RESUMO
Carbon tetrachloride (CCl4) is a halogenated hydrocarbon that is a colorless, clear liquid with a sweetish, ether-like, nonirritant odor. It was previously used in dry cleaning agents, refrigerants, and fire extinguishers. CCl4 toxicity is rarely observed. Two patients with acute hepatitis following exposure to a CCl4-containing antique fire extinguisher are presented. A son (patient 1) and father (patient 2) were admitted to the hospital with acute, unexplained elevated transaminases. After extensive questioning, they reported recent exposure to a large amount of CCl4 when an antique firebomb shattered in their home. Both patients cleaned the debris without personal protective equipment and slept in the contaminated area. The patients presented to the emergency department (ED) at varying times between 24 and 72 hours after CCl4 exposure. Both patients received intravenous N-acetylcysteine (NAC); patient 1 also received oral cimetidine. Both recovered uneventfully without sequelae. Extensive workup for other causes of elevated transaminases was unremarkable. Serum analyses for CCl4 were also unremarkable due to the delay between exposure and hospital presentation. CCl4 is a potent hepatotoxin. CCl4 metabolism via cytochrome CYP2E1 produces its toxic metabolite, the trichloromethyl radical. This radical covalently binds to hepatocyte macromolecules and causes lipid peroxidation and oxidative damage with ensuing centrilobular necrosis. Treatment is not well established, but NAC is likely beneficial via glutathione repletion and antioxidant effects. Cimetidine blocks cytochrome P450 and, thus, metabolite formation. Cimetidine may also promote the stimulation of regenerative processes acting on DNA synthesis. CCl4 toxicity is rare and infrequently reported in current literature but should be maintained in the differential of acute hepatitis. Two patients presenting nearly identically - at two different ages but from the same household - offered a clue to this enigmatic diagnosis.
RESUMO
Hypokalemia and hyperosmolar hyperglycemic syndrome (HHS) are two reversible but potentially fatal disorders that are important to identify and treat urgently. A 43-year-old patient presented to the ED with altered mental status and slurred speech, difficulty communicating, left-sided facial droop, and stool incontinence according to emergency medical services. This was preceded by 1.5 weeks of nausea, vomiting, polydipsia, and weight loss. On presentation, the patient was found tachycardic and tachypneic, with uncertain neurological deficits on physical exam, hyperglycemia, and electrocardiogram (EKG) abnormalities. Lab data were consistent with hyperosmolar hyperglycemic nonketotic coma. This case provides two important clinical scenarios in which cardiac EKG abnormalities and focal neurological deficits are the product of hyperosmolality and electrolyte abnormalities. Hypokalemia with EKG abnormalities consistent with a potential ischemic disease can progress into wide complex tachycardia and ventricular fibrillation. Hyperosmolar hyperglycemia may manifest with focal neurological deficits and without the classical presentation of a coma. Careful consideration of EKG and lab values in the context of clinical presentation may provide clues to resolvable etiologies. We report a case of a patient who presented to the ED with hypokalemia and HHS, both reversible but potentially fatal disorders that are important to identify and urgently treat.