Splenic Abscess

Background
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]

Epidemiology
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]

Etiology
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]

Splenic infarct. Selective splenic

arteriogram showing extravasation of contrast from the splenic artery at the splenic hilum prior
to angioembolization.
Alcoholics, diabetics, and patients who are immunosuppressed are among the most susceptible to
splenic abscesses.[6, 12] . Rarely, splenic abscess can be caused by a parasitic infection such as
brucellosis[15] or umbilical catheterization in the newborn.[16]

athophysiology
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, 17]

This patient has a splenic abscess due

to pneumococcal bacteremia. Note that the massively enlarged spleen is readily visible, with
minimal retraction in the left upper quadrant.

Resected spleen (same as in the

above image) with abscesses caused by pneumococcal bacteremia. Note the discrete abscesses
adjacent to normal parenchyma.
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
See the list below:

Aerobes (in most published cases)

o

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]

Indications
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.[21]
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.
Early diagnosis and percutaneous drainage can increase the chance to preserve the spleen and,
hence, its immunologic function.[22]
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.