2011 N09 CO Poisoning

An Evidence-Based Approach September 2011
Volume 8, Number 9
To Pediatric Carbon Monoxide Author
Abby M. Williams, MD
Poisoning Clinical Fellow, Division of Pediatric Emergency Medicine,

Department of Pediatrics, Monroe Carell Jr. Children’s
Hospital at Vanderbilt, Nashville, TN
Abstract Peer Reviewer
Tommy Y. Kim, MD, FAAP

This article focuses on the evidence-based treatment of carbon mon- Assistant Professor of Emergency Medicine and Pediatrics,
Loma Linda Medical Center and Children’s Hospital, Loma
oxide (CO) poisoning, the most common preventable toxic exposure Linda, CA
that results in death in children 12 years old and younger. Evidence James W. Rhee, MD, FAAEM
suggesting that CO poisoning should be considered in the differen- Assistant Professor of Medicine and Pediatrics, Director of
Medical Toxicology Sections of Emergency Medicine and
tial diagnosis of pediatric patients with nonspecific complaints is Pediatric Emergency Medicine, The University of Chicago,
examined, and the use of carboxyhemoglobin levels to determine Chicago, IL
severity of CO exposure is reviewed.
CME Objectives
Case Presentation Upon completion of this article, you should be able to:
1. Describe the mechanisms by which CO is a harmful
exposure.
You have just arrived for your 7AM shift on a chilly January morning when 2. Identify patients at risk for CO poisoning.
an unresponsive 21-month-old girl is brought in by emergency medical 3. Recognize the signs and symptoms of CO poisoning.
4. Create a treatment and follow-up plan for any patient
services. On arrival to the ED, she is noted to be lethargic and flaccid. She after CO exposure.
is immediately placed on a cardiorespiratory monitor and the following 5. Discuss the controversies related to hyperbaric
oxygen therapy for CO poisoning.
vital signs are obtained: temperature 37.5°C (99.5°F), heart rate 154 beats
per minute, respiratory rate 32 breaths per minute, blood pressure 86/57 Acknowledgment
mm Hg, and oxygen saturations of 99% on face mask oxygen. On physical
examination, you note sluggish opening of her eyes to voice. She moans and A very special thank you to the author’s local toxicology
expert, Dr. Donna Seger, for her suggestions in the writing
localizes to pain, and her skin is pale. She is not apneic or cyanotic. Other of this review.
than her altered level of consciousness, the rest of her physical examination
Prior to beginning this activity, see “Physician CME
is normal. She appears to be managing her airway appropriately. Emer- Information” on back page.
gency medical services reports that a serum glucose obtained in route was
98 mg/dL.
AAP Sponsor Medicine, University of Medicine and Medicine Department, Chief - Tommy Y. Kim, MD, FAAP Gary R. Strange, MD, MA, FACEP
Dentistry of New Jersey; Director, Pediatric Emergency Medicine Assistant Professor of Emergency Professor and Head, Department
Martin I. Herman, MD, FAAP, FACEP Pediatric Emergency Medicine, Division, Medical Director - Pediatric Medicine and Pediatrics, Loma of Emergency Medicine, University
Professor of Pediatrics, UT College Children’s Medical Center, Atlantic Emergency Department, University Linda Medical Center and of Illinois, Chicago, IL
of Medicine, Assistant Director of Health System; Department of of Florida Health Science Center Children’s Hospital, Loma
Emergency Services, Lebonheur Christopher Strother, MD
Emergency Medicine, Morristown Jacksonville, Jacksonville, FL Linda, CA
Children’s Medical Center, Assistant Professor,Director,
Memorial Hospital, Morristown, NJ Alson S. Inaba, MD, FAAP,
Memphis, TN Brent R. King, MD, FACEP, FAAP, Undergraduate and Emergency
Ran D. Goldman, MD PALS-NF FAAEM Simulation, Mount Sinai School of
Editorial Board Associate Professor, Department Pediatric Emergency Medicine Professor of Emergency Medicine Medicine, New York, NY
Jeffrey R. Avner, MD, FAAP of Pediatrics, University of Toronto; Attending Physician, Kapiolani and Pediatrics; Chairman, Adam Vella, MD, FAAP
Professor of Clinical Pediatrics Division of Pediatric Emergency Medical Center for Women & Department of Emergency Medicine, Assistant Professor of Emergency
and Chief of Pediatric Emergency Medicine and Clinical Pharmacology Children; Associate Professor of The University of Texas Houston Medicine, Director Of Pediatric
Medicine, Albert Einstein College and Toxicology, The Hospital for Sick Pediatrics, University of Hawaii Medical School, Houston, TX Emergency Medicine, Mount Sinai
of Medicine, Children’s Hospital at Children, Toronto, ON John A. Burns School of Medicine, Robert Luten, MD School of Medicine, New York, NY
Montefiore, Bronx, NY Honolulu, HI; Pediatric Advanced
Mark A. Hostetler, MD, MPH Clinical Professor, Pediatrics and
Life Support National Faculty Michael Witt, MD, MPH, FACEP,
T. Kent Denmark, MD, FAAP, FACEP Professor of Pediatrics and Emergency Medicine, University of
Representative, American Heart FAAP
Medical Director, Medical Simulation Emergency Medicine, University of Florida, Jacksonville, FL
Association, Hawaii and Pacific Medical Director, Pediatric
Center; Associate Professor of Arizona Children’s Hospital Division
Island Region Ghazala Q. Sharieff, MD, FAAP, Emergency Medicine, Elliot Hospital
Emergency Medicine and Pediatrics, of Emergency Medicine, Phoenix, FACEP, FAAEM Manchester, NH
Loma Linda University Medical AZ Andy Jagoda, MD, FACEP Associate Clinical Professor, Children’s
Center and Children’s Hospital, Madeline Matar Joseph, MD, FAAP, Professor and Chair, Department Hospital and Health Center/University Research Editor
Loma Linda, CA of Emergency Medicine, Mount
FACEP of California, San Diego; Director Lana Friedman, MD Fellow,
Sinai School of Medicine; Medical
Michael J. Gerardi, MD, FAAP, Associate Professor of Emergency of Pediatric Emergency Medicine, Pediatric Emergency Medicine,
Director, Mount Sinai Hospital, New
FACEP Medicine and Pediatrics, Assistant California Emergency Physicians, San Mount Sinai School of Medicine,
York, NY
Clinical Assistant Professor of Chair for Pediatrics - Emergency Diego, CA New York, NY
Accreditation: EB Medicine is accredited by the ACCME to provide continuing medical education for physicians. Faculty Disclosure: Dr. Williams, Dr. Kim, Dr. Rhee, and their related parties
report no significant financial interest or other relationship with the manufacturer(s) of any commercial product(s) discussed in this educational presentation. Commercial Support: This issue of
Pediatric Emergency Medicine Practice did not receive any commercial support.
Her mother arrives 20 minutes later and states relationship of Sudden Unexpected Infant Death
that the child is previously healthy, and she was in her Syndrome (SUIDS) and CO poisoning. Omalu et al
normal state of health when she placed her in the crib at reported a link between SUIDS and CO poisoning4
bedtime. Mother says she went to check on her daughter while Variend and Forrest reported no association
this morning when she did not wake at her normal time in a series of 50 infants who died unexpectedly.5
and found her unresponsive with vomitus in the crib. Further evaluation is necessary to elucidate a link
She has not had any fevers, upper respiratory symptoms, between SUIDS and CO poisoning.
diarrhea, or rashes. There is no history of trauma, and Carbon monoxide poisoning is frequently as-
the child has been in the care of her mother. When ques- sociated with inhalation injuries. When associated
tioned about sick contact exposure, the child’s mother with a thermal burn, it is easier to recognize a CO
states that she has not been feeling well, with headache exposure. However, CO poisoning may go unrec-
and nausea upon waking this morning; however, she is ognized and undetected, leading to morbidity and
currently feeling better. mortality.6 Carbon monoxide poisoning often pres-
What other history would you like to obtain from the ents to the emergency department (ED) as a constel-
mother? What diagnostic tests and therapies do you want lation of non-specific symptoms. It is not detectable
to start? on routine drug screens. The clinician must pay close
While you are entering your orders, the nurse calls attention to the details of the history and have a high
you to the bedside because the patient has started to seize. index of suspicion in order to avoid missing this
potentially lethal exposure.
Introduction
Critical Appraisal Of The Literature
Carbon monoxide is an odorless, colorless gas re-
leased from the incomplete combustion of burning The literature review was launched with Ovid
hydrocarbons. Carbon monoxide has been called a MEDLINE® and PubMed searches for articles on
“great imitator” and “silent killer.” Carbon monox- CO poisoning from 1965-2010. Keywords included
ide poisoning is the most common preventable toxic CO poisoning and inhalation injury. All searches were
exposure resulting in death in children 12 years and limited to the English language, human subjects, and
younger.1 In this age group, it is typically an unin- children ages 0-18 years. Of 251 articles identified,
tentional poisoning. In adolescents, especially males, 88 are provided for the reader’s reference. Further-
CO poisoning may be intentional.2 It has also been more, a search of the Cochrane database revealed
described as a form of child abuse by caregivers.3 one review on the use of hyperbaric oxygen (HBO)
Finally, there has been mixed evidence between the for CO poisoning. Additionally, the 2008 data from
the 26th Annual Report of the American Association
of Poison Control Centers (AAPCC) (http://www.
Table Of Contents aapcc.org) National Poison Data System (NPDS)
Abstract........................................................................ 1 was reviewed for details regarding CO poisoning
Case Presentation.......................................................1 in children. The bibliographies of the best articles
Introduction................................................................2 were also reviewed, and references were pulled from
Critical Appraisal Of The Literature....................... 2 these articles.
Epidemiology, Etiology, And Pathophysiology..... 2 Unfortunately, there are only very limited case
Differential Diagnosis................................................ 3 series and case reports in the literature describing
Prehospital Care......................................................... 3 CO poisoning in children. Most of the published
Emergency Department Evaluation........................ 5 data is inferred from published data in adults. The
Diagnostic Studies...................................................... 6 most recent studies in the literature focus on fast,
Clinical Pathway For Management Of Carbon easy, non-invasive, and inexpensive ways to detect
Monoxide Poisoning In Children..........................7 CO levels in a patient as well as newer technologies
Treatment..................................................................... 8 to detect neurological damage as a result of expo-
Prognosis..................................................................... 9 sure. There is much debate regarding HBO therapy.
Controversies And Cutting Edge.............................9 Most of the published data are from the 1980s and
Risk Management Pitfalls For Carbon Monoxide come from regional burn centers and coastal areas
Poisoning............................................................... 10 where hyperbaric chambers are available.
Cost-Effective Strategies..........................................11 For information on carbon monoxide exposure
Special Circumstances............................................. 12 in adult patients, see the February 2011 Emergency
Disposition................................................................ 12 Medicine Practice article, “Diagnosis And Manage-
Summary................................................................... 12 ment Of Carbon Monoxide Poisoning In The Emer-
Case Conclusion....................................................... 12 gency Department.”
References.................................................................. 13
CME Questions......................................................... 15
Pediatric Emergency Medicine Practice © 2011 2 ebmedicine.net • September 2011

Epidemiology, Etiology, And Once inhaled, CO has a very high affinity for
hemoglobin and binds with it to form carboxyhemo-
Pathophysiology globin (COHb). The affinity of CO for hemoglobin
is 210 to 270 times higher than oxygen’s affinity;
Carbon monoxide is a gas released from the burn-
therefore, only small amounts of CO are necessary
ing of carbonaceous materials and is frequently as-
to cause harm.21 Thus, the amount of COHb formed
sociated with smoking, house fires, vehicle exhaust,
is directly related to the concentration of CO at the
and inadequate ventilation with heaters, genera-
time of exposure and the length of time exposed.
tors, and wood or gas stoves. Carbon monoxide
Formation of COHb causes a shift in the oxyhemo-
poisoning commonly occurs during the winter
globin dissociation curve to the left (Figure 1, page
months and after natural disasters when use of
4) and leads to hypoxemia.
space heaters and generators is increased. Howev-
Even more harmful than hypoxemia, CO causes
er, it can also occur during the summer months and
oxidative stress by poisoning the cytochrome oxi-
in open air environments. It has been described in
dase enzyme in the mitochondria and platelet heme
children swimming behind a boat where engine ex-
protein, which results in direct neuronal and cardiac
haust is released7-9 or riding in the back of pickup
injury via necrosis and apoptosis.22-23 One study has
trucks.10 Much of the surveillance data published
cited inhibition of 76% of the cytochrome oxidase
in the literature describes the circumstances of CO
activity after acute CO poisoning.24 To take this one
poisoning in relationship to natural disasters in the
step further, cytochrome oxidase dysfunction in the
United States and abroad.11-19
brain has been associated with lipid peroxidation
The Centers for Disease Control and Prevention
that may explain the neurological symptoms de-
collected poison control data after Hurricane Ike in
scribed in CO poisoning.25-26
Texas during September 2008. The resulting study
linked improper generator use with 82% to 87% of
CO exposures. Seven deaths were reported in this Differential Diagnosis
study.12 In another study related to Hurricane Ike,
Fife et al describe that 75% of poisonings within 36 Carbon monoxide poisoning typically presents with
hours of landfall of Hurricane Ike were from genera- a constellation of vague, nonspecific symptoms that
tors powering televisions and video games.14 This make it easy to mistake for other illnesses. A his-
article, creatively entitled “Dying To Play Video tory of fire or other exposure can help the practitio-
Games” alludes to the idea that generators are not ner make the diagnosis. However, in less clear cut
only used to power refrigerators and air condition- instances, such as the child in the case presentation,
ing units as previously suspected but also to power there may be a very broad differential diagnosis.
sources of entertainment. Another article published (See Table 1.)
by Muscatiello et al discussed 264 people from 155
households who were diagnosed with CO poison- Prehospital Care
ing during power outages related to a snow storm.
Via telephone interviews, this group showed that in A study recently published by an aeromedical
many households, portable generators were oper- service determined that their most commonly
ated in an enclosed space or too close to the home, transported toxicologic emergency was CO poison-
and gas ranges were used for heat.11 Van Sickle et al ing.27 The overall goal of prehospital management
studied the effects of 4 major hurricanes in 2004 and of patients with CO exposure is rapid recognition
collected data from 10 Florida hospitals to identify of the exposure, removal from the environment,
subjects diagnosed with CO poisonings.17 Using assessment of the airway, and placement of 100%
telephone interviews, the authors found that 74% of
affected households did not own a generator prior to
the hurricanes, and 86% did not have a CO detector. Table 1: Differential Diagnosis Of Patients
Sixty-seven percent of those interviewed reported Presenting With Carbon Monoxide Poisoning
receiving some CO safety educational information
before the incident. • Viral syndrome, such as influenza
Other studies have attempted to classify risk • Headache (tension, migraine, etc)
factors and trends in CO poisoning. Mendoza and • Meningitis
Hampson collected data on 250 consecutive chil- • Stroke
dren treated with HBO for severe CO poisoning.20 • Seizure disorder
• Gastroenteritis
In this study, 94% of poisonings were unintentional
• Non-accidental injury
and occurred in November, December, and January.
• Other ingestion leading to altered mental status
Intentional poisonings occurred only in adolescents; • Sudden Unexpected Infant Death Syndrome (SUIDS)*
71% were male. Minorities were affected more often
than non-Latino whites (P < 0.001). *The evidence for SUIDS is scanty5
September 2011 • ebmedicine.net 3 Pediatric Emergency Medicine Practice © 2011

Figure 1. Pathophysiological Mechanisms Of Carbon Monoxide Poisoning
Reprinted with permission from: Weaver LK. Carbon monoxide poisoning. NEJM. 2009;360:1217-1225. Copyright
2009, Massachusetts Medical Society.

supplemental oxygen. Additionally, the child potential CO exposures.
should be placed on continuous cardiorespiratory Cho et al described the presenting symptoms
monitoring with pulse oximetry. When available, a in 30 children ages 2 to 17 years diagnosed with
co-oximetry reading may be obtained by the trans- CO poisoning over a 10-year span.35 In this case
porting provider. series, presenting symptoms included conscious-
In the case of CO exposure associated with ness disturbance (86.7%), seizure (23.3%), headache
smoke inhalation, transporters should systemati- and dizziness (10%), and vomiting (3.3%). Another
cally assess the patient’s “ABCs” to the best of their smaller series reported varying results with a higher
ability and evaluate for signs of trauma or burns. incidence of nausea (100%), headache (93%), vomit-
Carbon monoxide poisoning in the setting of a fire ing (75%), lethargy (63%), syncope (56%), and visual
may lead to significant airway edema and airway disturbances (21%). Only one subject in this series had
obstruction. The transporter should rapidly assess a seizure.28 This study claims that children are prone
the child for burns sustained to the face, singed eye- to lethargy and syncope at significantly lower COHb
brows, burned hair in the nares, and/or oral swell- levels than are reported in adults. From a sample of
ing, and placement of an endotracheal tube to secure 74 subjects, Yarar et al reported altered mental state,
the airway should be considered. The child should dizziness, headache, nausea, vomiting, and syncope
continue to receive 100% supplemental oxygen via as the most common chief complaints.36 Interestingly,
the endotracheal tube. If not intubated, the prefer- 6 of the 74 subjects (8.1%) had no complaints. Four of
able means of oxygen delivery is by non-rebreather the 6 subjects had an initial COHb level considered to
at 100% oxygen. be at a toxic level (COHb level of 20%-40%). Finally,
Clarke et al reported euphoria or elevated moods
Emergency Department Evaluation in 10 children after acute mass exposure to CO in a
school for children with special needs.37
Important Historical Questions Baker et al reported the incidence of CO poison-
The best way to diagnose CO poisoning is to ask the ing in children presenting with nonspecific flu-like
right questions, such as: symptoms to an urban children’s hospital ED.38 The
authors found that 24 of 46 subjects with flu-like
• Was the child in a fire? symptoms and at least 1 risk factor for CO poisoning
• Was the child in an environment with an indoor heat- had elevated COHb levels. Interestingly, just being a
ing device or generator? motor vehicle passenger was considered a risk factor
• Do other members of the child’s household or environ- in this series. This study further illustrates the impor-
ment suffer from non-specific headaches or nausea? tance of considering CO poisoning on the differential
• What underlying medical conditions does the child diagnosis of all children with nonspecific symptoms.
have that may predispose them to severe symptoms at Although some studies have suggested that the
low CO levels? presence of fever or diarrhea would rule out CO
• Is the child presenting with a complaint that could be exposure,38 other studies have challenged this idea.
related to CO poisoning (See Table 2.) There have been case reports of children present-
• Do the child’s symptoms abate when they move to a ing with febrile illnesses in the setting of acute CO
new environment (such as going outdoors)? poisoning,31,33,39 thus making it more difficult to
differentiate between poisoning and viral illness.
When a child presents to the ED from a fire, most Diarrhea, which has not been reported in adults with
practitioners would immediately consider the pos- acute CO poisoning, has been reported in infants
sibility of CO exposure. A practitioner should have
a low threshold to consider CO poisoning during
periods of cold weather and natural disasters as the Table 2. Reported Presenting Complaints In
use of indoor heating devices and generators is more Pediatric Carbon Monoxide Poisoning
common. However, it is the more elusive presenta-
tion that challenges the practitioner to consider CO • Headache
poisoning on the differential diagnosis. • Nausea/vomiting
Most of the data describing signs and symptoms • Syncope
of CO poisoning originate from studies of the adult • Dizziness
population. This is unfortunate as children often ex- • Changes in mental status/confusion/lethargy
hibit symptoms at lower COHb levels than adults.28 • Weakness
• Seizure
Many of the presenting symptoms in children are
• Euphoria
described as isolated case reports.29-34 Patients pre-
• Visual disturbance
senting with headaches, nausea, vomiting, syncope, • Fever
changes in mental status, weakness, confusion, or • Diarrhea
euphoria without cause should be questioned about • No complaints

after CO exposure.33,39 A summary of historical com- Complete resolution of the neurological symptoms
plaints in pediatric CO poisoning is listed in Table 2. have been described in case series and case reports
In addition to symptoms, the use of indoor heat- in children.28,43,45 In Cho’s series of 30 children with
ing devices and generators are important questions acute CO poisoning, 16.7% progressed to DNS
to ask. Inquiring if other members of the household consisting of ataxia, dysmetria, personality changes,
or environment where the child resides have non- dystonia, rigidity, focal weakness, and enuresis with-
specific symptoms such as headache and nausea in 3 to 14 days.35 All symptoms completely resolved
may also be helpful. For more chronic exposures, within 2 months. The authors of this article allude to
asking if the symptoms only occur in one environ- presentation with seizures, hypotension, and more
ment and then abate when going to a new environ- severe metabolic acidosis as risk factors for develop-
ment such as walking outdoors may provide a clue. ment of DNS. Case reports have recognized CO poi-
Finally, it is important to inquire about any underly- soning as a cause of reversible sensorineural hearing
ing medical conditions that may predispose a patient loss,46 transient motor tics and vocalizations,45 cen-
to more severe symptoms at lower CO levels. For tral diabetes insipidus,47 and acute hydrocephalus
example, patients with sickle cell disease, leukemia, resulting in the death of a 2-year-old boy.32
or other types of anemia may require more aggres- There is even less reported in the literature of
sive treatment. the neuropsychological effects of CO poisoning in
children. Several studies in children have reported
Important Physical Findings cognitive impairment and a decline in school func-
The physical examination findings of CO poison- tion post-exposure.48-49 Difficulty with school perfor-
ing in children is poorly described in literature. It is mance can be detrimental during childhood and is
traditionally taught that patients with CO poisoning a major problem after CO exposure; however, it is
present with a “cherry red” appearance; however, this often very difficult to study memory and concentra-
is an insensitive and typically a post-mortem finding. tion deficits in a child due to developmental chal-
Evaluation for co-morbidities such as airway com- lenges and limited validated tools. Finally, many of
promise, singed facial hair, and dermal burns is an the studies discussing DNS in kids are flawed due to
important part of the physical examination. Finally, inappropriate or inadequate long-term follow-up to
cutaneous blisters unrelated to thermal burns have track evolution of DNS symptoms.
been reported in adults.44 This was thought to be the
result of compression alone versus compression and Diagnostic Studies
CO oxidative damage. As CO can have a detrimen-
tal effect to the neurological and cardiac systems, Pulse Oximetry
patients should be examined for any abnormalities on Pulse oximetry should not be used in the diagnosis
neurological and cardiac examinations. of CO poisoning. Hemoglobin molecules become
Due to its high oxygen demand, the heart is saturated at very low partial pressures of oxygen,
vulnerable to the hypoxia that results from CO poi- and oxygenated hemoglobin and COHb have the
soning; however, the presenting cardiac signs of CO same absorption coefficient. As a result, pulse oxim-
exposure in pediatrics have been described only in etry has been proven to give falsely elevated oxygen
case reports.31,39,40-42 In these accounts, the children saturation levels in the setting of CO poisoning.50
presented with sinus tachycardia, presence of a gal-
lop (S4), and signs of cardiogenic shock. Co-oximetry And Carboxyhemoglobin Levels
Patients may present with various neurological Carboxyhemoglobin levels may be determined by
symptoms such as fatigue, altered mental status, either a noninvasive CO-specific pulse oximeter or
syncope, muscle weakness,31 posturing,30,43 as well a blood test known as a co-oximeter. A co-oximeter
as a positive Babinski sign. The key components of is a blood gas analyzer that measures oxygenated
the neurological examination focus on evaluation of hemoglobin, COHb, deoxygenated hemoglobin, and
strength, coordination, and gait. methemoglobin levels.51 There is no difference in
the value between an arterial and venous sample,52
Delayed Neurological Sequelae which is an important advantage in pediatrics where
Some patients will exhibit delayed neurological arterial blood samples are often difficult to obtain.
sequelae (DNS). Delayed neurological sequelae may However, it still requires a venous blood sample.
be solely neurological or neuropsychological symp- This test provides an accurate value of oxygenated
toms. Unfortunately, adequate measures to predict hemoglobin and level of COHb at the specific time
who is most susceptible to DNS are lacking. Delayed in which the serum is collected. Unfortunately, it
neurological sequelae have been described in the does not factor in information about the length of
literature to occur several days to weeks after CO time the child was exposed to CO or the CO clear-
poisoning in patients who had previous resolution ance after removal of the patient from the exposure.
of symptoms or who were initially asymptomatic. Some practitioners and transporters may have

Clinical Pathway For Management Of Carbon Monoxide
Poisoning In Children
Was the patient involved in a known

NO YES
carbon monoxide exposure?
Are the history and/or symptoms suggestive of a Was the patient involved in a fire or are they at risk
potential CO exposure? for inhalational injury?
NO YES NO YES
• Start 100% oxygen. (Class II) Is there evidence

CO exposure
• Perform work-up. (Class II) NO of or risk for
unlikely.
• Consult toxicology. (Class II) airway edema?
YES
Is the patient pregnant?

NO YES Intubate.
(Class I)
What is the severity of the presenting symptoms?
Abbreviations:
Asymptomatic/
Moderate/Severe CO, carbon monoxide;
Mild
HBO, hyperbaric oxygen;
PICU, pediatric intensive care unit.
On oxygen for at
Do symptoms
least 4 hours
continue despite
and now symp-
oxygen therapy?
toms resolved?
YES NO NO YES
Discharge home Admit to general Admit to general Consider HBO therapy after toxi-
with follow-up. ward. ward or PICU. cology consult. (Class III)
Class Of Evidence Definitions

Each action in the clinical pathways section of Pediatric Emergency Medicine Practice receives a score based on the following definitions.
Class I Class II Class III Indeterminate tatives from the resuscitation
• Always acceptable, safe • Safe, acceptable • May be acceptable • Continuing area of research councils of ILCOR: How to De-
• Definitely useful • Probably useful • Possibly useful • No recommendations until velop Evidence-Based Guidelines
• Proven in both efficacy and • Considered optional or alterna- further research for Emergency Cardiac Care:
effectiveness Level of Evidence: tive treatments Quality of Evidence and Classes
• Generally higher levels of Level of Evidence: of Recommendations; also:
Level of Evidence: evidence Level of Evidence: • Evidence not available Anonymous. Guidelines for car-
• 1 or more large prospective • Non-randomized or retrospec- • Generally lower or intermediate • Higher studies in progress diopulmonary resuscitation and
studies are present (with rare tive studies: historic, cohort, or levels of evidence • Results inconsistent, contradic- emergency cardiac care. Emer-
exceptions) case control studies • Case series, animal studies, tory gency Cardiac Care Committee
• High-quality meta-analyses • Less robust RCTs consensus panels • Results not compelling and Subcommittees, American
• Study results consistently posi- • Results consistently positive • Occasionally positive results Heart Association. Part IX. Ensur-
tive and compelling Significantly modified from: The
Emergency Cardiovascular Care ing effectiveness of community-
Committees of the American wide emergency cardiac care.
Heart Association and represen- JAMA. 1992;268(16):2289-2295.
This clinical pathway is intended to supplement, rather than substitute for, professional judgment and may be changed depending upon a patient’s individual
needs. Failure to comply with this pathway does not represent a breach of the standard of care.
Copyright © 2010 EB Medicine. 1-800-249-5770. No part of this publication may be reproduced in any format without written consent of EB Medicine.

access to pulse CO-oximetry. This noninvasive Lactate Level
device has been proven to be a reliable diagnostic The presence of a lactic acidosis of greater than 10
technique in adults that could facilitate faster diag- mmol per liter is an indicator of cyanide intoxica-
nosis of a CO poisoining;53-55 however, more pedi- tion, but it is not a good indicator of CO poisoning.66
atric studies still need to be done to corroborate its However, it bears mention in this article because
efficacy. cyanide intoxication and CO poisoning are closely
Carboxyhemoglobin levels have been tra- associated in the setting of house fires.
ditionally used by physicians to diagnose CO
poisoning and may have some clinical utility; Muscle Enzymes And Cardiac Biomarkers
however, they are an insensitive diagnostic test. Since CO poisoning causes myocardial ischemia, el-
Unfortunately, reports in adults and children evations in creatine kinase (CK), creatine kinase with
have shown a lack of a direct correlation between muscle-brain subunits (CK-MB), and troponins may
presenting signs and symptoms, COHb levels, and assist the clinician in determining the severity of CO
prognosis.26,29,56-58 Despite this, it is traditionally poisoning and the effect on the heart.
thought that symptoms begin to occur at CoHb
levels of > 15%. Toxic levels occur at > 20%, with Electrocardiogram
symptoms ranging from nausea and headache to Since CO has a direct toxic effect on the myocardium,
confusion and disorientation; furthermore, neu- an electrocardiogram (ECG) should be considered
rological deficits are noted at > 40%. Irreversible in suspected cases of CO poisoning. The most com-
damage, seizures, cardiopulmonary arrest, and mon ECG finding is sinus tachycardia in the setting
death occur at > 50%.59-61 Children may become of hypoxemia.40 Furthermore, a prolonged corrected
symptomatic at lower COHb concentrations than QT (QTc) interval has been reported in a case series
previously reported in the adult population.33,62 of adults and children67 as well as 2 case reports of
Crocker and Walker reported more severe neuro- children40,68 in the setting of acute CO toxicity. As a
logic and physiologic changes in children starting prolonged QT interval may be congenital or associat-
at 15%.28 In another large observational study of ed with other ingestions and exposures, these studies
150 children, Chou et al reported that COHb levels may be reporting an incidental finding. Finally, one
as low as 1.1% were associated with symptoms.63 case report of 3-year-old twin girls reported delayed
These values may be low due to a delay in presen- supraventricular tachycardia after CO exposure.30
tation that allowed for some clearing of COHb or Although these ECG findings are not specific for CO
oxygen therapy in route that may falsely reduce toxicity, these studies demonstrate the importance of
the measured COHb level at presentation. This obtaining an ECG for all acutely poisoned patients.
study teaches us to use caution when obtaining
COHb levels and to not assume that a low COHb Head Computed Tomography/Brain Magnetic
level is reassuring. Finally, in a case series of 3 Resonance Imaging
adolescent girls who had the same exposure and
Head imaging is not necessarily indicated for a child
individual laboratory data that showed similar
with CO poisoning unless there are associated neu-
COHb concentrations, the patients exhibited a
rological symptoms.
variety of neurological manifestations.64
Many small studies have been published to
The conclusion from these studies is that COHb
attempt to characterize changes on head imaging
levels are not a reliable method to predict expected
in patients with CO poisoning. In adults and chil-
symptoms or outcomes, and there should not be too
dren, neuroimaging by magnetic resonance imaging
much focus on the absolute number in the ED. The
(MRI) routinely demonstrates gray matter involve-
COHb level gives the clinician information about the
ment, in particular in the basal ganglia,69-71 while
level at the time; however, it does not give the clini-
other studies have disputed this and reported more
cian any information about length of exposure, time
white matter hyperintensities.72-74 Furthermore, MRI
since exposure, or interventions performed since
findings do not necessarily correlate with present-
exposure.
ing symptoms75 or long-term neurological deficits.76
In conclusion, MRI is unlikely to be a very helpful
Breath Analysis
diagnostic tool in the acute setting.
Shenoi et al described the use of a CO breath ana- There have been case reports in children of com-
lyzer in a random sample of 470 children ages 5 to 20 puted tomography (CT) scans that acutely showed
years to estimate CO exposure.65 The breath ana- decreased white matter attenuation in the frontal
lyzer correlated well with co-oximetry. However, it lobes77 and basal ganglia47 as well as cerebellar
is not as universally useful as it can only be used in hypodensities78 in the setting of CO poisoning. The
children old enough to cooperate with instructions above findings on CT scans of children with altered
to blow into the device. mental status may prompt the clinician to consider
CO poisoning on the differential diagnosis.

Treatment 100% oxygen in a chamber that is pressurized to 2
to 3 atmospheres and is so specialized that it is only
Any patient with suspected CO poisoning should available at a limited number of centers. Hyperbaric
be kept on a cardiorespiratory monitor with pulse oxygen works by increasing the partial pressure of
oximetry. Vital signs should be obtained every hour oxygen and shifting the oxygen dissociation curve
while being observed in the ED. back to the right. Risks of HBO treatment include
The antidote for CO poisoning is oxygen. Pa- the risk of transport to the HBO therapy center,
tients with suspected and/or confirmed CO poi- barotrauma, pneumothorax, claustrophobia, oxygen
soning should immediately be placed on oxygen at toxicity, and limited access to the patient. In a series
100%. This may be delivered via a well-fitted face of 22 children treated with HBO therapy for a vari-
mask or endotracheal tube. There should not be a ety of reasons (including CO poisoning), Keenan et
delay in oxygen delivery while awaiting co-oximetry al reported hypotension, bronchospasm, hemotym-
or laboratory results. In adults, the half-life of CO panum, and progressive hypoxemia as the complica-
is 320 minutes on room air, 80 minutes on 100% tions of HBO therapy.79
normobaric oxygen, and 23 minutes on 100% hy- The efficacy of HBO therapy for CO poisoning
perbaric oxygen. In a series of 177 subjects, Klasner has been a hot topic of research. Part of the debate
et al reported that children actually have a shorter stems from the fact that most of the studies in the
CO half-life than adults.62 However, the major flaw literature do not describe well the details of the envi-
of this study is that it only evaluated 2 separate CO ronment where the exposure occurred or the length
levels in time rather than a series of points. Physi- of CO exposure and do not have adequate and
ologically, if children do in fact have a shorter CO validated follow-up for DNS. Weaver et al published
half-life, it is thought to be due to a higher minute a recent randomized controlled trial with a favorable
ventilation. It is traditionally taught that patients outcome from HBO therapy.80 In this trial, 152 symp-
with any significant exposure should receive inhaled tomatic adult patients received either 3 HBO therapy
oxygen at 100% for 12 hours. sessions or normobaric oxygen treatment sessions.
Subjects received neuropsychological testing after
Prognosis the first and third chamber sessions, then at 2 weeks,
6 weeks, 6 months, and 12 months. This study
Prognosis is difficult to assess for CO exposure. As reported that 3 HBO treatment sessions reduced the
stated previously, the COHb level at presentation risk of neurological and cognitive sequelae (P < 0.05)
does not predict long-term neurological outcome. in adults for symptomatic CO poisoning.
However, smoke inhalation is a known comorbidity However, most of the current adult literature
that has a higher association with death. Chou et al does not report a favorable outcome after HBO
reported predictors of mortality for children with therapy. A Cochrane review of HBO therapy was
CO poisoning with and without smoke inhalation. published in 2000 in order to assess its usefulness in
They found that patients with mortality from smoke preventing neurologic sequelae as compared to nor-
inhalation had a higher initial COHb level, lower mobaric oxygen.81 This review identified 6 random-
initial body temperature, and greater incidence in ized controlled trials that only included nonpreg-
respiratory and cardiac arrest in the field compared nant adults, of which 3 were utilized in the primary
to those who survived.63 For patients with evidence analysis. This review of HBO therapy showed that
of acute myocardial ischemia, case reports have “no conclusive evidence of benefit exists for patients
documented complete recovery of cardiac function with severe CO poisoning.” Additional randomized
at follow-up.31,40 controlled trials are needed to further evaluate its
use. This conclusion was echoed in 2005 by Buckley
et al in a systematic review that included 4 of the
Controversies And Cutting Edge same articles as the Cochrane review as well as 2
more recent articles.82 One of those articles was the
The primary controversies regarding CO poisoning randomized controlled trial published by Weaver
center around the use of HBO therapy, neuropsychiat- (mentioned previously). These authors used a Bayes-
ric testing for DNS, and the usefulness of COHb lev- ian analysis of the 6 review articles and concluded
els for determining symptoms and prognosis (which that there is still uncertainty about the utility of HBO
is discussed in the Diagnostic Studies section on therapy and recommended establishing strict guide-
page 6).26 The controversial use of carbon monoxide lines for initiation of HBO therapy.
as treatment is also discussed in this section. Since publication of the Cochrane review and
the review by Buckley, there have been new adult
Hyperbaric Oxygen Therapy studies published. In 2010, Annane et al performed
A possible, yet controversial, treatment modality is 2 randomized controlled trials in parallel in adults.83
the use of HBO or high pressure oxygen. Hyperbaric The first arm consisted of 2 groups where subjects
oxygen therapy involves having the patient breathe received either 6 hours of normobaric oxygen or 4

Risk Management Pitfalls For Carbon Monoxide Poisoning
1. “I did not consider carbon monoxide on the 6. “I saw the burns on the patient’s face, but he
differential diagnosis.” was breathing fine, so I didn’t think he needed
Patients with carbon monoxide poisoning intubation.”
typically present with a constellation of non- Delay in securing the airway in a patient
specific complaints such as headache, nausea, involved in a fire with evidence of facial burns
vomiting, and lethargy. As it is more common and inhalation injury can be detrimental.
in winter months when viral syndromes are Airway edema may not occur for hours after
frequent reasons for visits to the emergency inhalation injury, and once recognized, it may
department, it is a diagnosis that may be be very difficult to secure the airway at that
easily overlooked. A good clinician should time. All children presenting with evidence of
inquire about potential carbon monoxide burns to the face and airway should have an
exposures for any patient presenting with endotracheal tube placed and be given 100%
non-specific complaints. oxygen via the tube.
2. “The patient has a normal oxygen saturation, 7. “I know the diagnosis is carbon monox-
so there is no evidence of hypoxia.” ide poisoning, so my evaluation is com-
Hemoglobin molecules become saturated at plete.”
very low partial pressures of oxygen, so the Children with carbon monoxide exposure
clinician cannot rely on a pulse oximetry to and toxicity also present with co-morbidities
show evidence of hypoxia. Carbon monoxide such as inhalation injury, dermal burns, and
exposure cannot be diagnosed using oxygen cyanide poisoning. The clinician should
saturation readings. consider these co-morbidities in addition to
treating with oxygen.
3. “The child was only exposed to a low level of
carbon monoxide, so this is not a significant 8. “The COHb level was very low, so it is okay to
exposure.” discharge the child home.”
Carbon monoxide has a higher affinity for Relying on the COHb level as an absolute
hemoglobin than oxygen, so it only takes indication of symptoms, clinical course, and
a small amount to cause toxicity. Smaller prognosis is dangerous. Studies have shown
volumes of exposure for a longer time may be that children can be symptomatic at low COHb
just as toxic as a high volume exposure for a levels.
short period of time.
9. “The child is at baseline mental status after
4. “Carbon monoxide poisoning only occurs in oxygen therapy. I can send him home because
enclosed spaces.” there is nothing else to do.”
There have been reports of children with carbon Do not forget to counsel parents about
monoxide toxicity in open air environments delayed neurological sequelae. This includes
while riding in the back of cars and trucks and neurological as well as neuropsychological
while playing outside near generators. problems that occur several days to weeks after
exposure. Ideally, the primary care physician
5. “I will just wait for the laboratory work-up to should be involved in follow-up, and the child
come back before treating the patient.” may be referred to a neurologist.
Oxygen is the antidote for carbon monoxide
poisoning. Delay in treatment with 100% oxygen 10. “It is up to the family to handle the environ-
while awaiting results of diagnostic tests may ment where the exposure occurred.”
increase morbidity and mortality. Anyone Social work may be involved during the
suspected of carbon monoxide exposure should emergency department visit to assist the family
be placed on 100% oxygen via facemask while in ensuring a safe, carbon monoxide-free
work-up is pending. environment and providing carbon monoxide
monitors for the home. Furthermore, local
fire departments and gas companies may be
involved to provide any additional assistance
and deem the home safe.

hours of normobaric therapy plus 1 HBO therapy Crocker and Walker reported no morbidity
session. The second arm also consisted of 2 groups and mortality among 16 children who received
where subjects received either 4 hours of normobaric HBO.28 Once again, the circumstances of the
oxygen plus 1 HBO therapy session (same as one of exposure (length of time, etc) were not described.
the groups in the first arm) or 4 hours of normobaric All of these subjects presented with nausea and/
therapy plus 2 HBO therapy sessions spaced by 6 or vomiting, 12 had headaches, and 11 were
to 12 hours. Both of these trials were terminated lethargic. These subjects were followed by paren-
early after an interim analysis of 385 patients when tal interview and review of the medical records.
it was determined that those who received 2 HBO Although 2 had some form of DNS (1 with chronic
therapy sessions had a lower recovery rate (P = headaches and 1 with memory difficulties),
0.007), and there was no significant difference in both had complete resolution of symptoms at 9
outcome between the 2 groups in the first arm of the months. One other child exhibited poor school
trial. Thus, HBO therapy was not shown to improve performance that had been described prior to her
recovery after CO exposure and may have worsened exposure. Regarding the use of HBO therapy for
outcomes in this more recent large, randomized treatment of cardiac arrest after CO poisoning, one
controlled trial in adults. small consecutive case series reported universal
There are no largely powered and randomized mortality among 18 adults and children.84
publications in the literature that report neurologi- A final special consideration is the pregnant
cal outcomes for children treated with HBO therapy. teenage girl who presents after CO exposure. The
Only a few small studies have evaluated HBO presence of fetal hemoglobin means that the dis-
therapy in children with CO poisoning limited by sociation curve is already shifted slightly to the left.
insufficient follow-up. Two of these studies are men- Carbon monoxide exposure further shifts this curve,
tioned below. thus making the fetus more susceptible to the effects
In an observational study, Rudge reported that of CO. Data has suggested that pregnant women
13 of 14 children under the age of 2 had complete and their fetuses do the best with HBO therapy after
recovery after receiving HBO therapy.58 However, CO poisoning.85-86
“complete recovery” is inadequately defined, as the In summary, there is insufficient information in
authors assumed that lack of return for repeat HBO the literature regarding use of HBO therapy for the
therapy implied recovery. There was no follow-up if treatment of children with CO exposure. The best
the children had deficits in memory, concentration, analyses in nonpregnant adults are inconclusive or
or school performance. Finally, the length of expo- do not support HBO therapy. It is recommended that
sure was not described. the clinician work in consultation with a toxicologist
Cost-Effective Strategies
1. When CO poisoning is suspected, the patient 3. Consult toxicology colleagues and/or your local
should be placed immediately on oxygen while poison control early.
the work-up is pending. Consultation may reduce the pursuit of
100% oxygen is the antidote to CO poisoning. unnecessary tests and expensive therapies such
Its administration is safe and easy. When it as hyperbaric oxygen. These colleagues can best
is initiated early in the evaluation, it reduces guide the clinician in which patients should be
the patient’s length of stay and morbidity and admitted and which can be safely discharged
mortality. home.
2. Do not follow the COHb levels too closely. 4. If a patient is deemed safe to discharge home,
A positive COHb level only confirms an ensure that the environment where the expo-
exposure, and a negative result does not rule- sure occurred has been cleared and the fam-
out an exposure. A good history is the best way ily has a good safety plan to prevent further
to make the diagnosis of a CO exposure and exposures. This may be done in conjunction
poisoning. Once an exposure is suspected, the with a social worker, fire department, or local
child should be placed on 100% oxygen for at gas company.
least 4 hours regardless of the absolute level This may reduce repeat ED visits by the patient
result. (Caveat: some institutions’ recommend and fresh exposures, thus freeing up resources
100% oxygen for a minimum of 8 or 12 hours; for other patients.
clinicians should follow their institution’s
protocols for use of 100% oxygen.)

or the local poison control for regional recommenda- Inhalation Injuries
tions and institutional preferences regarding the use Children with inhalation injury plus CO poisoning
of HBO therapy. are at much higher risk of death than just CO poi-
soning or thermal burn alone.59,63 Inhalation injury
Delayed Neurological Sequelae is a complex problem that is comprised of direct
As discussed previously in the Important Physical damage to the lungs from both heat and chemical
Findings section (page 6), there are no adequate irritation from smoke plus cellular impairment due
measures to predict which patients are most to mitochondrial poisoning from CO and cyanide.
susceptible to DNS. It is difficult to obtain good Upon arrival to the ED, it is imperative that the air-
baseline neuropsychological testing at the time of way is thoroughly assessed by evaluating for facial
presentation to compare to follow-up examinations. burns, singed facial/nasal hair, soot in the airway,
Furthermore, there is no clear-cut evidence that stridor, hoarse voice, wheezing, or shortness of
treatment with HBO improves outcomes or reduces breath. If there is any indication of airway compro-
the development of DNS. Additionally, it is more mise and the child has not already been intubated
difficult to perform complete neuropsychological by emergency medical services, an endotracheal
testing on children as compared to adults. More- tube is indicated as airway edema may progress
over, as stated previously, COHb levels are not quickly and result in a difficult airway to secure in
good measures at presentation to determine who the matter of a few hours. Oxygen at 100% may be
will develop DNS. administered via the endotracheal tube once place-
ment is confirmed. Patients with thermal burns
Carbon Monoxide Exposure As Treatment should also receive appropriate fluid resuscitation.
Interestingly, Bauer and Pannen have recently Finally, there is an associated risk of cyanide poi-
published a review suggesting that not all exposures soning with thermal burns and inhalation injury.
to CO are necessarily bad.88 They state that CO is Traditionally, the antidote for cyanide poisoning is
produced in animal models as an anti-inflammatory, sodium thiosulfate; however, in children hydroxo-
anti-oxidant, and anti-apoptotic, thus it is recently cobalamin (CYANOKIT®) may be more advanta-
thought to be a mediator of host protection. As a geous because of its rapid onset of action and fewer
result, there has been some evidence that small, side effects as compared to sodium thiosulfate.59
controlled exposures of CO may exert a beneficial
effect for certain conditions such as shock, sepsis, Comorbidities
ischemia/reperfusion, organ transplantation, and It is conceivable that patients with comorbidities
inflammation. Unfortunately, there are few human where hypoxia may be detrimental, such as sickle
studies available, and the authors of this review cell anemia or thalassemia, may be at increased risk
stress that additional randomized controlled trials from the effects of CO exposure. There is no data in
are necessary to further evaluate the potential utility the literature to support this statement; however, it
of CO for treatment purposes. may be an initial consideration while obtaining the
past medical history.
Special Circumstances
Disposition
Hyperbaric Oxygen Therapy
If HBO therapy is utilized, there are special pediat- Admission is indicated if the patient has moder-
ric needs that should be accommodated.87 The HBO ate to severe symptoms at presentation, persistent
therapy chamber should have infant- and child-specific neurological or cardiac symptoms, significant
equipment and be capable of keeping the child at an thermal burns, evidence of cyanide poisoning, or
appropriate temperature. Personnel comfortable with a comorbidity that warrants closer monitoring (ie
the administration of pediatric appropriate treatments sickle cell anemia). However, if the patient has
and sedation medications should be present and avail- been maintained on oxygen for at least 4 hours,
able. It may be necessary for a pediatric advanced life has returned to baseline mental status, and has
support-trained medical professional to remain physi- no evidence of persistent neurological or cardiac
cally present in the chamber with the child for safety symptoms, it may be safe to discharge the patient
and protection. Children tend to become very agitated home. All dispositions should be formulated
in a monochamber. Alert and older children should be in conjunction with the local poison control or
instructed on techniques to maintain Eustachian tube a consulting toxicologist. Guardians should be
function. If this is not possible, as in with an infant or counseled on the possibility of DNS and difficul-
intubated child, myringotomies should be considered ties with schoolwork after CO exposure. Close
prior to HBO therapy. Finally, if the child is awake, follow-up with a primary care provider or neu-
child-friendly distraction techniques and parental pres- rologist is recommended. The school administra-
ence may be employed to reduce anxiety. tion and teachers should be notified to watch for

any changes in school performance. Finally, safety that the child’s neurological examination improved after
measures should be discussed with the child’s several hours on oxygen. She had no further seizures and
guardian, and CO poisoning prevention infor- is currently at her baseline mental status. Social work
mation should be provided, and for suspected comes by while you are visiting to assist the family with
home exposures, the local fire department or gas obtaining safe heating methods for the home and arranges
company may be notified to safely clear the home for a home CO monitor. Once discharged, the child and
prior to return of the patient(s) to prevent further mother will stay at the grandmother’s home until the heat
exposure to the patient or others. is properly resumed in their home.
Summary References
Carbon monoxide is present in our daily environ- Evidence-based medicine requires a critical ap-
ments and is the most common toxicologic cause praisal of the literature based upon study methodol-
of preventable morbidity and mortality. Clinicians ogy and number of subjects. Not all references are
must stay vigilant, especially in the winter months, equally robust. The findings of a large, prospective,
as to avoid missing the nebulous presentation of randomized, and blinded trial should carry more
CO poisoning. Clinicians cannot rely on presenting weight than a case report.
symptoms and COHb levels to predict prognosis but To help the reader judge the strength of each
should immediately begin treatment by administra- reference, pertinent information about the study,
tion of 100% oxygen. Further treatment with HBO such as the type of study and the number of patients
therapy should be determined in conjunction with a in the study, will be included in bold type following
toxicologist. Prior to discharge, close follow-up and the reference, where available.
safety precautions should be arranged.
1. Bronstein AC, Spyker DA, Cantilena LR, et al 2008 An-
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syndrome in a child following carbon monoxide poisoning.
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71. Tuchman RF, Moser FG, Moshe SL. Carbon monoxide free by completing the following test. Monthly on-
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imaging findings in chronic carbon monoxide intoxication.
Acta Radiol. 2005; 46:322-327. (Prospective; 16 subjects)
74. Muller NG, Gruber O. High-resolution magnetic resonance 1. How does CO poisoning occur?
imaging reveals symmetric bitemporal cortical necrosis after a. It is released into the air from incomplete
carbon monoxide intoxication. J Neuroimaging. 2001;11:322- combustion of hydrocarbons and
325. (Case report; 1 subject) accidentally inhaled by bystanders in the
75. Prockop LD. Carbon monoxide brain toxicity: clinical, mag-
netic resonance imaging, magnetic resonance spectroscopy,
environment.
and neuropsychological effects in 9 people. J Neuroimaging. b. It is released into the air from incomplete
2005; 15:144-149. (Case series; 9 subjects) combustion of hydrocarbons and
76. Kesler SR, Hopkins RO, Blatter DD, et al. Verbal memory deliberately inhaled in a suicide attempt.
deficits associated with fornix atrophy in carbon monoxide c. It occurs when small children ingest soil and
poisoning. J Int Neruopsychol Soc. 2001;7:640-646. (Prospec-
tive; 69 subjects)
dust particles around the house.
77. Finelli PF, DiMario FJ Jr. Hemorrhagic infarction in white d. A and B
matter following acute carbon monoxide poisoning. Neurol- e. All of the above
ogy. 2004;63:1102-1104. (Case series; 3 subjects)
78. Fan HC, Wang AC, Lo CP, et al. Damage of cerebellar white

2. What are the primary goals of emergency Physician CME Information
medical services with evaluating a child with a Date of Original Release: September 1, 2011. Date of most recent review: August
known CO exposure? 10, 2011. Termination date: September 1, 2014.
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An Evidence-Based Approach September 2011

Poisoning Clinical Fellow, Division of Pediatric Emergency Medicine,

Abstract Peer Reviewer

Tommy Y. Kim, MD, FAAP

Pediatric Emergency Medicine Practice © 2011 2 ebmedicine.net • September 2011

September 2011 • ebmedicine.net 3 Pediatric Emergency Medicine Practice © 2011

Pediatric Emergency Medicine Practice © 2011 4 ebmedicine.net • September 2011

September 2011 • ebmedicine.net 5 Pediatric Emergency Medicine Practice © 2011

Pediatric Emergency Medicine Practice © 2011 6 ebmedicine.net • September 2011

Was the patient involved in a known

• Start 100% oxygen. (Class II) Is there evidence

Is the patient pregnant?

What is the severity of the presenting symptoms?

Class Of Evidence Definitions

September 2011 • ebmedicine.net 7 Pediatric Emergency Medicine Practice © 2011

Pediatric Emergency Medicine Practice © 2011 8 ebmedicine.net • September 2011

September 2011 • ebmedicine.net 9 Pediatric Emergency Medicine Practice © 2011

Pediatric Emergency Medicine Practice © 2011 10 ebmedicine.net • September 2011

September 2011 • ebmedicine.net 11 Pediatric Emergency Medicine Practice © 2011

Pediatric Emergency Medicine Practice © 2011 12 ebmedicine.net • September 2011

September 2011 • ebmedicine.net 13 Pediatric Emergency Medicine Practice © 2011

Pediatric Emergency Medicine Practice © 2011 14 ebmedicine.net • September 2011

September 2011 • ebmedicine.net 15 Pediatric Emergency Medicine Practice © 2011

Direct all questions to: Subscription Information:

Pediatric Emergency Medicine Practice © 2011 16 ebmedicine.net • September 2011

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