Keywords

FormalPara Learning Objectives

  • To understand the imaging spectrum of different types of infections and their potential mimics in the abdomen and pelvis.

  • To understand differentiating features of abdominal infections with imaging in various organs in the abdomen and pelvis taking into consideration relevant clinical background information and the main risk factors.

2.1 Introduction

Intra-abdominal infections are the second leading cause of death in critical care settings with the incidence in the USA estimated to be 3.5 million cases per year [1]. In both developing and developed countries with a myriad of etiologies, abdominal infections pose a high risk of morbidity and mortality. Impairments to the immune system, potentially lead to higher rates and impact long-term outcomes in predisposing conditions such as malignancy or immunocompromise [2,3,4]. Predisposing host factors include barrier disruption, such as skin or mucosa, anatomic obstruction, pre-existing malignancies, immunosuppression including chemotherapy, surgical procedures, interventions, and medical device site infections. The common infectious agents can be categorized into viral including COVID-19, bacterial including gram-negative and positive, acid-fast bacilli, and nosocomial such as clostridium difficile, fungal such as candida, aspergillus, mucor and parasitic such as echinococcus. The organ systems and sites involved with infections include gastrointestinal and genitourinary tracts, hepatobiliary, pancreas, peritoneum, retroperitoneum, and abdominal wall. Based on the organ system involvement diverse imaging modalities can be utilized including plain radiographs, fluoroscopy, ultrasound (US), computed tomography (CT) including dual energy, magnetic resonance imaging (MRI), and molecular imaging techniques such as positron emission tomography (PET). Distinct imaging features about the site and etiology of infection can help clinch early diagnosis and improve patient outcomes. The purpose of this chapter is to discuss the underlying risk factors and mechanisms of infections and to present the variety of imaging manifestations of abdominal and pelvic infections.

2.2 Risk Factors for Infections

Abdominal infections can occur de novo or in a setting of numerous risk factors such as barrier disruption, such as skin or mucosa, anatomic obstruction, pre-existing malignancies, tumor burden, immunosuppression including chemotherapy, surgical procedures, interventions, and medical device site infections [5].

2.2.1 Barrier Disruption

The cornerstone defense mechanism for the body against infections includes the skin and mucosal surfaces. The destruction of these barriers by predisposing conditions such as trauma, catheter placement, vascular compromise, malignancy, radiation therapy, and chemotherapy [6]. The mucosal barrier injury occurs in four phases: inflammation, apoptosis, ulceration, and healing [7].

2.2.2 Anatomic Obstruction

The presence of anatomic obstructions such as gastrointestinal, hepatobiliary, and urinary tracts can be a predisposing factor for post-obstructive infections. Small or large bowel obstruction which can be due to adhesions, strictures, or tumors can be challenging to clinically manage as it can contribute to bowel ischemia, perforation, fistulas, peritonitis, and abdominopelvic abscesses, typically polymicrobial. Hepatobiliary obstruction can result in recurrent cholangitis and hepatic abscesses. Urinary tract obstruction may cause hydronephrosis which can progress to complicated pyelonephritis, and renal and prostatic abscesses [5].

2.2.3 Vascular Compromise

Vascular occlusion can lead to poor circulation and thereby ischemia and infarction which facilitates infection in an organ. Decrease in arterial flow from iatrogenic, thrombus, or malignant causes while venous compromise can from direct tumor extension or mass effect result in complications such as bowel perforation and abscess formation [8].

2.2.4 Pre-existing Malignancy

While solid organ malignancies such as carcinoma and sarcoma commonly lead to disruption of natural barriers and obstruction, hematological malignancies, such as lymphoma, acute myeloid leukemia, and chronic lymphocytic leukemia can cause severe prolonged immunosuppression and neutropenia in addition to barrier disruption, thereby predisposing to infections.

2.2.5 Immunosuppression

Chemotherapy and marrow infiltration-induced immunosuppression causes febrile neutropenia with an absolute neutrophil count <of 1500 cells per mm3 (severe neutropenia <500 cells per mm3)[9]. This clinical condition can lead to polymicrobial bacterial infections commonly enteric Gram-negative bacteria, Staphylococcus aureus, and clostridium [3, 10, 11]. Additionally, viral infections and invasive fungal infections, such as candida and aspergillus, can occur[12, 13]. Imaging features of these infections can help detect and manage any potential complications.

2.2.6 Prior Radiation

Acute radiation leads to inflammation and mucosal barrier injury depending upon the dose and the field of radiation, thereby causing the entry of infectious pathogens into the body and bloodstream [14]. The most common manifestations of acute radiation injury include mucositis, esophagitis, and esophageal dysmotility, colitis, and anorectal complications. Chronic radiation can lead to fibrosis with stricture or fistula formation causing obstruction, stasis, and viscus perforation, superinfection, and abscess formation [14, 15]. Another potential mechanism of chronic radiation-induced injury that may predispose to infection is vascular sclerosis leading to tissue hypoperfusion. Some of the radiation-induced changes such as small bowel wall thickening and mucosal hyperenhancement, and luminal narrowing [15].

2.2.7 Medical Devices

Medical devices including drainage and peritoneal dialysis catheters, vascular access catheters, stents, and shunts can not only be the vehicle for introducing infectious pathogens such as skin-colonizing staphylococci but can also complicate the management [16]. Superficial infections can spread along the skin or abdominal wall muscles and cause peritonitis and abdominopelvic abscesses. While biliary stents can lead to cholangitis and recurrent obstruction, ureteric stents and percutaneous nephrostomy tubes can cause acute and chronic pyelonephritis and bacteremia [17, 18]. Timely diagnosis with multimodality imaging can help in surveillance of these infections and prevention of complications.

2.2.8 Surgery

The global incidence of surgical site infections is 11 % [19]. These can be minor such as surgical wound infections or major such as anastomotic bowel and biliary leaks which may need additional surgical interventions. Presence of adhesions, obstruction, leaks, and fistula can predispose to surgical site infection. Imaging can help identify, characterize, and manage these complications.

Key Point

The recognition of the predisposing condition can help identify the potential pathogenesis and imaging spectrum of infection for early diagnosis and prompt management

2.3 Imaging in Abdominal Infections

Imaging plays an essential role in evaluating infections within the abdomen and pelvis and can facilitate early detection and management, thus truly adding value to patient care with potential to improve outcomes. Although abdominal radiographs have been largely replaced by cross-sectional imaging, they play an important role for the surveillance of bowel obstruction and pneumoperitoneum and to evaluate implanted devices and catheters [20]. Ultrasound is additional imaging modality which can be used as bed side technique to assess hepatobiliary, genitourinary, and gynecologic infections and related pathologies. For assessment of gastrointestinal infectious etiologies, ultrasound is however limited due to the inability of sound to travel through the bowel gas. Other factors limiting usage of this technique include operator dependence, patient compliance, and body habitus. Thereby, for the workup of patients with abdominal infections and for nonspecific complaints such as abdominal pain, fever, or unknown sepsis, contrast-enhanced CT (CECT) has become the diagnostic modality of choice. Recently, dual energy CT (DECT) with material density images and iodine quantification can help detect and evaluate infectious disease processes. MRI is a useful problem-solving tool for better characterization for hepatobiliary or pancreatic infections and to differentiate from infection mimics such as inflammatory or autoimmune etiologies and malignancies [21]. While CT remains the preferred imaging modality, MRI can not only help with the diagnosis of microbial infection but also in the longitudinal tracking of the bacterial infection [22]. For the bacterial and viral infections, MRI can help in detection of local inflammation, edema formation, and tissue characterization such as assessment of water content and diffusivity as manifestation of immune response. While radiation dose accompanying the CT scan, could favor use of MRI in certain clinical circumstances, longer acquisition time and compromised image quality due to motion artifacts, need of longer breath hold and following commands can limit the diagnostic utility of MRI. Radionuclide studies, such as using indium-111 white blood cell scan, are most useful for vascular graft infection, and their larger use have been superseded by cross-sectional imaging[23]. Combination of radionuclide uptake with SPECT/CT can improve localization while FDG PET/CT can both localize and quantitate the degree of infection [24]. White light imaging and linked color imaging endoscopy have been used, for example, in diagnosis of Helicobacter pylori infection with high sensitivity and specificity. Functional imaging largely remains a research tool with clinical potential uncertain for diverse infectious conditions.

Key Point

The imaging pattern of manifestation of infection is dependent upon the infecting organism and organ system.

2.3.1 Gastrointestinal Tract Infections

Gastrointestinal tract immune system is dependent upon a number of components which include gastric acid, bowel flora, and motility apart from the humoral and cell-mediated immune defenses [25]. Disruption of any of these protective mechanisms can ensue an infectious disease process. Compared to immunocompetent individuals, gastrointestinal infections in immunosuppression leads to a high rate of morbidity and mortality. Common pathogens infecting the gastrointestinal tract causing colitis include Gram-negative bacilli such as shigella (S. dysenteriae, S. flexneri, S. boydii, and S. sonnei), Escherichia coli, Clostridium difficile, and Salmonella and viruses such as cytomegalovirus (CMV) [26]. In developing countries, mycobacterial tuberculosis infections are common involving most frequently causing terminal ileitis and cecal colitis, lymphadenopathy, and peritonitis. Imaging manifestations of bacterial infections on CECT and MRI include bowel wall thickening, with enhancement and edema, fat stranding, perforation, abscess, neutropenic enterocolitis, and secondary peritonitis. Accurate diagnosis is based on a combination of clinical history, symptoms, imaging findings, and serological and laboratory tests. The management is most often conservative, and interventions and surgery are reserved for complications such as perforation or bleeding.

Apart from the bowel wall, perirectal and perianal infections can also occur with pre-existing conditions such as cancer and radiation presenting as diarrhea, tenesmus, and hematochezia [27]. Acute proctitis (<6 months) occurs due to mucosal inflammation, and chronic proctitis occurs due to microvascular insufficiency from obliterative endarteritis [28]. The resulting vascular compromise leads to intestinal ischemia, transmural fibrosis and possibly strictures, ulcerations, fistulas, and perforation [28]. CECT demonstrates mural stratification and wall thickening at the radiation site. Fistulas can be better evaluated with fluoroscopy. MRI with high soft-tissue resolution can delineate the extent and degree of sphincter involvement of fistulous tracts and perirectal and perianal abscesses (Fig. 2.1) [29].

Fig. 2.1
Two M R I of the lower abdomen highlight the perianal abscess in the ischiorectal fossa.

Axial post-gadolinium T1-weighted fat-suppressed image (a, b) showing perianal abscess (red arrow) in the left ischiorectal fossa extending superiority into the perirectal region in a patient of Crohn’s disease. The perianal fistula track is located at 5 o’clock position on the left side

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2.3.1.1 Clostridioides Difficile Colitis

C. difficile, a Gram-positive anaerobic infection commonly occurs after a few weeks of use of antibiotics that disrupt the normal bowel flora and is most common cause of nosocomial bowel infections (Fig. 2.2) [30]. While often the infection can be mild, it is not infrequent that it can be fulminant leading to hypotension, or ileus to necessitate hospitalization [31]. The severe manifestations of infection include megacolon, perforation, and septicemia, with mortality rates of up to 25% [31] Usually, the infection involves the entire colon and less commonly segmental [30, 31]. CECT features include mucosal ulcers, pseudomembrane, wall thickening, submucosal edema, mucosal hyperenhancement, and pericolic fat stranding, which later evolve to lack of enhancement and sloughing. The transmural edema with wall thickening along with mucosal hyperemia produce the “accordion sign” where the orally administered contrast is trapped between edematous haustral folds [32]. Presence of irregular mucosal with polypoid protrusions can result in wall nodularity and “thumbprinting” on contrast enema and radiographs [32]. Radiologically, if the colonic diameter is more than 6 cm, toxic megacolon is suspected. The management is usually medical, except for complicated cases where surgery may be required.

Fig. 2.2
Four M R I of the lower abdomen highlights the wall thickening of the rectosigmoid colon, which is lightly shaded.

Axial T2-weighted fat-suppressed images (a, b) of an elderly female with clostridium difficile colitis following prolonged use of antibiotics show diffuse wall thickening of the rectosigmoid colon with evidence of enhancement on axial (c) and coronal (d) fat-suppressed post-contrast T1-weighted image

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2.3.1.2 Neutropenic Enterocolitis

Neutropenic enterocolitis is also called as neutropenic colitis or typhlitis and is a potentially life-threatening complication of chemotherapy, more commonly seen in hematological malignancies such as acute myeloid leukemia and following cytotoxic chemotherapy. The condition occurs in severely neutropenic patients (cell count <500 cells per mm3) typically in the third week of chemotherapy [33]. The most common site of involvement is cecum and patients often present with right lower quadrant pain [34]. The risk of this condition is increased in the presence of prior inflammation such as diverticulitis, malignancy, and postoperative state [33]. The infection is most commonly polymicrobial although bacterial organisms such as Gram-negative bacilli, Gram-positive cocci, and anaerobes, and fungal pathogens such as candida can also cause the condition [33]. Multipronged approach of clinical, laboratory, and imaging features is critical for diagnosis. CECT is the imaging modality of choice with findings including wall thickening, submucosal edema, mucosal hyperenhancement, fat stranding in the region of cecum and ascending colon with possible terminal ileum involvement (Fig. 2.3). The complications can include perforation, pneumatosis, extraluminal gas, and pericolic fluid [32, 35]. For pediatric population, thickened bowel wall of more than 10 mm on US with clinical and laboratory findings can provide diagnosis [36]. Imaging differentials include cecal diverticulitis and pseudomembranous colitis.

Fig. 2.3
Three M R I and a P E T of the abdomen with a cluster of circular patches focusing on wall thickening of the colon.

Axial post-contrast CT (a) and PET (b) image showing colonic wall thickening and uptake within the small bowel and colon which worsens on follow-up post-contrast CT axial (c) and coronal (d) image obtained 2 weeks later in a patient of necrotizing enterocolitis

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2.3.1.3 Gastrointestinal Tuberculosis

Due to factors such as stasis, presence of lymphoid tissue, and closer contact of bacilli with the enteric mucosa, the most common site of tubercular involvement in gastrointestinal tract is ileocecal region in about 64% of cases [37]. The lesions can be ulcerative and ulcero-hypertrophic in bowel and show confluent granulomas and caseation necrosis in the bowel and adjacent lymph nodes[38]. Rarely, duodenum and esophagus can be involved. Plain X-ray abdomen may show enteroliths, features of obstruction like dilated bowel loops with multiple air fluid levels or presence of air under diaphragm in case of perforation. There may be evidence of calcification as calcified lymph nodes, calcified granulomas, and hepatosplenomegaly. On barium studies, accelerated intestinal transit; hyper-segmentation of the barium column, precipitation, flocculation and dilution of the barium, stiffened and thickened folds, narrowing of bowel lumen and strictures can be seen. CECT and CT enterography can show wall thickening in the cecum and terminal ileum with asymmetric thickening of the IC valve and associated lymphadenopathy with areas of low attenuation suggestive of caseous necrosis (Fig. 2.4) [39, 40]. Strictures can be seen in ileum and sometimes jejunum.

Fig. 2.4
Three M R I of the sagittal, coronal, and axial section of the abdomen highlight the region of pelvic bones and wall thickening. Arrows point to the colonic wall thickening.

An adult male patient with tuberculous colitis demonstrating diffuse colonic wall thickening (white arrow) and ascites (*) on sagittal (a), coronal (b), and axial post-contrast (c) images

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2.3.1.4 Viral Enterocolitis

Viral infections such as CMV have a high morbidity and mortality (42%), commonly affecting the colon, stomach, and esophagus [41]. CECT and MRI imaging features are non-specific including wall thickening, ascites, and lymphadenopathy. In complicated cases, mucosal ulcers and ischemia or perforation-related changes can occur. Differential diagnosis apart from other infectious etiologies include graft versus host disease in a setting of stem cell transplant. Another common viral agent which affects the gastrointestinal tract is Norovirus, causing gastroenteritis[42]. Non-specific CT findings include low attenuation small bowel wall thickening and distension with fluid [43]. Differential diagnosis includes neoplastic bowel infiltration and mural hemorrhage where the bowel wall is hyperdense [44].

Recently, COVID-19 commonly affects the gastrointestinal tract and could at times precede pulmonary involvement. While CECT is the modality of choice for the detection of bowel involvement, US and MRI can help management and follow-up. CECT findings include involvement of ascending colon, transverse colon, and descending colon with features of bowel wall thickening, mucosal hyperenhancement, low attenuation submucosal edema, bowel dilation, pericolic fat stranding and lymphadenopathy [45, 46]. Complications such as pneumatosis intestinalis are rare and can secondarily be contributed by chronic bowel ischemia, obstruction, and autoimmune etiologies. Portal and mesenteric vein thrombosis are typically seen in COVID-19 infection [47]. Isolated case reports of appendicitis have also been reported [48].

2.3.1.5 Fungal Infections

In patients with acute leukemia, diabetes, cancer and immunocompromised states, fungal infections in the gastrointestinal tract are increasingly common with pathogens including Aspergillus, Candida, and Mucor [49, 50]. CECT shows gastrointestinal tract wall thickening and stranding, lymphadenopathy, peritoneal and retroperitoneal thickening, hepatic and splenic microabscesses, vascular compromise, and infarcts [51]. Both aspergillus and mucor are angio-invasive with highest mortality in about half the cases with mucor. Additionally, large ulcers with irregular edges can be seen within the stomach and the colon. Candida infections can cause ulcers, peritonitis, and infarcts in solid organs [52].

2.3.2 Hepatobiliary Infections

Hepatobiliary infections comprise of infectious cholangitis, hepatitis (acute and chronic viral), bacterial, mycobacterial, parasitic (such as echinococcal and amoebiasis), fungal, and gastrointestinal or systemic infections involving the liver secondarily due to portal circulation and the organ [53].

2.3.2.1 Liver Abscesses

The routes of spread of liver abscess include biliary, hematogenous, or contiguous with infections resulting from bacterial or fungal colonization [21]. Predisposing factors include the presence of malignancy, biliary tract disease, post-interventions, and surgery. While CECT is the imaging modality of choice, MRI can provide information on possible communication of abscesses with the biliary tract and to differentiate hepatic abscesses from necrotic metastases. Compared to the latter, abscesses demonstrate a rather thin and homogeneous wall, and greater restricted diffusion with lower ADC values [54]. Area of diffusion restriction on MRI correlate with high T2 signal while in necrotic tumors these correlates to intermediate T2 signal intensity. For abscesses larger than 6 cm, or risk of impending perforation, percutaneous drainage is often required [55]. Fungal infections such as hepatosplenic candidiasis, the most common form of chronic disseminated candidiasis usually sets in a predisposing hematologic malignancy after chemotherapy [56]. The typical manifestation includes multifocal peripheral hepatic, splenic, and renal cortical microabscesses demonstrable on US, CT, and MRI [57]. US shows microabscesses as hypoechoic or as a “bull’s eye” lesion with peripheral hypoechoic fibrosis and central hyperechoic inflammation [58]. CECT and MRI can demonstrate innumerable tiny microabscesses, hypoattenuating on CT and variable on MRI: T1 hypointense ad T2 hyperintense when acute and hypointense peripheral rim on T1 and T2 with central hyperintensity on T1-weighted images when subacute and hypointense on all sequences when in chronic phase. These can calcify in chronic phase with differentials including metastases, lymphoma, and sarcoidosis.

2.3.2.2 Cholangitis

Obstructing stones, malignant or non-malignant stricture, biliary stents, and choledochojejunostomy can lead to acute or ascending cholangitis presenting with Charcot’s triad including abdominal pain, fever, and jaundice [59]. Acute suppurative cholangitis refers to cholangitis with the presence of pus in the biliary tract occurring in elderly patients >70 years of age, smokers, and in patients with impacted biliary stones or procedure related [51, 60]. Common bacterial agents include E. coli (31%), Klebsiella pneumoniae, Enterococcus faecalis, and Streptococcus species. Indwelling plastic biliary stents predispose to enterococcus and polymicrobial infections [60]. CECT and MRI images show central, diffuse, or segmental biliary ductal dilation with smooth symmetric and diffuse bile duct wall thickening most pronounced in the central ducts. While the ductal dilation can be assessed on US, early, and intense enhancement of the thickened bile duct walls and the liver parenchyma may demonstrate wedge-shaped peripheral patchy peribiliary enhancement, most marked in the arterial phase. US and MR cholangiopancreatography (MRCP) can determine the presence of tumors or stones in the central bile ducts (Fig. 2.5). Pus may be seen on CT as hyperdense material within the distended ducts. Inspissated bile or sludge may also be hyperdense on CT; MRI, especially DWI, can be more specific for identifying purulent material, as it demonstrates restricted diffusion with very low signal intensity on ADC map but no internal enhancement. Cholangitis can be complicated by bacteremia and sepsis, hepatic abscesses, portal vein thrombosis, and bile peritonitis [60].

Fig. 2.5
Four M R cholangiopancreatography of the axial section of the abdomen. Arrows point to the biliary thickening. The light circular patch appears on the left in the images on the top.

An adult female with cholangitis. Coronal MRCP (a) image showing left-sided mild ductal dilatation. The plastic stent can be visualized in the common bile duct on axial T2-weighted image (b). Axial subtracted (c) and non-subtracted (d) fat-suppressed post-contrast delayed images show the biliary thickening and enhancement

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2.3.2.3 Viral Infections

Viral hepatitis can result from hepatitis A virus infection commonly in developing countries and reactivation of hepatitis B and hepatitis C in patients with known chronic hepatitis after receiving chemotherapy [59, 60]. The resultant periportal edema and parenchymal injury can be seen on US as “starry sky” appearance due to increased echogenicity of the portal triads, and on MRI as diffusely heterogeneous signal intensity of the liver with hyperintense T2 signal. CECT and post-contrast MRI images show early and heterogenous hepatic enhancement. Recently, COVID-19 has been shown to cause liver injury due to its cytopathic effect with elevation of liver enzymes such as ALT, AST, and GGT. There have been reports of moderate micro-vesicular steatosis and lobular and portal activity in liver biopsy specimens of COVID-19 patients [61, 62].

2.3.2.4 Parasitic Infections

There are a number of parasitic infections that can affect the liver and biliary tree with the most common being amebic infection, hydatid disease, schistosomiasis, fascioliasis, and clonorchiasis [63, 64]. Amoebiasis, an infection of the large intestine can spread to the liver leading to abscess formation appearing on US as solitary, unilocular, and hypoechoic round or oval mass commonly in right hepatic lobe. There may be evidence of internal echoes and posterior acoustic enhancement. Associated diaphragmatic disruption with rupture into the pleural space or pericardium is highly suggestive of an amebic liver abscess [64]. CT appearance is of a circumscribed lesion with central fluid attenuation and peripheral rim enhancement (target” or “double-rim” appearance) with or without septations, fluid-debris levels, and rarely gas or hemorrhage [58]. MRI shows central low T1- and high T2-signal, peripheral rim enhancements and perilesional edema. The amoebic abscess usually responds to medical management with drainage needed for larger ones. In a setting of a suspected liver abscess with associated thickening/inflammation of the right colon, an amebic abscess should be considered.

Echinococcal liver disease is caused by echinococcosis granulosus and multilocularis infections. On US, the appearance can range from a pure cyst to a lesion that mimics a solid mass [65]. Echinococcal cysts can be easily differentiated from simple hepatic cysts by the presence of a wall of varying thickness and additional signs such as the presence of daughter cysts demonstrating a “spoke-wheel” pattern [64]. Another is the “water-Lily” sign, in which wavy floating membranes are seen within the hydatid cavity resulting from detachment of the endocyst. When the patient is repositioned, multiple echogenic foci can be seen to move within the hydatid cavity giving the “snowstorm” sign. These echogenic foci result from rupture of daughter cysts that leads to scolices passing into the hydatid cyst fluid forming a white sediment that is then referred to as “hydatid sand.” When the hydatid cyst degenerates and becomes nonviable, it can appear heterogeneous with hypoechoic and hyperechoic content, mimicking a solid mass. This is the “ball of wool” sign. Finally, a hydatid cyst can partially or completely calcify over time [66]. If the calcifications are more central in location, that usually indicates a nonviable cyst. CT shows high attenuation of the echinococcal cyst walls and the internal floating membranes with peripheral enhancement and non-enhancing central content. Daughter cysts and calcifications similar to that on US can be seen. MRI shows a T1 and T2 hypointense peripheral rim of pericyst with internal floating membranes and daughter cysts. The E. multilocularis can infiltrate along the biliary tracts towards the hepatic hilum and cause peritoneal seeding of infection, transdiaphragmatic intrathoracic spread of disease, and superinfection (Fig. 2.6) [67].

Fig. 2.6
Two M R I of the axial section of the abdomen. Arrows pointing to bile ducts highlight the cystic lesion and enhancement. The light-shaded circular spot is exposed at the center.

Axial T2-weighted image (a) of an adult male shows hyperintense complex solid and cystic lesion infiltrating along the bile ducts (white arrow) with mild ductal dilatation in a patient with Echinococcus multilocularis infection. Axial delayed post-contrast image (b) shows heterogenous enhancement

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2.3.3 Genitourinary Tract Infections

2.3.3.1 Obstructive Uropathy

Obstructive uropathy due to the presence of tumor, ureteral reflux from loss of the ureterovesical junction competency, indwelling catheters and stents, and pelvic radiation can predispose to urinary tract infections. The level of urinary tract obstruction can be the ureter, bladder, or urethra, leading to urinary stasis, a major risk for bacterial colonization and infection [68]. Additionally, urinary tract obstruction also impairs the renal function. The obstruction at the level of ureters can occur due to retroperitoneal adenopathy, pelvic or ureteric malignancies or radiation-induced stricture [69]. The major diagnostic imaging modalities include US and CECT which can demonstrate hydroureteronephrosis and asymmetric nephrogram for detection of ureteral obstruction. In lower urinary tract obstruction, such as due to prostatomegaly or strictures, US can also help evaluate the presence of post-void residual urine. The filling defects in the collecting system or ureters including mass lesion or stones can be better assessed on CT urography using a split bolus technique or a 3-phase study. The level of obstruction and etiologies pertaining to soft-tissue mass can be better evaluated with MRI. Accuracy in diagnosis helps in clinical management typically requiring decompression using retrograde ureteral stents or percutaneous nephrostomy tubes.

2.3.3.2 Renal and Urinary Bladder Infections

Urinary bladder infections can occur with E. coli and other Gram-positive cocci, Gram-negative enterobacteriaceae and candida [70]. The predisposing factors for urinary bladder infection include indwelling Foley’s catheter or suprapubic catheter, obstructive uropathy, and prior surgical interventions such as bladder tumor resection with or without intestinal urinary pouches. While the bacterial infections frequently can be diagnosed early and effectively managed, fungal organisms such as C. albicans can lead to renal microabscesses or larger abscesses, fungal balls or chronic disseminated candidiasis [54]. [71]. Renal infections can occur due to ascending urinary tract infection or hematogenous dissemination. The initial presentation of renal infection is pyelonephritis which can evolve and complicate into renal abscess in the setting of bacteremia or fungemia. Prompt and early diagnosis can ensure medical management with favorable outcome prior to the development of complications that may need percutaneous or surgical aspiration [72]. On US, the presence of pyelonephritis demonstrates a heterogenous appearance of renal cortex with reduced flow on Doppler. On CECT and MRI, the appearance is of a wedge-shaped or rounded area of streaky cortical enhancement (Fig. 2.7). The presence of renal abscess can demonstrate central hypodensity on CT and T2 hyperintensity on MRI with evidence of diffusion restriction.

Fig. 2.7
Four M R I of the 2 axial and 2 coronal sections of the abdomen. Arrows highlight the renal abscess. It enhances the light patch at the bottom of the images.

Axial (a) and coronal (b) post-contrast CT images of an adult male shows heterogenous focus of evolving renal abscess at the upper pole of the ectopic single kidney. Axial (c) and coronal (d) non-contrast CT images of an adult male with diabetes shows air within the anterior interpolar cortex of the left kidney suggesting emphysematous pyelonephritis and evolving abscess

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2.3.3.3 Prostatic Infections

Infections in the prostate gland can occur contiguously such as from urethra or bladder infections or secondary to procedures such as cystoscopy, prostate biopsy, urethral/suprapubic catheter placement, brachytherapy, cryotherapy, or radiation [73]. Chemotherapy and bacteremia are additional systemic factors in cancer patients that increase the risk of developing prostatic abscess. Clinically, patients present with dysuria, urgency, frequency, sensation of incomplete voiding, and suprapubic or perineal pain. On CT and MRI, the inflamed gland can demonstrate enlarged and edematous appearance. The presence of central hypoechoic areas on US, low attenuation on CT and T2 hyperintensity on MRI correlate with possibility of a prostatic abscess. MRI provides better imaging characterization for prostatic abscess assessment, and both CT and MRI can demonstrate a unilocular or multilocular rim enhancing collection commonly in the transition zone or central zone of the prostate (Fig. 2.8) [73].

Fig. 2.8
Two C T images of the coronal and axial section of the abdomen focusing on the prostatic abscess. The R O I, area, circumference, diameter, mean, minimum, maximum, and standard deviation of the circled portion are listed in image b.

Coronal (a) and axial (b) post-contrast CT images of an adult male showing low attenuation within the prostate gland consistent with prostatic abscess

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2.3.4 Peritoneal and Abdominal Wall Infections

Intra-abdominal and abdominal wall infections can occur due to secondary involvement from adjacent site or in a setting of immunosuppression, cancer, radiation, and interventions such as paracentesis, surgery, and medical devices. The inflammation of the peritoneum (peritonitis) can be infectious or non-infectious such as due to irritation by blood or bile. The gastrointestinal etiologies for peritonitis include bowel obstruction and perforation and anastomotic dehiscence. Additional causes include cancer, ischemia, infectious enterocolitis, ulcers, and radiation can lead to bowel perforation. Surgery, indwelling peritoneal dialysis catheters, non-tunneled catheters and shunts also predispose to infection. The complicated peritonitis can lead to a systemic inflammatory response that with a mortality rate of up to 30% [73, 74]. Patients present with generalized abdominal pain, tenderness, guarding, and fever. Pathogens in peritonitis depend upon the cause, as pathogens in the upper gastrointestinal tract differ than those of the lower. US can be used to evaluate for ascites and collections, and to guide aspiration, but CECT is the modality of choice in imaging peritonitis to identify a source and look for intra-abdominal abscesses. Typical imaging features are ascites, peritoneal enhancement, and thickening, which is typically smooth with infectious etiology, but could less commonly be nodular or irregular, a feature favoring carcinomatosis.

2.3.4.1 Peritoneal Devices

Patients with advanced abdominal malignancies often develop refractory ascites requiring indwelling peritoneal catheters associated with a significantly increased infection risk. Simple fluid collections or ill-defined fluid around devices can be due to seromas and post-surgical changes; however, the development of an enhancing wall or new gas pockets without recent intervention is concerning for abscess formation. Additional peritoneal devices include peritoneal infusion catheters, dialysis catheters, ventriculoperitoneal shunts, and surgical drains; any of those can be complicated by peritonitis from translocation of skin flora or from bowel perforation, albeit the latter is rare. Peritonitis is also an uncommon risk following percutaneous gastrostomy tube placement. Management consists of antibiotics and removal of the causative device, with surgery in cases of frank perforation.

2.3.4.2 Intra-abdominal Abscesses

Non-visceral abscesses are polymicrobial and either peritoneal or retroperitoneal with the former due to a complication of peritonitis and/or perforation. Retroperitoneal abscesses can be caused by hollow viscous perforation or by hematogenous, lymphatic, or local spread of infection. Clinical symptoms include fever and abdominal discomfort. For example, a perirectal abscess may cause diarrhea, and an abscess in contiguity with the bladder may cause urinary symptoms. CECT and MR imaging demonstrate a rim enhancing fluid collection with surrounding inflammatory changes. For >3 cm abscess, drainage is required. If untreated, abscesses may extend to adjacent structures, erode into vessels (causing pseudoaneurysms, hemorrhage, and thrombosis), rupture, or less commonly fistulize, eventually leading to bacteremia and septic shock with high mortality rates [74].

2.3.4.3 Abdominal Wall Infections

Skin and soft-tissue infections (SSTI) in the abdominal wall can be very serious in immunocompromised patients, particularly those with vascular pathologies such as endarteritis obliterans (seen with radiation therapy). SSTIs include cutaneous infections in addition to deeper subcutaneous, muscular, and fascial infections such as cellulitis, necrotizing fasciitis, and pyomyositis. Deep SSTI infections can be caused by skin injury or skin disruption from surgery, catheter and line insertions, radiation treatment, and primary or metastatic tumors. Cellulitis is a clinical diagnosis, but imaging features include skin thickening with subcutaneous fat stranding, edema, and inflammation. The presence of subcutaneous gas on non-contrast CT that spreads along fascial planes is usually worrisome for necrotizing fasciitis, requiring early and aggressive management with drainage and surgical debridement (Fig. 2.9). Vesicocutaneous and enterocutaneous fistulas due to tumors, radiation therapy, or surgical complications can lead to SSTIs. Imaging with US, CT, or MRI can be helpful in delineating the predisposing factor, differentiating acute versus fibrotic fistula track as well as the number and relationships of tracts, and evaluating for any associated drainable abscesses.

Fig. 2.9
Six C T images of 2 coronal, 2 sagittal, and 2 axial views of the abdomen. In A, B, D, and E, arrows highlight the abdominal wall air and fluid. In D and E, arrows point to the peritoneal enhancement.

Coronal (a, d), sagittal (b, e) and axial (c, f) post-contrast CT images of two adult female patients showing anterior abdominal wall air and fluid containing collections (white arrows). Note the peritoneal enhancement and thickening (red arrows)

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2.4 Conclusion

Radiologists should be familiar with the risks of infection and identify the most common imaging manifestations of infections. Imaging plays an important role in diagnosis, management, and prognosis of infectious processes in the abdomen and pelvis in patients with oncologic conditions, including those affecting the gastrointestinal, hepatobiliary, and genitourinary systems, in addition to non-visceral and abdominal wall infections, and those associated with medical devices, radiation, and surgical procedures.

Take-Home Messages

  • Infections of the abdomen and pelvis have significant impact on patient morbidity and mortality.

  • Imaging plays an important role in the diagnosis and management of patients with intra-abdominal infections.

  • Imaging manifestation of abdominal infections can be varied depending on the type of microbial, pathogenesis, and organ system involved.

  • Early recognition of imaging signs of infection along with identification of mimics is essential for prompt diagnosis and management.