Karboksihemoglobinemia

Karboksihemoglobinemia, also known as carboxyhemoglobinemia, is a form of hypoxia caused by elevated levels of carboxyhemoglobin in the blood after exposure to carbon monoxide (CO). CO binds to hemoglobin with high affinity, forming carboxyhemoglobin and reducing both the blood’s oxygen content and the release of oxygen to tissues.

Pathophysiology: CO’s strong affinity for hemoglobin shifts the oxygen-hemoglobin dissociation curve to the left, diminishing oxygen delivery to organs. At higher exposures, CO can also impair cellular respiration by inhibiting mitochondrial enzymes, contributing to tissue hypoxia.

Causes and risks: The most common sources are smoke inhalation from fires, exposure to vehicle exhaust in enclosed spaces, and faulty furnaces or gas heaters. Cigarette smoke adds to CO exposure. Vulnerable groups include pregnant individuals, children, and people with cardiovascular disease or underlying lung conditions.

Clinical presentation and diagnosis: Symptoms range from headache, dizziness, and nausea to confusion, weakness, syncope, or seizures, depending on exposure level. Cherry-red skin is a classic description but unreliable for diagnosis. Diagnosis requires measurement of carboxyhemoglobin, typically by co-oximetry on blood samples; pulse oximetry can be misleading and may appear normal.

Management and prognosis: Immediate management involves removing the person from exposure and administering 100% oxygen, usually via a non-rebreathing mask. In selected cases with significant neurologic symptoms, high CO-hemoglobin levels, or specific risk factors, hyperbaric oxygen therapy may be considered. Prompt treatment generally improves outcomes, while delays increase the risk of lasting neurologic sequelae. Prevention includes proper ventilation, maintenance of combustion devices, and the use of CO detectors.