Faculty Bibliography

STUDY OBJECTIVE/OBJECTIVE:Previous studies have suggested that the initial emergency department (ED) lactate concentration may be an important prognostic indicator for inhospital mortality from acute drug poisoning. We conduct this cohort study to formally validate the prognostic utility of the initial lactate concentration in a larger, distinct patient population with acute drug overdose. METHODS:This observational, prospective, cohort study was conducted during 5 years at 2 urban teaching hospitals. Consecutive adult ED patients with acute drug overdose had serum lactate levels tested as part of clinical care. The primary outcome was inpatient fatality. Receiver operating characteristics were plotted to determine optimal cut points, test characteristics, area under the curve, odds ratios, and 95% confidence intervals (CIs). RESULTS:Of 3,739 patients screened, 1,406 were analyzed (56% women; mean age 43.1 years) and 24 died (1.7%). The difference in mean initial lactate concentration was 5.9 mmol/L (95% CI 3.4 to 8.1 mmol/L) higher in patients who died compared with survivors. The area under the curve for prediction of fatality was 0.85 (95% CI 0.73 to 0.95). The optimal lactate cut point for fatality was greater than or equal to 5.0 (odds ratio 34.2; 95% CI 13.7 to 84.2; 94.7% specificity). Drug classes for which lactate had the highest utility were salicylates, sympathomimetics, acetaminophen, and opioids (all area under the curve ≥0.97); lowest utility was for diuretics and angiotensin-converting enzyme inhibitors. CONCLUSION/CONCLUSIONS:Initial lactate concentration is a useful biomarker for early clinical decisionmaking in ED patients with acute drug overdose. Studies of lactate-tailored management for these patient populations are warranted.

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

Background: Extracorporeal membrane oxygenation (ECMO) is a rescue therapy for patients with acute respiratory distress syndrome (ARDS) and refractory cardiogenic shock. Patients with diphenhydramine overdose can develop severe cardiotoxicity, including wide-complex tachycardia leading to cardiac arrest. There are no reported cases of confirmed diphenhydramine poisoning successfully treated with ECMO Hypothesis: ECMO is effective in severe diphenhydramine poisoning with ARDS and refractory cardiogenic shock. Methods: Single-patient chart review. Case: An 18-year-old female with a history of depression was brought to the emergency department (ED) after being found unresponsive in her car with an empty package of diphenhydramine and empty bottle of ibuprofen Initial emergency medical services (EMS) vital signs were BP 60 mmHg/palp, HR 114 bpm, and RR 12 bpm. Bag-valve mask ventilation was initiated en route to the hospital. In the ED, the patient was unresponsive and then began actively seizing. Cardiac monitoring revealed a wide-complex tachycardia, and then the patient went into a pulseless electrical activity (PEA) cardiac arrest Return of spontaneous circulation occurred after 6 min of CPR during which she was intubated and received intravenous sodium bicarbonate, epi-nephrine, dextrose, calcium, and normal saline. Despite vasopressors and maximum ventilator support, the patient developed ARDS and refractory cardiogenic shock. She was placed on veno-arterial (VA) ECMO. The patient received VA ECMO for 3 days, then veno-venous (VV) ECMO for 11 days, and mechanical ventilation foratotalof21 days. Her course was complicated by rhabdomyolysis, acute kidney injury requiring dialysis, acute liver failure, and compartment syndrome of her left lower extremity necessitating fasciotomy. She was discharged to inpatient rehabilitation neurologically intact 30 days after presentation. A serum diphenhydramine concentration obtained in the ED on arrival was 6000 ng/mL (50-100 ng/mL). Acetaminophen, salicylate, and urine toxicology testing were all negative. Discussion: We believe this is the first case of confirmed diphenhydra-mine poisoning successfully treated with ECMO. This case report supports the use of ECMO in poisonings with cardiovascular collapse secondary to a cardiac toxin. Conclusion: ECMO can be used as a life-saving treatment modality in severe diphenhydramine overdose refractory to conventional therapy

STUDY OBJECTIVE/OBJECTIVE:To assess the efficacy of 10mg intramuscular (IM) methadone in patients with opioid withdrawal syndrome (OWS). METHODS:This was a prospective observational, convenience sample of patients presenting to the ED with mild to moderate OWS. Evaluations included the Clinical Opiate Withdrawal Scale (COWS), Withdrawal Symptoms Scale (WSS), Altered Mental Status Scale (AMSS) and a physician assessment of the patient's WSS (MDWSS). After enrollment, 10mg of IM methadone was administered and patients were reassessed at 30min post-methadone administration. The primary outcome was the change in COWS at baseline and after methadone administration. Secondary outcomes were the differences between AMSS, and WSS post-methadone. RESULTS:Fifty-seven patients had COWS scores recorded at baseline and 30min. Fifty-six had mild to moderate OWS. The COWS improved a mean of 7.6 after methadone administration (P<0.001). The improvement was greater among patients presenting with moderate versus mild withdrawal (mean decrease=-9.1 vs. -5.5, P<0.001). Patients were more likely to self-score themselves as having withdrawal compared to MDs (93.6% vs. 76.6% respectively, P=0.027). Of the 62 patients with baseline and follow-up WSS by self-assessments, 69% improved post-methadone administration. In addition, the AMSS score remained the same or improved among 86% of cases with measurements at baseline and follow-up. CONCLUSION/CONCLUSIONS:A single IM dose of 10mg methadone in the ED reduces the severity of acute mild to moderate OWS by 30min. Larger prospective, randomized controlled, and blinded studies would be needed to confirm these results.

Epidemiological data, including prevalence, for cannabinoid hyperemesis syndrome (CHS) remain largely unknown. Without these data, clinicians often describe CHS as "rare" or "very rare" without supporting information. We seek to estimate the prevalence of CHS in a population of patients presenting to a socioeconomically and racially diverse urban Emergency Department of a public hospital. This study consisted of a questionnaire administered to a convenience sample of patients presenting to the ED of the oldest public hospital in the United States. Trained Research Associates (RAs) administered the questionnaire to patients between the ages of 18-49 years who reported smoking marijuana at least 20 days per month. The survey included questions related to CHS symptoms (nausea and vomiting) and Likert scale rankings on eleven symptom relief methods, including "hot showers." Patients were classified as experiencing a phenomenon consistent with CHS if they reported smoking marijuana at least 20 days per month and also rated "hot showers" as five or more on the ten-point symptom relief method Likert scale for nausea and vomiting. Among 2,127 patients approached for participation, 155 met inclusion criteria as smoking 20 or more days per month. Among those surveyed, 32.9% (95% CI, 25.5% - 40.3%) met our criteria for having experienced CHS. If this is extractable to the general population, approximately 2.75 million (2.13 - 3.38 million) Americans may have suffered from a phenomenon similar to CHS.

Because salicylism is a clinical diagnosis, the serum concentration should be interpreted in conjunction with the clinical presentation. A 26-year-old man presented to the Emergency Department with abdominal painand had extremely elevated serum triglycerides (>7000 mg/dL). Ethanol, acetaminophen, and salicylate concentrations were checked because of concern of self-injurious behavior, which returned at 13.1 mg/dL, undetectable, and >100 mg/dL, respectively. His basic metabolic panel revealed a bicarbonate of 23 mEq/L and an anion gap of 11. An arterial blood gas showed a pH 7.39 and a PCO2 of 36.6 mmHg. On physical examination, he was awake and alert, and had a respiratory rate of 12–14/min. The possible effect of hyperlipidemia to falsely elevate the salicylate concentration was recognized. He was treated for severe hypertriglyceridemia and as his triglyceride level dropped, his repeat salicylate concentration was <1 mg/dL. Since dfferent sized lipoproteins contribute variably to serum sample turbiditythey have the potential to interfere with the absorption of light thereby producing erroneous laboratory results . Clinicians need to be aware of the implications of severe hyperlipidemia and interference to prevent clinical errors based on false positive laboratory results