Atypical Shu (PTT) Induced by Chronic Drinking of Cocaine: A Case

The thrombocytopenia associated with cocaine consumption has been well documented]. Severe thrombocytopenia usually occurs within 3 weeks of intravenous or inhaled cocaine abuse. Microangiopathic hemolytic anemia (MHA) associated with cocaine is rare. We would like to report a case of cocaine-induced atypical hemolyticus uremic syndrome. Clinical Observation: this is a 29-year-old Causasian patient, followed in a psychiatric center under duress for 6 years for behavioral disorders, hallucinations and attacks on others related to schizophrenia. He is known for drug addiction and heroin, cannabis and cocaine. The patient was found on the ground by the firefighters at 10:53 a.m. when he had been out on leave from 4:30 p.m. the day before in a context of hypothermia at 28°C, unconscious. On arrival in intensive care, the vital parameters were: blood pressure 105/56mmHg, PAM: 70 mmHg, heart rate 60 beats/min, saturation 96%, Weight: 92.7 Kg, Height: 167 cm. Patient sedated, curarized. The initial assessment showed a blood glucose level of 7.16 mmol/l; Urea: 6.6 mmol/l; Creatinine: 130 μmol/l with a peak at 790 μmol/l; Potassium: 6.06 mmol/l; Myoglobin: 316,000 μg/l, LDH: 782 IU/l; CK: 23.086 IU; HCO3: 17.5 mmol/l, Lactate: 4.7 mmol/l (-1.3); Hemoglobin: 17.7 g/dl (12 - 18), Hematocrit: 53.2% (34 - 52); Platelets: 261 G/l 90 - 1.2); Fibrinogen: 3.72 g/l; blood and urine toxin assays were positive for Cocaine, Cannabis, benzodiazepines and opiates. The initial evolution was quickly favorable on the hemodynamic and neurological level with ad integrum recovery after stopping sedation and rapid self-extubation. However, the renal function continues to deteriorate, he becomes anuric, the EER was started continuously by CVVHF in view of the suspicion of acute renal failure by rhabdomyolysis. The appearance of stigmata of TMA with a collapsed haptoglobin at 0.20 g/l (VN: 0.34 - 2), schistocytes at 2.1% (VN: <1%) and moderate thrombocytopenia at 114,000/mm3 led his transfer to the Nephrology Intensive Care Unit. The secondary evolution was marked on the nephrological plan by an improvement of the renal function after a rise of the creatinine until a peak with 790 μmol/l then constant fall with 372 μmol/l, a resumption of the diuresis allowing the stop of the dialysis sessions. The etiological assessment of TMA came back in favor of a TTP secondary to cocaine consumption with a collapsed ADAMST 13 activity < 10%, the anti-ADAMST 13 were negative. Conclusion: We reported a case of atypical HUS (PTT) induced by chronic cocaine use with a collapsed ADAMST 13 activity.