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.

Diagnostic use of physicians' detection of urine fluorescence in a simulated ingestion of sodium fluorescein-containing antifreeze.

STUDY OBJECTIVE: We sought to assess physicians' ability to accurately determine the presence or absence of sodium fluorescein (SF) in urine at a concentration corresponding to that present after ingestion of a toxic amount of commercial automotive antifreeze. METHODS: We studied 2 different urine specimen evaluation formats--one presenting isolated specimens, and the other presenting specimens grouped for comparison--to determine whether the visual clues afforded by grouped comparison aided the accuracy of the evaluation. On each study day, 3 urine specimens (1 control specimen obtained before SF administration and 2 specimens obtained after SF administration) were obtained from each of 9 or 10 volunteers. Each of these 27 or 30 urine specimens were presented sequentially and in random order to 2 emergency physicians during separate evaluation time periods. Each physician was asked to classify each specimen as fluorescent or nonfluorescent (sequential format). After a rest period, each physician, again separately, was asked to look at the same 27 or 30 urine specimens, this time all together in a test tube rack so that grouped comparisons were possible. The physicians again classified each sample as either fluorescent or nonfluorescent (grouped format). We assessed sensitivity, specificity, and accuracy of the evaluation by each presentation format (sequential or grouped). RESULTS: Mean examiner sensitivity, specificity, and accuracy for detecting the presence of SF in urine using the sequential presentation format were 35%, 75%, and 48%, respectively, whereas the same test performance indices were 42%, 66%, and 50%, respectively, when the grouped format was used. CONCLUSION: Wood's lamp determination of urine fluorescence is of limited diagnostic utility in the detection of SF ingestion in an amount equivalent to toxic ingestion of some ethylene glycol--containing automotive antifreeze products.

Intravenous pyridoxine-induced metabolic acidosis.

STUDY OBJECTIVE: Pyridoxine hydrochloride, the antidote for isonicotinic acid hydrazide (INH)--induced seizures, is available in solution at a concentration of 100 mg/mL at a pH of less than 3. Pyridoxine is often infused rapidly in large doses for INH-induced seizures. Effects of pyridoxine infusion on base deficit in amounts given for INH poisoning have not been studied in human subjects. We hypothesized that this infusion would result in transient worsening of acidosis. METHODS: We conducted a randomized, controlled crossover trial in human volunteers. Five healthy volunteers (mean age, 35 years; range, 29 to 43 years) were randomized to receive intravenous placebo (50 mL of normal saline solution) or 5 g of pyridoxine (50 mL) over 5 minutes. A peripheral intravenous catheter was established in each arm, and a heparinized venous blood sample was obtained for base deficit at baseline and 3, 6, 10, 20, and 30 minutes after infusion. After at least a 1-week washout period, the volunteers were assigned to the alternate arms of the experiments, thus acting as their own control subjects. Data were analyzed by using the 2-tailed paired t test, controlling for multiple comparisons. RESULTS: No difference was noted between groups at baseline. A statistically significant increased base deficit was noted after the pyridoxine infusion versus control at 3 to 20 minutes but not at 30 minutes (P =.1). Maximal mean increase in base deficit (2.74 mEq/L) was noted at 3 minutes. CONCLUSION: A transient increase in base deficit occurs after the infusion of 5 g of pyridoxine in normal volunteers.

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.

Atropine use in Centruroides scorpion envenomation.

BACKGROUND: Systemic scorpion envenomation may be associated with hypersalivation and respiratory distress. Atropine can dry secretions, but is not recommended for stings from many foreign scorpions, since it exacerbates adrenergic toxicity to the cardiopulmonary system. Serious adrenergic effects, however, are rare with Centruroides sculpturatus envenomation. CASE SERIES: Five cases of Grade IV C. sculpturatus envenomation whose treatment included atropine were found on retrospective review at one poison control center located in a scorpion-endemic area. No clinically significant adverse effects of atropine were noted. In 3 cases, atropine's reversal of hypersalivation and respiratory distress obviated the need for further interventions.

Medicare expenditures on unsuccessful out-of-hospital resuscitations.

Numerous studies have shown the futility of continued emergency department (ED) resuscitative efforts for victims of out-of hospital cardiac arrest when prehospital resuscitation has failed. Nevertheless, these patients continue to arrive in the ED, where they create a strain on resources. To assess the economic cost of this, Medicare expenditures were determined for resuscitative efforts on victims of atraumatic, out-of-hospital cardiac arrest subsequently pronounced dead in the ED. Charts of patients pronounced dead in the ED of a 65,000-visit urban teaching hospital during 1995 were reviewed. Selected patients met the following criteria: 1) Medicare recipient age 65 or over; 2) atraumatic, out-of-hospital arrest; 3) transported to the ED by an EMS crew authorized to perform advanced cardiac life support interventions. A total of 105 cases were identified that met inclusion criteria and for which Medicare had claims on file corresponding to the date of death. Ambulance service payments ranged from $105-$391; mean = $263. Physician service payments ranged from $8-$106; mean = $65. Payments for Medicare Part A (hospital facility) ranged from $59-$1,025; mean = $436. The total Medicare reimbursement was $80,197, mean = $764. This annualizes to a national expenditure projection of $58 million. Failed out-of-hospital resuscitation for Medicare patients is associated with poor outcome and high cost. Termination of these efforts in the prehospital arena is unlikely to affect outcome, and would result in considerable cost savings on physician and hospital facility charges. Compassionate protocols that recognize these principles should be developed and implemented.

Acute cyanide toxicity caused by apricot kernel ingestion.

A 41-year-old woman ingested apricot kernels purchased at a health food store and became weak and dyspneic within 20 minutes. The patient was comatose and hypothermic on presentation but responded promptly to antidotal therapy for cyanide poisoning. She was later treated with a continuous thiosulfate infusion for persistent metabolic acidosis. This is the first reported case of cyanide toxicity from apricot kernel ingestion in the United States since 1979.

Recurrent near-syncope with flushing.

Episodic vasomotor instability with flushing is an uncommon presentation that is suggestive of an endocrine etiology. This report is the case of a 42-year-old woman who presented to the ED 5 times in a 2-week period for recurrent, self-limited episodes of light-headedness associated with tachycardia, hypertension, and flushing. The patient's diagnosis eluded detection in both the outpatient and the inpatient settings for several months. The clinical diagnosis was ultimately confirmed by biochemical test samples obtained in the ED during a subsequent symptomatic event. The differential diagnosis of this patient's presentation includes pheochromocytoma, carcinoid syndrome, medullary thyroid carcinoma, systemic mastocytosis, and other endocrine and toxicologic diseases. ED management of the patient with transient yet significant vasomotor changes includes a workup for syncope, initiation of focused biochemical investigations, referral to the appropriate consultant, and consideration for admission.