In a city where cover bands are judged on whether they can sell the song in the first eight bars, Steven Chen, MD, MPH, MS-HPEd, opened his Converge 2026 session on inpatient dermatology with an analogous claim: the skin tells you what is wrong before the chart does. Dermatologists, he reminded the audience, do a physical and history, not a history and physical. Start with the exam. The history follows. Across five cases, he walked hospitalists through a practical framework for the cutaneous eruptions that most often land on a consult pager, with particular attention to what the admitting team can and should do before dermatology arrives.
Case 1: Stevens-Johnson Syndrome and Toxic Epidermal Necrolysis (SJS/TEN)
A 69-year-old man with follicular lymphoma on bendamustine and rituximab was started on trimethoprim-sulfamethoxazole for Pneumocystis pneumonia (PCP) prophylaxis. Two weeks later, he presented with fevers, myalgias, and a dusky, macular, atypical-targetoid eruption with mucosal involvement and a positive Nikolsky sign. By hospital day three, the rash had progressed beyond 10% of body surface area, evolving from Stevens-Johnson Syndrome (SJS) into Toxic Epidermal Necrolysis (TEN). Dr. Chen emphasized the differential between true target lesions (concentric, raised, three zones) and the macular targetoid lesions of SJS and TEN, which carry a fundamentally different prognosis. Management starts with stopping the offending agent (most commonly antibiotics, antiepileptics, or nonsteroidal anti-inflammatory drugs administered four to 21 days prior), good wound care, considering burn unit transfer, avoiding debridement, and consulting ophthalmology and gynecology or urology early. Antibiotics should be reserved for documented sepsis. The severity-of-illness score for Toxic Epidermal Necrosis (SCORTEN) remains the standard prognostic tool, though a 2018 multicenter U.S. cohort suggested observed survival exceeds SCORTEN predictions, with prognosis worsening sharply above 40% body surface area. The 2022 Cochrane review found etanercept may reduce disease-specific mortality, and 2024 spatial proteomics work in Nature implicated JAK1, opening the door to ruxolitinib and other JAK inhibitors as emerging adjuncts alongside intravenous immunoglobulin (IVIG), steroids, and burn unit care.1,2
Case 2: Drug Reaction with Eosinophilia and Systemic Symptoms (DRESS)
A 55-year-old man, five weeks into nafcillin for methicillin-susceptible Staphylococcus aureus bacteremia, developed a confluent erythematous eruption with facial swelling, myalgias, and arthralgias. DRESS classically begins two to six weeks after first exposure to the culprit drug, most often antiepileptics, antibiotics, or antivirals. Mortality approaches 10%, driven primarily by hepatotoxicity. Diagnosis is clinical, supported by the RegiSCAR scoring system; biopsy is non-specific. Importantly, neither rash nor eosinophilia is required to make the diagnosis. Workup should include a complete blood count (CBC) with differential, liver function tests, and blood urea nitrogen with creatinine, with attention to atypical lymphocytes, lymphadenopathy, and hepatosplenomegaly. Steroids are first-line, often intravenous, given for bowel edema, with a long taper. Cyclosporine has the strongest second-line evidence. Viral reactivation (human herpesvirus-6, Epstein-Barr virus, cytomegalovirus) is increasingly recognized, and a thyroid-stimulating hormone test (TSH) should be checked two to three months out, given the risk of autoimmune thyroiditis. The teaching point hospitalists should not miss is to build a drug chart. Lay every medication against the rash timeline, and the latency window almost always names the culprit.
Case 3: Purpura Fulminans
A 44-year-old man walked into the emergency department with flu-like symptoms a day after a dog bite and developed retiform purpura while in the CT scanner. Purpura fulminans represents microvascular occlusion in the skin, essentially disseminated intravascular coagulation visible at the bedside, and is a true emergency. The angular, stellate, geographic edges of retiform purpura are the visual signature. The differential includes encapsulated organism sepsis (especially in asplenic patients), tick-borne illness, catastrophic antiphospholipid syndrome, and protein C or S deficiency. History should specifically probe splenectomy, immunization status, animal exposures, and travel. This patient grew Capnocytophaga canimorsus and died within 72 hours. Recognizing retiform morphology early enough to escalate antibiotics, resuscitation, and intensive care is the single most actionable hospitalist skill in this category.
Case 4: Pyoderma Gangrenosum (PG)
A 72-year-old woman developed exquisitely tender, expanding, undermined ulcers at her surgical site after a laparoscopic-converted-to-open cholecystectomy. Neutrophilic dermatoses, including pyoderma gangrenosum, Sweet syndrome, and Behçet syndrome, all exhibit pathergy, meaning surgical debridement makes them dramatically worse. Stopping the surgical team from debriding is sometimes the most important consult recommendation of the day. Diagnosis is clinical and one of exclusion, supported by biopsy with tissue culture to rule out infection. Treatment is immunosuppression, typically prednisone 1 mg/kg, often co-administered with antibiotics until cultures return. For patients with known pyoderma gangrenosum facing future surgery, expectant management with perioperative steroid or cyclosporine coverage is reasonable.
Case 5: Cutaneous Small Vessel Vasculitis (CSVV)
Palpable purpura on the lower extremities is the classic presentation, most often reactive to a drug or infection. Cutaneous small vessel vasculitis is a clinical descriptor, not synonymous with IgA vasculitis, leukocytoclastic vasculitis, or Henoch-Schönlein purpura. Direct immunofluorescence sensitivity for IgA deposition drops off after 48 hours, so timing matters if biopsy is pursued. Most cases respond to trigger removal and topical steroids; systemics are reserved for ulceration. Antineutrophil cytoplasmic antibodies, cryoglobulins, rheumatoid factor, antinuclear antibodies, and complement should be sent when the clinical picture suggests systemic vasculitis.
Key Takeaways
- Each drug rash carries a characteristic latency window: exanthematous at one to two weeks, SJS or TEN at one to three weeks, DRESS at two to six weeks, and urticaria within hours.
- Retiform purpura signals vasculopathy or vasculitis until proven otherwise.
- Early recognition of neutrophilic dermatoses can be tissue- and life-saving.
- Not every vasculitis needs an exhaustive workup if the trigger is obvious.
- And when in doubt, call dermatology early, ideally before the rash sings its second verse.
Dr. Migliore is an assistant professor of medicine at Columbia University College of Physicians and Surgeons, and director of general medicine consult and perioperative services, as well as a medicine attending physician, at Columbia University Medical Center, both in New York.
References
- Pathak GN, et al. From the Cochrane Library: systemic interventions for Steven-Johnson Syndrome (SJS), Toxic Epidermal Necrolysis (TEN), and SJS/TEN overlap syndrome. JMIR Dermatol. 2024 Jan 30;7:e46580. doi: 10.2196/46580.
- Nordmann TM, Anderton H, Hasegawa A, et al. Spatial proteomics identifies JAKi as treatment for a lethal skin disease. 2024;635(8040):1001-1009. doi:10.1038/s41586-024-08061-0.
