Splenic Abscess 

Abscesses of the spleen have been reported periodically since the time of Hippocrates. He postulated that 1 of 3 courses was followed by a patient with a splenic abscess: (1) the patient might die; (2) the abscess might heal; or (3) the abscess might become chronic and the patient may live with the disease.^[1]

Splenic abscess is a rare entity, with a reported frequency of 0.05-0.7%.^{[2, 3]} Its reported mortality rate is still high, up to 47%, and can potentially reach 100% among patients who do not receive antibiotic treatment.^[4] Appropriate management can decrease the mortality to less than 10%.^[5]

The timely and widespread use of imaging methods (eg, computed tomography [CT] scanning, ultrasonography) facilitates early diagnosis and guides treatment, thus improving the prognosis.^[6]

Frequency

Published autopsy statistics suggest that splenic abscess is rare (0.05-0.7%); the incidence may depend on the study population.^{[2, 3]} For example, the incidence of splenic abscesses in Denmark was 0.056% per 1000 somatic hospital discharges per year or 0.0049% per year of all hospital deaths.^[3]

The literature suggests a wide variability of causative pathogens, demography, and clinical material.^[2]

Splenic abscesses have diverse etiologies.^[7] The most common is hematogenous spread originating from an infective focus elsewhere in the body. Infective endocarditis, a condition associated with systemic embolization in 22-50% of cases, has a 10-20% incidence of associated splenic abscess.^[8] Other infective sources include typhoid, paratyphoid, malaria, urinary tract infection, pneumonias, osteomyelitis, otitis, mastoiditis, and pelvic infections. Pancreatic, other retroperitoneal, and subphrenic abscesses, as well as diverticulitis, may contiguously involve the spleen. Splenic trauma is another well-recognized etiologic factor. Splenic infarction resulting from systemic disorders (see the image below), such as hemoglobinopathies (especially sickle cell disease), leukemia, polycythemia, or vasculitis, can become infected and evolve into splenic abscesses.^{[2, 4, 9, 10, 11, 12, 13, 14]}

Alcoholics, diabetics, and patients who are immunosuppressed are among the most susceptible to splenic abscesses.^{[6, 12]}

Splenic abscesses occur in a variety of clinical scenarios, as shown in the images below. Published studies suggest that preexisting splenic tissue injury and bacteremia are required to form a basis for an abscess.^{[2, 15]}

Published scenarios are grouped below:

• Hematogenous embolization to a previously normal spleen - Typical examples include patients with septic endocarditis who have abused IV drugs and patients undergoing chemotherapy who develop fungemia, resulting in a splenic abscess. Typically, patients in this category either are immunosuppressed or have an overwhelming bacteremia. This group of patients is expected to expand and include analogous groups from the domains of transplantation and HIV/AIDS.
• Hematogenous spread in the presence of previously altered splenic architecture - This group includes patients with single splenic infarcts (from trauma) or multiple splenic infarcts (from sickle cell disease or vasculitis). Bacteremia from an intercurrent infection (eg, pneumonia, cholecystitis, central line sepsis) can colonize a splenic avascular area and form an abscess, as depicted in the image below.
• Contiguous spread - This includes direct involvement from a pancreatic abscess, gastric or colonic perforations, or subphrenic abscesses.

Microbiology

• Aerobes (in most published cases)

  • Gram-positive cocci -Streptococcus, Staphylococcus, Enterococcus (predominant in most reports)
  • Gram-negative bacilli -Escherichia coli, Klebsiella pneumoniae, Proteus,Pseudomonas species, Salmonella species (occasionally predominant)
• Anaerobes -Peptostreptococcus, Bacteroides, Fusobacterium,Clostridium, Propionibacterium acnes
• Polymicrobial (up to 50% of cases)
• Fungal -Candida
• Unusual flora -Burkholderia pseudomallei (occasionally reported in melioidosis), actinomycotic and mycobacterial abscesses, most typically seen in immunosuppressed patients.^[5]

The history and physical examination are not sufficiently reliable to make the diagnosis of splenic abscess. However, information derived from the history and physical examination can suggest this diagnosis. Therefore, the clinician must maintain a high index of suspicion, particularly in the above-listed higher risk clinical scenarios and patient groups.^[16]

History

The signs and symptoms of splenic abscess have been well described but are not very specific. Therefore, splenic abscess remains a substantial diagnostic challenge. The classical triad of fever, left upper quadrant pain, and splenomegaly is seen in only about one third of patients.

The symptoms of splenic abscess can be variable and depend on the location, size, and progression of the process. They can also be acute, subacute, or chronic. Deep-seated, small abscesses can be painless and accompanied by septic symptoms.^[17]

• Fever (>90%) can be moderate, continuous, intermittent, or even absent.
• Abdominal pain (>60%) typically occurs suddenly, with a punctum maximum in the left hypochondrium (>39%). Remember that pain usually signifies perisplenitis.^[18]
• Involvement of the diaphragmatic pleura can cause shoulder pain. The associated eponym is the Kehr sign, although there is no clear demonstration that Kehr either described it or suffered from it.
• Pleuritic chest pain around the left lung base (>15%) is aggravated by coughing or forced expiration.
• General malaise and other constitutional and dyspeptic symptoms can be included, all of which can also be seen in a variety of other septic conditions.

Physical examination 

• Abdominal tenderness (>50%) may or may not be accompanied by muscle guarding in the left upper quadrant. There may be edema of the soft tissues overlying the spleen. Costovertebral tenderness may also be noted.
• Splenomegaly (< 50%) is less frequently observed, probably because of early diagnosis resulting from the widespread use of imaging methods.
• Chest findings are nonspecific and reportedly include dullness at the left lung base (>30%), left basilar rales (>21%), or elevation of the left hemidiaphragm (>15%).

Once the diagnosis of a splenic abscess has been made, the patient must be admitted to the hospital and treated. Treatment depends on the patient's overall condition, comorbidities, and primary disorder (if any), as well as the size and topography of the abscess.^[19]

Empiric broad-spectrum antibiotics have a primary role in the initial management of splenic abscesses. The success of antibiotic therapy is not affected by the presence of multiple abscesses or by a polymicrobial flora. The choice of antibiotics is tailored to the culture results.

Percutaneous drainage has gained acceptance as an effective and less invasive treatment method than surgical intervention in selected patients. The reported success rate of percutaneous drainage is 67-100%. Such drainage preserves the spleen and avoids the risk of overwhelming postsplenectomy infections. Percutaneous drainage can also be used as a bridge to elective surgery in patients who are clinically unstable or in patients who have multiple comorbidities.

Percutaneous drainage is likely to be useful in patients who have unilocular or bilocular collections and if the character of the abscess content permits a minimally invasive drainage. Multilocular abscesses, ill-defined cavities, septations, and necrotic debris typically do not respond to percutaneous drainage.

Surgery is reserved for patients who are stable and not amenable to percutaneous drainage. Depending on available expertise, laparoscopic or open procedures can be considered.

The normal adult spleen weighs up to 150 grams, measures 4 x 7 x 11 cm, and represents the largest single accumulation of lymphoid tissue in the body. The spleen lies beneath the left hemidiaphragm and is attached to the stomach, left kidney, and diaphragm by the gastrosplenic, lienorenal, and phrenolienal ligaments. The gastrosplenic ligament contains the short gastric vessels, which can be injured easily during interventions in the area.

Anomalies of the spleen must always be considered, including wandering spleen, polysplenia, asplenia, or accessory spleen. Accessory spleen is the most common of the splenic anomalies (>1% of all patients). Solitary or multiple accessory spleens can be found in the splenic hilum, pancreas, lesser sac, retroperitoneum, liver, or gut mesentery.

The size and location of a splenic abscess determines its relationship with the surrounding organs and the possible routes for extension or fistulization. Small solitary or multiple abscesses tend to remain contained by the splenic capsule. Advanced abscesses in the spleen's upper pole can fistulize into the pleura. Abscesses originating from the lower pole can involve the splenic flexure and communicate with the colonic lumen. The stomach and pancreas can be affected in an analogous way.^[20]

Contraindications to percutaneous drainage include the following^{[6, 11, 19]} :

• Multiloculated or debris-filled abscess
• Multiple small abscesses
• Uncontrollable coagulopathy
• Poorly defined abscess on CT scan or ultrasonogram
• Diffuse ascites
• No safe route for drainage

Relative contraindications to percutaneous drainage include the following:

• Splenic abscesses secondary to spread from a contiguous process, such as other large primary abscesses (eg, pancreatitis, perforated colon cancer) that cannot be eradicated by this method
• Abscess rupture
• A phlegmonous or poorly characterized lesion on CT scan or ultrasonogram