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HBOT Treatment for Carbon Monoxide Poisoning Therapy


Increased exposure to carbon monoxide (CO), which is a poisonous gas requires exposure to oxygen to counteract the side effects of the former. Carbon monoxide poisoning is quite lethal and leads to fatalities in severe cases. This is due to the high affinity of haemoglobin (Hb) to the slightest amount of carbon monoxide. The affinity of carbon monoxide to haemoglobin is about 200 times that of oxygen to haemoglobin. CO poisoning also manifests itself in cellular metabolism by impeding mitochondrial functions and therefore cellular respiration. Haemoglobin facilitates the dissolution of oxygen into blood plasma therefore hampering its functioning reduces the amount of oxygen in the blood. Some of the most common symptoms of CO poisoning that patients suffer from include loss of memory, attention and concentration span, excessive headaches and fatigue, drowsiness, and vomiting, among others. In some cases, the patients are unable to walk and contain their urine and stool. The brain and the heart are the most affected body parts by CO poisoning hence the numerous symptoms affecting even the most basic body processes. Due to their high metabolisms, the two key organs require high amounts of oxygen concentration at all times to function optimally.

Hyperbaric oxygen therapy (HBOT) attempts to take the body back to normalcy by aiding in the conversion of carboxyhaemoglobin (COHb) back to its regular and functional state haemoglobin. In its functional state, haemoglobin can carry up to four oxygen molecules. Carboxyhaemoglobin reduces the amount of oxygen transported by the blood to the cells and body tissues. In excessively high amounts, carboxyhaemoglobin also affects the body’s inflammatory responses to various stimuli. HBOT also takes care of the damaged vascular endothelium for the vessels supplying blood to the brain. The reduction of neutrophil action reduces occurrences of such phenomena as tissue edema and cerebral hypoxia. The brain can get back to an optimal phase of performance.

HBOT is highly recommended for severe cases of CO poisoning where patients have lost consciousness, severe cognitive functioning and memory, as well as the ability to move. In this case, COHb is normally higher than 30% in the body. It is also used by pregnant women as well as infants in severe cases where they require high efficacy. HBOT is also used alongside various drugs by recovering patients of CO poisoning. This form of treatment is complementary and is essential for those who are boosting their cognitive and motor functions after being on the receiving end of CO poisoning. It is also recommended for patients dealing with end-organ ischemia/damage such as those treating their kidneys. Some of the neurological symptoms that call for HBOT include cardiac dysfunction, neuronal injury or complete damage, dementia, regular seizures, and comas. Placing patients under 100% oxygen at this point is key since it will reduce the severity of what they are going through.

Compared to normobaric oxygen and other forms of oxygen supplementation, hyperbaric oxygen is more rapid and effective in action. Patients are protected from such phenomena as lipid peroxidation in the brain. This way, their memory, and cognitive functioning are restored with time. Exposure of CO poisoning patients to HBOT has immediate results as improvements in the patients are seen. 1-2 hours of HBOT reduce the effects of carbon monoxide poisoning by more than 50%; the half-life of CO is about 300 minutes. Patients can recover in hours for slight symptoms to several days for dire cases.

Sources

Lawson-Smith, P., Jansen, E. C., Hilsted, L., & Hyldegaard, O. (2010). Effect of hyperbaric oxygen therapy on whole blood cyanide concentrations in carbon monoxide intoxicated patients from fire accidents. Scandinavian Journal of Trauma, Resuscitation and Emergency Medicine, 18(1), 32–41. https://doi.org/10.1186/1757-7241-18-32

Millar, I., & Scheinkestel, C. (2007). Hyperbaric oxygen for acute carbon monoxide poisoning. Carbon Monoxide Poisoning, 7(6), 391–402. https://doi.org/10.1201/9780849384189.

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