Multiple drugs

Abstract

Various toxicities: 21 case reports In a case series involving cases from the National Poison Data System (NPDS), 21 patients (14 female and 7 male), aged 2–88 years were described, who developed various toxicities following accidental ingestion, overdose or medication errors secondary to various medications. Among these 21 patients, 8 patients also exhibited lack of efficacy while being treated with various medications [not all dosages, routes, time to reactions onsets and outcomes stated]. This report describes a 16-year old girl (case 108), who exhibited lack of efficacy while being treated with methylthioninium chloride for acute sodium nitrite poisoning. The girl intentionally ingested sodium nitrite powder (purchased online). An emergency medical services (EMS) initially found her responsive, but she became unresponsive and cyanotic enroute to the emergency department (ED). She was then intubated and ventilated. She became bradycardic, and went into pulseless electrical activity arrest, and was resuscitated with CPR, epinephrine and sodium bicarbonate. Additionally, she received IV methylthioninium chloride [methylene blue] 1 mg/kg over 1 hour and a second dose 30 minutes later. However, her methemoglobin (MetHgb) remained elevated despite treatment. She was transfused blood. She was found to have no cardiac activity and asystole. She died 2 h after ED arrival. As per autopsy findings, she was died due to sodium nitrite poisoning. This report describes a 19-year old boy (case 111), who exhibited lack of efficacy while being treated with hydroxocobalamin for acute sodium azide poisoning. The boy called EMS around 1 hour after ingesting sodium azide in a suicide attempt. He was found to be agitated, tachycardic, lethargic, tachypneic, hyperpnic, labored breathing and intermittently answering questions. He received hydroxocobalamin, along with unspecified IV fluids; however, no effect was noted. Over day 1 he became more somnolent requiring intubation and ventilation. Thereafter, he received sodium bicarbonate drip for worsening acidosis. His hypotension was treated with norepinephrine. His low potassium, phosphorus and magnesium partially responded to replacement therapy. Around 18 hours post ingestion, he developed shock and needed increased vasopressor support. He had severe global hypokinesis and suffered pulseless electrical activity with return of spontaneous circulation after 10 minutes of CPR and advanced cardiovascular life support. However, he had second pulseless electrical activity arrest. After 20 minutes of resuscitation efforts he was declared dead (19 hours after ingestion). As per autopsy findings, he was died due to sodium azide poisoning. This report describes a 41-year-old woman (case 369), who exhibited lack of efficacy while being treated with dopamine, norepinephrine, vasopressin, sodium bicarbonate, magnesium and epinephrine for cardiogenic shock. The woman made a tea and brownie from taxus leaves and ingested after reading about its toxicity on the internet. Two hour post ingestion, she told her counselor who triaged her to the ED. She had no symptoms for the first 90 minute, but then developed tachycardia, QRS widening and then ventricular fibrillation. She was coded for 20 minute, receiving amiodarone, lidocaine and sodium bicarbonate with return of spontaneous circulation. She was started on dopamine for hypotension, and received IV lipidemulsion. She had further episodes of cardiac arrest with return of spontaneous circulation. She was transferred to a tertiary care center in refractory cardiogenic shock for ECMO evaluation. She received increased doses of dopamine, norepinephrine and vasopressin but lost pulses. CPR was started, and received sodium bicarbonate, magnesium and epinephrine. Her condition continued to deteriorate, resuscitation efforts were stopped, and she died 9 hours after ingestion. As per autopsy findings, she was died due to taxus leaves poisoning. This report describes a 10-year-old girl (case 380), who developed acute respiratory distress syndrome, pulseless electrical activity, unresponsive, aspiration, acute anoxic injury, cerebral oedema with ischemic changes and central diabetes insipidus secondary to methadone poisoning, which was accidentally ingested instead of cough medicine. The girl accidentally ingested her mother’s liquid methadone twice, instead of cough medicine. Later that night she developed respiratory distress, and her grandfather performed CPR. An emergency medical services found her in pulseless electrical activity (PEA). She was found to be unresponsive in PEA during physical exam. Thus, she was intubated, and received epinephrine enroute to the ED. Her urine was positive for methadone and methadone metabolite. She received several rounds of epinephrine and sodium bicarbonate with return of spontaneous circulation. She was then intubated and received unspecified IV fluids. Chest X-ray showed aspiration and she developed acute respiratory distress syndrome. Her head CT showed acute anoxic injury. Additionally, she developed central diabetes insipidus. Based on the prognosis, the family opted for institution of comfort measures, and she died 6 hours post presentation. Autopsy findings showed cerebral oedema with ischemic changes, along with blood methadone level 0.24 mg/L. As per autopsy findings, she was died due to methadone poisoning. This report describes a 14-year-old girl (case 381), who developed vomiting, lethargy, aspiration, drowsiness, hypotension, worsening of renal and hepatic function and cardiac arrest secondary to amlodipine, colchicine and fenofibrate poisoning for suicide. The girl intentionally ingested a family member’s medications after writing a suicide note. She vomited repeatedly but did not tell anyone until the following morning, when she was transported to the ED. Available medications included amlodipine, colchicine and fenofibrate. Physical examination showed lethargy, BP 84/66, HR 120, RR 20, O2 sat 99% body tempreture 37°C. Laboratory investigations showed pH 6.95, pCO2 77, sodium 141, potassium 3.6, chloride 106, CO2 22, blood urea nitrogen 21, creatinine 1.8, glucose 98, albumin/globulin ratio 13, AST 257, ALT 54, WBC 44, haemoglobin 17.9, hematocrit 50.7, INR 1.9, creatine phosphokinase 523 and lipase 666. She was found to be drowsy upon arrival to the ED which improved after unspecified IV fluid and antiemetic. In the ICU she become more hypotensive and had a cardiac arrest. She was intubated (after aspirating), ventilated and received sodium bicarbonate, calcium and epinephrine with return of spontaneous circulation. Thereafter, her BP declined (BP 63/36, HR 147), and she developed worsening renal (creatinine 2.4) and hepatic (INR 2.8) function. She shortly died. Antemortem peripheral blood showed colchicine 44 ng/mL. As per autopsy findings, she was died due to amlodipine, colchicine and fenofibrate poisoning. This report describes a 17-year-old girl (case 386), who developed nausea, vomiting, sore throat, unresponsive, jaundice, sinus tachycardia, potential cerebral oedema, intracranial pressure increased, shock and refractory intracranial hypertension secondary to paracetamol poisoning due to intentional paracetamol overdose. The girl presented to the ED for sore throat with vomiting. Her paracetamol [acetaminophen] level was found to be 30 microg/mL, and was discharged. She was then re-admitted on the following day as she was unresponsive with jaundice and sluggish pupils. Physical examination showed BP 115/79, HR 127, O2 sat 100%, body temperature 37°C. Laboratory investigations showed AST 6332, ALT 7489, INR 13 and lactate 8.6. ECG showed sinus tachycardia. She was only responsive to pain, had icteric sclerae and jaundice, pupils 7mm and sluggish. Thus, she received acetylcysteine [N-acetylcysteine], vitamin K and fresh frozen plasma. It was noted that she had intentionally ingested paracetamol overdose 3 days prior, and had been nauseated with vomiting for the past 2 days. On day 2 of admission, she was intubated and started on epinephrine drip. Her intracranial pressure (ICP) monitoring was initiated, and measured was as 90s. She received boluses of NaCL with ICP improvement. Her head CT revealed CSF narrowing and potential cerebral oedema. She received CRT, plasmapheresis and continued acetylcysteine. Laboratory investigations showed AST 1