Two days later (day 15), a necrotic area was seen at the open wound on the left flank (Figure 3). Development of sepsis was also noted with a white blood cell count of 23,000/µL, heart rate of 120 bpm, and lactic acid level of 4.4 mmol/L. Broad-spectrum intravenous antibiotics, vancomycin and piperacillin-tazobactam, were initiated. A repeat exploratory laparotomy revealed a multifocal necrotic bowel around the small bowel anastomosis and the rectal stump. Some areas of perforation were also noted around the anastomotic site. These areas were debrided, and the necrotic bowel was resected. Histopathological evaluation of resected specimen again revealed fungal aseptate hyphae consistent with the diagnosis of invasive GIM.
Subsequently, 2 days later (day 17), bloody output was noted from the nasogastric tube and abdominal surgical drains. The patient developed hemorrhagic shock refractory to blood transfusion, intravenous hydration, and inotrope therapy. Immediate laparotomy was performed, revealing an 8 × 4 cm area of perforation with necrosis at the previously seen gastric ulcer site along with active bleeding. Attempts to control the bleeding remained unsuccessful and the patient eventually died in the operating room.
Mucormycosis is a life-threatening, opportunistic, angioinvasive fungal infection. Most commonly it occurs in immunocompromised patients with predisposing conditions, including uncontrolled diabetes mellitus, hematologic malignancies, and solid organ transplant.2 Angioinvasion provides a pathway for the hematogenous spread for mucormycosis. It can also cause local ischemia and infarction, which leads to tissue necrosis.3 The mechanism of transmission of mucormycosis includes inhalation or ingestion of spores and direct inoculation into disrupted mucocutaneous surfaces.4 Although most commonly seen in rhinocerebral and pulmonary forms, mucormycosis can present as gastrointestinal, cutaneous, central nervous system, and disseminated forms.5
GIM accounts for 7% of the total reported cases and has a very poor prognosis with a mortality rate of 85%.6 In the gastrointestinal tract, the stomach is the most common site, followed by the colon and ileum.7 Predisposing risk factors for GIM include malnutrition, uremia, typhoid fever, and penetrating trauma.1,8 The clinical features of GIM vary, including fever, abdominal pain, nausea, vomiting, diarrhea, gastrointestinal bleed, or gastrointestinal perforation.9 Diagnosis is confirmed with direct microscopy and histopathological evaluation from a tissue biopsy, which can be obtained endoscopically or during surgery.10 Recommended management of GIM is a combination of surgical debridement and intravenous antifungal therapy. Rapid initiation of antifungal therapy has been noted to improve survival, but a delay in treatment greater than 6 days has shown to double the mortality rates.11
Although there is no clear consensus regarding optimal antifungal therapy, amphotericin B is the advised first-line treatment. Liposomal amphotericin B can be used at higher doses and has a lower risk for nephrotoxicity. The recommended course of treatment duration is usually 4-6 weeks.12 Posaconazole is also an effective agent and can also be used for treatment in cases of polyene intolerance.13 Antifungal therapy alone is typically inadequate. Surgical debridement of necrotic tissue is often required for comprehensive treatment of invasive mucormycosis.14
Author contributions: G. Sehmbey and R. Malik acquired and analyzed the data and wrote the manuscript. D. Kosa, I. Srinivasan, K-Y Chuang, and S. Bellapravalu analyzed the data and wrote the manuscript. K-Y Chuang is the article guarantor.
Financial disclosure: None to report.
Previous Presentation: This case report was presented as a poster at the 2018 ACG Scientific Meeting; October 5–10, 2018; Philadelphia, Pennsylvania.
Informed consent was obtained for this case report.
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© 2019 The Author(s). Published by Wolters Kluwer Health, Inc. on behalf of The American College of Gastroenterology.
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