Carbon monoxide (CO) has the toxic effects of tissue hypoxia and produces various systemic and neurological complications. The main clinical manifestations of acute CO poisoning consist of symptoms caused by alterations of the cardiovascular system such as initial tachycardia and hypertension, and c...
Carbon monoxide (CO) has the toxic effects of tissue hypoxia and produces various systemic and neurological complications. The main clinical manifestations of acute CO poisoning consist of symptoms caused by alterations of the cardiovascular system such as initial tachycardia and hypertension, and central nervous system symptoms such as headache, dizziness, paresis, convulsion and unconsciousness. CO poisoning also produces myocardial ischemia, atrial fibrillation, pneumonia, pulmonary edema, erythrocytosis, leucocytosis, hyperglycemia, muscle necrosis, acute renal failure, skin lesion, and changes in perception of the visual and auditory systems. Of considerable clinical interest, severe neurological manifestations may occur days or weeks after acute CO poisoning. Delayed sequelae of CO poisoning are not rare, usually occur in middle or older, and are clinically characterized by symptom triad of mental deterioration, urinary incontinence, and gait disturbance. Occasionally, movement disorders, particularly parkinsonism, are observed. In addition, peripheral neuropathy following CO poisoning usually occurs in young adults.
Carbon monoxide (CO) has the toxic effects of tissue hypoxia and produces various systemic and neurological complications. The main clinical manifestations of acute CO poisoning consist of symptoms caused by alterations of the cardiovascular system such as initial tachycardia and hypertension, and central nervous system symptoms such as headache, dizziness, paresis, convulsion and unconsciousness. CO poisoning also produces myocardial ischemia, atrial fibrillation, pneumonia, pulmonary edema, erythrocytosis, leucocytosis, hyperglycemia, muscle necrosis, acute renal failure, skin lesion, and changes in perception of the visual and auditory systems. Of considerable clinical interest, severe neurological manifestations may occur days or weeks after acute CO poisoning. Delayed sequelae of CO poisoning are not rare, usually occur in middle or older, and are clinically characterized by symptom triad of mental deterioration, urinary incontinence, and gait disturbance. Occasionally, movement disorders, particularly parkinsonism, are observed. In addition, peripheral neuropathy following CO poisoning usually occurs in young adults.
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