Faculty Bibliography

BACKGROUND:We report a patient with a massive hydroxychloroquine overdose manifested by profound hypokalemia and ventricular dysrhythmias and describe hydroxychloroquine toxicokinetics. CASE REPORT/METHODS:A 20-year-old woman (60 kg) presented 1 h after ingesting 36 g of hydroxychloroquine. Vital signs were: BP, 66 mmHg/palpation; heart rate, 115/min; respirations 18/min; oxygen saturation, 100% on room air. She was immediately given intravenous fluids and intubated. Infusions of diazepam and epinephrine were started. Activated charcoal was administered. Her initial serum potassium of 5.3 mEq/L decreased to 2.1 mEq/L 1 h later. The presenting electrocardiogram (ECG) showed sinus tachycardia at 119 beats/min with a QRS duration of 146 ms, and a QT interval of 400 ms (Bazett's QTc 563 ms). She had four episodes of ventricular tachydysrhythmias requiring cardioversion, electrolyte repletion, and lidocaine infusion. Her blood hydroxychloroquine concentration peaked at 28,000 ng/mL (therapeutic range 500-2000 ng/mL). Serial concentrations demonstrated apparent first-order elimination with a half-life of 11.6 h. She was extubated on hospital day three and had a full recovery. CONCLUSION/CONCLUSIONS:We present a massive hydroxychloroquine overdose treated with early intubation, activated charcoal, epinephrine, high dose diazepam, aggressive electrolyte repletion, and lidocaine. The apparent 11.6 hour half-life of hydroxychloroquine was shorter than previously described.

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

Objective: Aggressive gastric emptying is often withheld in poisoning due to concerns over safety and efficacy. Despite this, endoscopy performed by emergency medicine physicians demonstrates significant retention of residual drug products many hours after ingestion [1]. Decedents may also demonstrate significant drug retention [2]. We developed a novel video technique in an attempt to improve the safety, efficacy, and completeness of orogastric lavage.
Method(s): Using SolidWorksTM (Dassault Systems, Waltham, MA, 2018), we designed and produced a special Y-adapter with a polylactic acid medium using a 3D Printer (Monoprice, Rancho Cucamonga, CA, 2018) to permit side hole insertion of a disposable AmbuR aScopeTM three intubating bronchoscope (Columbia, MD, 2018) into a standard 40 Fr orogastric lavage tube (OGT). This allowed bronchoscope placement into the orogastric tube (OGT) with an air-tight seal and the ability to visualize through a distal side port. To simulate overdose, 50 pills (acetaminophen 500 mg/diphenhydramine 25mg tablet) were placed into the mannequin stomach with 200 mL of tap water. The mannequin was positioned in the left lateral decubitus position; the apparatus was assembled; and gastric lavage was accomplished with 2 L of tap water.
Result(s): We were able to easily visualize tube passage and placement into the stomach to an appropriate depth, appreciating an initially cloudy solution with numerous pill fragments. The adapted system then permitted lavage under constant bronchoscope visualization. Gastric contents were easily ascertained through the distal ports, and the stomach could be evaluated to the pylorus to exclude bezoars or remaining pill fragments. After lavage, a clear solution with no remaining evidence of pill slurry was evident. After extensive lavage, using the bronchoscope, only a small amount of pill fragments were visualized in the fundus.
Conclusion(s): This study demonstrates a proof of concept, linking visualization with OGT placement and active lavage. If these findings can be confirmed in vivo, our novel device may help clarify the indications, improve the safety and efficacy, and define the endpoints of orogastric lavage

Objective: Digoxin toxicity is determined largely by physical examination and electrocardiogram (ECG) findings; concentrations serve for confirmation. Some reports suggest decreased digoxin sensitivity in younger patients. We report a case of an infant with a very elevated digoxin concentration successfully managed conservatively. Case report: A 2-month-old boy (3.1 kg) with a past medical history of congestive heart failure was admitted to the hospital for vomiting and failure to thrive. The patient was started on oral digoxin, ordered as 0.015 mg twice daily. Due to a medication error, he was instead given 0.15mg twice a day for four days. His only other medication was furosemide. He had no new symptoms or change in the frequency of his vomiting. During a new medication reconciliation, the error was discovered. At that time, his vital signs were blood pressure 88/43mmHg, heart rate 123 beats/minute, respiratory rate 52, temperature 36.9 degreeC, and oxygen saturations 100% (on supplemental oxygen). His electrocardiogram (ECG) showed a sinus rhythm at 122 beats/minute with normal intervals. There was no evidence of increased automaticity or any arrhythmias. A serum digoxin concentration drawn 5 hours after his last dose was 16 nmol/L. Other laboratory findings at that time were notable for a potassium of 5.2mmol/L with slight hemolysis and a creatinine of 3.5 mumol/g. Repeat laboratory tests 8 hours after his last dose revealed a digoxin concentration of 15 nmol/L, potassium 5.3mmol/L (hemolyzed), creatinine 2.7 mumol/g and magnesium 0.72 mmol/L. He remained hemodynamically stable despite occasional episodes of vomiting. No cardiac ectopy or other events were noted. Oral digoxin was withheld and Digifab was not given. Repeat digoxin concentrations on day 1, 2, 4 and 5 were 9.6, 4.9, 2.9 and 1.92 nmol/L, respectively.
Conclusion(s): Digoxin toxicity often manifests with cardiac and constitutional symptoms. While toxicity is usually expected with elevated digoxin concentrations, only 63% of infants with a digoxin concentration greater than 6.4 nmol/L developed toxicity [1]. In fact, some evidence suggests that infants have decreased sensitivity to digoxin [2]. In this case the significantly elevated post-distribution digoxin concentration with no clear signs or symptoms of toxicity supports this presumption

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)