Acute CO poisoning is a systemic toxic disease caused by inhalation of high concentrations of CO, mainly damage to the central nervous system. Its causes are: occupational, lifestyle and other factors, and in China it is mostly caused by lifestyle factors. Acute CO poisoning is divided into mild, moderate and severe poisoning. The main manifestations of mild and moderate poisoning are headache, dizziness, palpitation, nausea, vomiting, weakness of limbs, blurred consciousness and even coma, but the duration of coma is short, and the person can be awakened sooner after being rescued from the scene, and there are generally no obvious complications. The blood HbCO concentration ranges from 10% to 50%. Some patients show EEG abnormalities. In severe poisoning, the degree of consciousness impairment reaches deep coma or decortical state. Often, there is dental closure, tonic generalized spasm, and urinary and fecal incontinence. Some patients may suffer from cerebral edema, pulmonary edema, severe myocardial damage, shock, respiratory failure, upper gastrointestinal bleeding, skin blisters or patchy skin redness, muscle swelling and necrosis, liver and kidney damage, etc. The blood HbCO concentration may be higher than 50%. Most patients have abnormal EEG. Acute CO poisoning late onset encephalopathy refers to the emergence of neuropsychiatric symptoms after recovery from acute poisoning consciousness impairment and after a pseudo-healing period of 2 to 60 days. The common clinical manifestations are as follows: a. Mental disorders: loss of orientation, significant decrease in calculating power, memory loss, slow reaction, inability to take care of themselves, some patients show dementia, or hallucinations, delusions, incoherent speech, behavioral disorders, etc. b. Extrapyramidal symptoms: dull face, increased muscle tone, slow movement, small gait, loss of accompanying movement of both upper limbs, small writing syndrome and Parkinson’s syndrome. c. Cone system nerve damage: manifesting mild hemiparesis, pseudobulbar palsy, positive pathological reflexes or urinary incontinence. d. Focal cortical dysfunction: such as aphasia, blindness, dysgraphia, dyscalculia, etc., or secondary epilepsy. Cranial CT examination may reveal pathologically hypodense areas in the brain. EEG may reveal moderate or high abnormalities. Diagnosis and differential diagnosis: Acute CO poisoning can be diagnosed based on the history of exposure to high concentrations of CO inhalation and symptoms and signs of acutely occurring central nervous system damage, combined with the results of timely determination of HbCO in blood, on-site hygienic investigation and measurement of CO concentration in air, and after excluding other etiologies. Acute CO poisoning should be differentiated from cold, hypertension, food poisoning, diabetes mellitus, cerebrovascular accident, sleeping pill poisoning and other diseases. The differential diagnosis of delayed encephalopathy needs to be made with other disorders with similar symptoms. Treatment: Quickly remove the poisoned person from the poisoning site to a ventilated place, loosen the collar, pay attention to warmth, and closely observe the state of consciousness. Timely and effective oxygen administration is the most important treatment principle for acute CO poisoning. All poisoned patients should be treated with hyperbaric oxygen, which can accelerate the clearance of HbCO in the patient’s blood and rapidly correct tissue hypoxia. The method is to inhale pure oxygen with 2 to 2.5 atmospheric pressure movable mask for 60 minutes once a day, generally 10 to 20 times for mild poisoning, 20 to 30 times for moderate poisoning, and 30 to 50 times for severe poisoning. Patients with delayed encephalopathy should have a sufficient course of hyperbaric oxygen therapy according to their specific condition. Symptomatic and supportive therapy: According to the condition, therapeutic drugs to relieve cerebral edema and improve cerebral blood circulation, maintain respiratory and circulatory function and antispasmodic, etc. are used. For patients with late-onset encephalopathy, treatment includes hyperbaric oxygen, glucocorticoids, vasodilators, neurophilic nutrients and anti-Parkinson’s disease drugs. For patients with moderate or severe intoxication, they should rest for two weeks and be closely observed for two months after they are comatose and awake.