In the winter months, remain vigilant for CO poisoning, as the presenting signs are often nonspecific.
Dr Stiller is Chief, Section of Maternal-Fetal Medicine, Department of Obstetrics and Gynecology, Bridgeport Hospital, Bridgeport, Connecticut, and Clinical Professor of Obstetrics and Gynecology, Yale School of Medicine, New Haven, Connecticut.
Neither of the authors has a conflict of interest to report in respect to the content of this article.
Carbon monoxide (CO) is a colorless and odorless gas that is a byproduct of combustion and has the potential to quickly reach hazardous concentrations in poorly ventilated areas. In fact, accidental household CO poisoning is the most frequent cause of poisoning in pregnancy.1 Some of the more common sources of CO production include running vehicles, poorly maintained heating equipment, clogged chimneys, and poorly ventilated gas appliances. In cold winter months, it is important to remain vigilant for CO poisoning, as the presenting signs are often nonspecific.
The maternal symptoms of acute CO poisoning range from relatively mild and nonspecific (eg, headaches, nausea, and vomiting) to more severe (eg, altered mental status or coma) as maternal levels of carboxyhemoglobin (COHb) increase. In nonsmoking women, the normal level of COHb ranges from 1% to 3%, but it can reach as high as 9% in those who smoke. In acute poisoning, levels may reach 30%–50%.
The effects of CO poisoning on the developing fetus depend greatly on the gestational age of exposure and the dose. As a general rule, fetal injury is more likely when acute maternal CO poisoning is associated with more severe symptoms such as loss of consciousness. An anoxic event during the early gestational ages of embryogenesis or shortly after may be associated with anatomical malformations such as limb abnormalities or microcephaly, specifically in fetuses that survive to viability.2 At later gestational ages, severe exposures can be associated with the fetal neurological sequelae of anoxia, including but not limited to hypoxic ischemic encephalopathy, hypotonia, and cerebral palsy. Mortality rates for fetuses may be as high as 67% in severe intoxications. Generally, mild maternal exposures presenting with only headaches and nausea are more likely to result in favorable fetal outcomes.3
Signs of fetal CO toxicity may include decreased movement and changes in heart rate. Affected fetuses may exhibit a Category II heart rate pattern, defined by tachycardia, in most cases with minimal variability and the absence of accelerations.5 The diagnosis of maternal CO poisoning remains challenging due to nonspecific signs and symptoms in the mother, such as headaches, nausea and vomiting, and altered mental status. It is important, then, to maintain a high level of suspicion during the winter months when evaluating patients with these symptoms, especially women who have been exposed to areas where combustion is occurring, such as fireplaces, stoves, running automobiles, or portable generators.
The first step in treating CO poisoning is to remove the patient from the source of toxicity. Obtain vital signs and pulse co-oximetry, and perform a focused neurological exam. As soon as CO intoxication is suspected, administer 15L/min of 100% oxygen via a non-rebreather mask and place the patient on a cardiac monitor to evaluate for myocardial ischemia. Obtain a COHb level to help diagnose and determine exposure levels in conjunction with the total clinical picture to help guide therapy. The table outlines a recommended course of action and investigative steps.6
With hyperbaric oxygen (HBO) therapy, oxygen is delivered under a higher atmospheric pressure, thereby increasing the oxygen content of blood and facilitating oxygen exchange. It greatly decreases the time to elimination of CO from circulation. One important factor to bear in mind is the lag time required to eliminate CO from fetal circulation. Continue oxygen therapy for approximately 5 times longer than what is required to neutralize maternal levels.
Knowing whether HBO is available at your facility, and what your facility’s policy is regarding its use is important. The general consensus across the literature is to initiate HBO therapy if maternal COHb levels exceed 20%, if there are maternal signs of neurological compromise including altered mental status or coma, or if there are signs of fetal hypoxia, such as abnormal fetal heart rate tracing patterns or decreased fetal movements.7 The only absolute contraindication to HBO therapy is an untreated pneumothorax, but an ongoing risk-benefit analysis must be performed with respect to the fetus. Initial animal model studies suggested the possibility of adverse fetal outcome from HBO therapy, but multiple human subject case reports during pregnancy have not supported those concerns.8
The majority of CO poisoning incidents are mild and the fetal outcomes are good. However, risk of fetal mortality is much higher with exposures that are severe and life threatening. The number of CO poisoning episodes can be reduced with a strong focus on primary prevention via patient education materials, which are available from the CDC and include instructions for safe heating practices and proper CO detector use.9
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8. Elkharrat D, Raphael JC, Korach JM, et al. Acute carbon monoxide intoxication and hyperbaric oxygen in pregnancy. J Intensiv Care Med. 1991;17(5):289–292.
9. Centers for Disease Control and Prevention. Carbon Monoxide Poisoning: Frequently Asked Questions. http://www.cdc.gov/co/faqs.htm. Accessed October 29, 2015.