You receive notification that EMS is bringing in a 14-year-old hockey goalie after a syncopal event. EMS inform you that he is the first of many potential victims en route after multiple players and spectators at a local ice rink began complaining of different symptoms. According to EMS, a noninvasive pulse CO-oximeter reported his COHb level at 21%. His GCS score was 14 at the scene due to confusion and disorientation, his vital signs were stable, and he was given oxygen by nonrebreather face mask. His blood glucose was 115 mg/dL. On arrival, the patient’s vital signs are normal with an oxygen saturation of 100% on 15 L/min of oxygen by nonrebreather face mask. The goalie complains of severe 9/10 frontal headache, nausea, and ringing in his ears. On physical examination, his face is flushed, and he is diaphoretic with an otherwise normal physical examination and mental status. His CBC, electrolytes, and arterial blood gas analysis are in the normal range. His COHb level is 19%. His ECG is normal. As you prepare to manage the patient and other potential victims, you ask yourself: What was the source of this poisoning and are others in danger? What are the most common symptoms of carbon monoxide poisoning in children? What are the treatment goals? What are the indications for consulting with a hyperbaric medicine specialist?
A 2-month-old girl is brought to the ED by her mother with a chief complaint of “lethargy.” The baby was in her usual state of health until this morning when she had to be aroused by her mother. The infant fed poorly, having a weak latch and feeding for only 5 minutes. The mother notes that she herself has been feeling nauseous and has a mild headache, and wonders if the baby caught her “virus.” On examination, the infant’s vital signs are: temperature, 36.9°C (98.4°F); heart rate, 155 beats/min; blood pressure, 76/42 mm Hg; respiratory rate, 46 breaths/min; oxygen saturation, 99% on room air. The baby is lethargic on examination, arousing and crying for IV placement, but then quickly falling asleep again. She has a normal cardiorespiratory and abdominal examination. Grasping reflex is not present bilaterally and moro reflex is diminished. She has diminished truncal tone but intact reflexes. You consider the broad differential for the lethargic-appearing infant: Sepsis? Nonaccidental trauma? Cardiac arrhythmia? Adrenal insufficiency? The patient is started on 5 L/min of oxygen by face mask. Her blood glucose is 80 mg/dL. She is given a 20 mL/kg bolus of normal saline and antibiotics. A head CT shows normal anatomy with no acute bleeding or infarction. Her ECG is normal for her age. The COHb returns with the blood gas at 28%. You ask yourself: What are the next steps in treatment of CO poisoning in an infant? Can a baby be referred for hyperbaric oxygen therapy? Who should be called regarding home safety concerns? What was the source of the CO and who else is at risk? Should the mother be treated?
A 6-year-old girl is brought to the ED by EMS after being rescued from a 3-alarm fire at an apartment complex. The girl was found in her bed by the fire department. According to the rescuer, the room was hot with smoking carpet and filled with thick smoke. In the ambulance, the girl was minimally responsive to painful stimuli. Her vital signs were remarkable for tachycardia, with a heart rate around 130 beats/min, but were otherwise stable. In the ED, her heart rate remains 130 beats/min, her blood pressure is now 68/36 mm Hg, her respiratory rate is 24 breaths/ min, and her oxygen saturation is 100% on 15 L/min by nonrebreather mask with an oxygen reservoir. The girl has a GCS score of 8, with eye opening only to painful stimuli and nonlocalization of pain. Her speech is not comprehensible. There are soot debris and superficial burns to her face and neck, with a demarcation line representing the blanket. She has a normal cardiorespiratory and abdominal examination. The patient is intubated with a 5.0 cuffed endotracheal tube. Soot was noted in the larynx. She is ventilated at 24 breaths/ min with 100% oxygen and given 40 mL/kg of lactated Ringer’s solution with an improvement in her blood pressure to 100/62 mm Hg. The venous blood gas results show a mixed metabolic and respiratory acidosis and her lactate result is 12.4 mmol/L. Her COHb level is 18%. Her cyanide level is pending. As you begin to think about the next steps, you wonder: How should comorbid CO and cyanide poisoning be treated? Given that the patient has burns, CO poisoning, and suspected cyanide poisoning with critical care needs, can she possibly still be a candidate for hyperbaric oxygen therapy? What can you advise her parents about her prognosis and potential complications?
Carbon monoxide (CO) has been called a “silent killer.” It is formed by the incomplete combustion of hydrocarbon fuels and, as it is both clear and odorless, is undetectable by the human senses. It rapidly diffuses into the pulmonary circulation and competes with oxygen to bind the hemoglobin molecule, thereby impairing oxygen delivery.
The toxic effects of CO poisoning have been known for centuries. As early as the 4th century BC, Aristotle cautioned that coal fumes lead to a “heavy head” and death.1 Until the mid 20th century, coal was the primary heating fuel in the urban United States, and accidental CO-related fatalities from improper ventilation or heater malfunction were not uncommon.2 With cleaner-burning fossil fuels, more efficient engines, and advances in energy technology, CO levels in the air and rates of CO poisoning have fallen. In 1923, Henderson and Haggard measured CO from a moving car in New York City and found levels in city traffic to range from 10 to 290 parts per million (ppm); today, air levels are generally less than 1 ppm.3
Despite a historical decline, CO remains one of the leading causes of poisoning-related emergency department (ED) visits, with 50,000 cases annually in the United States.4-7 CO poisoning is responsible for 500 unintentional, non–fire-related deaths annually in the United States, more than any other gas.4,8 The incidence of CO poisoning has a seasonal and geographic association with cold climates, peaking during winter months and occurring at higher rates in high-altitude states, notably the north and Midwest.4,7,9 However, cases occur year-round, so clinicians must remain suspicious for less-common and evolving sources of exposure.10
The presentation of CO poisoning can range from mild and nonspecific to critical illness, depending on the level and duration of the exposure and host factors. Because symptoms can mimic a myriad of conditions and a source of exposure is not always known, the diagnosis may remain hidden if clinicians are not vigilant in maintaining an awareness and suspicion for CO poisoning.
The mainstay for treatment of CO poisoning is oxygen therapy. In severe cases, the emergency clinician must weigh the risks and benefits of transfer to a center with capabilities for hyperbaric oxygen (HBO) therapy, the evidence for which remains controversial.
In this issue of Pediatric Emergency Medicine Practice, the current state of diagnosis and management of CO poisoning in children in the ED is reviewed. The unique developmental and physiologic traits of children with this condition will be considered. The current epidemiology of CO poisoning is defined and put it into a historical context to better understand how sources and prevention strategies for CO poisoning have evolved over time. Current research topics are explored, including noninvasive detection, laboratory and radiographic markers for disease severity, HBO therapy, and other therapies for the treatment of CO poisoning.
A PubMed search strategy, developed in consultation with a medical librarian, searched all English-language human studies related to CO published from November 2009 through January 2015. A combination of the following search terms were used: carbon monoxide poisoning, carbon monoxide, ACOP, poison, toxicology, toxicity, poisoning, CO poisoning, CO toxicity, human, humans, adult, infant, infancy, child, pediatric, pediatrics, middle age, teen, adolescent, adolescents, adolescence, children, patient, patients, and age. This strategy yielded 477 articles; 211 were relevant to this review topic.
The review was then extended to include bibliographic references of relevant literature prior to the queried date range including review articles that cite studies dating back to 1950.11,12 Clinical guidelines and policies from relevant professional organizations related to CO poisoning that were published over the past 30 years were searched. The American College of Emergency Physicians (ACEP) published an evidence-based Clinical Policy on critical issues in the management of adult patients presenting to the ED with acute CO poisoning.13 The Cochrane Database of Systematic Reviews had a single review that was most recently updated in 2011 related to CO regarding the use of HBO.14
A targeted search on the use of HBO in children was performed. A PubMed query with the terms carbon monoxide and hyperbaric was performed for English-language review articles and clinical trials from January 1985 through February 2015. This strategy yielded 133 publications that were reviewed. Limiting the search in PubMed to only pediatrics yielded 17 results, of which there were several review articles and case series on HBO therapy use in pediatric CO poisoning, but no randomized controlled trials or case-control studies. None of the review articles cite any randomized controlled trials of HBO use in pediatric CO poisoning.
Neil B. Hampson, Susan L. Dunn. Symptoms of carbon monoxide poisoning do not correlate with the initial carboxyhemoglobin level. Undersea & Hyperbaric Medicine. 2012;39(2):657665. Available at: http://www.ncbi.nlm.nih.gov/pubmed/22530449. Reproduced with permission from the Undersea and Hyperbaric Medical Society.
Evidence-based medicine requires a critical appraisal of the literature based upon study methodology and number of subjects. Not all references are equally robust. The findings of a large, prospective, randomized, and blinded trial should carry more weight than a case report.
To help the reader judge the strength of each reference, pertinent information about the study, such as the type of study and the number of patients in the study is included in bold type following the references, where available. The most informative references cited in this paper, as determined by the authors, are noted by an asterisk (*) next to the number of the reference.
Theodore E. Macnow, MD;Mark L. Waltzman, MD, FAAP
September 2, 2016
October 2, 2019
Upon completion of this article, you should be able to:
Physician CME Information
Date of Original Release: September 1, 2016. Date of most recent review: August 15, 2016. Termination date: September 1, 2019.
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