Delayed encephalopathy after carbon monoxide poisoning

Introduction to delayed encephalopathy after carbon monoxide poisoning Delayed encephalopathy after depletion of carbon monoxide poisoning (DEACMP) refers to acute carbon monoxide poisoning in patients with acute carbon monoxide poisoning after the recovery of acute poisoning symptoms, after several days or weeks of normal or near normal "false healing" reappears to acute dementia A group of neuropsychiatric symptoms. Carbon monoxide poisoning (CMP), also known as gas poisoning, is a carbon monoxide that enters the human body through the respiratory tract and combines with hemoglobin to form carboxyhemoglobin, which reduces or loses the oxygen carrying capacity of normal hemoglobin, causing hypoxia in whole body tissues, but lacking in brain tissue. Oxygen-induced diseases with advanced neurological dysfunction. basic knowledge The proportion of illness: 0.002% Susceptible people: no special people Mode of infection: non-infectious Complications: headache, dizziness, disturbance of consciousness, intelligent disorder, vascular Parkinson's syndrome

Causes of delayed encephalopathy after carbon monoxide poisoning

CO is inhaled by the body (50%):

Carbon monoxide (CO) is a colorless, odorless, odorless gas with a specific gravity of 0.967. It is extremely stable in nature, is not easily decomposed by itself, and is not easily oxidized. It has a highly toxic effect on the nervous system.

The cause of CO poisoning is very clear. It is caused by the inhalation of CO produced by carbonaceous substances in the case of insufficient combustion. The patients who are emitted are most commonly used indoors to ignite coal stoves or gas-fired water heaters, and the doors and windows are poorly closed and ventilated, or The rainy weather is low, the wind blows into the chimney, and the CO gas flows back into the room, causing the indoor concentration to rise and causing poisoning. In the past decade, the sporadic cases of CO poisoning have changed from the previous cities to the urban-rural integration and rural areas. Due to the improvement of living standards, the adobe houses have been converted into brick houses or villa buildings, and the heating facilities are relatively lagging behind. The coal stoves are still mainly used for heating or installing earth heating. Due to the lack of attention to ventilation, the number of patients with CO poisoning increases year by year, using gas. Improper water heaters are not uncommon for those who are poisoned.

Pathological changes (20%):

Once CO enters the body, it rapidly combines with hemoglobin to form carboxyhemoglobin (HbCO). The binding ability of CO and hemoglobin is 300 times that of oxygen, but the dissociation speed is 3600 times slower than oxygen, which makes it easy for hemoglobin to lose oxygen carrying capacity. The tissue is hypoxic. In addition, CO can also bind to the divalent iron of reduced cytochrome oxidase, which is more important for tissue hypoxia. Because brain tissue is the least tolerant to hypoxia, the brain is the first to be affected. Followed by the heart.

Acute CO poisoning 24h death, blood and internal organs are cherry red, tissue and organs are congested, there are different sizes of hemorrhage, after brain tissue hypoxia, the first involved is the rapid expansion of blood vessels in the brain, anaerobic glycolysis of brain tissue Increased, brain tissue edema, mainly cell edema, accumulation of acidic metabolites in the brain, blood-cerebrospinal fluid barrier destruction, increased vascular permeability, can cause interstitial cerebral edema, severe vascular endothelial cell swelling, bleeding Small blood vessel thrombosis, the cerebral cortex may appear parallel to the surface of the banded necrosis such as white line, called stratified necrosis, sometimes diffuse or local, sometimes visible globus pallidus or cystic cavity.

Microscopically, the cerebral cortex has a ischemic change of diffuse nerve cells, which is often evident in the third layer. The more typical change is the disappearance of stratified nerve cells. Long white banded lesions can be seen under low magnification. Sometimes it can be seen by careful observation of the naked eye. It is called pseudo-stratified necrosis (pseudolaminarn ecrosis). The deep white matter fibers of the brain are demyelination, which can be aggregated into pieces. The myelin sheath is swollen and spheroid, and the axons are also curved and fractured. And destruction, etc., it is generally believed that the frontal lobe and temporal lobe damage are relatively heavy, followed by the basal nucleus, globus pallidus, striatum, cerebellar dentate nucleus and thalamus, and in the case of delayed encephalopathy, extensive demyelination with white matter The lesion is mainly, the myelin sheath is swollen, broken or disappeared, the axon is bent, and the fracture is broken. The mechanism causing this change is mostly the direct action of hypoxia and the secondary degeneration caused by the degeneration of nerve cells, especially small blood vessels. Swelling degeneration of venous endothelial cells causes blood flow delay or thrombosis, which is also the pathological basis of myelin loss.

Foreign pathological studies have confirmed that the main pathological changes of delayed encephalopathy after acute CO poisoning are extensive demyelination of cerebral white matter, similar to allergic encephalomyelitis, but the latter is heavier. Domestic pathological reports are more common. Symmetrical softening lesions on both sides of the globus pallidus, followed by focal or lamellar degeneration and necrosis of the second and third layers of the cerebral cortex, extensive demyelination of the white matter, and most prominent in the frontal or parietal lobe. Long-term brain atrophy can be seen.

Inhalation of exhaust gases (20%):

In addition, in industrial production, the inhalation of exhaust gas generated in the production process such as steel, cement, building materials and chemicals is also one of the causes of CO poisoning.

Prevention of delayed encephalopathy after carbon monoxide poisoning

Pay attention to the heating and ventilation of coal stoves, use gas water heaters correctly, and avoid CO poisoning. In addition, in industrial production, pay attention to safe production and prevent CO poisoning caused by inhalation of exhaust gas. Early treatment is very important to prevent delayed encephalopathy after carbon monoxide poisoning.

Delayed encephalopathy complications after carbon monoxide poisoning Complications, headache, dizziness, consciousness disorder, intelligent disorder, vascular Parkinson's syndrome

A common headache, dizziness, disturbance of consciousness or a different degree of mental retardation, a small number of patients will leave Parkinson's syndrome.

Symptoms of delayed encephalopathy after carbon monoxide poisoning Common symptoms Carbon monoxide poisoning Gait instability, nausea, weakness, flushing, tinnitus, vertigo, palpitations, slow coma

1. The main manifestations of acute CO poisoning: closely related to the concentration of carboxyhemoglobin in the blood, according to clinical manifestations, can be divided into 3 levels:

(1) mild poisoning: carboxyhemoglobin in the blood is 10% to 20%, the patient feels headache, dizziness, tinnitus, nausea, vomiting, palpitations, weakness, and may have a transient coma.

(2) Moderate poisoning: carboxyhemoglobin in the blood is 30% to 40%. In addition to the above symptoms, the complexion appears flushed, the lips are cherry red, the pulse is fast, sweaty, irritated, gait is unstable, and it can be drowsiness. State, even coma.

(3) severe poisoning: carboxyhemoglobin in blood is more than 50%, glascow coma scale can be less than 3 points, the patient's limb muscle tension is increased, sputum hyperreflexia, bilateral pathological reflex positive, quickly fall into Coma, can last for hours or days.

2, delayed encephalopathy after acute CO poisoning: acute CO poisoning after the condition improved for several days or weeks, some patients may re-emerge, the symptoms are mental symptoms, slow response, low intelligence, increased limb muscle tension, urine Incontinence, even coma.

DEACMP occurs in middle-aged and elderly people. It is reported in foreign countries as 2.8% to 11.8%. Among the 30 cases reported in China, 66.6% of people over 50 years old, and the older the incidence rate, the harder it occurs, the children rarely under 10 years old. However, it is not directly related to the severity of the patient's poisoning.

For patients with acute CO poisoning, it is necessary to be on guard against the occurrence of delayed encephalopathy, clinically after a period of waking period, and then appear mental disorders, intelligent changes, increased muscle tone and incontinence and other symptoms of neurological dysfunction Delayed encephalopathy should be considered. Combined with head CT or MRI, extensive white matter damage can be diagnosed.

Examination of delayed encephalopathy after carbon monoxide poisoning

1, blood routine: the total number of white blood cells and neutrophils can be increased.

2 , carboxyhemoglobin: can be found in the blood, there are two simple carboxyhemoglobin determination method for reference:

1 add alkali method: take 1 to 2 drops of the patient's blood, dilute with distilled water 3 ~ 4ml, add 10% sodium hydroxide 1 ~ 2 drops to mix, normal blood is green, when there is carboxyhemoglobin in the blood, blood retention The red color is unchanged.

2 boiling method: take appropriate amount of blood in a small test tube, set fire to boil, if it is brick red, suggesting CO poisoning, normal gray-brown.

3, EEG: can be expressed as diffuse alpha wave inhibition or disappearance, symmetry diffuse high amplitude slow wave.

4, ECG: may have arrhythmia, tachycardia, conduction block and myocardial ischemia changes.

5, head CT and MRI: patients with mild and moderate acute CO poisoning, CT can be normal, severe CT can be expressed as cerebral edema, one side or double basal ganglia ischemic low-density changes.

Delayed encephalopathy can be manifested as leukoaraiosis, MRI manifested as cerebral periventricular white matter and bilateral semi-oval center symmetric fusion lesions, low signal in T1 weighted phase, and T2 weighted phase high signal, lesions can affect subcortical The inner capsule, the outer capsule and the basal ganglia may have ischemic necrosis. When the condition is serious, pseudo-stratified necrosis can be seen on the T1-weighted phase.

Diagnosis and diagnosis of delayed encephalopathy after carbon monoxide poisoning

diagnosis

The general diagnosis of acute CO poisoning is not difficult. According to the environmental conditions of patients with CO poisoning, the patient has typical clinical manifestations. The whole brain is mainly caused by neurological disorders, the focal localization signs are relatively lacking, the lips are cherry red, and the blood is detected. Carbon oxyhemoglobin can be used to determine the diagnosis.

Differential diagnosis

Delayed encephalopathy should be differentiated from other brain injuries, infections and cerebrovascular diseases and metabolic encephalopathy such as hypoglycemic encephalopathy.

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