Poisoned by carbon monoxide

Introduction Carbon monoxide poisoning is a poisoning caused by inhalation of the product through the respiratory tract when the carbonaceous material is incompletely burned. The mechanism of poisoning is that the affinity of carbon monoxide and hemoglobin is 200-300 times higher than that of oxygen and hemoglobin. Therefore, carbon monoxide is easily combined with hemoglobin to form carboxyhemoglobin, which causes hemoglobin to lose its ability to carry oxygen and cause tissue asphyxia. It has toxic effects on whole body tissue cells, especially on the cerebral cortex. When people realize that carbon monoxide poisoning has occurred, it is often too late. Because the cerebral cortex that controls the movement of the human body is the first to suffer from paralysis, it is impossible to achieve a purposeful voluntary movement. The hands and feet are not listening. Therefore, carbon monoxide poisoning people are often unable to carry out effective self-help.

Cause

Carbon monoxide (CO) is a colorless, odorless, odorless gas. The density is 1.291. The concentration of CO in the air reaches 12.5%-74%, posing a risk of explosion. Industrially, the blast furnace gas and the furnace contain 30% to 35% of CO, and the water gas contains 30% to 40% of CO. In the steelmaking, coking, kiln and other industries, the furnace door or kiln door is not tightly closed during the production process, and a large amount of CO can escape from the gas pipeline leakage. When the indoor diesel locomotive or train passes through the tunnel, the CO in the air can reach harmful concentrations. The CO content of the guns produced by the mines is also high. A large amount of CO is produced when coal mine gas explosion. The chemical industry synthesizes ammonia, methanol, acetone, etc. to be exposed to CO.

In daily life, smoking a pack a day can increase the blood carboxyhemoglobin (COHb) concentration to 5% to 6%. Living 8 hours in a smoking environment is equivalent to smoking 5 cigarettes. The CO content of the gas produced by the coal stove can be as high as 6% to 30%. CO poisoning can occur when the interior doors and windows are closed, the chimney has no chimney, or the chimney is clogged, leaking, tumbling, and using a gas heater shower in a poorly ventilated bathroom. The CO concentration in the air at the scene of the fire can be as high as 10%, and poisoning can also occur.

an examination

Related inspection

Dynamic electrocardiogram (Holter monitoring) blood oxygen saturation

1. Determination of carboxyhemoglobin in blood

Normal human blood carboxyhemoglobin content can reach 5% to 10%, a small amount from endogenous carbon monoxide, O.4% to O.7% mild carbon monoxide poisoning, blood carboxyhemoglobin can be higher than 10% Moderate poisoning can be higher than 30%, and severe poisoning can be higher than 50%. However, the determination of carboxyhemoglobin in blood must be timely. After 8 hours of exposure to carbon monoxide, carboxyhemoglobin can be reduced to normal and may not be in parallel with clinical symptoms.

2. EEG

It has been reported that 54% to 97% of patients with acute carbon monoxide poisoning can find abnormal EEG, which is characterized by an increase in low amplitude and slow wave. Generally, the theta waves and delta waves in the forehead and ankle are often associated with clinical disturbances of consciousness. Some comatose patients can also have special three-phase waves, similar to the waveforms in hepatic coma. Pseudo paroxysmal spine slow waves or slow and slow waves. Some patients with acute carbon monoxide poisoning may have a long-term abnormality of ESD.

3. Brain evoked potential examination

In the acute phase of delayed carbon monoxide poisoning and late encephalopathy, the visual evoked potential VEP100 prolonged latency, the abnormal rates were 50% and 68%, respectively, and the recovery period was reduced to 5% and 22% of the median nerve somatosensory evoked potential (SEP). See N32 and other long-term latent components selective damage, the abnormal rate of both types of patients are more than 70%, and the recovery of brainstem auditory evoked potential (BAEP) abnormality is closely related to the degree of disturbance of consciousness, and poisoning The outcome of the disease is parallel.

4. Brain imaging examination

In patients with carbon monoxide poisoning, the CT scan of the brain in the acute phase and the occurrence of delayed encephalopathy showed that the main abnormalities were bilateral cerebral cortical white matter and a symmetrical sensation of density reduction in the globus pallidus or internal capsule. Later, ventricular enlargement or sulcal widening was observed. The abnormal rates were 41.2% and 87.5%, respectively. The prognosis of patients with abnormal brain CT was better. The patients with CT abnormalities had more than 48 hours of coma. However, there is no CT change in the early stage of delayed encephalopathy. The above CT abnormalities are usually found after 2 weeks of delayed onset of encephalopathy, so it is not as sensitive as brain evoked potentials and EEG.

5. Blood, urine, cerebrospinal fluid routine test

The total number of peripheral red blood cells, white blood cells and neutrophils increased. The number of white blood cells in severe poisoning was higher than 18×109/L. One-fifth of patients with urinary protein can be positive in patients with 40% urine sugar. Cerebrospinal fluid pressure and routine majority are normal.

6. Blood biochemical examination

Serum ALT activity and transient increase in non-protein nitrogen. Lactate and lactate dehydrogenase activity increased after acute poisoning. Serum AST activity also began to increase in the early 24 hours to the highest value. If it exceeds the normal value by 3 times, it often indicates that the condition is severe or there is complication with rhabdomyolysis, the blood creatine phosphokinase (CPK) activity is significantly increased. . Blood gas examination shows that the blood oxygen partial pressure normal blood oxygen saturation can be normal, the blood pH is lowered or normal, and the blood carbon dioxide partial pressure often has a compensatory decrease in blood potassium.

7. Electrocardiogram

Some patients may have ST-T changes, as well as ventricular premature contractions, conduction block, or transient sinus tachycardia.

Differential diagnosis

Light weight: The poisoning time is short, and the blood carboxyhemoglobin is 10%-20%. It is characterized by early symptoms of poisoning, headache, dizziness, palpitations, nausea, vomiting, weakness of the limbs, and even short-term fainting. Generally, the mind is still awake, inhaling fresh air, and leaving the poisoned environment, the symptoms quickly disappear, generally leaving no sequelae. 89 of them were mildly poisoned.

Medium: The poisoning time is slightly longer, and the carboxyhemoglobin in the blood accounts for 30%-40%. On the basis of mild symptoms, collapse or coma may occur. The skin and mucous membranes are cherry red that is unique to gas poisoning. If the rescue is timely, it can be quickly awake, fully recovered within a few days, and generally has no aftereffects.

Heavy: found too late, inhaled too much gas, or inhaled a high concentration of carbon monoxide in a short period of time, blood carboxyhemoglobin concentration is often more than 50%, patients with deep coma, various reflexes disappear, incontinence, quadriplegia Cold, blood pressure drops, shortness of breath, will die quickly. The longer the general coma, the more serious the prognosis, often leaving sequelae such as dementia, memory and comprehension, limb paralysis. According to the history of CO exposure, suddenly fainted, the skin mucosa cherry red, the diagnosis is generally no difficulty. When the medical history is difficult, it should be differentiated from cerebrovascular accident, meningitis, and diabetic ketoacidosis. The determination of HbCO in blood has diagnostic value. According to the exposure history of inhaled higher concentrations of carbon monoxide and the symptoms and signs of acute central nervous system damage, combined with the results of timely determination of blood carboxyhemoglobin (HbCO), on-site hygiene investigation and determination of carbon monoxide concentration in the air, and exclude other After the cause, it can be diagnosed as acute carbon monoxide poisoning.

The material in this site is intended to be of general informational use and is not intended to constitute medical advice, probable diagnosis, or recommended treatments.