Contribution of serum ethanol concentration to the osmol gap: a prospective volunteer study.

BACKGROUND: The contribution of ethanol ([EtOH]) to the osmol gap (OG) is commonly described by the formula [EtOH (mg/dL)]/k, where k is assumed to be 4.6 (one-tenth of its molecular weight) if ethanol behaves ideally in solution. However, several studies on convenience samples of patients suggest that ethanol does not behave ideally and that k may be significantly different from this ideal constant. OBJECTIVES: To determine prospectively the relationship between serum ethanol concentration and total serum osmolality in a group of healthy volunteers. METHODS: Experimental subjects ingested 20 mL of 100% ethanol diluted in sugar-free soda at a rate of one drink every 10 min, up to a maximum of seven drinks. Control subjects ingested 20 mL of water diluted in sugar-free soda at the same rate. Blood samples were obtained at baseline and then at every 20 min for 180 min to measure serum [EtOH] concentration, electrolytes, glucose, and osmolality (via freezing-point depression). The OG was calculated by subtracting predicted osmolality from measured osmolality. The OG was then divided by [EtOH] to determine the coefficient of ethanol's contribution to total serum osmolality. RESULTS: A total of 10 volunteers (five men and five women; mean age, 38.8 years, and range, 28-49 years) participated in and completed the study. Eight (four male and four female) were in the experimental group, and two (one male and one female) were in the control group. Mean peak [EtOH] was 229 mg/dL (median, 223.5 mg/dL; IQR, 171-273 mg/dL) and a linear relationship between [EtOH] and OG (Pearson coefficient of 0.98) was found. Using covariate correction for each subject's baseline OG, k was calculated to be 4.25 (95% CI, 4.13-4.38) averaged over all participants. CONCLUSIONS: In this volunteer study, the coefficient describing the contribution of ethanol to serum osmolality (k) was found to be 4.25. This indicates that ethanol contributes more to total serum osmolality than would be predicted for an ideal solute.

Rattlesnake envenomations: unusual case presentations.

Rattlesnake envenomations are common in some areas of the United States. Although fatal rattlesnake envenomations are rare and usually preventable, morbidity may be significant. Patients may present with localized edema, hypotension, coagulopathy, or thrombocytopenia. Patients with progressive swelling or severe coagulopathy are typically treated with Crotalidae polyvalent antivenin. We present a series of 4 patients with unusual complications of rattlesnake envenomation to illustrate the wide spectrum of disease that may be encountered. These case presentations include anaphylaxis to rattlesnake venom, an acute airway emergency, progressive and marked edema with a large pleural fluid collection, and death.

Epidemiology and hospital course of rattlesnake envenomations cared for at a tertiary referral center in Central Arizona.

OBJECTIVE: To describe the demographics and primary inpatient treatment of victims of rattle-snake bites (RSBs) referred to a teritiary referral poison treatment center in central Arizona, and to compare the frequency of local tissue complications and hematologic toxicity during hospitalization in children with those for adults. METHODS: This was a chart review of patients diagnosed as having RSB by a toxicology service between July 1994 and April 2000. Data collected included: age, sex, date, bite location, time to and length of hospitalization, time to and amount of antivenin, serial hematologic studies, and inpatient complications. RESULTS: Of 241 patients admitted, 236 charts met inclusion criteria. The majority of RSB victims were male (81%). Children (< or =13 years) represented 22%. Most RSBs (78%) occurred between April and September. Mean time (+/-SEM) to presentation was 1.7 +/- 0.2 hours. Antivenin was administered to 77% of patients, with an average (+/-SEM) of 28.5 +/- 0.9 vials administered. Hematologic abnormalities included: coagulopathy (60%), hypofibrinogenemia (49%), and thrombocytopenia (33%). No statistically significant difference in the above parameters was detected between upper- and lower-extremity envenomations, or between children and adults. Immediate antivenin reactions occurred in 36% of patients. Hemorrhagic bullae formation occurred in 22%, occurring most frequently in upper extremities. Operative procedures were required in 3.4% of patients. Hospitalization averaged 2.5 +/- 0.1 days. There was no fatality. CONCLUSIONS: In Arizona, RSB victims were typically adult males with upper-extremity bites. Hematologic abnormalities were common. Local tissue complications were more common with upper-extremity envenomations. No statistically significant difference was detected in frequency of hematologic disorders or local tissue complications when children were compared with adults.

Combined ingestion and subcutaneous injection of elemental mercury.

A 40-year-old man with a history of schizophrenia and inflammatory soft tissue lesions after self-injection of elemental mercury presented to the Emergency Department. Multiple skin abscesses associated with fever required operative debridement. An incidental finding of oral mercury ingestion was followed clinically and did not result in complications. Exposure to elemental mercury through injection or ingestion is an uncommon event, but one the Emergency Physician may encounter. Subcutaneous mercury injection should be managed with local wound debridement, whereas ingestions are rarely of clinical significance.

Hypertonic sodium bicarbonate is effective in the acute management of verapamil toxicity in a swine model.

STUDY OBJECTIVE: This study was conducted to determine whether hypertonic sodium bicarbonate would improve the hypotension associated with severe verapamil toxicity compared with volume expansion. METHODS: The study design used a nonblinded acute animal preparation. Twenty-four anesthetized and instrumented swine were poisoned with verapamil delivered at a rate of 1 mg/kg per hour for 10 minutes followed by incremental increases of 1 mg/kg per hour every 10 minutes until the endpoint of a mean arterial blood pressure of 45% of baseline was achieved. Animals alternately received either 4 mEq/kg of hypertonic sodium bicarbonate intravenously over 4 minutes or similar volumes of 0.6% sodium chloride in 10% mannitol (control). The main outcome parameter followed was mean arterial pressure. In addition, physiologic parameters including cardiac output, heart rate, pH, PCO (2), PO (2), plasma ionized calcium, sodium, and potassium were monitored. RESULTS: Verapamil toxicity, as defined by a mean arterial pressure of 45% of baseline, was produced in all animals following an average verapamil infusion dose of 0.6+/-0.12 mg/kg. This dose produced an average plasma verapamil concentration of 728.1+/-155.4 microgram/L, with no significant difference between groups. Swine treated with hypertonic sodium bicarbonate experienced a significant increase in mean arterial pressure (>50%) and cardiac output (>30%) over the first 20 minutes that slowly equilibrated with the control group over the remainder of the experiment. As expected, plasma sodium concentrations were elevated significantly in the sodium bicarbonate group while plasma potassium concentrations were decreased significantly. Finally, there was a significant decrease in plasma ionized calcium concentration in the sodium bicarbonate-treated group compared with controls. CONCLUSION: Hypertonic sodium bicarbonate reversed the hypotension and cardiac output depression of severe verapamil toxicity in a swine model.

Failure of intravenous N-acetylcysteine to reduce methemoglobin produced by sodium nitrite in human volunteers: A randomized controlled trial.

STUDY OBJECTIVE: To determine whether intravenous N -acetylcysteine (NAC) produces a clinically significant decline in sodium nitrite-induced methemoglobinemia in human volunteers. METHODS: We conducted a randomized, control crossover trial with each subject serving as his own control. Methemoglobinemia was induced with intravenous sodium nitrite (4 mg/kg) administered over 10 minutes starting at time 0. At time 30 minutes, subjects were randomly assigned to treatment with intravenous NAC for 100 minutes (150 mg/kg over 1 hour followed by 14 mg/kg per hour for 40 minutes) or administration of an equal volume of 5% dextrose in water. Each subject received the alternative treatment after an interval of at least 1 week. Blood methemoglobin concentrations were measured by multiwavelength co-oximetry at time 0, 15, 30, 50, 70, 90, 110, and 130 minutes. Area under the methemoglobin concentration-time curve (AUC) between 30 and 130 minutes was compared between groups using a 2-tailed, paired t test. RESULTS: There were no statistically significant differences in the control and treatment groups with respect to baseline hemoglobin or methemoglobin concentrations, as well as nitrite-induced methemoglobin concentrations at the initiation of treatment (0.85+/-0.06 g/dL, 0.88+/-0.04 g/dL; mean+/-SEM; P =.31). Mean AUC for the control group (77.1+/-5.7 g x min/dL) was significantly lower than the mean AUC for the treatment group (84.5+/-4.7 g x min/dL); P =.01). CONCLUSION: Intravenous NAC failed to enhance methemoglobin reduction in this model.

Crack cocaine ingestion with prolonged toxicity requiring electrical pacing.

CASE REPORT: We report a 38-year-old man who experienced prolonged toxicity lasting over 16 hours from the time of ingestion of 1/4 ounce of crack cocaine. His illness included status epilepticus, wide and narrow complex bradyarrhythmias, ventricular arrhythmias, and delayed hyperthermia. His bradyarrhythmias were refractory to medicinal intervention and responsive to application of an external pacemaker. The patient recovered to his baseline state over the ensuing 48 hours.

Renal failure and corrosive airway and gastrointestinal injury after ingestion of diluted diquat solution.

A 66-year-old man ingested 200 mL of Dexol Industries Weed and Grass Killer Concentrate (Torrance, CA), which contains 1.84% diquat dibromide, a herbicide structurally similar to paraquat. He remained asymptomatic for 8 hours, and then a sore throat and vomiting developed. Twenty hours after ingestion, esophagitis, mucositis, epiglottitis, and acute renal failure developed, from which he slowly recovered. This is the first report of systemic diquat toxicity from ingestion of a diluted diquat solution.