British Journal of Radiology 74 (2001),1145-1147 © 2001 The British Institute of Radiology
Disseminated aspergillosis inciting intestinal ischaemia and obstruction
S S Shah, MD
B A Birnbaum, MD
and
J E Jacobs, MD
Department of Radiology, Hospital of the University of Pennsylvania, 3400 Spruce Street, Philadelphia, PA 19104, USA
Correspondence: Bernard A Birnbaum, MD
 |
Abstract
|
|---|
Invasive aspergillosis is an opportunistic infection that characteristically affects the immunocompromised host, resulting in a high degree of morbidity and mortality. Although the portal of entry is usually pulmonary, there are rare reports of invasive aspergillosis localized to the gastrointestinal tract. In addition, haematological spread may develop, with life threatening disseminated infection involving the vital organs and the gastrointestinal tract. Although disseminated infection is well recognized, the CT findings of gastrointestinal disease have not been reported to our knowledge. We describe the CT findings in a patient with invasive aspergillosis involving the gastrointestinal tract, which resulted in intestinal ischaemia complicated by small bowel obstruction.
|
Introduction
|
|---|
Disseminated aspergillosis is a rapidly progressive and highly lethal infection that typically affects the immunocompromised patient [1–3]. Gastrointestinal invasion may occur and result in serious complications such as bowel obstruction and angioinvasion with secondary bowel ischaemia, necrosis and perforation [1, 2, 4]. Although disseminated aspergillosis involving the bowel is a well recognized clinical entity, CT findings of invasive aspergillosis in the gastrointestinal tract have not been reported to date. We report the CT findings of a patient with histopathologically proven invasive aspergillosis that caused intestinal ischaemia and small bowel obstruction.
|
Case report
|
|---|
A 68-year-old Caucasian man with acute myelogenous leukaemia and refractory anaemia was admitted to our tertiary care institution for induction chemotherapy. 9 days after receiving idarubicin and cytarabine therapy the patient developed fever (39°C), experienced abdominal cramping and diarrhoea, and was noted to be neutropenic (300 white blood cells mm-3) and thrombocytopenic (10 000 platelets mm-3). The patient received iv vancomycin for a suspected iv line infection, and iv gentamycin, cefipime and metronidazole were commenced for broad-spectrum coverage. Blood and sputum cultures were negative. After 36 h of non-localizing abdominal pain and obstipation, physical examination was unremarkable, as was a chest radiograph. Abdominal radiographs showed dilated loops of small bowel compatible with possible evolving or partial small bowel obstruction.
Immediate surgical intervention was deferred owing to the patient's neutropenic high risk status. The patient was treated with nasogastric suction, and serial abdominal radiographs were obtained. The patient's abdominal symptoms improved with conservative management, although nasogastric tube outputs remained high and fever continued. CT of the abdomen and pelvis was obtained 5 days after admission to hospital, using both iv and oral contrast media. The proximal abdomen was imaged using 7 mm collimation and a helical pitch of 1.3:1, while the pelvis was imaged using 5 mm collimation and a helical pitch of 1.5:1. CT demonstrated evidence of a partial small bowel obstruction with moderate homogeneous intestinal wall thickening proximal to the transition zone and mild inflammatory stranding within the mesentery (Figure 1
). The intestinal wall thickening was suspicious of bowel oedema or ischaemia. There was no evidence of pneumoperitoneum, pneumotosis or vascular thrombosis. Following the CT study, a bone marrow biopsy demonstrated continued blast proliferation with leukogenic cells, indicating no response to chemotherapy.
View larger version (153K):
[in this window]
[in a new window]
|
Figure 1. Contrast enhanced axial CT demonstrates moderate circumferential thickening of a short segment of jejunum (white arrow) with a homogeneous enhancement pattern and mild inflammatory stranding of the adjacent mesentery (arrowheads). The proximal jejunum is mildly dilated (open arrow). Pelvic ileal loops (not shown) appeared collapsed, consistent with the clinical findings of partial small bowel obstruction.
|
|
At this time, 7 days after the onset of symptoms, the patient experienced localizing right lower quadrant tenderness and further CT of the abdomen and pelvis was performed using oral and iv contrast media. This study demonstrated collapsed distal ileum with circumferential homogeneous mural thickening involving the intestine at the transition zone with dilatation of the proximal small bowel, compatible with moderate grade obstruction (Figure 2). Associated mesenteric inflammation was noted, although no discrete mass lesion was identified at the transition zone. The decision was made to halt chemotherapy and initiate blood, platelet and white cell transfusions. 72 h later, with continued thrombocytopenia and an absolute neutrophil count of 0 mm-3, the patient underwent exploratory laparotomy with segmental resection of ischaemic-appearing small bowel. Histopathological examination of the surgical specimens demonstrated two 5 cm resected sections of mid jejunum and proximal ileum with transmural ischaemia, ulceration and Aspergillus fungal forms invading the intestinal arterioles.
View larger version (139K):
[in this window]
[in a new window]
|
Figure 2. Contrast enhanced axial CT, performed 3 days after Figure 1 , shows increased jejunal thickening (arrow) suspicious of mural ischaemia, with progressive inflammation of the peri-enteric fat. There is now fluid within the left paracolic space.
|
|
The patient developed post-operative sepsis and could not be weaned from ventilatory support. The patient's condition rapidly deteriorated despite broad spectrum antibiotic coverage and pressor agents. Ventilatory support was withdrawn and the patient died 72 h after the operation.
|
Discussion
|
|---|
Aspergillus is an inhaled fungus ubiquitous in nature. The organism may present with a broad pathogenic spectrum that includes limited allergic reactions of the nasal sinuses and lower respiratory tract, colonization and fungus ball formation in hosts with normal immunity, semi-invasive infection of the pulmonary parenchyma and bronchi in the mildly immunodeficient patient, and severe opportunistic invasive infection that may be complicated by systemic dissemination [1]. Disseminated aspergillosis is a highly lethal and rapidly progressive fungal infection that characteristically affects immunocompromised patients with a history of haematological malignancy, corticosteroid treatment or cytotoxic chemotherapy [1]. Almost one-quarter of those with invasive pulmonary aspergillosis develop disseminated infection with Aspergillus sp. via hematogenous spread [2]. Of these patients, there is a reported incidence of gastrointestinal involvement of 41–47% [2, 3].
Patients are rarely diagnosed with bowel involvement prior to autopsy because the typical symptoms of abdominal pain, obstruction and gastrointestinal bleeding are usually eclipsed by the septic manifestations of systemic infection. The first reported ante-mortem diagnosis of invasive aspergillosis of the colon was established by surgical laparotomy with sigmoid and right hemicolectomy in 1983 [4]. Weingrad et al [5] documented a case of aspergillosis as an unusual cause of perforated appendicitis in 1982. To our knowledge, invasive intestinal aspergillosis has otherwise only been reported sporadically in the non-radiology literature.
Aspergillus, in particular A. fumigatus, is the second most common opportunistic mycosis in patients with malignancies, following Candida sp. [3]. The portal of entry in disseminated aspergillosis is invariably considered to be the lungs [1, 2]. Fulminant infection in the lungs may lead to haematogenous spread of the fungal organism to the bloodstream, vital organs and gastrointestinal tract. Two prior case reports of invasive aspergillosis involving the bowel in patients receiving chemotherapy, paralleling the case we are presenting, showed normal chest radiographs throughout their hospitalization, which suggests the bowel may have been the initial portal of entry [6, 7]. There is a paucity of literature describing gastrointestinal aspergillosis. The majority of reports describe primary infection with invasive Aspergillus in the pulmonary system with subsequent dissemination [3]. It has been proposed that chemotherapeutic toxicity may alter normal gastrointestinal immunity to allow entry of Aspergillus by disrupting mucosal barriers [2]. However, further study is required to elucidate the exact mechanism of the organism's portal of entry in patients with gastrointestinal involvement and whether concomitant or prior pulmonary infection is truly necessary.
Aspergillus has a marked tendency to invade blood vessels and therefore exhibits vascular occlusion, peripheral areas of haemorrhage and areas of secondary infarction [6]. These areas are usually surrounded by superimposed necrotizing inflammatory tissue reactions [3]. Aspergillus hyphae also proliferate in infarcted tissue and can extend radially into adjacent tissue. These pathological features are identical in the lung, as well as in any organ involved with disseminated disease.
Treatment for invasive aspergillosis is prompt initiation of iv amphotericin B. Whether 5-fluorocytosine therapy is helpful remains controversial [8]. The mortality of disseminated infection with Aspergillus is almost 90%, and treatment should therefore be empirical in those with suspected infection [7].
As this case demonstrates, CT findings of invasive intestinal aspergillosis may be entirely non-specific. Our patient presented with CT findings of small bowel obstruction secondary to segmental mural thickening of the small intestine. No obstructing soft tissue mass was identified and the bowel wall appeared homogeneously enhanced, without evidence of mural stratification or a "target sign". The presence of peri-enteric inflammation within the subtended mesentery was an important secondary finding that suggested an inflammatory or infectious aetiology as the cause of the patient's intestinal obstruction.
In summary, despite the presence of a normal chest radiograph disseminated aspergillosis should be considered in the CT differential diagnosis when an immunocompromised patient presents with the above findings.
Received for publication July 16, 2001.
Accepted for publication August 14, 2001.
|
References
|
|---|
-
Watts JC, Chandler FW. Aspergillosis. In: Connor DH, et al, editors. Pathology of infectious diseases. Stamford, CT: Appleton & Lange, 1997:933–41.
-
Young RC, Bennett JE, Vogel CL, Carbone PP, DeVita VT. Aspergillosis: the spectrum of disease in 98 patients. Medicine 1970;49:147–73.[Medline]
-
Prescott RJ, Harris M, Banerjee SS. Fungal infections of the small and large intestine. J Clin Pathol 1992;45:806–11.[Abstract/Free Full Text]
-
Kinder RB, Jourdan MH. Disseminated aspergillosis and bleeding colonic ulcers in renal transplant patients. J R Soc Med 1985;78:338–9.[Medline]
-
Weingrad DN, Knapper WH, Gold J. Aspergillus peritonitis complicating perforated appendicitis in adult acute leukemia. J Surg Oncol 1982;19:5–8.[Medline]
-
Marterre WF, Mong AT, Pulito AR. Locally invasive aspergillosis of the bowel. J Ped Surg 1992;27:1611–3.[Medline]
-
Cohen R, Heffner JE. Bowel infarction as the initial manifestation of disseminated aspergillosis. Chest 1992;101:877–9.[Abstract/Free Full Text]
-
Davies SF, Sarosi GA. Aspergillosis in the immunocompromised patient. In: Al-Doary Y, Wagner GE, editors. Aspergillosis. Springfield, IL: Thomas, 1985:96–114.
Top
Abstract
Introduction
