Clinical manifestations
Acute hydrogen sulfide poisoning generally develops rapidly, with clinical manifestations dominated by brain and/or respiratory system damage, and may also be accompanied by organ dysfunction such as the heart. Clinical manifestations can vary significantly depending on factors such as exposure to hydrogen sulfide concentrations.
1. Central nervous system damage is the most common:
(1) Headache, dizziness, fatigue, ataxia, and mild impairment of consciousness may occur after exposure to higher concentrations of hydrogen sulfide. Eye and upper respiratory tract irritation often presence.
(2) After exposure to high concentrations of hydrogen sulfide, encephalopathy manifests as yarrow, headache, dizziness, irritability, irritability, delirium, epileptiform convulsions, and generalized tonic and parocular seizures. Coma may occur suddenly; Dyspnea or cardiac arrest after respiratory arrest may also occur. Fundus examination shows that some cases have optic nerve papillary edema. Some cases may be accompanied by pulmonary edema.
Symptoms of encephalopathy often appear earlier than respiratory symptoms. It may take some time for mucosal irritation to occur.
(3) Shock-like death can occur after exposure to extremely high concentrations of hydrogen sulfide, that is, respiratory arrest within seconds or minutes after exposure, and cardiac arrest may occur after a few minutes; They may also fall into a coma immediately or within minutes and die from respiratory arrest. Death can occur unaware, with immediate loss of smell when the smell of hydrogen sulfide is detected, and in a few cases, a disgusting sweet taste can be detected in the moment before coma. There are generally no aura symptoms before death, but breathing may occur first and deeply and rapidly, followed by respiratory arrest.
Coma usually occurs at the scene of an accident in acute poisoning, and the degree varies depending on the concentration and time of exposure to hydrogen sulfide, and may occasionally be accompanied by or without respiratory failure. Some cases can be resuscitated after leaving the accident site or on the way to the hospital. Patients who still maintain vital signs when they arrive at the hospital, such as those without hypoxic encephalopathy, tend to recover faster. People who are in a coma for a long time may have headache, dizziness, vision or hearing loss, disorientation, ataxia, or epileptiform convulsions after resuscitation, and most cases can fully recover. Two cases of delayed encephalopathy have been reported, both of which resuscitated after 2 days of deep coma, regained coma after 1.5 days and 3 days, and resuscitated after 2 weeks and 1 month, respectively.
The central nervous system symptoms are extremely serious, while the mucosal irritation symptoms are not obvious, and the irritation symptoms may not have occurred due to the short contact time. or because the systemic symptoms are severe and easy to attract attention.
Patients with early or only brain dysfunction without morphological changes in acute intoxication have poor sensitivity to electroencephalography and brain anatomy imaging such as electronic computed tomography (CT) and magnetic resonance imaging (MRI), while abnormal single-photon emission electron computed brain scan (SPECT)/positron emission scan (PET) correlates well with clinical manifestations and neuroelectrophysiological examinations. If one case was in a decorticular state after a deep coma after poisoning, CT showed that there were foci of reduced density in the bilateral globus pallidus. The CT and MRI of the head of the other patient in a poisoned coma were not abnormal. PET examination 3 years after the accident showed abnormal metabolism in the bilateral temporal lobe, subparietal lobe, left thalamus, and striatum. After half a year, SPECT showed a decrease in bilateral lenticular nucleus flow, and there was no abnormality in the cerebral cortex. Patients have hyposmia, extrapyramidal signs, memory deficits, etc.
Fifteen cases with a history of repeated acute hydrogen sulfide poisoning were reported to have symptoms such as fatigue, drowsiness, headache, agitation, anxiety, and memory loss.
2. Respiratory system damage: chemical bronchitis, pneumonia, pulmonary edema, acute respiratory distress syndrome, etc. may occur. A small number of cases of poisoning can be dominated by clinical manifestations of pulmonary edema, while neurological symptoms are mild. May be accompanied by ocular conjunctivitis. Keratitis.
3. Myocardial damage: In the course of poisoning, some cases may experience palpitations, shortness of breath, chest tightness or angina-like symptoms; A small number of cases developed myocardial infarction-like manifestations after recovery from coma and improvement of poisoning symptoms for 1 week. The ECG shows an acute myocardial dead pattern, but it may disappear quickly. Its disease is mild, the course of the disease is short, the prognosis is good, and the diagnosis and treatment method is different from that of myocardial infarction caused by coronary arteriosclerosic heart disease, so it is considered to be diffuse toxic myocardial damage. Myocardial enzyme profiling can be abnormal to varying degrees.
Diagnosis of acute hydrogen sulfide poisoning is mainly based on:
1. Have a clear history of exposure to hydrogen sulfide The smell of rotten eggs in the patient's clothing and exhalation can be used as indicators of exposure. Hydrogen sulfide can be produced or measured at the scene of the accident. Patients can use the smell of rotten eggs before the onset of the disease as a reference.
2. Clinical characteristics: Clinical manifestations dominated by brain and/or respiratory system damage mentioned above.
3. Laboratory examination: There are currently no specific laboratory examination indicators. (1) The increased content of hydrogen sulfide or sulfide in the blood can be used as an absorption index, but it is inconsistent with the severity of poisoning, and its half-life is short, so blood should be collected within a short time after stopping contact. (2) The urinary thiosulfate content can be increased, but it can be disturbed by factors such as measurement time and dietary sulfur content. (3) sulfhemoglobin (SHb) in the blood cannot be used as a diagnostic indicator, because hydrogen sulfide does not bind to normal hemoglobin to form sulfhemoglobin, which has nothing to do with the mechanism of poisoning; Many studies have shown that hydrogen sulfide does not have significant concentrations of sulfur in human and animal blood. (4) The sulfur content in the blood and tissues of the corpse can be disturbed by factors such as the decomposition of the corpse, which affects its reference value.
4. Differential diagnosis: Shock-like deaths at the accident site should be distinguished from acute poisoning with other chemicals such as carbon monoxide or cyanide, acute cerebrovascular disease, myocardial infarction, etc., and from suffocation caused by entering an environment containing high concentrations of chemicals such as methane or nitrogen caused by air hypoxia. Other symptoms should also be differentiated from similar illnesses of other causes or trauma from falls after coma.