Case Presentation: A 61-year-old man with type 2 diabetes mellitus was admitted for surgical resection of left fifth metatarsal due to osteomyelitis refractory to prolonged antibiotic use. Vital signs on admission were all within normal limits; significant lab values included ESR 79 mm/hr, CRP 7.07 mg/dL, and WBC 9.2 k/uL. Following surgical debridement and amputation, treatment with vancomycin and cefepime was initiated. On postoperative day 4, he developed a painful, palpable maculo-papular purpuric rash primarily on the posterior of his calves, with fewer lesions on the dorsum of the hands, and sparing the palms and soles. No acute changes in his vital signs, CBC or serum chemistries were noted. HIV and HCV studies returned negative. Vancomycin and cefepime were held. Dermatology consultants performed bedside exam and biopsy. The rash improved with topical clobetasol 0.05%. Antibiotic regimen was changed to doxycycline monotherapy. Biopsy results revealed superficial and deep perivascular neutrophilic infiltrate with focal fibrinoid degeneration, extravasated erythrocytes, and occasional eosinophils, all consistent with leukocytoclastic vasculitis (LCV). Topical steroids were continued for symptom relief.

Discussion: The development of a purpuric rash acutely during an inpatient setting is uncommon and therefore presents a diagnostic challenge to internists. However, these pathologies can be quickly recognized, diagnosed, and treated when approached systematically and with an understanding of their underlying pathophysiology. Purpuric rashes, or lesions that do not blanch with pressure or with diascopy, typically are indicative of vascular damage or vessel wall inflammation. Two common mechanisms for vascular infiltration include direct invasion by infectious pathogen or immune-mediated inflammation. Purpuric rashes caused by infection, and likely to be seen in the hospital, include the petechial and purpuric hemorrhages seen in meningococcemia and Rocky Mountain spotted fever, and both may be identified by their associated symptoms of fever, headache, or photophobia. Purpura driven by immune-mediated inflammation includes idiopathic thrombocytopenic purpura, DIC, cryoglobulinemia, Sweet syndrome (also known as acute febrile neutrophilic dermatosis) and Henoch-Schonlein purpura (a subtype of LCV). More broadly, LCV or cutaneous small-vessel vasculitis, refers to infiltration of neutrophils, many undergoing apoptosis, into blood vessel walls in response to drug exposure (antibiotics, HCTZ), hepatitis C virus, or autoimmune connective tissue disease, however most cases are idiopathic.

Conclusions: In summary of this initial differential for inpatient palpable purpura, remember, you don’t want to MISS this RAsH (Meningococcemia, ITP, Septic vasculitis, Sweet syndrome, Rocky Mountain spotted fever, Autoimmune, or Henoch-Schonlein purpura). Findings will be circular lesions, primarily in dependent areas, and biopsy will show abundant neutrophils with little or no immunoglobulin. Treatment is based in first detecting or ruling out reversible underlying causes and correcting them, with topical steroids for symptom relief only.

IMAGE 1: Palpable purpura in dependent areas consistent with leukocytoclastic vasculitis

IMAGE 2: Scattered palpable purpura seen in leukocytoclastic vasculitis