INTRODUCTION: We present a case of a 26-year-old man who was involved in a mining accident. He was trapped for approximately 42 hours with carbon monoxide levels measured at 1300 parts per million within the mine shaft. The patient had a significant decrement in his cognitive function, and had reduced cardiac function. After 3 treatments with hyperbaric oxygen, the patient survived. He had gradual, but dramatic improvement in his cardiovascular and neurologic function.
CASE PRESENTATION: A 26-year-old male was involved in a mining accident caused by an explosion igniting methane gas. He was trapped in the mine for approximately 42 hours. Rescuers were delayed 12 hours after the explosion due to high concentrations of carbon monoxide and methane gas in the shaft. Air near where the miners were last known to be stationed contained 1,300 parts per million of carbon monoxide (400 parts per million is the maximum considered safe). Our patient was found alive, and was the only survivor found. He was noted to be in respiratory distress and had an altered sensorium. The patient was intubated, placed on mechanical ventilation and taken to a nearby hospital. Initial carboxyhemoglobin levels were inaccurate. The patient was stabilized and transferred to our institution for hyperbaric oxygen therapy. Carboxyhemoglobin levels at the previous tertiary care center were reported as 20%. Upon arrival to our institution, the patient was in multisystem organ failure. Echocardiography revealed an ejection fraction of 20% with global hypokinesis. Computerized tomography of the brain revealed multiple focal areas of hemorrhage within the subcortical white matter. The globus pallidus was spared. The patient received three treatments of hyperbaric oxygen therapy at 3 atmospheres for 30 minutes and 2.4 atmospheres for 60 minutes. He demonstrated significant improvement in all aspects of his care. His ejection fraction improved to 35% with normal wall motion. His neurological status improved significantly as he is currently mobile, is communicative and has his cognitive functions intact.
DISCUSSIONS: Carbon monoxide (CO) is a tasteless and odorless gas caused by incomplete combustion of carbon based compounds. In the US, 1000-2000 accidental deaths occur each year. CO binds oxygen at 240 times that of oxygen consequently decreasing oxygen carrying capacity of blood. The severity of carbon monoxide poisoning is a function of the duration of exposure and the concentration of the gas. The initial carboxyhemoglobin level correlates poorly with outcome. Mechanisms of acute carbon monoxide poisoning include hypoxia, reduced cellular oxygen metabolism, lipid perioxidation leading to oxidative injury, and damage to vascular endothelium. Persistent or delayed neurologic sequalae can ensue. It may also lead to myocardial injury leading to increased long term mortality. Standard treatment includes removal from exposure site, administration of supplemental oxygen, and general supportive care. The half life of carboxyhemoglobin is approximately 320 minutes which is decreased to 23 minutes with hyperbaric oxygen treatment. Furthermore, hyperbaric oxygen therapy has been shown to decrease morbidity and mortality. It has also been shown to decrease the delayed neurological sequalae associated with carbon monoxide poisoning. To our knowledge, this is the first reported case of a patient surviving long term exposure to lethal doses of carbon monoxide levels after hyperbaric oxygen therapy.
CONCLUSION: Carbon monoxide poisoning remains an important cause of accidental and intentional injury worldwide. This is the first case reported of a patient surviving prolonged periods of carbon monoxide exposure at lethal doses after treatment with hyperbaric oxygen. We recommend the use of hyperbaric oxygen therapy in patient with sustained and toxic levels of carbon monoxide that have neurologic and cardiac toxicity.
DISCLOSURE: Anil Singh, None.