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Disseminated enteroinvasive aspergillosis in a critically ill patient without severe immunocompromise

Disseminated enteroinvasive aspergillosis in a critically ill patient without severe... JSCR 2013; 11 (3 pages) doi:10.1093/jscr/rjt091 Case Report Disseminated enteroinvasive aspergillosis in a critically ill patient without severe immunocompromise 1,* 2 2 2 2 ´ ´ Jennifer H. Fieber ,Jorunn Atladottir , Daniel G. Solomon , Linda L. Maerz , Vikram Reddy , 3 2 Kisha Mitchell-Richards and Walter E. Longo 1 2 Yale University School of Medicine MD Candidate, New Haven, CT, USA, Yale Department of Surgery, New Haven, CT, USA and Yale Department of Pathology, New Haven, CT, USA *Correspondence address: c/o Walter Longo, Yale Department of Gastrointestinal Surgery, PO Box 208062, New Haven, CT 06520-8062, USA. Tel: þ1-520-471-7013; Fax: þ1-203-785-2615; E-mail: jennifer.fieber@yale.edu Received 4 September 2013; accepted 22 September 2013 Invasive aspergillosis (IA) is a rapidly progressive and often fatal infectious disease described classically in patients who are highly immunocompromised. However, there has been increas- ing evidence that IA may affect critically ill patients without traditional risk factors. We present a case of a 47-year-old man without conventional risk factors for IA who presented with impend- ing sepsis and proceeded to have a complicated hospital course with a postmortem diagnosis of invasive gastrointestinal aspergillosis of the small bowel. INTRODUCTION distended and diffusely tender but without rebound tenderness or guarding. The rectal examination was positive for gross Aspergillus is a ubiquitous fungus that causes opportunistic blood. A non-contrast abdomen and pelvis computed tomog- infections in the immunocompromised patient population and raphy (CT) scan was significant for pancolitis and the patient has a high mortality. Up to 60% of patients with invasive pul- was started on antibiotics. monary aspergillosis will have extrapulmonary dissemination Emergency general surgery was consulted, and the patient of disease [1]. The gastrointestinal tract is the third most was transferred to the surgical intensive care unit (SICU). The common location for dissemination [2]. The presentation of patient developed hypotension requiring vasopressors and invasive gastrointestinal aspergillosis (IGA) most commonly respiratory failure requiring mechanical ventilation. Over the includes abdominal pain and gastrointestinal bleeding but next 2 days, leukocytosis and lactic acidosis normalized, and may rarely present as an acute abdomen [2, 3]. Diagnosis of the patient was weaned off vasopressors and extubated. IGA infrequently occurs before autopsy [4]. We present Clostridium difficile antigen was negative and antibiotics were a unique case of IGA leading to intestinal infarction and narrowed. ultimately death in a critically ill patient. On hospital day 6, the patient complained of sudden onset sharp abdominal pain and developed peritoneal signs on abdominal examination. Non-contrast abdominal CT scan CASE REPORT demonstrated pneumoperitoneum, colitis and ascites. In the A 47-year-old man with a history of hepatitis C, hemophilia A context of the patient’s co-morbidities, the patient was deemed too high a surgical risk for exploratory laparotomy. managed on home Factor VIII and, recently, diagnosed ulcera- The patient was taken to the operating room for a loop ileos- tive colitis on prednisone 40 mg for 10 days was transferred to our facility for concern for toxic megacolon and admitted to tomy rescue procedure. Intraoperatively, the small bowel appeared normal, and ascites appeared clear. The patient was the medical intensive care unit (MICU). Admission vital signs extubated postoperatively and initially improved. were temperature 34.48C, heart rate 96 bpm, blood pressure 107/51, respiratory rate 14 breaths per minute and oxygen sat- On postoperative day 3, he developed supraventricular tachycardia, respiratory failure requiring mechanical ventila- uration 97% on 3 l/min by nasal cannula. On physical ex- amination, the patient was cachectic and his abdomen was tion, hypotension requiring vasopressors and large-volume Published by Oxford University Press and JSCR Publishing Ltd. All rights reserved.# The Author 2013. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/ by-nc/3.0/), which permits non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited. For commercial re-use, please contact journals.permissions@oup.com. Page 2 of 3 J.H. Fieber et al. Figure 1: Hemorrhagic bowel with dark purple–black areas of gangrene and Figure 2: Admixed blood clot and fecal material, focally adherent to the foci of serosal fibrinopurulent exudate. granular, friable mucosa with associated exudate and edema. serosanguinous ascites drainage from the intra-abdominal drain. Concurrently, intraoperative ascites cultures grew Candida, Methicillin-resistant Staphylococcus aureus, and E. coli and appropriate antibiotic therapy was initiated. Sputum cultures grew 1þ Aspergillus fumigatus. A repeat endotracheal (ET) aspirate culture was negative for fungus, and a non-contrast chest CT scan demonstrated no evidence of a fungal pneumonia. For the next week, the patient remained intubated but was successfully weaned off vasopressors, and his abdominal examination improved. On postoperative day 14, peritoneal signs and acute hypotension requiring vasopressors recurred. The patient devel- oped black ileostomy output, bleeding from the intra-abdominal drain and bright red blood per rectum. The patient underwent an emergent exploratory laparotomy. Intraoperatively, the small bowel was necrotic from the distal jejunum to the distal ileum. Seventy-three centimeters of small bowel were resected, and a Figure 3: Transmural necrotic, hemorrhagic and congested bowel wall. primary anastomosis was performed. Postoperatively, the patient had profuse, uncontrollable intra-abdominal bleeding and remained hemodynamically un- stable. Despite massive transfusion and aggressive attempts to correct coagulopathy, the patient continued to deteriorate. Goals of care were changed to comfort measures, and the patient died the next morning. Concomitantly, a third ET aspirate culture was positive for 2þ A. fumigatus. The family refused autopsy. Pathologic evaluation of the resected bowel revealed hemor- rhagic, gangrenous bowel (Fig. 1) and granular friable, ulcer- ated mucosa (Fig. 2). Microscopically, there were areas of transmural bowel necrosis (Fig. 3) and fungi within the bowel wall, artery wall and lumen (Fig. 4). Gomori Methenamine Silver stain was characteristic of Aspergillus species (Fig. 5). DISCUSSION We present a case of fatal IGA in a critically ill patient with Figure 4: Mononuclear cells associated with scattered neutrophils and newly diagnosed ulcerative colitis managed with low-dose prominent fungal hyphae in subserosal arteries and invading vessel walls. Disseminated enteroinvasive aspergillosis in a critically ill patient Page 3 of 3 corticosteroids and coagulopathy. His gastrointestinal symp- toms were nonspecific and readily explained by his comorbid- ities. Our patient did have comorbidities known to impact immune function, including critical illness, short course corticosteroid use, malnutrition and liver dysfunction but was not considered to be at high risk of developing IA. When the initial sputum culture grew A. fumigatus,the possibility of IA was investigated through imaging that was not consistent with fungal infection and a negative repeat ET aspirate culture. The initial sputum culture was thought to be a contaminant or colonization. We believe that our patient had a primary subclinical lung infection with secondary angioinva- sion of the small bowel leading to this severe complication. In conclusion, the diagnosis of IGA is difficult, especially in nontraditional hosts, but should be considered as part of the differential diagnosis in critically ill patients with nonspecific gastrointestinal symptoms. Figure 5: Gomori Methenamine Silver stain highlighting fungal forms, some dichotomous, with frequent septation, characteristic of Aspergillus species. REFERENCES steroids, hemophilia A and hepatitis C. Traditional risk factors for IA include neutropenia, stem cell transplants, organ 1. Eggimann P, Chevrolet JC, Starobinski M, Majno P, Totsch M, Chapuis B, et al. Primary invasive aspergillosis of the digestive tract: report of two transplants and advanced AIDS [4]. Steroid courses longer cases and review of the literature. Infection 2006;34:333–8. than 3 weeks and prednisone dosage 1.25 mg/kg/day also 2. Walsh TJ, Anaissie EJ, Denning DW, Herbrecht R, Kontoyiannis DP, increase risk of IA [5, 6]. Critical illness is increasingly being Marr KA, et al. Treatment of aspergillosis: clinical practice guidelines of the Infectious Diseases Society of America.ClinInfectDis considered as possible risk factor of IA in non-neutropenic 2008;46:327–60. patients [7]. 3. Hori A, Kami M, Kishi Y, Machida U, Matsumura T, Kashima T. Clinical The diagnosis of IA is difficult in classically high-risk significance of extra-pulmonary involvement of invasive aspergillosis: a retrospective autopsy-based study of 107 patients. J Hosp Infect patients, as symptoms are ill defined, radiologic studies are only 2002;50:175–82. suggestive of the diagnosis and cultures are not sensitive [8]. 4. Segal BH, Walsh TJ. Current approaches to diagnosis and treatment of Invasive aspergillosis provides a further diagnostic challenge in invasive aspergillosis. Am J Respir Crit Care Med 2006;173:707–17. critically ill patients, as symptoms can often be explained 5. Gustafson TL, Schaffner W, Lavely GB, Stratton CW, Johnson HK, Hutcheson RH, Jr. Invasive aspergillosis in renal transplant recipients: through other aspects of the patient’s presentation [6]. correlation with corticosteroid therapy. J Infect Dis 1983;148:230–8. Diagnostic methods for IA have only been thoroughly studied 6. Meersseman W, Vandecasteele SJ, Wilmer A, Verbeken E, in traditional immunocompromised patients [8]. Differentiating Peetermans WE, Van Wijngaerden E. Invasive aspergillosis in critically ill patients without malignancy. Am J Respir Crit Care Med colonization from invasive infection in positive ET culture 2004;170:621–5. aspirates continues to be difficult, and the value of newer 7. Garnacho-Montero J, Amaya-Villar R, Ortiz-Leyba C, Leon C, antigen-based testing in non-neutropenic patients has been Alvarez-Lerma F, Nolla-Salas J, et al. Isolation of Aspergillus spp. from the respiratory tract in critically ill patients: risk factors, clinical questioned [4, 6, 9]. Invasive testing for histopathological presentation and outcome. Crit Care 2005;9:R191–9. diagnosis is often contraindicated in critically ill patients. 8. Dimopoulos G, Frantzeskaki F, Poulakou G, Armaganidis A. Invasive The diagnosis of IGA was extremely challenging in our aspergillosis in the intensive care unit. Ann N Y Acad Sci 2012;1272:31–9. 9. Blot SI, Taccone FS, Van den Abeele AM, Bulpa P, Meersseman W, patient because of his complex clinical presentation and lack Brusselaers N, et al. A clinical algorithm to diagnose invasive pulmonary of classic risk factors. He presented with gastrointestinal aspergillosis in critically ill patients. Am J Respir Crit Care Med bleeding, colitis and sepsis in the context of ulcerative colitis, 2012;186:56–64. http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Journal of Surgical Case Reports Oxford University Press

Disseminated enteroinvasive aspergillosis in a critically ill patient without severe immunocompromise

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Published by Oxford University Press and JSCR Publishing Ltd. All rights reserved. © The Author 2013.
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Abstract

JSCR 2013; 11 (3 pages) doi:10.1093/jscr/rjt091 Case Report Disseminated enteroinvasive aspergillosis in a critically ill patient without severe immunocompromise 1,* 2 2 2 2 ´ ´ Jennifer H. Fieber ,Jorunn Atladottir , Daniel G. Solomon , Linda L. Maerz , Vikram Reddy , 3 2 Kisha Mitchell-Richards and Walter E. Longo 1 2 Yale University School of Medicine MD Candidate, New Haven, CT, USA, Yale Department of Surgery, New Haven, CT, USA and Yale Department of Pathology, New Haven, CT, USA *Correspondence address: c/o Walter Longo, Yale Department of Gastrointestinal Surgery, PO Box 208062, New Haven, CT 06520-8062, USA. Tel: þ1-520-471-7013; Fax: þ1-203-785-2615; E-mail: jennifer.fieber@yale.edu Received 4 September 2013; accepted 22 September 2013 Invasive aspergillosis (IA) is a rapidly progressive and often fatal infectious disease described classically in patients who are highly immunocompromised. However, there has been increas- ing evidence that IA may affect critically ill patients without traditional risk factors. We present a case of a 47-year-old man without conventional risk factors for IA who presented with impend- ing sepsis and proceeded to have a complicated hospital course with a postmortem diagnosis of invasive gastrointestinal aspergillosis of the small bowel. INTRODUCTION distended and diffusely tender but without rebound tenderness or guarding. The rectal examination was positive for gross Aspergillus is a ubiquitous fungus that causes opportunistic blood. A non-contrast abdomen and pelvis computed tomog- infections in the immunocompromised patient population and raphy (CT) scan was significant for pancolitis and the patient has a high mortality. Up to 60% of patients with invasive pul- was started on antibiotics. monary aspergillosis will have extrapulmonary dissemination Emergency general surgery was consulted, and the patient of disease [1]. The gastrointestinal tract is the third most was transferred to the surgical intensive care unit (SICU). The common location for dissemination [2]. The presentation of patient developed hypotension requiring vasopressors and invasive gastrointestinal aspergillosis (IGA) most commonly respiratory failure requiring mechanical ventilation. Over the includes abdominal pain and gastrointestinal bleeding but next 2 days, leukocytosis and lactic acidosis normalized, and may rarely present as an acute abdomen [2, 3]. Diagnosis of the patient was weaned off vasopressors and extubated. IGA infrequently occurs before autopsy [4]. We present Clostridium difficile antigen was negative and antibiotics were a unique case of IGA leading to intestinal infarction and narrowed. ultimately death in a critically ill patient. On hospital day 6, the patient complained of sudden onset sharp abdominal pain and developed peritoneal signs on abdominal examination. Non-contrast abdominal CT scan CASE REPORT demonstrated pneumoperitoneum, colitis and ascites. In the A 47-year-old man with a history of hepatitis C, hemophilia A context of the patient’s co-morbidities, the patient was deemed too high a surgical risk for exploratory laparotomy. managed on home Factor VIII and, recently, diagnosed ulcera- The patient was taken to the operating room for a loop ileos- tive colitis on prednisone 40 mg for 10 days was transferred to our facility for concern for toxic megacolon and admitted to tomy rescue procedure. Intraoperatively, the small bowel appeared normal, and ascites appeared clear. The patient was the medical intensive care unit (MICU). Admission vital signs extubated postoperatively and initially improved. were temperature 34.48C, heart rate 96 bpm, blood pressure 107/51, respiratory rate 14 breaths per minute and oxygen sat- On postoperative day 3, he developed supraventricular tachycardia, respiratory failure requiring mechanical ventila- uration 97% on 3 l/min by nasal cannula. On physical ex- amination, the patient was cachectic and his abdomen was tion, hypotension requiring vasopressors and large-volume Published by Oxford University Press and JSCR Publishing Ltd. All rights reserved.# The Author 2013. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/ by-nc/3.0/), which permits non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited. For commercial re-use, please contact journals.permissions@oup.com. Page 2 of 3 J.H. Fieber et al. Figure 1: Hemorrhagic bowel with dark purple–black areas of gangrene and Figure 2: Admixed blood clot and fecal material, focally adherent to the foci of serosal fibrinopurulent exudate. granular, friable mucosa with associated exudate and edema. serosanguinous ascites drainage from the intra-abdominal drain. Concurrently, intraoperative ascites cultures grew Candida, Methicillin-resistant Staphylococcus aureus, and E. coli and appropriate antibiotic therapy was initiated. Sputum cultures grew 1þ Aspergillus fumigatus. A repeat endotracheal (ET) aspirate culture was negative for fungus, and a non-contrast chest CT scan demonstrated no evidence of a fungal pneumonia. For the next week, the patient remained intubated but was successfully weaned off vasopressors, and his abdominal examination improved. On postoperative day 14, peritoneal signs and acute hypotension requiring vasopressors recurred. The patient devel- oped black ileostomy output, bleeding from the intra-abdominal drain and bright red blood per rectum. The patient underwent an emergent exploratory laparotomy. Intraoperatively, the small bowel was necrotic from the distal jejunum to the distal ileum. Seventy-three centimeters of small bowel were resected, and a Figure 3: Transmural necrotic, hemorrhagic and congested bowel wall. primary anastomosis was performed. Postoperatively, the patient had profuse, uncontrollable intra-abdominal bleeding and remained hemodynamically un- stable. Despite massive transfusion and aggressive attempts to correct coagulopathy, the patient continued to deteriorate. Goals of care were changed to comfort measures, and the patient died the next morning. Concomitantly, a third ET aspirate culture was positive for 2þ A. fumigatus. The family refused autopsy. Pathologic evaluation of the resected bowel revealed hemor- rhagic, gangrenous bowel (Fig. 1) and granular friable, ulcer- ated mucosa (Fig. 2). Microscopically, there were areas of transmural bowel necrosis (Fig. 3) and fungi within the bowel wall, artery wall and lumen (Fig. 4). Gomori Methenamine Silver stain was characteristic of Aspergillus species (Fig. 5). DISCUSSION We present a case of fatal IGA in a critically ill patient with Figure 4: Mononuclear cells associated with scattered neutrophils and newly diagnosed ulcerative colitis managed with low-dose prominent fungal hyphae in subserosal arteries and invading vessel walls. Disseminated enteroinvasive aspergillosis in a critically ill patient Page 3 of 3 corticosteroids and coagulopathy. His gastrointestinal symp- toms were nonspecific and readily explained by his comorbid- ities. Our patient did have comorbidities known to impact immune function, including critical illness, short course corticosteroid use, malnutrition and liver dysfunction but was not considered to be at high risk of developing IA. When the initial sputum culture grew A. fumigatus,the possibility of IA was investigated through imaging that was not consistent with fungal infection and a negative repeat ET aspirate culture. The initial sputum culture was thought to be a contaminant or colonization. We believe that our patient had a primary subclinical lung infection with secondary angioinva- sion of the small bowel leading to this severe complication. In conclusion, the diagnosis of IGA is difficult, especially in nontraditional hosts, but should be considered as part of the differential diagnosis in critically ill patients with nonspecific gastrointestinal symptoms. Figure 5: Gomori Methenamine Silver stain highlighting fungal forms, some dichotomous, with frequent septation, characteristic of Aspergillus species. REFERENCES steroids, hemophilia A and hepatitis C. Traditional risk factors for IA include neutropenia, stem cell transplants, organ 1. Eggimann P, Chevrolet JC, Starobinski M, Majno P, Totsch M, Chapuis B, et al. Primary invasive aspergillosis of the digestive tract: report of two transplants and advanced AIDS [4]. Steroid courses longer cases and review of the literature. Infection 2006;34:333–8. than 3 weeks and prednisone dosage 1.25 mg/kg/day also 2. Walsh TJ, Anaissie EJ, Denning DW, Herbrecht R, Kontoyiannis DP, increase risk of IA [5, 6]. Critical illness is increasingly being Marr KA, et al. Treatment of aspergillosis: clinical practice guidelines of the Infectious Diseases Society of America.ClinInfectDis considered as possible risk factor of IA in non-neutropenic 2008;46:327–60. patients [7]. 3. Hori A, Kami M, Kishi Y, Machida U, Matsumura T, Kashima T. Clinical The diagnosis of IA is difficult in classically high-risk significance of extra-pulmonary involvement of invasive aspergillosis: a retrospective autopsy-based study of 107 patients. J Hosp Infect patients, as symptoms are ill defined, radiologic studies are only 2002;50:175–82. suggestive of the diagnosis and cultures are not sensitive [8]. 4. Segal BH, Walsh TJ. Current approaches to diagnosis and treatment of Invasive aspergillosis provides a further diagnostic challenge in invasive aspergillosis. Am J Respir Crit Care Med 2006;173:707–17. critically ill patients, as symptoms can often be explained 5. Gustafson TL, Schaffner W, Lavely GB, Stratton CW, Johnson HK, Hutcheson RH, Jr. Invasive aspergillosis in renal transplant recipients: through other aspects of the patient’s presentation [6]. correlation with corticosteroid therapy. J Infect Dis 1983;148:230–8. Diagnostic methods for IA have only been thoroughly studied 6. Meersseman W, Vandecasteele SJ, Wilmer A, Verbeken E, in traditional immunocompromised patients [8]. Differentiating Peetermans WE, Van Wijngaerden E. Invasive aspergillosis in critically ill patients without malignancy. Am J Respir Crit Care Med colonization from invasive infection in positive ET culture 2004;170:621–5. aspirates continues to be difficult, and the value of newer 7. Garnacho-Montero J, Amaya-Villar R, Ortiz-Leyba C, Leon C, antigen-based testing in non-neutropenic patients has been Alvarez-Lerma F, Nolla-Salas J, et al. Isolation of Aspergillus spp. from the respiratory tract in critically ill patients: risk factors, clinical questioned [4, 6, 9]. Invasive testing for histopathological presentation and outcome. Crit Care 2005;9:R191–9. diagnosis is often contraindicated in critically ill patients. 8. Dimopoulos G, Frantzeskaki F, Poulakou G, Armaganidis A. Invasive The diagnosis of IGA was extremely challenging in our aspergillosis in the intensive care unit. Ann N Y Acad Sci 2012;1272:31–9. 9. Blot SI, Taccone FS, Van den Abeele AM, Bulpa P, Meersseman W, patient because of his complex clinical presentation and lack Brusselaers N, et al. A clinical algorithm to diagnose invasive pulmonary of classic risk factors. He presented with gastrointestinal aspergillosis in critically ill patients. Am J Respir Crit Care Med bleeding, colitis and sepsis in the context of ulcerative colitis, 2012;186:56–64.

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Published: Nov 4, 2013

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