Pediatric emergency medicine trisk 326

FIGURE 67.8 Frostbite. Child played in the snow for a prolonged period on a cold day wearing
sneakers.

Friction Blisters
Blisters usually occur in areas predisposed to trauma or friction such as on the
heels after walking or playing sports or due to new, possibly poorly fitted, shoes.
However, a persistent history may suggest EB, which may not always present in
infancy in milder subtypes such as EB simplex as discussed above. See Table
67.2 for differentiation of the various types.
Occasionally, accidental burns or burns secondary to child abuse are seen.
Abused children may have cigarette burns or have had their feet dipped in
scalding water.

Frostbite
Fingers, toes, feet, nose, cheeks, and ears are affected by extreme cold. After
exposed areas are damaged by the cold temperature, symptoms occur on
rewarming. Erythema, swelling, and burning pain occur at first, followed by
vesicles and bullae (at times hemorrhagic ( Fig. 67.8 )) within 24 to 48 hours.
Prevention is most important with appropriate protection of these sites from
extreme cold.


LABORATORY EVALUATION
If there is no clear etiology of what led to the blister, the laboratory tests
described next can be helpful.

Gram Stain
The Gram stain of fluid from an intact blister will be positive in impetigo and in a
secondarily infected lesion. It will be negative, however, in all other conditions.

Tzanck Smear

Multinucleated giant cells will be present on a Tzanck smear of material scraped
from the base of an intact, freshly opened vesicle caused by herpes simplex,
herpes zoster, and primary varicella. The Tzanck smear is not sensitive so
additional testing is required if negative.

Rapid Slide Test for Direct Immunofluorescence
Fluorescent-tagged monoclonal antibody is applied to cells scraped from the
blister base and can differentiate HSV-1, HSV-2, or varicella-zoster virus. Results
can be available in 1 to 2 hours.

Bacterial or Viral Cultures
Cultures help confirm an etiologic diagnosis when Gram stain, Tzanck smears,
and DIF are negative or indeterminate.

Polymerase Chain Reaction
An alternative or adjunct to traditional culture techniques, polymerase chain
reaction techniques allow for amplification of DNA or RNA present within a
specimen and rapid identification of the etiologic pathogen, including HSV, VZV,
and enterovirus. The technique is useful even when the pathogen present is no
longer viable.

Skin Biopsy
For perplexing cases undiagnosed by clinical and/or simple laboratory evaluation,
dermatologic consultation and skin biopsy are required.
If the picture on histology is compatible with erythema multiforme, DIF should
be considered. DIF will be negative in erythema multiforme but will be positive
in bullous pemphigoid (linear IgG and C3 on the basement membrane), DH
(granular IgA at tips of dermal papillae of uninvolved perilesional skin), and
CBDC (linear IgA on the basement membrane) though DIF can occasionally be
negative in CBDC.

Indirect immunofluorescence can be performed to test for circulating
antibodies. Circulating IgG is found in bullous pemphigoid; circulating IgA is
found in CBDC.

CONCLUSION
Vesiculobullous diseases have a variety of presentations and several key features
that may help to distinguish them from one another. While characteristic features
in some make diagnosis straightforward, many of the blistering disorders require
further diagnostic evaluation in order to confirm diagnosis. Treatment is aimed at
the underlying pathogenesis.
Suggested Readings and Key References
Chandler DJ, Fuller LC. A review of scabies: an infestation more than skin deep.
Dermatology 2019;235(2):79–90.
Fine JD, Bruckner-Tuderman L, Eady RA, et al. Inherited epidermolysis bullosa:
updated recommendations on diagnosis and classification. J Am Acad
Dermatol 2014;70(6):1103–1126.
Fine JD, Mellerio JE. Extracutaneous manifestations and complications of
inherited epidermolysis bullosa: part I. Epithelial associated tissues. J Am Acad
Dermatol 2009;61(3):367–384; quiz 385–386.
Fine JD, Mellerio JE. Extracutaneous manifestations and complications of
inherited epidermolysis bullosa: part II. Other organs. J Am Acad Dermatol
2009;61(3):387–402; quiz 403–404.
Juckett G. Arthropod bites. Am Fam Physician 2013;88(12):841–847.
Lai-Cheong JE, McGrath JA. Kindler syndrome. Dermatol Clin 2010;28(1):119–
124.
Lara-Corrales I, Pope E. Autoimmune blistering diseases in children. Semin
Cutan Med Surg 2010;29(2):85–91.
Méni C, Bruneau J, Georgin-Lavialle S, et al. Paediatric mastocytosis: a

systematic review of 1747 cases. Br J Dermatol 2015;172(3):642–651.
Mintz EM, Morel KD. Clinical features, diagnosis, and pathogenesis of chronic
bullous disease of childhood. Dermatol Clin 2011;29(3):459–462, ix.
Pavlek L, Schmidt J. Visual diagnosis: vesicular rash in a neonate. Pediatr Rev
2017;38(9):e32–e34.
Sansaricq F, Stein SL, Petronic-Rosic V. Autoimmune bullous diseases in
childhood. Clin Dermatol 2012;30(1):114–127.
Torrelo A, Alvarez-Twose I, Escribano L. Childhood mastocytosis. Curr Opin
Pediatr 2012;24(4):480–486.


CHAPTER 68 ■ RASH: DRUG ERUPTIONS
MELINDA V. JEN

DRUG ERUPTIONS
The spectrum of cutaneous drug eruptions ranges from the relatively benign,
where the medication can be continued if essential, to the severe, where there can
be significant morbidity and mortality. Thus, prompt and accurate diagnosis is
critical and can be lifesaving. The primary morphology of the eruption helps
guide the clinician to a diagnosis. Herein, we summarize the most salient features
of the most common drug reactions, with a particular focus upon their primary
morphologies.

URTICARIA
Urticaria (hives, wheals) consists of erythematous, edematous papules and
plaques that can coalesce into larger polycyclic, arcuate, and annular plaques (
Figs. 68.1 and 68.2 ). A key diagnostic feature is that individual lesions are
transient, resolving within 24 hours, but with new lesions appearing elsewhere.
As they resolve, purpuric macules secondary to capillary leak and
hyperpigmentation may remain. Pruritus and angioedema, particularly of the

eyelids, hands, and feet, are common.
Urticaria results from IgE degranulation of mast cells. Although the most
common cause of urticaria is infection, medications can sometimes trigger
urticaria. Urticaria typically appears within the first 2 weeks of starting the culprit
medication. Cephalosporins, β-lactam antibiotics, sulfonamides, and
anticonvulsants are common causes of drug-induced urticaria. Some medications,
such as nonsteroidal anti-inflammatory drugs (NSAIDs), may cause urticaria
through both immunologic and nonimmunologic pathways (via increased
leukotriene synthesis).
Urticaria is often confused for erythema multiforme (EM). The key features
differentiating urticaria from EM are morphology, individual lesion duration,
symptomology, and distribution. Urticaria can be annular, polycyclic, and arcuate,
but does not have the classic target appearance of EM. Additionally, urticaria
does not vesiculate, while the central areas of EM lesions may be bullous. As
noted above, individual lesions of urticaria last less than 24 hours, while lesions
of EM are fixed and take several days to resolve. If symptomatic, urticaria is
pruritic while EM may itch or burn. Urticaria can occur anywhere on the body,