Volume 31 Number 9 September 2017

Little Monsters
Continuing trends in global interdependence and shifting
climate changes have triggered an increase in the number
of patients presenting with parasitic infections. Emergency
physicians must be aware of the unique life-threatening
complications posed by these insidious organisms and
be prepared to discern relevant diagnostic information,
including details about diet and recent travel, by initiating
an expeditious examination of any patient with signs of
parasitic or tropical disease.

Too Hot to Handle

The spectrum of heat-related illnesses is notoriously
broad, ranging from mild discomfort to fulminant organ
failure and death. Emergency clinicians must be prepared
to recognize high-risk patients and initiate proper cooling
methods
Lumbar rapidly,(LP)
puncture whileis avoiding therapies
used in the that might be
diagnostic
ineffectiveoforcentral
evaluation even deleterious. It is particularly
nervous system important
(CNS) processes,
to differentiate
most commonly in heat-related illness from
cases of suspected other mimics
infection and such
as sepsis, and remain vigilant about
subarachnoid hemorrhage. Less commonly, the complications that
can arise isasused
procedure cellular injury progresses.
for therapeutic purposes (eg, in cases
of idiopathic intracranial hypertension).

THE OFFICIAL CME PUBLICATION OF THE AMERICAN COLLEGE OF EMERGENCY PHYSICIANS

IN THIS ISSUE
Lesson 17 n Heat-Related Illness . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 3
LLSA Literature Review . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 11 Critical Decisions in Emergency Medicine is the official
Critical ECG . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 12 CME publication of the American College of Emergency
Physicians. Additional volumes are available to keep
Lesson 18 n Parasitic Infections . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 13 emergency medicine professionals up to date on
Critical Procedure . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 19 relevant clinical issues.

Critical Image . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 20
EDITOR-IN-CHIEF
CME Questions . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 22 Michael S. Beeson, MD, MBA, FACEP
Drug Box/Tox Box . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 24 Northeastern Ohio Universities,
Rootstown, OH

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 Too Hot to Handle
Heat-Related Illness

LESSON 17

By Anna Schlechter, MD and Timothy Ruttan, MD

Dr. Schlechter is a pediatric emergency medicine fellow and Dr. Ruttan is a clinical
assistant professor at the University of Texas at Austin Dell Medical School at
Dell Children’s Medical Center of Central Texas.

Reviewed by Michael S. Beeson, MD, MBA, FACEP

OBJECTIVES
On completion of this lesson, you should be able to:
1. Distinguish the different forms of heat-related illness.
2. List the clinical and laboratory abnormalities that may
accompany heat stroke.
3. Explain the treatment options and proper dispositions for
the various forms of heat-related illness.
4. Identify patients who are at high risk of developing heat-
related illness.
5. Differentiate heat-related illness from other pathologies
that may present similarly.
FROM THE EM MODEL
6.0 Environmental Disorders
6.6 Temperature-Related Illness
CRITICAL DECISIONS
n What clinical findings can help distinguish
different forms of heat-related illness?
n What clinical, laboratory, and imaging
abnormalities are reliable indicators of heat
stroke?
n What treatments should be initiated in the field
and emergency department?
n Which patients are at high risk of heat-related
illness?
n What other pathologies can mimic heat-related
illness?
n Which cases warrant hospital admission?

Heat-related illness encompasses a spectrum of pathologies ranging from minor complaints, including
rashes and heat exhaustion, to life-threatening disorders such as heat stroke, which poses a mortality risk of
12% in adults.1 The etiology of heat-related illness includes excess heat production, decreased heat transfer to the
environment, or a combination of the two.

September 2017 n Volume 31 Number 9 3

 CASE PRESENTATIONS
■ CASE ONE
A 15-year-old high school athlete
arrives via ambulance with nausea
and dizziness. It is late August and
he is wearing a tight-fitting polyester
jersey, which is drenched in sweat.
EMS was called when he became
disoriented and short of breath
during football practice. On the
field, paramedics noted the boy to
be tachycardic with a temperature of
38.8°C (102°F). He vomited twice
during transport.
He has no chronic medical
prob­lems, although he is currently
taking a stimulant for the treatment
of attention-deficit/hyperactivity
disorder (ADHD). His vital signs are
blood pressure 120/83, heart rate 110,
respiratory rate 26, temp­erature 38°C
(100.4°F), and oxygen saturation
98% on room air. He answers the
emergency clinician’s questions
appropriately, but appears tired.
When body temperatures rise above
41°C (105.8°F), proteins denature and
cells undergo apoptosis or necrosis; this
dangerous cascade can cause irreparable
harm to multiple organ systems. Time is
of the essence, so emergency clinicians
must be prepared to rule out other
diagnoses that can mimic heat-related
illness (Table 1) and initiate cooling
measures rapidly.
CRITICAL DECISION
What clinical findings can help
distinguish different forms of
heat-related illness?
Rashes
Heat rash (also termed miliaria
rubra, sweat rash, or prickly heat) has
an erythematous, pruritic appearance;
papules and pustules result from a
combination of heat exposure and the
obstruction of sweat glands, which can
become clogged with material from the
stratum corneum produced by excess
sweating.2 Rashes most often are seen in
areas of friction, where skin rubs against
skin or clothing. Although symptoms can
4 Critical Decisions in Emergency Medicine
■ CASE TWO
A disabled 83-year-old woman
arrives via ambulance after being
found seizing in her home. The
temperature outside is unusually warm
(96°F with 100% humidity). The
woman is accompanied by her niece,
who states that the patient’s home has
no air conditioning and its windows
are painted shut. EMS reports
an initial temperature of 40.2°C
(104.4°F). Intramuscular midazolam
was administered on scene, which
resolved her seizing. She was intubated
prior to transport, and cooling with
water spray and fans was initiated.
Upon arrival, the patient’s vital
signs are blood pressure 82/36, heart
rate 149, and rectal temperature 103°F
(39.4°C). Her skin is hot and dry, and
she is minimally responsive to painful
stimuli.
develop in any age group, they are more
common in children, whose sweat glands
are underdeveloped. It is important for
clinicians to distinguish this benign
and generally self-limiting rash from
other common dermatological findings,
including viral exanthems or other
infectious etiologies.
Edema
Heat edema, another benign process,
results from the microvascular transudate
of fluid and peripheral vasodilation as
the body attempts to shunt warm blood
to the periphery.3 In contrast to the
lower-extremity edema often seen in
patients with heart failure, heat-related
swelling is not associated with volume
overload. Rather, these patients typically
are suffering from relative hypovolemia
caused by inadequate replacement of
volume losses.2 Although heat edema
usually is lower-extremity dependent, it
also can be found in the hands. An abrupt
transition from a cold environment to
a warmer one may precipitate swelling.
Given that the disorder frequently is
found in older adults with existing
cardiac, renal, and/or liver comorbidities,
■ CASE THREE
A 2-month-old girl arrives via
ambulance after being left in a hot car
for approximately 20 minutes. The
child’s father reports thinking he had
dropped her off at daycare; however,
he returned to his car after waiting in
line at the post office to find her still
buckled into her car seat.
When EMS reached her, she was
crying and appeared to have vomited
and sweated through her clothing.
On scene, the infant’s vital signs were
heart rate 180, respiratory rate 40,
rectal temperature 39.3°C (103°F), and
oxygen saturation 98% on room air.
Paramedics initiated cooling with ice
packs to the neck, axilla, and groin.
Upon arrival in the emergency
department, her rectal temperature
is 38.2°C (100.8°F). She is noted to
have an erythematous papular rash
consistent with miliaria rubra on the
abdomen, chest, and bilateral axilla.
it is important to distinguish the
underlying etiology to help guide
diagnostic and therapeutic efforts.
Syncope
Heat syncope, which results
secondary to peripheral vasodilation and
venous pooling, is particularly common
in unacclimated patients. The disorder
usually results after a rapid change
in position (eg, going from sitting to
standing), and generally improves when
the patient is supine. It is important to
note that, unlike in some of the more
serious heat-related illnesses, patients
with heat syncope do suffer from an
elevated core body temperature.3 As
always, a careful history and physical
examination, in addition to other studies
as indicated, is important to distinguish
benign cases from more serious but
relatively rare etiologies.
Cramps
Heat cramps are painful spasms
that often affect large muscle groups,
especially the legs (eg, the calves,
quadriceps, and hamstrings). They can
occur either during or immediately after
exertion, and can be triggered by muscle
overload/fatigue, dehydration, and
electrolyte deficiencies.4 It is important
to note that core body temperature will
not exceed the critical threshold of 40°C
(104°F) in these patients.
Heat Stress, Exhaustion,
and Stroke
Heat stress is defined as the initial
degree of discomfort felt when the
body tries to respond to a thermal load.
There is some physiological strain that
may manifest as decreased exercise
performance; however, by definition, the
core temperature stays within normal
limits.5 Although the threshold for heat
stress varies between patients, it depends
more on the degree of acclimatization
to the environment than on baseline
physical fitness. This is an important
point, as fit individuals who fail to
acclimate may still experience significant
and unexpected symptoms.
If heat stress progresses, core
temperatures can reach between
38°C (100.4°F) and 40°C (104°F),
resulting in heat exhaustion. Beyond
decreased exercise performance, other
symptoms may include tachycardia,
sweating, weakness, headache, thirst,
nausea, and vomiting. 5 Although some
patients may experience transient
confusion, overall mentation is normal.
Dehydration is common, but its severity
will vary depending largely on the
degree of fluid intake during the period
of heat exposure.
Heat stroke, a further progression of
heat stress, is defined as a temperature
above 40°C (104°F) accompanied
by central nervous system (CNS)
dysfunction.3 Patients may present with
altered mental status (AMS) manifested
as slurred speech, ataxia, delirium,
hallucinations, or seizure activity. In
severe cases, obtundation or coma may
result in airway compromise.6 Vital
signs often are unstable; tachycardia and
hypotension are both commonplace and
concerning. While patients can exhibit
symptoms much like those seen with
heat exhaustion, there are two important
distinguishing signs that indicate heat
stroke: AMS and anhidrosis (although
the latter is not a universal finding).
As with other heat-related illnesses,
heat stroke may be exertional or
nonexertional. The nonexertional type
(ie, classic heat stroke) frequently is
seen during heat waves and in humid
environments. It tends to develop more
slowly and typically is seen in older
patients or those with comorbidities that
prevent behavioral adaptation.
Although exertional heat stroke also
occurs with more frequency during heat
waves and in humid environments, it
also can be seen in cooler months in a
highly motivated athlete. In addition,
exertional illness evolves more rapidly
over the course of hours rather than
days, and tends to be the result of sports,
occupational exposure, or other high-risk
activities such as illegal border crossings.7
CRITICAL DECISION
What clinical, laboratory, and
imaging abnormalities are
reliable indicators of heat stroke?
Although the definition of heat-related
illness includes specific temperature
indices, the core temperature may no
longer be elevated by the time a patient
arrives at the hospital, as cooling is likely
to have been initiated during transit. For
this reason, it is especially important
to be aware of the clinical signs and
laboratory abnormalities consistent
with heat stroke; an accurate diagnosis
is imperative, even in the absence of a
characteristic elevated temperature.
Overall, the indicators of heat stroke
are secondary to the denaturation
of bodily proteins, which manifests
as multisystem organ damage and
a resultant systemic inflammatory
response.8 Although no single laboratory
finding is pathognomonic for heat stroke,
consideration of potential abnormalities
in the appropriate clinical context
allows the clinician to make the correct
diagnosis and initiate treatment.
Mental status changes such as
confusion or delirium generally are not
seen until the rectal temperature exceeds
40°C (104°F). Protein denaturation
and more severe damage begin when
the patient’s temperature reaches 41°C
(105.8°F). Encephalopathy and seizures
may follow and are associated with poor
outcomes, even with optimal treatment.
Changes in mental status primarily
stem from hypotension and diminished
cerebral perfusion, which causes cerebral
ischemia.1 Of note, many patients at
high risk for heat-related complications,
including small children and those
who are elderly or disabled, may be
particularly difficult to assess at baseline
for the harbingers of more serious illness.
An initial computed tomography (CT)
scan of the head may be normal or may
show signs of cerebral edema. This
finding frequently is noted with repeat
imaging later in the hospital course, as
the illness progresses.
Hypotension is common in patients
with core temperatures above 42°C
(107.6°F). Vasodilation occurs and
the cardiac index increases as the
body attempts to expel excess heat.
When the heart becomes overloaded,
the myocardium can be impaired;
electrocardiogram (ECG) findings
may look identical to those seen in
patients with coronary ischemia, even
in the absence of structural lesions.1
Patients who develop acute respiratory
distress syndrome can be challenging
to oxygenate. This complication can
be visualized on chest x-ray or lung
ultrasound.
Electrolyte anomalies such as
hyponatremia (secondary to salt loss
from sweat) or hypernatremia (secondary
to volume depletion) may be evident on
laboratory tests. Blood gases frequently
reveal a metabolic acidosis as a result
of perfusion abnormalities and protein
breakdown. Gastrointestinal (GI)
abnormalities can run the gamut from
diarrhea (in mild cases) to hemorrhage
(in cases of severe thermal damage to
the GI tract) and continued injury that
evolves even after resuscitation and
normalization of vital signs.
The liver frequently is damaged during
heat stroke, as it is a major site of heat
production and typically has the highest
temperature of any other organ in the
body. Profound shock states can further
complicate the clinical course by causing
hypoperfusion and laboratory patterns
consistent with shock liver. Transferase
levels continue to rise, peaking 48 to
72 hours after injury before gradually
returning to normal within 14 days. In
severe cases, liver biopsies may reveal
September 2017 n Volume 31 Number 9 5
 damage to the heart and vascular system,
TABLE 1. Signs, Symptoms, and Treatment of Heat-Related Illness endotoxins released from the heat-
Condition Signs/Symptoms Treatment injured GI tract, or a variety of other
NORMAL BODY TEMPERATURE AT PRESENTATION inflammatory mediators that impact
Miliaria rubra Pruritic erythematous rash with Cool patient
normal mediators of vascular resistance.1
papules and pustules in Remove excess clothing
areas of skin friction Avoid lotions Lactate concentrations often are
Heat edema Swelling that often affects the Elevate the extremities elevated in the initial stages as a result of
lower extremities Remove patient from hot environment hypoperfusion and organ damage.
Heat syncope Transient loss of consciousness Remove patient from hot environment
due to dehydration/rapid Oral rehydration with salt-containing CRITICAL DECISION
change in position fluids
IV rehydration if needed What treatments should
Heat cramps Pain to the large muscle Oral hydration, stretching, massage be initiated in the field and
groups If elevated CPK, renal dysfunction
or hyponatremia, give IV fluids emergency department?
and correct electrolyte anomalies; The most critical step when managing
consider admission
heat-related illness is to remove the
ELEVATED BODY TEMPERATURE AT PRESENTATION
Heat exhaustion Body temp. ≤40°C (104°F) Remove from hot environment patient from the environment that has
Tachycardia, sweating, nausea, Oral rehydration caused the symptoms. In the field, this
vomiting, weakness, fatigue, Normal saline bolus can be as simple as placing the patient
mild confusion Check electrolytes in the back of an air-conditioned
Close observation/admission
ambulance and removing all clothing
Heat stroke Body temp. >40°C (104°F) ABCs with intubation if necessary
CNS dysfunction (eg, ataxia, Fluid resuscitation to facilitate cooling. Such actions
delirium, hallucinations, Cooling measures are especially important in humid
seizures, slurred speech) Avoid antipyretics and dantrolene environments.
May have obtundation or Benzodiazepines for seizure activity Although there are normal variations
coma Chest x-ray, head CT
Vital signs with tachycardia CBC, PT/PTT/INR, fibrinogen, CMP, UA,
within tightly controlled limits, 37°C
and hypotension CK, ABG (98.6°F) is the normal body temperature
Multisystem organ failure Admission across all populations.2 Normal skin is
nearly constant at 35°C (95°F), creating
the temperature gradient necessary
areas of cholestasis and necrosis.1 (resulting from the dilutional effects of to dissipate heat from the core to the
Despite these abnormalities, a spon­ rehydration), shortened red blood cell periphery.2 Methods of cooling include
taneous return of hepatic function is half-life after heat stroke, and increased conduction, convection, radiation, and
likely; few patients ultimately require rigidity and osmotic fragility of the red evaporation. Conduction is direct heat
transplantation. Prolonged prothrombin blood cell membrane.1 Platelets can be transfer to an adjacent, cooler object
time also is frequently seen as a result of normal or decreased, and may decline (eg, application of an ice pack or cooling
liver dysfunction. steadily in the first 24 hours after insult.9 blanket). Convection is the transfer of
Renal insufficiency is a frequent Finally, disseminated intravascular heat to a gas or liquid moving over the
finding in heat stroke. Prerenal azotemia, coagulation (DIC) is seen in nearly body. Heat transfer occurs when a gas
the most common complication, is 50% of patients with heat stroke; in or liquid is colder than the body (as with
marked by an elevation of blood urea such cases, laboratory tests will reveal the use of fans or water immersion).
nitrogen to a greater degree than prothrombin time (PT) and partial Radiation refers to the emission of
creatinine levels.1 Rehydration usually thromboplastin time (PTT) prolongation electromagnetic heat waves, a process
corrects these laboratory abnormalities and D-dimer elevation. Some patients that does not require direct contact or
within a few days, and dialysis is rarely may bleed, while others can experience air motion. Evaporation, which occurs
necessary in the presence of supportive a period of hypercoagulability (as is when water vaporizes from the skin
care measures. That said, serum typical in any patient with disseminated and respiratory tract, is the body’s most
creatinine phosphokinase (CPK) levels intravascular coagulation). These effective mechanism for dissipating
may be elevated as a result of muscle abnormalities generally resolve after excess heat, with concomitant reduction
breakdown and rhabdomyolysis. Such a few days in patients who are able to in skin temperature of 0.58 kcal per
elevations also may worsen kidney injury survive the initial insult. milliliter of sweat.10 Evaporation is the
and increase the risk of dialysis or long- Shock can result from hypovolemia mechanism employed with sweating,
term renal impairment. caused by sweat loss. Patients may have misting, or the use of a fan.
Hematological abnormalities, low vasomotor tone, even after volume A core tenet of reducing body
which are common in patients with repletion and normal temperature has temperature is the removal of all
heat stroke, may be accompanied by been achieved. This complication is clothing, which increases the surface
a rapidly declining hematocrit levels believed to be the result of thermal area exposed to convective air currents.2

6 Critical Decisions in Emergency Medicine

The addition of fans increases convection
and evaporation-mediated heat transfer;
however, both become less effective as
ambient temperature and relative humidity
increase.11 In fact, the physiologically
effective evaporation of sweat ceases when
humidity exceeds approximately 75%;
sweating becomes essentially ineffective
at 95% relative humidity.2 Morbidity is
reduced drastically if cooling measures
begin within 30 minutes of insult.12
Cooled, slightly hypotonic oral
solutions should be given, as treatments
with high osmolality can slow gastric
emptying and delay the movement of cool
fluids to the small intestine.2 Cold-water
gastric lavage, peritoneal lavage, and
rectal or bladder lavage have not been
proven to be beneficial and can result in
water intoxication.2
Minor heat-related illnesses may be
treated at home rather easily. Patients
with miliaria rubra simply should be
placed in a cool environment, and any
clothing should be replaced with clean,
dry (preferably cotton) clothing. Lotions,
which can obstruct infants’ sweat glands,
should be avoided until the rash resolves.13
Signs of heat edema necessitate removal
from the hot environment. The patient’s
extremities should be elevated and/or
compression stockings should be applied.3
Diuretics have no role in the treatment
of heat-related swelling.2 Heat cramps
can be treated with removal from the hot
environment. rest, stretching, and oral or
IV hydration with isotonic fluids.
Similarly, the mainstay of treatment
for heat syncope is removal from the
hot environment and oral hydration. If
orthostatic hypotension persists despite
oral rehydration, normal saline (NS) may
be beneficial.14 More aggressive evaluation
is warranted in any patient at risk for
Heat stroke should be treated much
like any other life-threatening condition.
Patients should be resuscitated with
fluids as needed, and intubated if
necessary. Cooling measures should
be initiated immediately with cool
water spray, air conditioning, and ice
packs placed to the neck, groin, and
axilla.5 Although immersion therapy
in ice water is the most effective form
of cooling, it is infrequently used in
emergency departments due to its
tendency to disrupt other resuscitation
efforts. Ice packs are more commonly
used to augment evaporative and
convective methods. While there
have been no studies to definitively
support the use of chilled IV fluids over
standard room-temperature fluids, some
studies suggest that they may improve
outcomes.15
Recommendations vary regarding
the temperature at which cooling
should be discontinued. Some
sources cite a core temperature of
38.6°C (101.4°F) as the benchmark
for discontinuation, while others
recommend a goal of 38.9°C
(102.0°F) or 39°C (102.2°F).1,6,16,17 A
benzodiazepine should be given to any
patient who is seizing, per standard
protocol; additional treatment for
status epilepticus should be pursued as
indicated. When managing a seizing
patient, especially one with exertional
heat stroke, it is important to consider
and treat other potential etiologies such
as hyponatremia.
FIGURE 1. National Weather Service Heat Index Chart
80 82
40 80 81
45 80 82
Relative Humidity (%)
Hypotension should be managed
as distributive shock; vasodilation
moves a large proportion of blood
volume to the periphery, although
some patients may present with
concomitant hypovolemia. 2 The use
of permissive hypotension during the
cooling phase, which enables gradual
peripheral vasoconstriction and central
redistribution of the circulating volume,
can help avoid the pulmonary vascular
congestion sometimes seen with
overly aggressive fluid resuscitation. 2
Vasopressors may be administered
if blood pressure does not respond
adequately to fluid resuscitation alone.6
Agents that have predominant alpha-
adrenergic effects (eg, norepinephrine)
should be eschewed, as they pose
a theoretical risk of peripheral
vasoconstriction, which could decrease
core cooling. 2 In the rare case of
clinical hemorrhage, patients should
be managed with fresh frozen plasma
and platelets.9 Muscle relaxants,
benzodiazepines, and neuroleptic agents
may be used to inhibit shivering, which
will add to the heat burden in a heat
stroke patient.
Medications such as acetaminophen,
ibuprofen, and dantrolene should be
avoided; they do not appear to be
effective for the treatment of heat-
related illness, and actually may be
deleterious. Imaging (eg, chest x-ray or
head CT) should be used to evaluate
for multisystem organ dysfunction, a
finding that warrants admission to the
84 86 88 90 92 94 96 98 100 102 104 106 108 110
83 85 88 91 94 97 101 105 109 114 119 124 130 136
84 87 89 93 96 100 104 109 114 119 124 130 137

cardiac disease or other causes of syncope. 50 81 83 85 88 91 95 99 103 108 113 118 124 131 137
Patients with heat exhaustion should 55 81 84 86 89 93 97 101 106 112 117 124 130 137
60 82 84 88 91 95 100 105 110 116 123 129 137
stop exercising and be placed in a cool
65 82 85 89 93 98 103 108 114 121 128 136
environment. Any excess clothing should 70 83 86 90 95 100 105 112 119 126 134
be removed, and oral rehydration with 75 84 88 92 97 103 109 116 124 132
slightly hypotonic salt-containing fluids 80 84 89 94 100 106 113 121 129
should be initiated. Most patients improve 85 85 90 96 102 110 117 126 135
90 86 91 98 105 113 122 131
with these measures alone; however,
95 86 93 100 108 117 127
if symptoms persist, blood should be 100 87 95 103 112 121 132
evaluated for electrolyte abnormalities
Likelihood of Heat Disorders with Prolonged Exposure or Strenuous Activity
and a 20-mL/kg normal saline bolus
should be administered for volume Caution Extreme Caution Danger Extreme Danger
repletion as needed.

September 2017 n Volume 31 Number 9 7


TABLE 2. Drugs That May
Increase Risk of Heat-Related
Illness2,13
Psychiatric and Neurological Drugs
Anti-Parkinsonian drugs
Antipsychotic agents
• Lithium
• Tricyclic antidepressants
• Selective serotonin reuptake
inhibitors
• MAO inhibitors
Over-the-Counter Medications
Antihistamines
Decongestants
Laxatives
Salicylates
Diuretics
Ergogenic stimulants (eg, ephedrine)
Cardiac Drugs
Beta blockers
Calcium channel blockers
Drugs of Abuse
Methamphetamine
Cocaine
Ethanol
Methylenedioxypyrovalerone
(ie,“bath salts”)
Ecstasy
Jimson weed
Mushrooms
Phencyclidine
intensive care unit. Laboratory testing
generally should include a complete
blood count (CBC); comprehensive
metabolic panel (CMP); urinalysis (UA);
and PT/PTT/international normalized
ratio (INR), fibrinogen CPK, and
arterial blood gas (ABG) measurements.
An ECG also may be warranted,
depending on the patient’s history and
presentation. Delays in the termination
of cooling, especially with axillary and
groin ice packing, can result in local
tissue destruction from cold-induced cell
death, localized tissue inflammation,
and ischemia.17 Patients who undergo
cooling are at risk for a physiological
phenomenon called afterdrop,
the process by which peripheral
blood vessels that were previously
vasoconstricted to divert warm blood
to the body’s core become dilated after
rewarming techniques are started.18 The
vasodilation causes a sudden circulatory
return of cold, deoxygenated, low pH,
lactic acid-rich blood. Unless active core
rewarming techniques (eg, IV fluids and
humidified oxygen) are implemented
simultaneously, this process can lead
8 Critical Decisions in Emergency Medicine
to prolonged hypothermia and cardiac surface area-to-body mass ratios, which
dysrhythmias, despite adequate passive causes increased heat absorption.6
rewarming techniques.18,19 Patients taking stimulants or drugs
with anticholinergic properties (secondary
CRITICAL DECISION to decreased sweating) are more prone to
Which patients are at high risk heat-related illness.13 Multiple prescription
of heat-related illness? and over-the-counter drugs are associated
with hyperthermia (Table 2). Those
Infants who are tightly bundled
undergoing vigorous exercise over
during warm and humid summer
prolonged time periods (Figure 1),
months are particularly vulnerable
including military personnel (especially
to heat-related illness, as are young
new recruits), also are at increased risk. It
children left in hot cars or directly
is important to note that heat stroke is the
exposed to the sun. Patients who are
third leading cause of death among high
incapable of leaving an inhospitable
school athletes.22
environment (eg, the very young, elderly,
or disabled) also may be prone to CRITICAL DECISION
dehydration due to a limited capacity to
What other pathologies can
obtain proper fluids. Some medications
can limit the body’s natural ability to mimic heat-related illness?
adapt to heat, putting these populations The differential diagnosis of the
at further risk for adverse outcomes highly febrile patient (core temperature
(Table 2). Limited social networks also >41°C) with AMS extends well beyond
can make it difficult for elderly adults to heat stroke, and it is important not
escape the heat or seek help within an to have diagnostic foreclosure in the
appropriate time window. absence of a corroborating history.
There are several physiological Maximum febrile temperatures rarely
differences that put children at particular exceed 41°C (105.8°F); at such a point,
risk of heat-related illness. An immature hyperpyrexia originating from the central
hypothalamus makes infants less capable thermoregulatory center is less likely.
of using compensatory mechanisms to Differential diagnoses (Table 3) include
dissipate heat.20 Furthermore, the total toxicological etiologies (eg, malignant
sweating capacity is decreased in young hyperthermia, overdose), metabolic
children, which renders evaporative (eg, hyperthyroidism) or neurological
cooling less effective. Pediatric patients (eg, stroke, meningitis) abnormalities, and
also have a smaller blood volume than infections (eg, cerebral malaria or sepsis).
adults, reducing their ability to transfer Patients with sepsis may have
warm blood into the periphery to cool altered mental status; high fever; and
the central core.6,21 Due to their higher laboratory findings consistent with
basal metabolic rates, children produce disseminated intravascular coagulation
more endogenous heat per kilogram than and end-organ failure. As previously
older patients.6 They also have higher noted, it can be challenging to confirm
n Overcooling patients; this procedure should be continued only until the
patient’s core temperature reaches 39°C (102.2°F).
n Using dantrolene to treat heat-related illness. It is important to remember that
heat-related illness is a distinct disease process from malignant hyperthermia.
n Managing heat-related illness with antipyretic agents. Such treatments are
ineffective and potentially deleterious.
n Failing to recognize alternative pathologies such as sepsis, meningitis, or drug
toxicity in a patient with signs of heat-related illness (eg, elevated temperature).
if a temperature of 40.2°C (104.4°F)
represents sepsis or downtrending heat
stroke, given that some cooling likely
is to have occurred during transport
to the emergency department. A
high index of suspicion must be kept
throughout the initial evaluation; if the
history or examination are equivocal
(eg, a patient found down with limited
additional history), it is reasonable
and prudent to initiate antibiotics
empirically while awaiting definitive
cultures or additional details. A
conundrum still exists on such issues
as the use of vasopressors, which may
be harmful in patients with heat stroke
but are recommended in cases of sepsis.
An infant presenting with
hyperpyrexia can be particularly
challenging to manage. The core
temperature may be elevated if the
child was over-bundled and placed in
a warm environment.23 If the history
and examination are consistent with
hyperthermia secondary to heat
exposure, it may be reasonable to employ
a period of observation with supportive
care rather than proceeding with a full
febrile infant workup. In this instance,
antipyretics should be avoided and
infants should have a rectal temperature
assessed every 15 to 30 minutes. If the
temperature improves with supportive
care alone, a sepsis evaluation can
potentially be avoided, especially if close
follow-up with the child’s pediatrician
can be arranged.23
A deleterious elevation of body
temperature also may be seen in cases
of malignant hyperthermia, a disorder
caused by an abnormal ryanodine
receptor (a type of calcium channel
receptor in the smooth endoplasmic
reticulum). Such patients almost always
present after treatment with a triggering
agent such as a depolarizing muscle
relaxant or a volatile halogenated
anesthetic. The triggering agent coupled
with skeletal muscle rigidity and
hypercapnia should help to distinguish
malignant hyperthermia from heat-
related illness. It is important to note
that although dantrolene works well to
treat malignant hyperthermia, it is not
effective in the treatment of heat stroke.
Hyperpyrexia can be seen in
patients with drug toxicity caused by
n Heat stroke is defined as a temperature >40°C (104°F) accompanied by AMS.
n Evidence of organ damage, including elevated LFTs, edematous changes on
head CT, and DIC may manifest in the days immediately following heat stroke.
n Although hematological laboratory studies may be abnormal in patients
with heat stroke, treatment with fresh frozen plasma and platelets should be
administered only if clinical hemorrhage develops.
n If shock persists after rehydration of patient, appropriate vasopressor therapy
should be initiated.
anticholinergic medications, stimulants, increased risk for severe complications.
and salicylates; serotonin syndrome; Patients with signs of multiorgan
neuroleptic malignant syndrome; dysfunction should admitted to an
ethanol withdrawal; or drug-induced intensive care setting.
fever.24 When available, the patient’s Characteristics associated with the
history can be extremely helpful in need for admission included advanced
distinguishing between these etiologies. age, comorbidities, male sex, and low
In addition, broad laboratory testing and socioeconomic status.25 The majority
empirical treatment can be helpful in of heat-related deaths occur in patients
pinpointing the underlying reason for the older than 65 years, and those with
hyperthermia. cardiovascular disease or mental illness.26
Most experts agree that children with
CRITICAL DECISION heat stroke should be admitted to a
Which cases warrant hospital pediatric critical care unit, where they
admission? can undergo appropriate monitoring and
Patients with benign forms of heat- treatment for ongoing and delayed end-
related illness such as heat rash, heat organ dysfunction.
cramps, and heat syncope can be safely Conversely, the practice at many
discharged to home with appropriate major endurance events (eg, marathons)
education. Patients with suspected heat has been to observe and carefully
syncope cane be discharged; however, it monitor the minority of athletes
is important to rule out other pathologies who are healthy at baseline with no
that may mimic a syncopal episode, comorbidities, recover rapidly and
including arrhythmia, stroke, or seizure. completely with cooling, and have
Similarly, patients with heat stress or no subsequent symptoms or signs
heat exhaustion can be rehydrated in the of complications. Such patients
emergency department, observed until generally can be discharged after an
vital signs normalize, and discharged appropriate period of observation with
home with appropriate precautions and arrangements for proper follow-up.
follow-up care. A thorough reexamination should be
Most patients with heat stroke performed prior to discharge. Those
should be hospitalized for a period who fail to improve within a few hours
of observation. Indications for despite care may be developing late
admission include hypotension, seizure, complications of heat injury, including
encephalopathy, persistent oliguria, rhabdomyolysis, acute kidney injury,
symptoms of rhabdomyolysis, persistent disseminated intravascular coagulation,
electrolyte abnormalities, evidence of or acute liver failure, and should be
persistent acute kidney injury, significant admitted for observation and diagnostic
ongoing diarrhea and vomiting, testing. 27 Admission is required if the
significant gastrointestinal bleeding, vital reexamination reveals any concerning
sign abnormalities, alterations in mental findings or if new or recurrent
status despite appropriate treatment, or an symptoms develop.
September 2017 n Volume 31 Number 9 9
 CASE RESOLUTIONS
■ CASE ONE
The athlete was cooled with
misted water spray, and ice packs
were placed to his neck and axilla.
Despite the administration of oral
fluids, he continued to feel unwell
and had a second episode of emesis.
Laboratory tests revealed mild
hypernatremia consistent with
dehydration, but were otherwise
within normal limits. The patient’s
symptoms largely resolved
following a 20-mL/kg NS bolus at
room temperature. He tolerated 16
ounces of oral rehydration solution,
and was discharged to home with
a diagnosis of heat stress. Prior
to discharge, the teenager was
cautioned about the importance
of breaks during exercise, proper
acclimatization, and hydration.
Organ damage does not always
manifest with laboratory abnormalities
early in the course of illness, and
clinicians should monitor patients with
possible heat injury closely. For those
without severe symptoms or grossly
abnormal laboratory results, a reasonable
approach is to reexamine the patient
and recheck the relevant studies on an
outpatient basis every 24 to 48 hours to
assess organ function.
Summary
Heat-related illness runs the gamut
from relatively mild disorders, including
miliaria rubra and heat stress, to life-
threatening processes such as heat stroke.
Emergency clinicians must be prepared
to initiate proper cooling rapidly and
understand which therapies might be
ineffective or even deleterious. A proper
history and physical examination should
also be performed to rule out other
diagnoses that can mimic heat-related
illness (eg, sepsis or toxicity). It also is
important to be aware of complications
that can arise as cellular injury progresses,
so that proper care can be administered in
the hours following heat insult.
10 Critical Decisions in Emergency Medicine
■ CASE TWO
Ice packs were placed to the elderly
woman’s axilla and groin. Two large-bore
IVs and two 20-mL/kg NS boluses were
administered at room temperature. A chest
x-ray confirmed appropriate endotracheal
tube placement, and no signs of acute
respiratory distress syndrome (ARDS) were
visualized. A head CT was consistent with
mild cerebral edema. Due to persistent
hypotension, a third 20-mL/kg NS bolus
was administered.
Laboratory studies revealed prerenal
azotemia, thrombocytopenia, metabolic
acidosis, elevated aspartate aminotrans­
ferase and alanine aminotransferase,
and coagulo­pathy. She subsequently was
admitted to the ICU, where she developed
multisystem organ failure consistent with
nonexertional heat stroke (eg, DIC, ARDS,
acute renal failure requiring hemodialysis,
and hypotension requiring vasopressors).
Her liver function tests continued to rise in
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1. Jardine DS. Heat illness and heat stroke. Pediatr Rev.
2007;28(7):249-258.
2. Atha WF. Heat-related illness. Emerg Med Clin North
Am. 2013; 31(4):1097-1108.
3. Howe AS, Boden BP. Heat-related illness in athletes.
Am J Sports Med. 2007;35(8):1384-1395.
4. Bergeron MF. Muscle cramps during exercise- is it
fatigue or electrolyte deficit? Curr Sports Med Rep.
2008;7(4):S50-S55.
5. Bouchama A, Knochel JP. Heat stroke. N Engl J Med.
2002;346(25):1978-1988.
6. Greenfield B, Clingenpeel J. Pediatric heat-related
illness. Emerg Med. 2016;33:249-256.
7. Ruttan T, Stolz U, Jackson-Vance S, et al. Validation
of a temperature prediction model for heat deaths
in undocumented border crossers. J Immigr Minor
Health. 2013;15(2):407-414.
8. Leon LR, Helwig BG. Heat stroke: role of the
systemic inflammatory response. J Appl Physiol.
2010;109(6):1980-1988.
9. Jardine DS, Bratton SL. Using characteristic changes
in laboratory values to assist in the diagnosis of
hemorrhagic shock and encephalopathy syndrome.
Pediatrics. 1995;96(6):1126-1131.
10. Platt M, Vicario S. Heat illness. In: Marx JA, eds.
Rosen’s Emergency Medicine: Concepts and Clinical
Practice. 7th ed. St. Louis, MO: Elsevier; 2009:1882-
1892.
11. Wyndham CH, Strydom NB, Cooke HM, et al.
Methods of cooling subjects with 
hyperpyrexia. J
Appl Physiol. 1959;14(5):771-776.
12. Heled Y, Rav-Acha M, Shani Y, et al. The “golden
hour” for heatstroke treatment. Mil Med.
2004;169(3):184-186.
13. Santelli J, Sullivan JM, Czarnik A, Bedolla J. Heat
illness in the emergency department: keeping your
cool. Emerg Med Pract. 2014;16(8):1-21; quiz 21-22.
14. Bergeron MF. Muscle cramps during exercise- is it
fatigue or electrolyte deficit? Curr Sports Med Rep.
2008;7(4):S50-S55.
15. Moore TM, Callaway CW, Hostler D. Core
temperature cooling in healthy volunteers after
rapid infusion of cold and room temperature saline
solution. Ann Emerg Med. 2008;51:153-159.
the initial 72 hours of hospitalization. A
repeat head CT on day 4 revealed marked
cerebral edema, and life support was
withdrawn on day 6.
■ CASE THREE
The overheated infant received a
peripheral IV with a 20-mL/kg bolus
of NS at room temperature. Her rectal
temperature was monitored every 30
minutes for the next 4 hours, but gradually
normalized.
As the child’s temperature improved, so
did her rash. She was able to tolerate oral
rehydration and formula without emesis,
although she continued to have loose,
non-bloody stool. Neither a septic workup
nor empiric antibiotics were initiated,
since heat exposure was felt to be the likely
source of her core temperature elevation.
Child protective services (CPS) was
notified, and the patient was discharged to
home with a family member, in accordance
with a CPS safety plan.
16. Casa DJ, McDermott BP, Lee EC, et al. Cold water
immersion: the gold standard for exertional
heat stroke treatment. Med Sci Sports Exerc.
2007;35(3):141-149.
17. Stewart TE, Whitford AC. Dangers of prehospital
cooling: A case report of afterdrop in a patient with
exertional heat stroke. J Emerg Med. 2015;49(5):630-
633.
18. Nuckton TJ, Claman DM, Goldreich D, et al.
Hypothermia and afterdrop following open water
swimming: the Alcatraz/San Francisco Swim Study.
Am J Emerg Med. 2000;18(6):703-707.
19. MacKenzie MA, Hermus AR, Wollersheim HC,
et al. Thermoregulation and afterdrop during
hypothermia in patients with poikilothermia. Q J
Med. 1993;86(3):205-213.
20. Charkoudian N. Human hermoregulation from the
autonomic perspective. Auton Neurosci. 2016;196:1-2.
21. Wendt D, van Loon LJ, Lictenbelt WD.
Thermoregulation during exercise in the heat:
strategies for maintaining health and performance.
Sports Med. 2007;37(8):669-682.
22. Coris EE, Ramirez AM, Van Durme DJ. Heat illness
in athletes: the dangerous combination of heat,
humidity and exercise. Sports Med. 2004;34(1):9-16.
23. Cheng TL, Partridge JC. Effect of bundling and
high environmental temperature on neonatal body
temperature. Pediatrics. 1993;92(2):238-240.
24. Khoujah D, Hu K, Calvello EJ. The management of the
hyperthermic patient. Br J Hosp Med. 2011;72(10):571-
575.
25. Pillai SK, Noe RS, Murphy MW, et al. Heat illness:
predictors of hospital admissions among emergency
department visits- Georgia, 2002-2008. J Community
Health. 2014;39(1):90-98.
26. Christenson ML, Geiger SD, Anderson HA. Heat-
related fatalities in Wisconsin during the summer of
2012. WMJ. 2013;112(5):219-223.
27. Moran DS, Gaffin SL. Clinical management of heat-
related illnesses. In: Wilderness Medicine, Auerbach
PS. (Ed), Mosby, St. Louis; 2001: 290.

Trauma Airway Management
Horton CL, Brown CA, and Raja AS. Trauma Airway Management. J Emerg Med. 2014, 46(6):814-820.
The successful airway management
of a trauma victim hinges on rapid,
decisive action. Clinicians must identify
patients who require emergent intubation
by answering three critical questions.
• Is there a failure to maintain or
protect the airway? A trauma airway
can be assessed by calculating the
Glasgow Coma Scale Score (scores
<12 indicate significant brain injury
requiring intubation). Testing the
gag reflex is not recommended as it
can induce vomiting. Better clinical
indicators of airway protection include
the patient’s ability to phonate,
swallow, and handle secretions.
• Is there a failure of oxygenation
or ventilation? This can be gauged
by evaluating respiratory effort,
exhalation of carbon dioxide, and
oxygen saturation. Such failures
can indicate impending respiratory
collapse.
• Is there a need for intubation based
on the anticipated clinical course? The
opportunity to intubate early and in a
controlled setting should be seized in
patients with comorbid conditions.
If any of these questions can be answered
in the affirmative, the clinician must
proceed to the best intubation method
based on the patient’s stability and the
availability of equipment.
The LEMON mnemonic (look
externally, evaluate 3-3-2 rule, Mallampati
score, obesity/obstruction and neck
mobility) will help predict patients in
whom direct laryngoscopy will be difficult.
The MOANS mnemonic (mask seal,
obesity/obstruction, age >55, no teeth and
Critical Decisions in Emergency Medicine’s series of LLSA reviews features articles articles from ABEM’s 2017 Lifelong Learning and
Self-Assessment Reading List. Available online at acep.org/llsa and on the ABEM website.
The LLSA
Literature Review
By Grace Landers MD, LT (MC), and Daphne Morrison-Ponce MD, LCDR(MC)
Naval Medical Center, Portsmouth, VA
Reviewed by Andrew J. Eyre, MD
stiff lungs) helps predict difficult mask weight (a lower dose is required in cases
ventilation. Rapid sequence intubation of shock). Ketamine (1.5 mg/kg) is an
(RSI) is believed to be the safest and most alternative to etomidate, especially to
successful approach in patients who lack facilitate awake intubations. The paralytic
difficult airway characteristics. of choice remains succinylcholine
It is paramount to use an algorithmic (1-1.5 mg/kg) due to its short duration
approach and plan for adjunct methods and rapid onset. Rocuronium
any time a difficult airway is predicted. (1.0 mg/kg) is a viable alternative when
However, when the need for immediate succinylcholine is contraindicated.
intubation forces the clinician to act, a Although trachea-bronchea injuries
single “best attempt” (best device and are relatively rare, they should be
most experienced operator) RSI followed considered in any trauma patient with
by a surgical airway is recommended. dyspnea, respiratory distress, hoarseness,
According to the LEMON or dysphonia accompanied by pain,
algorithm, cervical spine immobilization neck ecchymosis, swelling, or soft-tissue
automatically predicts a possible crepitus. Such cases should be managed
difficult airway; in such cases, manual with awake intubation techniques,
immobilization outside the collar is tracheostomy, or cricothyrotomy.
required. While direct laryngoscopy and Otherwise, unguided placement of a
RSI have not been shown to significantly large-bore endotracheal tube or positive-
affect clinical outcomes regarding c-spine
pressure ventilation can quickly complete
stabilization, the use of video-enhanced
a partial tracheal transection.
devices may be beneficial.
******
Patients with suspected head injuries The views expressed in this article are those of the authors
may benefit from pretreatment with and do not necessarily reflect the official policy or position
of the Dept. of the Navy, Dept. of Defense or the United
lidocaine (1.5 mg/kg) and fentanyl States Government.
(2-3 mg/kg) to mitigate the rise in We are military service members. This work was prepared
as part of our official duties. Title 17 U.S.C. 105 provides
intracranial pressure associated with that ‘Copyright protection under this title is not available
for any work of the United States Government.’ Title 17
laryngeal manipu­lation. Etomidate U.S.C. 101 defines a United States Government work as a
(0.3 mg/kg) can be used for induction; work prepared by a military service member or employee
of the United States Government as part of that person’s
dosing should be based on lean body official duties.
KEY POINTS
n Delays in securing an advanced airway can compromise patient management.
n Airway deterioration can be prevented by performing a rapid clinical assessment
and utilizing an airway algorithm to guide trauma management.
n Clinicians should maintain a high level of suspicion for tracheobronchial injury and
plan for difficult airway management.
n Appropriate use of advanced airway tools, surgical airways, and consultation with
specialists is important for the successful management of any trauma patient.
September 2017 n Volume 31 Number 9 11
 A 45-year-old man with lightheadedness.

The Critical ECG

Sinus rhythm with second-degree atrioventricular block type 1 By Amal Mattu, MD, FACEP
Dr. Mattu is a professor, vice chair, and
(Mobitz I, Wenckebach), rate 60, high left ventricular voltage, benign director of the Emergency Cardiology
early repolarization (BER). Mobitz I characterized by regular P waves Fellowship in the Department of
Emergency Medicine at the University
(here, the atrial rate is approximately 80/min and regular) with progressive of Maryland School of Medicine in
Baltimore.
prolongation of the PR interval until a P wave fails to conduct to the
ventricle, producing a pause in the ventricular response. ST-segment
elevation (STE) is noted in leads V2-V4. The presence of a slight upstroke at the end of the QRS complex in leads V3-V4
and lead II, producing what is sometimes referred to as a “fishhook appearance” at the end of the QRS complex,
is characteristic of BER. Acute myocardial infarction (MI) and BER can sometimes be confused. Helpful clues that
distinguish acute MI and exclude BER include the presence of reciprocal ST-segment depression in some leads, any
convex upward ST-segment elevation, or evolving changes noted on serial ECGs. Additionally, the STE of BER is rare in
the elderly, especially elderly women, and usually localized to the anterior and lateral precordial leads.

From Mattu A, Brady W, ECGs for the Emergency Physician 2. London: BMJ Publishing; 2008:11,23. Reprinted with permission.

12 Critical Decisions in Emergency Medicine

 Little Monsters
Parasitic Infections

LESSON 18

By Alex H. Wang, MD; and Theresa M. Nguyen, MD

Dr. Wang is a global health fellow at Global Emergency Care in Masaka,
Uganda. Dr. Nguyen is assistant professor of emergency medicine at Loyola
University Medical Center in Maywood, Illinois.
Reviewed by Walter L Green, MD, FACEP

OBJECTIVES
On completion of this lesson, you should be able to:
CRITICAL DECISIONS
1. Identify the most common and life-threatening
manifestations of parasitic infections. n What symptoms are of greatest concern when
2. Recognize which patients are at highest risk. evaluating a suspected parasitic infection?
3. Detail the appropriate workup, diagnosis, and n How should a suspected parasitic infection
management that should be initiated in the emergency initially be assessed?
department.
n What diagnostic tests can help identify
4. Explain the treatment options for infections caused by
various classes of parasites. specific parasitic infections?
5. List strategies for counseling patients on the prevention n Which treatments should be initiated in the
of parasitic infections during future travel. emergency department?
n Which patients can be safely discharged?
FROM THE EM MODEL
10.0 Systemic Infectious Disorders
10.4 Protozoan/Parasites

Continuing trends in global interdependence and shifting climate changes have triggered an increase in the
number of patients presenting with parasitic infections. Emergency physicians must be aware of the unique life-
threatening complications posed by these insidious organisms. Relevant diagnostic information, including details
about diet and travel, combined with an expeditious examination of high-risk patients can help mitigate the potentially
deadly sequelae of these microscopic invasions.

September 2017 n Volume 31 Number 9 13

 CASE PRESENTATIONS
■ CASE ONE
An otherwise-healthy 44-year-
old man arrives via ambulance after
having a witnessed generalized tonic-
clonic seizure. He is accompanied by
his wife, who reports that the patient
recently returned from a trip to Central
America, where he had frequent
exposures to farms and wild animals.
The patient does not recall any recent
trauma; he denies weight loss, headache,
and nausea, and states he felt “perfectly
fine” until right before the episode.
His vital signs are blood pressure
115/78, heart rate 76, respiratory rate
18, temperature 37.4°C (99.3°F), and
oxygen saturation 98% on room air.
The patient is alert and oriented to
person and place but not to time. A full
neurological examination is significant
for papilledema, but does not reveal
any other focal deficits.
■ CASE TWO
An ill-appearing 14-year-old
girl presents with palpitations and
tachycardia. She was diagnosed with
Considering the broad spectrum of
parasitic infections, their vastly different
presentations, and the general lack of
emphasis on tropical diseases during
medical training, it is up to the clinician
to discern relevant symptoms and findings
and initiate appropriate treatment.
Broadly defined, a parasite is an organ­
ism that lives on or within a host organism,
deriving resources at the expense of its
host. There are three classes of parasites
that cause disease in humans: protozoa,
helminths, and ectoparasites. Protozoa
account for a diverse group of unicellular
organisms classified based on motility
(eg, ciliated, flagellated, amoeboid, and
sporozoan eukaryotes). Helminths are
large, multicellular organisms generally
visible to the naked eye in their adult
stages. There are three primary groups of
helminths that cause disease in humans:
roundworms, flatworms, and tapeworms.
Here, we will specifically address protozoa
and helminths.
14 Critical Decisions in Emergency Medicine
a viral syndrome 2 weeks ago, after
presenting with fever, shortness of
breath, and headache. Her mother
reports a family trip to Brazil one
month ago.
Her vital signs are blood pressure
100/56, heart rate 158, respiratory rate
18, temperature 38.4°C (101.2°F), and
oxygen saturation 92% on room air.
An electrocardiogram (ECG) shows low
QRS voltage, prolonged QT intervals,
and T-wave inversions. A chest x-ray
is remarkable for bilateral pleural
effusions and cardiomegaly. The heart
examination is notable for tachycardia
as well as a new “blowing” holosystolic
murmur, best appreciated at the apex.
The head, eyes, ears, nose, and throat
(HEENT); lung; and abdominal
examinations are normal, and no
stigmata of endocarditis were found.
■ CASE THREE
A 62-year-old woman arrives
via ambu­lance with profuse watery
diarrhea and altered mental status
(AMS). Staff at her nursing home
CRITICAL DECISION
What symptoms are of greatest
concern when evaluating a
suspected parasitic infection?
Parasitic infections can involve
multiple organ systems and a broad
variety of symptoms (Table 1). While
a large proportion of patients are
asymptomatic, emergency physicians
should be prepared to recognize acute
and often deadly presentations.
Neurocysticercosis, which occurs when
Taenia solium larvae are acquired via the
fecal-oral route (Figure 1), is a leading
cause of acquired epilepsy in developing
countries. The ingested cysticerci cross
into the bowel wall following activation
from gastrointestinal fluids, and encyst
in tissues and terminal organs. While
most patients remain asymptomatic,
roughly 2% of infections encyst in the
eye, manifesting as proptosis, visual
disturbances, or vision loss.1 More
commonly, cysticerci encyst in the central
called 911 when the patient became
disoriented. They report that she
has been having mild abdominal
cramping and 10 to 12 bowel
movements every day for the past
2 weeks, despite the administration
of loperamide. She has a history
of multiple myeloma, but has had
no fever, foreign travel, or recent
antibiotic use. Her stool is watery,
non-bloody, non-foul smelling, and
without mucus.
Her vital signs are blood pressure
96/65, heart rate 110, respiratory
rate 14, tempera­ture 37.8°C (100°F),
and oxygen saturation 97% on
room air. The patient opens her eyes
to voice and mutters in incoherent
sentences. The HEENT examination
is significant for dry mucous
membranes. Distal pulses are 1+
in all four extremities. Skin turgor
is decreased. Her abdomen is soft
and nontender without any masses,
rebound, or guarding. The heart and
lung examinations are unremarkable.
nervous system (CNS) and compress
neurological structures. These lesions
present as seizures more than 50%
of the time, and commonly result in
intracranial hypertension, cognitive
dysfunction, and focal neurological
deficits. Papilledema is the most common
sign of neurocysticercosis (seen in ≤28%
of patients); in a small percentage of cases,
inflammatory host reactions result in
encephalitis or stroke-like presentations.2
Chagas disease can be recognized
either in the acute or chronic form. It is
spread by triatomine “kissing bugs” that
deposit feces containing Trypanosoma
cruzi into the bloodstream, which
subsequently invade host cells (Figure 2).
In the acute phase, most patients are
asymptomatic. Nonspecific symptoms
such a fever, malaise, headache, and
anorexia can be present. Classically, the
most recognized marker of the acute
phase of Chagas disease is a painless
unilateral swelling of the eye called
Romaña’s sign, seen in 20% to 50% of
acute cases. Patients also may present
with fever, persistent tachycardia or a
nonpruritic rash. The chronic phase
can present weeks to months after the
initial infection. Symptomatic patients
may suffer from arrhythmias, congestive
heart failure, thromboembolism,
megaesophagus, and toxic megacolon.
Cryptosporidiosis, a common cause
of traveler’s diarrhea worldwide, is
spread as a resistant oocyst via the
fecal-oral route. Episodes generally are
self-limiting; however, the disease can
have a severe and often fatal clinical
course in vulnerable populations. In
immunocompromised patients, infection
principally is localized to the distal
small intestine and respiratory tract,
presenting as mild watery diarrhea
and cough. Although symptoms most
frequently resolve in 2 to 3 weeks, they
can recur after a brief period of recovery.
In the immunocompromised, fulminant
disease can cause the passage of more
than 21 stools each day for more than 2
months, leading to failure to thrive and
malabsorption. Rarely, cryptosporidiosis
disseminates into numerous organ
systems and causes complications such
as esophagitis, appendicitis, cholangitis,
pancreatitis, and intestinal perforation.3
FIGURE 1. Lifecycle of Cysticercosis
p Oncospheres develop
i into cysticerci in muscles.
Ž Oncospheres hatch,
penetrate intestinal
wall, and circulate
to musculature.
Humans acquire the
infection by ingesting
raw or undercooked
meat from infected
animal host.
 Embryonated eggs and/or
gravid proglottids are
ingested by pigs or humans.
p
i p
d
Œ
Eggs or gravid proglottids in feces
and passed into environment
COURTESY OF THE US CENTERS FOR DISEASE CONTROL AND PREVENTION
CRITICAL DECISION
How should a suspected parasitic
infection initially be assessed?
The presentation of a parasitic
infection differs dramatically depending
on its etiology and location, duration, and
stage of infection. In the undifferentiated
patient, parasites may not be high on
the list of potential diagnoses; however,
specific elements of the history are
essential to consider. The clinician should
determine dates and locations of travel,
including layovers, to narrow down
specific infections based on incubation
periods. It also is important to obtain
details regarding trip accommodations,
exposures to animals and insect bites,
and sources of drinking water. Travel
and food consumption history also
should be emphasized, given that many
of these diseases are transmitted in
tropical climates and via the fecal-oral
route.4 Knowledge of the geography
and epidemiology of where parasites are
endemic can be useful. Familiarity with
parasitic lifecycles, means of transmission,
and intermediate hosts can further
narrow the differential diagnosis.
The mechanisms by which parasites
cause acute disease generally fall into
two categories: mass effect and host
inflammatory response. The host
inflammatory response elicits systemic
Cysticerci may develop
in any organ, being more
common in subcutaneous
tissues as well as in the
brain and eyes.
 for eosinophilia may be useful in disting­
 can be initiated, although testing is
Scolex attaches
to intestine.
‘
Adults in small intestine.
Infective stage =pi
Diagnostic stage =p d
symptoms via a Th2-type pattern
with the production of interleukins,
immunoglobulins, and activation of mast
cells. 5 A high parasitic load can increase
the risk of mass effect-induced symptoms
such as intestinal obstruction (eg, heavy
ascariasis).6 Acute interventions should
be targeted at blunting the inflammatory
response or decreasing the parasitic load.
Of note, antiparasitic drugs can cause
a Jarisch-Herxheimer-like reaction to
dying organisms.7
Parasitic infections typically do not
require definitive therapy in the emergency
department unless a causative agent is
detected by the presence of eggs, worm
segments, or cysts. In the rare case of
life-threatening illness, routine emergency
algorithms should be applied with no
change in management specific to the
parasitic etiology. Stabilization is essential
in any patient with systemic disease (eg,
seizure, anaphylaxis, or organ failure).
A seizure secondary to
neurocysticercosis should be managed
much like any other first-time
seizure; priorities include securing the
airway if necessary, administering
fluids for hypotension, and treating
with benzodiazepines or phenytoin.
Arrhythmia in cases of Chagas disease
may require antiarrhythmic agents
and/or cardioversion in addition to a
cardiology consultation. Patients with
cryptosporidial infections require fluid
resuscitation and electrolyte replacement.
Protozoan infections present with a
wider range of symptoms and tend to be
more acute, whereas helminth infections
predominantly manifest with chronic sym­
ptomatology. An initial CBC to look
uishing between the two. Eosinophilia
(>500/uL) is common in helminth
infections but not in protozoan infections.8
Stool studies for ova and parasites also
neither sensitive nor specific and cannot
distinguish between classes of helminths.
CRITICAL DECISION
What diagnostic tests can help
identify specific parasitic infections?
The diagnosis of cysticercosis
relies on radiographic imaging and
serological studies alongside clinical and
September 2017 n Volume 31 Number 9 15

FIGURE 2. Triatomine Vector
of Chagas Disease
epidemiological data.9 A patient may
have clinical disease from a single or
small number of cysticerci with negative
serological results but visible lesions on
imaging. Parasites also may reside in
locations other than the brain; in such
cases, CNS imaging may be negative
and serological results might be positive,
indicating an antibody response to
lesions elsewhere (eg, the spinal cord).
The location and characteristics of the
lesions on imaging, especially on magnetic
resonance imaging (MRI), are essential to
determine the best treatment modalities.
A fundoscopic examination must be
performed prior to initiating therapy
in patients with visual or neurological
changes. Lumbar puncture, which can
help exclude other diagnoses, may show
elevated white blood cells. Otherwise,
computed tomography (CT) of the
brain is useful for identifying calcified
cysticerci; on the other hand, MRI may
be more sensitive for smaller lesions
and intraventricular and subarachnoid
involvement. MRI also can better identify
associated degenerative changes around
cysticerci or the pathognomonic finding
of a scolex. If imaging is not diagnostic,
the Centers for Disease Control (CDC)
recommends a serum enzyme-linked
immunoelectrotransfer blot assay (EITB).
However, these tests are dependent on the
number, type, and location of the cysts.
Chagas disease may be diagnosed
in either the acute or chronic phases of
infection. In acute cases, a peripheral
blood smear can identify the infectious
larval agents. Polymerase chain reaction
(PCR) assays also are highly specific and
may be positive before trypomastigotes
can be detected on blood smear. These
tests are less relevant in chronic cases, in
which the level of parasitemia decreases
per its natural course. There is no gold
16 Critical Decisions in Emergency Medicine
standard approach for diagnosing chronic hypertension, edema, or hydrocephalus
infection, which relies on at least two if present. Commonly used antiepileptic
positive serological tests performed in drugs include phenytoin, carbamazepine,
parallel. These may be enzyme-linked levetiracetam, and topiramate. Because
immunosorbent or immunofluorescent seizures recur in as many as 40%
antibody assays, which can assess for of patients with first-time seizure,
whole parasite lysate or recombinant research supports the administration
antigens. Auxiliary evaluations may be of antiepileptic therapy for 6 to 12
required for the different manifestations months after radiographic resolution of
of disease, including echocardiography the lesion(s).10 For patients who present
for heart failure, ECG monitoring with hydrocephalus or herniation,
for arrhythmia, and endoscopy for endoscopic or open surgical resection
megaesophagus. should be considered. The initiation of
Tests for Cryptosporidium typically antihelminthic therapies (eg, albendazole
are not included in routine ova and or praziquantel) and anti-inflammatory
parasite testing. It is incumbent on the agents are almost never regarded as
clinician to request specific studies for medical emergencies; an infectious disease
this parasite if there is a high index of specialist should be consulted prior to
suspicion. Multiple stool samples collected administration of these medications.
on separate days may be necessary, The treatment of Chagas disease
since Cryptosporidium can be excreted is complicated and should be tailored
intermittently. Infection also may be to each case based on the phase and
diagnosed by microscopy, PCR, or manifestation of the disease and the
immunohistological testing. Although patient’s demographic group. The only
specimens usually are present in stool, antiparasitic agents with proven efficacy
they also can be detected in duodenal against Chagas are benznidazole and
aspirates, bile secretions, and respiratory nifurtimox; however, both drugs are
secretions. A microscopic evaluation can contraindicated in pregnant women and
be performed on wet mount and stained in patients with severe renal or hepatic
slides. These are complemented by enzyme dysfunction. Particularly in its chronic
immunoassays against the oocyst wall, phase, the disease may present with
which have increased sensitivity. However, cardiac symptoms such as heart failure,
the gold standard for diagnosis is PCR. arrhythmia, or thromboembolism,
or gastrointestinal symptoms such as
CRITICAL DECISION megacolon or megaesophagus, both of
Which treatments should be which can be treated symptomatically.
Progression of either disease will require
initiated in the emergency
endoscopic or surgical intervention.
department? The acute treatment of Chagas-induced
The acute treatment of neurocysticer­ heart failure generally is supportive,
cosis should be focused on the control although particular caution should be
of seizures with antiepileptic agents employed with the use of beta-blockers,
and the management of intracranial as bradycardia is common. In these
n When assessing a returned traveler, it is imperative to obtain detailed information
about travel dates, modes of transportation, sources of water, outdoor exposures,
and contact with animals.
n Be familiar with what laboratory testing for parasites is available at your institution.
n Refer to the CDC website or The Yellow Book for additional information regarding
tropical infections and travel recommendations.
n Consult an infectious disease specialist as soon as a parasitic infection is
suspected.
situations, cardiac pacing may be
offered for heart block or sinus node
dysfunction. Amiodarone is the preferred
agent for Chagas-induced ventricular
arrhythmias; catheter ablation and
implantable cardioverter-defibrillator
placement also may be considered.
Antithrombotic therapy should be
initiated based on the patient’s Chagas
cardioembolism risk score.11 Cardiac
tamponade, which can occur secondary
to pericardial effusion, may require
pericardiocentesis (in rare cases).
Most immunocompetent patients with
cryptosporidiosis will recover without
treatment. Diarrhea should be managed
with fluid replacement; however, those
with severe and prolonged symptoms
may require additional supportive
care such as antimotility agents
and enteral or parenteral nutrition.
Nitazoxanide is the first-line therapy
for immunocompromised patients older
than 1 year. However, nitazoxanide
alone is not effective in HIV-infected
patients, who also require appropriate
control with antiretroviral therapy.12
Adjunct therapy with paromomycin and
azithromycin may improve outcomes
in immunocompromised patients
with a volume loss greater than 10
liters per day, and in those who failed
nitazoxanide monotherapy.
CRITICAL DECISION
Which patients can be safely
discharged?
Acute interventions are unnecessary
for the vast majority of parasitic
infections. Those with confirmed
infections may require an infectious
disease consultation to determine
long-term management. However,
n Failing to consider parasitic infections as part of the differential diagnosis. At
the same time, clinicians shouldn’t assume that illness in a returned traveler is
secondary to a tropical disease or parasitic infection.
n Failing to discuss preventative strategies for future travel and ensuring adequate
follow-up care prior to discharge.
n Treating all cases of traveler’s diarrhea with antibiotics. Most cases will resolve
with supportive care alone.
TABLE 1. Life-Threatening Presentations of Parasitic Infections
Organ system Presentation Notable parasites
Cardiovascular Anaphylaxis13 Echinococcus sp. (Hydatid disease)
Anemia14,15 Necator americanus (New-world hookworm)
Trichuris trichiura (Whipworm)
Diphyllobothrium latum (Fish tapeworm)
Babesia sp. (Babesiosis)
Plasmodium sp. (Malaria)
Cardiomyopathy16 Trypanosoma cruzi (Chagas disease)
Trichinella sp. (Trichinosis roundworm)
Taenia solium (Cysticercosis)
Entamoeba histolytica (Amoebiasis)
Pulmonary Acute Respiratory Strongyloides stercoralis (Threadworm)
Distress Syndrome17 Babesia sp. (Babesiosis)
Plasmodium sp. (Malaria)
Gastrointestinal Appendicitis18 Enterobius vermicularis (Pinworm)
Taenia sp. (Beef tapeworm)
Trichuris trichiura (Whipworm)
Ascaris lumbricoides (Giant roundworm)
Entamoeba histolytica (Amoebiasis)
Cholangitis19 Fasciola hepatica (Common liver fluke)
Clonorchis sinensis (Chinese liver fluke)
Opisthorchis sp. (Southeast Asian liver fluke)
Ascaris lumbricoides (Giant roundworm)
Echinococcus sp (Hydatid disease)
Gastroenteritis20 Cryptosporidium parvum (Cryptosporidiosis)
Cyclospora cayetanensis (Cyclosporiasis)
Isospora belli (Isosporiasis)
Giardia lamblia (Giardiasis)
Entamoeba histolytica (Amoebiasis)
Peritonitis21 Entamoeba histolytica (Amoebiasis)
Echinococcus sp. (Hydatid disease)
Ascaris lumbricoides (Giant roundworm)
Strongyloides stercoralis (Threadworm)
Neurological Encephalitis Toxoplasma gondii (Toxoplasmosis)
Trypanosoma cruzi (Chagas disease)
Seizure Taenia solium (Neurocysticercosis)
Entamoeba histolytica (Amoebiasis)
Echinococcus sp. (Hydatid disease)
stable patients with normal vital signs, that parasitic-induced mass effect can
unremarkable test results, and adequate cause emergent presentations such as
follow-up plans can be discharged appendicitis, pancreatitis, cholangitis,
safely. Hospitalization may be required, peritonitis, and obstruction. Such findings
depending on the severity and etiology of more commonly are found with helminth
the organ systems affected. It is crucial infections. Although such manifestations
to maintain a higher index of suspicion are rare in the United States, they can be
and a lower threshold for intervention in life-threatening. An emergency surgery
children and the immunosuppressed, in consultation may be pertinent.
whom parasitic infections can have long- In high-risk populations, it is necessary
term and devastating consequences. to emphasize preventative measures. Basic
It also is important to consider hygiene and sanitation are paramount,
particularly in relation to the consumption
of water and food products. Although
these practices are most important during
travel abroad, they remain relevant
domestically. T. solium infection is found
in low-income countries in Latin America,
Asia, and sub-Saharan Africa, where
free-range pigs are common. Human
access to latrines often is limited in such
settings, resulting in the contamination of
water sources and further propagating the
parasitic lifecycle.
Chagas disease, which is found in
September 2017 n Volume 31 Number 9 17
 CASE RESOLUTIONS
■ CASE ONE
The returned traveler with a
first-time seizure was evaluated with
an initial workup that included a
CBC, basic metabolic panel (BMP),
and hepatic and toxicology panels,
which were within normal limits. The
patient’s ECG was unremarkable. A
CT head was negative for intracranial
mass lesions or hydrocephalus, but
revealed local hypoattenuation in the
left temporal lobe. A funduscopic
examination showed papilledema,
and a lumbar puncture revealed an
intracranial pressure of 220 mm H 2O.
An MRI with gadolinium
enhancement revealed a solitary
cystic lesion in the left temporal lobe
surrounded by a perifocal edema
with a bright nodule in the cyst.
An electroencephalogram showed
intermittent left temporal slowing
without epileptic activity. Stool sample
analyses were unremarkable, and an
enzyme-linked immunoelectrotransfer
blot assay detected no antibodies
against T. solium in serum or
cerebrospinal fluid.
the tropical climates of the Americas,
is spread by triatomine bugs that nest
in the crevices of houses often made
of mud and clay. These insects are
nocturnal and feed on humans while
they sleep. Clean rooms, mosquito nets
and insecticides can decrease the risk
of infection. Cryptosporidiosis is a very
tenacious organism that is prevalent
globally. Oocysts are resistant to alcohol-
based sanitation as well as treatment
with chlorine and iodine; however, they
are sensitive to extreme heat. In settings
where drinking water is suspect, boiling
for at least 1 minute prior to consumption
can prevent infection.
Summary
Continuing trends in global
interdependence and shifting climate
changes are likely to increase the
prevalence of parasitic infection.
Emergency clinicians must be able to
discern relevant information from a
patient’s physical examination and
18 Critical Decisions in Emergency Medicine
A diagnosis of neurocysticercosis was
made and carbamazepine was initiated.
Infectious disease was consulted
regarding admission.
■ CASE TWO
The teenage girl received a full infec­
tious workup, including blood, sputum,
and urine cultures; empirical treatment
with IV vancomycin and cefepime also
was initiated. Bedside echocardiography
confirmed a large pericardial effusion,
significant mitral regurgitation, and
septal dyskinesia. The patient was taken
to the cardiac catheterization laboratory
for emergent pericardiocentesis. During
the procedure, she experienced an
episode of wide-complex monomorphic
tachycardia and was cardioverted.
Her peripheral blood smear was
notable for T. cruzi parasites, confirming
a diagnosis of acute Chagas heart
disease. Infectious disease recommended
treatment with benznidazole. The girl’s
heart rate and vital signs eventually
stabilized, and she was discharged home
after an uncomplicated hospital course.
comprehensive history, including details
about recent travel and dietary habits.
Pediatric and immunocompromised
patients warrant particular attention,
particularly with respect to comorbidities
and malnutrition. The acute diagnosis
of these infections may be dependent
on the exclusion of other common
manifestations. Eosinophilia, stool
sample testing, and immunohistological
or serological assays may be suggestive.
REFERENCES
1. García HH, Gonzalez AE, Evans CA, et al. Taenia
solium cysticercosis. Lancet. 2003;362(9383):547-556.
2. Singhi P. Neurocysticercosis. Ther Adv Neurol Disord.
2011;4(2):67-81.
3. Hunter PR, Nichols G. Epidemiology and
clinical features of Cryptosporidium infection in
immunocompromised patients. Clin Microbiol Rev.
2002;15(1):145-154.
4. Lo RR V 3rd, Gluckman SJ. Fever in the returned
traveler. Am Fam Physician. 2003;68(7):1343-1350.
5. MacDonald AS, Araujo MI, Pearce EJ. Immunology
of parasitic helminth infections. Infect Immun.
2002;70(2):427-433.
6. Villamizar E, Méndez M, Bonilla E, et al. Ascaris
lumbricoides infestation as a cause of intestinal
obstruction in children: experience with 87 cases. J
Pediatr Surg. 1996;31(1):201-205.
7. Barar FSK. Essentials of Pharmacotherapeutics. New
Delhi, India: S. Chand & Company; 2006.
■ CASE THREE
The elderly woman with AMS and
profuse diarrhea initially was managed
for severe hypovolemia. A 16-gauge IV
was placed in her right cephalic vein,
and fluid resuscitation with normal
saline was initiated. Her laboratory
tests were remarkable for a hemoglobin
level of 8.9 g/dL and a white blood cell
count of 3300/mm3. Serum potassium
was depressed at 2.4 meq/L. Routine
blood cultures and a PCR evaluation for
cytomegalovirus were negative.
Stool sample analyses were
remarkable for 2 to 3 polymorpho­
nuclear leukocytes/hpf with mild
mucus but no visible blood. A fecal
occult blood test was negative, and no
pathogen was seen on Gram stain. A
cryptosporidial infection was suspected,
so a stool sample was submitted for
further analysis via acid-fast stain to
evaluate for oocysts. Infectious disease
was consulted regarding admission and
further treatment. The patient ultimately
was discharged home in stable condition
after her diarrhea resolved with IV fluid
resuscitation and electrolyte replacement.
8. Schulte C, Krebs B, Jelinek T, et al. Diagnostic
significance of blood eosinophilia in returning
travelers. Clin Infect Dis. 2002;34(3):407-411.
9. Del Brutto OH, Rajshekhar V, White AC Jr, et al.
Proposed diagnostic criteria for neurocysticercosis.
Neurology. 2001;57(2):177-183.
10. Carpio A, Hauser WA. Prognosis for seizure recurrence
in patients with newly diagnosed neurocysticercosis.
Neurology. 2002;59(11):1730-1734.
11. Sousa AS, Xavier SS, Freitas GR, Hasslocher-
Moreno A. Prevention strategies of cardioembolic
ischemic stroke in Chagas’ disease. Arq Bras Cardiol.
2008;91(5):306-310.
12. Abubakar I, Aliyu SH, Arumugam C, et al. Treatment of
cryptosporidiosis in immunocompromised individuals:
systematic review and meta-analysis. Br J Clin
Pharmacol. 2007;63(4):387-393.
13. Langer JC, Rose DB, Keystone JS, et al. Diagnosis
and management of hydatid disease of the liver.
A 15-year North American experience. Ann Surg.
1984;199(4):412-417.
14. Farid Z, Patwardhan VN, Darby WJ. Parasitism and
anemia. Am J Clin Nutr. 1969;22(4):498-503.
15. Hatcher JC, Greenberg PD, Antique J, et al. Severe
babesiosis in Long Island: review of 34 cases and their
complications. Clin Infect Dis. 2001;32(8):1117-1125.
16. Kirchhoff LV, Weiss LM, Wittner M, Tanowitz
HB. Parasitic diseases of the heart. Front Biosci.
2004;9:706-723.
17. Cook GA, Rodriguez H, Silva H, et al. Adult respiratory
distress secondary to strongyloidiasis. Chest.
1987;92(6):1115-1116.
18. da Silva DF, da Silva RJ, da Silva MG, et al. Parasitic
infection of the appendix as a cause of acute
appendicitis. Parasitol Res. 2007;102(1):99-102.
19. Carpenter HA. Bacterial and parasitic cholangitis.
Mayo Clin Proc. 1998;73(5):473-478.
20. Stürchler D. Parasitic diseases of the small intestinal
tract. Baillieres Clin Gastroenterol. 1987;1(2):397-424.
21. Bethony J, Brooker S, Albonico M, et al. Soil-
transmitted helminth infections: ascariasis, trichuriasis,
and hookworm. Lancet. 2006;367(9521):1521-1532.

EMPTYING AN INTRATHECAL PUMP RESERVOIR
Contraindications
While there are no absolute contra­
indications in the truly emergent situation,
relative contraindications include
overlying infection and coagulopathy.
Risks and Benefits
The primary risks of accessing the
pump reservoir include the introduction
of infection, failure to access the device or
remedy the clinical situation, and damage
to nearby structures. Theoretically, the
procedure could result in the delivery of
unwanted medication if the reservoir’s
pressure is increased or its contents are
partially injected into subcutaneous space
during the drainage process.
Emptying the reservoir in cases
of overdose can decrease the amount
of medication exposure and prevent
further toxicity. Depending on the type,
concentration, and amount of drug that
remains, drainage may be beneficial.
Alternatives
There is limited literature about
the appropriate resuscitation and
management of patients with medication
overdose due to intrathecal pumps.
Alternative treatments include irrigation
of the cerebrospinal fluid (CSF) through
spinal catheters placed at multiple levels,
The Critical
Procedure
Intrathecal drug delivery, which relies on a small “pain
pump” surgically implanted under the skin, has become an
increasingly common method for relieving chronic pain. As
such, emergency clinicians must be prepared to manage the
treatment’s potential complications, including medication
overdose (a rare side effect most commonly caused by device
malfunction or programming errors).
By Steven J. Warrington, MD, MEd
Dr. Warrington is director of the Emergency
Medicine Residency Program and academic chair of
the Department of Emergency Medicine at Orange
Park Medical Center in Orange Park, Florida.
and withdrawal of large volumes of Special Considerations
CSF via lumbar puncture. It may be necessary to remove the
Reducing Side Effects contents of the pump reservoir in cases
of suspected overdose. The clinician
Medtronic discourages the use of
also should be aware of the potential
an open syringe when emptying certain
pumps. High pressures in the reservoir for life-threatening withdrawals with
may result in the ejection of its contents. certain medications. Of note, emptying
A three-way stopcock or extension tubing the pump contents and supportive care
with clamp is recommended. Ultrasound are not always enough; further lifesaving
guidance may be beneficial. interventions might be needed.
TECHNIQUE
1. Obtain consent if possible and notify staff.
2. Consider adjunct therapies to support the patient’s cardiopulmonary status.
Patients may continue to deteriorate both during and following the procedure.
3. Obtain and assemble necessary equipment: 22-gauge needle, syringe (≥ 20 mL),
3-way stopcock or extension set with clamp, antiseptic agent, ultrasound probe cover
(optional), and ultrasound (optional).
4. Locate the device and fill port. (The fill port should be in the center of the device.)
5. Prepare the site with antiseptic and insert the needle directed at the fill port; advance
until it touches the bottom of the fill reservoir. The passage through subcutaneous
tissue typically can be felt, as can the silicone septum and metal bottom of the
reservoir.
6. Open the clamp/stopcock and slowly aspirate (remember to close if the volume
exceeds the capacity of one syringe).
7. Stop the procedure when bubbles stop forming and negative pressure is felt OR
wait 5 seconds after the fluid can no longer be aspirated.
8. Remove the needle, record the results/procedure (including volume of medication
aspirated), and reevaluate the patient.
9. Contact the pump manufacturer when able.
September 2017 n Volume 31 Number 9 19
 The Critical Image
A 36-year-old man presents with 2 days of headache and nausea; his By Joshua S. Broder, MD, FACEP
symptoms are similar to those he’s experienced with previous migraines. Dr. Broder is an associate professor and the
However, unlike in prior episodes, he awoke this morning with a pulsatile residency program director in the Division
“swishing” sound in his left ear, coinciding with his heartbeat. He also noted of Emergency Medicine at Duke University
Medical Center in Durham, North Carolina.
drooping of his left upper eyelid and a small left pupil. His vital signs are blood
pressure 165/92, heart rate 89, respiratory rate 16, temperature 37.0°C (98.6°F),
and oxygen saturation 100% on room air.
The patient is alert and in no distress. His examination is notable for a constricted left pupil relative to the right, and ptosis of the left
eye. Photographs of the patient’s eyes are shown in Image A (cropped from single photograph, with equal illumination of both pupils).
A noncontrast computed tomography (CT) scan of the brain is normal, and a CT angiogram of the head and neck is performed.

B B. A CT angiogram of the brain

Narrowed demonstrates a narrowed left internal
Normal internal carotid artery as it passes through the
internal carotid carotid canal. Compare with the normal
carotid artery right internal carotid artery. Because the
artery within carotid canal develops congenitally in
within carotid concert with the carotid artery, the fact
carotid canal that the canal is of normal size indicates
canal
that the vascular stenosis is acquired —
in this case, from focal dissection of the
carotid artery.

KEY POINTS
n Horner syndrome is characterized
by ptosis, miosis, and anhydrosis.
The condition can be congenital or
acquired, and results from interruption
of sympathetic fibers anywhere along
their course from the hypothalamus
to the superior chest.1 Etiologies are
varied, including vascular aneurysms
and dissections, masses, demyelinating
disease, brainstem stroke, and infections.
n The sympathetic nerves follow the
Zoomed view course of the carotid artery through the
from Image B carotid canal in the petrous temporal
bone. When a vascular cause is
suspected, CT imaging should include
an unenhanced scan of the brain and
CT angiography from the aortic arch
through the neck and brain, as multiple
vascular abnormalities may coexist.

20 Critical Decisions in Emergency Medicine

 C
Zoomed view from Image C

Normal
internal
carotid
artery

C. CT angiogram of the neck. A second

vascular abnormality is seen — in this
case, an irregularity of the left internal
carotid artery at the level of the first
cervical vertebra (C1), suggesting vascular
dissection.
Irregular
region of
internal
carotid
artery

D
Zoomed view from Image D

Pseudoaneurysm D. A curved planar reconstruction

of internal shows the abnormality from Image C,
carotid artery and reveals that this actually is a
pseudoaneurysm of the internal carotid
artery at this level.

CASE RESOLUTION
The patient underwent carotid angiography to stent the affected internal carotid artery.

1. Flaherty PM, Flynn JM. Horner syndrome due to carotid dissection. J Emerg Med. 2011;41:43-6

September 2017 n Volume 31 Number 9 21

 CME
Reviewed by Lynn Roppolo, MD, FACEP

Qualified, paid subscribers to Critical Decisions in Emergency Medicine may receive

CME certificates for up to 5 ACEP Category I credits, 5 AMA PRA Category 1
Credits™, and 5 AOA Category 2-B credits for completing this activity in its entirety.

QUESTIONS Submit your answers online at acep.org/newcriticaldecisionstesting; a score of 75%

or better is required. You may receive credit for completing the CME activity any time
within three years of its publication date. Answers to this month’s questions will be
published in next month’s issue.

1
Which of the following etiologies can cause heat
syncope? 6 Cooling should be continued until the patient’s
core temperature reaches what level?
A. Hypothalamic dysfunction A. 37°C (98.6°F)
B. Peripheral vasodilation B. 39°C (102.2°F)
C. Potassium deficiency C. 40°C (104°F)
D. Seizure activity D. 41°C (105.8°F)

2 What core body temperature is consistent with

heat stress? 7 When should blood products be administered to a
patient with heat stroke?
A. Between 38°C (100.4°F) and 38.9°C (102°F) A. When clinical hemorrhage is apparent
B. Between 38°C (100.4°F) and 40°C (104°F) B. When hemoglobin levels are <8
C. >40°C (104°F) C. When PT, PTT/INR are critically prolonged
D. <38°C (100.4°F) D. Within the first 30 minutes of insult

3 Which of the following cooling methods is

widely accepted as ideal? 8 Which of the following patients is at lowest risk
for heat-related illness?
A. Administration of cooled IV fluids A. 4-week-old infant
B. Ice packs placed to the neck, axilla, and groin B. 20-year-old man with asthma
C. Immersion C. 38-year-old woman with hypertension
D. Misting and fans D. 80-year-old man with congestive heart failure

4 At what point do liver function tests peak in

patients with heat stroke? 9 Which of the following symptoms is consistent
with heat exhaustion?
A. 5 to 7 days after insult A. Ataxia
B. 24 to 48 hours after insult B. Mild confusion
C. 48 to 72 hours after insult C. Slurred speech
D. Immediately upon presentation D. Transient loss of consciousness

5 Which of the following drugs is least likely to

increase a patient’s risk of heat-related illness?
10 Which disease is most likely to manifest with
symptoms that mimic heat-related illness?
A. Fluoroquinolones A. Dengue fever
B. Jimson weed B. Myocardial infarction
C. Laxatives C. Squamous cell carcinoma
D. Tricyclic antidepressants D. Thyroid storm

22 Critical Decisions in Emergency Medicine

11
Which of the following organisms does not
typically cause cardiomyopathy?
16 A patient with known neurocysticercosis presents
with seizures for the second time in the past year.
What is the most appropriate therapy?
A. Echinococcus sp. (Hydatid disease)
B. Entamoeba histolytica A. Albendazole
C. Taenia solium (Cysticercosis) B. Dexamethasone
C. Nifurtimox
D. Trypanosoma cruzi (Chagas disease)
D. Phenytoin

12 A 35-year-old Peace Corps volunteer presents with
fever, malaise, and rash. His initial workup should
include which of the following tests?

17 T. solium cysticerci most commonly encysts in
which of the following locations?
A. Cortex
A. Blood cultures/urinalysis/lumbar puncture B. Eye
B. Complete blood count/basic metabolic C. Muscle
panel/blood cultures D. Ventricle
C. Electrocardiogram/echocardiogram/Chagas
polymerase chain reaction test
D. Parasitic panel
18
Which of the following is the most common
complication of acute Chagas disease?
A. Arrhythmia

13 Which of the following is the most common
sign/symptom of neurocysticercosis?
B. Dysphagia
C. Hepatosplenomegaly
D. Intestinal perforation
A. Headache/encephalopathy
B. Headache/seizure
C. Papilledema/altered mental status
D. Papilledema/seizure 19
A 44-year-old woman with HIV presents with
4 days of watery diarrhea. She has been
noncompliant with her antiretroviral regimen.
Stool microscopy confirms oocysts suggestive of

14
What is the appropriate treatment regimen
for acute Chagas disease?
cryptosporidiosis. What is the most appropriate
management?
A. Amiodarone
A. Fluid resuscitation
B. Benznidazole B. Immediate administration of nitazoxanide
C. Corticosteroids C. No intervention
D. Supportive care D. Treatment of immunocompromised state

15 Which of the following prophylactic measures
is inappropriate for the prevention of Chagas
20 Which of the following findings on a complete
blood count may be indicative of parasitic
disease? infection?
A. Chagas vaccine A. Anemia
B. Home improvement B. Eosinophilia
C. Mosquito net use C. Leukocytosis
D. Prenatal serological screening of high-risk D. Thrombocytopenia
populations

ANSWER KEY FOR AUGUST 2017, VOLUME 31, NUMBER 8

1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 18 19 20
B B A C C A D C C D C D B C A D A B D B

September 2017 n Volume 31 Number 9 23

 Drug Box
TRANEXAMIC ACID (LYSTEDA)
By Frank Lovecchio, DO, MPH, FACEP, Maricopa
Medical Center, Phoenix, Arizona
Recent studies suggest that tranexamic acid may be
lifesaving following traumatic and postpartum bleeding.
A synthetic analog of the amino acid lysine, the drug
prevents the body’s enzymes from breaking down
blood clots and serves as an antifibrinolytic by reversibly
binding lysine receptor sites on plasminogen or plasmin,
thus preserving fibrin’s matrix.
Indications and Dosing
Cyclic heavy menstrual bleeding:
1,300 mg 3x/day (3,900 mg/day) PO for up to 5 days
during menstruation
Tooth extraction in patients with hemophilia (in
combination with factor replacement therapy):
10 mg/kg IV immediately before surgery, then
10 mg/kg 3-4x/day; may be used for 2-8 days
Trauma-associated hemorrhage (off-label use):
1,000-mg IV over 10 min (loading dose), followed
by 1,000 mg over 8 hours
Note: Every effort should be made to administer
within 3 hours of injury.
Other off-label uses include elective cesarean
section, acute hereditary angioedema attacks,
intracranial hemorrhage associated with
thrombolytics (plasminogen-activator), postpartum
hemorrhage, prevention of perioperative bleeding
associated with cardiac or spinal surgery and dental
procedures (in patients on oral anticoagulants), blood
conservation during total hip replacement, and
traumatic hyphema.
Precautions
• Side effects include hypotension (with rapid IV
injection); and more commonly, back pain, muscle
aches, nasal symptoms, and headache.
• Hypersensitivity to tranexamic acid is the only
contraindication.
• Pregnancy risk factor B
Tox Box
BUPROPION OVERDOSE
By Matthew Riddle, MD, and Christian A. Tomaszewski, MD, MS, MBA,
FACEP, University of California, San Diego
Mechanism
Bupropion (Wellbutrin, Zyban) is a monocyclic antidepressant, structurally
similar to amphetamine, which inhibits neuronal reuptake of dopamine and
norepinephrine. It is a widely prescribed antidepressant with additional uses,
including smoking cessation, ADHD, obesity, sexual dysfunction, and even
recreational use (IV, IN, PO).
Pharmacokinetics
• Commonly prescribed in sustained and extended-release preparations,
although immediate-release also is available.
• Rapidly absorbed from gastrointestinal tract with peak concentrations in
3-5 hours with half-life >20 hours.
Clinical Presentation
• Neurological symptoms (eg, delirium, lethargy, confusion, tremors, and
seizure) are most common.
­— Up to 20% of patients seize following acute overdose.
­— Status epilepticus is rare.
• Cardiac effects include tachycardia and QRS widening, wide-complex
tachydysrhythmias, bradycardia, and cardiac arrest.
Diagnostic Evaluation
• No specific test for bupropion overdose.
• Can cause false-positive amphetamine on urine drug screen.
• ECG, renal, and liver panels may be useful.
Management
• Management generally is supportive.
• Decontamination (use cautiously due to aspiration risk from rapid deterioration).
• Activated charcoal may be useful if administered <1 hour post ingestion.
• Consider whole bowel irrigation for ingestions of >10 extended-release pills
due to possible bezoar formation.
• Use benzodiazepines to manage seizures.
• QRS prolongation >120 ms can be treated with sodium bicarbonate.
• ECMO has been used successfully to treat refractory shock.
Disposition
• May discharge if patient remains asymptomatic >6 hours post ingestion.
• After ingestion of sustained or extended-release preparations, patients.
should be considered at risk for seizures for at least 18 hours, or as long as
symptoms persist.