Carbon Monoxide Toxicity.

Carbon monoxide accounts for thousands of deaths worldwide each year. Clinical effects can be diverse and include headache, dizziness, nausea, vomiting, syncope, seizures, coma, dysrhythmias, and cardiac ischemia, and severe toxicity generally affects the nervous and cardiovascular systems. Because of its complex pathophysiology, effects of toxicity can be acute or delayed. The diagnosis can be elusive, as carboxyhemoglobin levels do not always correlate with the degree of poisoning. Even when the diagnosis is certain, appropriate therapy is widely debated. Normobaric oxygen is the standard therapy, and the efficacy of hyperbaric oxygen is unclear.

Calcium channel blocker toxicity.

Calcium channel blockers continue to be used for the management of a wide variety of adult and pediatric conditions including hypertension, angina pectoris, atrial arrhythmias, Raynaud phenomenon, and migraine headaches. With increased use comes increased potential for misuse and abuse. This article serves as a review of calcium channel blocker physiology with emphasis on presentation and management of the pediatric patient with calcium channel blocker toxicity.

Toxicity associated with carbon monoxide.

Carbon monoxide is an insidious poison that accounts for thousands of deaths each year in North America. Clinical effects maybe diverse and include headache, dizziness, nausea, vomiting,syn-cope, seizures, coma, dysrhythmias, and cardiac ischemia. Children, pregnant women, and patients who have underlying cardiovascular disease are particularly at risk for adverse out-comes. Treatment consists of oxygen therapy, supportive care, and, in selected cases, hyperbaric oxygen therapy.

Carbon monoxide poisoning.

CO is an insidious poison with many sources of exposure. CO poisoning produces diverse signs and symptoms, which often are subtle and can be misdiagnosed easily. Failure to diagnose CO poisoning may result insignificant morbidity and mortality and allow continued exposure to a dangerous environment. In the ED, a high index of suspicion must be maintained for occult CO exposure. Headache, particularly when associated with certain environments, and flulike illness in the wintertime with symptomatic cohabitants should raise the index of suspicion in the ED significantly for occult CO poisoning. Emergency treatment of CO poisoning begins with inhalation of supplemental oxygen and aggressive supportive care. HBOT accelerates dissociation of CO from hemoglobin and may prevent DNS. Absolute indications for HBOT for CO poisoning remain controversial, although most would agree that HBOT is indicated in patients who are comatose, are neurologically abnormal, have a history of loss of consciousness with their exposure, or have cardiac dysfunction. Pregnancy with an elevated CO-Hgb level (>15-20%) also is widely considered an indication for treatment. HBOT may be considered in patients who have persistent symptoms despite NBO, metabolic acidosis, abnormalities on neuropsychometric testing, or significantly elevated levels. The ideal regimen of oxygen therapy has yet to be determined, and significant controversy exists regarding HBOT protocols. The emergency physician may be confronted with the difficult decision regarding disposition and even transfer to a hyperbaric facility. Often the local medical toxicologist, poison control center, or hyperbaric unit can assist the emergency physician with the decision-making process.

Hyperbaric oxygen therapy in acute ischemic stroke: results of the Hyperbaric Oxygen in Acute Ischemic Stroke Trial Pilot Study.

BACKGROUND AND PURPOSE: Hyperbaric oxygen therapy (HBO) has promise as a treatment for acute stroke. This study was conducted to evaluate the efficacy, safety, and feasibility of using HBO in acute ischemic stroke. METHODS: We conducted a randomized, prospective, double-blind, sham-controlled pilot study of 33 patients presenting with acute ischemic stroke who did not receive thrombolytics over a 24-month period. Patients were randomized to treatment for 60 minutes in a monoplace hyperbaric chamber pressurized with 100% O2 to 2.5-atm absolute (ATA) in the HBO group or 1.14 ATA in the sham group. Primary outcomes measured included percentage of patients with improvement at 24 hours (National Institutes of Health Stroke Scale [NIHSS]) and 90 days (NIHSS, Barthel Index, modified Rankin Scale, Glasgow Outcome Scale). Secondary measurements included complications of treatment and mortality at 90 days. RESULTS: Baseline demographics were similar in both groups. There were no differences between the groups at 24 hours (P=0.44). At 3 months, however, a larger percentage of the sham patients had a good outcome defined by their stroke scores compared with the HBO group (NIHSS, 80% versus 31.3%; P=0.04; Barthel Index, 81.8% versus 50%; P=0.12; modified Rankin Scale, 81.8% versus 31.3%; P=0.02; Glasgow Outcome Scale, 90.9% versus 37.5%; P=0.01) with loss of statistical significance in a intent-to-treat analysis. CONCLUSIONS: Although our HBO protocol appears feasible and safe, it does not appear to be beneficial and may be harmful in patients with acute ischemic stroke.