Diagnosis and management of carbon monoxide poisoning in the emergency department.

An 89-year-old female is found by her family, lying unconscious on her kitchen floor after they had been unable to reach her by phone for several hours. EMS is activated and when the paramedics arrive, they note that the gas oven is on, and there is thin, gray smoke coming from around the door. The house gas supply is turned off, windows are opened, and the family and the patient are immediately evacuated from the home. En route to the hospital, the patient is placed on high-flow oxygen at 15 liters per minute by non-rebreather mask. Her bedside glucose determination is 229 mg/dL. Vital signs are within normal limits during transport. She opens her eyes to sternal rub, and makes spontaneous movements of all extremities. Upon arrival to the ED, the patient becomes more alert and is able to respond to your questions. She tells you that she remembers putting a tray of calzones into the oven, after which she has no recall of the day's events. She has a past medical history of "well-controlled" hypertension, hyperlipidemia, and non-insulin-dependent diabetes. Her medications include hydrochlorothiazide 25 mg daily, lisinopril 10 mg daily, simvastatin 20 mg daily, and metformin 1000 mg twice daily. On physical examination, weight is 65 kg, blood pressure is 97/50 mm Hg, heart rate is 113 beats per minute, respiratory rate is 22 breaths per minute, temperature is 37.1 degrees C (98.8 degrees F), and oxygen saturation is 99% on 15 liters per minute via non-rebreather mask. She appears her stated age. Cardiopulmonary examination is remarkable only for tachycardia. Her abdomen is soft and non-tender with normal bowel sounds. Her skin is warm and dry, and there is no peripheral edema. Her cranial nerves are intact, with briskly reactive, symmetric pupils. Motor and sensory examination is non-focal, and cerebellar testing is notable only for an intention tremor on finger-nose-finger test. Gait is normal and speech is fluent and without errors. Laboratory testing shows a hemoglobin of 10.3 g/dL and a leukocyte count of 11.7 x 10(9)/L. Electrolyte results fall within the normal range, and her serum creatinine is 1.7 mg/dL. Qualitative CK-MB and troponin I tests are positive, and the sample has been sent to the STAT lab for quantitative testing. Serum carboxyhemoglobin level is 15% with normal serum pH on an arterial blood gas. An ECG reveals deep, down-sloping inferior and lateral ST-segment depressions which were not present on a routine cardiogram 1 month prior. You have many questions about this patient's care. What symptoms and physical signs need to be addressed and treated? What additional diagnostic testing should be performed? What treatment regimen is appropriate and what should be avoided? What are the risks or delayed complications from her illness? Are there special considerations for this or other patient populations?

The effects of intravenous calcium in patients with digoxin toxicity.

BACKGROUND: Digoxin is an inhibitor of the sodium-potassium ATPase. In overdose, hyperkalemia is common. Although hyperkalemia is often treated with intravenous calcium, it is traditionally contraindicated in digoxin toxicity. OBJECTIVES: To analyze records from patients treated with intravenous calcium while digoxin-toxic. METHODS: We reviewed the charts of all adult patients diagnosed with digoxin toxicity in a large teaching hospital over 17.5 years. The main outcome measures were frequency of life-threatening dysrhythmia within 1 h of calcium administration, and mortality rate in patients who did vs. patients who did not receive intravenous calcium. We use multivariate logistic regression to ensure that no relationship was overlooked due to negative confounders (controlling for age, creatinine, systolic blood pressure, peak serum potassium, time of development of digoxin toxicity, and digoxin concentration). RESULTS: We identified 161 patients diagnosed with digoxin toxicity, and were able to retrieve 159 records. Of these, 23 patients received calcium. No life-threatening dysrhythmias occurred within 1 h of calcium administration. Mortality was similar among those who did not receive calcium (27/136, 20%) compared to those who did (5/23, 22%). In the multivariate analysis, calcium was non-significantly associated with decreased odds of death (odds ratio 0.76; 95% confidence interval [CI] 0.24-2.5). Each 1 mEq/L rise in serum potassium concentration was associated with an increased mortality odds ratio of 1.5 (95% CI 1.0-2.3). CONCLUSION: Among digoxin-intoxicated humans, intravenous calcium does not seem to cause malignant dysrhythmias or increase mortality. We found no support for the historical belief that calcium administration is contraindicated in digoxin-toxic patients.

Severe hydrogen sulfide exposure in a working adolescent.

We describe an occupational exposure to hydrogen sulfide gas in a 16-year-old boy. While cleaning the reoxygenation tank of a fish hatchery, he and an adult supervisor lost consciousness. The adult died, and the adolescent regained consciousness briefly when emergency medical services personnel administered oxygen. At a local emergency department, he was intubated for respiratory distress. He was transferred to a tertiary care facility for additional management and, over the next 2 weeks, had a recovery to normal function. Hydrogen sulfide is a colorless, malodorous gas that results from the decay of organic material. It is a byproduct of industry and agriculture. The mechanism of its toxicity is related primarily to inhibition of oxidative phosphorylation, which causes a decrease in available cellular energy. Although there is some anecdotal evidence to suggest that the early use of hyperbaric oxygen is beneficial, supportive care remains the mainstay of therapy. This report highlights the sources of exposure, management, and need for more stringent application of safety regulations in industries in which adolescents are employed.