What Is Carbon Monoxide Poisoning?

Carbon monoxide poisoning is the product of incomplete combustion of carbonaceous substances through inhalation through the respiratory tract and causes poisoning. The poisoning mechanism is that the affinity of carbon monoxide and hemoglobin is 200-300 times higher than the affinity of oxygen and hemoglobin, so carbon monoxide is easily combined with hemoglobin to form carboxyhemoglobin, which causes hemoglobin to lose its ability and function to carry oxygen, causing tissue suffocation. It has a toxic effect on the tissue cells of the whole body, especially the cerebral cortex.

Basic Information

nickname

gas poisoning

English name

carbon monoxide poisoning

Visiting department

Emergency Department

Common causes

Caused by inhalation of excessive combustion of carbonaceous substances

Common symptoms

Severe headache, dizziness, and palpitations; severe cases are flushed, and lips are cherry-red

Contagious

no

Clinical manifestations of carbon monoxide poisoning

The clinical manifestations are mainly hypoxia, the severity of which is proportional to the saturation of HbCO. Mild patients have headache, weakness, dizziness, and difficulty breathing during work. HbCO saturation is 10% to 20%. Symptoms aggravated, the patient's lips were cherry red, nausea, vomiting, confusion, collapse, or coma, and HbCO saturation reached 30% to 40%. In severe cases, a deep coma accompanied by high fever, increased muscle tone in the extremities, and paroxysmal or tonic spasticity, HbCO saturation> 50%. Patients often have brain edema, pulmonary edema, myocardial damage, arrhythmia, and respiratory depression, which can cause death. In some patients, blisters and redness may appear on the skin of the chest and limbs, mainly due to autonomic neurotrophic disorders. After recovering from a coma, some patients with acute CO poisoning will be unconscious again after 2 to 30 days of sham healing, and will suffer from post-psychiatric neuropathy such as dementia sclerosis, tremor paralysis syndrome, sensory dyskinesia, or peripheral neuropathy. Also known as delayed encephalopathy with acute carbon monoxide poisoning. Long-term exposure to low concentrations of CO may cause headache, dizziness, memory loss, inattention, and palpitations.

Light

The poisoning time is short, and the carboxyhemoglobin in the blood is 10% -20%. The symptoms are early symptoms of poisoning, headache, dizziness, palpitations, nausea, vomiting, weakness in the limbs, and even short-term fainting. Generally, the patient is still awake, inhales fresh air, and escapes from the poisoning environment. The symptoms quickly disappear, and generally no sequelae are left.

2.Medium

The poisoning time is slightly longer, and the oxyhemoglobin in the blood accounts for 30% to 40%. On the basis of mild symptoms, collapse or coma may occur. The skin and mucous membranes have a cherry red characteristic of gas poisoning. If the rescue is timely, you can wake up quickly and recover completely within a few days. Generally, there are no sequelae.

3.Heavy

It was found that the time was too late, too much gas was inhaled, or high concentrations of carbon monoxide were inhaled in a short period of time, the blood carboxyhemoglobin concentration was often above 50%, the patient showed deep coma, various reflections disappeared, incontinence, cold limbs, Blood pressure drops, shortness of breath, and death quickly. Generally, the longer the coma, the more serious the prognosis, and the sequelae of dementia, memory and understanding, and paralysis often remain.

Carbon monoxide poisoning test

1. Determination of carboxyhemoglobin in blood

The content of carboxyhemoglobin in normal people's blood can reach 5% to 10%, and a small amount of it comes from endogenous carbon monoxide, which is 0.4% to 0.7%. The carbhemoglobin in the blood of mild carbon monoxide poisoning can be higher than 10% , Moderate poisoning can be higher than 30%, 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, the carboxyhemoglobin can be reduced to normal and it can not be parallel to clinical symptoms.

2. EEG

It has been reported that 54% to 97% of patients with acute carbon monoxide poisoning can find abnormal EEG, showing low-wavelength and slow-wave increase. Generally, theta waves and delta waves in the frontal and temporal regions are often related to clinical conscious disturbances. Some patients with coma may also have special three-phase waves, similar to those in liver coma; pseudo paroxysmal slow waves or slow spikes and slow waves. In some patients with acute carbon monoxide poisoning, abnormal EEG abnormalities in the later stage can persist for a long time.

3. Brain Evoked Potential Examination

In the acute phase of carbon monoxide poisoning and delayed encephalopathy, the latency of visual evoked potential VEP100 is prolonged, and the abnormal rates are 50% and 68%, respectively. The recovery period can be reduced to 5% and 22% of the median neurosensory evoked potential (SEP) examination. Seen in N32 and other medium and long latent components, the selectivity is impaired, and the abnormal rate of both types of patients is more than 70%. With the improvement of consciousness, the abnormality of brainstem auditory evoked potential (BAEP) is closely related to the degree of disturbance of consciousness and is related to poisoning. The outcomes of the conditions are parallel.

4. Brain Imaging

Patients with carbon monoxide poisoning who underwent craniocerebral CT examinations in the acute phase and late-onset encephalopathy showed that the main abnormality was bilaterally subcortical white matter and pale globules or inner sacs showing roughly symmetrical density-reduced areas. Later, ventricular enlargement or sulcus widening The abnormal rate was 41.2% and 87.5% without abnormal brain CT. The prognosis was better, and those with CT abnormality had a coma time of more than 48 hours. However, there is no CT change in the early stage of delayed encephalopathy. The above CT abnormalities are generally not visible until two weeks after the onset of the symptoms of delayed encephalopathy, so it is not as sensitive as the evoked potentials and EEG.

5. Routine tests for blood, urine, and cerebrospinal fluid

The total number of peripheral red blood cells, total white blood cells, and neutrophils increased. In severe poisoning, the number of white blood cells above 18 × 10 ⁹ / L had a severe prognosis. 1/5 of the patients may have urine protein positive in 40% of patients. Cerebrospinal fluid pressure and routine are mostly normal.

6. Blood biochemical examination

Transient increase in serum ALT activity and non-protein nitrogen. Lactate and lactate dehydrogenase activities increased after acute poisoning. Serum AST activity also began to increase 24 hours to the highest value in the early stage. If it is 3 times higher than normal, it often indicates that the disease is severe or there are comorbidities with rhabdomyolysis, and the blood creatine phosphate kinase (CPK) activity is significantly increased . Blood gas examination shows normal blood oxygen partial pressure, blood oxygen saturation can be normal, blood pH is reduced or normal, blood carbon dioxide partial pressure is often compensatory, and blood potassium can be reduced.

7. ECG

ST-T changes can be seen in some patients, and pre-ventricular contractions, conduction blocks, or transient sinus tachycardia can also be seen.

Diagnosis of carbon monoxide poisoning

Clinical diagnosis can be made based on the history of CO exposure, sudden coma, and cherry red on the skin and mucous membranes.

1. There are conditions and contact history of gas generation. Occupational poisoning is often collective, and living poisoning is often caused by winter fires and poor indoor ventilation. People in the same room also have poisoning performance. The use of water heaters is also an important cause of gas poisoning.

2. Mild poisoning patients have dizziness, headache, fatigue, palpitations, nausea, vomiting, and blurred vision.

3. In severe cases, the skin is cherry-red, breathing and pulse are accelerated, limbs are strengthened, consciousness is impaired, and they are in a deep coma or even corpse. Eventually due to lung failure. Heart failure and death.

4. After rescue from severe patients, after 2 to 60 days of sham healing, symptoms of delayed encephalopathy may appear, manifested as dementia. Tremor paralysis, hemiplegia. Seizures, sensory dyskinesias, etc.

5. Carboxyhemoglobin (HBCO) was positive in blood. The blood HBCO concentration of mild poisoning is 10% to 30%, the blood HBCO concentration of moderate poisoning is 30% to 40%, and the blood COHB concentration of severe poisoning can be as high as 50%.

Complications of carbon monoxide poisoning

The course of the disease can be complicated by pulmonary fever, pulmonary edema, and heart disease.

Carbon monoxide poisoning treatment

Treatment medication

Mannitol, hypertonic glucose, diuretics, dexamethasone.

2. Principles of treatment

(1) General treatment Breathe fresh air; keep warm; inhale oxygen; patients with weak breath or stop breathing must take artificial respiration immediately; hibernation therapy can be used if necessary;

(2) Prevention and treatment of cerebral edema.

(3) Supportive therapy.

3. Remedy measures

Quickly move the patient to a place with fresh air, rest in bed, keep warm, and keep the airway open.

(1) Correcting hypoxia Quickly correct the state of hypoxia. Inhalation of oxygen can accelerate the dissociation of COHb. Increase CO emissions. When inhaling fresh air, it takes about 4 hours to release half of CO from COHb. When inhaling pure oxygen, it can be shortened to 30 to 40 minutes, and inhaling 3 atmospheres of pure oxygen can be reduced to 20 minutes. Hyperbaric oxygen chamber treatment can increase the dissolved oxygen in the blood, increase the partial pressure of oxygen in the arteries, make the oxygen in the capillaries easily diffuse into the cells, and quickly correct tissue hypoxia. When breathing is stopped, artificial respiration should be performed as early as possible, or breathing should be maintained with a ventilator. Critical patients can consider plasma exchange.

(2) Prevention and treatment of cerebral edema After severe poisoning, cerebral edema can reach its peak within 24 to 48 hours. Dehydration therapy is important. At present, the most commonly used is 20% mannitol, a rapid intravenous drip. After 2 to 3 days, the phenomenon of increased cranial pressure improves, and can be reduced. Furosemide can also be injected for dehydration. Adenosine triphosphate and adrenal glucocorticoids such as dexamethasone also help relieve brain edema. If frequent seizures are present, diazepam is the drug of choice, and phenytoin is given intravenously after the seizures have stopped.

(3) Treatment of infection and control of high fever should be used for pharyngeal swab, blood and urine culture, and broad-spectrum antibiotics should be selected. High thermal energy can affect brain function. Physical cooling methods can be used, such as an ice cap on the head and an ice pack on the body surface to keep the body temperature around 32 ° C. Such as chills or difficulty in temperature drop during the cooling process, hibernation drugs can be used.

(4) Promote the metabolism of brain cells Apply the energy mixture. Commonly used drugs are adenosine triphosphate, coenzyme A, cytochrome C, and a large number of vitamin C.

(5) Prevention and treatment of complications and comorbidities Nursing work during coma is very important. Keep the airway open and perform tracheotomy if necessary. Turn over regularly to prevent pressure ulcers and pneumonia. Pay attention to nutrition and nasal feeding if necessary. Patients with acute CO poisoning should recover from coma for 2 weeks as much as possible to prevent neurological and cardiac complications. If there are later symptoms, give appropriate treatment.

Prognosis of carbon monoxide poisoning

The lighter can fully recover within a few days, and the severe can develop neurological sequelae. If you are exposed to a too cold environment during treatment, it is likely to be complicated by pneumonia.

Prevention of carbon monoxide poisoning

1. It should be widely publicized that there should be safety settings (such as chimneys, small ventilation windows, wind buckets, etc.) when using coal fires indoors, explaining the possible symptoms of gas poisoning and common sense of first aid, especially the harm and severity of gas to small infants. Coal furnace chimneys should be installed reasonably. Coal furnaces without chimneys should be placed outdoors at night.

2. Do not use obsolete water heaters, such as inline water heaters and flue water heaters, both of which are explicitly prohibited by the state from being produced and sold; do not use overdue service water heaters; install professional water heaters. Install, dismantle, and modify burning appliances. When showering in winter, do not close the doors and windows of the bathroom tightly, and do not shower for too long.

3. Do not allow the engine to idle for a long time when driving; do not open the air conditioner too long when the vehicle is stopped; even during driving, always open the windows to allow convection of air inside and outside the car. If you feel unwell, stop and rest; if you feel dizzy, heavy, or have weak limbs when driving or riding an air-conditioned vehicle, open the window in time to breathe fresh air.

4. Install carbon monoxide alarms where carbon monoxide is likely to be generated. Carbon monoxide alarm is a device specifically used to detect the concentration of carbon monoxide in the air. It can promptly alarm when the concentration of carbon monoxide exceeds the standard. Some can forcibly open windows or exhaust fans to keep people away from carbon monoxide.