Carbon Monoxide Toxicity in the Wilderness

November 1, 2018
By Jessica Duke, MD

Imagine you are working as medical staff at Everest Base Camp when you spot one of the climbers stumbling through camp. You approach the climber, introduce yourself, and ask him if he needs assistance. He tells you that he is looking for the bathroom, but also complains of a headache and feeling dizzy. You ask a few more questions and discover that the climber’s group just arrived to camp several hours ago. He and his wife were cold and tired so they cooked themselves an early dinner in their tent then went straight to bed. They did not drink alcohol and he did not have a headache before going to sleep. He woke up having to urinate so got up to use the bathroom. His wife is still asleep in the tent. You bring the climber to the medical tent where he is found to have an oxygen saturation of 86%, normal for someone at Everest Base Camp. After starting the climber on oxygen, you go check on his wife. You discover that her skin is flushed and that she is difficult to arouse. You note a kerosene lamp burning inside the tent and quickly pull her outside. What is causing these symptoms and what is the appropriate treatment?


At first, you may have thought that the ataxic climber with a headache was suffering from high altitude cerebral edema. All sickness at altitude is altitude sickness until proven otherwise, right? Well, in this case you astutely picked up on the fact that the patient cooked dinner in his tent, which raised your suspicion for carbon monoxide (CO) poisoning In the wilderness setting, CO toxicity most commonly occurs by fuel combustion from stoves or lanterns in enclosed spaces, such as tents or snow shelters. When you checked on the patient’s wife, you found her flushed and sedated with a kerosene lamp burning inside the tent, confirming your suspicion. You saved her life by considering this diagnosis and quickly removing her from the toxic environment.


CO is a colorless and odorless asphyxiant gas that binds to hemoglobin in red blood cells creating carboxyhemoglobin (COHgb). CO has an affinity for hemoglobin over 200 times that of oxygen. Bound CO prevents oxygen uptake by hemoglobin and significantly reduces the blood’s oxygen carrying capacity. CO also interferes with cellular oxidation and reduces the function of all high oxygen demand tissues (heart, brain, lungs). The half-life of COHgb is approximately 300 minutes when breathing room air at sea level, 60 to 90 minutes with 100% oxygen at sea level, and 20 minutes with hyperbaric oxygen at 3 atmospheres of pressure. 


Signs and symptoms of CO toxicity vary based on exposure, duration, and the health and age of the individual. At higher altitudes, the reduction of partial atmospheric pressure potentiates clinical toxicity from CO. Mild CO toxicity is a great imitator of acute mountain sickness (AMS), presenting with headache, dizziness, and nausea. Patients with severe CO toxicity have symptoms that mimic high altitude cerebral edema (HACE) and high altitude pulmonary edema (HAPE), including flushed skin, tachycardia, hypotension, cardiac arrhythmias, progressive confusion, ataxia, seizures, CNS depression, and non-cardiogenic pulmonary edema.


When assessing a patient with these symptoms at altitude, it may be difficult to differentiate between CO poisoning and high altitude sickness. Unfortunately, oxygen saturation via a pulse oximeter is an unreliable indicator of CO poisoning and carboxyhemoglobin levels correlate poorly with clinical toxicity and outcome. Therefore, it is paramount to obtain a thorough history and physical. Make sure to consider CO poisoning in your differential and to ask about the use of stoves or lanterns inside an enclosed tent or snow shelter. Luckily, treatment for CO poisoning is similar to altitude illness. Most importantly, remove the patient from the toxic environment. If available, administer supplemental oxygen and consider using a Gamow bag to increase the air pressure around the patient. If symptoms are severe or do not rapidly improve with supplemental oxygen, the patient will need to be evacuated with rapid descent to a hospital for possible hyperbaric therapy.