Venoarterial extracorporeal membrane oxygenation for the management of massive amlodipine overdose.

A 50-year-old man was admitted to the intensive care unit with respiratory failure and shock after suffering a massive overdose of amlodipine, lisinopril and hydrochlorothiazide. Despite mechanical ventilation, vasopressors, calcium gluconate, hyperinsulinemia-euglycemia therapy, methylene blue and intravenous fat emulsion, the patient's respiratory and hemodynamic status deteriorated. Venoarterial extracorporeal membrane oxygenation (ECMO) was initiated to provide cardiopulmonary support in the setting of profound respiratory failure and refractory shock. The patient was placed on ECMO 19 hours after arrival to the hospital, after which vasopressor and ventilatory requirements decreased significantly. The patient was decannulated from ECMO after 8 days and was discharged home after a 56-day hospitalization. Early institution of ECMO should be considered for the management of respiratory failure and refractory shock in the setting of calcium channel blocker overdose when medical therapies are insufficient.

The MALAdy of metformin poisoning: Is CVVH the cure?

Inadvertent or intentional metformin overdose can result in death from refractory lactic acidosis. We report a death from metformin-induced refractory lactic acidosis despite aggressive care. A 49-year-old hypertensive diabetic female presented 1 hour after ingesting 60 tablets of 500 mg metformin and 20 combination tablets of 12.5 mg hydrochlorothiazide/20 mg lisinopril. She was awake and alert, with a blood glucose of 579 mg/dL. Chemistry panel revealed lactic acidosis and acute renal failure (arterial blood gas pH, 7.18; pCO(2), 15 mm Hg; pO(2), 127 mm Hg; HCO(3), 6 mmol/L; lactate, 9.6 mmol/L; and creatinine, 1.2 mg/dL [0.8 mg/dL previously]). She received normal saline, sodium bicarbonate, and insulin. On arrival to the intensive care unit she was obtunded, with a blood pressure of 40/25 mm Hg and had worsening acidosis and poor oxygenation (arterial blood gas pH, 6.79; pCO(2), 55; pO(2), 57; HCO(3), 8.4; and base excess of -25 on 100% fractional inspired oxygen). She was intubated and received additional fluid boluses, bicarbonate, and norepinephrine. Continuous veno-venous hemofiltration (CVVH) was started 6 hours after her ingestion. Metformin was 380 microg/mL on CVVH initiation. The patient developed pulseless electrical activity 30 hours after her ingestion, which recurred 20 minutes later. The family requested no further resuscitation. She died 31.5 hours after her ingestion. Metformin concentrations decreased to 97 microg/mL 28 hours after the ingestion on CVVH, with a first-order elimination half-life of 11.3 hours (r(2) = 0.99) and a clearance of 56.2 mL/min. Further investigations on the place of CVVH in the management of the poisoned patient with MALA unable to hemodynamically tolerate conventional hemodialysis may be needed.

Acute oxcarbazepine, benazepril, and hydrochlorothiazide overdose with alcohol.

An epiletic patient, suffering from partial complex seizures and hypertension, ingested approximately 42 g of oxcarbazepine (OXC) and an undefined number of tablets containing an association of benazepril and hydrochlorothiazide along with some glasses of wine. Four hours later he was brought to the emergency room. He was stuporous and gradually became unconscious. Therefore he was intubated and, approximately 6 hours after the overdose, transferred to the intensive care unit, where he underwent a 4-hour hemodialysis. Even if this procedure did not accelerate the elimination of the prodrug nor its active metabolite (monohydrocarbazepine), 3 hours after the end of dialysis the patient was fully recovered.

Delayed hypoglycemia in a child after ingestion of a single glipizide tablet.

This is the first report to describe the delayed onset of hypoglycemia in a child after ingestion of one tablet of glipizide. A 2-year-old boy was observed to ingest 5 mg glipizide and 25 mg hydrochlorothiazide. Activated charcoal was administered within 35 minutes of ingestion. Hypoglycemia (serum glucose 49 mg/dL) developed 11 hours later. Emergency physicians must be aware of the potential for delayed hypoglycemia in children with single-tablet ingestions of glipizide. Prolonged monitoring of glucose levels is warranted.

Electromechanical dissociation 48 hours after atenolol overdose: usefulness of calcium chloride.

Electromechanical dissociation (EMD) occurred in a 20-year-old woman 48 hours after an overdose of atenolol, despite intensive treatment of the beta-blocker poisoning (gastric lavage, charcoal, glucagon, epinephrine, atropine, correction of electrolyte abnormalities, administration of fluids, cardiac pacing, and mechanical ventilation). Administration of calcium chloride during EMD repeatedly restored blood pressure. Therefore it may have a role to play in management of atenolol overdose.

Quinine overdose: review of toxicity and treatment.

Quinine sulfate is a commonly prescribed remedy for idiopathic nocturnal leg cramps and is now available "over the counter." A 24-year-old man ingested 8 g (a commonly dispensed quantity) of quinine sulfate in a suicide attempt. Despite hemoperfusion begun 10 h after ingestion, the patient died. This report reviews the toxic manifestations of quinine and the currently available modes of treatment.

Central nervous system and cardiac manifestations of hydrochlorothiazide overdosage; treatment with hemodialysis.

A patient with end-stage renal failure inadvertently received high-dose hydrochlorothiazide as treatment for hypertension, resulting in CNS and cardiac toxicity. These toxic manifestations were successfully treated with hemodialysis. A hydrochlorothiazide dialysance of 62.5 mL/min was demonstrated. The possibility of hydrochlorothiazide toxicity should be considered in any patient with renal insufficiency who exhibits unexplained arrhythmias or symptoms related to the CNS.

Dyazide-induced reversible acute renal failure associated with intracellular crystal deposition.

Acute interstitial nephritis due to Dyazide therapy, ie, a combination of hydrochlorothiazide (25 mg) and triamterene (50 mg), has been recently reported in the literature. This had been characterized by nonoliguric renal failure after a long latent period (weeks) following exposure to the drug. Pathologic data have indicated a drug-induced hypersensitivity reaction. We report here one case of oliguric acute renal failure after a massive Dyazide intoxication. Based on the results of the renal biopsy and clinical course, we propose that the oliguria was secondary to a direct toxic effect on the tubules, and intrarenal obstruction was secondary to triamterene crystals and crystal-laden cells. In addition, pathologic findings also suggested a moderate hypersensitivity reaction. After hemodialysis and short-term steroid therapy, the patient achieved complete recovery of renal function within 12 days. Recent knowledge of triamterene-induced nephrolithiasis helps to explain the pathogenesis of acute renal failure in this patient, and is briefly reviewed here.

Clonidine poisoning. A complex problem.

Clonidine hydrochloride poisoning in children has become more frequent with increasing availability of this drug. We report four cases of accidental clonidine poisoning that demonstrate the various signs and symptoms of clonidine poisoning. The most frequent and significant toxic effects are depression of consciousness, bradycardia, hypotension, and respiratory depression. Ventilatory support must be available if apnea occurs. Bradycardia can be treated with atropine sulfate, epinephrine chloride, dopamine hydrochloride, or tolazoline hydrochloride. Hypotension is treated with intravenous fluids and dopamine, reserving tolazoline for refractory cases. Hypothermia is common but is of minor clinical significance. Paradoxical hypertension should be treated with tolazoline. Clonidine may not be detected in body fluids by routine toxicology-screening procedures, so poisoning should be suspected on clinical grounds.