Faculty Bibliography

Background: Aluminum phosphide (AlP) is a highly toxic fumigant that is restricted in the USA. When exposed to humidity or water, AlP generates phosphine gas, a mitochondrial toxin that can produce cardiovascular collapse, respiratory failure, metabolic acidosis, and death. Hypothesis: The use of extracorporeal life support (ECLS) in patients with severe AlP toxicity increases chances of survival. Methods: Single-patient chart review. Case: A 3-year-old girl with no significant past medical history presented to the emergency department with 10 h of cough and vomiting. Symptoms started after her father placed AlP pellets throughout the house for rodent control. Of note, her 47-year-old mother, 16-year-old brother, and 21-year-old sister all presented at the same time with minor gastrointestinal and upper respiratory symptoms that resolved quickly. The patient's vital signs were BP 60/40 mmHg, HR 150 beats/min, RR 25 breaths/min, T 99.5 degreeF, O2 Sat 100%. She was noted to be somnolent and had dry mucous membranes with delayed capillary refill. Venous blood gas showed pH 7.32; PCO2 28 mmHg, calculated HCO3 14 mEq/L, and a lactate 4.2 mmol/L. Anion gap was 29 mmol/L. ECG showed diffuse ST segment depressions. She remained hypotensive despite intravenous fluids and was started on IV dopamine. She was transferred to an ECLS center 2 h after presentation. Shortly after transfer, the patient had a ventricular tachycardia arrest and was connected to veno-arterial ECLS after 90 min of resuscitation. She was started on IV N-acetylcysteine and oral vitamin E as well as intravenous L-carnitine. Her hospital course was complicated by ventricular dysrhyth-mias, seizures and bacteremia, hepatic injury, pulmonary edema and acute kidney failure requiring dialysis. Cardiac function slowly improved, and the patient was weaned off ECLS on day 15 of admission with an intact mental status and no reported neurologic sequelae. Discussion: Phosphine poisoning is challenging for the provider since it is often lethal, has no specific antidotes and rarely occurs in the USA. Conclusion: Early transfer to an ECLS-capable center and aggressive treatment in aluminum phosphide toxicity may be associated with better outcomes

Objective: Despite the known risk of cyanide toxicity in house fires and the well demonstrated benefit of hydroxocobalamin in cyanide poisoning, many first responders do not routinely administer hydroxocobalamin. In addition, there is a paucity of data regarding prehospital hydroxocobalmin use. We present two cases in which hydroxocobalamin administration at the scene of a house fire appeared to prevent death in one patient. Case series: Case 1: A 52-year-old woman with no known significant past medical history was found unresponsive in front of a house fire. Intravenous (IV) access was established and the patient was intubated on scene by Emergency Medical Services (EMS) personnel. Hydroxocobalamin 5 g, was administered IV on scene. On arrival to the Emergency Department, she was tachycardic (118 bpm) and hypertensive (220/97mmHg). Initial blood gas analysis showed pH 6.9, PCO2 57mmHg, HCO3 14 mEq/L, and a lactate 13 mmol/L. She was given sodium thiosulfate 12.5 g IV. Her carboxyhemoglobin level was 36.9% and she was transferred for hyperbaric oxygen therapy. Although the patient's hospital course was complicated by pneumonia, she was extubated on day 5 of admission and later discharged with no reported neurological complications. Case 2: Concurrently, another patient, a 64-year-old man with a prior history of seizure disorder and prior cerebrovascular accident was pulled from the same building on fire. He was found to be in cardiac arrest with pulseless electric activity. He was given hydroxycobalamin 5 g IV and thiosulfate 12.5 g IV in addition to epinephrine 1 mg twice on scene by EMS, with return of spontaneous circulation. His carboxyhemoglobin level was 43% and a head computed tomography showed evidence of anoxic brain injury. Unfortunately, he expired in the Emergency Department shortly after presentation. A pre-hospital blood sample was obtained and tested for cyanide, revealing a concentration of 24 mumol/L (toxic range >20 mumol/L) Conclusion: Cyanide poisoning from house fires is well recognized. Hydroxocobalamin has a proven efficacy as a cyanide antidote when administered in a timely fashion. However, a large number of EMS systems in the US do not carry hydroxocobalamin or any other cyanide antidote. Here, we report on the administration of pre-hospital hydroxocobalamin after a house fire in two patients, one with a confirmed toxic cyanide concentration. These cases should lead to a discussion about EMS antidote stocking of hydroxocobalamin and the need for future research on this subject

Objective: Both acute and chronic salicylism constitute a significant cause of mortality and morbidity in poisoned patients. While some authors have suggested that there is no need to screen for salicylate toxicity in the absence of a history or an anion gap acidosis, here we present a case of non-anion gap acidosis in a patient with significant salicylate poisoning. Case report: A 59-year-old man with no known significant past medical history was brought to the Emergency Department with depressed mental status. On arrival, he was tachypneic (26/ minutes) with shallow respirations, temperature of 37.3 degreeC, blood pressure 129/79 mmHg, heart rate 81 bpm, and oxygen saturation 94% on room air. Venous blood gas analysis showed: pH 7.4 and pCO2 28mmHg. Initial blood tests revealed: sodium 135 mmol/L, potassium 4.6mmol/L, chloride 105 mmol/L, bicarbonate 19mmol/L, blood urea nitrogen 19 mmol/L, creatinine 132 mumol/ L, glucose 6.7mmol/L, and anion gap 11 mmol/L (normal range 8-16 mmol/L). He was intubated and a subsequent arterial blood gas showed: pH 7.14 and pCO2 77 mmHg. Blood salicylate concentration obtained on initial screening was 0.61 mmol/L (therapeutic < 0.22 mmol/L). Intravenous bicarbonate infusion was started, he was given multi-dose activated charcoal and hemodialysis performed. He was extubated five days after admission and medically cleared on day 7 of admission. Conclusion: Significant salicylate ingestion is a well-recognized cause of elevated anion gap metabolic acidosis. Sporer et al. suggested that there is no need to screen for salicylate ingestion in the absence of anion gap acidosis [1]. However, here we demonstrate the presence of a non-anion gap metabolic acidosis associated with a clinically severe salicylate ingestion. There are multiple explanations for this phenomenon. Multiple chemistry analyzers including the one used at our hospital uses a proprietary ion-sensitive chloride electrode. With this analyzer, salicylate concentrations of 0.145 mmol/L and more than 0.43 mmol/L are known to cause a 4% and 15% false increase in chloride concentrations, respectively. This can erroneously cause a normal or even negative anion gap. In addition, acute salicylism occasionally causes proximal renal tubular dysfunction that can contribute to a non-anion gap acidosis. Clinicians should be compulsive about screening for salicylates in undifferentiated poisoned patients as routine chemistry tests may be insufficient to show salicylate toxicity