Faculty Bibliography

Objective: In-flight pain emergencies are responsible for 17% of medical diversions on commercial airlines [1]. While the Federal Aviation Authority mandates that airlines carry aspirin in the emergency medical kit (EMK), some airlines carry opioids. This case highlights the risks associated with in-flight administration of opioid analgesics from an ill-equipped EMK. Case report: The poison center was consulted about a 38-yearold, opioid-naive woman who was brought to an emergency department directly from the airport following a transatlantic flight on a large European airliner. She had normal vital signs but was somnolent and nauseous with bilateral miosis. In her possession was a physician note attesting that she had complained of leg pain during the flight and was given buprenorphine (400 mug sublingual) and aspirin (300mg oral) from the emergency medical kit on board the flight. In the absence of hypoventilation, we recommended against naloxone administration. The patient was admitted to the intensive care unit for monitoring and discharged home 24 hours later without sequelae. We investigated the EMK contents of the patient's airline and were extremely concerned by our findings. The quantity of buprenorphine (30 x 200 mug tablets), its convenient location within the lid compartment (next to the stethoscope and face mask), and the relative scarcity of naloxone (2 x 0.4 mg ampules) were all striking. While buprenorphine has a ceiling effect on respiratory depression in healthy volunteers, its high mu-opioid receptor affinity makes it difficult to treat with standard doses of naloxone [2]. Many physicians are also unfamiliar with analgesic buprenorphine doses which are 10-fold lower than doses used for opioid medication assisted therapy. Lastly, sublingual buprenorphine has a peak therapeutic effect 1-4 hours following administration: too late and too long for pain on a plane for shorter flights.
Conclusion(s): The large quantity of easily-accessible buprenorphine in an airline's EMK directly contributed to this patient's overdose. While the patient did not suffer permanent injury, she was subjected to many medical tests and hospitalized for 24 hours in a costly ICU bed. We seriously question the role of buprenorphine in the management of in-flight pain crises. (Table Presented)

Objective: To highlight the variety of possible complications that may arise following ingestion of 35% hydrogen peroxide. Case report: A 40-year-old woman presented to the emergency department (ED) with blood-tinged emesis episodes following unintentional ingestion of 35% hydrogen peroxide. She complained of epigastric pain radiating to her right shoulder, headache, sore throat, and chest pain. Her triage vital signs were blood pressure 111/87 mmHg, heart rate 103/min, respiration rate 19/min, temperature 37.2 degreeC, oxygen saturation 96% (room air) with unremarkable initial physical exam aside from epigastric and diffuse abdominal tenderness. There was no obvious caustic injury to the oropharynx. Later, the patient complained of blurry vision. Initial testing was notable for elevated troponin (0.286 ng/ mL, reference <0.08 ng/mL), Non-specific T wave inversions were seen on the electrocardiogram (ECG). A computerised tomography (CT) scan of chest and abdomen showed diffuse gastric pneumatosis and pneumobilia without obvious evidence of coronary air emboli. A head CT showed no acute infarct or pneumocephalus. She was transferred for hyperbaric oxygen therapy; after one session her symptoms resolved, except for continued blurred vision. Additional evaluation including echocardiography and magnetic resonance imaging (MRI) was planned, but she left against medical advice before these were completed. At ophthalmology follow-up, she reported return to normal vision; however, she had left homonymous hemianopia, likely due to the ingestion.
Conclusion(s): Both gastrointestinal and neurologic complications following 35% hydrogen peroxide ingestion are reported as well as successful treatment with hyperbaric oxygen [1-2]. However, to our knowledge, this is the first case with cardiac involvement as evidenced by the elevated troponin concentration and an unusual case of homonymous hemianopia. We believe that these novel findings may be complications caused by paradoxical gas emboli that transited through a patent foramen ovale; a mechanism that has been described with iatrogenic air emboli [3], but not after hydrogen peroxide ingestion. This illustrates the variety of possible complications following ingestion of industrial strength hydrogen peroxide

Objective: Isopropyl alcohol ingestion is reported to cause ketosis without acidosis. We report a case of confirmed isopropyl alcohol ingestion associated with an anion gap metabolic acidosis with no preceding hypotension. Case report: A 15-year-old female with a past medical history of depression presented to the emergency department after being found somnolent at home. Thirty minutes prior to arrival, she drank 300mL of 70% isopropyl alcohol. She had one episode of vomiting and was intubated for airway protection. Initial vital signs were blood pressure 115/66mmHg, heart rate 86 beats/minutes, respiratory rate 20/minute, temperature 36.3 degreeC, and oxygen saturations 100% (on supplemental oxygen). Electrocardiogram (ECG) showed sinus rhythm (92 beats/minute) with normal intervals. Venous blood gas analysis showed pH 7.2, PCO2 50.4 mmHg, and lactate 0.34 mmol/L. Basic metabolic profile showed sodium 137mmol/L, potassium 2.9mmol/L, chloride 105mmol/L, bicarbonate 24mmol/L, blood urea nitrogen 11mmol/L, creatinine 244 mumol/L, glucose 9 mmol/L, and anion gap 8mmol/L. Measured serum osmoles were 353 mOsm/L with a calculated osmolar gap of 65. Ethanol, acetaminophen and salicylate were undetectable. Urine ketones were undetectable but serum acetone was 21 mg/dL. Repeat laboratory tests seven hours after admission were arterial blood gases pH 7.21, PCO2 27 mmHg, lactate 1.1mmol/L, with sodium 141mmol/L, potassium 3.5mmol/L, chloride 102mmol/L, bicarbonate 15mmol/ L, blood urea nitrogen 10mmol/L, creatinine 244 mumol/L, glucose 8 mmol/L and anion gap 23. Given the rising anion gap and elevated lactate, a loading dose of fomepizole 15mg/kg in addition to thiamine and folate were administered. She was started on continuous veno-venous hemofiltration (CVVH) 15 hours post-admission for 2 hours and was later switched to hemodialysis. Toxic alcohol concentrations sent after 2 hours of CVVH were isopropyl alcohol 69 mg/dL and acetone 82mg/dL. Ethylene glycol and methanol were undetectable. She completed 4 hours of hemodialysis, with resolution of acidosis. Following extubation, she admitted to ingesting only isopropyl alcohol.
Conclusion(s): Isopropyl alcohol is either eliminated unchanged via kidneys or lungs or is metabolized by alcohol dehydrogenase to acetone, the latter eliminated by the liver or lungs. However, rodent studies show that acetone may be further metabolized to lactate, generating formate, which can contribute to an anion gap metabolic acidosis. While this pathway may explain the acidosis and hyperlactemia in our patient, it has not been demonstrated in humans. The development of acidosis in this patient is puzzling and unexpected

Background: Alcoholic ketoacidosis (AKA) is a metabolic derangement caused by poor nutritional status and an altered oxidation-reduction state in patients with alcohol use disorder (AUD). During starvation, fatty acids undergo beta-oxidation, with resulting ketone and ketone-like byproducts causing both an elevated osmolar gap and an elevated anion gap metabolic acidosis. Ingestion of toxic alcohols (TAs), such as methanol or ethylene glycol, also produces an elevated osmolar gap, and subsequently an elevated anion gap metabolic acidosis. It is difficult to distinguish AKA from TA ingestion clinically, many hospitals do not provide timely serum TA concentrations, and the cost of unnecessary fomepizole and/or hemodialysis is significant. The aim of this study is to identify risk factors suggestive of AKA when TA ingestion is the primary alternative differential diagnosis. We hypothesize that a positive ethanol concentration will be predictive of the diagnosis of AKA.
Method(s): This is a retrospective analysis of data from a single Poison Control Center (PCC) from 2000 to 2019. A structured query language search (SQL) of Toxicall

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.