Pediatric emergency medicine trisk 346

TABLE 70.3GIANOTTI–CROSTI SYNDROME: INFECTIOUS DISEASE ASSOCIATIONS Viral Epstein–Barr virus most common, cytomegalovirus, enteroviruses, influenza and parainfluenza viruses, hepatitis v

TABLE 70.3

GIANOTTI–CROSTI SYNDROME: INFECTIOUS DISEASE

ASSOCIATIONS

Viral 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

Bacterial Bartonella henselae, Borrelia burgdorferi, Neisseria

meningitidis, Streptococcus pyogenes

Other

inflammatory

triggers

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 long-term 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