A benign cause of a striking purpuric rash in a 24-month-old previously healthy boy: a case report

Introduction

Background

The sudden onset of purpuric rash with edema in an infant is a clinical red flag that prompts urgent evaluation. Life-threatening causes such as sepsis or meningococcemia must be excluded first, while non-life-threatening vasculitides such as immunoglobulin A (IgA) vasculitis may also enter the differential diagnosis (1). Despite more than 400 documented cases of Finkelstein-Seidlmayer vasculitis [also known as acute hemorrhagic edema of infancy (AHEI)], its dramatic appearance continues to trigger extensive laboratory investigations and empirical therapy, including antibiotics or corticosteroids (2,3).

Rationale and knowledge gap

Recent systematic reviews clarify several misconceptions regarding this vasculitis. Fever occurs in only a subset of patients, and preserved general condition is now regarded as the defining diagnostic feature (4). Updated reviews also confirm that most cases are post-infectious or post-vaccination, and that there are no confirmed reports of medication-triggered disease (5). Extracutaneous involvement is uncommon, occurring in only 10–15% of cases (6). Furthermore, immunopathologic studies show that IgA deposition is present in only ~25% of Finkelstein-Seidlmayer vasculitis cases, compared with nearly 100% in IgA vasculitis (7). These nuances are still insufficiently recognised in clinical practice, contributing to diagnostic uncertainty and overtreatment.

Objective

We report a thriving 24-month-old boy who developed striking centrifugal purpura with genital involvement during a viral illness, while remaining systemically well. This case highlights bedside diagnostic cues that support quaternary prevention by helping clinicians distinguish benign vasculitis from severe causes of purpura and avoid unnecessary interventions. We present this article in accordance with the CARE reporting checklist (available at https://pm.amegroups.com/article/view/10.21037/pm-25-126/rc).

Case presentation

A 24-month-old previously healthy boy presented with a single fever episode of 38.3 ℃ that resolved without antipyretics, along with mild upper respiratory symptoms (rhinorrhea, cough) that had begun approximately 72 hours before the onset of cutaneous findings. On the day before admission, purpuric lesions appeared on his lower limbs, initially interpreted as insect bites. Within 48 hours the rash spread centrifugally to upper limbs, ears, cheeks and genital region. Non‑pitting edema developed on the face, extremities, palms and soles.

The child remained systemically well, with preserved appetite and mood. He was fully vaccinated according to the national immunization schedule, with no recent vaccinations preceding symptom onset. No further fever or mucosal, gastrointestinal, articular, or urinary symptoms occurred. At the time of emergency department evaluation, the child remained well, with only mild residual rhinorrhea. Examination revealed nummular, palpable, non-blanching purpuric plaques with well-defined borders on the limbs, ears, cheeks, and scrotum, with edema most evident in dependent areas (Figure 1).

Figure 1 Clinical presentation of Finkelstein-Seidlmayer vasculitis. (A) Symmetrical purpuric and ecchymotic lesions with associated non-pitting edema on the trunk and lower limbs. (B) Edema and purpuric rash affecting the eyelid, cheek, and forehead. (C) Multiple nummular purpuric plaques distributed over the arm and thigh. This image is published with the consent from the patient’s parents.

Cardiopulmonary, abdominal, and neurological examinations were normal, and hemodynamic status was stable.

Initial laboratory evaluation included: hemoglobin 11.8 g/dL (normal 10.5–13.5 g/dL); white blood cells 9,500/µL (normal 6,000–17,000/µL); platelets 233,000/µL (normal 150,000–450,000/µL); C-reactive protein (CRP) 4.9 mg/L (normal <1 mg/L); erythrocyte sedimentation rate (ESR) 19 mm/h (normal <20 mm/h); normal renal function, liver enzymes, and coagulation parameters.

Given the child’s good general condition, the presence of non-pitting inflammatory edema and symmetrical purpura, a clinical diagnosis of Finkelstein-Seidlmayer vasculitis was made. The patient was managed expectantly with supportive care. Lesions and edema resolved within one week without recurrence.

All procedures performed were in accordance with institutional and national ethical standards and with the Declaration of Helsinki and its subsequent amendments. Written informed consent was obtained from the patient’s parents for publication of this case report and the accompanying clinical images. A copy of the written consent is available for review by the editorial office of this journal.

Discussion

Key findings

This case exemplifies a classic presentation of Finkelstein-Seidlmayer vasculitis in a well-appearing infant, characterized by symmetrical purpura and non-pitting edema with spontaneous resolution. Although histology was not pursued, recent literature shows that biopsy is rarely required when the bedside picture is typical and evolution is self-limited (4).

Centrifugal extension to the genital region has been occasionally described but remains uncommon in reported series (8,9). Additional dermatologic analyses detail other uncommon presentations that may mimic more alarming pathology (10).

The complete resolution within days without corticosteroids, antibiotics, or hospitalization aligns with contemporary evidence reinforcing this vasculitis as benign and self-limited (2).

Strengths and limitations

A strength of this report is the detailed chronological description of symptom onset, evolution, and resolution, alongside clinical photographs. Another strength is the explicit application of recent diagnostic concepts—particularly the emphasis on purpura and non-pitting edema in a well-appearing infant (11).

The main limitation is the absence of histopathology; however, biopsy is not routinely required when the bedside picture is pathognomonic and spontaneous improvement is observed (4,12).

Comparison with similar researches

Finkelstein-Seidlmayer vasculitis is a rare, self-limiting form of leukocytoclastic vasculitis, typically affecting infants aged 4 to 24 months. Most cases are reported following mild infections or occasionally after vaccination, with no confirmed reports of medication-induced disease (13). Fever is present in only a subset of patients, and recent reviews emphasise that the diagnostic hallmark consists of purpura and non-pitting edema in a well-appearing infant (11). Extracutaneous involvement is uncommon, occurring in only 10–15% of cases (6). Despite the alarming cutaneous presentation, systemic involvement is rare and the prognosis is excellent.

A structured comparison with mimicking conditions is crucial in distinguishing this benign vasculitis from life-threatening causes of purpura. Sepsis or meningococcemia must be excluded first; in contrast to these fulminant conditions, our patient remained hemodynamically stable and well-appearing. Erythema multiforme lacks true purpura or edema. Hemorrhagic urticaria is typically pruritic and migratory. Serum sickness–like reactions usually present with fever, joint involvement, lymphadenopathy, and older age. IgA vasculitis tends to affect older children and is associated with systemic manifestations; moreover, IgA deposition is present in only ~25% of Finkelstein-Seidlmayer vasculitis cases compared with nearly 100% in IgA vasculitis (7). Suspicion of child abuse becomes unlikely when lesions are bilateral, symmetrical, and the child remains well.

Explanations of findings

This vasculitis is characterised by sudden onset of painful, non-pitting edema associated with purpuric, nummular, or ecchymotic lesions. Although fever may occur, it is not universal (11). The child’s preserved condition, normal laboratory studies, and absence of extracutaneous involvement are consistent with the known benign behaviour of the disease (6).

Although a biopsy can confirm leukocytoclastic vasculitis, recent literature indicates that histology is seldom required in classic cases, and laboratory investigations primarily serve to rule out sepsis, coagulopathy, renal disease, or systemic inflammation (12). In our patient, centrifugal progression from the lower limbs to the trunk and genital region, followed by full resolution within days without medication, illustrates the self-limited course that supports a conservative, watch-and-wait approach (2).

Implications and actions needed

Recognising these clinical patterns allows clinicians to distinguish Finkelstein-Seidlmayer vasculitis from severe etiologies and reinforces the principles of quaternary prevention (14).

Management is expectant and supportive. Hydration, monitoring, and reassurance are the main measures. Corticosteroids, antihistamines, and antibiotics have no proven impact on disease course and are not routinely indicated (2,14). Hospital admission is unnecessary unless systemic compromise or diagnostic uncertainty persists (14).

Accordingly, this case demonstrates that conservative outpatient management is safe, avoids iatrogenic harm, and reduces caregiver anxiety. Greater awareness of updated diagnostic criteria is needed to minimise overtreatment.

Conclusions

This report underscores the importance of recognising Finkelstein-Seidlmayer vasculitis (AHEI) in infants presenting with dramatic purpura and edema. It highlights uncommon features such as genital involvement and centrifugal spread that may raise suspicion for this benign vasculitis even in dramatic presentations. Early recognition not only avoids overtreatment and extensive investigations but exemplifies quaternary prevention by minimising iatrogenic harm and offering timely reassurance to families (7). Contemporary assessments show that extracutaneous involvement is uncommon—reported in only 10–15% of cases—which supports the safety of conservative management (6). Updated systematic reviews reinforce that most cases follow infections or vaccinations rather than medication exposure (5), while modern dermatologic analyses have corrected longstanding misconceptions regarding lesion morphology and disease severity, further reducing diagnostic uncertainty (10).

Acknowledgments

None.

Footnote

Reporting Checklist: The authors have completed the CARE reporting checklist. Available at https://pm.amegroups.com/article/view/10.21037/pm-25-126/rc

Peer Review File: Available at https://pm.amegroups.com/article/view/10.21037/pm-25-126/prf

Funding: None.

Conflicts of Interest: All authors have completed the ICMJE uniform disclosure form (available at https://pm.amegroups.com/article/view/10.21037/pm-25-126/coif). The authors have no conflicts of interest to declare.

Ethical Statement: The authors are accountable for all aspects of the work in ensuring that questions related to the accuracy or integrity of any part of the work are appropriately investigated and resolved. All procedures performed were in accordance with institutional and national ethical standards and with the Declaration of Helsinki and its subsequent amendments. Written informed consent was obtained from the patient’s parents for publication of this case report and the accompanying clinical images. A copy of the written consent is available for review by the editorial office of this journal.

Open Access Statement: This is an Open Access article distributed in accordance with the Creative Commons Attribution-NonCommercial-NoDerivs 4.0 International License (CC BY-NC-ND 4.0), which permits the non-commercial replication and distribution of the article with the strict proviso that no changes or edits are made and the original work is properly cited (including links to both the formal publication through the relevant DOI and the license). See: https://creativecommons.org/licenses/by-nc-nd/4.0/.

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