Avoiding Common Errors in the Emergency Department - Book 1

Consider balanced fluids in the resuscitation of patients with DKA.
An initial bolus dose of insulin is no longer recommended prior to the
initiation of an insulin infusion.
Do not administer a bolus of insulin to pediatric DKA patients.
Do not administer insulin until the potassium level is >3.5 mEq/L.
Sodium bicarbonate is not indicated in the treatment of patients with
DKA.

SUGGESTED READINGS

Chua HR, Schneider A, Bellomo R. Bicarbonate in diabetic ketoacidosis—A
systematic review. Ann Intensive Care. 2011;1(1):23.

Chua HR, Venkatesh B, Stachowski E, et al. Plasma-Lyte 148 vs. 0.9% saline for
fluid resuscitation in diabetic ketoacidosis. J Crit Care. 2012;27(2):138–145.

Goyal N, Miller JB, Sankey SS, et al. Utility of initial bolus insulin in the treatment
of diabetic ketoacidosis. J Emerg Med. 2010;38(4):422–427.

Kitabchi AE, Umpierrez GE, Miles JM, et al. Hyperglycemic crises in adult
patients with diabetes. Diabetes Care. 2009;32(7):1335–1343.

Mahler SA, Conrad SA, Wang H, et al. Resuscitation with balanced electrolyte
solution prevents hyperchloremic metabolic acidosis in patients with diabetic
ketoacidosis. Am J Emerg Med. 2011;29(6):670–674.

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113

DO NOT RELY ON ORTHOSTATIC
VITAL SIGNS TO DIAGNOSE
VOLUME DEPLETION

ANAND K. SWAMINATHANGORDONWU , MD, MPH ,
MD

Orthostatic blood pressure measurements are commonly thought to be useful
in the assessment of intravascular volume status. Orthostatic hypotension
(OH) is defined as:

1) A reduction in systolic blood pressure (SBP) of at least 20 mm Hg
2) A reduction in diastolic blood pressure (DBP) of at least 10 mm Hg
3) An increase in heart rate (HR) of at least 30 beats per minute (bpm)

To meet the definition of OH, one of the above criteria must be met when
measured at least 3 minutes after standing from a supine position. In
addition, patients should also experience symptoms of OH. These symptoms
can include light-headedness, dizziness, blurred vision, nausea, palpitations,
headache, or weakness that resolves with recumbence.

OH is very common. Data from large studies on unselected elderly
nursing home patients demonstrate that the rate of OH ranges from 28% to
50%. Studies in adolescents show similar rates, with ~44% of patients
exhibiting orthostatic changes. It is important to remember that OH is simply
an exam finding and not a disease.

In an attempt to clarify the significance of OH, Raiha and colleagues
performed a prospective cohort study. The authors demonstrated that
systolic, or mean, blood pressure changes with standing did not predict

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mortality at 10 years. However, a decrease in DBP of at least 10 mm Hg with
standing was associated with an increase in vascular mortality (odds ratio of
2.7). This association disappeared in multivariate analysis when the authors
adjusted for underlying conditions, such as cardiovascular disease. They
hypothesized that patients with more labile DBPs likely had significant
comorbid conditions that predisposed them to events like myocardial
infarction and stroke.

To further investigate the efficacy of OH as a marker of intravascular
volume depletion, Witting and colleagues performed tilt table testing on
healthy volunteers after blood donation of <600 mL. In adult patients
younger than 65 years of age, a change in HR of >20 bpm or a change in
SBP >20 mm Hg had a sensitivity of 47% and a specificity of 84% for
volume depletion. Sensitivity and specificity values were similar in patients
older than 65 years of age. The results of this study suggest that a finding of
OH, either by a drop in SBP or increase in HR, is not specific enough to state
with confidence that moderate volume depletion is present. Importantly, just
because the patient does not have OH, it does not mean they have a normal
intravascular volume. In addition, emergency providers often overestimate
the utility of OH in elderly patients. As Witting and colleagues have shown,
there is no statistically significant difference between OH in the elderly
compared with younger patients as a clinical predictor of volume status.

Building on the work of prior studies, McGee and colleagues assessed
the utility of OH symptoms. In their systematic review, the authors
demonstrated that the complaint of symptomatic OH had little predictive
value in regard to mild to moderate volume loss. However, in patients with
severe blood loss (600 to 1,100 mL), there was a dramatic increase in
sensitivity (97%) and specificity (98%) in patients who were unable to stand
for vital signs measurements secondary to severe dizziness. In this subset of
severely symptomatic patients, the inability to stand served as an excellent
predictor of severe volume loss. Otherwise, simply the complaint of nausea
or dizziness with standing was not clinically useful and should not be
routinely used as a measure of intravascular volume status.

KEY POINTS

Patients should be standing for at least 3 minutes before orthostatic
vital signs are measured.
OH is very common. Up to 55% of patients may have vital sign
changes consistent with OH. This does not mean that they have

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intravascular volume depletion.
OH measurements are neither sensitive nor specific in mild to
moderate intravascular volume depletion.
Orthostatic vital sign measurements in the elderly patient are not a
useful clinical predictor of volume status.
If the patient is symptomatic and unable to stand for vital sign
measurements, the patient is more likely to have intravascular volume
loss of at least 600 mL.

SUGGESTED READINGS

American Autonomic Society, American Academy of Neurology Consensus
Conference. Consensus statement on the definition of orthostatic hypotension,
pure autonomic failure and multiple system atrophy. Clin Auton Res.
1996;6:125–126.

McGee S, Abernethy WB, Simel DL. Is this patient hypovolemic? JAMA.
1999;281(11): 1022–1029.

Raiha I, Luutonen S, Piha J, et al. Prevalence, predisposing factors and prognostic
importance of postural hypotension. Arch Intern Med. 1995;155:930–935.

Stewart JM. Transient orthostatic hypotension is common in adolescents. J Pediatr.
2002;140:418–424.

Witting MD, Wears RL, Li S. Defining the positive tilt test: A study of healthy
adults with moderate acute blood loss. Ann Emerg Med.
1994;23(6):1320–1323.

554

114

HHS: WHEN HIGH SUGARS HAVE
GOT YOU DOWN!

STEPHANIE LAREAU, MD, FAWM, FACEP

Though diabetic ketoacidosis (DKA) is often the first endocrine emergency
considered in the patient with hyperglycemia, it is critical for the emergency
provider (EP) to include hyperglycemic hyperosmolar state (HHS) in the
differential diagnosis. Failure to consider HHS can result in significant
delays in treatment and, ultimately, increased patient morbidity and mortality
for this critical condition.

The diagnostic criteria for HHS include a serum glucose value >600
mg/dL, serum osmolality >320 osm/kg, a pH above 7.3, a serum bicarbonate
>15 mEq/L, and the absence of ketonuria. In contrast to DKA, many patients
with HHS will present with symptoms of neurologic dysfunction. These
symptoms can include altered mental status, lethargy, seizure, or unilateral
deficits that mimic a stroke. Since HHS is more common in elderly patients
with Type II diabetes, it can sometimes be difficult to determine if mental
status changes are acute, especially in those with dementia. Furthermore,
debilitated nursing home patients are at increased risk of HHS. These
patients often have impaired access to hydration or are receiving numerous
medications that can alter sensorium. It is critical to maintain a high index of
suspicion for HHS in hyperglycemic patients with altered mental status,
confusion, or lethargy.

The emergency department evaluation of patients with HHS should
include a search for the precipitating etiology. The most common precipitant
of HHS is infection (i.e., pneumonia, urinary tract infection, sepsis). Other
precipitants include myocardial infarction, stroke, medications, renal failure,
and head injury (i.e., subdural hematoma). As a result, the emergency
department evaluation may include an electrocardiogram, computed

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tomography of the head, chest radiograph, urinalysis, and laboratory studies
(i.e., complete blood count, comprehensive metabolic panel, troponin,
medication levels, lactate).

Patients with HHS have significant intravascular volume depletion. In
fact, the average fluid deficit in HHS is ~9 L! Therefore, appropriate fluid
resuscitation is critical. Patients who develop HHS often have numerous
comorbid conditions, including cardiac and renal dysfunction. As a result,
they may not be able to tolerate rapid, large volume resuscitation. Rapid
administration of fluids can lead to pulmonary edema and respiratory
compromise. An isotonic crystalloid should be administered and the patient
monitored closely for signs of fluid overload.

Despite the absence of ketoacidosis and an elevated anion gap, patients
with HHS benefit from an insulin infusion to control hyperglycemia. An
insulin infusion is initiated at 0.1 U/kg. In contrast to patients with DKA,
conversion to a dextrose infusion is usually not required as hyperglycemia is
corrected. Patients can be transitioned to subcutaneous insulin treatment
when they are able to tolerate oral nutrition. Given the need for close
monitoring to prevent hypoglycemia, hypokalemia, and volume overload,
patients with HHS are typically admitted to an intensive care unit or
intermediate care unit. It is important that the inpatient team continues the
evaluation for the precipitating cause of the HHS. Finally, medication
adjustments and patient and caretaker education are provided on discharge to
prevent recurrence of the condition.

KEY POINTS

Consider HHS in the hyperglycemic patient with altered mental status.
The average fluid deficit in patients with HHS is ~9 L.
Rapid administration of fluids can lead to pulmonary edema and
respiratory compromise.
An insulin infusion is initiated at 0.1 U/kg for patients with HHS.
In contrast to patients with DKA, conversion to a dextrose infusion is
usually not required as hyperglycemia is corrected.

SUGGESTED READINGS

Anna M, Weinreb JE. Hyperglycemic hyperosmolar state. In: De Groot LJ, Beck-
Peccoz P, Chrousos G, et al. eds. Endotext. South Dartmouth, MA:

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MDText.com, Inc., 2000.
Kitabchi AE, Umpierrez GE, Miles JM, et al. Hyperglycemic crises in adult

patients with diabetes: A consensus statement from The American Diabetes
Association. Diabetes Care. 2009;32(7):1335–1343.
Pasquel FJ, Umpierrez GE. Hyperosmolar hyperglycemic state: A historic review
of the clinical presentation, diagnosis, and treatment. Diabetes Care.
2014;37(11):3124–3131.
Wolfsdorf JI, Allgrove J, Craig ME, et al. Diabetic ketoacidosis and hyperglycemic
hyperosmolar state. Pediatr Diabetes. 2014;15:154–179.

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115

DO NOT OVER TREAT HYPO- OR
HYPERNATREMIA

NICOLE CIMINO-FIALLOS, MD AND WAN-TSU WENDY
CHANG, MD

Sodium disturbances are common in the emergency department and can
easily stump the emergency provider (EP). Treatment of sodium disorders is
based on the lab value, the time course of illness, and the etiology.
Mismanagement of the patient with hypo- or hypernatremia can quickly
worsen the patient’s outcome. The following chapter discusses critical pearls
in the treatment of patients with hypo- and hypernatremia.

HYPONATREMIA—ADD A PINCH OF SALT

Hyponatremia is defined as a serum sodium value <135 mEq/L.
Hyponatremia can cause cerebral edema, which may lead to cerebral
herniation. The clinical presentation of patients with hyponatremia can range
from asymptomatic to seizure and coma. All patients should be evaluated for
the cause of hyponatremia, as this will assist in management decisions. For
example, postoperative and intracranial etiologies for hyponatremia often
require urgent correction. It is also important to determine the time course of
illness. Patients who have a sudden drop in sodium levels are likely to be
more symptomatic and require urgent treatment than those patients who have
a slower decrease in sodium levels. Patients with seizure or coma due to
hyponatremia require immediate treatment. Asymptomatic patients rarely
require emergent therapy.

For patients who require emergent treatment (seizure, coma), administer
a 100 mL bolus of hypertonic saline over 10 minutes. The goal is to increase
the serum sodium level by 4 to 6 mEq/L over 6 hours. An increase in sodium

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by 4 to 6 mEq/L will alleviate most symptoms and prevent cerebral
herniation. It is important not to increase sodium levels by more than 8
mEq/L in 24 hours. Overcorrection of sodium can easily occur and cause
significant adverse effects. Correction by more than 8 mEq/L in the first 24
hours can increase the risk for osmotic demyelination syndrome, seizure, and
cerebral herniation. If patients deteriorate from too rapid of a correction of
hyponatremia, desmopressin with D5W should be administered to lower
sodium values.

For the patient who does not require emergent treatment, hyponatremia
should be treated at a much slower rate. In these patients, it is important to
begin with an assessment of intravascular volume status. Patients with
hypovolemia or euvolemia may simply need fluid administration. These
patients can receive 0.9% normal saline with free water restriction in addition
to treatment of the etiology of hyponatremia. For hypervolemic patients,
furosemide can be administered along with fluid restriction for treatment.

HYPERNATREMIA—WATER IT DOWN

Hypernatremia is defined as a serum sodium >145 mEq/L. Coma, seizure,
and death can result from the shrinkage of cerebral cells as they lose free
water. As serum osmolality increases, patients develop excessive thirst,
weakness, agitation, ataxia, and neurologic deficits.

Most patients with hypernatremia have chronic hypernatremia that has
developed over 48 hours or longer. It is important not to rapidly normalize
the serum sodium level. Because of the time required for cerebral adaption to
elevated sodium, patients with chronic hypernatremia are at significant risk
for cerebral edema with rapid correction. Instead, treatment should aim to
lower the serum sodium level by 10 mEq/L over 24 hours. When the serum
sodium level is >154 mEq/L, start with 0.9% normal saline rather than a
more hypotonic fluid. Once the serum sodium level falls below 154 mEq/L, a
hypotonic solution, such as D5W or 0.45% normal saline, can be used. In
order to determine the amount of fluid that should be administered, it is
important to calculate the free water deficit. The free water deficit can be
calculated using the following formula:

In patients with chronic hypernatremia, the free water deficit should not
be replaced all at once. To select an infusion rate for hypotonic fluid in the
patient with chronic hypernatremia, use the following formulas:

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It is important to search for and treat the etiology of hypernatremia while
replacing the free water deficit. Despite appropriate therapy, hypernatremia
may not correct appropriately if the patient is having continued loss of free
water. Be sure to monitor electrolytes frequently after the initiation of
therapy. If serum sodium levels are not improving after 4 hours of therapy,
recalculate the free water deficit and adjust the infusion rate. If the patient’s
sodium has corrected too quickly (at a rate that will decrease the serum
sodium by more than 10 mEq in 24 hours), stop the infusion and recheck
serum sodium in 2 to 4 hours. One potential reason for the failure of sodium
to correct appropriately is the use of D5W. This fluid can cause
hyperglycemia and free water loss due to glycosuria. For patients who fail to
correct appropriately and have received D5W for free water replacement,
change the intravenous fluid to 0.45% normal saline.

KEY POINTS

Treatment of sodium disorders depends on the cause, time course of
illness, and severity of symptoms.
For patients who require emergent treatment of hyponatremia,
administer a 100-mL bolus of hypertonic saline over 10 minutes.
When correcting hyponatremia, the goal is to correct by 4 to 6 mEq in
the first 24 hours.
Calculate the free water deficit in patients with hypernatremia. Do not
replace the free water deficit all at once, as this can result in cerebral
edema.
Treatment of hypernatremia should aim to lower the serum sodium
level by 10 mEq/L over 24 hours.

SUGGESTED READINGS

Olsso K, Öhlin B, Melander O. Epidemiology and characteristics of hyponatremia
in the emergency department. Eur J Intern Med. 2013;24:110–116.

Pfennig CL, Slovis CM. Sodium disorders in the emergency department: A review
of hyponatremia and hypernatremia. Emerg Med Pract. 2012;14(10):1–26.

Sterns RH, Silver SM. Salt and water: Read the package insert. QJM.
2003;96:549–552.

Verbalis JG, Goldsmith SR, Greenberg A, et al. Diagnosis, evaluation and

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treatment of hyponatremia: Expert panel recommendations. Am J Med.
2013;126(10 Suppl 1):S1–S42.

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116

A 3-PRONGED APPROACH TO THE
TREATMENT OF HYPERKALEMIA

ERICA B. SHAVER, MD AND CHRISTOPHER S. KIEFER,
MD

Disorders of potassium (K+) regulation are commonly encountered in the
emergency setting. Hyperkalemia, defined as a K+ level >5.0 mEq/L, is the
most lethal electrolyte disorder. Given that K+ is the body’s major
intracellular cation, even small shifts across cellular membranes can lead to
an array of symptoms including nausea, fatigue and muscle weakness. As K+
levels increase, cardiac membrane instability, electrocardiogram (EKG)
changes, and lethal arrhythmias can occur. Hyperkalemia is diagnosed by
serum measurement or suggested by classic EKG abnormalities. Classic
EKG changes associated with hyperkalemia include peaked T waves (Figure
116.1), a widened QRS complex, and bradycardia that can lead to the classic
“sine wave” morphology (Figure 116.2).

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Figure 116.1 Peaked T waves in hyperkalemic patient.

Figure 116.2 “Sine wave” pattern in a profoundly hyperkalemic
patient.

Never delay treatment of a patient with classic EKG signs of
hyperkalemia while waiting for a serum K+ level. If concerning EKG
changes are noted, it is imperative to initiate treatment to prevent cardiac
arrhythmias and circulatory collapse. Similarly, the treatment of a patient

563

with classic EKG changes should not be delayed due to a serum K+ level that
may not correlate. Patients with normal K+ levels at baseline generally
exhibit EKG changes earlier compared with patients who have chronically
elevated potassium levels. These patients often tolerate higher levels before
EKG changes are noted. Importantly, EKG abnormalities alone are not
indicative of the degree of K+ elevation.

This chapter will discuss a simple 3-pronged approach to the treatment of
hyperkalemia: stabilize, redistribute, and reduce.

STABILIZE

Calcium is the cornerstone of cardiac membrane stabilization in patients with
EKG changes associated with hyperkalemia. Importantly, calcium does not
change serum K+ levels. Nonetheless, failure to administer calcium can lead
to life-threatening arrhythmias from hyperkalemia. Calcium should be
administered prior to the results of serum K+ levels, especially in patients
with chronic kidney disease. Two calcium formulations are commonly given
for hyperkalemia: calcium chloride and calcium gluconate. Given the
potential for peripheral vein injury, calcium chloride should be administered
through a central venous line. Calcium chloride contains three times the
elemental calcium as does calcium gluconate. As a result, calcium gluconate
requires higher doses for similar clinical effect.

REDISTRIBUTE

Redistribution of serum K+ is facilitated by administration of albuterol,
insulin with glucose, and sodium bicarbonate. Redistribution measures do
not eliminate K+ from the body, but rather shift K+ to the intracellular
compartment.

Albuterol shifts K+ across cell membranes via a secondary messenger
system. Recent studies have reported a decrease of K+ by ~0.6 to 1.0 mmol/L
in patients given high-dose (10 to 20 mg) nebulized albuterol. Standard doses
(5 mg) of nebulized albuterol can be helpful but do not achieve optimal
effects.

Insulin shifts extracellular K+ across the cell membrane via the Na-K
ATPase enzyme. In order to avoid hypoglycemia associated with insulin
administration, intravenous dextrose is administered concomitantly with 10
units of regular insulin in patients with a serum glucose <250 mg/dL. It is
important to note that insulin is cleared via the kidney. Patients with renal

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insufficiency may have delayed clearance of insulin and require additional
dextrose to prevent hypoglycemia.

The use of sodium bicarbonate in the treatment of acute hyperkalemia
remains controversial. A recent literature has questioned the efficacy of
bicarbonate at lowering serum K+ levels. A recent Cochrane review reported
that the evidence for bicarbonate use in hyperkalemia is equivocal. An
additional recent review emphasized that there is no significant decrease in
serum K+ with bicarbonate and advised against routine usage.

REDUCE

Total body serum K+ can be reduced through hemodialysis, increased urinary
excretion, or a binding resin in the stool. Hyperkalemic patients who present
with fluid overload and normal renal function may benefit from loop diuretic
medications. Loop diuretics work on the loop of Henle and increase K+
excretion in the urine. Other potassium-depleting diuretics, such as thiazide
diuretics, are not as effective as loop diuretic agents.

Hyperkalemic patients with hypovolemia and acute kidney injury and
normal urine output may benefit from intravenous fluid resuscitation. Fluid
administration in this group of patients may reduce serum K+ through
dilution and potassium excretion through improved renal perfusion.

Sodium polystyrene (Kayexalate) is a cation exchange resin administered
orally or rectally that exchanges sodium for K+ and eliminates K+ via the
gastrointestinal tract. The evidence advocating the use of Kayexalate to treat
hyperkalemia originates from a single study published in the 1960s that
demonstrated a reduction in serum K+ in patients with acute and chronic
renal failure. Recent literature, however, recommends against routine
administration of Kayexalate in the hyperkalemic patient due to an
unpredictable reduction of serum K+ and an increased risk of colonic
necrosis.

Oliguric or anuric patients with hyperkalemia will require hemodialysis
to definitively remove K+ from the body. Early consultation with nephrology
for hemodialysis should be obtained in patients with oliguria, anuria, or end-
stage renal disease.

KEY POINTS

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Never delay treatment of a patient with classic EKG signs of
hyperkalemia while waiting for a serum K+ level.
Calcium chloride contains three times the elemental calcium as does
calcium gluconate.
High-dose albuterol (10 to 20 mg) can decrease K+ by ~0.6 to 1.0
mmol/L.
Recent literature recommends against the routine administration of
sodium polystyrene.
Consult nephrology early for hemodialysis in patients with oliguria,
anuria, or end-stage renal disease.

SUGGESTED READINGS

Kovesdy CP. Management of hyperkalemia: An update for the internist. Am J Med.
2015;128:1281–1287.

Mahoney BA, Smith WAD, Lo D, et al. Emergency interventions for
hyperkalemia. Cochrane Database Syst Rev. 2005;18:2.

Sterns RH, Rojas M, Bernstein P, et al. Ion-exchange resins for the treatment of
hyperkalemia: Are they safe and effective. J Am Soc Nephrol.
2010;21:733–735.

Weisberg LS. Management of severe hyperkalemia. Crit Care Med.
2008;36:3246–3251.

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117

KNOW HOW TO RECOGNIZE AND
TREAT THYROID STORM

HENDERSON D. MCGINNIS, MD

Thyroid storm is an extreme version of hyperthyroidism with a mortality rate
that approaches 30%, even with treatment. The recognition and management
of thyroid storm can be difficult in the emergency department (ED). Often,
patients present with nonspecific symptoms that can easily be misdiagnosed
as more common ED conditions (i.e., sepsis). The following chapter will
focus on the clinical presentation, diagnosis, and management of patients
with thyroid storm.

Recall that the pituitary gland secretes thyroid-stimulating hormone
(TSH), which prompts the thyroid gland to secrete thyroid hormone. Most
thyroid hormone is released from the thyroid gland as thyroxine (T4), the
physiologically inactive form, while the remainder is released as
triiodothyronine (T3), the active form. T4 is converted to T3 in the peripheral
tissues. When enough thyroid hormone is present, further release of TSH is
inhibited. Under normal circumstances, this feedback mechanism remains in
balance. When this balance becomes interrupted, the thyroid gland can
become over- or underactive.

Thyroid storm typically presents with elevated temperature,
hypertension, tachycardia (often beyond that expected for the elevated
temperature), and altered sensorium. The altered sensorium is usually
hyperactivity and can vary anywhere from feelings of anxiety to coma. These
signs and symptoms can be easily overlooked, especially in the evaluation of
a patient with vague complaints. Additional clinical findings include tremors,
diaphoresis, thinning hair, exophthalmos, and goiter. Patients with thyroid
storm may also manifest signs and symptoms of high-output congestive heart
failure, such as pulmonary edema, jugular venous distention, and increased

567

dyspnea on exertion. Some would call thyroid storm the “great imitator,” as
it can present similarly to other more common ED diagnoses.

The diagnosis of thyroid storm should be based on the clinical
presentation. Scoring tools for thyroid storm have been published, but no tool
has been shown to be superior and these tools are not commonly utilized in
the ED. The diagnosis is confirmed with thyroid function testing; TSH, free
T3, and free T4 levels should be obtained. Patients with thyroid storm
usually have a low TSH level and elevated T3, T4, or both. Though
exceedingly rare, a TSH-producing tumor can demonstrate a normal, or
elevated, TSH level in conjunction with a high T4 and T3. This tumor should
be considered in patients with these lab findings and signs and symptoms of
thyrotoxicosis.

The ED management of thyroid storm includes decreasing circulating
thyroid hormone levels, reducing the effects of thyroid hormone, treating the
presumed etiology, and providing supportive care. These treatment steps
should be initiated prior to the results of confirmatory laboratory tests in
patients with thyroid storm. Initial management begins with the
administration of beta-blocker medications. During thyroid storm, there is an
increased expression of beta1-adrenergic receptors, which results in many of
the clinical manifestations. Though any beta-blocker can be used,
propranolol is generally the medication of choice, as it also blocks the
peripheral conversion of T4 to T3. The emergency provider should target a
heart rate <100 bpm with the use of a beta-blocker agent. Heart rate control
will also improve hemodynamics in patients with high-output heart failure
due to thyroid storm. If patients are intolerant to beta-blockers,
nondihydropyridine calcium channel blockers may be used with similar
efficacy. Importantly, these agents will not block the peripheral conversion
of T4 to T3.

Antithyroid medications (i.e., thionamides, iodine) should be
administered after a beta-blocker agent has been given. The thionamides,
propylthiouracil (PTU) and methimazole, block new thyroid hormone
synthesis and should be administered before iodine. Both are administered
orally and have been shown to be equally effective. Similar to propranolol,
PTU blocks the peripheral conversion of T4 to T3. Iodine will further inhibit
thyroid hormone synthesis but should be given at least 1 hour after the
administration of a thionamide medication. If iodine is administered before a
thionamide agent, it will provide substrate for new hormone synthesis and
increase hormone levels. Lastly, glucocorticoid medications block the
peripheral conversion of T4 to T3 and should be administered to patients
with life-threatening features of thyroid storm.

568

A critical component in the ED treatment of thyroid storm is temperature
management in the setting of fever. A common pitfall is to provide active
cooling through the use of cooling blankets, cooled intravenous fluids, and
ice packets. However, active cooling methods are contraindicated in thyroid
storm. Active cooling will precipitate peripheral vasoconstriction and can
worsen hypertension. Temperature management in thyroid storm should
consist only of passive cooling techniques, such as a reduction in room
temperature and the removal of clothing.

KEY POINTS

Consider thyroid storm in the patient with altered mental status and
fever.
Begin treatment for thyroid storm while awaiting confirmatory lab test
results.
Propranolol is the recommended beta-blocker agent of choice and can
inhibit the peripheral conversion of T4 to T3.
Provide iodine therapy at least 60 minutes after the administration of
PTU or methimazole.
Passive cooling is the preferred method for temperature management
in patients with thyroid storm.

SUGGESTED READINGS

Akamizu T, Satoh T, Isozaki O, et al. Diagnostic criteria, clinical features, and
incidence of thyroid storm based on nationwide surveys. Thyroid.
2012;22(7):661–679.

Bahn RS, Burch HB, Cooper DS, et al. Hyperthyroidism and other causes of
thyrotoxicosis: Management guidelines of the American Thyroid Association
and American Association of Clinical Endocrinologists. Thyroid.
2011;21(6):593–646.

Devereaux D, Tewelde SZ. Hyperthyroidism and thyrotoxicosis. Emerg Med Clin
North Am. 2014;32(2):277–292.

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118

UNDERSTAND THE ROLE OF
MAGNESIUM IN THE TREATMENT

OF HYPOKALEMIA

FARHAD AZIZ, MD AND JUSTIN BOONE ROSE, MD

Hypokalemia is a common electrolyte abnormality seen in the general
population. Causes of hypokalemia include decreased potassium intake,
increased entry of potassium into cells, increased gastrointestinal loss, and
increased urinary loss. Hypokalemia has many clinical manifestations, some
of which can be life threatening and include cardiac arrhythmias and
respiratory depression. The primary treatment for hypokalemia is potassium
supplementation, along with the identification and correction of the cause of
hypokalemia. Unfortunately, exogenous potassium supplementation does not
always replete potassium to normal levels. The most common reason for the
failure to reach normal potassium levels is that an inadequate amount of
potassium is administered for the level of hypokalemia. Another common
cause of hypokalemia that is refractory to supplementation is
hypomagnesemia. It is essential for the emergency provider to normalize
magnesium levels in order to treat hypokalemia.

The majority of potassium is stored within the cells of the body. Oral
intake of potassium-rich foods or potassium supplements (i.e., potassium
chloride, potassium phosphate, potassium bicarbonate, potassium gluconate)
can increase potassium levels. Potassium chloride is the preferred method of
oral potassium administration, given its rapid absorption. In addition to
potassium supplementation, treatment of hypokalemia also includes the
prevention of continued potassium loss (gastrointestinal or urinary sources).

Despite appropriate doses of supplemental potassium, it is common to

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have difficulty reaching a normal serum level. Hypomagnesemia is a
concurrent electrolyte abnormality seen in up to 60% of patients with
hypokalemia. Magnesium is absorbed predominantly in the small intestine
via active and passive pathways. Magnesium is then filtered through the
renal glomeruli. Magnesium can be lost through gastrointestinal or renal
secretion. Magnesium deficiency can worsen hypokalemia and cause it to be
refractory to treatment.

The majority of potassium secretion occurs in the distal convoluted
tubules and the cortical collecting duct, while the majority of potassium
reabsorption occurs in the proximal tubule and loop of Henle. Magnesium
plays a critical role in potassium homeostasis by decreasing potassium
secretion and increasing its excretion within the kidney. In the distal
convoluted tubule and cortical collecting duct, potassium is absorbed into the
cell across the basolateral membrane via a Na+/K+-ATPase pump. Once
within the cell, potassium is secreted into the urine via the ROMK channel.
Magnesium inhibits this channel and lowers the amount of potassium
secreted into the luminal fluid. When the body has a magnesium deficiency,
there is no longer inhibition of this channel and potassium is readily secreted
into the lumen and excreted in the urine.

Common causes of hypomagnesemia include malnutrition, vomiting,
diarrhea, and malabsorption. The most important step is to consider
concomitant hypomagnesemia in the setting of hypokalemia that is refractory
to treatment. The treatment for hypomagnesemia is magnesium
supplementation and identification of the etiology. Once magnesium is
repleted, potassium repletion can occur and has a higher chance of success.
Normal serum magnesium level ranges from 1.5 to 2.4 mg/dL. In mild to
moderate hypomagnesemia (1.0 to 1.5 mg/dL), 1 to 4 g of magnesium sulfate
can be administered intravenously (IV) at a maximum rate of 1 g/hour. In
severe symptomatic hypomagnesemia, 1 to 4 g of magnesium sulfate can be
administered IV over 5 to 60 minutes. Intravenous doses should be decreased
by 50% in patients with renal insufficiency. Faster rates of infusion can result
in an increase in urine magnesium excretion. Oral preparations of
magnesium include magnesium chloride and magnesium oxide. These have
limited bioavailability but are useful for outpatient therapy.

KEY POINTS

Hypomagnesemia is present in up to 60% of patients with
hypokalemia.

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Hypokalemia is difficult to correct before magnesium is replaced.
Search for the cause of hypokalemia and hypomagnesemia.
IV replacement is the preferred route to replace magnesium.
In severe hypomagnesemia, 1 to 4 g of magnesium sulfate can be
administered IV over 5 to 60 minutes.

SUGGESTED READINGS

Ayuk J, Gittoes NJ. Contemporary view of the clinical relevance of magnesium
homeostasis. Ann Clin Biochem. 2014;51(Pt 2):179–188.

Cohn JN, Kowey PR, Whelton PK, et al. New guidelines for potassium
replacement in clinical practice: A contemporary review by the National
Council on Potassium in Clinical Practice. Arch Intern Med.
2000;160:2429–2436.

Kraft MD, Btaiche IF, Sacks GS, et al. Treatment of electrolyte disorders in adult
patients in the intensive care unit. Am J Health Syst Pharm.
2005;62:1663–1682.

Rose BD, Post TW. Hypokalemia. In: Rose BD, Post TW, eds. Clinical Physiology
of Acid–base and Electrolyte Disorders. 5th ed. New York: McGraw-Hill,
2001:836.

Whang R, Flink EB, Dyckner T, et al. Magnesium depletion as a cause of
refractory potassium repletion. Arch Intern Med. 1985;145:1686–1689.

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119

KNOW HOW TO INTERPRET THE
VENOUS BLOOD GAS

JOSHUA (JOSH) NICHOLS, MD AND COREY HEITZ, MD

The decision to obtain a venous blood gas (VBG) or an arterial blood gas
(ABG) can be a challenge for the emergency provider (EP). It is sometimes
difficult to know when either test is indicated. Importantly, a VBG can save
time, spare the patient the pain of an arterial blood draw, avoid arterial
injury, and avoid potential arterial thrombosis and ischemia.
Notwithstanding, it is critical for the EP to know how to interpret the results
of the VBG. This chapter discusses the correlation of the pH, arterial partial
pressure of carbon dioxide (PaCO2), arterial partial pressure of oxygen
(PaO2), the bicarbonate (HCO3), and lactate levels obtained with a VBG
compared to that of an ABG.

PH

The pH of the VBG correlates well with the pH of an ABG. In two large
meta-analyses, authors demonstrated that the mean difference between the
venous and arterial pH is between 0.033 and 0.035. The VBG pH has shown
good correlation in patients with acidosis (i.e., diabetic ketoacidosis) and
alkalosis, where the pH ranges from 7.05 to 7.61.

There are two clinical instances where the provider must be wary of the
pH from a VBG. There are insufficient data to support using venous pH in
patients with mixed acid-base disorders. Additionally, few studies have been
conducted that correlate venous and arterial pH in the hypotensive patient,
who has a systolic blood pressure <90 mm Hg. In one small study, authors
showed that the arterial to venous pH difference increased slightly in
hypotensive patients compared to normotensive patients; however, this

573

increase was not statistically significant. Due to the relative paucity of
studies that have examined pH from a VBG in the setting of hypotension, the
EP should consider an ABG pH in patients with shock.

CARBON DIOXIDE

The partial pressure of carbon dioxide (PCO2) of the VBG is an important
measurement. Unfortunately, the PCO2 from a VBG does not correlate well
enough with the PaCO2 of the ABG to be used simply as a surrogate marker.
At normal PCO2 levels, the VBG and ABG PCO2 do correlate well. This
association does not hold well in patients with hypercapnia. However, the
PCO2 from a VBG can be used to screen for hypercapnia. A venous PCO2
value that is <45 mm Hg has been shown to have a negative predictive value
of 100% for a PaCO2 that is >50 mm Hg. If the VBG PCO2 is normal,
hypercapnia can reliably be excluded. If the VBG PCO2 is >45 mm Hg, the
EP should obtain an ABG to measure PaCO2 and determine if there is
clinically relevant hypercapnia.

OXYGEN

The partial pressure of oxygen (PO2) from a VBG correlates poorly with the
PaO2 from an ABG. In one study, authors estimated the VBG PO2 was ~37
mm Hg less than the ABG PaO2. In this study, the 95% confidence interval
was sufficiently wide to make any correlation between the two values. A
notable exception to this is in cases of cyanide toxicity, where the EP may
see arterialization of the VBG PO2 due to binding of cyanide to cytochrome
c oxidase. This halts the electron transport chain and prevents conversion of
oxygen to water. In this instance, VBG PO2 may be within 10% difference of
the ABG PaO2.

BICARBONATE

As with pH, the VBG HCO3 correlates well with arterial HCO3. In two large
meta-analyses, the mean difference between venous and arterial HCO3 was
1.03 to 1.41. The small mean difference and a narrow confidence interval
make venous estimation of arterial HCO3 clinically useful in most cases.
However, the EP must be cognizant of the patient’s underlying medical
conditions. In one study that compared venous and arterial pH in patients

574

with an exacerbation of chronic obstructive pulmonary disease (COPD) who
had hypercapnic respiratory failure, individual arterial and venous HCO3
measurements differed by as much as −6.24 to +10.0 mmol/L. This suggests
that the HCO3 from a VBG may be less useful in these patients. Although
not entirely clear, this poor level of agreement may be due to COPD, which
causes a baseline chronic metabolic alkalosis combined with an acute
respiratory acidosis. This finding highlights the poor understanding of VBG
and ABG correlation in mixed acid-base disorders.

LACTATE

VBG lactate correlates well with arterial lactate at normal levels (<2
mmol/L). A systematic review showed that at normal levels, the mean
difference between venous and arterial lactate is 0.25 mmol/L. However, the
authors noted that in studies that included hemodynamically unstable trauma
patients and patients with higher lactate levels, there was a weaker
correlation between arterial and venous lactate.

KEY POINTS

The VBG is appropriate for estimating arterial pH and HCO3, unless
the patient is hypotensive or there is suspicion of a mixed acid-base
disorder.
The VBG PCO2 can be used to screen for hypercapnia. There is poor
correlation with PaCO2 at values >45 mm Hg.
The VBG PO2 is not clinically useful, except in cases of suspected
cyanide toxicity.
The VBG lactate correlates best with ABG lactate at values <2
mmol/L.
ABG is preferable to VBG in patients with shock, severe trauma, and
mixed acid-base disorders.

SUGGESTED READINGS

Baskin S, Brewer T. Cyanide poisoning. In Sidell F, Takefuji E, Franz D, eds.
Medical Aspects of Chemical and Biological Warfare. Washington, DC: Office
of the General Surgeon, 1997:271–286.

Bloom BM. The role of venous blood gas in the emergency department: A

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systematic review and meta-analysis. Eur J Emerg Med. 2014;21:81–88.
Byrne AL. Peripheral venous and arterial blood gas analysis in adults: Are they

comparable? A systematic review and meta-analysis. Respirology.
2014;19:168–175.
Kelly AM. Review article: Can venous blood gas analysis replace arterial in
emergency medical care. Emerg Med Australas. 2010;22:493–498.
Kelly AM. Validation of venous pCO2 to screen for arterial hypercarbia in patients
with chronic obstructive airway disease. J Emerg Med. 2005;28:377–779.

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120

KNOW THE INDICATIONS FOR
BICARBONATE THERAPY

KIMBERLY BOSWELL, MD

The use of sodium bicarbonate in the emergency department (ED) has varied
over generations. Bicarbonate has been used to treat numerous conditions,
such as diabetic ketoacidosis (DKA) and in the prevention of contrast-
induced nephropathy (CIN) for patients undergoing computed tomography
studies. Recent literature, however, has challenged the utility and safety of
bicarbonate administration for several disease processes. Currently, there are
only a few indications for bicarbonate use in the ED. This chapter discusses
the utilization and controversies of bicarbonate therapy in the ED.

The foundation of DKA treatment includes aggressive fluid resuscitation,
electrolyte management, and insulin. Bicarbonate is no longer recommended
to treat the acidosis associated with DKA, unless the patient’s pH falls below
6.9. If bicarbonate is given for a pH < 6.9, it should be given in small
aliquots (100 mEq) and infused over 1 to 2 hours. The venous pH should be
checked every 2 hours and bicarbonate should be stopped when the pH is
above 7.0. The controversy surrounding bicarbonate therapy in DKA is
primarily twofold. First, there is little evidence to support the benefit of its
administration, and there are several possible side effects, including a
paradoxical decrease in the cerebral pH and a decrease in serum potassium
levels. Second, there is evidence to suggest that it decreases the clearance of
ketones. Importantly, its use in pediatrics is discouraged due to its
association with cerebral edema. The routine use of bicarbonate therapy in
DKA should no longer be considered a pillar of treatment and should be
reserved for the most critically ill patients.

Lactic acidosis can be the result of numerous disease processes or
injuries and reflects hypoperfusion of tissues. The use of sodium bicarbonate

577

to treat lactic acidosis remains controversial and generally should be
considered when the pH is <7.1 and the serum bicarbonate is <6. Profound
acidosis negatively impacts patient hemodynamics through a reduction in
cardiac contractility and a decreased response to catecholamines. This, in
turn, leads to arteriolar vasodilation and can result in various arrhythmias.
For patients with a pH > 7.1, it is recommended that treatment focus on the
etiology of lactic acidosis rather than administration of bicarbonate. Several
studies have demonstrated that there is little difference in the administration
of bicarbonate compared to saline with respect to cardiac output and mean
arterial pressure in the patient with a pH > 7.1. In fact, it is important to
remember that the administration of exogenous bicarbonate can effect
electrolyte balance and result in hypocalcemia, hypernatremia, and
hypokalemia. In addition, exogenous bicarbonate stimulates arterial and
tissue production of carbon dioxide. The goal of bicarbonate treatment in
severe lactic acidosis is simply to achieve a pH > 7.1 while simultaneously
treating the etiology.

Another controversial topic is the administration of bicarbonate to
prevent CIN. The belief that alkalinization protects the kidneys from free
radical damage fostered the belief that bicarbonate therapy would be
beneficial in CIN prophylaxis. However, the mechanism by which contrast
affects the kidney is not well understood. Many randomized trials and meta-
analyses have demonstrated equivocal outcomes when bicarbonate was
compared with normal saline. In 2012, the Kidney Disease: Improving
Global Outcomes Guidelines recommended simple administration of isotonic
fluids for volume expansion for CIN prophylaxis. This recommendation
remains current.

Severe, life-threatening hyperkalemia remains an important an indication
for the use of bicarbonate in the ED. Bicarbonate shifts extracellular
potassium to the intracellular compartment in order to maintain an
electrically neutral environment. Interestingly, there have been no studies
that actually demonstrate an immediate or significant benefit (acute change
in the serum potassium level) with bicarbonate. It is important to note that
administration of bicarbonate should not be the only intervention employed
in the acute treatment of hyperkalemia. The administration of calcium,
insulin and glucose, and beta-2 agonists is still indicated.

KEY POINTS

Bicarbonate should not be used in the routine treatment of DKA,

578

unless pH drops below 6.9.
Administer bicarbonate to patients with a severe lactic acidosis (pH <
7.1).
Bicarbonate therapy can induce hypokalemia, hypernatremia, and
hypocalcemia.
Bicarbonate therapy is not indicated for prophylaxis of CIN.
Administer bicarbonate to the patient with severe hyperkalemia who is
not responding to traditional therapies, such as insulin and glucose and
beta-2 agonists.

SUGGESTED READINGS

Kraut JA, Kurtz I. Use of base in the treatment of severe academic states. Am J
Kidney Dis. 2001;38(4):703–727.

Kraut JA, Madias NE. Treatment of acute metabolic acidosis: A pathophysiologic
approach. Nat Rev Nephrol. 2012;8(10):589–601.

Latif KA, Freire AX, Kitabchi AE, et al. The use of alkali therapy in severe
diabetic ketoacidosis. Diabetes Care. 2002;25(11):2113–2114.

Okuda Y, Adrogue HJ, Field JB, et al. Counterproductive effects of sodium
bicarbonate in diabetic ketoacidosis. J Clin Endocrinol Metab.
1996;81(1):314–320.

Solomon R, Gordon P, Manoukian SV, et al.; on behalf the BOSS Trial.
Randomized trial of bicarbonate or saline study for the prevention of contrast-
induced nephropathy in patients with CKD. Clin J Am Soc Nephrol.
2015;10(9):1519–1524.

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SECTION VII
ENVIRONMENT

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121

NOT SO FAST! REWARMING THE
COLD PATIENT

KUBWIMANA MOSES MHAYAMAGURU, MD, EMT-P AND
CHRISTOPHER G. WILLIAMS, MD, FAWM

Whoever said “take your time,” “slow is smooth, smooth is fast,” “measure
twice and cut once,” and “slowly but surely” may well have been speaking of
hypothermia treatment. We will discuss how this sage advice pertains to the
hypothermic patient later. First, though, let us review the mechanics of
normal thermoregulation and heat transfer from the body.

THERMOREGULATION

A normal body temperature is said to be 36.4°C to 37.5°C. Achieving a
normal body temperature is the result of balancing heat production and heat
loss. The vast majority of heat leaves the body through the skin via radiation,
evaporation, conduction, and convection. The majority of remaining heat loss
occurs via respiration.

Thermal regulation is controlled by the anterior hypothalamus. There are
factors/conditions that can alter thermoregulation, and they include extremes
of ages, endocrine disorders, malnutrition, and hypoglycemia, which all tend
to limit heat production. Other things that can interfere with
thermoregulation include breakdowns in skin integrity (e.g., burns, road rash)
or inappropriate vasodilation in the periphery (e.g., mediations, spinal cord
injuries, sepsis). Hypothermia has been defined as a core body temperature
≤35°C (95°F). It is commonly subdivided into three levels of severity: mild
hypothermia (32°C to 35°C [90°F to 95°]), moderate hypothermia (28°C to
32°C [82°F to 90°F]), and severe hypothermia, which equals a core
temperature <28°C (82°F). At temperatures approaching 30°C, humans

581

become altered—even to the point of coma—and cardiac dysrhythmias may
occur. At 23°C, apnea is common.

TREATMENT OF HYPOTHERMIA

Noninvasive passive external rewarming tends to be enough for patients with
mild hypothermia. A basic thing like covering up the patient with dry
clothing in a warm room generally suffices.

For moderate hypothermia, more aggressive external rewarming is
indicated with the use of heated blankets, hot pads, hot water bottles, and
chemical warmers. In the case of severe hypothermia, invasive rewarming
attempts should be undertaken. This includes cardiopulmonary bypass or
intravenous rewarming. Intracavitary lavage has grown out of favor.

Patients with mild hypothermia can have intense shivering and cold
white/pale skin. Patients with moderate hypothermia have altered mental
status in the form of dysphasia, amnesia, confusion, or apathy—symptoms
mimicking many pathologies. In addition, they tend to be hyporeflexic and
have ataxia or loss of fine motor skills. Patients with severe hypothermia lose
complete ability to shiver; they may be delirious or comatose and have fixed
and dilated pupils, oliguria, bradycardia, hypotension, and pulmonary edema.
Keeping these signs and symptoms in mind is vital. It is not unheard of for a
patient to be found with ataxia and decreased level of consciousness,
delivered to the ED not shivering, and ending up being intubated for
suspicion of other causes of altered mental status (AMS) without considering
their core temperature as the possible etiology.

Perhaps the greatest threat in the resuscitation of hypothermic patients is
dysrhythmia. This can result in a refractory ventricular fibrillation and is
associated with jostling or manhandling the patient. Care should be taken
both prehospital and in the resuscitation bay when transferring the patient,
placing pads, performing procedures, etc. A second, more insidious threat is
the afterdrop phenomenon. This occurs as rewarming of the body causes
stagnant, frigid blood in the periphery to circulate back toward the core,
leading to a paradoxical drop in core temperature. This author has met
Greenlandic Inuits who report witnessing this event frequently. One of these
Inuits (who is himself a physician) teaches that arms and lower legs should
be kept out of warming blankets and away from heating pads until the core is
sufficiently warmed.

It is also important to note that a patient may not necessarily be dead
when found down, cold, cyanotic, and without apparent cardiac or
respiratory activity. As the saying goes, “a patient is not dead until they’re

582

warm and dead.” The American Heart Association (AHA) recommends
rewarming patients up to 35°C before declaring resuscitative efforts futile
and withdrawing support. (Obviously, this only applies to cases where cause
of death is ambiguous or potentially environmental). The AHA has a
modified AHA algorithm for hypothermic resuscitation. Some things to
remember are as follows: administration of code drugs and defibrillation
should be withheld until rewarming to at least 28°C is achieved, and
acquiring an EKG may be difficult on cold skin, for which the use of pin
electrodes is an option.

In addition to VF and afterdrop, some potential complications to keep in
mind while rewarming the severely hypothermic patient include hypokalemia
and hypophosphatemia, hypoglycemia, rewarming-related hypertension,
bladder atony, paralytic ileus, coagulopathy, and rhabdomyolysis. Every
patient should be monitored during and after rewarming, with attention paid
to the above complications.

KEY POINTS

Slow is smooth; smooth is fast: Avoid rough movements and handle
the victim gently for all procedures to avoid VF.
Preexisting or concurrent conditions may be the exacerbating force
leading to hypothermia.
When in doubt, adequately warm the core before the extremities to
prevent afterdrop.
Resuscitation should be continued until the absence of cardiac activity
is documented after raising the body temperature to a level of 28°C to
30°C.

SUGGESTED READINGS

Brugger H, Durrer B, Elsensohn F, et al. Resuscitation of avalanche victims:
Evidence-based guidelines of the international commission for mountain
emergency medicine (ICAR MEDCOM): Intended for physicians and other
advanced life support personnel. Resuscitation. 2013;84(5):539–546.

Cohen DJ, Cline JR, Lepinski SM, et al. Resuscitation of the hypothermic patient.
Am J Emerg Med. 1988;6(5):475–478, ISSN 0735–6757,
http://dx.doi.org/10.1016/0735-6757(88)90251-3.

Durrer B, Brugger H, Syme D. Advanced challenges in resuscitation: Special
challenges in ECC—hypothermia. Resuscitation. 2001;50(2):243–245, ISSN

583

0300–9572, http://dx.doi.org/10.1016/S0300-9572(01)00389-6.
Petrone P, Asensio JA, Marini CP. Management of accidental hypothermia and

cold injury. Curr Probl Surg. 2014;51(10):417–431.
European Resuscitation Council. Part 8: Advanced challenges in resuscitation:

Section 3: Special challenges in ECC 3A: Hypothermia. Resuscitation.
2000;46(1–3):267–271.

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122

ACCLIMATIZE OR DIE OR DESCEND

CLINTON G. KEILMAN, MD

ACUTE MOUNTAIN SICKNESS

Acute mountain sickness (AMS) is an intolerance to hypoxia that usually
occurs in the first few days of travel to altitudes above 8,200 ft. The
symptoms can start as early as 2 hours, but rarely after 36 hours at altitude.
Rapid rate of ascent, higher altitudes, unacclimatization, increased physical
exertion, and genetic predisposition all increase the risk and severity of
AMS. The hallmark sign of AMS is headache, which is usually bitemporal,
throbbing, and worse with the Valsalva maneuver. Symptoms that can
accompany the headache are nausea, vomiting, anorexia, GI disturbance,
dizziness, dyspnea on exertion, malaise, and lassitude. AMS typically
resolves in 1 to 2 days and is self-limiting and not life threatening. AMS does
not have neurologic findings aside from headache. If neurologic findings are
present, it is likely that AMS has progressed to high-altitude cerebral edema
(HACE). The Lake Louise consensus definition for AMS is the presence of
headache and at least one of the following: gastrointestinal problems, fatigue
or weakness, dizziness or light-headedness, and difficulty sleeping.

Prevention

As with nearly all medical conditions, prevention is far superior to treatment.
The Wilderness Medical Society has presented recommendations for the
prevention/prophylaxis of AMS. These include taking ≥2 days to arrive at
3,000 m and limiting subsequent sleeping elevation to <500 m/d,
acetazolamide 125 mg bid, and/or dexamethasone 4 mg bid. These
recommendations are nuanced depending on an individual patient’s risk
category for high-altitude illness, so the reader is referred to the WMS
consensus guidelines for details. The bottom line is that if a patient follows a

585

proper ascent profile, the use of acetazolamide or dexamethasone can be
avoided in most cases.

Treatment

For mild AMS, stop the ascent to allow time to acclimatize and treat with
analgesics and antiemetics for symptomatic relief. Acetazolamide 125 to 250
mg bid can be used to speed up acclimatization or one should descend by
1,600 ft or more until symptoms resolve. To treat moderate to severe AMS,
use dexamethasone 4 mg PO, IM, IV q6h, oxygen 2 L/minute, and
acetazolamide 250 mg bid. (Think “DOA,” if you don’t want your patients
“dead on arrival.”) Descend if possible, but if unable to descend, treat with
portable hyperbarics.

HIGH-ALTITUDE CEREBRAL EDEMA

HACE is an encephalopathy with the cardinal symptoms of ataxia and
change in consciousness (confusion, somnolence, coma) with focal
neurologic signs and seizures being uncommon. AMS progression to HACE
usually requires 1 to 3 days, but can happen as quickly as 12 hours. The use
of labs can be helpful in ruling out other conditions; however, imaging has a
minor role. “Computed tomography (CT) may show compression of sulci
and flattening of gyri, and attenuation of signal more in the white matter than
gray matter. MRI is more revealing, with a characteristic high T2 signal in
the white matter, especially the splenium of the corpus callosum, and most
evident on diffusion-weighted images.” The Lake Louise consensus
definition for HACE is the presence of one of the following: presence of a
change in mental status and/or ataxia in a person with AMS or the presence
of both mental status changes and ataxia in a person without AMS.

Treatment

Treatment for HACE is similar to that for AMS but is more urgent.
Immediately descend, and if you cannot descend, treat with portable
hyperbarics. A portable hyperbaric bag compressed to two psi is the
equivalent of descending 5,250 ft. In addition to descending, treat early with
dexamethasone 8 mg PO, IM, or IV and then 4 mg q6h and oxygen 2 to 6
L/min.

HIGH-ALTITUDE PULMONARY EDEMA

High-altitude pulmonary edema (HAPE) usually occurs on day 2 to 4 on

586

altitudes >8,200 ft and is the most common cause of death at altitude. The
Lake Louise consensus defines HAPE as a minimum of two of the following
symptoms: dyspnea at rest, cough, weakness or decreased exercise
performance, chest tightness, or congestion. In addition, there must be a
minimum of two of the following signs: crackles or wheezing in at least one
lung field, central cyanosis, tachypnea, or tachycardia. If recognized early,
this condition is easily reversible.

Treatment

The treatment of HAPE is similar to HACE in that you must descend but you
must also minimize exertion. If one cannot descend, treat with portable
hyperbarics, oxygen 2 to 6 L/min, and add nifedipine 30 mg PO q12h
(sildenafil or tadalafil as an alternative) to reduce pulmonary artery pressure
and resistance.

KEY POINTS

Most EM providers will not see this in the ED unless it is a severe
case because most will resolve by the time they reach an ED.
When faced with questions about a patient with symptoms at altitude,
descent is always the right answer.
Early recognition is key to treat and prevent further deterioration of
the patient.

SUGGESTED READINGS

Auerbach P. Wilderness Medicine. Philadelphia, PA: Elsevier/Mosby, 2012.
Luks A, McIntosh S, Grissom C et al. Wilderness medical society practice

guidelines for the prevention and treatment of acute altitude illness: 2014
Update. Wilderness Environ Med. 2014;25(4):S4–S14.
Sutton J, Houston C, Coates G. Hypoxia and Molecular Medicine. Burlington, VT:
Queen City Printers; 1993.
Swenson E. Pharmacology of acute mountain sickness: Old drugs and newer
thinking. J Appl Physiol. 2016;120(2):204–215.
doi:10.1152/japplphysiol.00443.2015.

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123

AGGRESSIVE COOLING IS
(ALMOST) ALWAYS THE CORRECT

APPROACH TO THE CRITICAL,
ENVIRONMENTALLY

HYPERTHERMIC PATIENT

CHRISTOPHER G. WILLIAMS, MD, FAWM

During a December storm in 1790, local physician, James Currie, stood
helplessly from the shore near Liverpool Harbor while a number of
American crewmen floundered and succumbed to the 40-degree waters.
Unable to maintain their grasp to the surrounding rigging and flotsam, many
drowned. Following this ordeal, Dr. Currie began to undertake a series of
human experiments involving cold water immersion (CWI). It is from these
limited experiments of only a handful of euthermic, healthy subjects that the
phenomenon known as the “Currie response” was derived. This argues that
an individual placed rapidly into a cold environment will vasoconstrict,
shiver, and temporarily maintain or elevate his or her temperature (by 0.1°C
to 0.2°C total). These findings crept into modern medical teaching along with
the dogma that hyperthermia should only be treated with a few strategically
placed ice packs, evaporative cooling with tepid-to-warm water, avoidance
of CWI, etc. For about 200 years, the medical community, including
emergency physicians, has practiced beneath this well-meant but poorly
derived conclusion that cooling measures should be implemented cautiously.

Just as the severity of thermal burns is a function of heat intensity and
duration of contact, hyperthermia resulting in end-organ damage should be

588

viewed similarly. Consequently, aggressive treatments are indicated to limit
the amount of time a patient remains hyperthermic. Unlike the treatment of
severe hypothermia, when premature and overly aggressive correction can
result in afterdrop phenomena, arrhythmias or refreezing injuries,
hyperthermic patients tolerate—in fact require—as timely a correction as
safely feasible. Time can mean neurons, nephrons, myocytes, and
hepatocytes, so cool them, and cool them quickly.

Heat-related illness is the leading cause of morbidity and mortality
among US high school athletes, as well as military recruits during training.
Heat waves annually kill many thousands, predominantly among the
extremes of age and those of lower socioeconomic means. Heat illness in
general should be viewed as a spectrum involving minor symptoms such as
heat edema, heat rash, heat cramps, heat syncope, or moderate-to-severe
symptoms, namely, heat exhaustion, heat injury (implying end-organ
damage), and heat stroke (CNS impairment).

Upon arrival to the emergency department, a patient suspected of
moderate-to-severe heat illness may require more than simple passive
cooling measures. Heat is dissipated via conduction, convection, radiation,
and evaporation. Remove all clothing, especially constrictive clothing such
as uniforms or football pads. Skin temperatures can be misleading, so core
temperature should be obtained either rectally or via a temp-sensing Foley
catheter. (Be aware that the rectum is well insulated, so as cooling efforts
take effect, the measured temperature may actually lag behind the core
temperature.) Typically, a core temperature >40°C correlates with severe
heat injury or heat stroke, but this is not absolute. Hyperthermia + CNS
dysfunction = heat stroke. A temperature <40°C or the presence of sweating
should not dissuade a thoughtful clinician from making the diagnosis of heat
stroke.

Dehydration is associated with decreased sweat rates and increased core
temperatures, so begin efforts to rehydrate. Oral rehydration is sufficient for
mild-to-moderate cases where end-organ derangement is not in question. IV
fluids, typically crystalloids, are very commonly given in these patients, but
should not be given dogmatically; the goal should be euvolemia. Keep in
mind that symptomatic exercise-associated hyponatremia may present with
similar symptoms as heat exhaustion or heat stroke, such as weakness, ataxia,
and altered mentation. Encouraged consumption of free water in
hyponatremic patients thought to be merely dehydrated has yielded
catastrophic consequences.

So what about this “Currie response”? Studies and practical experience
show that in dangerously hyperthermic patients, CWI does not result in

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shivering or temperature gains. Whatever peripheral vasoconstriction occurs
is insufficient to counteract the effects of aggressive cooling measures.
Studies of CWI show cooling rates of hyperthermic patients at 0.2°C/minute
to 0.35°C/minute, orders of magnitude faster than other conventional cooling
methods. However, unless your patient is an otherwise healthy victim of
exertional heat stroke (EHS), the need for monitoring, managing airway,
evaluating for comorbid conditions, etc. may make immersive therapy
unfeasible.

There are expensive, name-brand options for rapidly cooling the critical
patient. These usually come in the form of pads or blankets and have the
added benefit of tighter monitoring of core temperature, avoidance of
overcooling, and maintaining a desired temperature. (The latter two are not
usually a factor in the treatment of environmentally hyperthermic patients.)
In many emergency departments, infrequent use and nursing unfamiliarity
makes the placement and use of these proprietary systems slow and
impractical. Perhaps the most common method of active cooling that does
not limit monitoring is the use of evaporation/convection. After clothing is
removed, hospital sheets or towels may be loosely draped over the patient
and doused with cold water. A box fan or a floor fan (snail fan) should be
obtained—call hospital maintenance if necessary—and directed at the
patient. As long as active cooling efforts are under way, the sheets should be
turned or replaced when warmed up and rewetted when dry. This has been
shown to decrease core temperature on average 0.04°C/minute to
0.1°C/minute. It is likely that adding ice packs to the patient augments this
cooling rate.

KEY POINTS

Hyperthermic injury is a time-sensitive process; so cool the patient!
Aggressive cooling efforts will not cause critically hyperthermic
patients to paradoxically shiver and raise their temperature.
Evaluate for concomitant dehydration and do not miss hyponatremia.
Cease active cooling measures when core temperature <39°C.

SUGGESTED READINGS

Auerbach PS. Wilderness Medicine. 6th ed. Philadelphia, PA: Elsevier/Mosby,
2012.

Della-Giustina D, Ingebretsen R, eds. Advanced Wilderness Life Support:

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Prevention, Diagnosis, Treatment, Evacuation. 8th ed. Salt Lake City, Utah:
Wilderness Medical Society, 2013:68–78.
Lipman GS, Eifling KP, Ellis MA, et al. Wilderness Medical Society practice
guidelines for the prevention and treatment of heat-related illness: 2014 update.
Wilderness Environ Med. 2014;25(4 Suppl):S55–S65.
Platt M, Vicario S. “Heat illness.” In: Rosen P, Marx JA, eds. Rosen’s Emergency
Medicine: Concepts and Clinical Practice. 8th ed. Philadelphia, PA: Elsevier
Saunders, 2014: 1896–1905.

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124

SMOKE INHALATION: COMMONLY
OVERTREATED AND

UNDERTREATED ASPECTS

DENNIS ALLIN, MD, FACEP, FAAEM, FAEMS

Smoke inhalation is the most common cause of death from fires, increasing
the mortality of a 30% total body surface area (TBSA) burn by 70%. Smoke
inhalation generally occurs in enclosed spaces, and treatment involves the
management of multiple mechanisms of injury including thermal burns from
fire and inhalation of superheated gases, direct effects of inhaled chemical
irritants, and inhaled substances producing systemic toxicity.

THERMAL BURNS

With few exceptions, the thermal burns in the airway will occur in the
oropharynx with the dissipation of heat protecting the lower airways. The
signs suggesting upper airway thermal injury include

1) Stridor
2) Hoarseness
3) Carbonaceous sputum
4) Visible burns and blistering of the mucosa or face

In patients involved in an enclosed space fire with signs of potential
airway involvement, elective intubation should be considered prior to signs
of airway obstruction as deterioration of the airway can occur very rapidly
and, once present, will make endotracheal intubation nearly impossible due
to swelling and constriction of the airway. Methods to evaluate the glottis

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include rapid sequence induction, awake laryngoscopy with local anesthesia,
and fiberoptic laryngoscopy. Patients with obvious signs of airway thermal
injury will likely have concomitant pulmonary injury that will also require
early aggressive securing of the airway to manage the acute pulmonary
injury as well as to provide necessary pulmonary toilet.

SYSTEMIC TOXINS

Carbon monoxide is the product of incomplete combustion of carbon
compounds and thus a common component of smoke inhalation. Toxicity
generally relates to hypoxic stress from binding to hemoglobin and leftward
shift of the oxygen dissociation curve. There are, however, additional
mechanisms of direct interruption of cellular metabolism as well as
immunologic and inflammatory pathologic processes likely unrelated to
hypoxia that can evolve over time. These processes affect mainly neuro
tissue leading to delayed neurologic sequelae including headaches, motor
weakness, balance issues, and cognitive deficits. The diagnosis of carbon
monoxide toxicity is suspected in patients with potential exposure to carbon
monoxide with headache, dizziness, vomiting, altered mental status, loss of
consciousness, severe acidosis, and cardiovascular dysfunction, confirmed by
measurement of either venous or arterial carboxyhemoglobin levels.
Remember that measurements in the ED may be low and have poor
correlation with the level of toxicity due to administration of oxygen by EMS
providers. Any HbCO level >10% in a smoker, or >4% in a nonsmoker, is
indicative of CO exposure. Once confirmed, the primary treatment is 100%
oxygen.

The role of hyperbaric oxygen therapy in carbon monoxide poisoning
remains somewhat controversial, but the generally accepted indications to
refer a patient for hyperbaric oxygen treatment include prolonged loss of
consciousness, neurologic dysfunction, or cardiovascular dysfunction, but it
must be understood that the principle purpose of hyperbaric oxygen therapy
is the prevention of neurologic sequelae and that the patient should be stable
from an airway and pulmonary status. Even then, these patients require a
hyperbaric center capable of critical care, and the number of these centers in
the United States is decreasing. The Divers Alert Network reports that only
30% of the hyperbaric departments in the United States can take patients 24
hours a day. For these reasons, the treating physician should consider
carefully the risk versus benefit of overemphasizing the transfer of a patient
for hyperbaric oxygen therapy prior to managing the life-threatening
complications of thermal burns to the skin and airway as well as the
pulmonary injuries, particularly if this would require transfer over a long

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distance.

Cyanide toxicity is frequently a concomitant exposure with carbon
monoxide in enclosed space fires with smoke inhalation. Cyanide exerts its
toxic effects through binding to cytochrome c oxidase resulting in cellular
hypoxia and usually profound lactic acidosis. Patients may present much like
those with carbon monoxide poisoning with headache, nausea, altered mental
status, and coma, but without a confirmatory test, this toxin often goes
overlooked. With the introduction of hydroxocobalamin, the empiric
treatment of severe smoke inhalation patients should be considered as there
are few complications with this therapy and great potential benefit.

KEY POINTS

Do not wait for obvious signs of airway obstruction in patients
exposed to fires in enclosed spaces who display signs of smoke
inhalation. The airway can obstruct very quickly, and at that point,
endotracheal intubation may be nearly impossible.
Smoke inhalation patients with altered mental status and acidosis
should be considered for cyanide poisoning with early, empirical
treatment with hydroxocobalamin.
Pulse oximetry will be a poor indicator of carbon monoxide levels,
and at the time of ED presentation, the venous or arterial
carboxyhemoglobin level will have a poor correlation with the level of
symptoms or degree of toxicity.
Emergency hyperbaric oxygen therapy is relatively limited in
availability and thus may require long transports. The priorities in
smoke inhalation patients are airway management, prevention of
hypoxia, and treatment of thermal burns. Patients should be treated
with hyperbaric oxygen if stable and if available within a reasonable
distance.

SUGGESTED READINGS

Dries DJ, Endorf FW. Inhalation injury: Epidemiology. Pathology, treatment
strategies. Scand J Trauma Resusc Emerg Med. 2013;19:21–31.

Haponik EF, Summer WR. Respiratory complications in burned patients:
Diagnosis and management of inhalation injury. J Crit Care.
1987;135:121–143.

Thai A, Xiao J, Ammit AJ, et al. Development of inhalation formulations of anti-

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inflammatory drugs to potentially treat smoke inhalation injury in burn victims.
Int J Pharm. 2010;389(1–2):41–52.
Thom SR. Carbon monoxide mediated brain lipid peroxidation in the rat. J Appl
Physiol. 1990;68:997–1003.
Thom SR. Taber RL, et al. Delayed neuropsychologic sequelae after carbon
monoxide poisoning: Prevention by treatment with hyperbaric oxygen. Ann
Emerg Med. 1995;25:474–480.
Weaver LK, Hopkins RO, et al. Hyperbaric oxygen for acute carbon monoxide
poisoning. N Engl J Med. 2002:347(14):1057–1067.

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125

CO POISONING: IT TAKES MORE
THAN O2

BRYAN WILSON, MD AND CHRISTOPHER G. WILLIAMS,
MD, FAWM

Carbon monoxide is a colorless, odorless gas that is formed by the
incomplete combustion of carbon containing materials and that causes a wide
variety of nonspecific symptoms. While typical symptoms include headache,
dizziness, and nausea, there are reports of symptoms as varied as vomiting,
shortness of breath, and even fever with diarrhea. An exposure history such
as the use of a combustible fuel for heat in the winter or the use of an indoor
generator in an emergency can draw attention to the possibility of carbon
monoxide poisoning. A wide range of exposures including riding in a truck,
operating a natural gas forklift, swimming behind a boat, and hookah use are
more difficult to identify. The presence of characteristic physical exam
findings such as cherry-red skin, retinal flame hemorrhages, and cutaneous
bullae is uncommon and should not be relied upon. Despite being one of the
most common toxic exposures in industrialized countries and causing
hundreds of deaths per year, the diagnosis of carbon monoxide poisoning can
easily go unrecognized and requires a high index of suspicion. Suspicion of
carbon monoxide poisoning can be confirmed by laboratory detection of
carboxyhemoglobin (HbCO) or dissolved serum carbon monoxide.

The toxicity of carbon monoxide results from several pathophysiologic
effects. The first is impairment of oxygen delivery by preferential binding to
hemoglobin with an affinity over 200 times greater than that of oxygen. The
effect of this hypoxemia is worsened by a concurrent left shift in the oxygen-
hemoglobin dissociation curve. Animal evidence strongly suggests that
poisoning heavily relies on direct end-organ damage via inactivation of
mitochondrial cytochrome oxidase and the resulting metabolic stress and a

596

subsequent free radical–mediated inflammatory cascade. Additionally,
animal evidence suggests a neuroexcitatory effect of carbon monoxide,
which likely enhances the metabolic stress via increased demand. The typical
result of these pathways is neuronal cell death, myocardial dysfunction, and
long-term development of neuropsychiatric sequelae. Due to the need for
diffusion into end organs to mediate toxicity, dissolved serum carbon
monoxide levels are likely more predictive of prognosis than are
carboxyhemoglobin saturations. Children and fetuses are more susceptible to
carbon monoxide poisoning. Previously, this was thought to be due to an
increased affinity to fetal hemoglobin though emerging research indicates
this may be more attributable to a high metabolic and respiratory demand in
the setting of hypoxemia.

Administration of supplemental oxygen is the foundation of carbon
monoxide poisoning treatment as it helps to improve hypoxemia and speed
elimination of carbon monoxide. On room air, carboxyhemoglobin has a
half-life of ~200 minutes. High FiO2 via mask can decrease this to 75
minutes, while administration of 100% oxygen at 3 atmospheres of pressure
reduces it to 15 minutes. Some evidence suggests that hyperbaric oxygen
may confer additional benefit by more promptly restoring cytochrome
oxidase activity and minimizing the subsequent inflammatory process. While
there is currently insufficient evidence to strongly recommend for or against
the administration of hyperbaric oxygen, it should be considered in severe
poisonings. In particular, hyperbaric oxygen is frequently recommended for
patients with neurologic deficits, syncope, fetal distress, or
carboxyhemoglobin >10% in the setting of pregnancy. It is important to
weigh the risk of transporting a critically ill patient against the possible
benefits of hyperbaric oxygen.

Long-term considerations for these cases revolve around good
neuropsychiatric follow-up and source control. It is important to consider
sequelae and concurrent exposures when evaluating a patient with carbon
monoxide poisoning. Of particular note would be exposure to airway burns
or cyanide poisoning in the setting of a house fire. Cyanide is released
through the combustion of various plastic products. A serum lactate >10
mmol/L in the setting of smoke inhalation is strongly suggestive of cyanide
toxicity with 6 mmol/L often considered confirmatory in cases with a high
pretest probability. In the setting of concurrent carbon monoxide and cyanide
poisoning, hydroxocobalamin and sodium thiosulfate would be preferable to
the methemoglobinemia producing amyl nitrite and sodium nitrite. Other
sequelae include pulmonary edema, myonecrosis, compartment syndrome,
and acute kidney injury, and the patient should be closely monitored for
development of these complications.

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Many patients develop a varied range of neuropsychiatric complications
such as impaired cognition, mood abnormalities, and abnormal movements
in the days to weeks following a poisoning. It is important to ensure the
patient has good follow-up to monitor and manage these symptoms should
they occur. In addition, all reasonable efforts should be made to identify the
source of the exposure and have it contained. The importance of doing this is
underscored by high-profile cases such as the fatal carbon monoxide
poisoning of a young boy just 2 months after the fatal poisoning of an elderly
couple in the same hotel room.

KEY POINTS

Consider carbon monoxide poisoning in vague cases that “just don’t
make sense.”
Pediatric and fetal patients are particularly sensitive to carbon
monoxide.
Consider hyperbaric oxygen for severe cases with neurologic
manifestations.
Consider coexposures such as cyanide and sequelae such as hypoxic
insult or airway burns.
Attempt to identify and report the source of the exposure.

SUGGESTED READINGS

Buckley NA, et al. Hyperbaric oxygen for carbon monoxide poisoning. Cochrane
Database Syst Rev. 2011;(4):CD002041.

Centers for Disease Control and Prevention. Nonfatal, unintentional, non—fire-
related carbon monoxide exposures—United States, 2004–2006. MMWR Morb
Mort Wkly Rep. 2008;57(33):896–899.

Mendoza JA, Hampson NB. Epidemiology of severe carbon monoxide poisoning
in children. Undersea Hyperb Med. (2006);33(6):439–446.

Tomaszewski C. Carbon monoxide. In: Hoffman RS, Howland MA, Lewin N, et
al. eds. Goldfrank’s Toxicologic Emergencies. 10th ed. New York: McGraw
Hill, 2015.

Weaver LK. Clinical practice. Carbon monoxide poisoning. N Engl J Med.
2009;360:1217–1225.

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126

A RASH THAT IS MORE THAN
“JUST A RASH”

NASH WHITAKER, MD

Few things are more frustrating to emergency physicians (EP) than an
unexplainable rash. EP search for that one piece of history that will reveal the
diagnosis: “A new detergent? How about a pet? Perhaps new jewelry? Oh,
your child just had a cold?” Typical discharge instructions end with a similar
unfulfilling undertone—“It’s probably just a virus, it will go away.” Often,
this is true; however, missing a more serious pathology when presented with
a rash carries significant mortality and morbidity, as is the case with tick-
borne diseases.

Ticks are one of the most common vectors for zoonotic disease
worldwide. Diseases native to the United States include, but are not limited
to, Lyme disease, Rocky Mountain spotted fever (RMSF), tularemia,
ehrlichiosis, babesiosis, Q fever, Colorado tick fever, relapsing fever, and
anaplasmosis. It is important to recognize that tick-borne illnesses have a
geographic distribution and seasonal variation, being more common during
summer months when ticks are more active.

The majority of the tick-borne illnesses present initially similar to a viral
syndrome: fever, chills, malaise, myalgia, headache, and gastrointestinal
symptoms (nausea, vomiting, diarrhea, anorexia) are the typical compilations
in the acute phase.1 These subtle and ambiguous symptoms are seen daily in
emergency departments nationwide, making the diagnosis of a tick-borne
disease very challenging. Since the majority of patients never recall a tick
bite, EP must keep tick-borne disease in their differential diagnosis in all
patients presenting with a febrile rash.2 Of all tick-borne diseases, the three
most unique, “can’t miss” diagnoses for the EP are Lyme disease, RMSF,

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and tularemia.

For those patients who do present with an attached tick, it is worth noting
that there is almost no risk of transmission if the duration of tick attachment
is <72 hours.2 All patients with suspected tick-borne disease will require
follow-up either with their primary care physician or an infectious disease
specialist, depending on their level of illness. Antibiotics should not be
delayed in the setting of high clinical suspicion with any of these diseases.
Admission might be required depending on symptom severity and the ability
of the patient to tolerate oral antibiotics.

LYME DISEASE

Lyme disease, the most common tick-borne disease in North America, is
caused by the spirochete Borrelia burgdorferi.1 It is endemically located in
the northeastern coastal, mid-Atlantic, and north central states, but has been
reported in all contiguous 48 states.

There are three stages of Lyme disease. Erythema migrans (EM), a
pathognomonic skin eruption that forms at the site of the tick bite,
characterizes the early stage. This distinct, vasculitic, nonpruritic rash is
infamous for Lyme disease and typically appears 2 to 20 days after
exposure.3 Classically, it is described as a “bull’s-eye” consisting of a red
ring with central clearing. A rash is present in 80% of cases, but only 60% of
those who develop rash have the classic bull’s-eye appearance.3

Dissemination of the spirochetes leads to the middle and late stages of
the disease, which are characterized by a multitude of symptoms. The most
commonly described symptoms include a transient migratory polyarthritis,
A-V nodal block, pericarditis, meningitis, uveitis, or unilateral/bilateral facial
nerve paralysis. Additionally, multiple diffuse EM rashes may occur and aid
in the diagnosis.3

Lyme disease is a clinical diagnosis for the EP. Treatment includes
doxycycline or amoxicillin. Polymerase chain reaction or immunoassay
confirmation testing is available.

ROCKY MOUNTAIN SPOTTED FEVER

RMSF is the most severe of all tick-borne diseases in the United States. It
has a mortality rate of ~15% to 20%. Rickettsia rickettsii is the pleomorphic,
intracellular agent. Five states account for 60% of cases: North Carolina,
Missouri, Tennessee, Arkansas, and Oklahoma, but sporadic cases have been

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