Severe Alkalemia and hypokalemia after chronic exposure to alkaline water.

Consumption of alkaline electrolyzed water (AEW) has become increasingly popular for consumer use. Although these alkaline water products are now commonly used, they are of questionable health benefit. Some individuals believe that it may help their dyspepsia. Furthermore, there is a paucity of evidence on its toxicologic profile and adverse effects. This is a single case report of a 42-year-old female with a past medical history of gestational diabetes, necrotizing pancreatitis, presented to the Emergency Department for 3 weeks of lethargy, weakness, difficulty walking, and vomiting. She endorsed consuming 5  liters (L) of alkaline water daily for the past month. Initial labs showed pH 7.69, potassium 1.6meQ/L, sodium 133 meQ/L, chloride 65 mmol/L, magnesium 0.9 meQ/L, and bicarbonate 46 mmol/L, and lactate of 13.2 mmol/L. EKG showed sinus tachycardia with QTc of 630 milliseconds. Patient was treated supportively with intravenous fluids and electrolyte replacement. The potassium rose to 6.6 meQ/L, which then the patient was treated for hyperkalemia. After four days of intravenous fluid and electrolyte replacement, the patient's electrolytes and acid-base status normalized, and she was transferred to the medical floors for further management. This case report illustrates severe metabolic alkalosis and hypokalemia in the setting of chronic alkaline water exposure. It also is an example of alkalemia with hyperlactatemia, or "lactic alkalosis". To our knowledge, there is no previous literature reporting serious adverse effects of alkaline bottled water products.

Management of lamotrigine overdose using hemodialysis.

Lamotrigine [LTG] is primarily an anti-epileptic drug used to treat seizure disorders, depression, and bipolar disease. It is generally well tolerated with limited side effects reported during routine use. Adverse events after overdose include neurotoxicity in the form of sedation and seizure activity, as well as cardiopulmonary toxicity in the form of sodium-channel blockade and cardiovascular collapse. There is no consensus regarding the role of hemodialysis (HD) in management of lamotrigine toxicity. Based on pharmacological properties, LTG is a candidate for extracorporeal removal, however, the successful use of HD for the treatment of this poisoning is not well described. We report the case of a 44 year-old female after a LTG overdose that experienced prolonged sedation that was ultimately treated with HD with an excellent response.

Delayed hyperthermia from chlorfenapyr overdose.

We describe the hospital course of a 42-year-old patient who presented to the Emergency Department following an ingestion of an unknown quantity of chlorfenapyr, an organochlorine pesticide that acts as a mitochondrial uncoupler (MU). There is limited data on chlorfenapyr toxicity in humans, but reports indicate a 100% mortality rate after a 7-10 day quiescent period.3-6 Our patient was admitted for a 5-day asymptomatic observation period before becoming critically ill. Supportive care, antioxidant therapy, and late hemodialysis (HD) proved futile. The patient expired from complications due to uncontrollable hyperthermia on hospital day 6. This case represents the first reported fatality due to chlorfenapyr in North America, and illustrates: 1) its potency as a human toxin, 2) the futility of extracorporeal decontamination once late toxicity has set in; 3) the potential need for early and aggressive decontamination in the ED; and 4) the need for a better understanding of this unique poison.

Lipid emulsion therapy during management of the critically-ill poisoned patient: a prospective cohort study.

BACKGROUND: Despite conflicting data, intravenous lipid emulsion has emerged as a potential antidote. The "lipid sink" theory suggests that following intravenous administration of lipid, lipophilic drugs are sequestered in the vascular compartment, thereby reducing their tissue concentrations. This study sought to determine if survival is associated with the intoxicant's degree of lipophilicity. METHODS: We reviewed all cases in the Toxicology Investigators Consortium's lipid sub-registry between May 2012 through December 2018. Information collected included demographics, exposure circumstances, clinical course, management, disposition, and outcome. The primary outcome was survival after lipid emulsion therapy. Survival was stratified by the log of the intoxicant's octanol-water partition coefficient. We also assessed the association between intoxicant lipophilicity and an increase in systolic blood pressure after lipid emulsion administration. RESULTS: We identified 134 patients, including 81 (60.4%) females. The median age was 40 years (interquartile range 21-75). One hundred and eight (80.6%) patients survived, including 45 (33.6%) with cardiac arrest during their intoxication. Eighty-two (61.2%) were hypotensive, and 98 (73.1%) received mechanical ventilation. There was no relationship between survival and the log of the partition coefficient of the intoxicant on linear analysis (P = 0.89) or polynomial model (P = 0.10). Systolic blood pressure increased in both groups. The median (interquartile range) systolic blood pressure before lipid administration was 68 (60-78) mmHg for those intoxicants with a log partition coefficient < 3.6 compared with 89 (76-104) mmHg after lipid administration. Among those drugs with a log partition coefficient > 3.6, the median (interquartile range) was 69 (60-84) mmHg before lipid and 89 (80-96) mmHg after lipid administration. CONCLUSION: Most patients in this cohort survived. Lipophilicity was not correlated with survival or the observed changes in blood pressure. The study did not address the efficacy of lipid emulsion.

Removal of baclofen with hemodialysis is negligible compared to intact kidney excretion in a pediatric overdose: a case report.

INTRODUCTION: Severe baclofen toxicity can result in respiratory failure, hemodynamic instability, bradycardia, hypothermia, seizures, coma, and death. While hemodialysis (HD) is well-described in treating acute baclofen toxicity in patients with end-stage kidney disease or acute kidney injury, the utility of HD for patients with normal kidney function is uncertain. Implementing HD to speed recovery after a large acute baclofen ingestion is appealing, considering: (a) potential for prolonged coma and ventilator-associated morbidity, and (b) baclofen's low protein-binding, low molecular-weight, and moderate volume of distribution. METHODS: We report a 51 kg, 14-year-old girl who presented to the emergency department (ED) with hypotension, obtundation, and status epilepticus after an intentional ingestion of 1200 mg baclofen. Her post-intubation neurologic examination was concerning for coma. A 14-hour post-ingestion baclofen concentration was 882 ng/mL (therapeutic range 80-400 ng/mL). Three urgent-HD sessions were performed to reduce her time on the ventilator. RESULTS: The total baclofen removed in the first three-hour HD session was 3.05 mg. The total urinary elimination of baclofen 42 mg over 24-hours on day one. She was discharged without neurologic deficits to psychiatry on day-14. CONCLUSION: In this case, the amount of baclofen recovered during HD is negligible in comparison to the amount cleared by kidney elimination in this patient with normal kidney function.

Hand Compartment Syndrome Due to N-acetylcysteine Extravasation.

N-acetylcysteine (NAC) is the antidote for acetaminophen (APAP)-induced hepatotoxicity. Both intravenous (IV) and oral (PO) NAC formulations are available with equal efficacy. Adverse events from either preparation are rare. We describe a hand compartment syndrome after extravasation of NAC requiring emergent fasciotomy during phase three of treatment for suspected APAP toxicity. Extravasation injuries leading to compartment syndrome are rare. It is unclear whether IV NAC induced a direct tissue-toxic insult, or functioned as a space-occupying lesion to cause a compartment syndrome. Compartment syndrome from extravasation of NAC is possible. In cases where IV access is difficult, PO NAC is an alternative.

Bilateral hydronephrosis and cystitis resulting from chronic ketamine abuse.

Ketamine associated urinary dysfunction has become increasingly more common worldwide. Point-of-care ultrasound (POCUS) is an established modality for diagnosing hydronephrosis in the emergency department. We describe a case of a young male ketamine abuser with severe urinary urgency and frequency in which POCUS performed by the emergency physician demonstrated bilateral hydronephrosis and a focally thickened irregular shaped bladder. Emergency physicians should consider using POCUS evaluate for hydronephrosis and bladder changes in ketamine abusers with lower urinary tract symptoms. The mainstay of treatment is discontinuing ketamine abuse.

Severe sodium channel blockade and cardiovascular collapse due to a massive lamotrigine overdose.

BACKGROUND: Cardiac arrest due to lamotrigine (LTG) has been reported after co-ingestion with bupropion, but severe sodium channel blockade in the absence of other toxins has not been described. We report a case of cardiac arrest and status epilepticus following a massive LTG overdose. CASE REPORT: A 48 year-old female was brought to the ED with seizure-like activity subsequent to ingesting 7.5 g of LTG. Vital signs were HR 131, BP 107/68, T 99.4°F, RR 16. She was intubated in the ED for a low GCS. Initial ECG demonstrated a narrow-complex normal sinus rhythm, and her labs were unremarkable. Three hours after intubation she developed status epilepticus, and a pulseless wide-complex tachycardia. She was aggressively resuscitated during which time pulses were periodically reestablished, but lost each time seizures recurred. She was not stabilized until the convulsions were terminated with vecuronium. Her post-resuscitation ECG demonstrated a junctional tachycardia with a 3 mm R-wave in aVR. The LTG level was 74.7 mcg/ml (therapeutic: 3-14 mcg/ml). Comprehensive LC-MS/MS drug screen was negative for all screened compounds. DISCUSSION: This is the first report of cardiovascular collapse due to LTG with the highest drug concentration to date. CONCLUSION: The degree of neurologic and cardiovascular toxicity seen in this case are novel and illustrate the potential for severe sodium channel blockade after massive LTG poisonings. Drug levels are not clinically relevant in the acute setting due to the time delay in obtaining results, and recurrent seizure activity may be the only clinical finding that precedes severe cardiac toxicity.