OVERVIEW: What every practitioner needs to know

Are you sure your patient has a splenic abscess? What should you expect to find?

Key symptoms

  • Fever and other systemic symptoms are often the only symptoms of splenic abscess. Pain in the left upper quadrant, sometimes pleuritic in nature, and sometimes referred to the left shoulder may also be seen. Early satiety is another symptom that is noted occasionally.

Key physical findings

  • There are often no physical findings other than fever and systemic signs of infection. Splenomegaly may be present on exam in approximately 50% of cases and abdominal tenderness is similarly present approximately 50% of the time. Left-sided chest findings such as dullness, rales, or a rub at the base may be present. Less frequent signs include costovertebral angle tenderness, acscites, and hepatomegaly. A splenic rub may rarely occur.

How did the patient develop a splenic abscess? What was the primary source from which the infection spread?

  • Almost all splenic abscesses develop as a result of bacteremia (or fungemia) although a small percentage spread to the spleen from a contiguous site. Endocarditis is the most classic underlying condition that results in splenic abscess although urinary tract infection, surgical wound infections, and gastrointestinal infections that result in bacteremia also lead to splenic abscess.

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  • Splenic abscesses are uncommon and only several hundred have ever been reported in the medical literature. In autopsy series, the incidence has been between 0.2% and 0.7%. In one series of 540 intra-abdominal abscesses, none were in the spleen.

Which individuals are at greater risk of developing splenic abscess?

  • Bacteremia is the most common predisposing risk factor. Classically, endocarditis is associated with splenic abscess but any cause of bacteremia, ranging from typhoid fever, to line infection, to urinary tract infection, may result in splenic abscess.

  • Abnormalities of the spleen, either primary or secondary, are risk factors. For example, splenic trauma, accidental or medically induced, accounts for as many as 30% of splenic abscesses, although in more recent series, trauma is less frequently a predisposing factor.

  • Felty syndrome and amyloidosis predispose to splenic abscess. Other factors include hemoglobinopathies, intravenous drug use, and diabetes mellitus.

  • The frequency of immunosuppression, particularly human immunodeficiency virus (HIV) infection but also cancer chemotherapy and steroid use, as a predisposing factor in splenic abscess appears to be increasing and appears to be present in nearly a third of cases.

Beware: there are other diseases that can mimic splenic abscess:

  • Tumors, splenic infarction, or hematoma can mimic splenic abscess clinically and on imaging studies.

What laboratory studies should you order and what should you expect to find?

Results consistent with the diagnosis

  • Leukocytosis is present in the majority of patients.

  • No serum laboratory tests are helpful in the diagnosis of splenic abscess.

Results that confirm the diagnosis

  • Blood cultures have been reported positive in 24% to 60% of cases.

  • Other fluid cultures, polymerase chain reaction assays, etc. may be helpful.

  • Abscess fluid cultured at surgery or percutaneously is diagnostic.

What imaging studies will be helpful in making or excluding the diagnosis of splenic abscess?

  • Ultrasonography is the single most useful imaging modality. It is relatively inexpensive, can be performed at the bedside or in the field, and is quite sensitive (ranging from 70% to over 90% in various series). Demonstration of an area of decreased echodensity is consistent with an abscess. High resolution ultrasound can detect microabscesses. The size, architecture, and number of abscesses can be identified and ultrasonography is often used in conjunction with percutaneous drainage procedures.

  • Computed tomography (CT) scan is the most sensitive modality with greater than 90% sensitivity in most series. Splenic abscesses are often noted on CT scans used to elucidate a source of fever or looking generally for occult abdominal infection.

  • There is less experience with magnetic resonance imaging scans in the diagnosis of splenic abscess although it is probably similar in sensitivity to CT. However, it is more cumbersome, more expensive, less easily coupled to a drainage procedure, and would therefore appear to offer no advantage over CT or ultrasonography.

  • Radionuclide scans (such as Tc99 liver-spleen scans) were frequently used in the past, but are no longer considered useful in comparison to other modalities.

What consult service or services would be helpful for making the diagnosis and assisting with treatment?

General surgery and infectious diseases consults would be helpful.

If you decide the patient has splenic abscess, what therapies should you initiate immediately?

Key principles of therapy

Untreated, splenic abscess is nearly always fatal. Splenectomy is the standard treatment for splenic abscess and is certainly the treatment against which other therapies need to be measured. Splenectomy can be performed laparoscopically in many patients. Antimicrobials are used to treat underlying bacteremia or fungemia, to control sepsis, and stabilize the patient for surgery or percutaneous drainage. For pyogenic splenic abscesses, the mortality in those treated with antibiotics alone approaches 50%. For certain pathogens, however, such as fungi and mycobacteria, antimicrobials may be the sole therapy.

1. Anti-infective agents

If I am not sure what pathogen is causing the infection, what anti-infective should I order?

Empirical broad-spectrum antibiotic therapy should be initiated as soon as splenic abscess is suspected while awaiting surgical or percutaneous drainage. Empirical therapy should be active against staphylococci, streptococci, and gram-negative aerobic bacilli. For example, administer vancomycin 1g every 12 hours plus a third-generation cephalosporin such as ceftriaxone 1 to 2g every 12 hours.

Antimicrobial therapy for common causes of splenic abscess is summarized in
Table I. Note that therapy is adjunctive to definitive drainage procedure. Also, therapy needs to be directed to underlying cause of abscess, e.g. bacterial endocarditis or peritonitis.

Table I.
Organism Antibiotic Dose Situation
Streptococci (PCN MIC <0.1μg/mL) PenicillinCeftriaxoneCefotaxime 20–24 million units daily (divided every 4 hours)2–4g daily (divided every 12 hours)12g daily (divided every 6 hours) Most often secondary to bacterial endocarditis
Streptococcus pneumoniae (MIC >0.1μg/mL) Vancomycin ± rifampicin 2g daily (divided every 12 hours)1,200mg daily (divided every 12 hours)
Staphylococcus aureus Oxacillin 12g daily (divided every 4 hours) Most often secondary to bacterial endocarditis
Methicillin-resistant S. aureus Vancomycin 2g daily (divided every 12 hours)
Aerobic gram-negative rods CeftriaxoneCefotaxime 2–4g daily (divided every 12 hours)12g daily (divided every 6 hours) Secondary to urinary tract infection or peritonitis
Burkholderia pseudomallei Ceftazidime 8g daily (divided every 6 hours) Frequent cause in Southeast Asia

MIC, minimum inhibitory concentration; PCN, penicillin.

2. Other key therapeutic modalities

What other therapies are helpful for reducing complications?

  • Splenectomy is the mainstay of therapy although increasingly percutaneous drainage of abscess is being used. In either case, adjunctive antibiotics should be directed at the pathogens found at drainage. Percutaneous drainage rather than splenectomy is more successful for smaller (i.e. <4cm) and unilocular abscess. Historically, its initial use was in those patients thought unable to tolerate an open surgical procedure, but several series have shown that CT and ultrasound-guided percutaneous aspiration have success rates comparable with open surgical splenectomy with less initial morbidity and mortality.

  • Microabscesses can be accessed by percutaneous fine needle aspiration under CT or ultrasound guidance. In HIV-infected patients, in whom fungal or mycobacterial abscesses may be more frequent, this may be the preferred initial approach. Abscesses due to these pathogens are usually treated without drainage with antimycobacterial or antifungal drugs (see Table I).

What complications could arise as a consequence of splenic abscess?

What should you tell the family about the patient's prognosis?

  • Untreated splenic abscess is nearly always fatal. Treatment of pyogenic splenic abscess with antibiotics alone carries approximately 50% mortality. Combined with adjunctive antibiotics, surgical splenectomy or percutaneous drainage are successful in more than 90% of cases. The underlying diseases associated with splenic abscess, including those associated with immunosuppression, still carry considerable morbidity and mortality.

  • Removal of the spleen is associated with an increased risk of sepsis due to encapsulated bacteria, such as Neisseria meningitidis, Streptococcus pneumoniae, and Haemophilus influenzae, and with intraerythrocytic parasites, such as Plasmodium spp. and Babesia.

How do you contract a splenic abscess and how frequent is this disease?

Splenic abscesses are not common; however, the incidence may be increasing with intravenous drug use, immunocompromising drugs and conditions, and perhaps because of better detection. They are usually associated with another condition, including bacterial endocarditis, bacteremia, infection in an adjacent structure such as the peritoneum, immunocompromise, or splenic abnormalities.

What pathogens are responsible for this disease?

Bacterial

  • Streptococci, especially those causing endocarditis, also group A Streptococcus

  • Staphylococci, especially Staphylococcus aureus

  • Salmonellae, Pseudomonas, Escherichia coli, Enterococcus spp., Klebsiella spp., and Proteus spp

  • Occasionally anaerobic bacteria, especially in association with peritonitis

  • Burkholderia pseudomallei is a frequent cause in Southeast Asia

Tuberculous

Mycobacterial species, including both Mycobacterium tuberculosis and atypical mycobacteria (especially in association with immunosuppressive conditions such as HIV infection). The proportion of splenic abscesses due to mycobacteria has increased in recent series.

Fungal

Fungi are present in 7.1% to 25.8% of splenic abscesses in different series. The most common fungi are Candida.

How do these pathogens cause splenic abscess?

Almost all splenic abscesses develop as a result of bacteremia (or fungemia). A small percentage spread to the spleen from a contiguous site. Endocarditis is the most classic underlying condition that results in splenic abscess. Urinary tract infection, surgical wound infections, and gastrointestinal infections that result in bacteremia can also lead to splenic abscess.

What other clinical manifestations may help me to diagnose and manage splenic abscess?

History

Fever and other systemic symptoms are often the only symptoms of splenic abscess. Pain in the left upper quadrant, sometimes pleuritic in nature, and sometimes referred to the left shoulder may also be seen. Early satiety is another symptom that is noted occasionally.

Physical exam

There are often no physical findings other than fever and systemic signs of infection. Splenomegaly may be present on exam in approximately 50% of cases and abdominal tenderness similarly is present approximately 50% of the time. Left-sided chest findings such as dullness, rales, or a rub at the base may be present. Less frequent signs include costovertebral angle tenderness, ascites, and hepatomegaly. A splenic rub may rarely occur.

How can splenic abscess be prevented?

There are no prophylactic drugs that can be used and vaccines are not available.

WHAT'S THE EVIDENCE for specific management and treatment recommendations?

There are no published consensus guidelines for the treatment of splenic abscess. There are no prospective controlled trials of therapy for splenic abscess. All recommendations are based on published case series and expert opinion.

Buecker, A, Neuerburg, JM, Adam, GB. “MR-guided percutaneous drainage of abdominal fluid collections in combination with X-ray fluoroscopy: initial clinical experience”. Eur Radiol. vol. 11. 2001. pp. 670-4. (Series demonstrating ability to perform abscess drainage under magnetic resonance guidance and the relative usefulness of magnetic resonance for subphrenic locations.)

Ooi, LL, Leong, SS. “Splenic abscesses from 1987 to 1995”. Am J Surg. vol. 174. 1997. pp. 87-93. (287 cases reported between 1987 and 1995 demonstrating increasing rate in immunocompromised patients and intravenous drug users compared with earlier series.)

Madoff, LC, Mandell, GL, Bennett, JE, Dolin, R. “Splenic abscess”. Mandell, Douglas, and Bennett's Principles and Practice of Infectious Diseases. 2009. pp. 1055-7. (Textbook chapter reviewing splenic abscess.)

Lee, W-S, Choi, ST, Kim, KK. “Splenic abscess: a single institution study and review of the literature”. Yonsei Med J. vol. 52. 2011. pp. 288-92. (Recent series showing increasing incidence of immunocompromising conditions.)

Green, BT. ” Splenic abscess: report of six cases and review of the literature”. Am Surg. vol. 67. 2001. pp. 80-5. (Single institution study with useful literature review. All patients were successfully treated by either splenectomy or percutaneous drainage.)

Chun, CH, Raff, MJ, Contreras, L, Varghese, R, Waterman, N, Daffner, R, Melo, JC. “Splenic abscess”. Medicine (Baltimore). vol. 59. 1980. pp. 50-65. (Classic series including lengthy review of the early literature.)

Kang, M, Kalra, N, Gulati, M, Lal, A, Kochhar, R, Rajwanshi, A. “Image guided percutaneous splenic interventions”. Eur J Radiol. vol. 64. 2007. pp. 140-6. (A large series from India documenting the effectiveness of percutaneous aspiration and drainage of splenic lesions including bacterial, tuberculous, and malignant splenic processes.)

Tarantino, L, Giorgio, A, de Stefano, G, Farella, N, Perrotta, A, Esposito, F. “Disseminated mycobacterial infection in AIDS patients: abdominal US features and value of fine-needle aspiration biopsy of lymph nodes and spleen”. Abdom Imaging. vol. 28. 2003. pp. 602-8. (A small series (n=12) showing the high sensitivity of fine needle aspiration for diagnosis of mycobacterial splenic abscess in patients with HIV.)

Carbonell, AM, Kercher, KW, Matthews, BD, Joels, CS, Sing, RF, Heniford, BT. “Laparoscopic splenectomy for splenic abscess”. Surg Laparosc Endosc Percutan Tech. vol. 14. 2004. pp. 289-91. (A small series demonstrating the feasibility of laparoscopic splenectomy.)

Changchien, CS, Tsai, TL, Hu, TH, Chiou, SS, Kuo, C-H. “Sonographic patterns of splenic abscess: an analysis of 34 proven cases”. Abdom Imaging. vol. 27. 2002. pp. 739-45. (A series showing sonographic appearance of splenic abscesses and suggesting a poorer prognosis for multifocal abscesses.)

Sangchan, A, Mootsikapun, P, Mairiang, P. “Splenic abscess: clinical features, microbiologic finding, treatment and outcome”. J Med Assoc Thai. vol. 86. 2003. pp. 436-41. (Shows the high incidence of B. pseudomallei in splenic abscess in Thailand.)

Venkataramu, NK, Gupta, S, Sood, BP, Gulati, M, Rajawanshi, A, Gupta, SK, Suri, S. “Ultrasound guided fine needle aspiration biopsy of splenic lesions”. Br J Radiol. vol. 72. 1999. pp. 953-6. (One of the early studies of fine needle aspiration demonstrating ability of the technique to define etiologic diagnoses of splenic processes, both infectious and noninfectious.)

DRG CODES and expected length of stay

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