How long is the aggravating period of delayed encephalopathy?

summary

Delayed encephalopathy after carbon monoxide poisoning, we need to seize the time to carry out treatment, refers to a group of neuropsychiatric symptoms of acute dementia in patients with carbon monoxide poisoning after the recovery of acute poisoning symptoms for several days or weeks. How long is the aggravating period of delayed encephalopathy in patients with the disease?, Now let's take a concrete look.

How long is the aggravating period of delayed encephalopathy?

First, the cause of CO poisoning is very clear, which is caused by the inhalation of CO produced by carbon containing substances when they are not fully burned. The most common cases of sporadic patients are burning coal stove or gas-fired water heater indoors, and the doors and windows are not well ventilated, or it is rainy on cloudy days, the air pressure is low, the wind blows into the chimney, and the CO gas countercurrent indoors, causing the indoor concentration to rise, causing poisoning. In recent years, the sporadic cases of CO poisoning have changed from urban to rural areas. Due to the improvement of living standards, Adobe houses have been transformed into brick houses or villas, but the heating facilities are relatively backward, and coal stoves are still used for heating or earth heating is installed. Due to not paying attention to ventilation, the number of CO poisoning patients increased year by year. Improper use of gas water heater, causing poisoning is not uncommon.

Second, once co enters the body, it quickly combines with hemoglobin to form carboxyhemoglobin (HbCO). The binding ability of CO with hemoglobin is 300 times that of oxygen, but the dissociation speed is 3600 times slower than that of oxygen, which easily makes hemoglobin lose its oxygen carrying ability. It causes tissue hypoxia. In addition, CO can also combine with iron 2 of reduced cytochrome oxidase, which aggravates tissue hypoxia. Because the brain tissue has the worst tolerance to hypoxia, the brain tissue is the first affected, followed by the heart.

Third, the main pathological change of delayed encephalopathy after acute CO poisoning is extensive demyelination of white matter, which is similar to allergic encephalomyelitis, but the latter is more severe. The most common pathological report in China is bilateral globus pallidus symmetrical softening, followed by focal or lamellar degeneration and necrosis in the second and third layers of cerebral cortex and the surface white matter. Extensive demyelinating degeneration can be seen in the white matter of the brain, especially in the frontal or parietal lobe. Brain atrophy can be seen in the long course of the disease.

matters needing attention

(1) Hyperbaric oxygen therapy, time to more than 3 months or to patients awake（ 2) Dexamethasone was used, 10mg / D intravenous drip for more than one month（ 3) (4) delayed encephalopathy is often accompanied by hypermyotonia. Eperisone hydrochloride is the first choice. 50-100 mg, 2-3 times / d. Patients with tremor can use benhexol (Antan) 2-4 mg three times a day, or levodopa / Benserazide (Madopa) (250 mg each tablet) from 1 / 4 tablets in the morning, 1 / 2 tablets in the middle and 1 / 4 tablets in the evening, and then gradually increase to the amount of treatment, which can improve symptoms（ 5) For patients with long-term coma, pay attention to nutrition, give nasal feeding. Pay attention to turn over and passive exercise to prevent bedsore and limb contracture.