Intra-abdominal Fungal Infections
Intra-abdominal Fungal Infections
Major risk factors for Candida peritonitis include hollow viscus perforation, abdominal and thoracic surgery, surgical drains in situ, intravenous and urinary catheters, severe sepsis, and extensive Candida colonization. This infection is uncommon following simple perforations or when appropriate repair is achieved on the first intervention. However, presence of persistent dehiscence or multiple surgical interventions significantly increases the risk. Patients can present with diffuse peritonitis or localized abscesses. Although some patients present with vague clinical signs, others may present with the classic signs of bacterial peritonitis. For many years, there has been debate over the importance of Candida isolated from the sites of intra-abdominal infection. The organism is a normal commensal of the gastrointestinal tract and its isolation is often difficult to interpret. Generally, infection is suspected when the organism is cultured from samples obtained intraoperatively or directly from an intra-abdominal collection. When Candida is cultured from subsequently obtained drainage fluid samples, colonization is a possibility. However, although there are reports of 'colonized patients' recovering without antifungal therapy, ignoring these cultures can be dangerous, especially in the setting of critical illness or when Candida is repeatedly isolated. In the recent years, there has been a lowering in the threshold for treating such patients. Hematogenous dissemination from the peritoneum can occur. In a study of 93 patients with Candida peritonitis in ICUs, the mortality was 38%. Management of this form of candidiasis usually entails both surgical intervention and antifungal therapy. Antifungal regimens are similar to those used in candidemia. Echinocandins are preferred in critically ill patients, in those with prior azole exposure, and in those with fluconazole-resistant candidiasis.
Candida Peritonitis
Major risk factors for Candida peritonitis include hollow viscus perforation, abdominal and thoracic surgery, surgical drains in situ, intravenous and urinary catheters, severe sepsis, and extensive Candida colonization. This infection is uncommon following simple perforations or when appropriate repair is achieved on the first intervention. However, presence of persistent dehiscence or multiple surgical interventions significantly increases the risk. Patients can present with diffuse peritonitis or localized abscesses. Although some patients present with vague clinical signs, others may present with the classic signs of bacterial peritonitis. For many years, there has been debate over the importance of Candida isolated from the sites of intra-abdominal infection. The organism is a normal commensal of the gastrointestinal tract and its isolation is often difficult to interpret. Generally, infection is suspected when the organism is cultured from samples obtained intraoperatively or directly from an intra-abdominal collection. When Candida is cultured from subsequently obtained drainage fluid samples, colonization is a possibility. However, although there are reports of 'colonized patients' recovering without antifungal therapy, ignoring these cultures can be dangerous, especially in the setting of critical illness or when Candida is repeatedly isolated. In the recent years, there has been a lowering in the threshold for treating such patients. Hematogenous dissemination from the peritoneum can occur. In a study of 93 patients with Candida peritonitis in ICUs, the mortality was 38%. Management of this form of candidiasis usually entails both surgical intervention and antifungal therapy. Antifungal regimens are similar to those used in candidemia. Echinocandins are preferred in critically ill patients, in those with prior azole exposure, and in those with fluconazole-resistant candidiasis.
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