Hypokalemic Cardiac Arrest: Narrative Review of Case Reports and Current State of Science.

PURPOSE: Hypokalemic cardiac arrest is an uncommon occurrence in the emergency department. Electrocardiogram findings related to hypokalemic cardiac arrest include prolonged QT, U waves, and preventricular contractions leading to Torsades de Pointes and then arrest. Literature evaluating the prevalence of hypokalemic cardiac arrest is scarce, and its management is lacking. This review provides a summary of current literature, recommendations from current guidelines, and proposed management strategies of hypokalemic cardiac arrest. SUMMARY: Intravenous potassium administration is the treatment for hypokalemic cardiac arrest. Although the treatment for hypokalemic cardiac arrest is known, there is limited evidence on the proper procedure for administering intravenous potassium appropriately and safely. Owing to the time-sensitive nature of treating hypokalemic cardiac arrest, rapid administration of intravenous potassium (10 mEq/100 mL of potassium chloride over 5 minutes) is warranted. Concerns regarding rapid potassium administration are not without merit; however, a risk-benefit analysis and potential mitigation strategies for unwanted side effects need to be considered if hypokalemic cardiac arrest is to remain a reversible cause. It is imperative to identify hypokalemia as the cause for arrest as soon as possible and administer potassium before systemic acidosis, ischemia, and irreversible cell death. CONCLUSIONS: More evidence is necessary to support treatment recommendations for hypokalemic cardiac arrest; however, it is the authors' opinion that, if identified early during cardiac arrest, intravenous potassium should be administered to treat a reversible cause for cardiac arrest.

Meropenem as an antidote for intentional valproic acid overdose.

Valproic acid (VPA) is a broad-spectrum antiepileptic drug indicated for monotherapy and adjunctive therapy of seizures, and complex manic episodes associated with bipolar disorder [1]. While uncommon due to monitoring, VPA can cause toxicity at supratherapeutic levels [1, 2]. Traditional treatment for VPA toxicity is primarily supportive care, however activated charcoal, l-carnitine, and hemodialysis have been successful in removing free VPA [2]. An interaction between carbapenem antibiotics and VPA is well-established and listed in respective package inserts as a combination to be avoided due to decreased VPA efficacy [1, 3]. Recent literature suggests co-administration of meropenem with VPA reduces mean plasma VPA levels by 50-80% [4, 6]. This case report describes the successful use of carbapenems to intentionally lower toxic VPA levels in a 42 year old female that presented to the emergency department with VPA toxicity from an overdose with divalproex sodium.

A cool side effect of valproic acid administration: Single dose-induced hypothermia.

Thermoregulatory derangements secondary to valproic acid (VPA) administration, specifically hypothermia, have been reported throughout the literature, but a handful of times. This case report describes a 28-year-old male presenting status-post multiple tonic-clonic seizures, treated for persistent seizure activity refractory to benzodiazepines with valproic acid (VPA), levetiracetam, and fosphenytoin. After just over an hour, the patient's core temperature fell from 36.8 °C to 34.9 °C. Temperatures were repeated for confirmation, no further doses of VPA were administered, and the patient's temperature returned to normal over the next 7 h with the use of warming blankets. Levetiracetam and fosphenytoin were continued with no further reported development of hypothermia during the patient's admission. After reviewing other potential causes, a thorough drug database review was performed that found VPA to be the only medication administered with published reports of inducing hypothermia. The mechanism of thermoregulatory derangement associated with VPA is not clearly defined and much of the evidence surrounds alterations in gamma-aminobutyric acid (GABA) activity in animal studies. To our knowledge, this case report is the first reported case of VPA-induced hypothermia following a single dose in the emergency department and offers the potential that prompt return to normothermia is likely following discontinuation of the offending agent.

Adjunct Analgesic Use for Acute Pain in the Emergency Department.

Purpose: Multimodal analgesia is common practice in the postoperative setting, but the utility of adjunctive analgesia in the emergency department (ED) is less understood. The primary objective of this study was to analyze ED prescriber ordering habits for adjunct nonopioid pain medication for opioid-naïve patients who require intravenous (IV) morphine or hydromorphone for acute pain. Secondary objectives were to assess initial and total opioid consumption in morphine equivalent units (MEU), pain scores, and ED length of stay (LOS) between groups. Methods: A retrospective chart review of adult patients who presented to the ED at a large academic medical center and received IV morphine or hydromorphone for acute pain was conducted. Patients were analyzed according to initial opioid received and presence or absence of adjunct nonopioid analgesics. Results: A total of 102 patient charts were analyzed. Adjunctive nonopioid analgesics were ordered on 38% of patients. Patients who received an adjunct nonopioid analgesic received a smaller mean initial opioid dose than those who did not (4.73 vs 5.48 MEU, p = .08). Initial pain score reduction on the 11-point Numeric Rating Scale (NRS) did not differ between patients who received adjunct analgesics versus those who did not (3 vs 4, p = .75). Patients who received adjunct analgesics were associated with a decreased ED LOS (294 vs 342 minutes, p = .04). Conclusion: A small proportion of patients with acute pain received a nonopioid analgesic in conjunction to IV opioids. Further studies are warranted to assess the impact of adjunct analgesics for patients with acute pain.

Cobicistat: a new boost for the treatment of human immunodeficiency virus infection.

Ritonavir is commonly used as a pharmacokinetic booster for antiretroviral regimens in the management of human immunodeficiency virus infections. Limitations to ritonavir boosting include increased pill burden, adverse effects, and a wide range of clinically significant drug-drug interactions. Cobicistat is a new pharmacokinetic booster that is a selective inhibitor of cytochrome P450 3A, the main metabolizing pathway of several antiretrovirals. Cobicistat has been studied as a booster for elvitegravir, a second-generation integrase inhibitor, and protease inhibitors. Based on successful clinical trials, a new single-tablet regimen of elvitegravir, cobicistat, emtricitabine, and tenofovir has been approved for the management of treatment-naïve patients. Additional studies are underway investigating the safety and efficacy of cobicistat-boosted protease inhibitor regimens for both treatment-naïve and treatment-experienced patients. Cobicistat is well tolerated and may become a preferred booster for antiretroviral regimens, as it can be coformulated with several agents to create simpler regimens.