Etiology and pathogenesis of delayed encephalopathy in acute carbon monoxide poisoning

Delayed encephalopathy after acute carbon monoxide (CO) poisoning refers to a group of neuropsychiatric symptoms, mainly acute dementia, that reappears after a "false recovery period" of several hours to several weeks in which the symptoms disappear or basically disappear after acute CO poisoning. So what is the cause of the disease?

Causes

1. Incomplete combustion of carbon-containing substances in oxygen or insufficient oxygen supply can produce carbon monoxide. Living or working in this environment for too long can easily lead to delayed encephalopathy after carbon monoxide poisoning.

2. Combustible gases used in production, such as steel smelting, fertilizer production, manufacturing of phosgene, formic acid, and formic aldehyde, can also lead to carbon monoxide poisoning due to poor facilities or improper operation, and improper rescue can also cause toxic encephalopathy.

3. Burning coal or charcoal for heating in winter may cause carbon monoxide poisoning if the combustion is incomplete and the indoor ventilation is poor. In severe cases, encephalopathy may occur, especially when burning coal or charcoal at night. Due to low air pressure and closed doors and windows, carbon monoxide poisoning can occur. The incidence rate in Northeast China is very high every year.

【Pathogenesis】

CO is a highly toxic asphyxiating gas. After CO is inhaled into the body and enters the blood, it quickly combines with hemoglobin (Hb) to form stable carboxyhemoglobin (HbCO). The affinity of CO for Hb is 240 times greater than that of oxygen for Hb, and the dissociation rate of HbCO is 3600 times slower than that of oxyhemoglobin. HbCO cannot carry oxygen. At the same time, the presence of HbCO can shift the hemoglobin oxygen dissociation curve to the left, thus causing tissue hypoxia and tissue and organ damage. The brain tissue is most sensitive to hypoxia and is the first to be affected, forming a series of pathological injuries.

There is no clear pathogenesis of delayed encephalopathy. Some people believe that it is caused by secondary cerebrovascular lesions. Pathological manifestations include cerebral vascular dilation, congestion, hemorrhage around small vessels, infiltration of perivascular cells, brain edema, swelling of endothelial cells of some small blood vessels, narrowing of the lumen or even complete occlusion. Some people believe that delayed encephalopathy is caused by brain hypoxia damaging oligodendrocytes, thereby affecting myelin metabolism and formation. Pathological manifestations include extensive demyelination of the brain's white matter. The study by Gu Renjun et al. suggests that the levels of 5-hydroxytryptamine (5-HT), acetylcholine (Ach), dopamine (DA) in the blood and 5-HT and DA in the cerebrospinal fluid of patients with delayed encephalopathy are significantly decreased, while the level of Ach in the cerebrospinal fluid is increased. After treatment, there was varying degrees of recovery, indicating that 5-HT, Ach, and DA play a certain role in the occurrence of this disease.