Splenic Abscess

Etiology

Splenic abscesses most commonly arise from hematogenous spread but can also result from contiguous contamination, superinfected hematoma, or infarction.[5] They may occur in the context of trauma, splenic artery embolization, hemoglobinopathy, endocarditis, osteomyelitis, immunosuppression, pancreatic disease, intraabdominal surgery, or intravenous drug use.[14][15][16] Less frequently, parasitic infections may lead to abscess formation. A splenic abscess can also develop following procedures that generate septic emboli, such as tooth extraction or infective endocarditis, where embolism-induced infarction can progress to abscess formation.[17] In children, the primary causes include septicemia, hematologic malignancy, malaria, tuberculosis, Epstein-Barr virus, and typhoid fever, with rarer etiologies including appendicitis, tympanitis, and infective endocarditis. In some cases, the underlying cause remains undetermined.[16][18]

Certain conditions predispose individuals to splenic abscesses, including solid organ or hematopoietic stem cell transplantation, cirrhosis, end-stage kidney disease, malignancy, inflammatory bowel disease, and immunosuppression. The anatomical proximity of the pancreas allows for the contiguous spread of infection.[5][19][17] Immunosuppressive medications, such as monoclonal antibodies or steroids, further increase the risk. Reported cases include a 71-year-old woman who developed a splenic abscess following COVID-19 pneumonia and a patient who developed an abscess after a traumatic splenic injury managed with splenic preservation.[20][21] Direct bacterial spread from malignancies, such as left-sided colon cancer, has also been documented as a mechanism of infection.[10]

The microbial spectrum of splenic abscesses reflects their diverse etiologies. Common bacterial isolates include Escherichia coli, Streptococcus group D, Streptococcus anginosus, Proteus mirabilis, staphylococcus spp, Candida spp, Klebsiella pneumoniae, Pseudomonas aeruginosa, Bacteroides fragilis, Clostridium difficile, Serratia marcescens, and Enterococcus faecalis. More unusual organisms include Burkholderia pseudomallei, Mycobacterium tuberculosis, Solobacterium moorei, Atopobium rimae, Cutibacterium avidum, and Actinomyces israelii.[19] Case reports highlight rare pathogens, such as a 29-year-old man with diabetic nephropathy who was found to have splenic abscess caused by the anaerobic gram-positive coccus Lancefieldella rimae, a common causative agent of periodontal disease, and a 79-year-old Chinese woman with Campylobacter rectus, found in oral infections, isolated from multiple splenic collections.[1][22]     

Approximately 3% to 5% of patients with infective endocarditis will develop a splenic abscess. Endocarditis, which results in bacterial vegetation formation on the endocardium and cardiac valves, frequently leads to septic embolization and splenic infarction. A subset of these infarctions progresses to abscess formation. Individuals with diabetes and reduced right ventricular function are at increased risk.[23]

Aseptic abscess syndrome, a neutrophil-laden collection associated with inflammatory bowel disease, is a rare entity. An affected person may present with fever, abdominal pain, diarrhea, and weight loss. The syndrome is systemic, involves the spleen in over 70% of cases, and is prone to relapse.[24] Characterized by negative cultures, failure of antibiotics to resolve the collection, and rapid clinical improvement following a course of corticosteroids, the abscess may rarely be the first indication of a chronic inflammatory condition such as Crohn disease. An aseptic splenic abscess typically occurs in those whose known inflammatory condition has progressed despite pharmacologic treatment.[24][25][26]

Epidemiology

The incidence of splenic abscess is 0.1% to 0.7%. Splenic abscesses have a bimodal distribution, peaking in both the third and sixth decades. Two-thirds of splenic abscesses are solitary, and the remainder are multiple abscesses.[22] The incidence is increasing due to improved detection, increased intravenous drug use, and the greater number of immunocompromised individuals. Mortality remains high, especially in the immunocompromised, and a solitary abscess in an immunocompetent person carries a 15% mortality.[22][27][28] Aseptic abscess syndrome, which involves the spleen in nearly 75% of cases, has an incidence of less than 1%.[24]

In a retrospective study of 33 cases of splenic abscess, 58% of affected persons were men with underlying comorbidities, including diabetes, pancreatitis, and hematologic malignancy; the median age was 57. Escherichia coli, enterococcus, and anaerobes were the most common pathogens isolated. The distribution and incidence of splenic abscesses have changed in parallel with an evolution in the treatment of immunodeficiency syndromes and the changing etiology of hematologic neoplasms.[5] 

Splenic abscess in children is rare. The comorbidities associated with abscesses in adults are rarely present in pediatric cases. Affected children are usually older than 10 and are predominantly boys. A case report was published of a large splenic abscess in a 12-year-old composed of Salmonella spp group D who presented with an elevated erythrocyte sedimentation rate and C-reactive protein and no evidence for endocarditis or other comorbidities. Aseptic splenic abscess is also found in children, usually secondary to systemic diseases such as systemic lupus erythematosus, Behcet disease, inflammatory bowel disease, and pyoderma gangrenosum.[17][29]

Pathophysiology

A splenic abscess is often polymicrobial and arises via hematogenous spread in the setting of immunocompromise but may also occur through bacterial seeding of a hematoma or infarct. Splenic abscesses may also occur idiopathically. Comorbidities may promote the formation of a splenic abscess through effects on immune function and the microvasculature.[5] Contiguous spread occurs through microperforations and dissemination of microbes and tumors in the setting of malignancy. Immunosuppression compromises mucosal barriers and affects the innate capacity of the spleen to manage microbial intruders.[10]

When microbes spread hematogenously from primary sources, collections may occur in multiple spaces concurrently and are transferred to the spleen from adjacent gastrointestinal or thoracic cavity areas. An abscess may arise within a hematoma caused by trauma to vessels or parenchyma. Immune dysfunction, including alcoholism, cirrhosis, diabetes, and treatment with immunosuppressants, increases susceptibility to an abscess. Infectious disease may promote abscess formation. The splenic abscess identified in those with concurrent COVID-19 is postulated to emerge from a heightened inflammatory response, vein thrombosis, and as a consequence of the virulence of the infection.[20]

History and Physical

Fever is the most common presenting symptom of a splenic abscess, followed by abdominal pain, nausea, and vomiting. The triad of fever, left upper quadrant tenderness, and leukocytosis attributed to a splenic abscess is present in one-third of cases. The physical exam may reveal guarding in the left upper quadrant, a palpable abdominal mass, edema of the overlying soft tissues, costovertebral tenderness, splenomegaly, left basilar rales, and dullness at the left lung base.[10] Those with an aseptic abscess may present with fever, abdominal pain, weight loss, and skin lesions.[25]

Evaluation

Evaluating a suspected splenic abscess requires a combination of laboratory testing, radiographic imaging, and microbiologic studies to confirm the diagnosis and guide treatment. Blood cultures, general laboratory work, and imaging are critical components of the diagnostic process. Hematogenous dissemination often leads to multiple abscess collections, and cultures from blood or other abscesses can help guide therapy. Laboratory markers such as leukocytosis with a left shift, elevated C-reactive protein, erythrocyte sedimentation rate, and procalcitonin are commonly elevated but nonspecific. These markers are useful for assessing infection severity and monitoring treatment response.

Radiographic imaging provides more definitive diagnostic information. CT with contrast is the gold standard, revealing a hypodense collection with rim enhancement and providing information about surrounding structures.[19][30] If CT is inconclusive, magnetic resonance imaging may be useful, particularly when contrast is contraindicated. Ultrasound can be used as an initial screening tool or in resource-limited settings, showing an anechoic mass with irregular walls and moderate distal enhancement.[1][2][31] Additionally, ultrasound-guided aspiration can confirm the diagnosis and provide material for culture to improve targeted antimicrobial therapy. Plain radiographs may show secondary findings such as left pleural effusion, left diaphragmatic elevation, or fullness in the left upper quadrant.

If infective endocarditis is suspected, transthoracic or transesophageal echocardiography is warranted to evaluate for cardiac vegetations. Tuberculosis testing (eg, interferon-gamma release assay) should be considered in suspected tuberculosis cases, particularly in endemic regions or immunocompromised patients. Splenic abscess culture, when readily obtained via percutaneous aspiration, can significantly impact morbidity and mortality by guiding antibiotic selection.[19] Image-guided percutaneous drainage, particularly under CT or ultrasound guidance, can also serve a dual diagnostic and therapeutic role, expediting source control in appropriate cases.

Treatment / Management

Treatment for a splenic abscess is centered around source control using antimicrobial therapy, drainage, and, when needed, splenectomy. Early administration of antibiotics and drainage is important for splenic preservation. Admission is recommended for all patients with a splenic abscess. Broad-spectrum antibiotics are used initially while awaiting culture data and planning for intervention. Culture results then guide antibiotic selection.[14][32] Although historically, the gold standard for treating a splenic abscess has been splenectomy, study results have demonstrated the efficacy of less invasive approaches. Percutaneous aspiration may also be a safer option for patients with multiple risk factors that make them poor candidates for surgery. Drainage can be used as a bridge to surgery. Percutaneous aspiration is most successful when the abscess is unilocular or bilocular with a complete and thick wall without internal septations. Aspiration is easier when the abscess content is thin. Multiple or more viscous collections may not be amenable to a percutaneous approach. Likewise, poorly defined collections or those inaccessible percutaneously may require laparoscopic or open surgery for successful drainage. The surgical approach to drainage may be intraperitoneal, retroperitoneal, or transpleural.[4][16] (B3)

The patient's overall clinical condition, including medical comorbidities, should guide treatment. Antimicrobial therapy is prescribed per culture results. The median duration of antimicrobial therapy shown in the results of a retrospective study of persons with a splenic abscess was 45 days. Most persons in the study received multiple antimicrobials, including beta-lactam, vancomycin, fluoroquinolone, and metronidazole. Those whose cultures demonstrated yeast received an antifungal. In a retrospective study including 33 persons with a splenic abscess, several deteriorated clinically while on antimicrobial therapy, many of whom underwent subsequent splenectomy. A large number of persons with pancreatic etiology of their splenic abscess experience some treatment failure.[5][19] Immunocompromised individuals may be infected by atypical organisms, including opportunistic microbes such as Actinomyces, and often require splenectomy and prolonged antibiotics.[22](B2)

Percutaneous drainage is less likely to be successful in patients with a multilocular abscess, ill-defined cavities, necrotic debris, and viscous fluid. Contraindications for percutaneous drainage include multiple small abscesses; debris-filled, poorly defined, or difficult-to-access cavities; coagulopathy; and diffuse ascites. Pharmacologic treatment alone is generally not recommended if drainage is possible. Mortality rates of more than 50% have been reported in cases managed solely with antibiotics. Fungi, actinomycetes, or Mycobacterium should be considered in those who do not respond to antimicrobial therapy. Fungi respond well to antifungal treatment alone, but results from a study found that corticosteroid therapy could benefit this cohort. Splenectomy is required when conservative treatment is insufficient. Splenectomy can often be performed laparoscopically, and in certain cases, a partial splenectomy may be feasible. Laparoscopic splenectomy usually results in a shorter length of stay and less postoperative pain. Many surgical approaches have been described. Robotic splenectomy has not shown any improvement in patient outcomes over laparoscopic splenectomy.[19]

Individual clinical scenarios inform decision-making. A case is described of a young man with alcoholism who developed a splenic abscess in the setting of pancreatitis and pseudocysts impinging on the splenic vein, causing venous compression and thrombosis. He was not a candidate for splenectomy and underwent an endoscopic ultrasound-guided cystgastrostomy and embolization of the splenic artery.[33] Similarly, a patient with a splenic abscess secondary to a perforated duodenal ulcer underwent endoscopic-guided transgastric drainage.[34] The definitive treatment for those who develop a splenic abscess as a consequence of infective endocarditis often involves valve replacement.[23] (B3)

Treatment for those found to have an aseptic abscess consists of corticosteroids, anti-inflammatories, and immunosuppressants; monoclonal antibodies are also used, and relapse is common. Many diagnosed with an aseptic splenic abscess have a preexisting diagnosis of inflammatory bowel disease, although occasionally, the identification of a splenic abscess can precede the diagnosis. Abscesses typically resolve rapidly with corticosteroids. The anti-inflammatory colchicine is protective against recurrence. Splenectomy may be needed in cases of persistent recurrence.[24][25] In children, collections smaller than 3 cm are generally treated with intravenous antibiotics, often for 4 weeks. If nonresolving, ultrasound-guided drainage or splenectomy is performed. The efficacy of the antibiotic regimen is monitored with serial imaging.[17](B3)

Differential Diagnosis

Splenic abscesses arise from various infectious sources, including bacterial, parasitic, fungal, and mycobacterial. They are more common in immunocompromised individuals, including those with hematologic malignancies, those with a history of treatment with chemotherapeutics, intravenous drug abusers, and persons with acquired immune deficiency syndrome.[35][36] A splenic abscess often results from infections involving other organs, such as pneumonia, pneumothorax, empyema, pulmonary embolism, and nephroureterolithiasis. An abscess may also emerge from primary splenic diffuse large cell lymphoma.[6]

Pertinent Studies and Ongoing Trials

In a retrospective study on 474 patients with infective endocarditis, a splenic abscess was identified in 36 of these persons by CT, and many of these had splenic emboli. The concluding recommendation was to evaluate all persons with suspected splenic emboli for evidence of abscess.[37] Although the incidence of human immunodeficiency virus is declining, prevalence remains significant, and the etiology of a splenic abscess in this population can range from an opportunistic infection to malignancy, including tuberculosis, lymphoma, and an array of microbial sources.[8]

A cohort of adult persons diagnosed with aseptic abscess syndrome over nearly 20 years outlined an association with inflammatory bowel disease in 42% of cases. In this same study, relapse was reported to be 62%, most frequently within the same organ. Colchicine was found to be protective against relapse due to its effect on the migration of neutrophils.[25] A meta analysis of splenectomy versus image-guided drainage of splenic abscess demonstrated a mortality of 12% and a complication rate of 26% for splenectomy and a mortality of 8% and a complication rate of 10% for percutaneous drainage of a splenic abscess.[38]

A case is reported of a 71-year-old woman admitted with COVID-19 pneumonia and subsequently diagnosed with a splenic abscess. The authors note a significant increase in the incidence of related splenic abscesses. Further, they note that diagnosis may be delayed due to the clinical focus on pulmonary findings in a person with COVID-19.[20]

Prognosis

The prognosis of a person with a splenic abscess is markedly improved compared with earlier times. The availability of percutaneous CT-guided drainage offers a less invasive, clinically effective alternative to surgery. Laparoscopic splenectomy is now often used instead of open surgery, with faster recovery and shorter hospital stays.[2][19]

Complications

Complications of a splenic abscess include, but are not limited to, the following:

• Pneumothorax
• Hemorrhage
• Left-sided pleural effusion
• Splenic artery/vein thrombosis
• Subphrenic abscess
• Viscus perforation
• Pancreatic fistula
• Pancreatic duct injury
• Postsplenectomy thrombocytosis
• Pneumonia
• Adverse drug reaction