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THE JOURNAL OF PEDIATRICS  www.jpeds.

com Volume 251  December 2022

intervals to evaluate the caliber of the internal carotid artery. Lalitha Sivaswamy, MD
Although literature regarding the natural course of Horner Central Michigan University
syndrome is limited in children, resolution of symptoms Children’s Hospital of Michigan
can be expected in 6 months to a year.5 n Detroit, Michigan

Abdelrahman Alsherbini, MD
Children’s Hospital of MI References
Detroit, Michigan
1. Thanvi B, Munshi SK, Dawson SL, Robinson TG. Carotid and vertebral
artery dissection syndromes. Postgrad Med J 2005;81:383-8.
Nirupama Kannikeswaran, MD 2. Nielsen PJ. Upside down ptosis in patients with Horner’s syndrome. Acta
Central Michigan University Ophthalmol (Copenh) 1983;61:952-7.
Children’s Hospital of MI 3. Burlacu CL, Buggy CJ. Coexisting harlequin and Horner syndromes after
Detroit, Michigan high thoracic paravertebral anaesthesia. Br J Anaesth 2005;95:822-4.
4. Robertson JJ, Koyfman A. Cervical artery dissections: a review. J Emerg
Med 2016;51:508-18.
Diniece Barran, MD 5. Lubelski D, Pennington Z, Sciubba DM, Theodore N, Bydon A. Horner
Children’s Hospital of MI syndrome after anterior cervical discectomy and fusion: case series and
Detroit, Michigan systematic review. World Neurosurg 2020;133:e68-75.

Skin Findings of Impetigo Neonatorum and Staphylococcal


Scalded Skin Syndrome

A
4-week-old male infant presented with 5 days of (SSSS). Targeted MSSA therapy was initiated with oxacillin.
honey-crusted facial rash (Figure, A). He was The infant completed a 10-day course of antibiotics with
admitted to a local children’s hospital to initiate complete resolution of symptoms.
therapy. Initial intravenous line placement attempts This case illustrates the link between localized Staphylo-
triggered Nikolsky sign, with skin exfoliation at sites of coccus aureus infection (impetigo) and SSSS, which results
lateral pressure on the patient’s feet (Figure, B). Over the from systemic effects of exfoliative toxins A or B. Honey-
next 2 days, skin desquamation progressed over the legs crusted lesions, especially perioral lesions, are a hallmark of
and torso. A facial swab grew abundant methicillin- impetigo neonatorum, which results from localized infection
susceptible Staphylococcus aureus (MSSA), supporting the and toxin production by S aureus.1 Exfoliative toxins A and B
diagnosis of local impetigo neonatorum with disseminated, produced by S aureus can then travel through the blood-
toxin-mediated Staphylococcal scalded skin syndrome stream to distant sites leading to skin exfoliation as seen in

Figure. A, Honey-crusted facial lesions associated with impetigo neonatorum and B, desquamation over the soles of the feet
secondary to Staphylococcal scalded skin syndrome.

The authors declare no conflicts of interest.

J Pediatr 2022;251:216-7.
0022-3476/$ - see front matter. ª 2022 Elsevier Inc. All rights reserved.
https://doi.org/10.1016/j.jpeds.2022.08.013

216 Daniels and Rosen


December 2022 REDISCOVERING THE PHYSICAL EXAM

SSSS.2 Staphylococcal toxins were implicated in the References


pathophysiology of SSSS as early as 1970, when it was
demonstrated that Staphylococci fulfilled Koch 1. Brazel M, Desai A, Are A, Motaparthi K. Staphylococcal Scalded Skin Syn-
postulates in a neonatal murine model of SSSS.3 These toxins drome and Bullous Impetigo. Medicina 2021;57.
are serine proteases that cleave desmoglein-1,4 a protein 2. Kondo I, Sakurai S, Sarai Y. New type of exfoliatin obtained from staphylo-
coccal strains, belonging to phage groups other than group II, isolated from
required for keratinocyte-to-keratinocyte adhesion in the
patients with impetigo and Ritter’s disease. Infect Immun 1974;10:851-61.
stratum granulosum of the skin.5 Disruption of 3. Melish ME, Glasgow LA. The staphylococcal scalded-skin syndrome. New
desmoglein-1 results in large patches of sloughing skin and Eng J Med 1970;282:1114-9.
the presence of Nikolsky sign, in which a shearing force 4. Amagai M, Matsuyoshi N, Wang ZH, Andl C, Stanley JR. Toxin in bullous
results in the separation of the epidermis and creation of impetigo and staphylococcal scalded-skin syndrome targets desmoglein 1.
Nat Med 2000;6:1275-7.
an erosion.6 MSSA is implicated in the majority of cases of
5. Ladhani S, Joannou CL, Lochrie DP, Evans RW, Poston SM. Clinical, mi-
culture-proven SSSS in the US, with a small minority of crobial, and biochemical aspects of the exfoliative toxins causing staphy-
MRSA cases.7,8 n lococcal scalded-skin syndrome. Clin Microbiol Rev 1999;12:224-42.
6. Shakeri A. Pyotr Vasilyevich Nikolsky-The Man Behind the Sign. JAMA
Dermatol 2018;154:181.
Elizabeth A. Daniels, MD 7. Braunstein I, Wanat KA, Abuabara K, McGowan KL, Yan AC, Treat JR.
David A. Rosen, MD, PhD Antibiotic sensitivity and resistance patterns in pediatric staphylococcal
Department of Pediatrics scalded skin syndrome. Ped Dermatol 2014;31:305-8.
Washington University School of Medicine 8. Wang Z, Feig JL, Mannschreck DB, Cohen BA. Antibiotic sensitivity and
St. Louis, Missouri clinical outcomes in staphylococcal scalded skin syndrome. Pediatr Der-
matol 2020;37:222-3.

Purpuric Vesiculobullous Rash in IgA Vasculitis (IgAV)

A
previously healthy 18-year-old girl presented to
outpatient pediatrics clinic with an acute history of
lower extremity rash of legs, ankles, and feet, with
recent extension to her arms. She then developed significant
abdominal pain, joint pain, and hematuria. Findings of the
physical examination showed a discrete purpuric nonblanch-
ing, palpable rash on bilateral upper (Figure 1) and lower
(Figure 2) extremities, with multiple intact and ruptured
hemorrhagic vesiculobullous lesions of the legs and ankles.
Immunoglobulin A vasculitis (IgAV; formerly Henoch
Sch€onlein purpura) was suspected, but the significant
bullous appearance led to clinical confusion. A skin biopsy
was obtained, which demonstrated capillary IgA
Figure 1. Discrete purpuric nonblanching, palpable rash on
deposition, confirming the diagnosis. Prednisone 80 mg/ bilateral upper extremities.
d was initiated for severe symptoms, and all symptoms
resolved completely within 1 month without recurrence or
long-term complication over the next several months. the upper extremities or evolve into hemorrhagic bullous
IgAV is the most common systemic childhood vasculitis. lesions.2 In patients with unusual or incomplete
Annual global incidence is estimated to be 10-20 cases per presentation, biopsy of the affected organ can confirm
100 000 children. It can be seen at any age, including adult- histologic IgA deposition. Most cases of IgAV are self-
hood, but is most common in childhood, with peak inci- limiting, with excellent prognosis within the first month,
dence between 4 and 7 years of age.1 Presentation is but recurrent episodes can occur in about 25% of patients.3
generally acute, and the diagnosis should be based on the Treatment may be required during the acute phase for
finding of palpable purpura in the presence of a classical triad severe gastrointestinal or renal vasculitis sequelae. Renal
of abdominal pain, arthritis or arthralgia, and renal involve- involvement with IgAV nephritis is the most serious
ment. The nonthrombocytopenic palpable purpuric rash complication and is linked to long-term morbidity and
almost exclusively starts on the lower extremities and but- mortality, accounting for 1%-2% of all childhood end-
tocks (Figure 3). Rarely the rash may progress to involve stage renal disease.4 Thus, all patients with IgAV should
undergo active renal monitoring for at least 6-12 months
The authors declare no conflicts of interest. after the acute episode with routine urinalysis and blood
pressure checks.5,6 Of note, the presence of bullous lesions
J Pediatr 2022;251:217-8.
0022-3476/$ - see front matter. ª 2022 Elsevier Inc. All rights reserved. does not appear to be associated with more severe
https://doi.org/10.1016/j.jpeds.2022.08.006 extracutaneous disease.2
Toddler with Horner’s Syndrome 217

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