Carbon Monoxide Poisoning In Children: Diagnosis And Management In The Emergency Department

Table of Contents

 

1. Abstract
2. Case Presentations
3. Introduction
4. Critical Appraisal of the Literature
5. Epidemiology And Etiology
6. Pathophysiology
   1. Pathophysiology In Children And Infants
7. Prevention Of Carbon Monoxide Poisoning
8. Differential Diagnosis
9. Prehospital Care
10. Emergency Department Evaluation
    1. Initial Stabilization
       1. Primary Survey
    2. Patient Presentation
    3. Exposure History
    4. Physical Examination
    5. Delayed Neurologic Sequelae
11. Diagnostic Studies
    1. Arterial Blood Gas
    2. Carboxyhemoglobin
    3. Complete Blood Count
    4. Chemistries
       1. Creatine Kinase
       2. Cyanide
       3. Glucose
       4. Lactate
    5. Pregnancy Test
    6. Toxicology
    7. Urinalysis
    8. Electrocardiography
    9. Cardiac Markers (Creatine Kinase-MB Or Troponin T)
    10. Chest Radiography
    11. Computed Tomography
12. Treatment
    1. Hyperbaric Oxygen Therapy
13. Disposition
14. Special Populations And Circumstances
    1. Newborns
    2. Pregnancy
    3. Fire Victims
       1. Cyanide Poisoning
    4. Chronic Carbon Monoxide Exposure
15. Controversies And Cutting Edge
    1. Noninvasive Detection
    2. Novel Treatments
16. Summary
17. Risk Management Pitfalls In The Management Of Carbon Monoxide Exposure
18. Time- And Cost-Effective Strategies
19. Case Conclusions
20. Clinical Pathway For The Diagnosis And Management Of Carbon Monoxide Poisoning In Pediatric Patients
21. Tables and Figures
    1. Table 1. All Symptoms Reported By Patients With Acute Carbon Monoxide Poisoning Grouped By Organ System
    2. Table 2. Indications For Hyperbaric Oxygen Therapy After Carbon Monoxide Poisoning
    3. Table 3. Practical Considerations For The Pediatric Hyperbaric Patient
    4. Figure 1. The Effect Of Carboxyhemoglobinemia On Oxygen Content And Delivery
    5. Figure 2. A Multiplace Hyperbaric Oxygen Chamber
22. References
23. Acknowledgements

Abstract

Approximately 5000 children present to the emergency department annually with unintentional carbon monoxide poisoning. Children may be more vulnerable to carbon monoxide poisoning because of their increased metabolic demand and their inability to vocalize symptoms or recognize a dangerous exposure, and newborn infants are more vulnerable to carbon monoxide poisoning because of the persistence of fetal hemoglobin. Mild carbon monoxide poisoning may present as viral symptoms in the absence of fever. While headache, nausea, and vomiting are the most common presenting symptoms in children, the most common symptom in infants is consciousness disturbance. This review discusses the limitations of routine pulse oximetry and carboxyhemoglobin measurement in determining carbon monoxide exposure, and notes effects of co-ingestions and comorbidities. Although the mainstay of treatment is 100% oxygen, the current evidence and controversies in the use of hyperbaric oxygen therapy in pediatric patients is reviewed, along with its possible benefit in preventing delayed neurologic sequelae.

Case Presentations

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?

Introduction

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.

Critical Appraisal Of The Literature

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.

Risk Management Pitfalls In The Management Of Carbon Monoxide Exposure

1. “I found a COHb level of 27% in my obtunded 17-year-old patient who was trying to fix a boat motor in his garage. I am consulting the hyperbaric medicine facility. This seemed like a straightforward case of CO poisoning, so I didn't consider any other testing.”
   While this patient has a history and symptoms consistent with severe CO poisoning, emergency clinicians must always remain vigilant for co-intoxicants and comorbidities. Even without evidence of trauma on examination, a head CT may be warranted in patients with altered mental status, as trauma may cause or result from severe CO poisoning. Intoxication from other drugs of abuse can also be a precipitant to a situation of CO poisoning. Patients with severe CO poisoning warrant a full trauma evaluation and screening for drugs of abuse.
2. “The pulse oximeter reads 100% and the patient does not appear cyanotic, so that means he must not have a significant amount of COHb.”
   Routine pulse oximetry cannot distinguish between oxyhemoglobin and COHb and will falsely read a normal oxygen saturation in cases of CO poisoning. The machine does not reflect the true degree of hypoxemia in CO-poisoned patients. When available, pulse CO-oximetry may be able to give a sense of the patient’s COHb level. Laboratory COHb level is the only way to confirm the presence or absence of CO poisoning.
3. “I finally finished fellowship and bought a new home for my family. Should I be installing CO detectors and how often do they need to be checked?”
   At minimum, CO detectors should be placed on every level of the home and within 10 feet of every bedroom door. While CO-only detectors may be placed at any altitude in a room, combination CO/smoke detectors should be placed on or near the ceiling, since smoke rises. CO detectors should be tested monthly to ensure functionality.
4. “I have a 10-month-old boy with lethargy and a COHb level of 22%. I remember hearing that HBO therapy is controversial in adults and not well studied in this population. Should I still be consulting with a hyperbaric medicine facility?”
   While there are no randomized controlled trials for HBO in children and its use remains controversial, the available data suggest that it is probably safe and possibly efficacious in preventing delayed neurologic sequelae. There are many pediatric-specific considerations (ie, available pediatric-trained personnel, multiplace chambers, the need for myringotomy) in HBO therapy, and early consultation is recommended to ensure the proper considerations, equipment, and personnel are in place to not delay HBO therapy. Unstable patients should usually not be transported, as the risks of transport often outweigh the unclear benefit of HBO; however, stable intubated patients may be candidates for HBO therapy.
5. “I have an adolescent patient with altered mental status and headache who endorses smoking a waterpipe at a hookah bar but denies any drugs other than tobacco. I have heard that hookah smoking is clean, so it can't possibly cause acute CO poisoning.”
   Hookah (waterpipe) smoking has seen increased popularity in the United States, with 1 in 5 adolescents endorsing smoking hookah in the past year.¹⁴² Hookah smoking is sometimes misunderstood as a “clean” way of smoking, since the smoke passes through water; however, there are many case reports and series of acute CO poisoning from hookah smoking. A WHO report suggested that the amount of smoke inhalation from a 200-puff hookah smoking session is equivalent to smoking 100 cigarettes.¹⁴³
6. “I am seeing a 4-year-old afebrile child in the ED with headache and malaise. A kerosene heater was recently turned on for the winter, so I suspected CO poisoning. The COHb level in the child was only 4%, so this must not be the source of his symptoms.”
   Literature in children suggests that normal levels of COHb may be ≤ 2%. In a study of children presenting to the ED with afebrile viral symptoms who had a potential source of CO exposure, more than 50% of the children had elevated (> 2%) COHb levels and all had symptomatic improvement with oxygen administration.⁴⁹ A mild elevation in COHb may indicate an exposure source, and a more-severe poisoning may be prevented if it is identified early.
7. “The parents of a 5-year-old boy with no significant past medical history are concerned that something at home has been causing daily morning headaches for the past month and a half. They have ensured that CO detectors are correctly installed and working, so CO poisoning must not be the etiology of his headaches.”
   Normal CO detector limits are based on preventing acute CO poisoning and will not alarm for lower levels of exposure, which may cause chronic CO poisoning. A COHb level in the ED will be helpful in diagnosing this patient. The parents should be advised that lower-limit CO alarms are available, and it is possible to call the fire department to have the home checked for subalarming CO levels.
8. “While serving as medical control, I was called by an EMS crew who were about to enter the house of a potential CO poisoning victim. They asked advice on initial management. I recommended removing the victim from the scene as quickly as possible.”
   The first priority for prehospital providers treating patients with suspected CO poisoning is to ensure scene safety. EMS personnel should not enter a potentially dangerous situation until it has been verified by the fire department or other agency that it is safe to do so. There are case reports of EMS personnel morbidity and mortality from CO poisoning in responding to a call.
9. “I read an article about how ice resurfacers might be a source of CO exposure. My 8-year-old hockey player presenting with headache, nausea, and vomiting has a postgame noninvasive pulse CO-oximeter level of 6%, so this must be CO poisoning.”
   Many ice resurfacers are now electric-powered and are not a source of CO. It would be odd for this player to be the only victim of CO poisoning in an arena, so other diagnoses (concussion, dehydration, or viral illness) must be considered. Noninvasive CO levels may be useful for screening purposes, but, with a precision of +/- 3% at 1 standard deviation, must be confirmed with blood COHb levels. NBO therapy should be given to the player pending the confirmatory test.
10. “My 17-year-old patient has been stressed out by school and studying too hard. She fell asleep in her car while in the garage. Thank goodness her mother happened to come home early from work and found her before it was too late. Her COHb level on presentation was 8%, it is now 2%. She was asymptomatic, so I sent her home.”
    Intentional CO poisoning is more common and more often fatal than unintentional CO poisoning. Comorbid mental health problems must always be considered in victims of CO poisoning. This patient warrants exploration of a possible suicide attempt prior to discharge and may require inpatient psychiatric hospitalization.

Tables And Figures

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.

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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.

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