“This case report presents a 67-year-old man with CO poisoning who developed delayed neurologic sequelae (DNS) due to delayed diagnosis and missed therapeutic window for HBOT. Investigation of CO poisoning requires taking a detailed history to avoid delays in diagnosis and treatment.”
“Carbon monoxide (CO) has a long controversial history of treatment, especially regarding hyperbaric oxygen. While the best therapeutic approach is vague, the diagnosis may be just as elusive. Typically, signs and symptoms range from headache to disorientation, cardiovascular ischemia, coma, and death. But, the signs and symptoms are largely variable and nonspecific.
The clinical features of CO poisoning depend on the ambient concentration of CO and the duration of exposure. Remember Haber’s Law: dose = concentration x time. This is an oversimplification of the dose effect relationship, however, as people “bring things” with them during an exposure — underlying disease(s), medications, age, and more can all influence susceptibility. For example, persons with underlying coronary heart disease have a greater risk of myocardial infarction and arrhythmias.
The astute clinician suspects CO poisoning based on vague symptoms in particular settings: enclosed space, multiple victims, fossil fuel combustion, etc. Among symptoms, the most reported is headache. But, other constitutional complaints may include malaise, nausea, and dizziness. Symptoms of acute poisoning are largely confined to alterations in mental status. So, probing questions of more serious symptoms are important, such as loss of consciousness and chest pain. Severe intoxication can lead to syncope, seizures, coma, chest pain, pulmonary edema, ventricular arrhythmias and marked lactic acidosis. With severe CO intoxication, always measure troponins and lactic acid.
Standard pulse oximetry does not differentiate carboxyhemoglobin (COHb) from oxyhemoglobin (more sophisticated devices like the CO Pilot™ are now available for field use, however). A COHb measurement is essential for determining exposure, but levels correlate imprecisely with the degree of poisoning and are not predictive of the development to delayed neurologic sequelae. Plus, other factors, like smoking, can affect COHb levels: nonsmokers may have up to 3 percent COHb at baseline; smokers may have levels of 10 to 15 percent. So, patient symptoms and signs guide management, not COHb levels. Thus, once the diagnosis of CO poisoning is established, repeat measurements are generally unnecessary.”
In 1998, the Iowa Department of Public Health (IDPH) and Iowa State University (ISU) Extension Department, with the assistance of local health departments, investigated a series of carbon monoxide (CO) poisonings associated with the use of liquified petroleum gas (LPG)-powered forklifts in light industry. In each episode, forklifts emitting high CO concentration levels were operated in inadequately ventilated warehouse and production facilities, which resulted in high CO accumulations. Employees at each site developed symptoms of CO poisoning, and some employees received inadequate or inappropriate medical care. This report summarizes the investigations and provides recommendations to prevent such incidents.
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