Avoiding Common Errors in the Emergency Department - Book 1

101

KNOW HOW TO DEAL WITH THE
DISPLACED PEG TUBE

JULIE Y. VALENZUELA, MD AND ROLANDO G.
VALENZUELA, MD, DTMH

As the number of physicians capable of placing percutaneous endoscopic
gastrostomy (PEG) tubes has increased, so has the number and type of PEG
tubes being placed. The PEG tube is placed for feeding access as well as for
gut decompression. Nearly 10% of patients with a PEG tube suffer some sort
of malfunction, with dislodgement occurring in 1.6% to 4.4% of patients. In
the emergency department (ED), we need to be familiar with PEG tubes and
comfortable with decision-making when these patients come to the ED
complaining of tube dislodgement.

The PEG tube consists of a single-lumen tube protruding into the
stomach, with a fixed internal bolster and a sliding external bolster. When
normally situated, there should be a 1 to 2 cm of movement of the tube
before reaching the external bolster. A gauze square is usually placed
between the skin and the external bolster to collect any moisture that may
gather. Normally, the skin surrounding the wound should be without
erythema, exudate, or drainage. Irritation dermatitis can occur at the insertion
site as well but should typically be a mild redness only. A common error is to
miss an infection (redness, pain, warmth, drainage, fever) at the insertion site
and to mistakenly ascribe symptoms and signs to irritation dermatitis. The
two must be carefully differentiated in each patient. Abscess, wound
infection, and necrotizing skin infection should be considered in patients who
show systemic signs of infection, remembering that patients who are
immunocompromised may not manifest all of the typical signs.

Dislodgement of a PEG tube occurs more frequently in the agitated,

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demented, or delirious patient. The decision to replace the PEG tube in the
ED depends on the amount of time elapsed since the PEG tube was placed,
as well as the amount of time the PEG tube has been dislodged.

The PEG tube’s initial placement involves controlled perforation of a
hollow organ with formation of a gastrocutaneous fistula. The PEG tube
holds the anterior stomach to the peritoneal wall. Eventually, the stomach
becomes attached to the abdominal wall as adhesions form. The tract is
considered mature in ~10 to 14 days, although the literature describes a range
of 1 week to 6 months. Maturation will take longer in elderly or
malnourished patients as well as those with acquired immune deficiency
disorder (AIDS), cancer, or diabetes; those who have undergone radiation
therapy; or those who have an otherwise compromised immune system.

When a tube becomes dislodged, history from the patient (and/or
caregiver) and examination are important. It is especially important to find
out the length of time that the PEG tube has been present, as well as how
long it has been out. PEG tubes that become dislodged before the month-long
maturation period is complete should not be replaced blindly. Lack of
maturation of the tract means that there is a high probability that the stomach
has fallen away from the abdominal wall. Blind placement of a PEG tube
may result in the tube being placed in the peritoneum. Moreover, these
patients should be considered to have a perforation, with initiation of
antibiotics, nasogastric tube placement, and surgical consultation. In these
cases, PEG tube replacement should be performed by a specialist using
endoscopic techniques in a controlled setting.

A PEG tube that has been present for over 1 month is considered mature,
and a replacement PEG tube can be replaced blindly into the fistula with
minimal risk to the patient. Replacement should not be delayed, as the
gastrocutaneous fistula will begin to close 4 to 48 hours after dislodgement.
Be sure to inflate the interior balloon. If a replacement PEG is unavailable, a
Foley catheter can be used to maintain patency of the tract and can be used
for feeding purposes until a replacement PEG tube can be inserted. It should
be noted that the mechanism for dislodgement, that is, trauma, or external
traction, can result in disruption of a mature tract and can result in peritoneal
placement if a PEG is inserted blindly. For this reason, confirmation of
placement should always be performed. This can be achieved using an
abdominal x-ray with radiopaque contrast injected into the tube.

Common errors in the ED management of these patients include

1) Failure to consult a specialist when an immature fistula track exists and
proceeding with blind replacement

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2) Failure to promptly maintain the fistula track and prevent its closure
with a Foley catheter or replacement PEG tube

KEY POINTS

Consider infection of the tract in a patient with redness and
tenderness, especially when systemic signs of infection are present.
A confirmatory dye study after tube replacement in a patient with a
mature fistula track.
In patients with immature tracts (<4 weeks), specialist consultation
should be obtained.

SUGGESTED READINGS

Jacobson G, Brokish PA, Wrenn K. Percutaneous feeding tube replacement in the
ED—are confirmatory X-Rays necessary? Am J Emerg Med.
2009;27(5):519–524.

Marshall JB, Bodnarcuk G, Barthel JS. Early accidental dislodgement of PEG
tubes. J Clin Gastroenterol. 1994;18(3):210–212.

McClave S, Neff RL. Care and long-term maintenance of percutaneous endoscopic
gastrostomy tubes. JPEN J Parenter Enteral Nutr. 2006;30:S27–S38.

Schrag S, Sharma R, Jalk NP, et al. Complications related to percutaneous
endoscopic gastrostomy (PEG) tubes. A comprehensive clinical review. J
Gastrointestin Liver Dis. 2007;16(4):407–418.

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102

COMMON PITFALLS IN POINT OF
CARE ULTRASOUND OF THE
GALLBLADDER!

KRISTIN BERONA, MD

Emergency point-of-care ultrasound to evaluate for gallbladder disease has
been utilized since the late 1980s. Emergency physicians are very good at
detecting gallstones and cholecystitis, with reported sensitivities from 88% to
96% for gallstones and 87% for cholecystitis. However, there are specific
tips and entities to be aware of to avoid missing gallstones or misinterpreting
other pathologies for gallstones and cholecystitis.

A complete and full evaluation of the gallbladder is necessary to not miss
stones. A full evaluation includes two views of the gallbladder in long axis
and in short axis interrogating from the fundus through the neck,
measurement of the anterior gallbladder wall, and measurement of the
common bile duct as medial as possible. Stones are generally hyperechoic
(bright), have a dense shadow, and are mobile. However, stones smaller than
4 mm may not shadow and stones impacted at the gallbladder neck may not
move. The gallbladder neck is an area that calls for meticulous evaluation
because gallstones there are often missed. To aid in evaluation of the
gallbladder neck, you can have the patient take a deep breath, or place the
patient in a left lateral decubitus position.

Another common misinterpretation is ironic: thinking that there are no
gallstones when the gallbladder is so full of stones that the gallbladder itself
is easy to miss, resulting in the clinician interpreting the scan as “contracted”
or “indeterminate.” When the gallbladder is completely full of stones, no bile
or hypoechoic area within the gallbladder is visible. This is called the “wall

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echo shadow” (WES) sign (see Figure 102.1). All that is seen is the
hyperechoic wall, another line of echoes from gallstones, and then a dense
shadow. The WES sign makes it very difficult to interpret wall thickness, but
it is important not to mistake it as negative for stones.

Figure 102.1 The wall echo shadow sign in a patient with a
gallbladder full of stones.

What about the false positives? There are many instances where we
might interpret the scan as positive for stones when they are not in fact
present. The most common mimicker of a stone is a gallbladder polyp. These
can be differentiated from stones in that they are not dependent or mobile
and do not shadow. Gallbladder polyps need outpatient follow-up, but the
patient is usually asymptomatic. Air in the duodenum adjacent to the
gallbladder can also be misinterpreted as positive for gallstones. The air in
the duodenum is hyperechoic, but does not have dense shadowing, and when
the patient is placed in left lateral decubitus, it becomes clear that the

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hyperechoic material (air) is outside of the gallbladder. Lastly, an ultrasound
artifact called edge artifact can mimic a stone because it creates a shadow.
Edge artifact occurs when the ultrasound beam encounters two different
tissues with contrasting sound propagation or hits a curved structure. The
change in beam direction causes the US beam to not be reflected back to the
transducer as expected and a shadow results. These shadows occur at the
edge of the gallbladder and will not have a hyperechoic stone associated.
Figure 102.2 demonstrates shadowing from both a stone and edge artifact.

Figure 102.2 Shadowing from both a stone and edge artifact.

Cholecystitis is diagnosed on ultrasound when there are gallstones or
sludge associated with secondary signs of infection: a positive sonographic
Murphy’s (maximal tenderness when ultrasound probe pushes directly over
the visualized gallbladder), gallbladder wall thickening (>3 mm), or
pericholecystic fluid. However, there are several entities aside from
cholecystitis that can cause gallbladder wall thickening, including a
contracted gallbladder (i.e., after eating), ascites, pancreatitis, or alcoholic

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hepatitis. In these cases, a thickened gallbladder wall needs to be taken in the
clinical context and laboratory findings.

KEY POINTS

A thorough evaluation of the gallbladder in two planes is your best
defense against misinterpretation. Look closely at the gallbladder
neck!
Be aware of entities that can be mistaken for stones: polyps, air in
duodenum, and edge artifact.
Contracted gallbladder, ascites, pancreatitis, and alcoholic hepatitis
can all cause gallbladder wall thickening—don’t be fooled into calling
cholecystitis.

SUGGESTED READINGS

Miller AH, Pepe PE, Brockman CR, et al. ED ultrasound in hepatobiliary disease. J
Emerg Med. 2006;30(1):69–74.

Scruggs W, Fox JC, Potts B, et al. Accuracy of ED bedside ultrasound for
identification of gallstones: Retrospective analysis of 575 studies. West J
Emerg Med. 2008;9(1):1–5.

Summers SM, Scruggs W, Menchine MD, et al. A prospective evaluation of
emergency department bedside ultrasonography for the detection of acute
cholecystitis. Ann Emerg Med. 2010;56(2):114–122.

Theodoro D. Hepatobiliary. In: Ma J, Matee, J, Blaivas M, eds. Emergency
Ultrasound. New York: McGraw Hill, 2008:169–922.

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SECTION V
CUTANEOUS

508

103

DON’T MISS NECROTIZING
FASCIITIS!

SHAUGHN KEATING, MD

Necrotizing fasciitis poses a particularly difficult diagnostic dilemma due to
its rarity and often subtle initial presentation. The term necrotizing soft tissue
infection (NTSI) is preferred as a more general descriptor of a collection of
bacteriologically distinct infections that share a final common pathway: rapid
necrosis of soft tissues, systemic toxicity, and high mortality if left untreated.
The diagnostic conundrum lies primarily in that the symptoms of early NTSI
are similar to that of cellulitis, leading to misdiagnosis, delayed treatment,
and high morbidity. Successful treatment requires early recognition, maximal
supportive care, and prompt surgical debridement.

NTSIs can be typed by their causal agent, and each has specific risk
factors. Type I NTSIs are polymicrobial infections that more commonly
affect those with impaired immune systems. They represent >80% of all
NTSIs. Common comorbidities include diabetes mellitus, morbid obesity,
and underlying kidney disease. Eponymous subtypes of Type I NTSIs have
also been historically classified by location. Fournier gangrene was described
in 1883 as gangrene foudroyante de la verge (“violent gangrene of the
penis”), a fulminant, morbid, perineal infection. Ludwig angina is an NTSI
of the deep oropharyngeal compartments and is caused by oral anaerobes.

Type II NTSIs are monomicrobial infections caused by Group A
streptococci (GAS) or Staphylococcus aureus. They are distinguished by the
virulence factors they produce. GAS M protein, protein F, streptococcal
inhibitor of complement, streptolysins, hyaluronidases, streptokinase, cell
envelope proteinases, and pyrogenic exotoxins and staphylococcal
leukocidin, modulins, and alpha-hemolysin allow them to spread rapidly and
cause toxic shock syndrome. While these infections are less common,

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representing 10% to 15% of NTSIs, their ability to affect healthy,
immunocompetent individuals with seeming minor trauma makes them
particularly dangerous.

A specific variant of monomicrobial Type II infection, clostridial
myonecrosis, is alternatively classified as a Type III NTSI. Clostridia are
obligate anaerobes and require deep inoculation in order to thrive. Infections
occur most often with local devascularization from surgery or intravenous
drug use or from complications of pregnancy such as retained products of
conception. Like Type II infections, clostridia produce an array of toxins that
potentiate its spread and systemic toxicity. These infections are notable for
their rapid spread and production of gas within fascial planes.

Regardless of type, the key to NTSI management is early diagnosis
leading to prompt debridement. Unfortunately, outward findings of erythema
and edema may be minimal or absent in early NTSIs because the soft tissues
affected are deep to the skin. Later in the course, violaceous bullae or
crepitus may appear. These findings are highly specific but insensitive and
suggest that significant tissue necrosis has already occurred. Differentiating
between cellulitis and early NTSI requires an understanding of the
underlying pathology. NTSIs impair and then destroy the underlying
vasculature of the soft tissues allowing for their rapid advance. Severe pain
out of proportion to exam is suggestive of this underlying tissue ischemia,
similar to mesenteric ischemia or limb arterial occlusion.

Once clinical concern is raised, laboratory tests and imaging are often
done, but may be of limited utility. Leukocytosis may be absent early in the
patient’s course, and nonspecific markers such as C-reactive protein fail to
distinguish between NTSI and cellulitis. Prior work on laboratory scoring
systems has failed to produce a sensitive and reliable tool to identify early
NTSIs. Gas along fascial planes in x-rays is pathognomonic but highly
insensitive. CT scans may show diffuse inflammation, necrosis, gas, or fluid
collections. In one study, when all these criteria were used, CT had a
negative predictive value of 100%. However, cellulitis, myositis, and other
nonnecrotizing myopathies can have similar findings, limiting specificity.
MRI has been suggested as a highly sensitive modality, but is limited by the
time taken to perform the study and similar issues with low specificity.

All patients with concern for NTSI should be started on maximal
supportive care and antibiotics, pending definitive treatment. The robust
inflammatory reaction often leads to large fluid shifts, and some patients may
require 10 to 20 L of IV fluids throughout their course. Prior to identification
of the causative bacteria, broad-spectrum IV antibiotics should be started
with both MRSA and broad gram-negative coverage, commonly vancomycin

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plus piperacillin/tazobactam. Clindamycin should also be started to suppress
bacterial toxin synthesis and may also modulate endogenous cytokine
production. IVIG has been investigated as an adjunctive therapy in severe
disease to suppress the inflammatory response and may improve survival, but
this is not yet part of standard emergency management.

Definitive diagnosis of NTSI requires surgery with direct inspection of
the tissues. Delay to first debridement increases mortality up to ninefold. If
high clinical concern exists, especially with late signs such as crepitus or
frank necrosis, surgical consultation should occur immediately, and further
diagnostic testing should not delay debridement. If the diagnosis remains
unclear, the Infectious Disease Society of America guidelines recommend
surgery after failure to respond to initial antibiotic therapy, defined as
reduction in fever, toxicity, and lack of advancement. Frequent reassessments
should be made with a low threshold to advocate for surgical management. If
there is no necrosis visualized with a small exploratory incision, the
procedure can be terminated with minimal risk. In an era when high-
resolution imaging has allowed the negative surgical rate for many
procedures to drop precipitously, there may be hesitation to perform a
surgery when the diagnostic testing is equivocal. The astute emergency
medicine provider may need to be an advocate for the patient given the
extreme risk-benefit ratio of a negative surgery compared with letting an
NTSI progress without debridement.

KEY POINTS

NSTIs may lack systemic toxicity or superficial skin findings early in
their course. NTSIs caused by GAS can affect young, healthy hosts
with minor or no apparent trauma.
Pain out of proportion to exam differentiates NTSI from cellulitis.
Crepitus, violaceous bullae, and skin sloughing are pathognomonic
late findings, but have low sensitivity.
Include clindamycin in NTSI treatment because it stops the bacterial
production of locally and systemically active toxins.
Definitive diagnosis and treatment can only be made with surgery and
debridement. Mortality increases with delayed surgical intervention,
so obtain surgical consultation early.
A negative exploratory incision has low risk. Advocate for surgical
exploration on all patients if there is high clinical concern or
progressive infection, even if imaging findings are nonspecific.

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SUGGESTED READINGS

Hussein QA, Anaya DA. Necrotizing soft tissue infections. Crit Care Clin.
2013;29(4):795–806.

Loudon I. Necrotising fasciitis, hospital gangrene, and phagedena. Lancet.
1994;344(8934): 1416–1419.

Stevens DL, Bisno AL, Chambers HF, et al. Practice guidelines for the diagnosis
and management of skin and soft-tissue infections. Clin Infect Dis.
2005;41(10):1373–1406.

Ustin JS, Malangoni MA. Necrotizing soft-tissue infections. Crit Care Med.
2011;39(9): 2156–2162.

Zacharias N, Velmahos GC, Salama A, et al. Diagnosis of necrotizing soft tissue
infections by computed tomography. Arch Surg. 2010;145(5):452–455.

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104

SJS AND TEN: ARE THEY
DIFFERENT?

ARUN NAIR, MD, MPH

WHAT IS SJS/TEN?

Recognize that these two entities are actually part of a spectrum with the
same underlying pathophysiology. It is acute disseminated epidermal
necrosis secondary to a hypersensitivity reaction to some nonnative agent—it
is most often due to a drug, but infections are not infrequently the cause. It is
the act of the epidermis separating from the dermis anywhere that is called
mucocutaneous. The pathophysiology is immune modulated and
multifactorial and super interesting, but you only need to know it in broad
strokes to provide excellent care. This is a burn, both on the outside and
inside, but with no associated thermal injury. The severity of the burn is
based on the body surface area (BSA) involved just like any other burn but
with one major caveat. There is often involvement of the unseen
mucocutaneous tissues—the alimentary, pulmonary, and genitourinary tracts
—which are not accounted for in traditional BSA calculations. Burnt skin
does not perform its usual functions, and it scars. The burn keeps growing if
the offending agent is still present. If you keep this overarching
understanding in mind, then the disease process and its treatment make
sense.

SKIN FINDINGS

Armed with the understanding that the epidermis is separating from the
dermis en masse, the skin findings including the Nikolsky sign should make
more sense. The epidermis is cleaving off the dermis as an intact layer or

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sheet and can be seen when a shear force is applied to the skin. Another way
this can be tested is with already formed blisters— if the entire blister can be
moved by applying gentle pressure to one side, it demonstrates that the
epidermal/dermal interface has been disrupted. This sign is nonspecific and
can be seen with other conditions, but its presence combined with any
mucosal lesion (most often seen on lips or in the mouth, but also remember
the conjunctiva and cornea) should cause serious consideration of a diagnosis
of the spectrum of SJS/TEN. Lesions can range from the pathognomonic flat
targetoid red and white lesion (not to be confused with the raised/edematous
blue, white, and red lesions of erythema multiforme target), which may
become confluent, develop into thin-walled blisters, or necrose into erosions.
As the disease process continues, sloughing off of large areas of skin can be
seen on palms, soles, tongue, etc. Except when the areas become
superinfected, there should be no significant edema or induration noted, and
the skin sheets should be thin and seem “topical.”

LOSS OF BARRIER

The epidermis’ job is to separate one’s insides from the outside world. It is
the first layer of protecting homeostasis, keeping our fluids and heat within
and preventing pathogens from without. Treatment of the skin findings in
SJS/TEN is the same as any other skin burn: provide analgesia, prevent
infection, and replace fluids and electrolytes as needed. Since there is no
thermal injury, the inflammatory response is not as exaggerated, and there
are less insensible losses. Replacing fluid at the rates recommended by the
Parkland formula will likely overestimate fluid deficit causing
“overressucitation” and its sequelae ranging from mild peripheral edema to
compartment syndrome and acute pulmonary edema. However, the patient
may require a large initial bolus to make up for fluid deficits depending on
time of presentation. Consider early ultrasound examination of IVC
collapsibility for estimating initial fluid status and placement of a Foley for
continuous urine output monitoring with a goal of 0.5 to 1 mL/kg/h.

As the inciting agent is often a drug, DO NOT dress the skin with
Silvadene (sulfa derivative) unless directed to do so by a burn specialist and
only if the causal agent has been definitively identified. The lesions should
be kept moist, protected, and sterile with nonadherent petroleum gauze. A
large percentage of patients with significant BSA involvement will go on to
develop skin infections. Try to prevent this as much as possible to avoid the
risk of adding another drug. Prescribing an antibiotic to someone undergoing
a hypersensitivity reaction is a risky option at best.

With the loss of the epidermis, the patient has lost his or her primary

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means of thermoregulation. Keep your patient as minimally exposed and for
the shortest time possible. Your patient may require warmed fluids or an
external heating device such as a Bair Hugger to maintain their temperature.

RECOGNIZE INTERNAL INVOLVEMENT

Our mucosal tissue allows for the diffusion of gases integral in ventilation
and oxygenation as well as the ciliary action responsible for mucus clearing
in our airways. Patients may progress to respiratory compromise from
pulmonary edema or obstruction and may require mechanical ventilation. In
this situation, care must be taken during intubation to not cause further
airway compromise by desquamating the tongue or other structures down
into the airway. The alimentary epithelia allow transport of everything from
ions to macromolecules and are integral in absorbing and retaining free water
—patients with significant GI involvement may require parenteral nutrition.
Our specialized corneal epithelia provide the transparency required for
proper vision. The fibrinous exudates caused by the loss of the mucosal layer
can cause scarring and stricture in luminal structures and can lead to
permanent loss of vision through corneal scarring. Early recognition and
management of these conditions are essential.

DISPOSITION

Don’t get too caught up in measuring BSA. If there’s minimal BSA
involvement, the patient looks good, and the causal agent is identified and
ceased, then the patient’s prognosis can be great and may get away with
hospital observation. If on the other hand, the size of lesions combined seems
bigger than the front of the torso, its >10%, and you should be calling your
local burn center ASAP for transfer. If its <10% but they look sick, better to
err on the side of transferring. Bad thermal or chemical burns go to the burn
center—the same applies here. Greater than 10% BSA means the patient in is
the overlap SJS/TEN phase and mortality >5%. If your patient is on this part
of the spectrum of SJS/TEN, the patient goes to the burn center. This is not
something for a novice practitioner to manage nor is this the patient that can
be admitted so that dermatology can see him or her once the weekend is
over. This level of mortality automatically necessitates ICU level of care and
requires the expertise that can only be delivered at a burn center. See Chapter
105.

Most importantly, try to identify the causal agent and cease exposure.
The disease process will continue to worsen as long as there is ongoing
exposure to the agent—stop all medications possible! The most important

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predictors of outcome are how early the exposure is stopped and how quickly
the patient is transferred to a burn center.

KEY POINTS

SJS/TEN is a spectrum of a hypersensitivity reaction to an offending
agent in which the mucocutaneous epidermis is separating from the
dermis en masse.
Don’t forget that the burn is also on the inside with consequences for
the GI, GU, and pulmonary systems.
Treat SJS/TEN the same as you would any burn - maintain
normothermia, replace fluid losses, and protect affected areas from
infection.
The most important predictors of patient outcomes are how early the
offending agent is stopped and how quickly they arrive at a burn
center - do not be the cause of the delay!

SUGGESTED READINGS

Endorf FW, Cancio LC, Gibran NS. Toxic epidermal necrolysis clinical guidelines.
J Burn Care Res. 2008;29:5.

Harr T, French LE. Toxic epidermal necrolysis and Stevens-Johnson syndrome.
Orphanet J Rare Dis. 2010;5:39.

McGee T, Munster A. Toxic epidermal necrolysis syndrome mortality rate reduced
with early referral to regional burn center. Plast Reconstr Surg.
1998;102:1018–1022.

Schwarts RA, Mcdonough PH, Lee BW. Toxic epidermal necrolysis part II.
Prognosis, sequelae, diagnosis, differential diagnosis, prevention, and
treatment. J Am Acad Dermatol. 2013;69(2):187.e1–e16.

Trent JT, Kirsner RS, Romanelli P, et al. Use of SCORTEN to accurately predict
mortality in patients with toxic epidermal necrolysis in the United States. Arch
Dermatol. 2004;140:7.

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105

THE SPECTRUM OF TEN

ALEXANDER JENSON, MD, MPH

Toxic epidermal necrolysis (TEN) is a severe form of an adverse
autoimmune reaction (usually drug induced) that involves keratinocyte death
and separation of the epidermis from the dermis of skin and mucous
membranes. It is part of a spectrum of severe epidermolytic reactions that
include Stevens-Johnson syndrome (SJS). Although rare, it still affects 2 per
million per year and has an overall mortality rate of 30%. In an emergency
department, rapid recognition (1), determination of severity (2), early
initiation of supportive care (3), and monitoring for life-threatening sequelae
(4) are essential.

RECOGNITION OF TEN

Although characterized by cutaneous and mucosal involvement, TEN is
frequently preceded by a prodrome consistent with a viral illness (cough,
fever, congestion, malaise). Typically, a few days after the prodrome, painful
erythematous macules develop symmetrically over the trunk, face, palms,
and soles. Over 90% of patients with TEN will have mucosal involvement,
including buccal, genital, and ocular (conjunctival or corneal) erythema and
erosions, which can cause dysphagia, visual changes, and pain. In the second
phase, these patches develop into bullae and detach. At presentation, skin can
vary from macules to blisters/bullae to erosions.

A history of present illness (HPI) must include discussion of recent
medications, as 80% to 95% of TEN cases develop as result of a drug
reaction, but the absence of this history should not prevent diagnosis as
identification of the offending drug often occurs post hoc. Drugs that can
commonly induce SJS/TEN can be divided simply into categories and
include antiepileptic drugs (carbamazepine, phenytoin, and phenobarbital),

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sulfonamides (notably Trimethoprim/Sulfamethoxazole [TMP/SMX]), and
antibiotics (including penicillins, cephalosporins, carbapenems, and
quinolones). Usually, the reaction begins between 1 and 8 weeks after
initiation of the agent, and for chronic medications, TEN risk drops
precipitously after 8 weeks. Other causes (although rare) for TEN include
infections such as Mycoplasma pneumoniae, cytomegalovirus, dengue fever,
a paraneoplastic reaction, immunizations, and even reactions to contrast
medium. Cohort studies have shown that patients with malignancy, HIV,
lupus, and collagen vascular disease are at higher risk of developing TEN
when exposed to these medications.

On exam, the hallmark rash is present over mucosal services (lips,
oropharynx, genitalia) and is notable for patches peripherally with
confluence over face, palms, soles, and trunk. The rash is painful and
progresses to blistering and epidermal sloughing, which can be precipitated
by lateral pressure (Nikolsky sign). The percentage of body area defines
TEN, with <10% body surface area (BSA) characteristic of SJS, 10% to 30%
of TEN/SJS overlap, and >30% for TEN.

Importantly, the differential for TEN includes IgA dermatosis,
paraneoplastic pemphigoid, and staphylococcal scalded skin syndrome,
which can all present with Nikolsky sign and bullae. Additionally, an
important distinction is made with drug eruption with eosinophilia and
systemic symptoms (DRESS), which has bullae and lip erosions, but without
epidermal sloughing and histologically distinct. Additionally, erythema
multiforme may resemble the early painful patches of TEN, although
epidermal death and bullae are infrequent.

SEVERITY OF TEN: SCORTEN

Given the high mortality rate of TEN, a rapid assessment of prognosis is
essential for prioritizing resources. As a result, the SCORTEN system has
been developed and validated repeatedly to guide prognosis, management,
and disposition for patients presenting with TEN.

The components of SCORTEN are age (>40 years), malignancy,
tachycardia (>120 bpm), percent of BSA (>10%) detached, serum blood urea
nitrogen (BUN) (>28 mg/dL), serum glucose (>252 mg/dL), and serum
bicarbonate (<20 mEq/L). Each is a binary variable that adds one point to the
score, up to 5 points. Each point adds to the relative risk of mortality during
hospitalization, from 3% (0 to 1 point) to 90% (5 points). The tool has been
validated at multiple burn units in the United States and abroad.

What does this mean for the Emergency Physician? Classic teaching is

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that a score of two or higher in SCORTEN should prompt ICU level care at a
burn center. However, it is important to remember that this is a progressive
process, and the patient’s initial presentation may be anywhere in the disease
course. If there is real concern for TEN, the patient needs a level of care that
can only be delivered at a burn ICU. Obviously, this decision should be made
in discussion with the local burn center and should also take into account
body surface involved, fluid repletion requirements, and other systemic
illness that may complicate care.

TREATMENT GUIDELINES FOR TEN: WHO,

WHAT, WHERE, AND WHY?

Before a discussion of who should be involved in the management of a
patient with TEN, it is crucial to stop the offending agent. In an ED setting,
this means both a good medication reconciliation and discussion with
dermatology. Unless absolutely necessary, cease all home medications if
TEN is suspected given the concern for complications.

Next, the who. This patient must be transferred to the local burn center
for management. Only a burn center has the combination of ICU experience
and large wound management. Multiple studies have shown that delayed
transfer to burn facilities directly increases mortality, so this patient should
be transferred as soon as reasonably possible.

Then, the where. Many TEN patients, especially those with other critical
illness, will require ICU level care, as discussed above. When discussing the
case with your local burn center, have a low threshold to advocate for a high
level of care for these patients, given complex fluid management and unseen
visceral organ involvement.

While disposition is important, what should be done in the ED prior to
transfer? Discuss with your local burn specialist regarding care, but there are
standards for management. First, fluids are a standard requirement for burns
and similarly for TEN/SJS. TEN differs from classic burns in two ways.
First, there is less microvascular injury, and cytokine response is less than in
a burn, decreasing the relative amount of insensible losses. Also, there is
heightened concern for pulmonary involvement in TEN, increasing potential
morbidity of overresuscitation and pulmonary edema. Nevertheless, these
patients may require up to 5 to 7 L/24 h of fluids. This should be titrated to
urine output of 0.5 to 1 mL/kg/h, as with other resuscitation. Given concern
for ureteral injury and close monitoring of output, a Foley catheter should be
placed.

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As with burns, bacterial superinfection is a common complication, and
ED care should start infection prevention. While transfer should not be
delayed for wound care, wounds should be cleaned if possible and should be
lightly covered with nonocclusive dressings as is standard in burn wound
management. Do NOT use sulfa-containing medications (Silvadene
included) as burn covering dressing prior to transfer, as this could have been
a cause of the TEN. Try to minimize dressing changes to reduce sloughing of
skin from contact. All intravenous lines should be placed as far away from
burned skin as possible.

In addition to supportive care (fluids, pain relief), TEN’s hallmark
mucosal involvement creates extradermal manifestations that the emergency
physician must be aware of and potentially manage early in this patient’s
care. Up to 25% of patients may have pulmonary involvement, including
bronchiectasis, bronchiolitis obliterans, and acute respiratory distress
syndrome (ARDS). Patients may frequently present with hypoxemia, but
with a normal initial chest radiograph (sloughing is typically not visible on
initial radiograph). Intubation may be complicated by oral and mucosal
lesions, and special care should be taken during laryngoscopy.

In addition to pulmonary complications, gastrointestinal and ocular
complications are common in TEN. These will both likely be managed at the
local burn center and are not a core component of ED management of TEN.
Prior to transfer, patients should be NPO, and ocular symptoms can be
managed with lubricating eye drops and erythromycin ointment.
Ophthalmology should be involved early to assess ocular manifestations and
lyse ocular adhesions but should not delay transfer to definitive care and
management.

Systemic treatments for disease modification (such as corticosteroids or
intravenous immunoglobulin) are controversial in TEN, with different data
showing minimal to no effect on prognosis or morbidity. Any initiation of
such therapy should be done in consultation with dermatology and/or the
local burn center, particularly in patients with underlying diseases that may
influence the pathogenesis of TEN.

TEN is a potentially life-threatening condition that must be recognized,
referred, and managed by every emergency clinician. Early initiation of
supportive care and transfer to the appropriate level of care is essential to
reduce mortality.

KEY POINTS

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TEN is an epidermolytic autoimmune reaction of the skin and mucous
membranes. It is pathophysiologically the same as SJS, but defined as
>30% BSA involvement.
The SCORTEN system for assessing TEN prognosis includes age,
malignancy, glucose, BUN, %BSA detached, and bicarbonate. A
score of 3 or higher prompts ICU admission.
Although similar to burns with the requirement for early aggressive
rehydration, less fluids are required in TEN, and careful monitoring of
pulmonary complications of overhydration is essential.
Pulmonary complications, including ARDS, are common in TEN. In
addition, gastrointestinal and ocular manifestations are common.
All patients with suspected SJS/TEN should be transferred as soon as
possible to a burn center. Basic wound care and fluid rehydration
should be initiated by the emergency physician prior to transfer.

SUGGESTED READINGS

Endorf FW, Cancio LC, Gibran NS. Toxic epidermal necrolysis clinical guidelines.
J Burn Care Res. 2008;29:5.

Harr T, French LE. Toxic epidermal necrolysis and Stevens-Johnson syndrome.
Orphanet J Rare Dis. 2010;5:39.

McGee T, Munster A. Toxic epidermal necrolysis syndrome mortality rate reduced
with early referral to regional burn center. Plast Reconstr Surg.
1998;102:1018–1022.

Schwarts RA, Mcdonough PH, Lee BW. Toxic epidermal necrolysis part II.
Prognosis, sequelae, diagnosis, differential diagnosis, prevention, and
treatment. J Am Acad Dermatol. 2013;69(2):187.e2.

Trent JT, Kirsner RS, Romanelli P, et al. Use of SCORTEN to accurately predict
mortality in patients with toxic epidermal necrolysis in the United States. Arch
Dermatol. 2004;140:7.

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106

MIMICS IN CELLULITIS

SHABANA WALIA, MD

There are many dermatologic conditions that can be strikingly similar to
cellulitis, especially on first presentation to the emergency department. While
some diagnoses are more chronic and indolent, others are life threatening and
crucial for the emergency physician to diagnose. Distinguishing between
cellulitis and other skin conditions can lead to a decrease in antibiotic use, a
decrease in the development of antibiotic resistance, as well as delays in
treatment of alternate and deadly diagnoses.

Cellulitis is an acute bacterial infection causing inflammation of the
epidermis, dermis, and underlying subcutaneous tissue. Group A-beta
hemolytic Streptococcus and Staphylococcus aureus are the most common
bacteria causing cellulitis. However, in children, and less commonly in adults
who are not responding to initial treatment, one must think of other causes of
cutaneous cellulitis. Haemophilus influenza type B is a severe form of
cellulitis that is accompanied by a respiratory infection. H. influenza cellulitis
can be differentiated from more common forms of cellulitis by physical
exam as the rash can have a characteristic blue-red-purple appearance. Other
uncommon forms of cellulitis are Vibrio vulnificus and Aeromonas
hydrophila, both of which are water-related organisms. A. hydrophila should
be suspected if there is a history of exposure to fresh water, if treatment for
streptococcal cellulitis fails, or if there are bullae and abscesses with foul-
smelling exudates on physical exam. V. vulnificus should be suspected if
there was an exposure to salt water, along with physical exam findings of
large bullae and vesicles. In more aggressive and serious stages, V. vulnificus
can progress to myositis and present similar to gas gangrene.

Erysipelas is a type of superficial cellulitis that involves the epidermis,
upper dermal layer, and the superficial lymphatic channels. On history, the
patient may describe a more rapidly progressing infection than cellulitis.

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Similar to cellulitis, the infected area of skin can be erythematous, warm, and
tender. In contrast, erysipelas can be differentiated by the raised margins and
sharply demarcated edges due to the superficial nature of the infection versus
the indistinct margins of cellulitis. Since Group A Streptococcus is the most
common cause of erysipelas, the treatment and clinical management are
often the same as for deeper forms of cellulitis.

Stasis dermatitis, commonly known as “Varicose eczema,” is often
misdiagnosed as cellulitis in the emergency setting. It is a complication of
long-standing chronic venous stasis, which is commonly a result of age-
related valvular insufficiency and less commonly surgery, previous DVTs,
and traumatic injury. Venous insufficiency leads to edema and extravasation
of blood cells, which can result in decreased blood flow to the tissues.
Patients with this condition will often have nontender, swollen, erythematous
legs with areas of hyperpigmentation and scaling ongoing for several months
to years. Stasis dermatitis can be secondarily infected with a superimposed
cellulitis or ulcers.

Lipodermatosclerosis or “sclerosing panniculitis” can be a complication
of long-standing chronic venous insufficiency and stasis dermatitis. The
proposed pathophysiology is similar to stasis dermatitis resulting in
decreased tissue perfusion, with the addition of further endothelial damage.
This damage causes microvascular thrombi formation, which results in tissue
infarction and the formation of fibroblasts and granulation tissue. On
physical exam, you should notice tapering of the lower third of the legs
resembling the upside-down “champagne bottle appearance,” as this disease
typically affects the bottom third of the lower legs. This finding may be the
only differentiating factor from cellulitis in the acute phase as patients can
also develop severe pain, warmth, and redness with indistinct margins of the
skin similar to cellulitis. The chronic phase is characterized by erythematous
indurated skin with browning discoloration and sclerotic plaques, thus more
easily differentiated from cellulitis.

Contact dermatitis is a skin reaction from an allergen or irritant that
results in skin inflammation. Differentiating cellulitis from dermatitis can be
simplified with a clear history from the patient. The presence of erythema or
a rash at the site of an allergen exposure is a clue to diagnosing this
condition. Patients may also complain of intense pruritus with the rash or
have a history of allergies. Physicians should inquire about the use of new
soaps, detergents, or topical creams. Contact dermatitis is a Type IV
hypersensitivity reaction and thus usually occurs 1 to 2 days after the
exposure. The condition improves with avoiding the offending allergen,
antihistamines and mild steroid cream. Antibiotics are not a mainstay of
treating contact dermatitis. Papular urticaria is another common

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hypersensitivity reaction that can occur after an insect bite. It consists of
pruritic papules surrounded by wheels or erythematous bases that can
progress to blisters and ulcers and tends to be localized near the insect bite.

The deadliest “can’t miss” mimic of cellulitis is necrotizing fasciitis.
Early on in the course of deep soft tissue infections, it can be extremely
difficult to detect differences on physical exam as these infectious can share
many characteristics with cellulitis such as erythema, warmth, localized
swelling, and tenderness. Necrotizing fasciitis involves the deep
subcutaneous tissues and spreads rapidly through the fascia and later can
involve the muscle. Though the infection is usually mixed, a wide range of
bacteria including gram-negative, gram-positive, and anaerobic bacteria have
been implicated. Pain out of proportion to the exam should always alert the
physician that a deeper soft tissue infection may be occurring. The
progression of the disease is much faster than other dermatologic conditions.
Within hours, the skin layers can become erythematous, swollen, and
crepitant and form abscesses. Gas can be seen on radiographs, but imaging
should never delay diagnosis. Early antibiotics, including broad and
anaerobic coverage, and most importantly early surgical debridement are the
treatment however, diagnosis is confirmed in the operating room by direct
visualization of the necrotic tissue.

These conditions are common mimics of cellulitis, though not an all-
inclusive list. Other physical presentations such as DVT, thromboembolism,
vasculitis, viral and drug-related exanthems, fungal infections, or malignancy
must be considered in the appropriate clinical setting. Most importantly, the
patient should be instructed to follow up with a primary physician within 24
to 72 hours of initial presentation of the acute rash. Dermatologic conditions
in immunosuppressed individuals or those not responsive to initial treatment
or recurrent/chronic rashes should prompt admission or urgent dermatology
follow-up.

KEY POINTS

Cellulitis most often presents unilaterally.
Stasis dermatitis, the most common mimic of cellulitis, results from a
long-standing history of chronic venous stasis and decreased tissue
perfusion.
Pain out of proportion to exam should prompt the emergency
physician to consider necrotizing soft tissue infections.
Observation and serial exams will aid in treatment and evaluation for

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alternate diagnoses.
A thorough history and physical exam will most often direct the
clinician in differentiating cellulitis from its mimics.

SUGGESTED READINGS

Blum CL, Menzinger S, Genné D. Cellulitis: Clinical manifestations and
management. Rev Med Suisse. 2013;9:1812–1815.

Hirschmann JV, Raugi GJ. Lower limb cellulitis and its mimics: Part I. Lower limb
cellulitis. J Am Acad Dermatol. 2012;67:163.e1–e12; quiz 175–176.

Keller EC, Tomecki KJ, Alraies MC. Distinguishing cellulitis from its mimics.
Cleve Clin J Med. 2012;79:547–552.

Westerman EL. Other disorders that mimic infectious cellulitis. Ann Intern Med.
2005;142:949.

Wolfson AB, Cloutier RL, Hendey GW, et al. Harwood-Nuss’ Clinical Practice of
Emergency Medicine. 6th ed. Philadelphia, PA: Wolters Kluwer, 2015.

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107

CHICKENPOX AND SHINGLES:
MORE THAN JUST A RASH

AARYN K. HAMMOND, MD

Chickenpox is a common and usually benign childhood illness caused by the
varicella-zoster virus. It is most often characterized and diagnosed by its
distinct pruritic vesicular rash in various stages across the body. However,
we must be cognizant of complications beyond the itchy rash and prepared to
treat what may result. The most common complication of chickenpox is
secondary superficial cutaneous bacterial infections. Infection is usually due
to Staphylococcus aureus or Streptococcus pyogenes. Localized cellulitis
may be treated with antibacterial agents. More severe infections such as toxic
shock syndrome and varicella gangrenosa have also been noted. Because
some studies have demonstrated a possible relationship between varicella
gangrenosa and NSAIDs, it is recommended that we avoid NSAIDS in the
treatment of fever and pain accompanied by chickenpox. In
immunocompromised children, bullous and hemorrhagic varicellas have
been seen and may be associated with thrombocytopenia or disseminated
intravascular coagulation.

Beyond the skin, chickenpox has also been found to cause pneumonitis
in immunocompetent populations and even more so in the
immunocompromised. Typically, pneumonitis is visible on chest radiographs
as diffuse interstitial nodular infiltrates. We must be suspicious of this
complication in those who present with dyspnea and cough in the context of
varicella rash. These cases should be treated aggressively with antiviral
medication and close observation, as there may be significant mortality in the
absence of treatment.

Another important complication of varicella infection is neurologic
disease. These may include cerebellar ataxia, encephalitis, transverse

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myelitis, meningitis, and Guillain-Barre syndrome. When the rash is noted
along with neurologic findings on exam, it is important to consider such
complications. The role of antiviral medications is unclear in varicella-
associated neurologic diseases. However, due to limited risks of treatment,
therapy is typically pursued in the case of viral encephalitis or severe disease.

After initial infection with varicella-zoster, the virus remains latent in
dorsal root ganglia and sometimes reactivates in the form of shingles, or
herpes zoster, as cell immunity decreases. Most cases of shingles occur after
the age of 50, and risk increases with age. Shingles typically presents as a
painful vesicular rash confined to one or two dermatomes, usually preceded
by 1 to 5 days of skin discomfort. Unlike chickenpox, treatment is
recommended for most cases as it has been shown to reduce symptoms,
severity, and complications. Valacyclovir and famciclovir are the antiviral
agents of choice, preferred over acyclovir. Typically, adjuvant
corticosteroids may be used in those without contraindications as they have
been shown to improve outcomes. It is also imperative to provide pain
control to those with shingles as this pain may be very severe.

The most common complication of shingles is postherpetic neuralgia.
The frequency increases with age, and it is diagnosed as pain persisting more
than 30 days after the onset of zoster rash. While not a dangerous
complication, the pain should not be underestimated and should be treated
aggressively. Data have shown that opioids, tricyclic antidepressants, and
gabapentin may be useful for treatment of pain.

In patients with zoster affecting the first division of the trigeminal nerve,
perform a detailed eye exam to evaluate for the presence of herpes zoster
ophthalmicus (HZO). Studies have shown that patients with eye redness in
the context of herpes zoster have high likelihood of having moderate to
severe disease. Other key features include photophobia, and rash in the
supratrochlear division, or Hutchinson sign (erythematous skin lesions on the
tip, side, or root of the nose). Not only do these patients require prompt
antiviral treatment, they should also have urgent ophthalmologic evaluation
as ocular diseases such as uveitis, keratitis, retinitis, and optic neuritis may
pose a threat to their vision. Another visual complication of HZO or remote
zoster in AIDS patients is acute retinal necrosis (ARN). This retinal injury is
caused by hematogenous spread. Although the disease is slowly progressive
in immunocompetent patients, in those with AIDS, it is very rapid and
progresses from ARN to retinal detachment and blindness, which may spread
bilaterally without treatment.

Important neurologic complications of shingles include contralateral
hemiparesis, encephalitis, and other nerve palsies. Contralateral hemiparesis

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may occur weeks to months after the development of rash. It is believed that
zoster reactivation in the trigeminal nerve is able to spread to the cerebral
arteries causing inflammation and ischemia causing contralateral
hemiparesis. Patients should be treated with corticosteroids and antivirals. Of
note, the infarction is irreversible despite treatment. Encephalitis associated
with zoster is one of the most dangerous complications. It typically presents
with fever, headache, and other neurologic findings in the context of recent
zoster infection. It is usually seen in patients with AIDS and despite
treatment often progresses to death. However, some reports note some
benefit with high-dose intravenous acyclovir.

KEY POINTS

Most patients with chickenpox will not require treatment. In contrast,
most patients who present with shingles within 72 hours of rash
development should be treated with valacyclovir or famciclovir.
In patients with varicella or zoster and respiratory complications,
evaluate for the presence of pneumonitis, and if diagnosed, treat
aggressively.
In patients with recent or ongoing varicella or zoster and neurologic
complaints, one should have high suspicion for encephalitis and
contralateral hemiparesis as these have potential for high morbidity
and mortality and should be treated aggressively.
Postherpetic neuralgia may be extremely painful, and adequate pain
management should be prescribed as necessary.
All patients with HZO and eye redness should receive urgent
ophthalmology evaluation.

SUGGESTED READINGS

Adam R, Vale N, Bona M, et al. Triaging herpes zoster ophthalmicus patients in
the emergency department: Do all patients require referral? Acad Emerg Med.
2010;17(11):1183–1188. doi:10.1111/j.1553-2712.2010.00875.x.

Galetta K, Gilden D. Zeroing in on zoster: A tale of many disorders produced by
one virus. J Neurol Sci. 2015;358(1–2):38–45. doi:10.1016/j.jns.2015.10.004.

Gnann J Jr. Varicella-zoster virus: Atypical presentations and unusual
complications. J Infect Dis. 2002;186(s1):S91–S98. doi:10.1086/342963.

Gnann J, Whitley R. Herpes zoster. N Engl J Med. 2002;347(5):340–346.
doi:10.1056/nejmcp013211.

Solomon C, Cohen J. Herpes zoster. N Engl J Med. 2013;369(3):255–263.

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doi:10.1056/nejmcp1302674.

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108

ERYTHEMA NODOSUM, NODULES,
AND HYPERSENSITIVITY

NICHOLAS RISKO, MD, MHS

Erythema nodosum (EN) is a delayed hypersensitivity reaction characterized
by tender subcutaneous nodules typically found in a bilateral, pretibial
distribution. EN rarely appears in emergency medicine literature; however, it
may herald serious underlying illness that would otherwise go unrecognized.
This chapter discusses management pearls for your next patient who presents
to the emergency department with EN.

EN has been shown to occur from a wide variety of exposures, although
up to 60% of cases are idiopathic.1 The annual incidence of EN ranges from
1 to 5 per 100,000,2 with women of reproductive age at higher risk.3–5 EN
may be preceded by a prodrome of 1 to 3 weeks that includes fever (60%),
malaise (67%), arthralgias (64%), arthritis (31%), and upper respiratory
symptoms.3 The arthralgias may persist up to 2 years after resolution of the
other symptoms.2 Less frequently noted systemic symptoms include
lymphadenopathy, hepatomegaly, splenomegaly, and pruritus.4 The lesions
themselves are typically found on extensor surfaces and are red, raised,
nonulcerative, and tender. They are a few centimeters in diameter and as they
heal take on a bruise-like appearance, moving from red to yellow, and finally
purplish.1,4

Your principal concerns when presented with a patient with EN are to
screen for dangerous causes and mimics. Leading causes are idiopathic
(55%), streptococcal infections (28% to 48%), sarcoidosis (11% to 25%),
drug reaction (3% to 10%), pregnancy (2% to 5%), and inflammatory bowel
disease (1% to 4%). Streptococcal infection is the leading cause in pediatric
populations. Rarer causes include lymphoma/leukemia, tuberculosis, HIV,

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HSV, viral hepatitis, histoplasmosis, and coccidioidomycosis.1,2,4,6

Other dangerous dermatologic conditions may present similarly in their
early stages. This differential includes cellulitis, erythema multiforme,
envenomated spider bites, toxic epidermal necrolysis, toxic shock syndrome,
bullous disease, Rocky Mountain spotted fever, and meningococcemia. Other
common mimics of less consequence to emergency management include
cutaneous vasculitis, nodular vasculitis, and superficial thrombophlebitis.1,7,8
Atypical presentations for EN are most commonly misdiagnosed as cellulitis,
trauma, or sarcoma.7,9,10

APPROACH TO THE PATIENT WITH ERYTHEMA

NODOSUM

Once you have ruled out other dangerous conditions, your initial screening
should assess for the most common causes of EN. All patients should receive
a chest x-ray to assess for sarcoidosis, tuberculosis, or other infections of the
lung. You may consider testing for tuberculosis exposure with a PPD.
Females of reproductive age should be tested for pregnancy. Ill-appearing
patients or patients with a history concerning for cancer should receive basic
blood work, with consideration of screening for HIV and viral hepatitis
status, as well as blood cultures for sicker patients.6

Patients with gastrointestinal symptoms may require diagnostics or
imaging in the emergency department or may simply be referred for
outpatient GI workup depending upon acuity of the presentation.

It is commonly recommended to screen for recent or active streptococcal
infection using throat cultures, rapid antigen test, or antistreptolysin-O
antibody titer, particularly in the patient with recent symptoms of
pharyngitis. However, because EN represents a late hypersensitivity process
and not active infection, this is unlikely to change your acute management
and should be balanced with available emergency department resources.2,4

If the workup does not identify a cause, you can provide reassurance to
the patient and referral to primary care follow-up. EN typically resolves
without treatment. Compression bandages and elevation of affected
extremities may help provide symptomatic relief. NSAIDs (typically
indomethacin or naproxen), as well as colchicine (2 mg for 3 days, 1 mg
daily for 2 to 4 weeks), may provide symptomatic relief. Potassium iodide
(400 to 900 mg/day) may be of benefit but is not without potential side
effects, including abdominal pain, nausea, vomiting, diarrhea, and swelling.
A short course of systemic steroids or injection of intralesional steroids may

531

provide limited benefit and but should be weighed against risks.11 Other
treatments inappropriate for the emergency department setting include
dapsone, methotrexate, and anti-TNF agents.2 If diagnostic confirmation of
EN is desired, refer to dermatology for a biopsy of the lesion.

KEY POINTS

EN is usually idiopathic, but the most common identified causes are
strep infection, sarcoidosis, pulmonary infection, systemic viral
infections, pregnancy, and drug reactions.
Beware of other dangerous rashes that may mimic EN.
Recommended emergency department diagnostics include the
following:

Most patients: chest x-ray, basic blood work, pregnancy test,
consider strep screening
GI complaints: imaging, stool studies, referral
Sick patients: blood cultures, HIV screening, viral hepatitis
screening
Most patients can be reassured that this will resolve on its own and be
safely discharged to primary care follow-up.
The safest and simplest option for symptomatic management is a
course of NSAIDs.

REFERENCES

1. Blake T, Manahan M, Rodins K. Erythema nodosum—A review of an
uncommon panniculitis. Dermatol Online J. 2014;20(4):22376.

2. Schwartz RA, Nervi SJ. Erythema nodosum: A sign of systemic disease. Am
Fam Physician. 2007;75(5):695–700.

3. Passarini B, Infusino SD. Erythema nodosum. G Ital Dermatol Venereol.
2013;148(4): 413–417.

4. Requena L, Requena C. Erythema nodosum. Dermatol Online J. 2002;8(1):4.
5. Requena L, Sanchez Yus E. Erythema nodosum. Semin Cutan Med Surg.

2007;26(2): 114–125.
6. Louthrenoo W, Lertprasertsuke N, Kasitanon N, et al. Erythema nodosum as a

manifestation of HIV infection. Asian Pac J Allergy Immunol.
2002;20(3):175–178.
7. Browne BJ, Edwards B, Rogers RL. Dermatologic emergencies. Prim Care.
2006;33(3): 685–695.
8. O’Neill JH Jr. The differential diagnosis of erythema nodosum. Del Med J.

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1991;63 (11):683–689.
9. Hyland-McGuire P, Guly H. Erythema nodosum—Diagnostic difficulties in

the accident and emergency department. J Accid Emerg Med.
1996;13(3):211–212.
10. Brady WJ, DeBehnke D, Crosby DL. Dermatological emergencies. Am J
Emerg Med. 1994;12(2):217–237.
11. Horio T, Imamura S, Danno K, et al. Potassium iodide in the treatment of
erythema nodosum and nodular vasculitis. Arch Dermatol. 1981;117:29–31.

SUGGESTED READINGS

Blake T, Manahan M, Rodins K. Erythema nodosum—A review of an uncommon
panniculitis. Dermatol Online J. 2014;20(4):22376.

Brady WJ, DeBehnke D, Crosby DL. Dermatological emergencies. Am J Emerg
Med. 1994;12(2):217–237.

Browne BJ, Edwards B, Rogers RL. Dermatologic emergencies. Prim Care.
2006;33(3):685–695.

Requena L, Requena C. Erythema nodosum. Dermatol Online J. 2002;8(1):4.
Schwartz RA, Nervi SJ. Erythema nodosum: A sign of systemic disease. Am Fam

Physician. 2007;75(5):695–700.

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109

CLASSIC IS NOT ALWAYS CLASSIC:
CLASSIC RASHES

DEBRA RAVERT, MD

Rashes can be intimidating. Many are nonspecific and innocuous, but some
are associated with significant pathology and cannot be overlooked. Rashes
are often associated with viruses and bacteria but can also be caused by
fungi, parasites, malignant processes, medications, and other chemicals. As
such, a thorough history must be taken that includes questions about risk
factors for immunosuppression, medication changes, allergies, and
exposures. Though considered “classic,” some of the rashes in this chapter
are rarely seen in clinical practice and warrant a review.

CLASSIC PEDIATRIC RASHES

Measles (rubeola)—historically known as first disease, caused by the
measles virus. The incidence of measles worldwide has declined sharply
since the advent of effective vaccination, and the WHO (World Health
Organization) has set a goal for elimination of measles in five of their six
regions by 2020. Measles is highly contagious, and populations need a 95%
immunization rate to control it. Recent outbreaks in underimmunized parts of
the United States underscore the need for practitioners to recognize the signs
and symptoms. The measles rash begins after several days of high fever,
cough, coryza, and conjunctivitis (the “three C’s”) and generally starts on the
face and spreads down the body, progressing from discrete macules to a
confluent rash (see Figure 109.1).

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Figure 109.1Classic measles rash.

Scarletina/scarlet fever—historically known as second disease, most
often caused by group A beta-hemolytic. Scarlet fever is generally preceded
by strep pharyngitis, with associated fever, sore throat, and headache. The
rash is distinguished by its “sandpaper” texture and on dark skin may be
more palpable than visible. Confirmation is with strep culture from
oropharynx, and first-line treatment is penicillin.

Rubella—historically known as third disease, caused by the rubella virus.
The rash of rubella is similar to the measles rash and similarly begins on the
face and spreads down the body. Associated symptoms are generally less
severe and include low-grade fever and malaise and patients are usually
nontoxic. Significant tender lymphadenopathy is classic for rubella. Rubella
is uncommon but important to recognize because of its teratogenicity.

Erythema infectiosum—still colloquially called fifth disease, caused by
parvovirus B19. The classic “slapped cheek” rash of fifth disease usually
follows several days after a mild prodrome of fever and rhinorrhea. The rash
is more common in children than adults, and associated polyarthralgia is
more common in adults than children. In a significant percentage of patients,
the facial rash is followed by a more diffuse, lacy rash over trunk, back, and
extremities. Fifth disease is mild and self limited in most patients but is
associated with anemia in sickle cell patients and immunosuppressed hosts.

535

Roseola—historically called sixth disease or exanthem subitum, caused
by human herpesvirus 6 and 7. Most common in very young children, the
roseola rash typically appears after a high fever as the child defervesces.
Patients usually have few associated symptoms, and the illness is self-
limiting.

CLASSIC TICK-BORNE ILLNESSES

Lyme disease—caused by Borrelia burgdorferi. The classic bulls-eye rash
(erythema migrans, Figure 109.2) generally appears within 2 weeks of a tick
bite, though as many as 30% of Lyme patients will not have the classic rash.
The rash itself begins at the site of the tick bite and becomes larger over
several days, usually maintaining distinct borders and associated with little to
no pain. Serology is usually negative at the time of the rash. First-line
treatment is 14 days of doxycycline.

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Rocky Mountain spotted fever (RMSF)—caused by Rickettsia rickettsii.
The rash of RMFS usually appears within 2 weeks of tick bite. The classic
rash of RMFS is petechial and progresses from wrists and ankles inward to
the trunk (Figure 109.3). Unfortunately, this distinctive pattern is absent in
up to 70% of patients. The petechial rash appears several days into the course
of illness even in those patients with a classical presentation, usually
following several days of fever and often a more generalized macular rash.
The disease is geographically more diverse than its name suggests, with
cases in all but two contiguous states. RMFS is the most lethal tick-borne
illness in the United States, and early recognition is essential to reducing
morbidity and mortality. Empiric treatment (first line is doxycycline) should
be started when RMFS is suspected and not deferred until serologic
confirmation.

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KEY POINTS

Rashes do not always look “classic.”
Consider rashes within their clinical context—onset, duration,
associated factors, vital signs, and overall appearance.
Although all of the rashes presented here are of viral or bacterial
origin, not all rashes are of infectious origin—don’t forget to inquire
about medications and exposures.
Some rashes look significantly different or are difficult to appreciate
on darker skin tones.
Tick-borne illnesses can be acquired in most of the United States and
need to be kept on the differential, especially in warmer months.

SUGGESTED READINGS

Allmon A, Deane K, Martin K. Common skin rashes in children. Am Fam
Physician. 2015;92(3):211–216.

Nathavitharana R. Diseases from North America: Focus on tick-borne infections.
Clin Med. 2015;15(1):74–77.

Ramdass P, Mullick S, Farber H. Viral skin diseases. Prim Care.
2015;42(4):517–567.

World Health Organization. (2012). Global Measles and Rubella Strategic Plan.
Geneva, Switzerland: World Health Organization. Retrieved from
http://www.measlesrubellainitiative.org/wp-content/uploads/2013/06/Measles-
Rubella-Strategic-Plan.pdf

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SECTION VI
ENDOCRINE/METABOLIC

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110

A NORMAL BICARBONATE VALUE
DOES NOT EXCLUDE AN ACID-
BASE DISTURBANCE

SETH T. STEARLEY, MD AND IAN BOYD, MD

Acid-base disturbances are one of the most difficult problems encountered in
emergency medicine. It is essential for the emergency provider to quickly
discern if a patient has an acid-base disturbance. Misdiagnosis of an acid-
base abnormality, or delayed therapy, can lead to serious complications.
Plasma bicarbonate concentration (HCO3), pH, and the arterial concentration
of carbon dioxide (pCO2) are critical in acid-base physiology. No value
should be evaluated in isolation.

Acid-base disturbances are commonly separated into metabolic or
respiratory disturbances. Metabolic disturbances cause a primary change in
HCO3, whereas respiratory disturbances cause a primary change in pCO2.
Although many emergency department (ED) patients have a pure metabolic
or respiratory disturbance, it is not uncommon to encounter patients with a
mixed acid-base disturbance.

The most common acid-base disturbance encountered in the ED is an
anion gap (AG) metabolic acidosis. The anion gap is calculated by the
following formula:

There are several “unmeasured” cations and anions (i.e., calcium,
magnesium and proteins, phosphate, sulfates, lactate) that maintain the
electrical neutrality of plasma. An increase in these unmeasured anions

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causes HCO3 to decrease and results in an AG metabolic acidosis. Often,
providers quickly look at the HCO3 on a basic metabolic panel as a clue to
the presence of an AG metabolic acidosis. Importantly, a significant acid-
base disturbance can be present with a normal HCO3 level. This is typically
seen in the setting of a mixed acid-base disorder. The classic example is a
patient who has both vomiting and diarrhea, which causes a concomitant
metabolic acidosis and metabolic alkalosis. The diarrhea leads to a loss of
bicarbonate and a metabolic acidosis, whereas the vomiting results in a
metabolic alkalosis.

Another example is the patient with a mixed metabolic acidosis and
respiratory acidosis. In these patients, the respiratory acidosis results in an
elevation in pCO2, which then shifts to HCO3. It is important to understand
that the kidneys regulate HCO3 in the setting of primary respiratory
problems. This renal compensation to changes in pCO2 can take hours to
days to reach equilibrium. Therefore, HCO3 can lag in compensation in
respiratory problems and therefore be “normal,” when in reality the body is
in a state of disequilibrium. It is important to evaluate for appropriate
compensation in all acid-base derangements. HCO3 concentration, in
respiratory disturbances, can be determined with the following equations:

If the expected HCO3 does not match the measured HCO3, then there is a
concomitant metabolic acidosis or alkalosis present.

Bicarbonate is one of the most important electrolytes in acid-base
physiology. Bicarbonate typically fluctuates with acute changes in metabolic

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and respiratory disturbances. Importantly, bicarbonate can be normal, or near
normal, despite the presence of a significant acid-base disturbance. Failure of
recognition can lead to serious complications to our patients and can further
complicate care.

KEY POINTS

HCO3, pH, and pCO2 should not be evaluated in isolation.
Evaluate for appropriate compensation in all acid-base disorders.
A normal HCO3 value should not be used to exclude an acid-base
disturbance.
Mixed acid-base disturbances can often result in a normal HCO3.
Renal HCO3 compensation to respiratory acid-base disorders can take
hours to days to reach equilibrium.

SUGGESTED READINGS

Chiu W, Jones KM, Chiu WC. Acid–base disorders. In: Farcy DA, Chiu WC,
Flaxman A, et al. eds. Critical Care Emergency Medicine. New York, NY:
McGraw-Hill; 2012:Chapter 21.

Hyneck M. Simple acid-base disorders. Am J Hosp Pharm. 1985;42(9):1992–2004.
Morris JE. Fluid, electrolyte, & acid base emergencies. In: Stone C, Humphries

RL, eds. Current Diagnosis & Treatment Emergency Medicine. 7th ed. New
York, NY: McGraw-Hill; 2011:Chapter 44.
Narins R, Emmett M. Simple and mixed acid-base disorders: A practical approach.
Medicine. 1980;59(3):161–187.
Nicolaou DD, Kelen GD. Acid-base disorders. In: Tintinalli JE, Stapczynski J, Ma
O, et al. eds. Tintinalli’s Emergency Medicine: A Comprehensive Study Guide.
New York, NY: McGraw-Hill; 2011.

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111

DON’T FORGET ABOUT
OCTREOTIDE FOR HYPOGLYCEMIA

HALEY M. RAPP, MD AND ERICA B. SHAVER, MD

Hypoglycemia is defined as a blood glucose concentration <50 mg/dL and
accounts for roughly 300,000 emergency department (ED) visits annually in
the United States. Most commonly, hypoglycemia occurs in patients with a
history of diabetes mellitus. The incidence of hypoglycemia has recently
decreased, due to improvements in medications and increased patient
education regarding diabetes treatment and control. Notwithstanding,
medications account for one of the most common etiologies of hypoglycemia
in ED patients.

The sulfonylurea class of medications is a mainstay in the treatment of
patients with diabetes. Commonly used sulfonylurea medications include
glyburide, glipizide, and glimepiride. These medications increase insulin
release by hyperpolarizing adenosine triphosphate–sensitive potassium
channels on pancreatic beta cells. This leads to a hyperinsulinemic state,
regardless of the blood glucose concentration. This can result in a profound
and prolonged hypoglycemia, because the counterregulatory response of the
adrenomedullary system to hypoglycemia is often impaired in diabetic
patients. The failed counterregulatory response to hypoglycemia is referred
to as hypoglycemia-associated autonomic failure. Sulfonylurea medications
have varying half-lives that can result in hypoglycemia that is not easily
reversed with dextrose alone.

The initial management of any patient presenting with hypoglycemia,
regardless of the cause, is rapid supplementation of glucose with either
intravenous (IV) dextrose or oral carbohydrate administration. The purpose
of IV dextrose administration is to create a relative hyperglycemic state.
However, in a patient taking a sulfonylurea medication, this hyperglycemic

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state further potentiates pancreatic insulin release, which then perpetuates the
vicious cycle of persistent hypoglycemia.

Traditional treatment of sulfonylurea-induced hypoglycemia has been the
administration of a continuous infusion of dextrose, sometimes for several
days. In recent years, octreotide has been utilized as an adjunctive treatment
for sulfonylurea-induced hypoglycemia. Octreotide is a long-acting
somatostatin analog that is used in the management of acromegaly, upper
gastrointestinal (GI) bleeding due to varices, and metastatic carcinoid
symptoms. In the setting of sulfonylurea-induced hypoglycemia, octreotide
acts by directly antagonizing the release of insulin from the pancreas.
Multiple studies have been performed to assess the safety, efficacy, and role
of octreotide in sulfonylurea-induced hypoglycemia. One randomized control
trial assessed the efficacy of octreotide plus IV dextrose administration
versus dextrose infusion alone and found that patients who received
octreotide had higher serum glucose concentrations and fewer hypoglycemic
events than did patients who received dextrose alone. Similar results have
been found in numerous retrospective analyses. The recommended dose of
octreotide for sulfonylurea-induced hypoglycemia is 1 to 2 mcg/kg given via
the IV or subcutaneous (SC) route every 8 hours for three doses. Side effects
of this medication are generally mild and predominantly limited to GI upset
(nausea, vomiting, diarrhea). Although more serious side effects such as
hypertension, arrhythmia, and syncope have been reported, these side effects
are typically seen in chronic use and are not usually reported in the short-
term use of octreotide for sulfonylurea-induced hypoglycemia.

Based on currently available evidence based data, patients who present to
the ED with suspected, or known, sulfonylurea-induced hypoglycemia or
hypoglycemia refractory to standard IV dextrose administration should be
given octreotide.

KEY POINTS

Review medications in any ED patient who presents with
hypoglycemia.
Sulfonylurea-induced hypoglycemia can be profound and prolonged.
Octreotide antagonizes the release of insulin from the pancreas.
The dose of octreotide in patients with sulfonylurea-induced
hypoglycemia is 1 to 2 mcg/kg IV or SC every 8 hours for 24 hours.
The primary side effects of octreotide are nausea, vomiting, and
diarrhea.

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SUGGESTED READINGS

Chan MM, Chan MM, Mengshol JA, et al. Octreotide: A drug often used in the
critical care setting but not well understood. Chest. 2013;144(6):1937–1945.

Cryer PE. Glycemic goals in diabetes: Trade-off between glycemic control and
iatrogenic hypoglycemia. Diabetes. 2014;63:2188–2195.

Dougherty PP, Klein-Schwartz W. Octreotide’s role in the management of
sulfonylurea-induced hypoglycemia. J Med Toxicol. 2010;6:199–206.

Dougherty PP, Lee SA, Lung D, et al. Evaluation of the use and safety of
octreotide as antidotal therapy for sulfonylurea overdose in children. Pediatr
Emerg Care. 2013;29(3):292–295.

Fasano CJ, O’Malley G, Dominici P, et al. Comparison of octreotide and standard
therapy versus standard therapy alone for the treatment of sulfonylurea-induced
hypoglycemia. Ann Emerg Med. 2008;50(4):400–406.

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112

PITFALLS IN THE MANAGEMENT OF
DKA

ANTHONY ROGGIO, MD

Diabetic ketoacidosis (DKA) is a critical metabolic derangement that is
commonly precipitated by acute illness (i.e., infection, myocardial infarction,
stroke) or medication noncompliance. The American Diabetic Association
and the International Society for Pediatric and Adolescent Diabetes provide
clinical guidelines for the management of patients with DKA.
Notwithstanding, these guidelines are complex and can be difficult to follow.
Given the mortality associated with DKA, it is imperative for the emergency
provider (EP) to be knowledgeable on several pitfalls that can occur in the
emergency department management of these critically ill patients.

INTRAVENOUS FLUIDS

Initial management of the DKA patient should begin with intravenous fluid
administration. Current guidelines recommend an initial bolus of 15 to 20
mL/kg of 0.9% normal saline. It is important to note that 0.9% normal saline
contains supraphysiologic concentrations of chloride. Hyperchloremia is
believed to be an inflammatory stimulus and is associated with adverse
effects on the renal, pulmonary, cardiovascular, and splanchnic organ
systems. Moreover, the strong ion difference of 0.9% normal saline is zero.
Thus, 0.9% normal saline will reliably induce a hyperchloremic metabolic
acidosis and potentially worsen the already disturbed acid-base balance in
patients with DKA.

Recently, balanced solutions (i.e., Plasma-Lyte) have been promoted as
better fluid choices in the resuscitation of critically ill patients. Balanced
solutions have lower concentrations of chloride and use organic ions as a

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substitute for bicarbonate. Studies that have compared the use of balanced
solutions to 0.9% normal saline in DKA patients have demonstrated a more
rapid closure of the elevated anion gap, increased mean arterial pressure, and
more rapid resolution of acidemia. Depending on the specific fluid, balanced
solutions also contain varying concentrations of electrolytes (i.e., potassium,
calcium, magnesium). While there are no current randomized trials that
demonstrate improved mortality with the use of balanced solutions, they are
a viable alternative intravenous fluid solution to 0.9% normal saline in the
management of DKA.

After an initial fluid bolus, maintenance fluids should be continued at a
rate of 250 to 500 mL/hour. A balanced solution should be considered for
patients with hyponatremia, whereas 0.45% normal saline should be
considered in patients who are hypernatremic or have normal sodium levels.

INSULIN

The administration of exogenous insulin is essential in the management of
DKA. Insulin reverses the ketogenesis that occurs in DKA and corrects the
metabolic acidosis. DKA patients can be stratified into mild, moderate, or
severe based on the mental status, pH, and serum bicarbonate level. This
stratification is listed in Table 112.1.

TABLE 112.1 DKA AND STRATIFICATION LEVELS

Historically, insulin has been given as a bolus dose of 0.1 U/kg, followed
by an insulin infusion. This administration strategy was felt to achieve
adequate serum levels of insulin in a short period of time. Recent literature,
however, has demonstrated that an initial bolus dose of insulin is not
required, provided that a continuous infusion is started at a rate of at least 0.1
U/kg/h. In addition, recent evidence has suggested that patients with mild or
moderate DKA can be safely managed with intermittent subcutaneous doses
of short- or medium-acting insulin preparations instead of an insulin
infusion. Importantly, subcutaneous insulin administration for DKA requires
further study and is not indicated in the treatment of patients with severe

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DKA.
Pediatric DKA patients are at risk for cerebral edema. Initiation of

insulin within the first hour of treatment or prior to fluid resuscitation has
been identified as a risk factor for cerebral edema. For this reason, an insulin
bolus should not be administered to pediatric DKA patients. Pediatric
patients should receive 1 or 2 boluses of intravenous fluids (20 mL/kg) prior
to the administration of any insulin.

Insulin administration should continue until the acidosis of DKA has
resolved. Once the blood glucose reaches a value of ~250 mg/dL, the type of
intravenous fluid should be changed to one that contains dextrose, in order to
maintain normoglycemia while the patient is treated with insulin. Once the
acidosis has resolved and the anion gap is closed, a long-acting insulin
should be administered via the subcutaneous route. The insulin infusion
should be continued for ~1 to 2 hours after administration of the long-acting
insulin in order to prevent rebound hyperglycemia or ketosis once the
infusion is stopped.

POTASSIUM

Many patients with DKA will have elevated levels of potassium, due to
electrolyte shifts from the acidosis. However, the majority of patients are
actually hypokalemic, due to loss of potassium in the urine from an osmotic
diuresis. Importantly, potassium levels will decrease even further with the
administration of insulin. Potassium repletion should begin when serum
potassium levels are below 5 mEq/L. If serum potassium levels are <3.5
mEq/L, potassium should be given prior to insulin administration in order to
prevent life-threatening hypokalemia.

SODIUM BICARBONATE

Contrary to conventional wisdom, the administration of sodium bicarbonate
may worsen intracellular acidosis and is a risk factor for cerebral edema in
pediatric DKA patients. Furthermore, bicarbonate has not been shown to
improve patient-centered outcomes in the management of DKA. As a result,
sodium bicarbonate is not recommended in the management of DKA, with
the possible exception of cardiac arrest secondary to profound acidosis.

KEY POINTS

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