Acute carbon monoxide poisoning (ACOP) is one of the common poisonings and the most common cause of acute poisoning deaths. The recommendations in the guideline are based on the Delphi grading criteria proposed by the International Infection Forum in 2001, and the literature involved in the guideline is divided into five levels from l to V according to the study methods and results, and the recommendation level of the recommendations is divided into A to E, with A being the highest level. Carbon monoxide (CO) is a colorless, odorless, non-irritating asphyxiating gas produced by carbonaceous substances during incomplete combustion, and is the most common asphyxiating gas in industrial production and living environments. The morbidity and mortality rate of ACOP are the top occupational and non-occupational hazards in China. Exposure pathway and toxicity 1, exposure pathway: CO enters the body through respiratory inhalation causing poisoning. (1) home life; (2) production; (3) coal mine gas explosion; (4) public places; (5) transportation; (6) agriculture and animal husbandry production. 2, toxicity: the amount of CO absorbed by the body depends on the amount of ventilation per minute, CO exposure time, CO concentration and environmental oxygen content. 3.Relationship between blood HhCO concentration and clinical manifestations: The blood HbCO concentration of patients is often inconsistent with their clinical manifestations. the HbCO concentration is affected by the time out of the environment and whether they receive oxygen therapy on the way. 4. Age distribution of poisoned patients: all age groups are involved. III. Clinical manifestations 1. Synergistic factors of the degree of poisoning: The degree of poisoning is influenced by the following factors: ① The greater the CO concentration and the longer the CO exposure time, the more severe the poisoning. ②The presence of other toxic gases (such as sulfur dioxide, methylene chloride, etc.) will enhance the toxicity. (③In high temperature environment, anemia, myocardial ischemia, cerebral blood supply deficiency, fever, diabetes and hypoxemia due to various reasons are serious. 2. Neurological system: (1) Toxic encephalopathy: (1) Whole brain symptoms: varying degrees of impaired consciousness, psychiatric symptoms, convulsions and epilepsy, etc. (2) Focal manifestations: such as hemiplegia, monoplegia, tremor, etc. (2) Cerebral edema: impaired consciousness. Vomiting, neck resistance, and optic papillary edema visible on fundus examination. (3) Brain herniation: deepening coma． Irregular breathing. Pupils are not equally round, and light response is absent. (4) Cortical blindness: caused by infarction, ischemia and poisoning of bilateral occipital lobes. (5) Peripheral nerve damage. (6) Cutaneous vegetative nerve dystrophy. 3, Respiratory system: (1) acute pulmonary edema; (2) acute respiratory distress syndrome (ARDS). 4. Circulatory system: shock and arrhythmia may occur in a few cases, and the incidence of acute left heart failure is extremely low. 5.Urological system: (1) pre-renal azotemia; (2) acute renal failure. 6. Shock: manifested as low blood pressure, narrow pulse pressure difference, fine pulse, wet and cold extremity endings, pale skin, prolonged capillary filling time, and oliguria or anuria. Complications mainly include: (1) rhabdomyolysis syndrome, which can cause acute renal failure. Abnormal sensation, severe pain, numbness, hypoesthesia or loss of sensation in the affected limb, etc. (2) cerebral infarction; (3) cerebral hemorrhage; (4) epileptic seizures or epilepsy. IV. Laboratory tests 1. Blood HbCO measurement, recommendation: HbCO has important reference significance for the diagnosis of ACOP. It should be used as the main examination item. Quantitative detection of blood HbCO concentration has high confidence (arterial blood gas analysis). Qualitative testing by colorimetric methods is prone to false positives and false negatives, and should be performed with contemporaneous healthy controls. Recommended grade: D. 2. Serum enzymatic tests, Recommendation: Abnormally high serum enzymes are meaningful for the diagnosis of ACOP. When the CO environment where the comatose patient is located is not clear and the differential diagnosis is difficult. The combination of abnormal increase in serum enzymology and blood gas analysis is an important laboratory indicator for the diagnosis of ACOP. Recommended grade: D. 3. Arterial blood gas analysis, Recommendation: Correction of hypoxemia and acid-base imbalance after ACOP is an important part of emergency resuscitation treatment. Comatose critically ill patients should be routinely tested in medical institutions that are in a position to do so. Recommended level: D. 4.Renal function test, Recommendation: Seriously ill patients should be routinely tested. Recommended level: D. 5, electroencephalogram examination: recommendation: not as a routine test items. Recommended level: D. 6.Cranial CT examination: Recommendation: Patients with severe ACOP should be used as routine examination items. Recommended level: D. 7.Brain magnetic resonance imaging (MRI): Recommendation: Patients with severe coma. This test should be performed promptly, especially when there is a differential diagnosis. Recommended level: D. 8.Electrocardiography: Recommendation: Patients with underlying diseases are prone to acute myocardial infarction, arrhythmia, acute cardiac insufficiency, etc., and should be selected according to the patient’s specific condition. Recommended grade: Grade D. V. Diagnosis and differential diagnosis 1. Diagnostic criteria The Diagnostic Criteria for Occupational Acute Carbon Monoxide Poisoning formulated by the Ministry of Health are followed. 2. Differential diagnosis (1) cerebral infarction (2) hemorrhagic cerebrovascular disease (3) diabetic ketoacidosis coma (4) hyperosmolar diabetic coma VI. Avoid accidental aspiration. 2. Oxygen therapy on site Use the oxygen absorbing device prepared on site to give oxygen therapy immediately. As a medicine, the application of “oxygen”, like any other medicine, should have clear indications, and the principle of ACOP on-site oxygen therapy is high flow and high concentration. (1) Nasal catheter oxygen administration: on-site oxygen therapy nasal catheter or nasal plug oxygen administration is the most economical and easy to implement method. The bilateral catheter method is more convenient than the unilateral catheter method, and the oxygen absorption effect is similar to the unilateral nasal catheter, which is one of the most acceptable methods for patients. (2) Mask method: ①Simple mask method: Simple mask is suitable for patients with severe hypoxia and no CO: retention. (②Oxygen storage bag mask: the group with oxygen storage bag is better than the normal mask group in terms of disappearance of patient’s symptoms and improvement of consciousness. (③Venturi mask: Venturi mask is used for the treatment of hypoxemia with hypercapnia. (3) Ventilator: The HDP-D high-frequency ventilation ventilator is used to give high-frequency jet ventilation and oxygen to poisoned patients at the scene of poisoning and in pre-hospital emergency at the first time. It is especially suitable for poisoning scene and pre-hospital emergency. This machine is suitable for patients who are unconscious but have a clear airway and not much sputum. (4) Portable hyperbaric oxygen chamber: However, no report has been seen on its application in ACOP medical clinic. Recommendation: On-site oxygen therapy as an essential rescue treatment measure after ACOP, all departments involved in rescue and treatment should create conditions to implement oxygen therapy immediately. The use of non-repetitive breathing mask (oxygen storage bag mask and Venturi mask) oxygen therapy is effective, practical and economical, and is firstly recommended. (Level D) 3. Early resuscitation treatment Recommendation: Early comprehensive, timely, appropriate, scientific and effective resuscitation treatment is essential for prognosis. (Grade C). 4.Hyperbaric oxygen therapy Recommendation: When available, early hyperbaric oxygen therapy can discharge CO from the body as soon as possible, which is beneficial for patients to wake up as soon as possible, reduce hypoxic injury and reduce the incidence of delayed encephalopathy. In the acute stage, patients should be sent to a hospital with hyperbaric oxygen chamber for hyperbaric oxygen therapy as soon as possible. Rigorous prospective, randomized, controlled and large sample clinical studies are needed for the treatment of ACOP with hyperbaric oxygen and prevention of delayed onset encephalopathy. (Level B) Pressure and frequency of hyperbaric oxygen therapy: Recommendation: Hyperbaric oxygen therapy pressure 0.20-0.25 MPa, duration of oxygen in the chamber 60 min, number of treatments according to the patient’s condition, but not more than 30 consecutive treatments. Whether oxygen is administered between hyperbaric oxygen treatments should be based on the results of blood gas analysis. Clarification of which modality is more beneficial requires a randomized controlled large sample multicenter study and is measured by neurocognitive experiments. (Grade C) 5. Intractable hypoxemia Recommendation: Patients with uncorrectable intractable hypoxemia and unstable vital signs should withhold hyperbaric oxygen therapy and mechanical ventilation should be considered. (Grade D) 6.Sub-hypothermia treatment Recommendation: Sub-hypothermia therapy can be applied to comatose patients at an early stage, and sub-cryogenic therapy should be continued for 3-5 d. Pay special attention to the rewarming process, and rewarming should not be too fast. (Grade C) 7. glucocorticoids Recommendation: ACOP patients with acute severe illness without obvious contraindications can be considered for improvement of severe illness with glucocorticoids according to the needs of the condition. Considering their adverse effects and limitations, glucocorticosteroids should not be used as routine treatment in ACOP yet. Further large sample studies are needed to make conclusive guidance. 8, dehydration drugs Recommendations: (1) dehydration drugs can be used in the early stage of ACOP with severe cerebral edema coma; (2) use with caution or not in the following cases: patients with combined cardiogenic pulmonary edema, existing renal insufficiency or oliguria, and cardiac insufficiency; (3) medullary loop diuretics can be used; (4) dehydration should be based on the patient’s condition, with reference to their vital signs, mental status, pupils, fundus changes and imaging changes should be mastered, with special attention to avoid excessive dehydration. (Grade D) 9. Gangliosides: Recommendation: There is not enough evidence-based clinical evidence to support the use in the acute phase of ACOP. (Grade D) 10. Anti-platelet aggregating agents Recommendation: Anti-platelet aggregating agents should be taken in patients with moderate to severe ACOP, especially in patients with combined hypertension, diabetes mellitus, cardiovascular disease, hyperlipidemia and other underlying diseases, and in patients of advanced age. (Grade C) 11, Edaravone Recommendation: The early application of edaravone in ACOP has certain efficacy in reducing cerebral edema and improving neurological function, which is recognized by clinicians and experts, but no large sample of randomized double-blind clinical studies have been seen. It can be applied in the acute phase in patients with severe COP. (Grade C) 12. Naloxone Recommendation: Naloxone is not recommended as a routine drug in the acute phase of COP. (Grade D) 13.Virocodone Recommendation: Pyrrolidone drugs protect or promote the functional recovery of nerve cells, have been used for many years in the treatment of ACOP, and there are reports of small sample clinical studies that they are effective, in addition, there are reports that they are effective in organic encephalopathy syndrome, no adverse effects have been reported, and they can be used in the acute phase of clinical use. (Grade D) VII. Prognosis of ACOP 1. Patients with mild ACOP can be rapidly removed from the scene of poisoning, breathe fresh air or oxygen, and treat symptomatically, and their symptoms can disappear. 2.Patients with moderate ACOP can be quickly removed from the poisoning scene, and after oxygen therapy and timely rescue treatment, most of them can be cured within a few days, but some of them have neurosis and peripheral nerve damage after the symptoms disappear, and some of them have delayed onset encephalopathy. The prognosis is affected by the time of carbon monoxide exposure, the promptness of resuscitation treatment, and the presence or absence of underlying diseases. The prognosis is as follows: (1) recovery; (2) residual sequelae; (3) impaired consciousness; (4) late onset encephalopathy; (5) death. VIII. Principles for determining the recovery status of ACOP I. The prognosis was determined quantitatively using four scoring criteria: Glasgow coma scale (GCS), Barthel index score, mini-mental state examination score (MMSE), modified muscle tone ( ashworth) score. 2. Time point for determining the rehabilitation status of ACOP: 1 month after ACOP. Recovery status: (1) healed, (2) recovered, 3) improved, 4) not healed. Late onset encephalopathy of carbon monoxide (CO) poisoning is a neurological disease with dementia, psychiatric symptoms and extrapyramidal abnormalities occurring after a period of seemingly normal pseudo-healing after the ACOP patient is conscious. 1. epidemiology 2. establishment of animal models of late-onset encephalopathy and related studies 3. expert consensus: the following factors predispose to late-onset encephalopathy: (1) age above 40 years. (2) Long duration of coma. (3) Having underlying diseases such as hypertension, diabetes mellitus, hyperlipidemia, etc. (4) Major mental stimulation during the pseudo-healing period. (5) Complications during acute intoxication, such as infection and cerebral infarction. (6) Premature discontinuation of treatment after acute intoxication or improper treatment during the acute period in moderate to severe patients. 4. Clinical manifestations: (1) pseudo-healing period; (2) onset process; 3) main symptoms and signs. 5. Main auxiliary examination features 6. Diagnostic criteria: (1) A clear history of ACOP. (2) There is a clear pseudo-healing period. (3) Typical clinical manifestations with dementia, psychiatric symptoms, increased muscle tone and tremor palsy. (4) Imaging changes: brain CT and MRI changes mainly occur in the centrum semiovale and parietal ventricles. Symmetrical lesions are common in the pallidum. The corpus callosum, hippocampus, subcortical U-fibers, and external capsule may also be involved, with cortical spongiosity changes. Late stage cerebral atrophy is seen. (5) The disease has a long course and is more difficult to treat. The course of the disease is generally 3-6 months, and a few patients have a disease course of up to 1 year, leaving different degrees of sequelae. Some patients are reported to heal spontaneously abroad, but there are few reports of spontaneous healing in China. 7. Differential diagnosis: (1) acute carbon monoxide toxic encephalopathy; (2) multi-infarct dementia; (3) subcortical arteriosclerotic encephalopathy; (4) Parkinson’s syndrome. 8. Treatment: (1) symptomatic supportive therapy; (2) hyperbaric oxygen (HBO) therapy; (3) medications: (1) donepezil, puzzle drugs, ziprasidone, new non-classical antipsychotics, and bromelain cryptotin. The use of these drugs has been reported, but no RCT studies are available. ②Piracetam, aniracetam, and olanzapine. Recommendation: Donepezil and pyrrolidone analogues protect or promote functional recovery of nerve cells and have been used for many years in the treatment of ACOP. Only small samples of clinical studies have reported that they are effective in the treatment of late-onset encephalopathy, in addition, they have been reported to be effective in organic encephalopathy syndrome, and no adverse effects have been reported, and they can be used in late-onset encephalopathy (grade D). ③Glucocorticoids: Recommendation: There is a lack of medical evidence as to whether the use of glucocorticoids in DNS can significantly improve the prognosis of patients and shorten the course of treatment, and the use of glucocorticoids is not recommended for elderly patients with reduced glucose tolerance or diabetes mellitus. ④Baclofen (Lioresal). Recommendation: It can be considered when muscle tone is significantly increased in ACOP patients, and should be reduced and discontinued promptly in patients with improved muscle tone from the original disease (Grade D). ⑤ Haloperidol. Start with a small dose, 1/4 tablet (0.5 mg) to start, usually 0.5 mg will be effective, ineffective can be increased, each time incremental 1/4 tablet (level D). Ten, the prognosis, late-onset encephalopathy is long, prolonged and difficult to heal, currently reported by HBO comprehensive treatment can make most patients return to the level of self-care or better, and those who are a little younger can still restore the ability to work. The improvement of the disease is characterized by increased speech, improved behavior, and active behavior; restoration of certain cognitive ability; gradual normalization of extra-pyramidal abnormalities such as increased muscle tone as the disease improves; and control of urination and defecation. Once the disease starts to improve, the changes can be seen every day, and the end point of recovery varies from person to person. The disease does not recur after it is cured.