Septal panniculitis presenting as tender erythematous nodules on the anterior shins.
Also known as: EN, septal panniculitis, erythema contusiforme
Overview
Acute, self-limited septal panniculitis characterized by symmetric, tender, erythematous, ill-defined subcutaneous nodules typically on the anterior shins. It represents a hypersensitivity reaction to a wide range of antigenic triggers rather than a primary skin disease.
Epidemiology
Most common form of panniculitis. Peak incidence 20-40 years; female predominance 3-5:1. Up to 50% of cases are idiopathic. Geographic variation reflects underlying infectious triggers (e.g., coccidioidomycosis in the southwestern US, tuberculosis worldwide).
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Question 1DermatologyMedium
A 29-year-old woman presents with a 10-day history of painful, tender, erythematous nodules over both anterior shins. She reports low-grade fever, malaise, and bilateral ankle pain. She takes no medications and is not pregnant. On exam she has several 2-4 cm poorly demarcated, deep, non-ulcerated tender nodules on both shins and mild ankle effusions. ESR and CRP are markedly elevated. A throat culture and ASO titer are pending. Which of the following is the most appropriate next diagnostic test?
ASerum angiotensin-converting enzyme
BLower-extremity venous ultrasound
CPosteroanterior chest radiograph
DPunch biopsy of a shin lesion
ESerum antinuclear antibody panel
Reveal answer & full explanation
Correct answer: C — Posteroanterior chest radiograph
ASerum angiotensin-converting enzyme
BLower-extremity venous ultrasound
CPosteroanterior chest radiograph✓
DPunch biopsy of a shin lesion
ESerum antinuclear antibody panel
Why Posteroanterior chest radiograph is correct
Bilateral tender shin nodules plus fever and ankle arthritis in a young woman are classic for erythema nodosum, and this triad raises strong suspicion for Löfgren syndrome (EN + bilateral hilar lymphadenopathy + ankle arthritis/fever), an acute form of sarcoidosis.
A chest radiograph is the essential next study in every patient with EN: it screens for the bilateral hilar adenopathy of sarcoidosis as well as pulmonary tuberculosis and endemic fungal disease (coccidioidomycosis, histoplasmosis), the other major systemic triggers.
Löfgren syndrome carries an excellent prognosis and usually resolves spontaneously, so identifying it on imaging changes counseling and management.
Why the others are wrong
Lower-extremity venous ultrasound is appropriate for suspected DVT or superficial thrombophlebitis, which produce a unilateral linear cord along a vein, not bilateral symmetric shin nodules, and would not explain the systemic findings.
Punch biopsy of a shin lesion is unhelpful because EN is a clinical diagnosis when classic nodules accompany a recognized trigger, and punch specimens are typically too shallow to capture the subcutaneous septal panniculitis; a deep incisional biopsy is reserved for atypical cases.
Serum antinuclear antibody panel is used to evaluate suspected lupus (including lupus panniculitis), but this presentation lacks lupus features, making it a low-yield, non-discriminating test and not the appropriate first step.
Serum angiotensin-converting enzyme — Löfgren syndrome is the leading suspicion, so a sarcoidosis marker is tempting, but serum ACE is neither sensitive nor specific for sarcoidosis and can neither show the bilateral hilar adenopathy that confirms Löfgren syndrome nor screen for tuberculosis; chest imaging comes first.
Question 2DermatologyMedium
A 28-year-old woman develops a sudden eruption of tender, warm, poorly demarcated erythematous nodules on both anterior shins two weeks after a sore throat. She also reports low-grade fever and aching ankles. The nodules are 2-4 cm, do not ulcerate, and are evolving through bruise-like color changes. Which of the following best explains the findings?
AMolecular mimicry by antibodies against streptococcal M protein
BIgE-mediated mast cell degranulation in the superficial dermal layers
CDirect bacterial invasion and proliferation throughout the dermis
DDelayed (type IV) hypersensitivity reaction within the fat septa
EImmune complex deposition causing leukocytoclastic vasculitis of dermal venules
Reveal answer & full explanation
Correct answer: D — Delayed (type IV) hypersensitivity reaction within the fat septa
AMolecular mimicry by antibodies against streptococcal M protein
BIgE-mediated mast cell degranulation in the superficial dermal layers
CDirect bacterial invasion and proliferation throughout the dermis
DDelayed (type IV) hypersensitivity reaction within the fat septa✓
EImmune complex deposition causing leukocytoclastic vasculitis of dermal venules
Why Delayed (type IV) hypersensitivity reaction within the fat septa is correct
Erythema nodosum is a delayed (type IV) hypersensitivity reaction to circulating antigens (here, streptococcal) that drives neutrophilic inflammation within the connective tissue septa of subcutaneous fat.
The septa widen and become infiltrated while the fat lobules are relatively spared, producing the defining histology of a septal panniculitis without vasculitis; Miescher radial granulomas are characteristic.
The clinical picture (tender, non-ulcerating bilateral shin nodules in a young woman after pharyngitis, with fever and arthralgias) fits the classic post-streptococcal trigger.
Why the others are wrong
IgE-mediated mast cell degranulation in the superficial dermal layers — the type I hypersensitivity mechanism of urticaria and anaphylaxis, producing transient wheals rather than deep tender subcutaneous nodules with septal panniculitis.
Direct bacterial invasion and proliferation throughout the dermis — describes cellulitis, which is unilateral, warm, expanding erythema without nodularity; erythema nodosum is a reactive immunologic process, not a skin infection, and symmetric shin nodules with bruise-like evolution after pharyngitis fit a reactive panniculitis.
Molecular mimicry by antibodies against streptococcal M protein — this type II cross-reactivity is the mechanism of acute rheumatic fever; its subcutaneous nodules are small, painless, and firm over bony prominences and extensor tendons, with central fibrinoid necrosis and palisading histiocytes on biopsy, not tender shin nodules with a septal panniculitis. The same preceding pharyngitis triggers erythema nodosum through a delayed-type reaction instead.
Immune complex deposition causing leukocytoclastic vasculitis of dermal venules — the preceding pharyngitis, fever, and aching ankles also fit a post-infectious immune complex vasculitis such as IgA vasculitis, but that process produces palpable purpura on dependent skin, not deep, tender subcutaneous nodules with bruise-like evolution; erythema nodosum is a septal panniculitis without vasculitis.
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Infections: streptococcal pharyngitis (most common identifiable cause in children and adults), tuberculosis, coccidioidomycosis, histoplasmosis, Yersinia, Salmonella, Mycoplasma, HIV, hepatitis B/C, EBV
A delayed (type IV) hypersensitivity reaction to circulating antigens produces neutrophilic inflammation within the connective tissue septa of subcutaneous fat. The septa widen and become infiltrated, while fat lobules remain relatively spared — the defining feature of septal panniculitis. Miescher radial granulomas (small histiocytic aggregates around central clefts) are characteristic on biopsy.
Clinical presentation
Symptoms
Sudden eruption of painful, tender, warm, erythematous nodules — typically over 1-2 weeks
Symmetric distribution on anterior shins, occasionally extending to thighs, forearms, or trunk
Prodromal or accompanying constitutional symptoms: low-grade fever, malaise, arthralgias
Lesions evolve through bruise-like color changes ('erythema contusiforme') over weeks and resolve without scarring
Signs / physical exam
1-5 cm poorly demarcated, deep, tender erythematous nodules
No ulceration (an important negative)
Joint tenderness or effusion (especially ankles) — common with Löfgren syndrome
Lymphadenopathy or hepatosplenomegaly if infectious or sarcoid trigger
Classic findings
Tender bilateral shin nodules in a young woman after streptococcal pharyngitis or sarcoidosis.
Differential diagnosis
Erythema induratum (nodular vasculitis) — Lobular panniculitis with vasculitis; tender nodules on posterior calves; often ulcerate; classically tuberculin-associated
Cellulitis — Unilateral, warm, expanding erythema with systemic signs; not nodular; responds to antibiotics
Thrombophlebitis — Linear cord along a vein, palpable thrombosed vessel, often after IV access; Doppler diagnostic
Cutaneous polyarteritis nodosa — Painful subcutaneous nodules with livedo reticularis on lower extremities; medium-vessel vasculitis on biopsy
Subcutaneous fat necrosis (post-trauma) — Localized nodules at site of trauma; lobular panniculitis with foamy macrophages
Lupus panniculitis — Indurated plaques, often on proximal limbs or face; lobular panniculitis with lymphocytic infiltrate
Diagnostic workup
Diagnostic criteria
Diagnosis is clinical when classic tender shin nodules accompany a recognized trigger. Deep incisional or excisional biopsy (punch biopsies often inadequate) showing septal panniculitis without vasculitis confirms the diagnosis when atypical features are present.
Labs
CBC, ESR, CRP (often markedly elevated)
ASO titer and throat culture for group A streptococcus
PPD or interferon-gamma release assay (IGRA) for tuberculosis
Hepatitis B and C, HIV serology
Stool studies for Yersinia / Salmonella in patients with GI symptoms
Pregnancy test in reproductive-age women
Medication review for hormonal contraceptives, sulfas, etc.
Imaging
Chest x-ray — essential to screen for sarcoidosis (bilateral hilar adenopathy of Löfgren syndrome) and pulmonary tuberculosis or coccidioidomycosis
Further imaging (chest CT, abdominal imaging) driven by clinical findings
Diagnostic algorithm
Trigger Category
Examples
Clue / Screen
Infection
Group A strep, TB, coccidioides, Yersinia, EBV, HIV
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