Derivation and validation of a formula to calculate the contribution of ethanol to the osmolal gap.

STUDY OBJECTIVES: We sought to evaluate the relationship between osmolal gap and serum ethanol level and derive a formula that can be used clinically to calculate the expected osmolal gap in the presence of ethanol. Some investigators have noted that the residual osmolal gap appears to increase as the ethanol level increases, and thus it is important to determine the exact relationship between these 2 values. METHODS: In part 1, a convenience sample of emergency department patients undergoing serum ethanol determination had sodium, urea, and glucose levels and osmolality determined on the same blood sample, and values were prospectively recorded. Predicted osmolality excluding ethanol was calculated with the following formula: 2 Na (mEq/L) + (Urea [mg/dL])/2.8 + (Glucose [mg/dL])/18. The osmolal gap was determined by subtracting the calculated serum osmolality excluding ethanol from the measured serum osmolality. Linear regression analysis was then used to derive a formula for the relationship between ethanol and the osmolal gap. This formula was then prospectively validated on a second convenience sample of patients. In part 2, we repeated this experiment in vitro by adding known amounts of ethanol to serum. RESULTS: We derived the formula to calculate the contribution of ethanol to the osmolal gap by using 98 observations. The mean ethanol level was 197.8 mg/dL (SD 138.5), with a range of 0 to 538.2 mg/dL. The relationship between ethanol and osmolal gap was linear, with a Pearson coefficient of correlation of 0.99. Linear regression analysis generated a model with the following formula: Osmolal gap=(Ethanol [mg/dL])/3.7 - 0.35 or, in SI units: Osmolal gap (mOsm/kg)=1.25 (Ethanol [mmol/L]) - 0.35 The 95% confidence interval (CI) for the multiplicative factor was 1/3.58 to 1/3.80 (or, in SI units, 1.21 to 1.28). The 95% CI for the additive constant was -2.19 to 1.50. We prospectively validated our formula on 128 patients. The mean residual osmolal gap for this group of patients was 0.84 mOsm/L (SD 5.65; range, -18.40 to 17.85 mOsm/L). The results of the in vitro experiments were similar. CONCLUSION: Our data suggest that the best formula for the calculation of the contribution of ethanol to osmolality is as follows: Ethanol (mg/dL)/3.7 or, in SI units: 1.25 (Ethanol [mmol/L])

Severe methemoglobinemia from topical anesthetic spray: case report, discussion and qualitative systematic review.

Few health care professionals realize that topical anesthetic spray can cause methemoglobinemia. We describe a 56-year-old woman who was transferred to our emergency department when severe cyanosis and chest pain developed after administration of topical oropharyngeal benzocaine and lidocaine during outpatient endoscopy. Investigations revealed a methemoglobin level of 51%. Despite rapid diagnosis and treatment with methylene blue, pulmonary edema consistent with adult respiratory distress syndrome developed, endotracheal intubation was required, and the patient suffered a lengthy course in the intensive care unit. This article presents a detailed discussion of the pathophysiology, diagnosis and treatment of methemoglobinemia, as well as a qualitative systematic review of the English literature on methemoglobinemia induced by topical anesthetic. The implications of this condition for emergency physicians are also outlined.

Cardiovascular toxicity after ingestion of "herbal ecstacy".

"Herbal Ecstacy" (sic) is an alternative drug of abuse usually containing both ephedrine and caffeine. Our literature search did not reveal any other reported cases of cardiovascular toxicity related to herbal "drugs of abuse." A case of cardiovascular toxicity following the ingestion of herbal ecstacy is presented. A 21-year-old male presented to the emergency department with an initial blood pressure of 220/110 mmHg and ventricular dysrhythmias after ingesting four capsules of herbal ecstacy. He was treated with lidocaine and sodium nitroprusside, and his symptoms resolved in 9 h. The pathophysiology and clinical course of ephedrine toxicity are discussed. Emergency physicians should consider ephedrine preparations in the differential diagnosis of patients presenting with a sympathomimetic toxidrome. Drugs of abuse containing "herbal" products can produce serious morbidity and mortality.

Renal failure caused by mushroom poisoning.

BACKGROUND: In the Pacific Northwest region of the US and in southwestern British Columbia, Canada, isolated cases of renal failure have occurred following ingestion of wild mushrooms. We report four cases in which toxic mushrooms were mistaken for the edible pine mushroom or matsutake (Tricholoma magnivelare). CASE REPORTS: Gastrointestinal symptoms started five to eight hours after ingestion and continued for several days. Three of the four patients were found to be in renal failure when they presented to the emergency department 5-6 days post ingestion. One patient, an elderly diabetic, had renal dysfunction the day following ingestion. All patients received hemodialysis and supportive care and regained renal function. DISCUSSION: Symptoms and time of onset are similar to those reported in previous cases of Amanita smithiana poisoning. This suggests that the mushroom involved in these cases may also be Amanita smithiana which contains nephrotoxic compounds. In one of the cases, stem ends of the mushrooms were available for examination. Cellular elements conforming to those described as being present in the species Amanita smithiana were seen on light microscopy. CONCLUSION: Mushroom field guides warn against mistaking Amanita smithiana for pine mushrooms. They are similar in size, color and habitat. It appears possible that Amanita smithiana mushrooms were eaten instead of pine mushrooms in these cases.