolysis, and possibly a direct effect of ecstasy itself.