Critical care clinics
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The majority of clinicians will encounter patients with heat-related illness in one form or the other. Early recognition and management are important to prevent morbidity and mortality. In children and elderly, the clinical signs may be subtle and in such situations a sound knowledge of heat-related illnesses is crucial. Besides diagnosing and treating heat-related illnesses, it is equally important to know how to prevent them as they are easily preventable.
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Individuals at extremes of age and those who have certain underlying medical conditions are at greatest risk for hypothermia. Hypothermia may occur during any season of the year and in any climate. Prompt recognition of hypothermia and early institution of the rewarming techniques are imperative for a successful outcome with minimal complications. Several rewarming techniques are available and the decision to use any of them depends on the degree of hypothermia, the condition of the patient, and the rewarming rate possible with the technique chosen.
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Envenomations are uncommon, challenging causes of critical care admissions. This article describes the diagnosis and treatment of envenomations that cause the most critical care admissions in the United States. Most are caused by the following animals: rattlesnakes, copperheads, cottonmouths, coral snakes, brown recluse spiders, and bark scorpions.
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The major physiologic stress encountered at high altitude is caused by the occurrence of hypobaric hypoxia. In this article, acute and chronic pulmonocardiac adaptation to altitude is reviewed, including possible genetic differences among highlanders from the Himalayan versus the Andean Mountains. The origin, symptoms, and treatment of acute mountain sickness and high altitude pulmonary edema are outlined. In addition, the prediction and prevention of pulmonary complications that may be encountered or exacerbated during commercial airflight are noticed.
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Carbon monoxide (CO) poisoning is common and frequently unrecognized since the signs and symptoms are relatively nonspecific. CO poisoning causes tissue hypoxia. Additionally, various animal studies have demonstrated that CO interferes with myoglobin, P450, and other enzyme function; causes lipid peroxidation through neutrophil activation; produces oxidative stress manifested by peroxynitrate deposition in endothelium; binds to cytochrome aa3, disrupting intracellular oxygen utilization; can cause neuroexcitotoxicity; and contributes to hippocampal cellular death through apoptosis. ⋯ CO poisoning, even when treated with supplemental oxygen can leave the patient with permanent neurocognitive or affective problems. Unfortunately, there appears to be no marker or constellation of signs or symptoms at presentation that predicts long-term outcome following CO poisoning. Given the neurocognitive sequelae following CO poisoning, increased awareness and prevention of CO poisoning is imperative.