Pediatric emergency medicine trisk 346

TABLE 70.3
GIANOTTI–CROSTI SYNDROME: INFECTIOUS DISEASE
ASSOCIATIONS
Viral

Bacterial
Other
inflammatory
triggers

Epstein–Barr virus (most common), cytomegalovirus,
enteroviruses, influenza and parainfluenza viruses,
hepatitis viruses (B, C), herpes simplex virus,
human herpes virus 6, human immunodeficiency
virus, pox virus, respiratory syncytial virus,
rotavirus
Bartonella henselae, Borrelia burgdorferi, Neisseria
meningitidis, Streptococcus pyogenes
Postimmunization (various)

GIANOTTI–CROSTI SYNDROME (PAPULAR
ACRODERMATITIS OF CHILDHOOD, PAPULOVESICULAR
ACROLOCATED SYNDROME)
Gianotti–Crosti syndrome (GCS) is a self-limited reactive phenomenon
clinically characterized by a blanchable papular and occasionally vesicular
exanthem characteristically distributed on the cheeks of the face, the
buttocks, as well as acral locations (arms and legs) ( Fig. 70.18 ). These
lesions exhibit variable pruritus. Early European and Japanese reports found
an association between GCS and hepatitis B virus infection, but cases in the
United States have been associated with other organisms, most notably EBV
( Table 70.3 ).

Evaluation for a specific etiology is often not necessary unless the history
or physical examination point to a specific etiology such as EBV or group A
beta-hemolytic streptococcal infection, for which treatment may be
necessary.
Antihistamines may reduce the pruritus but topical steroids may be of
limited benefit.
As with ULE, it is interesting to note that infection with molluscum
contagiosum can trigger a GCS-like eruption. This reactive GCS-like


phenomenon likewise, is of often shorter duration and is typically responsive
to topical steroid treatment, in contrast to conventional GCS.

CONCLUSION
Viral syndromes and papulosquamous disorders are a highly heterogeneous
group of skin disorders. While they share similar clinical characteristics with
one another, an awareness of their distinguishing features and their natural
histories will help in providing the patient a more accurate diagnosis, and
direct appropriate therapy accordingly.
Suggested Readings and Key References
Aronson PL, Yan AC, Mittal MK, et al. Delayed acyclovir and outcomes of
children
hospitalized
with
eczema
herpeticum.
Pediatrics
2011;128(6):1161–1167.
Berger EM, Orlow SJ, Patel RR, et al. Experience with molluscum
contagiosum and associated inflammatory reactions in a pediatric

dermatology practice: the bump that rashes. Arch Dermatol
2012;148(11):1257–1264.
Ganguly S. A randomized, double-blind, placebo-controlled study of
efficacy of oral acyclovir in the treatment of pityriasis rosea. J Clin Diagn
Res 2014;8(5):YC01–YC04.
Harms M, Feldmann R, Saurat JH. Papular-purpuric “gloves and socks”
syndrome. J Am Acad Dermatol 1990;23:850–854.
Knöpfel N, Noguera-Morel L, Latour I, Torrelo A. Viral exanthems in
children: a great imitator. Clin Dermatol 2019;37(3):213–226.
Moon AT, Castelo-Soccio L, Yan AC. Emergency department utilization of
pediatric dermatology (PD) consultations. J Am Acad Dermatol
2016;74(6):1173–1177.
Sugarman JL, Hersh AL, Okamura T, et al. Empiric antibiotics and
outcomes of children hospitalized with eczema herpeticum. Pediatr
Dermatol 2011;28(3):230–234.


CHAPTER 71 ■ RESPIRATORY DISTRESS
DEBRA L. WEINER, J. KATE DEANEHAN

INTRODUCTION
Respiratory distress is one of the most common chief complaints of children
seeking medical care. It accounts for nearly 10% of pediatric emergency
department visits and 20% of visits of children younger than 2 years. Twenty
percent of patients admitted to the hospital and 30% of those admitted to
intensive care units are admitted for respiratory distress. Primary respiratory
processes account for approximately 5% of deaths in children younger than 15
years and 20% in infants. In addition, respiratory distress contributes substantially
to deaths in patients with other primary processes. Respiratory arrest is one of the
five leading causes of death in pediatric patients. Respiratory distress is usually

reversible, but failure to treat the condition may result in cardiac arrest with longterm neurologic sequelae or death.

PATHOPHYSIOLOGY
The primary goals of respiration are to meet metabolic demands for O2 and to
eliminate CO2 . Secondary functions include acid–base buffering, host defense,
and hormonal regulation. Exchange of O2 and CO2 between the lungs and the
blood occurs at the alveolocapillary membrane and depends on adequate and
appropriately matched ventilation and perfusion.
Control of respiration is mediated by central and peripheral neural
mechanisms. Respiration is an intrinsic brainstem function of the respiratory
centers of the medulla. It is further influenced by the cerebellum, which alters
respiration with postural change; by the hypothalamus, which controls respiration
on a moment-to-moment basis; by the limbic system, which modulates respiration
in response to emotion; and by the motor cerebral cortex, which controls
volitional respiratory activity, including hyper- and hypoventilation and speech.
Impulses are transmitted from the brain via the vagus and spinal nerves to the
larynx, trachea, bronchi, bronchioles, and acini; the glossopharyngeal to the
pharynx; the hypoglossal (CN XII) to the tongue; and the spinal accessory (CN
XI) to accessory muscles. Cervical nerves (C2 to C4), the phrenic nerve (C3 to
C5), and the intercostal nerves (T1 to T12), innervate accessory muscles, the
respiratory diaphragm, and intercostal muscles, respectively.


Respiratory distress results from dysfunction or disruption of the respiratory
tract and/or systems that control or modulate respiration.
Respiratory failure is the inability to meet the metabolic demand for O2
(hypoxia) or to eliminate CO2 (hypercapnia). Criteria for defining respiratory
failure vary widely; one set of criteria is presented in Table 71.1 . Hypoxia can be
categorized on the basis of mechanism. Arterial hypoxemia results from an
inability to deliver adequate O2 to the blood, low atmospheric PO2 , diffusion

impairment, anatomic or physiologic shunt, or increased metabolic demand.
Anemic hypoxia is the result of the blood’s inability to deliver adequate O2 to
tissues as a result of decreased hemoglobin oxygen-carrying capacity.
Hypokinetic, ischemic, or stagnant hypoxia also results in an inability of the
blood to transport O2 to the tissues. Histotoxic hypoxia results from inability to
metabolize O2 at the tissue level as a result. Hypercapnia often contributes to
respiratory failure as a result of hypoxemia and is less commonly the primary
cause.
Infants are at an increased risk of respiratory distress compared with children
and adults because of anatomic and physiologic differences ( Table 71.2 ). These
differences result in greater risk of airway obstruction, less efficient respiratory
effort, limited respiratory reserve, and dysfunction of CNS respiratory control.

DIFFERENTIAL DIAGNOSIS
Establishing a diagnosis for respiratory distress in part depends on localizing the
pathology to a particular organ system. In addition to primary respiratory
etiologies, disease or dysfunction of other organ systems may indirectly result in
respiratory disturbance by compromising respiratory system function or by
stimulating compensatory respiratory mechanisms ( Tables 71.3 to 71.5 ).
Treatment of the underlying cause is essential for definitive treatment of the
respiratory distress.

Respiratory System
Respiratory distress may be caused by upper or lower airway obstruction or by
disorders of the parenchyma or interstitium. Upper airway obstruction is common
in infants and young children in part because of their airway anatomy and
physiology (see Chapter 75 Stridor ). The hallmark of complete upper airway
obstruction is inability to phonate (i.e., no speech, cry, or cough). Manifestations
of upper airway obstruction may also include nasal flaring, stertor or snoring,
gurgling, drooling, dysphagia, hoarseness, stridor, retractions, and paradoxical

chest/abdominal wall movement. In neonates, common causes include nasal