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carbon monoxide poisoning inspection, carbon monoxide poisoning diagnosis

carbon monoxide poisoning inspection, carbon monoxide poisoning diagnosis

Common inspections for carbon monoxide poisoning

Inspection Name Inspection Site Inspection Department Inspection Function
Urinary routines and other urological health care departments are often used in the urinary system...
Craniocerebral MRI Craniocerebral Nuclear Medicine Brain Surgery Cranial MRI Examination...
The six blood biochemistry department of blood, blood vessel and blood health care . Blood urea and muscle...
Chemical examination of cerebrospinal fluid of psychological brain surgery the cerebrospinal fluid of chemical ...
Carboxyhemoglobin Qualitative Test Systemic Blood Vessel Blood Carboxyhemoglobin...
Craniocerebral CT Craniocerebral Surgery Tumor Cranial CT can...
Evoked potential brain
- evoked by the brain ...
EEG Craniocerebral Health Care Department EEG examination right...
ECG heart care center aims to by heart ...
Mean red blood cell hemoglobin concentration blood vessel blood mean red blood cell blood...
Carboxyhemoglobin blood vessels - by detecting its egg...
1. Check:

1. Determination of carboxyhemoglobin in blood

The content of carboxyhemoglobin in the blood of normal people can reach 5% to 10%, of which a small amount comes from endogenous carbon monoxide, which is 0.4% to 0.7%. The carboxyhemoglobin in the blood of mild carbon monoxide poisoning can be higher than 10% , It can be higher than 30% in moderately poisoned patients, and higher than 50% in severely poisoned patients. However, the determination of blood carboxyhemoglobin must be timely. The carboxyhemoglobin can be reduced to normal after 8 hours of exposure to carbon monoxide, and there is no parallel relationship with clinical symptoms.

2. EEG

It is reported that 54% to 97% of patients with acute carbon monoxide poisoning can find abnormal EEG, which is manifested as an increase in low-amplitude slow waves. Generally, theta waves and delta waves in the frontal and temporal regions are more common and are often related to clinical consciousness disorders. Some patients with coma may also have special three-phase waves, similar to the waves in hepatic coma. False paroxysmal spikes and slow waves or slow spikes and slow waves. In some patients with acute carbon monoxide poisoning, the abnormality of EEG in the later stage of mental retardation can exist for a long time.

3. Brain evoked potential examination

In the acute phase of carbon monoxide poisoning and those with delayed encephalopathy, the latency of the visual evoked potential VEP100 is prolonged, and the abnormal rate is 50% and 68%, respectively. In the recovery phase, it can be reduced to 5% and 22% of the median nerve somatosensory evoked potential (SEP) examination. See N32 and other medium and long latent components are selectively damaged. The abnormality rate of both types of patients exceeds 70%, and the abnormality of the brainstem auditory evoked potential (BAEP) is closely related to the degree of consciousness disorder and poisoning. The outcome of the illness is parallel.

4. Brain imaging examination

In patients with carbon monoxide poisoning in the acute stage and when the delayed encephalopathy occurs, the main abnormality is that the white matter under the cerebral cortex and the globus pallidus or internal capsule appear roughly symmetrical reduced density areas. Later, the ventricles or sulci are enlarged. The abnormal rates were 41.2% and 87.5%, respectively. Those without abnormal brain CT had a better prognosis, and those with abnormal CT had a coma for more than 48 hours. However, there is no CT change in the early stage of delayed encephalopathy. The above-mentioned CT abnormalities are generally found only 2 weeks after the onset of delayed encephalopathy symptoms, so they are not as sensitive as brain evoked potentials and EEG.

5. Routine tests of blood, urine and cerebrospinal fluid

The total number of peripheral blood red blood cells, total white blood cells and neutrophils increased, and the number of white blood cells in severe poisoning was higher than 18×109/L. The prognosis is serious. One-fifth of patients may have urine sugar, and 40% of patients have urine protein positive. Cerebrospinal fluid pressure and routine are mostly normal.

6. Blood biochemical test

Serum ALT activity and non-protein nitrogen increased transiently. The activities of lactate and lactate dehydrogenase increase after acute poisoning. Serum AST activity also began to increase in the early stage and reached the highest value within 24 hours. If it exceeds 3 times the normal value, it often indicates that the condition is severe or there are comorbidities with rhabdomyolysis, and the blood creatine phosphokinase (CPK) activity is significantly increased. . Blood gas examination shows that the partial pressure of blood oxygen can be normal, and the blood oxygen saturation can be normal, the blood pH is reduced or normal, and the partial pressure of carbon dioxide in the blood often has a compensatory drop and blood potassium can be reduced.

7. Electrocardiogram

ST-T changes may occur in some patients, as well as ventricular premature contractions, conduction block, or transient sinus tachycardia.



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