Delayed encephalopathy

Some patients with acute CO poisoning recovered from coma and recovered to normal consciousness, but after 2 ~ 30 days of false recovery period, neuropsychiatric symptoms of encephalopathy appeared again, known as acute CO poisoning delayed encephalopathy. It is also referred to as "acute CO intoxication neurological sequelae" because of the "bipolar" clinical process. Common clinical manifestations are as follows:

1. Mental symptoms: sudden loss of orientation, indifferent expression, slow reaction, memory disorders, incontinence, life can not take care of themselves; Or appear vision, illusion, incoherent, behavior is abnormal, the expression is like acute dementia stupor model mental illness.

2. Brain focal lesion

1) Extrapyramidal nerve damage: most commonly seen in Parkinson's syndrome, the patient's extremities show lead tube or gearing muscle tension increase, slow movement, loss of both upper limbs during walking, accompanied by movement, hypergyrophy and static tremor. A small number of patients develop chorea.

2) nerve damage in the cone system: mild hemiplegia on one side or both sides, flexion and rigidity of the upper limbs, hypertonic tendon reflex, positive ankle clonus, leading to pathological reflex on one side or both sides, and motor aphasia or pseudobulbar paralysis may also occur.

3) Others: Cortical blindness, seizures, and parietal syndrome (agnosia, apraxia, apraxia, or miscount) have also been reported.

3. The effect of low concentration CO on human body

Whether long-term exposure to low concentrations of CO can cause chronic poisoning is still controversial. Data in recent years suggest that long-term exposure to low CO concentration may have two effects on human health:

1) Nervous system: dizziness, headache, tinnitus, fatigue, sleep disorder, memory loss and other symptoms of brain debilitating syndrome are more common. Neurobehavioral tests can find abnormalities, which can be recovered after being out of CO contact. Patients with persistent symptoms above often have a history of multiple mild acute CO poisoning.

2) Cardiovascular system: abnormalities such as arrhythmia, ST segment decline, prolonged QT interval, or right bundle branch block may occur in the electrocardiogram. When the COHB saturation of occupational contacts reached more than 5%, serum lactate dehydrogenase (LDH), hydroxybutyrate dehydrogenase (HBD) and creatine phosphokinase (CPK) increased, which may be related to myocardial damage. In addition, through population studies, it has been found that about 20% to 25% of smokers have blood COHB higher than 8% to 10%, and these people have a higher rate of sudden death from myocardial infarction than non-smokers. A study of 63 patients with coronary arteriosclerosis in recent 10 years found that after CO exposure increased the level of COHB from 0.6% to 2% and 3.9%, the time of myocardial infarction and angina pectoris appeared earlier, and the tolerance to exercise was significantly reduced. These data, combined with animal studies, suggest that the long-term effects of low CO concentrations may adversely affect the cardiovascular system. Its ability to bind to hemoglobin is 200 times that of oxygen.