In both industrial and domestic environments, the incomplete combustion of carbon-containing substances can produce carbon monoxide (CO). CO is a colorless, odorless, and tasteless gas with a specific gravity of 0.967. When CO concentrations in the air reach 12.5%, there is a risk of explosion. Acute carbon monoxide poisoning refers to the toxic effects caused by excessive inhalation of CO. It is a common type of poisoning encountered in daily life and occupational settings.
Etiology
In industrial settings, blast furnace gas and producer gas contain 30%–35% CO, while water gas contains 30%–40% CO. In processes such as steelmaking, coke production, and kiln firing, faulty sealing of furnace or kiln doors, gas pipeline leaks, or methane explosions in coal mines can release large amounts of CO, leading to inhalational poisoning. In fire incidents, CO concentrations in the air can reach as high as 10%, resulting in poisoning of individuals on site.
In daily life, the most common causes of CO poisoning involve the use of coal stoves for heating and gas leaks. Gases from coal stoves can contain 6%–30% CO. Improper precautions during their use can lead to poisoning. Smoking one pack of cigarettes per day can raise the blood carboxyhemoglobin (COHb) concentration to 5%–6%. Heavy, continuous smoking can also result in CO poisoning.
Pathogenesis
After inhalation, CO rapidly diffuses across the pulmonary capillary membrane and binds to hemoglobin in red blood cells, forming stable carboxyhemoglobin (COHb). CO has 240 times the affinity for hemoglobin compared to oxygen. Even at relatively low concentrations, CO can form significant amounts of COHb. COHb cannot carry oxygen and dissociates poorly. Its dissociation rate is only 1/3,600th that of oxyhemoglobin. CO binds to the heme group within hemoglobin, inhibiting the release of oxygen from the other three binding sites to peripheral tissues. This shifts the oxygen-hemoglobin dissociation curve to the left, exacerbating tissue hypoxia.
Furthermore, CO binds to the ferrous ion in reduced cytochrome oxidase, inhibiting cytochrome oxidase activity. This interference disrupts cellular respiration and oxidative processes, impeding the utilization of oxygen.
During CO poisoning, organs with fewer collateral blood vessels and high metabolic demands (e.g., the brain and heart) are most vulnerable to damage. Small blood vessels in the brain quickly become paralyzed and dilated. Under hypoxic conditions, adenosine triphosphate (ATP) in the brain depletes rapidly, leading to sodium pump dysfunction. Sodium ions accumulate within cells, triggering cerebral edema. Hypoxia causes endothelial swelling in blood vessels, resulting in cerebral circulatory impairment. The accumulation of acidic metabolic byproducts in the brain during hypoxia increases vascular permeability, further contributing to interstitial brain edema. Cerebral circulatory disorders can lead to the formation of cerebral thrombi, focal ischemic necrosis of the cerebral cortex and basal ganglia, as well as widespread demyelination, potentially causing delayed encephalopathy in some patients.
Pathology
In cases of acute carbon monoxide (CO) poisoning resulting in death within 24 hours, the blood appears cherry red, with congestion, edema, and petechial hemorrhages observed in various organs. For individuals who die several days after falling into a coma, the brain shows marked congestion and edema. Softening foci may appear in the globus pallidus, necrotic lesions in the cerebral cortex, and significant damage to the hippocampus due to its limited vascular supply. Cellular degeneration may be observed in the cerebellum. In some patients, scattered or focal demyelinating lesions can occur in the white matter of the cerebral hemispheres. The myocardium may exhibit ischemic damage or subendocardial multifocal infarctions.
Clinical Manifestations
Acute Poisoning
In healthy individuals, blood COHb concentrations can reach 5%–10%. Symptoms of acute CO poisoning are closely related to COHb concentrations in the blood and are influenced by preexisting health conditions, such as cardiovascular or cerebrovascular diseases, as well as physical activity levels at the time of poisoning. Acute CO poisoning is categorized into three grades based on severity:
Mild Poisoning
COHb concentrations range from 10% to 30%. Symptoms include varying degrees of headache, dizziness, nausea, vomiting, palpitations, and limb weakness. Patients with preexisting coronary artery disease may experience angina pectoris. Symptoms resolve rapidly after removal from the toxic environment and exposure to fresh air or oxygen therapy.
Moderate Poisoning
COHb concentrations range from 30% to 40%. Manifestations include chest tightness, shortness of breath, dyspnea, hallucinations, blurred vision, impaired judgment, motor incoordination, drowsiness, confusion, or light coma. The mucous membranes of the lips may appear cherry red. Patients typically recover to normal health with oxygen therapy, with no evident complications.
Severe Poisoning
COHb concentrations range from 40% to 60%. Symptoms progress rapidly to coma, respiratory depression, pulmonary edema, arrhythmias, or heart failure. Patients may exhibit signs consistent with a decorticate state. Some cases are complicated by inhalation pneumonia. Redness, swelling, and blisters may occur on pressure-exposed skin areas. Fundoscopic examination may reveal optic disc edema.
Delayed Neuropsychiatric Syndrome
Following recovery from consciousness disturbances caused by acute CO poisoning, patients may experience a "pseudo-recovery period" lasting 2 to 60 days, after which one or more of the following manifestations may occur:
- Mental and consciousness disorders: Symptoms such as dementia, stupor, delirium, or decorticate states may develop.
- Extrapyramidal neurological disorders: Damage to the basal ganglia can lead to parkinsonism, characterized by symptoms like flat affect, increased muscle tone in the limbs, resting tremor, and a shuffling gait.
- Pyramidal tract damage: Manifestations include hemiplegia, positive pathological reflexes, or urinary incontinence.
- Focal cortical dysfunction: Symptoms such as aphasia, blindness, inability to stand, and secondary epilepsy may occur.
- Damage to cranial or peripheral nerves: Manifestations may include optic nerve atrophy, auditory nerve damage, or peripheral neuropathy.
Patients who sustained acute brain injury during the initial period of CO poisoning have a higher likelihood of developing delayed neuropsychiatric syndrome.
Laboratory Examinations
Blood COHb Measurement
Direct spectrophotometric methods are commonly used to quantitatively measure COHb concentrations in clinical settings. Simplified qualitative methods, such as the alkali test, are also used. To perform this test, one or two drops of the patient’s blood are diluted with 3–4 ml of distilled water, followed by the addition of one to two drops of 10% sodium hydroxide solution. The mixture is then observed. With elevated COHb levels, the blood retains a pale red color after the addition of alkali, whereas normal blood turns green. This test typically shows positive reactions only when COHb concentrations reach 50% or higher.
Electroencephalography (EEG)
EEG findings may demonstrate diffuse low-amplitude slow waves, aligning with the progression of hypoxic encephalopathy.
Cranial CT Scan
Pathological hypodense areas may be observed in the brain during edema.
Diagnosis and Differential Diagnosis
The diagnosis of acute CO poisoning is based on a history of exposure to elevated concentrations of CO, rapid onset of neurological symptoms and signs, and timely blood COHb measurements. Occupational CO poisoning typically results from accidental events, and the exposure history is often clear. In cases of suspected domestic CO poisoning, environmental factors need to be evaluated, such as improper ventilation or leakage from stoves and chimneys, as well as whether other occupants in the same room experience similar symptoms.
Acute CO poisoning needs to be differentiated from conditions such as cerebrovascular accidents, concussions, meningitis, diabetic ketoacidosis, and coma caused by other intoxications. Blood COHb measurement serves as a valuable diagnostic indicator, but blood samples should ideally be collected within 8 hours of the patient’s removal from the toxic environment.
Treatment
Termination of CO Inhalation
Patients are moved to areas with fresh air to stop further carbon monoxide (CO) inhalation. Bed rest is maintained, body warmth is preserved, and the airway is kept unobstructed.
Oxygen Therapy
Oxygen Inhalation
Oxygen therapy is provided to individuals with poisoning, using nasal cannulas or oxygen masks. When breathing fresh air, the half-life of carboxyhemoglobin (COHb) is approximately 4 hours. Inhaling pure oxygen reduces this time to 30–40 minutes, while breathing pure oxygen at 3 atmospheres of pressure shortens it further to 20 minutes.
Hyperbaric Oxygen Therapy
Under hyperbaric conditions, treatment with 100% oxygen significantly reduces the half-life of COHb. This increases physically dissolved oxygen in the blood, enhances total oxygen content, improves oxygen release, and accelerates the elimination of CO. These effects rapidly correct tissue hypoxia, shorten coma duration and recovery time, and help prevent delayed encephalopathy resulting from CO poisoning.
A unified guideline for hyperbaric oxygen therapy indications does not currently exist. However, many hyperbaric oxygen centers use symptoms such as headache, nausea, or a COHb concentration >25% as key reference standards for recommending treatment. Additional clinical indications often considered include coma, brief loss of consciousness, ECG evidence of myocardial ischemia, and focal neurological deficits. For pregnant individuals, a COHb concentration exceeding 20% or signs of fetal distress are also considered indications for treatment.
Functional Support for Key Organs
For patients with severe coronary atherosclerotic lesions, there is a risk of cardiac arrest if COHb concentrations exceed 20%, making close cardiac monitoring essential. For CO poisoning cases not meeting hyperbaric oxygen therapy indications, 100% oxygen therapy is recommended until symptoms resolve and COHb levels drop below 10%. For patients with underlying cardiopulmonary diseases, treatment is continued until COHb levels drop below 2%.
Prevention and Treatment of Cerebral Edema
Cerebral edema following severe CO poisoning typically peaks within 24–48 hours. Alongside efforts to correct hypoxia, dehydration therapy is provided. Intravenous infusion of 20% mannitol at 1–2 g/kg is administered rapidly (10 ml/min), with dosage reduced once intracranial pressure improves after 2–3 days.
Corticosteroids may help alleviate cerebral edema, though their clinical utility remains to be confirmed. For frequent seizures, diazepam is typically used as a first-line treatment with an intravenous dose of 10–20 mg. Once seizures stop, intravenous phenytoin sodium is administered at 0.5–1 g, with repeat dosing every 4–6 hours as necessary.
Prevention and Management of Complications and Sequelae
Maintaining an unobstructed airway is critical. Intubation or tracheostomy is performed when necessary. Regular repositioning of patients is undertaken to prevent bedsores and hypostatic pneumonia. Nutritional support is provided, with enteral feeding as needed.
Cardiac Complications
Approximately 1/3 of patients with moderate to severe CO poisoning exhibit myocardial injury, and their long-term mortality rate is three times higher than those without myocardial damage. Therefore, early screening for cardiac enzymes following acute CO poisoning is recommended. Where feasible, myocardial imaging with nuclear technology may be employed to assess the extent of myocardial damage.
Prevention
Raising awareness about CO poisoning plays an important role in its prevention. The installation of exhaust pipes for indoor stoves reduces the risk of indoor gas accumulation. Proper sealing of chimney pipelines must be ensured to prevent leaks. In industrial settings, workers are expected to strictly follow safety operating protocols. Enhanced monitoring and alarm systems for CO concentrations in mine shaft environments are necessary. Entering environments with high CO concentrations requires the use of protective gas masks.