الفهرس 
Carbon Monoxide GasOnly 14 pages are availabe for public view
 |  | from | 99 |  |  |
| | | from | 99 | | |
Abstract
The main clinical magnifications of acute CO poisoning consist of symptoms caused by alterations of the cardiovascular system such as initial tachycardia and hypertension, and CNS symptoms such as headache, dizziness, paresis, convulsions and unconsciousness. Carbon monoxide poisoning also produces myocardial ischemia, atrial fibrillation, pneumonia, pulmonary edema, erythrocytosis, leucocytosis, hyperglycemia, muscle necrosis, acute renal failure, skin lesions and changes in perception of the visual and auditory systems. Severe neurological manifestations may occur days or weeks after acute CO poisoning. Delayed sequelae of CO poisoning are usually occur in middle or older ages.
Diagnosis of CO poisoning can be based upon general symptoms of toxicity, pulse oximeter measurement and laboratory diagnosis which is promising markers as serum S100B and serum specific enolase. Treatment of the CO poisoned patient begins with supplemental O2 and aggressive supportive care, including airway management, blood pressure support, and stabilization of cardiovascular status. Oxygen enhances dissociation of COHB and clearance from the blood by competing CO at the binding sites of hemoglobin and improving tissue oxygenation. Hyperbaric oxygen is the main standard treatment of CO poisoning. HBOT accelerates dissociation of CO from hemoglobin.