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)

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

Background: Severe baclofen toxicity (BT) can result in respiratory failure, hypotension or hypertension, bradycardia, hypothermia, seizures, coma and death. While hemodialysis (HD) is well-described in the treatment of BT in patients with end-stage renal disease (ESRD), the utility of HD in the treatment of acute BT in patients with normal renal function is less clear. Implementing HD to speed recovery after a large acute baclofen exposure is tempting, considering: a) the potential for prolonged coma and ventilator-associated morbidity, and b) baclofen's low protein binding (31%), small size (213 Da), and moderate volume of distribution (Vd =2.4 L/kg). We report the lack of efficacy of HD in a patient with an intentional baclofen overdose and normal kidney function. Case report: A 51-kg 14-year-old girl with no past medical history presented to the emergency department with hypotension, obtundation, and status epilepticus after an intentional ingestion of 1200 mg of baclofen. Her post-intubation neurologic exam was concerning for coma without any need for sedation. A 14-hour post-ingestion baclofen level was 882 ng/ml (therapeutic range 80-400 ng/ml). Urgent hemodialysis was performed due to her concerning neurologic status, with the goal of reducing her time on the ventilator. A Revaclear 300 dialyzer was used with an ultimate blood flow rate (Qb) of 300 ml/min and a dialysis fluid flow rate (Qd) of 400 ml/min. A total of three HD sessions were performed, with serum concentrations collected accordingly (Figure 1), and slow but progressive improvement in mental status. Baclofen concentrations were also systematically obtained in urine and dialysate during her hospital course. The total baclofen removed in the first three-hour HD session was 3.05 mg. The total amount of baclofen removed from urine over 24 hours on hospital day one was 42 mg, hospital day 2 was 9.2 mg, and hospital day 3 was 27.8 mg. A follow-up magnetic resonance imaging of the brain showed no evidence of anoxic brain injury. She was discharged without neurologic deficits to inpatient psychiatry on day 14. Case Discussion: There are few reports on the use of HD for acute BT in patients with normal renal function, and limited data on HD efficacy. Given the 12-fold increased quantity of baclofen recovered in urine during hospital day one in comparison to HD, the use of HD appears largely ineffective in enhancing elimination for patients with normal kidney function. Furthermore, baclofen was below the limit of detection in the dialysate on days 2 and 3. Post-HD rebound was consistent with redistribution given baclofen's larger volume of distribution. It is possible that the drug had already been distributed to tissue at the time HD was started, about 30 hours post-presentation, rendering elimination by HD ineffective.
Conclusion(s): The amount of baclofen recovered during hemodialysis is negligible in comparison to normal renal elimination in this patient with normal renal function