Pediatric emergency medicine trisk 309

with a low specific gravity. They may become severely dehydrated if the weight
loss is in excess of 3% to 5%. Constant observation should be maintained during
the water deprivation test to ensure patients do not covertly consume water and to
prevent severe dehydration. A trial of intranasal desmopressin (DDAVP) should
distinguish between DI and nephrogenic DI because patients with antidiuretic
hormone–deficient DI will respond to the exogenous hormone.
Unfortunately, even these tests are fraught with inaccuracies. Patients with
primary polydipsia who have chronic overhydration and diminished capacity to
concentrate urine may have a blunted response to water deprivation. In addition,
patients with DI and nephrogenic DI may produce hypertonic urine if the
glomerular filtration rate is decreased as severe dehydration ensues.
Radioimmunoassay for antidiuretic hormone can be helpful in confusing cases.
TABLE 64.3
LIFE-THREATENING CAUSES OF POLYDIPSIA
Diabetes insipidus (antidiuretic hormone deficient)
Nephrogenic diabetes insipidus
Diabetes mellitus
Primary polydipsia
Suggested Readings and Key References
Cermeroglu AP, Buyukgebiz A. Psychogenic diabetes insipidus in toddlers with
compulsive bottle-drinking: not a rare entity. J Pediatr Endocrinol Metab
2002;15(1):93–94.
Dabrowski E, Kadakia R, Zimmerman D. Diabetes insipidus in infants and
children. Best Pract Res Clin Endocrinol Metab 2016;30(2):317–328.
Di Iorgi N, Allegri A, Napoli F, et al. Central diabetes insipidus in children and
young adults: etiological diagnosis and long-term outcome of idiopathic cases.
J Clin Ednocrinol Metab 2014;99(4):1264–1272.
Dundas B, Harris M, Narasimhan M. Psychogenic polydipsia review: etiology,
differential, and treatment. Curr Psychiatry Rep 2007;9(3):236–241.
Kavanagh C, Uy N. Nephrogenic diabetes insipidus. Pediatr Cl N Am
2019;66(1):227–234.

Rose S, Auble B. Endocrine changes after pediatric traumatic brain injury.
Pituitary 2012;15(3):267–275.


CHAPTER 65 ■ RASH: ATOPIC/CONTACT
DERMATITIS AND PHOTOSENSITIVITY
JOY WAN

DERMATITIS
Dermatitis is the general term used to describe an itchy, eczematous rash. In
its acute form dermatitis is characterized by erythema, edema, exudation,
scattered papules or vesicles, scaling, and crusting. Chronic dermatitis is
characterized by lichenification (accentuated skin markings),
hyperpigmentation, hypopigmentation, and excoriations. Diagnosis of the
underlying cause of the dermatitis relies on patient history and physical
examination findings; histology is typically nonspecific. This chapter
highlights common causes of dermatitis in children, including atopic
dermatitis, nummular eczema, asteatotic eczema, dyshidrotic eczema,
lichen simplex chronicus, and contact dermatitis.

Atopic Dermatitis
Atopic dermatitis is the most common cause of dermatitis in children (
Table 65.1 ), occurring in 10% to 20% of children. It is a chronic and
relapsing condition characterized by pruritic eczematous papules, patches,
and plaques. There is often a personal or family history of allergic rhinitis,
hay fever, or asthma. Many patients have the onset of symptoms before 6
months of age, with most developing symptoms by 5 years of age. Heat,
stress, sweating, infection, and exposure to environmental (e.g., pet dander,
pollen) and contact allergens (e.g., fragrances, soaps) may precipitate flares.
The diagnosis is mainly based on typical history and physical

examination findings, and the American Academy of Dermatology has
developed criteria to summarize these features ( Table 65.2 ). The broad
differential diagnosis requires the exclusion of other skin conditions that
present in a similar fashion, including seborrheic dermatitis, scabies,
psoriasis, nutritional deficiencies (i.e., zinc), immune deficiencies, and
cutaneous lymphoma. Importantly, while superficial bacterial infections,


seborrheic dermatitis, and contact dermatitis may occur in isolation, they
may also coexist in a patient with atopic dermatitis.
The typical distribution can vary by age. Infants have lesions on the
cheeks, trunk, and extensor surfaces. Children show involvement of the
hands, feet, and flexor areas, such as the antecubital and popliteal fossae,
and the neck ( Fig. 65.1 ). In adolescents and adults, flexor areas, hands,
and feet are often involved. Xerosis (dry skin), ichthyosis vulgaris
(inherited fish-like scaling of the extremities and hyperlinear palms),
keratosis pilaris (follicularly based papules with cornified plugs in the upper
hair follicles), infraorbital eyelid folds (Dennie–Morgan sign), pityriasis
alba (scaly hypopigmented macules and patches on the cheeks), and
follicular accentuation may be seen.
The main factors to assess when caring for patients with atopic dermatitis
include pruritus, superinfection, and concomitant contact dermatitis. The
pruritus of atopic dermatitis may be severe, resulting in sleep disturbances
in the child and caretakers and difficulty concentrating in school and work.
The persistent itch-scratch cycle can also lead to severe excoriations in the
skin. This damage to the skin barrier, along with inherent defects in the skin
barrier and immunity that are associated with atopic dermatitis, makes
patients particularly susceptible to superinfections with bacteria
(Staphylococcus aureus or group A streptococcus), yeast (candida), and
viral infections (herpes simplex, enterovirus, and molluscum contagiosum).

The defective skin barrier in atopic dermatitis allows increased penetration
of contact allergens that is felt to explain the increased incidence of contact
dermatitis in this population (see below).
Management of atopic dermatitis includes minimizing triggers (irritants
and allergens) with “gentle skin care,” including an unscented soap,
fragrance-free laundry detergent, hypoallergenic shampoo and conditioner,
and regular application of thick unscented emollients immediately after
bathing. Repeated screening for new trigger contactants is important
because care providers may try new topical products in an effort to provide
relief.
Screening for infection is critical in all patients with atopic dermatitis
flares, including culturing active pustules for bacteria and obtaining a viral
culture or polymerase chain reaction (PCR) sample from vesicles or
erosions for herpes simplex virus, and in some cases, enterovirus. For


localized areas, use of a topical antibiotic that covers gram-positive
organisms is important. Empiric oral antibiotic or antiviral treatments may
be needed in more involved cases. Dilute bleach baths are helpful in
decreasing skin bacterial colonization and infections in atopic dermatitis
and may help minimize flares.
Atopic dermatitis on the cheeks of infants is best managed by applying
petrolatum-based ointments as a barrier prior to feeding and sleeping,
avoidance of irritants (e.g., wet wipes, drool, food, pacifiers), and low- to
mid-potency topical corticosteroids as needed.
Topical corticosteroids are the mainstay of treatment for most patients
with atopic dermatitis. One approach to minimize recurrences of localized
atopic dermatitis after flares is to use topical corticosteroids twice daily
during flares and then twice weekly for prevention. Alternatively, for more
diffuse atopic dermatitis, a more practical maintenance therapy may include

twice daily use of a low-potency topical steroid compounded into a thick
emollient (e.g., hydrocortisone 2.5% ointment mixed 1:1 with petrolatum).
Referral to dermatology and/or allergy may be helpful to further manage
moderate or severe atopic dermatitis. Particularly severe or persistent
dermatitis should prompt consideration of an underlying systemic disorder
associated with eczematous eruptions, such as immunodeficiencies or
nutritional deficiencies.