Emergency Department March 2018

Volume 20, Number 3

Management of Smoke Authors

Karalynn Otterness, MD

Inhalation Injury in Adults

Clinical Assistant Professor of Emergency Medicine, Stony Brook School
of Medicine, Stony Brook, NY
Christine Ahn, MD
Clinical Assistant Professor, Residency Assistant Program Director,
Abstract Department of Emergency Medicine, Stony Brook School of Medicine,
Stony Brook, NY

Peer Reviewers
Smoke inhalation injury portends increased morbidity and
mortality in fire-exposed patients. Upper airway thermal burns, Alex Manini, MD, MS, FACMT, FAACT
Professor of Emergency Medicine, Icahn School of Medicine at Mount
inflammation from lower airway irritants, and systemic effects Sinai, Elmhurst Hospital Center, New York, NY
of carbon monoxide and cyanide can contribute to injury. A Lewis S. Nelson, MD
standardized diagnostic protocol for inhalation injury is lacking, Professor and Chair, Department of Emergency Medicine, Rutgers New
Jersey Medical School, Newark, NJ
and management remains mostly supportive. Clinicians should
maintain a high index of suspicion for concomitant traumatic CME Objectives
injuries. Diagnosis is mostly clinical, aided by bronchoscopy Upon completion of this article, you should be able to:
and other supplementary tests. Treatment includes airway and 1. Diagnose and classify smoke inhalation injuries.
2. Recognize and treat carbon monoxide and cyanide toxicity.
respiratory support, lung protective ventilation, 100% oxygen or
3. Identify indications for intubation following smoke inhalation.
hyperbaric oxygen therapy for carbon monoxide poisoning, and
4. Initiate and monitor ventilation strategies and adjunctive therapies.
hydroxocobalamin for cyanide toxicity. Due to its progressive
Prior to beginning this activity, see “Physician CME Information”
nature, many patients with smoke inhalation injury warrant on the back page.
close monitoring for development of airway compromise. This issue is eligible for 4 trauma CME credits.

Editor-In-Chief
Andy Jagoda, MD, FACEP
Professor and Chair Emeritus,
Department of Emergency Medicine;
Director, Center for Emergency
Medicine Education and Research,
Icahn School of Medicine at Mount
Sinai, New York, NY
Associate Editor-In-Chief
Kaushal Shah, MD, FACEP
Associate Professor, Department of
Emergency Medicine, Icahn School
of Medicine at Mount Sinai, New
York, NY
Editorial Board
Saadia Akhtar, MD
Associate Professor, Department of Steven A. Godwin, MD, FACEP
Emergency Medicine, Associate Dean Professor and Chair, Department
for Graduate Medical Education,
Program Director, Emergency
Medicine Residency, Mount Sinai
Beth Israel, New York, NY
William J. Brady, MD
Professor of Emergency Medicine
and Medicine; Chair, Medical
Emergency Response Committee;
Medical Director, Emergency
Management, University of Virginia
Medical Center, Charlottesville, VA
Calvin A. Brown III, MD
Director of Physician Compliance,
Credentialing and Urgent Care
Services, Department of Emergency
Medicine, Brigham and Women's
Hospital, Boston, MA
Peter DeBlieux, MD Medicine, The University of
Professor of Clinical Medicine,
Interim Public Hospital Director
of Emergency Medicine Services,
Louisiana State University Health
Science Center, New Orleans, LA
Daniel J. Egan, MD
Associate Professor, Department
of Emergency Medicine, Program
Director, Emergency Medicine
Residency, Mount Sinai St. Luke's
Roosevelt, New York, NY
Nicholas Genes, MD, PhD
Associate Professor, Department of
Emergency Medicine, Icahn School
of Medicine at Mount Sinai, New
York, NY
Michael A. Gibbs, MD, FACEP
Professor and Chair, Department
of Emergency Medicine, Carolinas
Medical Center, University of North
Carolina School of Medicine, Chapel
Hill, NC
of Emergency Medicine, Assistant
Dean, Simulation Education,
University of Florida COM-
Jacksonville, Jacksonville, FL
Joseph Habboushe, MD MBA
Assistant Professor of Emergency
Medicine, NYU/Langone and
Bellevue Medical Centers, New York,
NY; CEO, MD Aware LLC
Gregory L. Henry, MD, FACEP
Clinical Professor, Department of
Emergency Medicine, University
of Michigan Medical School; CEO,
Medical Practice Risk Assessment,
Inc., Ann Arbor, MI
John M. Howell, MD, FACEP
Clinical Professor of Emergency
Medicine, George Washington
University, Washington, DC; Director
of Academic Affairs, Best Practices,
Inc, Inova Fairfax Hospital, Falls
Church, VA
Shkelzen Hoxhaj, MD, MPH, MBA
Chief Medical Officer, Jackson
Memorial Hospital, Miami, FL
Eric Legome, MD
Chair, Emergency Medicine, Mount
Sinai West & Mount Sinai St. Luke's; Robert Schiller, MD
Vice Chair, Academic Affairs for
Emergency Medicine, Mount Sinai
Health System, Icahn School of
Medicine at Mount Sinai, New York, NY
Keith A. Marill, MD
Assistant Professor, Department
of Emergency Medicine, Harvard
Medical School, Massachusetts
General Hospital, Boston, MA
Charles V. Pollack Jr., MA, MD,
FACEP
Professor and Senior Advisor for
Interdisciplinary Research and
Clinical Trials, Department of
Emergency Medicine, Sidney Kimmel
Medical College of Thomas Jefferson
University, Philadelphia, PA
Michael S. Radeos, MD, MPH
Associate Professor of Emergency
Medicine, Weill Medical College
of Cornell University, New York;
Research Director, Department of
Emergency Medicine, New York
Hospital Queens, Flushing, NY
Ali S. Raja, MD, MBA, MPH
Vice-Chair, Emergency Medicine,
Massachusetts General Hospital,
Boston, MA
Robert L. Rogers, MD, FACEP,
FAAEM, FACP
Assistant Professor of Emergency
Maryland School of Medicine,
Baltimore, MD
Alfred Sacchetti, MD, FACEP
Assistant Clinical Professor,
Department of Emergency Medicine,
Thomas Jefferson University,
Philadelphia, PA
International Editors
Chair, Department of Family Medicine, Peter Cameron, MD
Beth Israel Medical Center; Senior
Faculty, Family Medicine and
Community Health, Icahn School of
Medicine at Mount Sinai, New York, NY
Scott Silvers, MD, FACEP
Andrea Duca, MD
Associate Professor and Chair,
Department of Emergency Medicine,
Mayo Clinic, Jacksonville, FL
Corey M. Slovis, MD, FACP, FACEP
Professor and Chair, Department
of Emergency Medicine, Vanderbilt
University Medical Center, Nashville, TN
Ron M. Walls, MD
Professor and Chair, Department of
Emergency Medicine, Brigham and
Women's Hospital, Harvard Medical
School, Boston, MA
Critical Care Editors
William A. Knight IV, MD, FACEP
Associate Professor of Emergency
Medicine and Neurosurgery, Medical
Director, EM Advanced Practice
Provider Program; Associate Medical
Director, Neuroscience ICU, University
of Cincinnati, Cincinnati, OH
Scott D. Weingart, MD, FCCM
Associate Professor of Emergency
Medicine; Director, Division of ED
Critical Care, Icahn School of Medicine
at Mount Sinai, New York, NY
Senior Research Editors
Aimee Mishler, PharmD, BCPS
Emergency Medicine Pharmacist,
Maricopa Medical Center, Phoenix, AZ
Joseph D. Toscano, MD
Chairman, Department of Emergency
Medicine, San Ramon Regional
Medical Center, San Ramon, CA
Academic Director, The Alfred
Emergency and Trauma Centre,
Monash University, Melbourne,
Australia
Attending Emergency Physician,
Ospedale Papa Giovanni XXIII,
Bergamo, Italy
Suzanne Y.G. Peeters, MD
Attending Emergency Physician,
Flevo Teaching Hospital, Almere,
The Netherlands
Hugo Peralta, MD
Chair of Emergency Services,
Hospital Italiano, Buenos Aires,
Argentina
Dhanadol Rojanasarntikul, MD
Attending Physician, Emergency
Medicine, King Chulalongkorn
Memorial Hospital, Thai Red Cross,
Thailand; Faculty of Medicine,
Chulalongkorn University, Thailand
Stephen H. Thomas, MD, MPH
Professor & Chair, Emergency
Medicine, Hamad Medical Corp.,
Weill Cornell Medical College, Qatar;
Emergency Physician-in-Chief,
Hamad General Hospital,
Doha, Qatar
Edin Zelihic, MD
Head, Department of Emergency
Medicine, Leopoldina Hospital,
Schweinfurt, Germany

Go to the interactive PDF at www.ebmedicine.net/topics and click on the icon for a closer look at tables and figures.
Case Presentations
A 48-year-old man presents after being rescued from a
burning apartment. He complains of shortness of breath
and chest tightness. He is coughing up carbonaceous spu-
tum, has soot in his nares, and has 15% total body surface
area burns. He is mildly tachypneic, with an oxygen satu-
ration of 92%, and is wheezing. As you continue your
primary survey, you wonder what the indications are for
intubation in smoke inhalation, and the best approach to
this patient’s management...
As you are finishing your evaluation, the patient’s
72-year-old mother is brought in from the same fire. She
is obtunded, with 30% total body surface area burns on
her torso, extremities, and face. EMS reports that her
vital signs are: blood pressure, 100/65 mm Hg; pulse, 105
beats/min; respiratory rate, 16 breaths/min; oxygen satu-
ration, 90% on nonrebreather mask. She does not respond
to voice, although she moans and localizes to painful
stimuli. As the nurse is checking a fingerstick glucose and
placing her on a monitor, you begin your primary survey.
You ask your resident to describe the differential diagnosis
for altered mental status in a patient with smoke expo-
sure, while in the back of your mind, you begin to weigh
the testing and management priorities...
A little later in your shift, a 27-year-old woman who
is 18 weeks’ pregnant is triaged for shortness of breath,
cough, lightheadedness, mild confusion, and headache.
She was in the same apartment complex fire as your previ-
ous 2 patients. She cannot recall all the details because she
“fainted,” and she regained consciousness only when the
firefighters were evaluating her. The EMS crew mentions
that the carbon monoxide meter reading in the apartment
was elevated. Her vital signs are within normal limits.
You suspect carbon monoxide poisoning, but wonder
whether she is a candidate for hyperbaric treatment and
whether it is safe for the fetus...
Introduction
As these cases highlight, it is not uncommon for mul-
tiple patients who have been exposed to a serious fire
to present to the emergency department (ED) simulta-
neously, requiring urgent evaluation and stabilization.
Inhalation injuries contribute significantly to morbidi-
ty and mortality in fire-exposed patients, and their in-
juries can range in severity from minimal symptoms
to life-threatening injuries. The presence of smoke
inhalation injury (SII) is an independent predictor of
mortality, and it worsens the prognosis compared to
patients of similar age and burned total body surface
area (TBSA) without SII.1-3 In patients with cutane-
ous burns, the presence of a concomitant SII increases
fluid requirements, pulmonary complications, and
overall mortality.4 Likewise, patients with SII have in-
creased mortality when cutaneous burns are present.5
Data suggest that 5% to 10% of patients hospitalized
for burns have a concomitant SII, and that the pres-
Copyright © 2018 EB Medicine. All rights reserved. 2
ence of inhalation injury portends a 20% increased
mortality, which increases to 60% higher mortality if
secondary pneumonia develops.6 For these reasons,
inhalation injury is one of the criteria for transfer to
a burn center.7 The diagnosis and prognostication of
SII can be challenging due to the lack of standardized
severity scoring.1,8 Additionally, it is often difficult
to predict severity in the acute phase, since much of
the damage is not visible upon initial presentation.9
Various proposed grading schemes have not reliably
predicted patient outcomes.6
The insidious nature of SII, both in its delayed
development and associated poisoning exposures,
cannot be underestimated. The emergency clini-
cian’s ability to suspect, diagnose, and expertly
manage SII is crucial. Management is mainly sup-
portive, and some management strategies—such as
hyperbaric oxygen, proactive airway management,
and ventilation techniques—remain controversial.
Standardized diagnostic criteria for SII are lacking,
treatment strategies are suboptimal, and morbidity
and mortality remain high. This issue of Emergency
Medicine Practice presents a comprehensive review
of the existing literature, offers best-practice recom-
mendations on the management of patients with SII,
and highlights areas where further research is neces-
sary. For information about assessing and treating
patients with thermal burns, see the February 2018
issue of Emergency Medicine Practice, “Emergency
Department Management of Patients With Thermal
Burns,” available at www.ebmedicine.net/Burns.
Selected Abbreviations
ALI Acute lung injury
ARDS Acute respiratory distress syndrome
COHb Carboxyhemoglobin
CO Carbon monoxide
CN Cyanide
FiO2 Fraction of inspired oxygen
PaO2 Partial pressure of oxygen, arterial
SII Smoke inhalation injury
TBSA Total body surface area
Critical Appraisal of the Literature
A literature search was performed via PubMed
using the following main search terms: inhalation
injury, burns, inhalation, inhalation exposure, smoke
inhalation, chemical inhalation, carbon monoxide, carbon
monoxide poisoning, hydrogen cyanide, and cyanide.
Additional MeSH pairings were used to expand and
include airway management strategies, ED patient
population, and to limit the studies to those with
adult patients and published in English. Once a list
of pertinent studies was obtained, we selectively
reviewed reference lists to find additional relevant
articles. Overall, 1098 articles were identified and
Reprints: www.ebmedicine.net/empissues
87 were deemed applicable to be included. Many upper airway obstruction.5,12 Direct thermal damage
of the identified articles were retrospective studies, to epithelial cells denatures cell proteins and initi-
case reports, and literature reviews. Some prospec- ates the inflammatory cascade, which causes release
tive studies exist, but overall, we found a paucity of of reactive oxygen and nitrogen species. Activation
prospective, blinded, randomized controlled trials of poly(ADP-ribose) polymerase depletes cellular
pertaining to fire-related inhalation injury. adenosine triphosphate (ATP), which causes fur-
ther cell necrosis.10 The cumulative effects of local
Etiology and Pathophysiology inflammation and cellular death cause increased
permeability across the endothelial border, which
SII is caused by the cumulative effects of heat ex- contributes to edema of the supraglottic tissues, with
posure and the inhalation of chemicals, particulate potential for airway obstruction.10 Significant airway
matter, and toxic products of combustion such as edema can occur after intravenous (IV) fluid resus-
carbon monoxide (CO) and cyanide (CN).10 Clas- citation and, in many cases, this endpoint cannot be
sically, it is divided based upon anatomic location, predicted on initial evaluation.8 Fortunately, upper
and each subtype has distinct pathophysiologic fea- airway thermal injury is less common than the other
tures. The 3 important subtypes include: (1) upper subtypes of SII due to the large surface area of the
airway, (2) lower airway/lung parenchyma, and (3) supraglottic tissues, high flow rate of air through
systemic effects from metabolic cellular dysfunction. these structures, and efficient body processes to dis-
(See Table 1.) Often, all of these subtypes impact sipate heat and minimize such exposure.11
the patient simultaneously. Upper airway supra-
glottic injury typically results from thermal insult, Lower Airway and Lung Parenchymal Injury
whereas lower airway injury is due to chemical and Thermal injury is rarely a concern below the vo-
particulate insult.1,8 Important metabolic processes cal cords, as the heat of the inhaled gas is generally
are disrupted by CO and CN toxicities. The severity dissipated by the time it reaches this location.10,13
of SII is highly dependent on various factors, such Lower airway and lung parenchymal injury occurs
as the composition of inhaled gas (determined by from toxic effects of the chemicals and particles in
the type of burning material), host factors such as the inhaled smoke, and constitutes the majority of
underlying medical comorbidities, and the proxim- inhalation injuries.
ity and duration of the fire exposure.11 Furthermore,
inhaled substances can exert toxic effects via differ- Systemic Cellular Dysfunction of Carbon
ent mechanisms, including systemic cellular dys- Monoxide and Cyanide Exposure
function, ambient oxygen deprivation, and direct The combustion of certain substances, such as
irritation of the respiratory tissues.1 cotton, rubber, and plastic, produces toxic substanc-
es including chlorine, nitrogen dioxide, ammonia,
Upper Airway Thermal Injury sulfur dioxide, and aldehydes, which damage
Upper airway thermal injury can cause significant epithelial tissues of the airway.8 The more water-
edema of the mucosal tissue, which, in turn, can soluble toxins (such as ammonia) preferentially
produce airway obstruction. One-fifth to one-third of affect the upper airway, while the more poorly
patients hospitalized for SII may present with acute soluble toxins (such as chlorine) damage the bron-
chioles and lungs. Damaged tissues slough off and
combine with fibrin and other proteinaceous materi-
Table 1. Classification of Inhalation Injury als to form casts. Additionally, plasma, which
Injury Subtype Mechanism Clinical Consequences contains procoagulant factors, leaks into the airway
and promotes fibrin formation and further solidifica-
Upper airway Thermal burns • Airway edema/
injury from heat obstruction
tion of these proteinaceous fibrin casts.11 (See Figure
transfer 1, page 4. ) When coupled with an impaired
mucociliary transport system, this leads to physical
Lower airway/lung Chemical and • Fibrin casts that
obstruction of the lower airways.8 The toxic chemi-
parenchyma particulate obstruct lower airways
irritants • Inflammation
cals trigger release of neuropeptides, chemokines,
• Ventilation/perfusion
and other proinflammatory peptides such as sub-
mismatch stance P and neurokinins, all of which cause inflam-
• Atelectasis mation and edema of the lung parenchyma and
• Bronchospasm accumulation of fluid and mucous in the airways,
Systemic cellular Asphyxia/ • Lactic acidosis
decreasing lung compliance.11 Ventilation-perfusion
dysfunction from hypoxia • Central nervous mismatch ensues as the fibrin casts restrict airflow
carbon monoxide system insults and decrease ventilation, while the damaged tissue
and cyanide • Cardiovascular insults causes localized inflammation that increases blood
exposure flow.8,11 Surfactant is inactivated, alveoli collapse,

March 2018 • www.ebmedicine.net 3 Copyright © 2018 EB Medicine. All rights reserved.

and atelectasis ensues.4 The result of the intense
inflammatory response is acute respiratory distress
syndrome (ARDS).1
Many of the primary mechanisms of insult, in-
cluding epithelial cell damage, endobronchial debris
formation, inflammation, and atelectasis predispose
to secondary infections that contribute significantly
to morbidity and mortality. In a prospective obser-
vational study, elevation in inflammatory mark-
ers found in bronchial washings were associated
with development of bacterial pneumonia.14 Lastly,
through poorly understood mechanisms that may
involve neuropeptides, inhalation injury leads to
Figure 1. Soot and Bronchial Casts From
Smoke Inhalation
A CN produces an additive effect with CO to decrease
B
A: Bronchial soot. B: Bronchial casts.
Seung Ick Cha, Chang Ho Kim, Jae Hee Lee, et al. Isolated smoke
inhalation injuries: acute respiratory dysfunction, clinical outcomes,
and short-term evolution of pulmonary functions with the effects
of steroids. Burns. Volume 33, Issue 2. Pages 200-208. © 2007,
reprinted with permission from Elsevier.
Copyright © 2018 EB Medicine. All rights reserved. 4
bronchospasm, which further obstructs airflow.11
Smoke components such as CO and CN can also
cause toxicity via systemic effects.
CO is a colorless, odorless, tasteless gas that
results from incomplete combustion of carbon-con-
taining material, and it is an important cause of early
mortality in smoke-exposed patients.8 CO toxicity is
one of the most common causes of death in patients
with SII,10 and contributes to about 80% of smoke in-
halation-related deaths. CO is rapidly absorbed and
has a very high affinity for hemoglobin, binding to
hemoglobin with > 200 times the affinity of oxygen.
This displaces oxygen, shifts its dissociation curve
leftward, and impairs oxygen delivery to tissues.10
At the cellular level, CO acts as a competitive inhibi-
tor of cytochrome oxidase, which renders the cells
unable to use oxygen.4 The resultant cellular hypox-
ia is most prominently manifested in the tissues with
highest oxygen consumption, such as the central
nervous system and the cardiovascular system.15 CO
binds to myoglobin in myocytes, interfering with
cellular function and contributing to rhabdomy-
olysis, arrhythmias, and myocardial dysfunction.16
CO can cause cardiac injury in patients with normal
coronary arteries, and exacerbate underlying cardiac
or respiratory disease.
CN is formed by the incomplete combustion of
certain nitrogen-containing materials, particularly
the polymers that are commonly found in plastics
and other household products. Like CO, CN also
inhibits cytochrome oxidase, which halts produc-
tion of ATP in the electron transport chain. As a
result, oxygen utilization and aerobic respiration are
impaired, which causes profound lactic acidosis.12
tissue oxygenation and oxygen utilization, further
exacerbating the hypoxic state.4
Differential Diagnosis  
When SII is suspected, it is imperative to avoid
premature diagnostic closure. For example, patients
presenting from a fire may have concomitant trau-
matic injuries. Emergency clinicians must maintain
a broad differential and a high index of suspicion
for other medical and traumatic conditions because
critically ill patients may not be able to relay a
history. Traumatic injuries such as pneumothorax,
pericardial effusion or tamponade, and pulmonary
or cardiac contusions can mimic some of the signs
and symptoms of inhalation injury. Patients rescued
from a fire may have altered mental status for sev-
eral reasons, including head trauma, seizure, severe
CO poisoning, hypoxic encephalopathy, intoxication,
or hypoglycemia. Patients presenting with respira-
tory symptoms may have aspiration pneumonitis,
pneumonia, exacerbation of acute asthma or chronic
obstructive pulmonary disease, or ARDS.
Reprints: www.ebmedicine.net/empissues
Prehospital Care
Prehospital care of patients with SII prioritizes initial
stabilization and expeditious transport. Prehospital
providers should approach these patients assum-
ing they have concomitant traumatic injuries until
proven otherwise. The first priority is to ensure that
the rescuers are safe and the patient is separated from
the source of the fire in order to limit further smoke
exposure. As with any sick patient, initial assessment
and management focuses on the primary survey.
Airway management in the prehospital set-
ting warrants special consideration. If the patient’s
clinical status clearly necessitates immediate airway
management, then prehospital providers should
intervene accordingly. If endotracheal intubation is
difficult due to upper airway edema, adjuncts such
as bag-valve mask and laryngeal-mask airways
should be considered. For patients who are hypoxic
or wheezing, 100% supplemental oxygen and bron-
chodilators are indicated. Patients suspected to have
CO poisoning should also receive 100% supplemen-
tal oxygen. Large-bore IV access should be obtained,
and hypotension should be initially managed with
IV fluids.9 Often patients with SII will have signifi-
cant cutaneous burns, and pain should be managed
accordingly.
The available literature, although sparse, sup-
ports prehospital administration of hydroxocobala-
min for suspected acute CN poisoning in patients
with SII.17-19 Limited data (mostly animal studies, in
vitro studies, and case reports) suggest that hy-
droxocobalamin administration may interfere with
measurement and interpretation of carboxyhemoglo-
bin (COHb) levels and other blood tests.20-23 Clinical
use of hydroxocobalamin in suspected or confirmed
CN poisoning should not be withheld.
Emergency Department Evaluation
The initial approach to patients presenting with
burns and SII is similar to the trauma evalua-
tion. Particularly when the patient is critically ill,
evaluation begins with a primary survey to quickly
recognize and manage life threats. If the patient is
stable and has a normal primary survey, a secondary
survey and history should then be performed. If the
patient arrives altered or obtunded, history should
be obtained from alternate sources.
History
Since diagnosis of SII is largely clinical,4 the history
is key and should begin with questions about the
events leading up to the patient’s arrival. Ask about
the mechanism of exposure, and whether the fire
was in an enclosed space, since this increases the
likelihood of inhalation injury. The environment of
the fire is important, as the gases inhaled can vary,
March 2018 • www.ebmedicine.net
depending on what materials were combusted. The
length of exposure and proximity of the patient
to the fire are also key factors. Patients should be
questioned about presenting symptoms. Respira-
tory, cardiovascular, and neurological symptoms are
particularly relevant. Cough, shortness of breath,
carbonaceous sputum, voice change, and drooling
may be seen with SII. (See Table 2.)
Loss of consciousness is an important histori-
cal finding since it can be seen in patients with
CO or CN toxicity, and it often lengthens the time
the patient is exposed to the fire. Other symptoms
indicative of CO exposure are nonspecific and in-
clude headache, dizziness, myalgias, and nausea/
vomiting. In severe cases, altered mental status,
unresponsiveness, cardiovascular collapse, or death
may result.6
Clinical findings of CO toxicity are correlated
loosely to the COHb level. (See Table 3, page 6. )
However, other factors, including the rate and
length of exposure as well as pre-existing comorbidi-
ties, also significantly impact the clinical findings of
toxicity. Furthermore, many times patients’ injuries
do not follow this step-wise pattern, and often the
COHb level does not correlate with the clinical
presentation. CO poisoning causes short-term and
long-term neurologic symptoms, and some symp-
toms can occur as delayed sequelae after a period of
improvement. These symptoms are often subtle and
can include fatigue, memory deficits, affective
conditions, sleep disturbances, vertigo, neuropathy,
paresthesias, abdominal pain, and diarrhea. Other
long-term consequences include gait and motor
disturbances, peripheral neuropathy, hearing loss,
vestibular abnormalities, dementia, and psychosis.4
Delayed neurologic sequelae often resolve gradually
over months, but in 25% of the cases, can be perma-
Table 2. History and Physical Examination
Findings Suggesting Inhalation Injury
History
• Cough
• Shortness of breath
• Voice change/hoarseness
• Drooling
• Carbon monoxide/cyanide exposure symptoms: headache, nausea/
vomiting, dizziness, loss of consciousness, myalgias, altered mental
status, hyperventilation, hemodynamic compromise, shock, death
Physical Examination Findings
• Facial burns
• Airway edema
• Soot in nares/oropharynx
• Carbonaceous sputum
• Singed nasal hairs
• Lung sounds: rales, rhonchi, wheezing
• Stridor
• Vital signs: tachypnea or hypoxia
5 Copyright © 2018 EB Medicine. All rights reserved.
nent.24 Death occurs in approximately 3% of patients
medically treated for CO poisoning.25
CN poisoning can present with similar early
symptoms, including headache, dizziness, palpita-
tions, nausea, confusion, hyperventilation, or soot
in the mouth or sputum. Severe CN toxicity can
cause seizures, hemodynamic compromise includ-
ing hypotension and bradycardia and, ultimately,
cardiorespiratory arrest.23,26-28 A bitter-almond smell
may be present, but absence of this finding does not
exclude CN toxicity. The history should also assess
for potential concomitant traumatic injuries. The rest
of the history is similar to the standard ED evalu-
ation, including past medical history (especially
cardiorespiratory comorbidities, which may increase
morbidity and mortality), medications, allergies, and
last oral intake.
Physical Examination
Evaluation starts with assessment of the airway.
Examine the oral cavity looking for soft-tissue edema,
carbonaceous sputum, and soot in the oropharynx. Ab-
normal phonation, stridor, facial burns and/or edema,
soot in the nares or airway, and singed nasal hairs may
also indicate SII that could impair the airway. Note that
absence of the classic physical examination findings
does not exclude the possibility of SII.29
Once the airway is assessed and stabilized,
breathing is evaluated. Tachypnea is often present
and can indicate lower airway injury. Rales, rhonchi,
and decreased breath sounds may also indicate low-
er respiratory tract injury. Wheezing resulting from
bronchospasm may be heard on lung auscultation.
Oxygen saturation should be assessed; however, a
Table 3. Carboxyhemoglobin Levels and
Associated Symptoms15
Serum COHb Signs and Symptoms
Level (%)
0-10 Usually none; possible reduced
exercise tolerance
10-20 Headache, dyspnea with vigorous exertion
20-30 Headache, dyspnea with moderate exertion,
nausea, weakness, concentration difficulty,
ischemic electrocardiogram changes
30-40 Severe headache, impaired cognition, visual
disturbances, dizziness, nausea/vomiting,
cardiac ischemia
40-50 Confusion, exertional syncope, tachycardia,
tachypnea
50-60 Convulsions, collapse
60-70 Hypoventilation, coma; decreased cardiac output,
often fatal
> 70 Coma, respiratory failure; very likely fatal
Abbreviation: COHb, carboxyhemoglobin.
Copyright © 2018 EB Medicine. All rights reserved. 6
normal saturation does not exclude CO poisoning.
Following the breathing assessment, the cir-
culatory evaluation should be performed. Pulse,
blood pressure, capillary refill, and the skin should
be examined. IV or intraosseous access should be
obtained. IV fluid resuscitation should commence
if hypotension exists. Blood product transfusion
should be considered if the patient is hypotensive
and there is concern for a concomitant traumatic
injury. Disability evaluation includes obtaining the
Glasgow Coma Scale score and a basic neurologic
examination. Patients with alterations in mental
status could have hypoglycemia, seizures, shock,
hypoxia, brain or spinal cord injury, intoxication, or
severe SII with or without CO and/or CN toxicity.
The initial management involves assessing for and
treating these, as indicated.
The final portion of the primary survey involves
fully exposing the patient to facilitate a thorough
physical examination. In addition to evaluating inju-
ries, exposure also allows for calculation of TBSA for
cutaneous burns.
As with any critically ill patient, a secondary
survey, including a complete physical examination,
should be performed once the primary survey and
stabilizing measures are completed. Special atten-
tion must be paid to the assessment of mental status.
Since patients with CO poisoning may appear to be
alert, a more formalized evaluation, such as the Mini
Mental State Examination (MMSE), may be useful.
Link to MMSE: http://www.dementiatoday.com/
wp-content/uploads/2012/06/MiniMentalStateEx-
amination.pdf
Diagnostic Studies
Review of the American Burn Association National
Burn Repository, which included 9775 burn cases,
found that diagnosis by clinical findings was the
most commonly reported method.30 Some clues
suggesting increased risk for SII include closed-
space fire, advanced patient age, large burned body
surface area, and facial burns.29 While signs and
symptoms elicited from the history and physical
examination provide important clues to the presence
of inhalation injury, they do not provide diagnostic
certainty. Various diagnostic studies are often used
in conjunction with history and physical examina-
tion to aid in diagnosis and management.
Blood Gas and CO-Oximetry
The blood gas allows for evaluation of the patient’s
acid-base status. In the acute setting of SII, it is often
normal.31 As airway obstruction progresses, retention
of CO2 may occur. Decreased tissue perfusion can
lead to metabolic acidosis. The blood gas can vary,
depending on patient factors and clinical presenta-
tion, and it does not always demonstrate acidosis. For
Reprints: www.ebmedicine.net/empissues
example, in mild cases of CO toxicity, hyperventila-
tion may produce a respiratory alkalosis.32
For most purposes, a venous sample can be used
in lieu of an arterial sample. A venous blood gas can-
not be used for a PaO2 (partial pressure of oxygen
in arterial blood) level, however. Arterial blood gas
allows for calculation of PaO2 in order to determine
the PaO2/FiO2 (fraction of inspired oxygen) ratio,
which correlates with the degree of shunting. The
lower the PaO2/FiO2, the higher the mortality in
patients with SII.33 Note that PaO2/FiO2 can be influ-
enced by ventilator mode and IV fluid resuscitation,
so the ratio is less valuable as a diagnostic tool and
more valuable to trend response to therapy.1 Since
the PaO2 is usually normal in CO poisoning and the
PaO2 is what is used to calculate the oxygen satura-
tion on the blood gas, the blood gas oxygen satura-
tion is also often interpreted as normal. In severe
CO or CN poisoning, the venous PO2 may actually
be elevated due to reduced oxygen extraction at the
tissue level.
Patients suspected to have CO poisoning should
have a COHb level tested, most commonly by blood
CO-oximetry. Either an arterial or venous sample
can be obtained, as there is no statistically signifi-
cant difference between the two.16,34 A COHb level
is considered abnormal if it is > 3% in a nonsmoker
or > 10% in a smoker.34 However, significant toxic-
ity may exist despite a normal or near-normal level,
depending on the timing of the blood sample and
whether oxygen was administered prior to sample
collection.4,16,35 Furthermore, the level does not have
a strong correlation with the severity of poisoning or
clinical outcomes.
Pulse Oximetry
Pulse oximetry should be checked, as it can indi-
cate upper or lower airway pathology. However,
the pulse oximetry reading may be falsely normal
despite significant CO poisoning. In a retrospec-
tive study of 476 patients with CO intoxication,
approximately 68% of patients with COHb levels >
20% had normal vital signs, including pulse oxim-
etry.32 The pulse oximeter utilizes a wavelength that
is absorbed not only by oxyhemoglobin but also
by COHb, and thus it is often normal despite the
presence of CO toxicity since it cannot differentiate
oxyhemoglobin from COHb.16
Noninvasive Pulse CO-Oximetry
Noninvasive pulse CO-oximetry is a newer tech-
nology that uses multiple wavelengths of light
absorbed by oxyhemoglobin, COHb, deoxyhemo-
globin, and sometimes methemoglobin. The device
attaches to the patient’s finger and gives a reading
within seconds. The theoretical benefit is to quickly
recognize CO toxicity either in the prehospital or ED
triage setting, which would then expedite manage-
March 2018 • www.ebmedicine.net
ment. Because it is meant to be used as a screening
tool, the sensitivity should be high for noninvasive
pulse CO-oximetry to be useful. Though not widely
studied, the existing literature about its accuracy is
conflicting. One cross-sectional cohort study that
compared noninvasive pulse CO-oximetry readings
to laboratory COHb levels found that the nonin-
vasive readings were only 48% sensitive for COHb
levels > 15%.36 Further studies are warranted before
this technology can be routinely recommended.
Lactic Acid
The serum lactate level increases proportionally with
the rate of CN poisoning. In fire victims, a lactate
of 10 mmol/L is a sensitive and specific indicator
of CN intoxication.28 In patients with SII, a high
lactate level strongly suggests CN toxicity, and the
value correlates with the severity of toxicity.26 Some
retrospective trials and case reports suggest that an
elevated lactate level may be associated with serious
complications and is a marker of poor prognosis.37,38
Although often referenced due to its association
with CN toxicity, any condition that impairs tissue
perfusion can cause lactate to elevate. Important ex-
amples in the patient with SII include CO,39 hypoxia
due to upper or lower airway damage, and shock
due to trauma or burns.
Cyanide Testing
CN has a very short half-life and serum levels are
not often obtained in a timely fashion. For this rea-
son, when serum levels are measured, the levels are
often falsely low.26 In addition, the laboratory value
often takes a long time to result, sometimes several
days.40 As such, diagnosis of CN toxicity is mostly
clinical, and empiric treatment should be adminis-
tered when indications are met. If a serum blood CN
level is obtained at the scene or very shortly after ED
arrival, a level of 0.5 to 1 mg/L is considered mild,
1 to 2 mg/L is moderate, 2 to 3 mg/L is severe, and
> 3 mg/L is potentially lethal.26 In a multinational
prospective study, the most commonly seen mark-
ers of CN intoxication were dyspnea, depressed
GCS score, soot deposits (especially in the sputum),
and seizures. The authors suggest treatment with
hydroxocobalamin if any of these markers are pres-
ent.23 CN should also be suspected in cases of unex-
plained hypotension and severe lactic acidosis.26
Other Laboratory Testing
A fingerstick glucose test should be performed in
any patient with altered mental status. The basic
metabolic panel is useful for calculating an anion
gap, which can be elevated in acidotic states. It also
provides important information about the electrolytes
and renal function, which may be impaired due to
shock or hypoperfusion. A complete blood cell count
can be useful to trend the hemoglobin and hemato-
7 Copyright © 2018 EB Medicine. All rights reserved.
crit, especially in patients with concomitant traumatic
injuries. The creatine phosphokinase can be elevated
due to rhabdomyolysis, which may be seen in the
trauma setting. Beta HCG testing should be ordered
in all women of childbearing age, since pregnancy
may impact management decisions. Type and screen
is necessary in patients with traumatic injuries. Tro-
ponin levels should be checked in patients with SII. In
a retrospective study, troponin I levels were elevated
in CO poisoning, and were correlated with receipt of
hyperbaric oxygen therapy.35 Elevated troponin may
be a marker of poor outcome in patients with CO
poisoning.41
Electrocardiogram
In patients with SII, an electrocardiogram (ECG)
should be considered. CO exposure increases the
risk of dysrhythmias and myocardial ischemia.16
ECG is particularly useful if there is concern for CO
exposure, especially if the patient has any underly-
ing cardiorespiratory comorbidities, loss of con-
sciousness or syncope, or symptoms concerning for
possible cardiac ischemia. The presence of myocar-
dial injury may be an independent predictor of poor
outcomes in patients with severe CO poisoning.41
Chest X-Ray
Chest x-ray should be obtained in patients with SII;
however, it is often normal or nonspecific in the
acute setting.29 When present, suggestive findings
include peribronchial cuffing, perivascular haziness,
diffuse atelectasis, pulmonary edema, subglottic
edema, and bronchial wall thickening. However,
these findings are often absent at initial presentation.
If the initial chest x-ray shows pulmonary infiltrates,
Figure 2. Computed Tomography Scan Slice
With Radiologist’s Score Findings
John S. Oh, Kevin K. Chung. Admission chest CT complements
fiberoptic bronchoscopy in prediction of adverse outcomes in
thermally injured patients. Journal of Burn Care and Research.
2012. Volume 33, Issue 4. Pages 532-538. By permission of Oxford
University Press.
Copyright © 2018 EB Medicine. All rights reserved. 8
this is a sign of severe injury and portends a worse
prognosis.8 Patients can also have coexisting trau-
matic injuries that may be seen on x-ray.
Chest Computed Tomography
Usually used to supplement bronchoscopy, chest
computed tomography (CT) is another means of
evaluating the severity of inhalation injury, and has
the advantage over bronchoscopy of being nonin-
vasive and allowing for evaluation of the lower air-
ways. Findings such as increased interstitial mark-
ings, “ground glass” opacification, and consolidation
in conjunction with bronchoscopic findings show an
increase in endpoints such as pneumonia and acute
lung injury (ALI) or ARDS. (See Figure 2.) In a pro-
spective observational study, CT scans performed
within a few hours after smoke exposure were
predictive of SII. Bronchial wall thickness and per-
centage of luminal area were significantly higher in
patients with SII, compared to controls. These values
were also predictive of the number of mechanical
ventilation days, development of pneumonia, and
intensive care unit (ICU) length of stay.42 Another
retrospective study found that findings of inhala-
tion injury on chest CT (defined by the radiologist’s
score [RADS] scoring system) were predictive of the
composite endpoint of pneumonia, ALI/ARDS, and
death.43 However, the only statistically significant
correlation was for ALI/ARDS, with no statistically
significant difference in death or pneumonia.
To calculate a RADS score, 1-cm axial slices of
the lungs on chest CT are evaluated from the apex to
the diaphragm. For each slice, both the left and right
lung are divided into 4 quadrants, and each quad-
rant is assigned a score ranging from 0 to 3, depend-
ing on the highest severity of radiographic findings
found in that quadrant. (See Table 4.) The total score
for each CT slice is calculated by adding the 8 scores
(4 quadrant scores per lung), and then the scores
for each slice are added to determine the overall
RADS score of the CT scan. The overall RADS score
can then be divided by the total number of slices
Table 4. RADS Score to Grade Severity of
Inhalation Injury on Chest CT
Finding Score
Normal 0
Increased interstitial markings 1
Ground glass opacification 2
Consolidation 3
Abbreviations: CT, computed tomography; RADS, radiologist's score.
John S. Oh, Kevin K. Chung. Admission chest CT complements
fiberoptic bronchoscopy in prediction of adverse outcomes in
thermally injured patients. Journal of Burn Care and Research.
2012. Volume 33, Issue 4. Pages 532-538. By permission of Oxford
University Press.
Reprints: www.ebmedicine.net/empissues
to determine the “RADS per slice” score. An online inhalation injury based on bronchoscopic findings.
calculator for RADS scoring is available from (See Table 5.) In addition, bronchoalveolar lavage
www.MDCalc.com, at: washings can be evaluated for inflammatory bio-
• www.mdcalc.com/rads-radiologists-score- markers that may correlate with the severity of SII.46
smoke-inhalation-injury Most of the literature pertaining to the diag-
CT can also be used to construct a 3-dimensional nostic and prognostic capabilities of fiberoptic
virtual bronchoscopy, but the ability to evaluate blis- bronchoscopy is based upon retrospective data. One
tering and necrosis is limited.1 Furthermore, this has retrospective study showed that higher AIS scores
only been studied in a swine model, and cannot be correlated with increased COHb levels, increased
recommended, as human data are lacking. Limita- risk of ARDS, longer mechanical ventilation time,
tions of CT include determining the optimal timing and worsened oxygenation indices, with a trend to-
for performing the test and deciding what to do with ward multiorgan dysfunction and mortality.47 Other
abnormal radiographic findings in the setting of a studies have corroborated bronchoscopic findings as
negative bronchoscopy.1 being predictive of worsened outcomes, including
increased mortality.30,33,48 However, some of the lit-
Fiberoptic Bronchoscopy erature is conflicting; a retrospective study of 160 pa-
Besides the history and physical examination, fiber- tients found that bronchoscopy AIS grading did not
optic bronchoscopy is one of the more useful diag- correlate with mortality.49 Although standardized
nostic tests, although the optimal timing remains diagnostic criteria are lacking and further research
unknown. Fiberoptic bronchoscopy is currently from larger prospective trials is needed,50 fiberoptic
considered the gold standard for diagnosing SII, and bronchoscopy is one of the most commonly used
it has been the cornerstone of diagnosis since the tests to assess for SII. An ongoing study sponsored
1970s.44 It can evaluate the airway from the orophar- by the American Burn Association aims to develop a
ynx to the lobar bronchi. Positive findings include multimodal standardized scoring system for inhala-
mucosal erythema, edema, ulcerations or blistering, tion injury. An online calculator for AIS grading is
fibrin casts, charred tissue, or soot. The diagnostic available from www.MDCalc.com, at:
accuracy of fiberoptic bronchoscopy for SII is most • www.mdcalc.com/abbreviated-injury-score-ais-
frequently quoted in the literature as 86%.11,45 The inhalation-injury
abbreviated injury score (AIS) is the most commonly
used grading system that estimates the severity of Limitations of Fiberoptic Bronchoscopy
There are some limitations to fiberoptic bronchosco-
py, and for this reason SII remains a mostly clinical
Table 5. Abbreviated Injury Score Grading diagnosis in the ED. Fiberoptic bronchoscopy is an
Scale for Inhalation Injury on Bronchoscopy invasive test that is often not immediately available
in the ED, and may be falsely negative if performed
AIS Code Grade Class Description
too early in the patient’s clinical course. In patients
919201.2 0 No injury Absence of carbonaceous with burn shock, fiberoptic bronchoscopy might
deposits, erythema, edema,
miss inhalation injury if performed promptly after
bronchorrhea, or obstruction
1 Mild injury Minor or patchy areas of
injury, whereas a repeat bronchoscopic examination
919202.3
erythema, carbonaceous
24 to 48 hours later may be more accurate.29 In some
deposits, bronchorrhea, or burn patients, inhalation injury can be diagnosed
bronchial obstruction by fiberoptic bronchoscopy even if the patient is
919204.4 2 Moderate Moderate degree of erythema, completely asymptomatic.51 A further limitation of
injury carbonaceous deposits, bronchoscopy is that it can evaluate only the proxi-
bronchorrhea, or bronchial mal airways, whereas much of the morbidity and
obstruction mortality of smoke inhalation comes from lower
919206.5 3 Severe Severe inflammation
airway and lung parenchymal pathology.
injury with friability, copious
carbonaceous deposits,
bronchorrhea, or obstruction
Direct and Fiberoptic Laryngoscopy
919208.6 4 Massive Evidence of mucosal Though not well studied, laryngoscopy may be
injury sloughing, necrosis, considered as another tool to evaluate the upper
endoluminal obstruction airway. Findings include tissue erythema or edema,
soot in the airway, and mucosal blisters or erosions.
Abbreviation: AIS, abbreviated injury score. (See Figure 3, page 10. ) Laryngoscopy may be of
Joslyn M. Albright, Christopher S. Davis, Melanie D. Bird, et al. The
use when the emergency clinician is unsure whether
acute pulmonary inflammatory response to the graded severity of
the patient requires endotracheal intubation, espe-
smoke inhalation injury. Critical Care Medicine. Volume 40, Issue 4.
2012. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3290689/
cially when bronchoscopy is not immediately
Reprinted with permission of Wolters Kluwer Health, Inc. available. Compared to fiberoptic bronchoscopy,

March 2018 • www.ebmedicine.net 9 Copyright © 2018 EB Medicine. All rights reserved.

direct or fiberoptic laryngoscopy is less invasive, bet-
ter tolerated, and more widely available in emer-
gency settings.52 In a prospective study, 6 out of 11
patients had clinical signs and symptoms that were
worrisome for potential development of airway
obstruction. These patients were evaluated with
fiberoptic laryngoscopy, which obviated the need for
intubation in all 11 patients.53 Patients evaluated
with fiberoptic laryngoscopy should still be ob-
served closely, since symptoms may progress.
Conversely, in patients with subtle presentations
who have worrisome findings on laryngoscopy, the
clinician may choose to intubate earlier.
Other Clinical Testing
Radionuclide testing, most commonly utilizing
xenon 133, has also been used to diagnose SII. The
radioactive tracer is injected intravenously, under-
goes gas exchange, and is then exhaled. This process
permits visualization of the lower airways in order
Figure 3. Fiberoptic Laryngoscopy Views of
a Normal Airway and an Edematous Airway
A
B they have symptoms consistent with SII and there
A: Normal airway. B: Edematous airway.
Jimmy Toussaint, Adam J. Singer. The evaluation and management of
thermal injuries: 2014 update. Clinical and Experimental Emergency
Medicine. Volume 1, Issue 1, pages 8-18. Reprinted by Creative
Commons Attribution Non-Commercial License 3.0. Copyright ©
2014, The Korean Society of Emergency Medicine.
Copyright © 2018 EB Medicine. All rights reserved. 10
to diagnose an injury that is beyond the scope of
fiberoptic bronchoscopy. Failure to clear the radioac-
tive tracer after 90 seconds or segmental retention
of the tracer is considered a positive test.29 Unfor-
tunately, underlying lung diseases such as COPD
or asthma can result in a false-positive test.29 Also,
critically ill patients may not be suitable for trans-
port to the nuclear medicine department to undergo
this test.
Another clinical test that warrants mention is
pulmonary function testing, which can be used as a
screening tool. Due to increased pulmonary resis-
tance, SII causes decreased peak flow.29 However,
radionuclide testing and pulmonary function testing
do not significantly enhance diagnostic accuracy and
may not be worth the time and resources required to
perform them.11
Treatment
Airway Management
The 3 absolute indications for endotracheal intubation
include: (1) imminent threat of acute airway obstruc-
tion, (2) respiratory failure not responding to non-
invasive interventions, and (3) altered mental status
that impairs airway protection.54 If there are signs
of impending airway obstruction, including signifi-
cant edema or blistering of the oropharynx, stridor,
hoarseness, drooling, severe respiratory distress, or
hypoventilation, immediate endotracheal intubation
should be strongly considered. Similarly, obtunded
patients and those who are not protecting their air-
way require immediate intubation.
Ideally, when intubating, the individual most
experienced in airway management should place a
large endotracheal tube (> 7.5 cm outer diameter),
since many of these patients will undergo bronchos-
copy during their hospitalization.1 Because upper
airway edema may be present, the airway is often
difficult and this must be planned for accordingly.
Airway adjuncts, such as a bougie, laryngeal-mask
airway, video laryngoscope, and fiberoptic equip-
ment should be readily available. A backup plan
should be established and verbalized.
Although data are sparse, awake intubation
should be considered for patients strongly antici-
pated to have a difficult airway. The team should
anticipate the potential need for a surgical airway
and be prepared to perform one, if required. While
the need for airway establishment is sometimes
clear-cut, patients often fall into a “gray” zone where
is some concern about the development of delayed
airway obstruction and/or pulmonary insult, but
they are currently maintaining their airway and are
not in extremis. Much controversy exists about the
management of these patients, as the fear of direct
thermal injury leading to airway obstruction necessi-
Reprints: www.ebmedicine.net/empissues
tating immediate cricothyroidotomy29 or a “can’t in-
tubate/can’t oxygenate” situation looms large. Apart
from obvious cases where endotracheal intubation
is expected, it is also recommended for patients who
have deep burns to the face and neck, blistering or
edema of the oropharynx, hoarseness, stridor, or
large cutaneous burns > 40% TBSA.1,6,10,29
In the absence of obvious severe airway edema,
noninvasive positive-pressure ventilation (NIPPV)
can be useful in patients with mild to moderate
respiratory distress, provided they are cooperative
and alert.4,10,55 For more information on NIPPV, see
the February 2017 issue of Emergency Medicine Prac-
tice, “Noninvasive Positive-Pressure Ventilation for
Patients in Acute Respiratory Distress – An Update,”
at www.ebmedicine.net/NIPPV.
Fiberoptic or direct laryngoscopy using topi-
cal anesthesia can be used to visualize the airway
and determine the need for intubation. If normal,
intubation can be deferred, but the patient should
be monitored closely. After laryngoscopy, if intu-
bation is indicated, awake intubation with topical
anesthesia and moderate sedation is recommended
(eg, ketamine at a starting dose of 0.25-0.5 mg/kg
slow IV push, increasing by boluses of 10-20 mg as
needed).10,29,55 Paralytic agents should be used with
extreme caution, and other short-acting medications
such as fentanyl or midazolam can be considered.29
Once the airway is stabilized, the endotracheal tube
must be properly secured, as accidental extubation
can be life-threatening in the setting of edema.29 Ad-
hesive tape will not stick to burned skin; therefore
cotton ties (half-inch umbilical ties) are used to
secure the tube around the neck.29
IV fluids are administered for severe cutaneous
burns, and the combination of inhalation injury and
burn injury leads to increased fluid volume during
resuscitation.56 This can be harmful for inhalation
injury by causing worsened edema and obstruction,
which increases the risk of ARDS.7 Therefore, the
patient should be closely monitored to adjust fluid
administration based on the clinical condition.9
Mechanical ventilation is an independent pre-
dictor of mortality,57 and its use is not to be taken
lightly. Mechanical ventilation causes a release of
cytokines and leads to an inflammatory cascade
responsible for ventilator-associated lung injury, and
low tidal volume ventilation is traditionally used
to minimize these effects. In addition, the increased
positive pressure from mechanical ventilation causes
decreased venous return and leads to increased
fluid resuscitation,58 which has a negative impact on
airway and lung edema.
Tidal volumes should be initiated at 4 to 6 mL/
kg of predicted body weight, with plateau airway
pressure < 30 cm H2O, and a target oxygen satura-
tion > 92%.8,10,59 Permissive hypercapnia is accept-
able if targeted pH > 7.25.4,60 Various modes of
mechanical ventilation have been studied, and high-
March 2018 • www.ebmedicine.net
frequency percussive ventilation has emerged as
one of the more commonly endorsed lung protective
modes, as it is thought to clear sloughed respiratory
mucosa and plugs and decrease barotrauma.1 High-
frequency percussive ventilation was shown to be
associated with increased PaO2/FiO2 ratio and de-
creased need for rescue ventilation.61,62 (See Figure
4.) One study found, in the subset of patients with
≤ 40% TBSA, that use of high-frequency percussive
ventilation decreased lung inflammation and injury
histologically, increased compliance and ventilation,
and decreased incidence of ventilator-associated
pneumonia,63 with significant decrease in morbidity
and mortality.64
Other recruitment measures in the setting of
refractory hypoxia include positive end-expiratory
pressure (PEEP)60 and prone positioning. PEEP is
used to maintain oxygenation while keeping airway
plateau pressures < 30 cm H2O, and it can start at
8 cm H2O and be increased in 2.5-cm increments.8
PEEP increases arterial oxygenation by preventing
loss of lung compliance during mechanical venti-
lation and increased functional reserve capacity,8
while prone positioning was associated with an
increase in PaO2/FiO2.65
Figure 4. PaO2/FiO2 Ratio in High-Frequency
Percussive Ventilation Compared to Low-
Tidal-Volume Ventilation
450
HFPV
LTV
400
*
*
350
*
PaO2/FiO2 ratio
300
*
250
200
150
Before Day 0 Day 1 Day 2 Day 3 Day 4 Day 5 Day 6 Day 7
Asterisks denote P < .05
Abbreviations: FiO2, fraction of inspired oxygen; HFPV, high-frequency
percussive ventilation; LTV, low-tidal volume; PaO2, partial pressure
of oxygen, arterial.
Kevin K. Chung, Steven E. Wolf, Evan M. Renz, et al. High-frequency
percussive ventilation and low tidal volume ventilation in burns: a
randomized controlled trial. Critical Care Medicine. Volume 38, Issue
10. Pages 1970-1977. Used with permission of Wolters Kluwer Health,
Inc. DOI: http://dx.doi.org/10.1097/CCM.0b013e3181eb9d0b
11 Copyright © 2018 EB Medicine. All rights reserved.
 ClinicalClinical
Pathway For Emergency
Pathway Department
for Management Management
of Smoke Of Injury
Inhalation Multiple
Shocks

• Patient brought from fire scene

• Concern for smoke inhalation injury (eg, enclosed-space fire,
inhalation of smoke, cardiorespiratory or neurologic symptoms)

• Administer 100% oxygen (Class I) Signs of airway obstruction or respiratory failure?

• Obtain IV access (Comatose with hypoventilation, significant airway edema, upper
• Perform fingerstick glucose, lactate, troponin, ECG airway blistering, severe respiratory distress, or stridor)
• Consider x-ray
NO YES

• Perform primary and

secondary surveys Intubate (Class II)
• Consider CO/CN toxicity

Concern for CO toxicity? Concern for CN toxicity?

(Elevated COHb and/or symptoms: headache, loss of (Headache, loss of consciousness, altered mental status,
NO
consciousness, nausea/vomiting, dizziness, altered mental hyperventilation, elevated lactate, soot in oropharynx,
status, cardiac ischemia, hemodynamic instability) seizure, hypotension, bradycardia)

YES YES

• Continue 100% oxygen (Class I) • Administer hydroxocobalamin 5 g IV over 15 minutes (Class I)

• Consider transfer to burn center (Class II) Repeat once, if needed
• Consider hyperbaric oxygen therapy (Class III) • Consider transfer to burn center (Class I)

Presence of deep facial/neck burns,

large cutaneous burns > 40%TBSA,
or suspicion of pulmonary injury?

NO YES

• Transfer to monitored burn unit bed (Class I)

Consider observation in monitored setting (Class II)
• Consider further diagnostic studies, if available: laryngoscopy,
CT, bronchoscopy (Class II)
• Continue oxygen
• Consider nebulizers, suctioning, therapeutic bronchoscopy
(Class II)
• Consider inhaled adjunctive therapies (Class III)

Abbreviations: CN, cyanide; CO, carbon monoxide; COHb, carboxyhemoglobin; CT, computed tomography; ECG, electrocardiogram; IV, intravenous; TBSA,
total body surface area.

For Class of Evidence definitions, see page 13.

Copyright © 2018 EB Medicine. All rights reserved. 12 Reprints: www.ebmedicine.net/empissues

 In addition to being an effective tool to evalu- tissue plasminogen activator) in preclinical models
ate inhalation injury severity,66 bronchoscopy can show significantly lower pulmonary congestion,
also be used therapeutically to suction particulate decreased edema, decreased airway pressures, and
matter, secretions, and fibrin casts.8,29 Patients with decreased airway obstruction.70
burn TBSA of 30% to 59% with SII and pneumonia Prophylactic antibiotics have not been found
who received therapeutic bronchoscopy were found to be useful in preventing infection in burn pa-
to have decreased time on the ventilator, decreased tients,29,71 and instead increase the risk for exposure
ICU stay, and decreased hospital cost.66 to multidrug-resistant organisms. Further complicat-
ing the picture, it is difficult to distinguish burn-
Medical Adjuncts induced systemic inflammatory response syndrome
The use of bronchodilators has recently increased from sepsis, making it harder to decide when to
in the treatment of SII. Inhaled albuterol relaxes initiate antibiotic therapy. Broad-spectrum antibiot-
smooth muscle, decreases airway pressure, and ics should be initiated if suspicion for pneumonia is
improves PaO2/FiO2 in ovine models.50 Inhaled high.
epinephrine is thought to decrease hyperemia and Likewise, there is no conclusive evidence sup-
edema, aid bronchodilation, and lower airway pres- porting the use of corticosteroids to reduce airway
sures.1,5 Similarly, muscarinic receptor antagonists edema.13,72 In line with findings from older research,
such as tiotropium prevent airway smooth-muscle a prospective study evaluating 96 patients with
constriction. isolated inhalation injury found no improvement in
Inhaled nitric oxide, which is a potent vasodila- pulmonary function tests in those treated with corti-
tor, is another adjunct in SII treatment. Vasodilation costeroids versus those not treated.72 Corticosteroid
leads to decreased ventilation/perfusion mismatch, use is not recommended at this time.
decreased shunting, lower incidence of pulmonary
hypertension, and has proven promising in animal Treatment for Carbon Monoxide Poisoning
models.4 Some burn patients have benefited from The half-life of COHb on room air is 250 minutes,
inhaled nitric oxide with improved oxygenation at and on 100% oxygen, this is reduced to 40 to 60
doses of 5 to 20 ppm, and a trial of inhaled nitric ox- minutes.4,55 Hyperbaric oxygen therapy (HBOT)
ide can be considered when all other measures have (100% oxygen delivered at > 1.4 atm) further reduces
failed.67,68 the half-life of COHb, and has been used to treat
A single-center retrospective study showed CO toxicity.1,4,34 In one study, it was found to be
statistically significant survival benefit in SII patients beneficial, as the treatment group was found to have
when they were treated with inhaled heparin and lower rates of cognitive sequelae at 6 weeks and at
N-acetylcysteine (NAC).69 Anticoagulants are used 12 months after CO poisoning.73 A 2011 Cochrane
to decrease formation of fibrin casts, and NAC is review found the evidence for use of HBOT in treat-
a mucolytic and reducing agent that, theoretically, ment of CO to be inconclusive,74 and there are no
minimizes oxidative damage. Currently, a multi- established guidelines for its application. The 2017
center randomized controlled trial called HEPBURN American College of Emergency Physicians (ACEP)
is underway to assess the effects of nebulized Clinical Policy does not take a definitive stance on
heparin versus placebo in SII, which should provide recommending HBOT over normobaric therapy, but
further clarification. it does make a Level B recommendation that HBOT
Other combinations of aerosolized anticoagu- or high-flow normobaric therapy should be used
lants (eg, recombinant human antithrombin and in acute CO poisoning cases.75 Although, to date,

Class Of Evidence Definitions

Each action in the clinical pathways section of Emergency Medicine Practice receives a score based on the following definitions.
Class I Class II Class III Indeterminate
• Always acceptable, safe • Safe, acceptable • May be acceptable • Continuing area of research
• Definitely useful • Probably useful • Possibly useful • No recommendations until further
• Proven in both efficacy and effectiveness • Considered optional or alternative treat- research
Level of Evidence: ments
Level of Evidence: • Generally higher levels of evidence Level of Evidence:
• One or more large prospective studies • Nonrandomized or retrospective studies: Level of Evidence: • Evidence not available
are present (with rare exceptions) historic, cohort, or case control studies • Generally lower or intermediate levels of • Higher studies in progress
• High-quality meta-analyses • Less robust randomized controlled trials evidence • Results inconsistent, contradictory
• Study results consistently positive and • Results consistently positive • Case series, animal studies, • Results not compelling
compelling consensus panels
• Occasionally positive results

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 © 2018 EB Medicine. 1-800-249-5770. No part of this publication may be reproduced in any format without written consent of EB Medicine.

March 2018 • www.ebmedicine.net 13 Copyright © 2018 EB Medicine. All rights reserved.

no large prospective studies exist, a recent retro-
spective Taiwanese study of approximately 25,000
patients concluded that HBOT was associated with
decreased short-term and long-term mortality, par-
ticularly in younger patients (aged < 20 years) and
patients with acute respiratory failure.76 Therefore,
we recommend either HBOT or normobaric 100%
oxygen via nonrebreather mask or advanced airway4
as first-line therapy for CO treatment. Historically,
it was thought that indications for HBOT included
neurologic signs, cardiac ischemia, or syncope, and
elevated COHb level, with lower thresholds for
pregnant patients and those with cardiac history. Intubation can cause complications such as
Although this is not definitively supported by cur-
rent literature, these indications remain the most
logically applicable at this time. If uncertainty exists,
we recommend discussion with the local HBOT cen-
ter, medical toxicologist, or regional poison center.
For pregnant patients, HBOT should continue to
be strongly considered due to potential harm to the
fetus, although, again, there is no definitive evidence
to support this at this time.
Treatment for Cyanide Poisoning
Hydroxocobalamin is now the first-line therapy for
CN toxicity, and has been found to be as effective as
other antidotes, with lower rates of pneumonia de-
velopment and fewer ventilator days.77 A naturally
occurring analog of vitamin B12, hydroxocobalamin
binds to CN to form cyanocobalamin, which is
nontoxic and renally excreted.1,27 Treatment should
be initiated in any patient with severe inhalation
injury, unexplained hypotension, altered mental
status, elevated lactic acid, or high mixed venous
O2.8 The standard dose is 5 g IV over 15 min, with
one repeat dose, if necessary. Older therapies, such
as sodium nitrite given with sodium thiosulfate, are
now considered to be second-line therapy due to
increased risk of hypotension and methemoglobin-
emia.1,4,26 If hydroxocobalamin is not available and
CO inhalation has been ruled out, sodium nitrite
(300 mg IV) plus sodium thiosulfate (12.5 g IV) can
be used. If hydroxocobalamin is not available and
CO inhalation is present, sodium thiosulfate can be
used alone, but this is an inferior alternative, as it is
known that it does not penetrate intracellularly in
cerebral tissue.
Complications
Pneumonia is a common complication of inhalation
injury, due to direct mucosal injury and the result-
ing inflammatory response.1 Pneumonia was found
to be present in up to 50% of patients with inhala-
tion injury requiring urgent intubation.78 It has been
shown to independently increase burn mortality by
40%.5 When identified, treatment with antibiotics is
recommended.
Another common complication is airway and
Copyright © 2018 EB Medicine. All rights reserved. 14
pulmonary edema, often exacerbated by aggressive
IV fluid resuscitation. ALI is described as the onset
of decreased oxygen exchange and is defined by
PaO2/FiO2 < 300. More severe, ARDS is defined as
PaO2/FiO2 < 200. ALI and ARDS are characterized
by diffuse alveolar damage due to cytokine release
and increased permeability of the alveolar capillary
endothelium.59 Up to one-third of burn patients
require intubation, and in these patients, the preva-
lence of ARDS ranges from 33% to 54%, with in-
creasing mortality correlating to increasing severity
of ARDS.79  
barotrauma, suction catheter-related injuries, and
infectious complications such as tracheobronchitis or
ventilator-associated pneumonia.54 Ventilator-asso-
ciated pneumonia is associated with approximately
10% mortality, and is seen in 9% to 27% of ventilated
burn patients.10
Endobronchial polyps can form acutely or in a
delayed fashion, and tracheal stenosis is a delayed
complication that can develop months after the
injury. Other complications include bronchiectasis,
bronchiolitis, and vocal cord dysfunction.1 (See
Table 6.) Long-term follow-up involving pulmonary
function tests and laryngeal examinations allow for
detection and treatment of these complications.29
Special Populations
Pregnant Patients
Pregnant women were excluded from many of the
studies in our literature search, so there is a paucity
of data on which to base management decisions. An
important consideration in pregnancy is that cer-
tain medications cross the placenta, and this must
be kept in mind regarding treatment. The pregnant
patient should be regarded as 2 patients; however,
often the best way to protect the fetus is to optimize
maternal care. In the pregnant woman, maternal
CO poisoning and hypoxemia contributes to fetal
hypoxia, and the level of COHb in the fetus is 10% to
Table 6. Long-Term Complications of Smoke
Inhalation Injury
• Bronchiectasis
• Bronchiolitis obliterans
• Endobronchial polyposis
• Main bronchial stenosis
• Tracheal stenosis
• Vocal cord paresis, fixation, fusion; arytenoid dislocation
• Dysphonia (various causes)
Reprinted from Clinics in Plastic Surgery. Volume 36, Issue 4.
Leopoldo C. Cancio. Airway management and smoke inhalation injury
in the burn patient. Pages 555-567. Copyright 2009, with permission
from Elsevier.
Reprints: www.ebmedicine.net/empissues
15% higher than in the mother. Elimination of CO is
also slower in fetal blood. Due to the tendency of CO Figure 5. Imaging of Tracheal Wall Thickening
to accumulate in fetal blood, maternal COHb levels on X-Ray, Ultrasound, and Computed
are not a reliable means of evaluating fetal levels for Tomography
clinical therapeutic decisions.80 Although there is
concern for oxygen toxicity to the fetus with pro-
longed therapy, short-term HBOT can be considered
in pregnant women with elevated COHb, especially
if the fetus shows signs of distress.1 Because mater-
nal CO levels are not reliable to evaluate fetal COHb,
at this time there are no definitive recommendations
for cut-off levels for HBOT. Some authors suggest
delivery of the fetus if > 26 weeks’ gestation, as the
fetus would then be able to benefit from direct treat-
ment with 100% oxygen. However, this is a decision
that should be made in conjunction with the patient,
obstetrician, burn center, and hyperbaric center.80 A

Geriatric Patients
The elderly are at greater risk for mortality when
suffering from burns and/or inhalation injury, as
advanced age is one of the strongest independent
predictors of mortality in both populations, along
with %TBSA and the presence of inhalation in-
jury.81-83 The threshold to transport these patients as
soon as possible to burn centers should be low, so
they can receive appropriate care in the face of a life-
threatening disease.

Controversies and Cutting Edge B

Extracorporeal Membrane Oxygenation

The use of extracorporeal membrane oxygenation
(ECMO) in inhalation injury is promising, as it al-
lows for oxygenation and removal of CO2 without
the need to increase ventilator settings, and it al-
lows the lungs to heal. While there are case reports
of individuals with burn injuries who survived
after ECMO, the data are limited, and evidence is
inconclusive at this time.84 A 2017 retrospective
review identified 30 patients in the National Burn
Repository who received ECMO, and matched
them to those who did not, and found the ECMO
cohort was sicker, with significantly higher rates of
comorbidities, concomitant major thoracic trauma, C
pneumonia, acute renal failure, sepsis, ICU stay,
and mortality. The morbidity and mortality rates A: Chest x-ray, taken on admission after inhalation injury. Arrows point
were similar to those reported by the Extracorpore- out narrowing of the trachea.
al Life Support Organization. ECMO remains a pos- B: Transverse view of the tracheal ultrasound, taken on admission.
sible therapeutic option for a subset of inhalation Arrows point out hypoechoic thickening of the tracheal wall at the level
injury patients, especially when other treatment adjacent to the thyroid isthmus. T indicates the thyroid gland.
modalities have failed.85 C: Computed tomography scan, performed on admission. Arrows point
out thickening of the tracheal wall. T indicates the thyroid gland.
Point-of-Care Ultrasound Toru Kameda, Masato Fujita. Point-of-care ultrasound detection
of tracheal wall thickening caused by smoke inhalation. Critical
Though not well studied, point-of-care ultrasound
Ultrasound Journal. 2014;6(1):11. Used with permission by Creative
(POCUS) may be a promising tool to assist in diag- Commons Attribution License 4.0. Available at: https://www.ncbi.nlm.
nosis and management of SII. (See Figure 5.) A 2014 nih.gov/pmc/articles/PMC4105106/. Copyright 2014 Kameda and
case report described the use of POCUS to evaluate Fujita; licensee Springer.

March 2018 • www.ebmedicine.net 15 Copyright © 2018 EB Medicine. All rights reserved.

 Risk Management Pitfalls for Smoke Inhalation Injury
1. “The O2 saturation was normal, so I didn’t con-
sider CO toxicity.”
The standard pulse oximeter uses a wavelength
also absorbed by COHb, and it is often normal
in CO toxicity. For this reason, it is important
to obtain a COHb level via blood CO-oximetry.
Even with this value, significant toxicity
can occur at normal or near-normal levels,
depending on the timing of the sample and prior
administration of oxygen.
2. “The patient was hypoxic, so I set the vent set-
tings to volume control, FiO2 100%.”
Mechanical ventilation is an independent
predictor of mortality and its use should be
tailored to minimize the inflammatory effects it
elicits. High-frequency percussive ventilation
has emerged as a frequently utilized mode of
ventilation, especially in the burn unit. Initially
in the ED, low tidal volumes of 4 to 5 mL/kg
of predicted body weight, with plateau airway
pressure < 30 cm H2O, are recommended. Other
possible recruitment measures in the face of
persistent hypoxia include PEEP and prone
positioning. Also, 100% O2 is toxic in relatively
short order.
3. “The patient had normal vitals and appeared
well, so I didn’t anticipate airway compromise.”
The onset of SII can occur in the absence of
clinical signs or symptoms, as laryngeal edema
can take 24 hours to develop. An extended
period of observation is therefore recommended,
and if any concerning signs or symptoms of
inhalation injury are present, the patient should
be admitted to a burn unit for close monitoring
and possible bronchoscopy.
4. “I sent the CN level to the lab, and planned on
treating if the level came back elevated.”
CN has a very short half-life, and hospitals often
do not have the appropriate laboratory resources
to obtain immediate levels. Therefore, CN
levels are not helpful in the clinical setting, and
empiric therapy with hydroxocobalamin should
be initiated if concern for CN toxicity exists.
5. “I assumed the patient’s hypoxia and respiratory
distress were due to smoke inhalation injury.”
Underlying pathology such as a pericardial
effusion or tamponade, pneumothorax, and
pulmonary or cardiac contusions may need to be
considered when evaluating patients with SII, as
the symptoms are often similar.
Copyright © 2018 EB Medicine. All rights reserved. 16
6. “When the patient presented with altered men-
tal status, I assumed it was due to hypoxia and
chemical toxicity.”
The approach to burn patients should be similar
to that of trauma patients, as concomitant
traumatic injury is common. Patients should be
assessed with a primary survey, followed by a
secondary survey. Once the patient is stabilized,
occult trauma should be considered in the
workup of the patient, especially in the setting
of signs such as altered consciousness or pain.
7. “The initial chest x-ray was normal, so I wasn’t
concerned for SII.”
Chest x-rays should be obtained in patients
with inhalation injury to evaluate for other
etiologies, but the initial x-ray is often normal or
nonspecific. A negative x-ray is not sufficient to
rule out SII.
8. “The COHb level was only mildly elevated, so
I did not think CO toxicity was still a concern.”
Significant CO toxicity can be present with a
normal or near-normal COHb level, depending
on when the level was drawn and whether
oxygen was administered. Despite correction of
CO levels in the blood, cellular dysfunction can
persist long after initial exposure, and patients
with CO exposure require close monitoring and
extended follow-up.
9. “The patient was tachypneic and wheezing,
but he had a history of asthma, so I attributed
his symptoms to an asthma exacerbation.”
Signs such as tachypnea and wheezing,
along with others such as cough, dyspnea,
carbonaceous sputum, voice change, and
drooling are concerning for potential SII.
Underlying disorders such as acute asthma or
COPD exacerbation can present with similar
symptoms.
10. “The patient had only mild respiratory distress
initially, so I discharged him after 2 hours of
observation in the ED.”
Patients should be discharged from the ED only
if they are completely asymptomatic, without
concerning history for potential SII. Otherwise,
if any degree of inhalation injury is suspected,
the patient should be transferred to a burn center
and admitted for close monitoring and possible
bronchoscopic evaluation.
Reprints: www.ebmedicine.net/empissues
tracheal wall thickening, which was confirmed on
CT. 52 Transesophageal echocardiography has been
utilized in the ICU setting to guide IV fluid manage-
ment,86,87 and the extension of POCUS to evaluate
burn patients in the ED requires further study.
Disposition
The presence of inhalation injury is one of the
American Burn Association criteria for burn center
referral, so any patient with possible SII should be
transferred in an expeditious manner. Even if clini-
cal signs such as overt airway edema or hypoxia
are not present, if there is any concern for potential
inhalation injury based on history or other findings,
patients should be closely observed in a monitored
setting for 24 hours with a low threshold to intubate
if there is clinical worsening. Mucosal edema often
progresses and peaks over the course of 24 hours
after the burn, which makes close observation over
this time frame crucial.
Summary
Inhalation injuries are a prognostic indicator in
thermal burn patients, and they worsen morbidity
and mortality. A thorough history is key, and clinical
signs such as airway edema, carbonaceous sputum,
soot in the nares or oropharynx, facial burns and
edema, and singed nasal hairs can indicate potential
inhalation injury. Their absence, however, does not
exclude the possibility of SII, which can be insidi-
ous in onset. Mechanical ventilation is an indepen-
dent predictor of mortality, and can contribute to
ALI. Therefore, in patients without obvious need
for emergent intubation, the traditional approach
of prophylactic intubation could be replaced by
close observation in a monitored setting and pos-
sible bronchoscopic evaluation at 24 to 48 hours to
determine the degree of injury sustained and the
potential need for delayed intubation. In addition to
traditional diagnostic modalities such as CO-oxim-
etry and bronchoscopy, newer tests may be ben-
eficial in diagnosis including chest CT, lactate, and
troponin. Caution must be used when resuscitating
inhalation injury patients, as over-aggressive IV
fluid administration can lead to worsening airway
edema. Although HBOT remains controversial in the
treatment of CO toxicity, either HBOT or 100% nor-
mobaric oxygen remain the mainstays of treatment.
When any suspicion for CN toxicity exists, hydroxo-
cobalamin has replaced older kits as the first-line
therapeutic agent.
March 2018 • www.ebmedicine.net
Case Conclusions
Your first patient, the 48-year-old man who was short of
breath with carbonaceous sputum, soot in his nares, and
tachypneic and mildly hypoxic was immediately placed
on 100% oxygen, with rapid improvement in his oxygen-
ation. He was given inhaled albuterol, and his wheezing
improved. You considered BiPAP, but due to his marked
improvement, it was not needed. His COHb level was
3%, and he denied any symptoms such as nausea, dizzi-
ness, or headache. Troponin was negative. You contacted
the local burn center for transfer, as he would require close
monitoring and possible diagnostic bronchoscopy.
For the 72-year-old woman who was obtunded with
burns 30% TBSA, you decided to intubate due to her
significant hypoxia and obtundation. She was initially
placed on volume control with a low tidal volume of 6 mL/
kg at 100%, but due to difficulty with oxygenation, her
PEEP was increased to 8 mL, with some improvement.
She was borderline hypotensive, so you administered 1
L of normal saline, with moderate improvement in her
blood pressure. The patient was found to have a COHb
level of 16%, and her son stated she was not a smoker.
You empirically administered hydroxocobalamin 5 g IV x
1, and her blood pressure improved even further. Due to
her altered mental status and your inability to perform a
thorough history, you ordered a CT of her head, cervical
spine, chest, abdomen, and pelvis, which did not show
any traumatic injury. The burn center was contacted for
transfer and further management.
For the third patient, the 27-year-old pregnant
woman, her initial vital signs were normal, but you im-
mediately placed her on 100% nonrebreather mask. Other
vital signs were stable, and after a thorough primary and
secondary exam, you determined that she did not suffer
other traumatic injuries. Her symptoms improved, but
you obtained a COHb level of 17%. You called the local
hyperbaric oxygen center, and due to her pregnancy and
elevated COHb level, the decision was made for hyperbar-
ic oxygen therapy, after discussion with the patient and
her obstetrician.
Time and Cost-Effective Strategies
• Do not prophylactically intubate every patient
with facial burns. Studies evaluating broncho-
scopic findings in prophylactically intubated pa-
tients with facial burns are often not consistent
with severe SII findings; therefore, unnecessary
intubations could be potentially avoided.
• Consider a trial of NIPPV for patients with
milder symptoms without contraindications.
A period of observation in a closely monitored
setting with possible diagnostic bronchoscopy
in the setting of worsening symptoms is ac-
ceptable, in order to avoid iatrogenic effects of
mechanical ventilation.
• Treat patients empirically with hydroxocobala-
17 Copyright © 2018 EB Medicine. All rights reserved.
 min for possible CN toxicity. Symptoms of CN
toxicity are often nonspecific, while effects of
untreated toxicity can be severe. Hydroxoco-
balamin has proven beneficial, without serious
adverse reactions.
• Carefully consider the need to transfer to a
hyperbaric center. HBOT remains controversial
since conclusive evidence is lacking, and the
most recent ACEP Clinical Policy recommends
either 100% normobaric oxygen or hyperbaric
oxygen.
Key Points
• SII remains a largely clinical diagnosis which
can be aided by tests such as CT, laryngoscopy,
and bronchoscopy.
• Emergency clinicians must maintain a high
index of suspicion for concomitant traumatic in-
juries and other causes for altered mental status.
• Management is mostly supportive, including
close monitoring of the airway status, supple-
mental oxygen, and careful monitoring of IV
fluid resuscitation.
• Close observation is warranted, as initially
subtle signs and symptoms may progress.
• Clinicians should have a low threshold to treat
for concomitant CO and CN toxicities when
these toxic exposures are suspected.
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Evidence-based medicine requires a critical ap-
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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 is
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45. Garner JP, Jenner J, Parkhouse DA. Prediction of upper air-
way closure in inhalational injury. Mil Med. 2005;170(8):677-
682. (Review article)
46. Albright JM, Davis CS, Bird MD, et al. The acute pulmonary
inflammatory response to the graded severity of smoke in-
halation injury. Crit Care Med. 2012;40(4):1113-1121. (Prospec-
tive observational study; 60 patients)
47. Mosier MJ, Pham TN, Park DR, et al. Predictive value of
bronchoscopy in assessing the severity of inhalation injury.
J Burn Care Res. 2012;33(1):65-73. (Retrospective review; 32
patients)
48. Endorf FW, Gamelli RL. Inhalation injury, pulmonary
perturbations, and fluid resuscitation. J Burn Care Res.
2007;28(1):80-83. (Retrospective chart review; 80 patients)
49. Spano S, Hanna S, Li Z, et al. Does bronchoscopic evaluation
of inhalation injury severity predict outcome? J Burn Care
Res. 2016;37(1):1-11. (Retrospective review; 160 patients)
50. Palmieri TL. Inhalation injury: research progress and needs. J
Burn Care Res. 2007;28(4):549-554. (Review article)
51. Woodson LC. Diagnosis and grading of inhalation injury. J
Burn Care Res. 2009;30(1):143-145. (Review article)
52. Kameda T, Fujita M. Point-of-care ultrasound detection of
tracheal wall thickening caused by smoke inhalation. Crit
Ultrasound J. 2014;6(1):11-11. (Case report; 1 patient)
53. Muehlberger T, Kunar D, Munster A, et al. Efficacy of fiber-
optic laryngoscopy in the diagnosis of inhalation injuries.
Arch Otolaryngol Head Neck Surg. 1998;124(9):1003-1007.
(Prospective cohort study; 11 patients)
54. Cochran A. Inhalation injury and endotracheal intubation. J
Burn Care Res. 2009;30(1):190-191. (Review article)
55. McCall JE, Cahill TJ. Respiratory care of the burn patient. J
Burn Care Rehabil. 2005;26(3):200-206. (Review article)
56. Dries DJ. Key questions in ventilator management of the
burn-injured patient (second of two parts). J Burn Care Res.
2009;30(2):211-220. (Review article)
57. You K, Yang HT, Kym D, et al. Inhalation injury in burn
patients: establishing the link between diagnosis and prog-
nosis. Burns. 2014;40(8):1470-1475. (Prospective observation
study; 192 patients)
58. Mackie DP. Inhalation injury or mechanical ventila-
tion: which is the true killer in burn patients? Burns.
2013;39(7):1329-1330. (Editorial)
59. Peck MD, Koppelman T. Low-tidal-volume ventilation as
a strategy to reduce ventilator-associated injury in ALI and
ARDS. J Burn Care Res. 2009;30(1):172-175. (Review article)
60. Dries DJ. Key questions in ventilator management of the
burn-injured patient (first of two parts). J Burn Care Res.
2009;30(1):128-138. (Review article)
61. Chung KK, Wolf SE, Renz EM, et al. High-frequency percus-
sive ventilation and low tidal volume ventilation in burns: a
randomized controlled trial. Crit Care Med. 2010;38(10):1970-
1977. (Randomized control trial; 62 patients)
62. Reper P, Wibaux O, Van Laeke P, et al. High frequency per-
cussive ventilation and conventional ventilation after smoke
inhalation: a randomised study. Burns. 2002;28(5):503-508.
(Prospective randomized study; 35 patients)
63. Allan PF, Osborn EC, Chung KK, et al. High-frequency per-
cussive ventilation revisited. J Burn Care Res. 2010;31(4):510-
520. (Review article)
64. Hall JJ, Hunt JL, Arnoldo BD, et al. Use of high-frequency
percussive ventilation in inhalation injuries. J Burn Care Res.
2007;28(3):396-400. (Retrospective review; 122 patients)
65. Hale DF, Cannon JW, Batchinsky AI, et al. Prone positioning
improves oxygenation in adult burn patients with severe
acute respiratory distress syndrome. J Trauma Acute Care
Surg. 2012;72(6):1634-1639. (Prospective study; 18 patients)
66. Carr JA, Phillips BD, Bowling WM. The utility of bronchos-
copy after inhalation injury complicated by pneumonia in
19 Copyright © 2018 EB Medicine. All rights reserved.
 burn patients: results from the National Burn Repository. J
Burn Care Res. 2009;30(6):967-974. (Systematic review; 624
patients)
67. Kallet RH. Adjunct therapies during mechanical ventilation:
airway clearance techniques, therapeutic aerosols, and gases.
Respir Care. 2013;58(6):1053-1073. (Review article)
68. Sheridan RL, Hess D. Inhaled nitric oxide in inhalation
injury. J Burn Care Res. 2009;30(1):162-164. (Review article)
69. Miller AC, Rivero A, Ziad S, et al. Influence of nebulized un-
fractionated heparin and N-acetylcysteine in acute lung injury
after smoke inhalation injury. J Burn Care Res. 2009;30(2):249-
256. (Prospective comparative study; 30 patients)
70. Miller AC, Elamin EM, Suffredini AF. Inhaled anticoagula-
tion regimens for the treatment of smoke inhalation-associ-
ated acute lung injury: a systematic review. Crit Care Med.
2014;42(2):413-419. (Systematic review; 27 references)
71. Liodaki E, Kalousis K, Schopp BE, et al. Prophylactic antibi-
otic therapy after inhalation injury. Burns. 2014;40(8):1476-
1480. (Retrospective review; 58 patients)
72. Cha SI, Kim CH, Lee JH, et al. Isolated smoke inhalation in-
juries: acute respiratory dysfunction, clinical outcomes, and
short-term evolution of pulmonary functions with the effects
of steroids. Burns. 2007;33(2):200-208. (Prospective follow-
up study; 96 patients)
73. Weaver LK, Hopkins RO, Chan KJ, et al. Hyperbaric oxy-
gen for acute carbon monoxide poisoning. N Engl J Med.
2002;347(14):1057-1067. (Prospective randomized trial; 228
patients)
74.* Buckley NA, Juurlink DN, Isbister G, et al. Hyperbaric oxy-
gen for carbon monoxide poisoning. Cochrane Database Syst
Rev. 2011Apr 13(4):CD002041. (Systematic review; 6 trials,
1361 patients)
75.* Wolf SJ, Maloney GE, Shih RD, et al. Clinical policy: critical
issues in the evaluation and management of adult patients
presenting to the emergency department with acute carbon
monoxide poisoning. Ann Emerg Med. 2017;69(1):98-106.
(ACEP clinical policy)
76. Huang CC, Ho CH, Chen YC, et al. Hyperbaric oxygen
therapy is associated with lower short- and long- term
mortality in patients with carbon monoxide poisoning.
Chest. 2017;3692(17):30723-7. (Retrospective review; 25,737
patients)
77. Nguyen L, Afshari A, Kahn SA, et al. Utility and outcomes
of hydroxocobalamin use in smoke inhalation patients.
Burns. 2017;43(1):107-113. (Retrospective chart review; 273
patients)
78. Eckert MJ, Wade TE, Davis KA, et al. Ventilator-associated
pneumonia after combined burn and trauma is caused by
associated injuries and not the burn wound. J Burn Care
Res. 2006;27(4):457-462. (Retrospective chart review; 3388
patients)
79. Belenkiy SM, Buel AR, Cannon JW, et al. Acute respiratory
distress syndrome in wartime military burns: application of
the Berlin criteria. J Trauma Acute Care Surg. 2014;76(3):821-
827. (Retrospective chart review; 201 patients)
80. Roderique EJ, Gebre-Giorgis AA, Stewart DH, et al. Smoke
inhalation injury in a pregnant patient: a literature review
of the evidence and current best practices in the setting of a
classic case. J Burn Care Res. 2012;33(5):624-633. (Literature
review)
81. Colohan SM. Predicting prognosis in thermal burns with
associated inhalational injury: a systematic review of
prognostic factors in adult burn victims. J Burn Care Res.
2010;31(4):529-539. (Systematic review; 13 studies)
82. Edelman DA, White MT, Tyburski JG, et al. Factors affecting
prognosis of inhalation injury. J Burn Care Res. 2006;27(6):848-
853. (Retrospective chart review; 829 patients)
83. Kadri SS, Miller AC, Hohmann S, et al. Risk factors for in-hospi-
tal mortality in smoke inhalation-associated acute lung injury:
data from 68 United States hospitals. Chest. 2016;150(6):1260-
Copyright © 2018 EB Medicine. All rights reserved. 20
1268. (Retrospective cohort study; 769 patients)
84. Asmussen S, Maybauer DM, Fraser JF, et al. Extracorporeal
membrane oxygenation in burn and smoke inhalation injury.
Burns. 2013;39(3):429-435. (Systematic review, meta-analy-
sis; 29 studies)
85. Nosanov LB, McLawhorn MM, Vigiola Cruz M, et al. A
national perspective on ECMO utilization in patients with
burn injury. J Burn Care Res. 2017;39(2):10-14. (Retrospective
review; 30 patients)
86. Held JM, Litt J, Kennedy JD, et al. Surgeon-performed
hemodynamic transesophageal echocardiography in the
burn intensive care unit. J Burn Care Res. 2016;37(1):e63-e68.
(Retrospective observational study; 11 patients)
87. Maybauer MO, Asmussen S, Platts DG, et al. Transesopha-
geal echocardiography in the management of burn patients.
Burns. 2014;40(4):630-635. (Systematic review)
CME Questions
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below with your smartphone or visit
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1. Regarding smoke inhalation injury (SII),
which of the following is TRUE?
a. SII does not increase IV fluid requirements
when resuscitating a burn patient.
b. SII is an independent predictor of mortality.
c. Smoke inhalation, by itself, is an indication
for transfer to a burn center.
d. Criteria for diagnosing SII are based on
standardized bronchoscopic findings.
2. When evaluating a patient with SII, which of
the following is TRUE?
a. Primary and secondary survey must be
delayed until diagnosis is made.
b. Trauma is not usually a concern in patients
with SII.
c. Altered mental status in patients with SII is
always secondary to toxicities.
d. Patients with respiratory symptoms could
have aspiration pneumonia, acute asthma
or COPD exacerbation, or acute respiratory
distress syndrome.
Reprints: www.ebmedicine.net/empissues
3. Which of the following is appropriate prehos-
pital care for patients with possible SII?
a. If intubation is difficult due to airway
edema, do not place a laryngeal mask
airway, as this can cause additional swelling.
b. Hold off on administering 100% O2
immediately, as this can alter levels of CO
and make diagnosis more difficult.
c. Intubate the patient if there are any facial
burns, as this is indicative of severe SII.
d. Prehospital administration of
hydroxocobalamin is appropriate when
acute cyanide poisoning is suspected.
4. Regarding CO toxicity, which of the following
is correct?
a. Hyperbaric oxygen therapy is standard
therapy for patients with confirmed or
suspected CO toxicity.
b. Normobaric 100% is not helpful, as the half-
life of COHb is not altered significantly.
c. Lactate levels can be useful when evaluating
degree of CO toxicity.
d. Side effects from CO toxicity resolve once
COHb levels return to normal.
5. In the setting of SII, which of these diagnostic
tests is not clinically useful in a timely fash-
ion?
a. COHb level 9. When treating pregnant women who have
b. Lactic acid
c. Cyanide level a. Care of the fetus must be optimized first, as
d. Troponin
 the fetus has higher oxygen requirements.
6. Bronchoscopy, the best available test for evalu-
ation and diagnosis of inhalation injury:
a. Is based on a composite of CT scan findings,
laboratory values, and bronchoscopic
findings.
b. Will include findings of mucosal erythema,
edema, ulceration, fibrin casts, or charred
tissue.
c. Should be performed routinely immediately
upon suspicion of inhalation injury.
d. Effectively evaluates both proximal and
distal airways.
March 2018 • www.ebmedicine.net
7. Regarding ventilation of patients with SII,
which of the following is TRUE?
a. Hypoxia is life-threatening and requires
adjustments to the ventilator, such as
high tidal volumes and increased plateau
pressures.
b. Any increase in positive end-expiratory
pressure (PEEP) is dangerous in patients
with inhalation injury, and should not be
implemented.
c. Mechanical ventilation is potentially
dangerous and can lead to acute lung injury.
d. Pressure control remains the best mode
of ventilation, and other modes are
discouraged.
8. Regarding treatment for inhalation injury:
a. Bronchodilators such as albuterol
and epinephrine do not help, as the
pathophysiology of SII is quite different
from other obstructive disorders.
b. Inhaled anticoagulants are thought to lessen
the formation of fibrin casts.
c. Prophylactic antibiotics help to prevent
infection and ventilator-associated
pneumonia.
d. Empiric corticosteroids help prevent
ventilator-associated lung injury.
been exposed to CO:
b. Maternal COHb levels are a reliable means
of evaluating fetal COHb levels.
c. The elimination of CO is faster in fetal
blood.
d. There are no definitive recommendations for
cut-off levels for hyperbaric oxygen therapy.
10. For elderly patients exposed to fires, which of
the following is TRUE?
a. Age is an independent risk factor for
mortality. 
b. Elderly patients manifest fewer symptoms
compared to young patients.
c. Age is an indication for hyperbaric oxygen
therapy.
d. Elderly patients have increased fluid
requirements compared to young patients.
21 Copyright © 2018 EB Medicine. All rights reserved.
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POINTS & PEARLS
Points & Pearls is your digest version of each month’s
Emergency Medicine Practice issue

PEARLS
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 Physician CME Information
Date of Original Release: March 1, 2018. Date of most recent review: February 10, 2018.
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Education (ACCME) to provide continuing medical education for physicians. This activity
6
October 201
ber 10 has been planned and implemented in accordance with the accreditation requirements and
tcomes
Num
Volume 18,

Survival Ou policies of the ACCME.

Optimizing
Author Educa tion,
P te Medical
, MD, FACE Undergradua School of
Julianna Jungsor and Director of Johns Hopkins University

tients With
Profes Medicine,
Associate

For Adult Pa Cardiac Arrest

of Emergency
Department

Credit Designation: EB Medicine designates this enduring material for a maximum of 4 AMA PRA
MD
Baltimore,
Medicine,

Nontraumatic
wers
Peer Revie
Medical
Brady, MD
Chair,
Medicine;

, Univer
William J. Emergency Medicine and al Director, Emergency e, VA
Professor of
Emergency
Response
Comm ittee; Medic
sity of Virgini
a Medical
r, Charlottesvill
Cente Category 1 Credits™. Physicians should claim only the credit commensurate with the extent of
Abstract Management Health
significantly is, MD, FACE
P sity of Florida

their participation in the activity.

ine, Univer Research,
be improved matic Faheem Guirgsor of Emergency MedicMedicine, Division of
iac arrest can syste Profes of Emergency
ival after card resuscitative care. This ival Assistant Department
Patient surv tive improve surv Jacksonville,
pt and effec factors that defi- Jacksonville,
FL
with prom life support and rapid
zes the basic on technique successfully
ACEP Accreditation: Emergency Medicine Practice is approved by the American College of
CME Objec
tives able to:
review analy ding chest compressi should be
, inclu For patie nts who are tial. Tar- compl etion of this
article, you
uality basic life suppo
rt.
ced
outcome rhythms. care is essen nts Upon
elements of
high-q ines for advan
brillation of
shockable esuscitation patie Describe the basis and
current guidel
nsive postr ded for all
1.
evidentiary

Emergency Physicians for 48 hours of ACEP Category I credit per annual subscription.
ng
d, comprehe recommen en- Discuss the .
itoring of oxyg iac 2. life support interventions erations in postresuscita
tion care followi
resuscitate agement is
erature man addition to careful mon card tial consid
geted temp in agement of Describe essen neous circula
tion.
ols that may
be
rema in comatose, card iac rhythm. Man y emb olism , 3.
restora tion of sponta
rd resusc itation protoc
who and y, pulmonar standa
odynamics, cations to situations.
as pregnanc es, hypothermia, and
AAFP Accreditation: This Enduring Material activity, Emergency Medicine Practice, has been
List modifi resuscitation
ation, hem nces such 4.
ered in special
Inform ation”
msta ic caus consid
cian CME
arrest in circu and other toxicolog , see “Physi
dose . ing this activity back page.
opioid over mia are also reviewed Prior to beginn on the
coronary ische rs
r, MD
Robert Schille ent of Family Medicin
Internation
e, Peter Camer
al Edito
on, MD
Alfred
reviewed and is acceptable for credit by the American Academy of Family Physicians. Term
Director, The Centre,

of approval begins 07/01/2017. Term of approval is for one year from this date. Physicians
Chair, Departm Senior Academic
e, MD Medical Center; and Trauma
Eric Legom ncy Medicin
e, Beth Israel Emergency ity, Melbou
rne,
Chief of Emerge or of Medicine and Monash Univers
MD Hospital; Profess Faculty, Family School of
Daniel J. Egan, Department King’s County ncy Medicine, SUNY Community
Health, Icahn
New York,
NY Australia
Professor, Mount Sinai,
hief Associate e, Program Clinical Emerge Medicine, Medicine at e, MD

should claim only the credit commensurate with the extent of their participation in the activity.
ncy Medicin College of
Editor-In-C, MD, FACEP of Emerge ncy Medicin
e
Downstate , MD, FACEP
Giorgio Carbon ent of Emergency
Andy Jagoda Chair, Department
of Director, Emerge Sinai St. Luke's Brooklyn, NY Scott Silvers ent of Emergency Chief, Departm le Gradenigo,
Mount FL e Ospeda
Professor
and
Icahn School l Residency, NY MD Chair, Departm Clinic, Jacksonville, Medicin
Medicine, New York, Keith A. Marill, , Department of Medicine, Mayo Torino, Italy
Emergency Medica
Mount Sinai, l, New Roosevelt, ch Faculty ity FACEP s, MD
e at PhD Resear e, Univers MD, FACP, Peeter

Approved for 4 AAFP Prescribed credits.

of Medicin Genes, MD, Medicin Slovis, Suzanne Y.G. cy
Sinai Hospita Nicholas ent of Emergency Medical Center, Corey M. ent Medicine Residen l,
Director, Mount or, Departm Chair, Departm Emergency
Assistant Profess e, Icahn School of Pittsburgh Professor and Medicine, Vanderbilt Teaching Hospita
York, NY e, TN Director, Haga Netherlands
hief Emergency
Medicin
Sinai, New Pittsburgh,
PA of Emergency l Center, Nashvill The
Editor-In-C e at Mount Pollack Jr.,
MA, MD, University Medica The Hague,
Associate MD, FACEP of Medicin Charles V. MD of Hugo Peralta, MD Services, Hospital
of York, NY Advisor for Ron M. Walls, Chair, Department
Kaushal Shah, Department FACEP FACEP of Emerge
ncy a
Professor, Gibbs, MD, and Senior ch and Professor
and
Brigham and l Chair Buenos Aires, Argentin

AOA Accreditation: Emergency Medicine Practice is eligible for up to 48 American

Associate Icahn School Michael A. Department Professor Medicine,
Medicine, and Chair, y Resear
InterdisciplinarDepartment of Emergency Harvard Medica Italiano,
Emergency Sinai, New Professor e, Carolinas Hospital, ul, MD
e at Mount ncy Medicin ity of North Clinical Trials, Sidney Kimmen
l
Women's Rojanasarntik
of Medicin of Emerge Medicine, , MA Dhanadol Emergency
Univers
Emergency School, Boston Physician,
York, NY Medical Center, of Medicine, Chapel of Thomas Jefferso Attending Chulalo ngkorn
Carolina School Medical College lphia, PA Editors Medicine,
King Red Cross,
Editorial Board Critical Care Hospital, Thai

Osteopathic Association Category 2-A or 2-B credit hours per year.

Philade
Hill, NC University, Memorial of Medicin
e,
, MD, FACEP MPH MD, FACEP Thailand
Saadia Akhtar,
MD
Department
of Radeos, MD, Knight IV, ncy Thailand; Faculty University,
Professor,
A. Godwin
Dean Steven or and Chair, Departm nt
ent Michael S. or of Emerge
ncy William A. of Emerge
Associate Associate Professor Medical Chulalongkorn
Medicine, Profess Assista Assistant Profess Medical College Associate Neurosurgery, r
Emergency on, ncy Medicine, e, Weill York; e and Thoma s, MD, MPH
Educati H.
te Medical of Emerge ion Educat
ion, Medicin
University,
New Medicin
Midlevel Provide l Director,
Stephen ncy
& Chair, Emergel Corp.,
for Gradua r, Emergency Dean, Simulat of Cornell ent of Director, EM te Medica Professor
Program Directo cy, Mount Sinai of Florida
COM- Director, DepartmYork Program, Associa ity of Hamad Medica
University Research Medicine,

Needs Assessment: The need for this educational activity was determined by a survey
FL New ICU, Univers , Qatar;
Medicine ResidenYork, NY Jacksonville, Medicine, Medical College
Jacksonville, Emergency , Flushing,
NY Neuroscience OH Weill Cornell hief,
Beth Israel,
New FACEP Cincinnati, Physician-in-CDoha, Qatar
Henry, MD, Hospital Queens Cincinnati, Emergency
Gregory L. ent of MPH rt, MD, FCCM l Hospital,
Brady, MD e or, Departm ity MD, MBA, e, Scott D. Weinga or of Emergency Hamad Genera
William J. ncy Medicin Clinical Profess Univers Ali S. Raja, Emergency Medicin
Professor
of Emerge l Medicine, Vice-Chair, l, Associate
Profess of ED
e; Chair, Medica ttee; Emergency School; CEO, General Hospita Director, Division of Medicine Edin Zelihic,
MD ncy

of medical staff, including the editorial board of this publication; review of morbidity and
and Medicin n Medical ment, Massachusetts Medicine, ent of Emerge l,
Response
Commi of Michiga e Risk Assess Icahn School Head, Departm Hospita
Emergency r, Emergency Medical Practic MI Boston, MA Critical Care, New York, NY Leopoldina
MD, FACEP
, Sinai, Medicine, y
Medical DirectoUniversity of Virginia Inc., Ann Arbor, Rogers , at Mount nfurt, German
Robert L. rs Schwei
Management, Charlottesville, VA , MD, FACEP arch Edito
John M. Howell or of Emergency FAAEM, FACP or of Emergency
Medical Center, Senior Rese

mortality data from the CDC, AHA, NCHS, and ACEP; and evaluation of prior activities for
Profess
Clinical Profess Washington Assistant ity of BCPS
Brown III,
MD r The Univers i, PharmD,
Calvin A. Compliance, Medicine,
George DC; Directo Medicine, Medicine, James Damilin cist, Emergency
Physician Washington, School of
Director of Care University, Affairs, Best Practic
es, Maryland Clinical Pharma ’s Hospital and

Evidence-Based Management
and Urgent ic MD Joseph
Credentialing ent of Emerge
ncy of Academ l, Falls Baltimore, Room, St. Phoenix, AZ
Fairfax Hospita tti, MD, FACEP Medical Center,
Services, Departm and Women's Inc, Inova

emergency physicians.
Alfred Sacche Professor, MD
Toscano,
November 2016
Brigham Church, VA
Medicine, , MA MPH, MBA Assistant Clinical ncy Medicin
e,
Joseph D. of Emerge
ncy
Hospital, Boston Hoxhaj, MD, of Emerge Department
Department Chairman, Regional

Of Potassium Disorders In The

Shkelzen e, Baylor n University,
ncy Medicin San Ramon
ux, MD
Peter DeBlie Clinical Medicine, Chief of Emerge e, Houston, TX
Medicin
Thomas Jefferso
Philadelphia,
PA Medicine,
Medical Center,
San Ramon
, CA Volume 18, Number 11
Professor
of r College of Authors
Hospital Directo
Interim Public Medicine Services,

Emergency Department Target Audience: This enduring material is designed for emergency medicine physicians,
of Emerge
ncy
State Univers
ity Health John Ashurst, DO, MSc
Louisiana New Orleans, LA Director of Emergency Medicine
Science Center, Residency
Research, Duke Lifepoint
Conemaugh Memorial Medical
Center, Johnstown, PA
Shane R. Sergent, DO
Abstract Department of Emergency
Johnstown, PA
Benjamin J. Wagner, DO
Medicine, Conemaugh Memorial
Hospital, physician assistants, nurse practitioners, and residents.
Hypokalemia and hyperkalem Department of Emergency
ia are the most common elec- Medicine, Conemaugh Memorial

Goals: Upon completion of this activity, you should be able to: (1) demonstrate medical
trolyte disorders managed Johnstown, PA Hospital,
in the emergency departmen
diagnosis of these potentially t. The Peer Reviewers
life-threatening disorders
lenging due to the often vague is chal-
symptomatology a patient Camiron L. Pfennig, MD,

decision-making based on the strongest clinical evidence; (2) cost-effectively diagnose and
express, and treatment options may MHPE
Associate Professor of Emergency
may be based upon very little Medicine, University of South
data due to the time it may School of Medicine; Emergency
Medicine Residency Program
Carolina
take for laboratory values Greenville Health System, Director,
This review examines the to return. Greenville, SC

treat the most critical presentations; and (3) describe the most common medicolegal pitfalls
most current evidence with Corey M. Slovis, MD, FACP,
the pathophysiology, diagnosis, regard to FACEP
and management of potassium Professor and Chair, Department
disorders. In this review, classic of Emergency Medicine, Vanderbilt
University Medical Center,
paradigms, such as the use Nashville, TN
sodium polystyrene and the of CME Objectives
magnesium, are tested, and
routine measurement of serum
an algorithm for the treatment
potassium disorders is discussed. of
Upon completion of this article,
1. Identify the etiology of the
you should be able to:
depletion of potassium in patients
for each topic covered.
hypokalemia. with

Discussion of Investigational Information: As part of the journal, faculty may be presenting

2. Identify and manage the etiology
and underlying causes of hyperkalemia.
3. Describe the algorithmic management
hyperkalemia. of hypokalemia and
Prior to beginning this activity,

investigational information about pharmaceutical products that is outside Food and Drug
see “Physician CME Information”
Editor-In-Chief Daniel J. Egan, MD on the back page.
Andy Jagoda, MD, FACEP Associate Professor, Department Eric Legome, MD
Professor and Chair, Department Chief of Emergency Medicine, Robert Schiller, MD
Emergency Medicine, Icahn
of of Emergency Medicine, Program Chair, Department of Family
King’s County Hospital; Professor
International Editors

Administration-approved labeling. Information presented as part of this activity is intended

School Director, Emergency Medicine Medicine,
of Medicine at Mount Sinai, of
Beth Israel Medical Center; Peter Cameron, MD
Residency, Mount Sinai St. Clinical Emergency Medicine, Senior
Medical Luke's SUNY
Faculty, Family Medicine and
Director, Mount Sinai Hospital, Downstate College of Medicine, Academic Director, The Alfred
New Roosevelt, New York, NY Community Health, Icahn School
York, NY Brooklyn, NY of Emergency and Trauma Centre,
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Keith A. Marill, MD York, NY
Associate Editor-In-Chief

solely as continuing medical education and is not intended to promote off-label use of any
Assistant Professor, Department Scott Silvers, MD, FACEP Australia
of Research Faculty, Department
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Chair, Department of Emergency
School Emergency Medicine, University Giorgio Carbone, MD
Associate Professor, Department of Medicine at Mount Sinai, of Pittsburgh Medical Center, Medicine, Mayo Clinic, Jacksonville, Chief, Department of Emergency
of New FL
Emergency Medicine, Icahn York, NY Pittsburgh, PA Medicine Ospedale Gradenigo,
School Corey M. Slovis, MD, FACP,
of Medicine at Mount Sinai, FACEP

pharmaceutical product.
New Michael A. Gibbs, MD, FACEP Charles V. Pollack Jr., MA, Professor and Chair, Department Torino, Italy
York, NY MD,
Professor and Chair, Department FACEP of Emergency Medicine, Vanderbilt Suzanne Y.G. Peeters, MD
of Emergency Medicine, Carolinas University Medical Center, Nashville,
Editorial Board Medical Center, University
Professor and Senior Advisor
for TN Emergency Medicine Residency
Saadia Akhtar, MD of North Interdisciplinary Research Ron M. Walls, MD Director, Haga Teaching Hospital,
Carolina School of Medicine, and
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Hill, NC of
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Faculty Disclosure: It is the policy of EB Medicine to ensure objectivity, balance, independence,

Emergency Medicine, Associate Kimmel
Dean Steven A. Godwin, Medical College of Thomas and
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Professor and Chair, Department University, Philadelphia, PA Medical Hospital
Program Director, Emergency School, Boston, MA Italiano, Buenos Aires, Argentina
Medicine Residency, Mount of Emergency Medicine, Assistant Michael S. Radeos, MD,
Sinai MPH Dhanadol Rojanasarntikul,
Beth Israel, New York, NY Dean, Simulation Education, Associate Professor of Emergency Critical Care Editors MD
Attending

University of Florida COM-
William J. Brady, MD Jacksonville, Jacksonville,
FL
Professor of Emergency Medicine
Gregory L. Henry, MD, FACEP
and Medicine; Chair, Medical
Clinical Professor, Department
Emergency Response Committee;
Emergency
Medicine, Weill Medical College
William A. Knight IV, MD,
of Cornell University, New
York;
Research Director, Department
of
Emergency Medicine, New
of York
Hospital Queens, Flushing,
FACEP
Associate Professor of Emergency
Medicine and Neurosurgery,
Medical
Director, EM Midlevel Provider
transparency, and scientific rigor in all CME-sponsored educational activities. All faculty
Physician, Emergency
Medicine, King Chulalongkorn
Memorial Hospital, Thai Red
Cross,
Thailand; Faculty of Medicine,
Chulalongkorn University,
Thailand

participating in the planning or implementation of a sponsored activity are expected to disclose

Medical Director, Emergency Medicine, University NY Program, Associate Medical
of Michigan Medical School; Director, Stephen H. Thomas,
Management, University of CEO, Ali S. Raja, MD, MBA, MPH Neuroscience ICU, University MD, MPH
Virginia Medical Practice Risk Assessment, of Professor & Chair, Emergency
Medical Center, Charlottesville, Vice-Chair, Emergency Medicine, Cincinnati, Cincinnati, OH
VA Inc., Ann Arbor, MI Massachusetts General Hospital, Medicine, Hamad Medical
Scott D. Weingart, MD, Corp.,
Calvin A. Brown III, MD Boston, MA FCCM Weill Cornell Medical College,
John M. Howell, MD, FACEP Associate Professor of Emergency Qatar;

Director of Physician Compliance,
Credentialing and Urgent Care
Services, Department of Emergency
Medicine, Brigham and Women's
Hospital, Boston, MA
Clinical Professor of Emergency
Medicine, George Washington
University, Washington, DC;
Director
of Academic Affairs, Best
Practices,
Inc, Inova Fairfax Hospital,
Robert L. Rogers, MD, FACEP,
FAAEM, FACP
Assistant Professor of Emergency
Medicine, The University
of
Senior
Medicine, Director, Division
of ED
Critical Care, Icahn School
of Medicine
at Mount Sinai, New York, NY
to the audience any relevant financial relationships and to assist in resolving any conflict
Emergency Physician-in-Chief,
Hamad General Hospital, Doha,
Qatar
Edin Zelihic, MD
Head, Department of Emergency

of interest that may arise from the relationship. In compliance with all ACCME Essentials,
Falls Maryland School of Medicine, Research Editors Medicine, Leopoldina Hospital,
Peter DeBlieux, MD Church, VA Baltimore, MD Schweinfurt, Germany
James Damilini, PharmD,
Professor of Clinical Medicine, Shkelzen Hoxhaj, MD, MPH, BCPS
MBA Alfred Sacchetti, MD, FACEP Clinical Pharmacist, Emergency
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Baylor Assistant Clinical Professor, Room, St. Joseph’s Hospital
of Emergency Medicine Services, College of Medicine, Houston, and

Standards, and Guidelines, all faculty for this CME activity were asked to complete a full
TX Department of Emergency Medical Center, Phoenix,
Louisiana State University Medicine, AZ
Health Thomas Jefferson University,
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LA Philadelphia, PA
Chairman, Department of
Emergency
Medicine, San Ramon Regional

disclosure statement. The information received is as follows: Dr. Otterness, Dr. Ahn, Dr.
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Manini, Dr. Nelson, Dr. Mishler, Dr. Toscano, and their related parties report no significant
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Emergency Medicine Practice.... Biomarkers Inc; Consulting fees, EB Medicine.

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 Calculated
Decisions
Clinical Decision Support for Emergency Medicine Practice Subscribers
Abbreviated Injury Score (AIS)
for Inhalation Injury
Introduction: The Abbreviated Injury Score (AIS) classifies
Click the thumbnail above
inhalation injury severity based on bronchoscopic findings.
to access the calculator.
Points & Pearls
• The AIS may predict the development of acute
respiratory distress syndrome (ARDS), the length
of time on mechanical ventilation, and pro-
longed stay in the intensive care unit (ICU).
• Some studies have found a non-statistically
significant trend toward worse outcomes with a
higher AIS.
• AIS severity has not been consistently associ-
ated with mortality (Sheridan 2016).
• The AIS cannot reliably predict the need for
high fluid resuscitation requirements.
• A typical flexible bronchoscope is 5 mm in
diameter on average; hence, bronchoscopy
cannot identify narrower distal airway changes.
Thus, bronchoscopic findings cannot be relied
upon to accurately reflect the overall severity of
airway inhalation injury.
Advice
High AIS severity alone should not dictate manage-
ment decisions, which should be made in conjunc-
tion with a patient’s history, physical examination,
and laboratory findings.
Critical Actions
Macroscopic manifestations of airway abnormalities
may be delayed, falsely reassuring the clinician that
inhalation injury has not occurred (Hunt 1975).
CALCULATOR REVIEW AUTHOR
Pujan H. Patel, MD
Division of Pulmonary, Critical Care, and Sleep Medicine
Saint Louis University Hospital, St. Louis, Missouri
S1 www.ebmedicine.net
POWERED BY
Evidence Appraisal
The AIS criteria were first proposed by Endorf and
Gamelli in 2007. The purpose of their study was to
identify whether the severity of inhalation injury cor-
related better with pulmonary parameters (eg, lung
compliance, PaO2:FiO2 ratio) and acute fluid resus-
citation requirement than with bronchoscopically
assessed inhalation injury severity. They retrospec-
tively reviewed 80 adult patients with suspected
inhalation injury who required intubation, mechani-
cal ventilation, and flexible bronchoscopy within the
first 24 hours of admission. AIS criteria were used to
separate the patients into 2 groups of bronchoscop-
ic inhalation injury: a group with grades of 0 and 1,
and a group with grades of 2, 3, and 4. Character-
istics such as fluid resuscitation requirements, initial
oxygenation, lung compliance, and duration of me-
chanical ventilation were compared between the 2
groups; however, only decreased survival correlated
with bronchoscopic severity (P = .03).
Hassan et al (2010) also found a significant
increase (P < .01) in mortality with bronchoscopic
severity. They did not use the AIS criteria.
Since 2007, several studies have used the AIS
to try to tease out a clear relationship between the
bronchoscopic grade of injury and a range of clinical
outcomes, with varied results. For instance, in con-
trast to Endorf and Gamelli’s 2007 study, studies by
Albright et al (2012), Mosier et al (2012), and Spano
et al (2016) found that an increasing AIS grade did
not have a significant effect on mortality, with P
values of 0.21, 0.10, and 0.15, respectively.
Albright et al did show that increasing severity
was associated with longer ventilator days (P = .036)
and ICU stays (P = .04). Mosier et al (2012) noted a
significant association between AIS grade severity
and the development of ARDS at 24 hours (P < .01).
 Why to Use
• The AIS criteria have not been compared head-to-head with other bronchoscopic criteria; hence, for lack
of an alternative well-studied score, the AIS has been widely utilized as the predominant bronchoscopic
inhalation injury severity score in the literature.
• There is no universal consensus on diagnostic and grading criteria for inhalation injury. A multicenter pro-
spective cohort study by the American Burn Association is currently underway, with the goal of develop-
ing a scoring system for inhalation injury based on clinical, radiographic, bronchoscopic, and biochemical
parameters.

When to Use
Use the AIS for adult patients with suspected inhalation injury who are undergoing flexible bronchoscopy.

Next Steps
• Supportive treatment is the primary means of inhalation injury management, as very little is available in
the way of pharmacologic treatment once the inhalation injury has occurred.
• Bronchoscopy can play a therapeutic role in airway clearance, as necrotic tissue and eschar can result in
formation of pseudomembranes, sloughing of mucosa, and bronchial obstruction.
• Other measures include intensive bronchial hygiene, including:
• Bronchodilators, such as β2 agonists
• Frequent chest physiotherapy
• Early patient ambulation
• Upper airway edema can progress to respiratory failure necessitating intubation, particularly over the
first 24 hours after injury. If mechanical ventilation is required, a high-frequency percussive mode can be
considered, as some studies have shown benefit to this patient population. A lung-protective, low tidal
volume ventilation strategy (6-8 cc/kg of predicted body weight) is preferred in adults.
• Other supportive measures that have been used with varied success include prone positioning, extracor-
poreal membrane oxygenation (ECMO), inhaled anticoagulants (eg, heparin, antithrombin), and inhaled
N-acetylcysteine (NAC).
• Consider referring the patient to a designated burn center.

Use the Calculator Now • Hassan Z, Wong JK, Bush J, et al. Assessing the severity of
Click here to access the calculator. inhalation injuries in adults. Burns. 2010;36(2):212-216.
• Sheridan RL. Fire-related inhalation injury. N Engl J Med.
Calculator Creators 2016;375(5):464-469.
Frederick W. Endorf, MD and Richard L. Gamelli, MD • Hunt JL, Agee RN, Pruitt BA. Fiberoptic bronchoscopy in
Click here to read more about Dr. Endorf and Dr. Gamelli. acute inhalation injury. J Trauma. 1975;15(8):641-649.
• Spano S, Hanna S, Li Z, et al. Does bronchoscopic evalu-
References ation of inhalation injury severity predict outcome? J Burn
Original/Primary Reference Care Res. 2016;37(1):1-11.
• Endorf FW, Gamelli RL. Inhalation injury, pulmonary
Copyright © MDCalc • Reprinted with permission.
perturbations, and fluid resuscitation. J Burn Care Res.
2007;28(1):80-83.
Validation References
• Albright JM, Davis CS, Bird MD, et al. The acute pulmonary
inflammatory response to the graded severity of smoke
inhalation injury. Crit Care Med. 2012;40(4):1113-1121.
• Mosier MJ, Pham TN, Park DR, et al. Predictive value of
bronchoscopy in assessing the severity of inhalation injury.
J Burn Care Res. 2012;33(1):65-73.
Other References
• Walker PF, Buehner MF, Wood LA, et al. Diagnosis and
management of inhalation injury: an updated review. Crit
Care. 2015;19:351.

Emergency Medicine Practice • March 2018 S2 Copyright © 2018 EB Medicine. All rights reserved.
 RADS (Radiologist’s Score)
for Smoke Inhalation Injury
Introduction: The RADS (Radiologist’s Score) for Smoke
Inhalation Injury stratifies the severity of inhalation injury
Click the thumbnail above
to access the calculator. detected on a computed tomography (CT) scan of the chest.
Points & Pearls
• The RADS was derived from a sheep model and
validated retrospectively in human cohorts, with
limited validation in prospective clinical human
trials.
• Calculation of the RADS requires assessment of
each CT slice, which can be time-consuming.
• A higher RADS 24 hours after smoke inhalation
seems to correlate with greater smoke exposure
and severity of lung injury.
• Using chest CT scans in the evaluation of inhala-
tion injury has limitations, including the ques-
tionable optimal timing of CT and the interpre-
tation of abnormal CT findings in the setting of
a negative bronchoscopy.
Advice
The RADS should be used as an adjunct to clinical
history, examination, bronchoscopy, and arterial
blood gas data to determine the full clinical picture.
Critical Actions
As always, clinical judgment is paramount. Manage-
ment decisions should not be based solely on the
RADS.
Evidence Appraisal
The RADS tool was developed from an ovine study
of 20 anesthetized sheep who were intubated,
exposed to wood smoke, and then underwent CT
scans of the thorax at 6, 12, and 24 hours after
exposure (Park 2003). The study raised several ques-
tions, including whether smoke inhalation from the
combustion of materials other than wood would
behave in the same way; whether a normal CT result
would be sufficient to rule out significant injury; and
how the score would perform in direct comparison
to better-established diagnostic tools such as fiber-
optic bronchoscopy.
Oh et al conducted a retrospective study of
43 patients (25 with inhalation injury and 19 with-
CALCULATOR REVIEW AUTHOR
Pujan H. Patel, MD
Division of Pulmonary, Critical Care, and Sleep Medicine
Saint Louis University Hospital, St. Louis, Missouri
Emergency Medicine Practice • March 2018
Why to Use
Currently, no single tool accurately and reliably
risk stratifies and prognosticates outcomes for
patients with smoke inhalation injury. The RADS
can be a useful adjunct to determine the sever-
ity of inhalational injury to the lungs.
A multicenter prospective cohort study
sponsored by the American Burn Association is
currently underway, with the goal of develop-
ing a scoring system for inhalation injury based
on clinical, radiographic, bronchoscopic, and
biochemical parameters.
When to Use
• Use the RADS for patients with suspected or
diagnosed inhalation injury.
• The RADS is best used in conjunction with
flexible bronchoscopy.
Next Steps
• Supportive treatment is the primary means
of inhalation injury management. This in-
cludes intensive bronchial hygiene with the
following:
• Bronchodilators, such as β2 agonists
• Frequent chest physiotherapy
• Early patient ambulation
• Upper airway edema can progress to respi-
ratory failure necessitating intubation, par-
ticularly over the first 24 hours after injury. If
mechanical ventilation is required, a high-
frequency percussive mode of ventilation
has shown the most benefit in this patient
population (Cioffi 1991). A lung-protective,
low tidal volume ventilation strategy
(6-8 cc/kg of predicted body weight) is pre-
ferred for adults.
• Other supportive measures that have been
used with varied success include prone
positioning, extracorporeal membrane oxy-
genation (ECMO), inhaled anticoagulants
(eg, heparin, antithrombin), and inhaled
N-acetylcysteine (NAC).
• Consider referring the patient to a
designated burn center if any inhalation
injury is present, in accordance with the
American Burn Association guidelines.
S3 Copyright © 2018 EB Medicine. All rights reserved.
out); using multiple logistic regression analysis, • Cioffi WG Jr, Rue LW 3rd, Graves TA, et al. Prophylactic use
they found that inhalation injury on bronchoscopy of high-frequency percussive ventilation in patients with
correlated with an 8.3-fold increase in a composite inhalation injury. Ann Surg. 1991;213(6):575-580.
endpoint of pneumonia, acute lung injury/acute • August DL, Foster K, Richey K, et al. Computerized tomog-
respiratory distress syndrome, and death. Positive raphy correlates with ventilator days in inhalation injury:
bronchoscopy in conjunction with a RADS > 8 was preliminary data from the Inhalation Severity Injury Scoring
correlated with a 12.7-fold increase in the compos- System (ISIS) trial. Oral presentation at: Society of Thoracic
ite endpoints. Radiology Annual Meeting; March 16, 2014; San Antonio, TX.
We are not aware of any studies looking at inter-
rater reliability of the scoring system. Copyright © MDCalc • Reprinted with permission.
A prospective clinical trial is currently underway
to help answer many of the questions that have
been raised. Preliminary clinical data from the Inha-
lation Severity Injury Scoring System trial demon-
strated a positive correlation between the RADS and
ventilator days.

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References
Original/Primary Reference
• Oh JS, Chung KK, Allen A, et al. Admission chest CT
complements fiberoptic bronchoscopy in prediction of
adverse outcomes in thermally injured patients. J Burn Care
Res. 2012;33(4):532-538.
Other References
• Walker PF, Buehner MF, Wood LA, et al. Diagnosis and
management of inhalation injury: an updated review. Crit
Care. 2015;19:351.
• Enkhbaatar P, Pruitt BA, Suman O, et al. Pathophysiology,
research challenges, and clinical management of smoke
inhalation injury. Lancet. 2016;388(10052):1437-1446.
• Park MS, Cancio LC, Batchinsky AI, et al. Assessment of
severity of ovine smoke inhalation injury by analysis of com-
puted tomographic scans. J Trauma. 2003;55(3):417-427
• Putman CE, Loke J, Matthay RA, et al. Radiographic mani-
festations of acute smoke inhalation. AJR Am J Roentgenol.
1977;129(5):865-870.

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