Case Presentation: A 43-year-old female with a history of NASH cirrhosis and insulin dependent diabetes was sent from the Hepatology clinic for elevated Creatinine from 1.8 to 4.8 mg/dL. Her vital signs were stable and she was admitted for the management of suspected hepatorenal syndrome. Her hospital course was complicated by 5 weeks of ICU stay for a prolonged course of Norepinephrine infusion. Her renal function was finally stabilized around 2.5 mg/dL and she was transferred back to our medicine service on the day 39. Her MELD score at the time of transfer was 22. Her physical exam was notable for the painful erythema plus firm induration associated with localized paresthesia and a thickened cord along the vein on right forearm, which reportedly started 2 days prior. Thrombophlebitis was suspected since she had a peripheral intravenous catheter at the same location with no response to warm compress. Non-contrast CT, doppler and soft tissue ultrasounds were negative for any thrombosis or fluid collection. General surgery raised no concern of acute compartment syndrome. IV Vancomycin was started to treat as cellulitis with only mild improvement in erythema and firm induration. She then developed two small purpuric vesicles at the center of erythema, which resulted in larger, 2 to 3 cm-sized skin ulcerations with black eschars. The antibiotics were broadened to cover resistant gram-negatives and anaerobes with limited response. Skin biopsy was performed on the day 57 given the concern of other necrotic processes like Calciphylaxis, but the biopsy showed cutaneous abscess with mixed ribbonlike hyphae, consistent with Mucormycosis. Incision and drainage was performed and Amphotericin B infusion was started. She however deteriorated and deceased on the day 63.
Discussion: Rhizopus species are ubiquitously found in nature and can cause hospital-acquired infection in immunocompromised and diabetic patients. Though the majority of hospitalists may be more familiar with rhino-orbital-cerebral and pulmonary Mucormycosis, the skin is the most common site of hospital-acquired Mucor infection (57%) in one report. Intravenous catheters are one of the common portals of entry. The key discriminating symptoms would include severe pain out of proportion to the skin findings, firm indurated area with cellulitis, poor response to antibiotics, and delayed development of Ecthyma-like skin ulceration. The infection can cause ischemic infarction resulting in tissue necrosis and black eschar. Our case showed all of the above findings but it took more than 2 weeks from the onset to the diagnosis. Hospitalists rarely need to request skin biopsy for local erythematous lesions but cutaneous Mucormycosis is an exception. It is important to keep a high index of suspicion for cutaneous Mucormycosis when they encounter immunocompromised or diabetic patients with cellulitis refractory to broad-coverage antibiotics. Cutaneous Mucormycosis tends not to invade into deep tissue quickly, as was our case, but can be life-threatening if left untreated.
Conclusions: Since the true incidence of hospital-acquired cutaneous Mucormycosis is not available, hospitalists need to keep a high index of suspicion for this underrecognized mimicker of cellulitis in immunocompromised or diabetic patients.