Multiple drug overdose
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Various toxicities: case report A 51-year-old woman developed various toxicities, including minimal responsiveness, generalised tonic-clonic seizures, acute liver failure (ALF), rhabdomyolysis, acute tubular necrosis, acidosis, oliguria, Takotsubo cardiomyopathy, hypoxic hepatitis, cardiogenic shock, acute heart failure and coagulopathy following intentional overdose of enalapril, gamma aminobutyric acid/ glycine/melatonin/tryptophan/valerian root, hydrocodone, prednisone and tizanidine. Additionally, she exhibited false positive results for phencyclidine due to the ingestion of tizanidine. The woman, who had no significant medical history, presented to hospital after intentional polydrug overdose. After an argument with her husband, she ingested unknown quantities of enalapril, hydrocodone, prednisone tizanidine and gamma aminobutyric acid/glycine/melatonin/tryptophan/valerian-root [Alteril] pills. A few minutes after ingestion, she contacted emergency medical services and was transported to the emergency department. On arrival about an hour after ingestion, she appeared to be minimally responsive with a Glasgow Coma Scale of 12. She subsequently developed a generalised tonic-clonic seizure. Postictally, she was lethargic and exhibited fixed, dilated pupils, with the left pupil appearing slightly larger than the right one. Brain CT scan did not show any acute intracranial process. Initial laboratory analyses revealed normal renal function and liver biochemistries. However, the subsequent morning, she experienced a wide-complex ventricular tachycardia, hypotension (haemodynamic instability and acute heart failure) and another seizure. The woman was intubated, and she started receiving pharmacologic haemodynamic support. Repeat liver biochemistries on day 2 revaled the following: AST 2710 U/L, ALT 3116 U/L, ALP 48 U/L, total bilirubin 3.7 mg/dL, and INR 2.0 (coagulopathy). Due to concerns for ALF, she was administered acetylcysteine [N-acetylcysteine] and vitamin K. Urine toxicology screening was found to be positive for phencyclidine; however, her family denied any history of drug or alcohol abuse. Liver ultrasound demonstrated patent vasculature, normal liver parenchyma and no cholelithiasis or biliary ductal dilation. Creatine kinase was found to be increased at 1562 U/L, compatible with rhabdomyolysis. Her liver function continued to deteriorate, and she developed acute tubular necrosis, oliguria and acidosis, which necessitated initiation of continuous renal replacement therapy. Clinical prognosticative scoring systems for ALF indicated a poor transplant-free survival rate; therefore, she underwent evaluation for liver transplantation. However, echocardiogram showed severe wall motion abnormalities and a severely decreased ejection fraction of 19%. The mid anterior and distal anterior septum, mid inferior and distal inferior wall, entire apex and mid inferoseptal segment were akinetic; these findings suggested Takotsubo cardiomyopathy. Therefore, the ALF was attributed to hypoxic hepatitis in the backgrou
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