Medscape is available in 5 Language Editions – Choose your Edition here.


Splenic Infarct Treatment & Management

  • Author: Manish Parikh, MD; Chief Editor: John Geibel, MD, DSc, MSc, MA  more...
Updated: Dec 16, 2015

Approach Considerations

The indications that warrant surgical intervention include hematologic complications for the underlying disease process and persistent symptoms, such as sepsis, abscess, hemorrhage, or persistent pseudocyst formation.

Analysis of operative indications in the series of Nores et al revealed that patients with hematologic conditions were typically explored for complications of those conditions (69%), especially patients with nonmalignant conditions (90%), whereas patients with hematologic malignancies often (47%) underwent surgery for acute symptoms.[11] Complications of splenic infarction were a frequent indication (60%) for operation in patients with septic emboli.[11]

Pseudocysts usually are the result of prior trauma, with organization and liquefaction of the resultant hematoma, surrounded by a fibrous pseudocapsule. Small, asymptomatic pseudocysts (<4 cm) usually regress with time, whereas larger splenic cysts (>5 cm) require treatment because the risk of rupture can be as high as 25%.[22]

Splenic abscess can result from septic emboli or superinfection of a prior infarct. These have been managed traditionally by splenectomy, which can be technically challenging due to the intense surrounding inflammation and because of the scar tissue that surrounds the abscess. Indwelling percutaneous catheter drainage and appropriate antibiotic therapy can be used to treat selected cases of well-formed, unilocular abscesses.

An asymptomatic infarct without complication does not require surgical intervention. In fact, overall, most splenic infarcts do not require surgical intervention.


Medical Therapy

Surgery is indicated only in the presence of complications. Otherwise, the infarcted spleen can be left in situ, and the patient can be observed. Because of the rarity of this disorder and the largely anecdotal character of many reports, the roles of antibiotics and antiplatelet agents (for the treatment of thrombocytosis) have not been formally addressed. Similarly, no scientifically supported information exists regarding the possible increase in susceptibility to overwhelming postsplenectomy sepsis (OPSS) in these patients.

The principal mainstay of nonoperative therapy is analgesia with either narcotics or nonsteroidal anti-inflammatory drugs (NSAIDs) and close follow-up. Many of the altitude-related episodes in patients with sickle cell disease can be safely treated with supportive care rather than with splenectomy.[3] In certain circumstances, isolated splenic abscess can be treated with percutaneous drainage alone, and splenectomy can be avoided. However, a patient with multiple splenic abscesses usually will require splenectomy.


Surgical Therapy

For an infarcted spleen with any of the above-mentioned complications, splenectomy is required. Because of the (admittedly small) risk of fatal OPSS, splenic preservation is preferable whenever possible.

In cases of torsion of a wandering spleen, splenopexy with splenic salvage is the procedure of choice in the well-perfused, noninfarcted spleen. Techniques include suturing the spleen to the surrounding structures, wrapping the organ in omentum or mesh prior to suture fixation, or placing it in a surgically created retroperitoneal pouch. This has been reported laparoscopically.[23]

Complications, such as bleeding or pseudocyst formation, also may be amenable to splenic salvage using techniques of partial splenectomy.

Whereas a unilocular abscess can be managed successfully in select cases with percutaneous catheter drainage, some authors advocate splenectomy in all cases of splenic infarct and abscess, questioning the utility of preserving the residual, partially functioning spleen. This may be accomplished by using traditional open techniques or with laparoscopic techniques.

Perisplenic inflammation and dense adhesions can make splenectomy difficult. Another choice is to perform preoperative splenic artery embolization; this purposely infarcts the remaining spleen and minimizes blood loss, which otherwise can be quite profuse in these difficult dissections. Intraoperative ligation of the splenic artery at the superior margin of the pancreas in the lesser sac is another alternative to minimize blood loss if the spleen is enlarged.

Preparation for surgery

The choice of preoperative antibiotics should be guided by the patient's clinical status and associated comorbidities. A first-generation cephalosporin usually is adequate.

Appropriate preoperative hydration is essential in anticipation of potential blood loss.

If splenectomy (rather than splenic preservation) is planned, the patient should receive the pneumococcal and Haemophilusinfluenzae vaccine at least 2 weeks prior to the operation, if feasible.

Neoadjuvant chemotherapy in patients with hematologic malignancies (eg, chronic myeloid leukemia) can reduce spleen size and potentially increase the safety of the procedure.

Preoperative sequential compression devices and subcutaneous heparin can be used for deep vein thrombosis (DVT) prophylaxis.

Procedural details

The approach (eg, laparoscopy, midline laparotomy, or left subcostal incision) is determined by the underlying pathology/clinical scenario, as well as by the surgeon's preference. The presence of splenic infarct (or abscess) is not per se a contraindication for laparoscopy. Generally, the laparoscopic approach is contraindicated in emergency situations, such as hemorrhagic shock and spontaneous rupture. The surgeon's experience determines the point at which the enlarged spleen is too large to remove laparoscopically.

Because of the risk of lifelong susceptibility to infectious complications after splenectomy (particularly the rare but highly fatal OPSS), laparoscopic or open partial splenectomy should be attempted when feasible. Laparoscopic spleen-preserving distal pancreatectomy, with or without splenic-vessel preservation, has yielded promising results.[24]

Laparoscopic approach

For the laparoscopic approach, patient position is key to the success of this operation. Choices include the "hanging spleen" technique, in which the patient is in the lateral decubitus position (as described for laparoscopic adrenalectomy). Another option is the "leaning spleen" technique, in which the patient is at a 45º tilt. Both methods require a beanbag or jelly roll positioning pad. Once pneumoperitoneum is established, the splenocolic ligament is usually divided with ultrasonic shears. Next, the lesser sac is entered, and the short gastric vessels are divided.

If the surgeon prefers to "preligate," the splenic artery can be dissected along the superior border of the pancreas and divided with the vascular stapler. Otherwise, if feasible, the splenic vein and artery are exposed first and are dissected 1 cm proximal to the hilum, and they are usually divided with the vascular stapler. Then, the remainder of the spleen is released by dividing the peritoneal attachments with the ultrasonic scalpel.

In other scenarios, the attachments are divided first and the spleen is rolled anteriorly to expose the tail of the pancreas and the hilar vessels posteriorly. These vessels are then transected with the laparoscopic vascular stapler. The spleen is placed into an EndoCatch bag and is morcellated and extracted through the largest trocar site.

Other laparoscopic approaches are the supine approach (with set-up similar to laparoscopic Nissen fundoplication) and the hand-assisted approach. Laparoscopic partial splenectomy also has been described, including for splenic abscess, using the ultrasonic scalpel or radiofrequency ablation for parenchymal division.[25, 26]

Open approach

For the open approach, a standard midline incision or left subcostal incision (with possible Kehr extension up to the xiphocostal junction) may be used. Placing a large roll under the left flank often aids in exposure.

Usually, the gastrocolic ligament is opened outside the gastroepiploic arcade and the splenic artery is identified along the superior border of the pancreas and then ligated. Next, the spleen is completely mobilized by dividing the avascular splenophrenic and splenorenal ligaments. The splenocolic ligament is divided, and the spleen is mobilized into the wound. The tail of the pancreas is separated from the splenic artery and vein, the splenic vessels are ligated, and the spleen is extracted.

There are several techniques described for splenic repair.[22] The critical intraoperative maneuver regarding intraoperative splenic salvage entails fully mobilizing the spleen into the wound; this requires the division of one or two of the short gastric vessels combined with gentle dissection posteriorly, so that the capsule is not torn in the mobilization process.[16]

The use of postoperative drainage depends on the operative findings, including the presence of a frank abscess, and the proximity of the dissection to the pancreatic tail. The authors' preference is for closed suction drainage to be placed in the splenic bed, with early removal (ie, within 24 hours). There is some evidence that the routine use of drainage of the splenic bed in the absence of extrasplenic abscess or pancreatic injury is associated with an increased risk of local infection.

If concern exists regarding possible impingement upon the gastric wall during short gastric vessel division, a nasogastric tube may be left in place.


Postoperative Care

Following splenectomy or global infarct, administer pneumococcal vaccine and vaccine against Haemophilus (if not given preoperatively).

Postoperative thrombocytosis occurs frequently. Antiplatelet therapy is initiated for platelet counts higher than 1,000,000/μL. However, antiplatelet therapy is controversial in this circumstance, and its benefit has not been demonstrated with a randomized, prospective, controlled trial.

The authors' current preferences for DVT prophylaxis are the use of sequential compression devices prior to incision and the postoperative employment of early ambulation and subcutaneous heparin.

Postoperative pain management may include IV patient-controlled analgesia and possible epidural analgesia for cases requiring laparotomy.



Pulmonary complications (eg, pneumonia, atelectasis) were the most frequent complication (20%) in the series reported by Nores et al.[11] With the current trend toward a laparoscopic approach to splenectomy and partial splenectomy, this complication rate should be significantly reduced.

Postoperative abscess, fever, and wound infection constitute the second most common category of complications (~10%). The first line of treatment is radiologically guided percutaneous drainage and antibiotics. A missed injury to a viscus (eg, stomach or colon) should be ruled out.

Hemorrhage, though relatively infrequent, can follow splenectomy as a consequence of the intense perisplenic inflammation.

Because of the intimate association of the pancreatic tail and the splenic hilum, pancreatic injury can occur, especially in the setting of intense inflammation and/or abscess. The majority of these injuries resolve with nonoperative management, which includes wide drainage, the use of a somatostatin analogue to decrease exocrine pancreatic function, and either total parenteral nutrition (TPN) or enteral alimentation distal to the ligament of Treitz.

As a consequence of the intense inflammatory reaction that can accompany splenic abscess, dissection of the spleen from the greater curvature of the stomach can be difficult, and inadvertent, unrecognized injuries to the greater curve of the stomach do occur. With adequate external drainage and with no obstruction to normal gastric emptying, these can be treated expectantly with TPN or distal luminal alimentation and nasogastric tube decompression.

OPSS is the most serious postsplenectomy complication; it occurs rarely (0.5%) in adult patients but carries a prohibitive mortality in unvaccinated patients. For this reason, a trend away from splenectomy and toward splenic conservation has emerged.


Long-Term Monitoring

Follow-up is directed by the underlying cause of the infarction or abscess rather than by the absence of the spleen. Patients undergoing nonoperative management of splenic infarct, particularly a large infarct (when there is a concern that it will rupture), should be followed closely, with a low threshold for serial imaging.

Contributor Information and Disclosures

Manish Parikh, MD Assistant Professor of Surgery, Department of Surgery, New York University School of Medicine; Attending Surgeon, Director Laparoscopic and Bariatric Surgery, Bellevue Hospital

Manish Parikh, MD is a member of the following medical societies: Alpha Omega Alpha, American College of Surgeons, Society of American Gastrointestinal and Endoscopic Surgeons

Disclosure: Nothing to disclose.


H Leon Pachter, MD, FACS Chair, George David Stewart Professor, Department of Surgery, New York University Medical Center

H Leon Pachter, MD, FACS is a member of the following medical societies: American Association for the Surgery of Trauma, American College of Surgeons, American Surgical Association, American Trauma Society, New York Academy of Sciences, Society for Surgery of the Alimentary Tract, Society of Critical Care Medicine

Disclosure: Nothing to disclose.

Specialty Editor Board

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Received salary from Medscape for employment. for: Medscape.

Amy L Friedman, MD Professor of Surgery, Director of Transplantation, State University of New York Upstate Medical University College of Medicine, Syracuse

Amy L Friedman, MD is a member of the following medical societies: Association for Academic Surgery, International College of Surgeons, New York Academy of Sciences, Pennsylvania Medical Society, Philadelphia County Medical Society, Society of Critical Care Medicine, Association of Women Surgeons, International Liver Transplantation Society, Transplantation Society, American College of Surgeons, American Medical Association, American Medical Womens Association, American Society for Artificial Internal Organs, American Society of Transplant Surgeons, American Society of Transplantation

Disclosure: Nothing to disclose.

Chief Editor

John Geibel, MD, DSc, MSc, MA Vice Chair and Professor, Department of Surgery, Section of Gastrointestinal Medicine, and Department of Cellular and Molecular Physiology, Yale University School of Medicine; Director, Surgical Research, Department of Surgery, Yale-New Haven Hospital; American Gastroenterological Association Fellow

John Geibel, MD, DSc, MSc, MA is a member of the following medical societies: American Gastroenterological Association, American Physiological Society, American Society of Nephrology, Association for Academic Surgery, International Society of Nephrology, New York Academy of Sciences, Society for Surgery of the Alimentary Tract

Disclosure: Received royalty from AMGEN for consulting; Received ownership interest from Ardelyx for consulting.

Additional Contributors

Lewis J Kaplan, MD, FACS, FCCM, FCCP Associate Professor of Surgery, Division of Trauma, Surgical Critical Care, and Emergency Surgery, Perelman School of Medicine, University of Pennsylvania; Section Chief, Surgical Critical Care, Philadelphia Veterans Affairs Medical Center

Lewis J Kaplan, MD, FACS, FCCM, FCCP is a member of the following medical societies: American Association for the Surgery of Trauma, American College of Surgeons, Association for Academic Surgery, Association for Surgical Education, Connecticut State Medical Society, Eastern Association for the Surgery of Trauma, International Trauma Anesthesia and Critical Care Society, Society for the Advancement of Blood Management, Society of Critical Care Medicine, Surgical Infection Society

Disclosure: Nothing to disclose.


We wish to thank Amber A Guth, MD, FACS, Associate Professor, Department of Surgery, New York University Clinical Cancer Center, New York University School of Medicine, for her contribution to this article.

  1. Ebert EC, Nagar M, Hagspiel KD. Gastrointestinal and hepatic complications of sickle cell disease. Clin Gastroenterol Hepatol. 2010 Mar 4. [Medline].

  2. Franklin QJ, Compeggie M. Splenic syndrome in sickle cell trait: four case presentations and a review of the literature. Mil Med. 1999 Mar. 164(3):230-3. [Medline].

  3. Sheikha A. Splenic syndrome in patients at high altitude with unrecognized sickle cell trait: splenectomy is often unnecessary. Can J Surg. 2005 Oct. 48(5):377-81. [Medline]. [Full Text].

  4. O'Keefe JH Jr, Holmes DR Jr, Schaff HV, et al. Thromboembolic splenic infarction. Mayo Clin Proc. 1986 Dec. 61(12):967-72. [Medline].

  5. Ting W, Silverman NA, Arzouman DA, et al. Splenic septic emboli in endocarditis. Circulation. 1990 Nov. 82(5 Suppl):IV105-9. [Medline].

  6. Yu LK, Hsu CW, Tseng JH, et al. Splenic infarction complicated by splenic artery occlusion after N-butyl-2-cyanoacrylate injection for gastric varices: case report. Gastrointest Endosc. 2005 Feb. 61(2):343-5. [Medline].

  7. Olson JF, Steuber CP, Hawkins E, et al. Functional deficiency of protein C associated with mesenteric venous thrombosis and splenic infarction. Am J Pediatr Hematol Oncol. 1991 Summer. 13(2):168-71. [Medline].

  8. Torda A. Postpartum toxic shock syndrome associated with multiple splenic infarcts. Med J Aust. 2005. 182:93. [Medline]. [Full Text].

  9. Gupta BK, Sharma K, Nayak KC, et al. A case series of splenic infarction during acute malaria in northwest Rajasthan, India. Trans R Soc Trop Med Hyg. 2010 Jan. 104(1):81-3. [Medline].

  10. Desai DC, Hebra A, Davidoff AM. Wandering spleen: a challenging diagnosis. South Med J. 1997 Apr. 90(4):439-43. [Medline].

  11. Nores M, Phillips EH, Morgenstern L. The clinical spectrum of splenic infarction. Am Surg. 1998 Feb. 64(2):182-8. [Medline].

  12. Hayashi H, Beppu T, Okabe K, et al. Risk factors for complications after partial splenic embolization for liver cirrhosis. Br J Surg. 2008 Jun. 95(6):744-50. [Medline].

  13. Wu SC, Chen RJ, Yang AD, et al. Complications associated with embolization in the treatment of blunt splenic injury. World J Surg. 2008 Mar. 32(3):476-82. [Medline].

  14. Jaroch MT, Broughan TA, Hermann RE. The natural history of splenic infarction. Surgery. 1986 Oct. 100(4):743-50. [Medline].

  15. Joshi SC, Pant I, Shukla AN, et al. Splenic infarct as a diagnostic pitfall in radiology. J Cancer Res Ther. 2008 Apr-Jun. 4(2):99-101. [Medline].

  16. Pachter HL, Guth AA, Hofstetter SR. Changing patterns in the management of splenic trauma: the impact of nonoperative management. Ann Surg. 1998 May. 227(5):708-17; discussion 717-9. [Medline]. [Full Text].

  17. Antopolsky M, Hiller N, Salameh S, et al. Splenic infarction: 10 years of experience. Am J Emerg Med. 2009 Mar. 27(3):262-5. [Medline].

  18. Urban BA, Fishman EK. Helical CT of the spleen. AJR Am J Roentgenol. 1998 Apr. 170(4):997-1003. [Medline]. [Full Text].

  19. Balcar I, Seltzer SE, Davis S. CT patterns of splenic infarction: a clinical and experimental study. Radiology. 1984 Jun. 151(3):723-9. [Medline]. [Full Text].

  20. Kluger Y, Paul DB, Townsend RN. Enhanced rim around infarcted, traumatized spleen on computed tomographic scans: case report. J Trauma. 1994 Mar. 36(3):436-7. [Medline].

  21. Goerg C, Schwerk WB. Splenic infarction: sonographic patterns, diagnosis, follow-up, and complications. Radiology. 1990 Mar. 174(3 Pt 1):803-7. [Medline]. [Full Text].

  22. Pachter HL, Hofstetter SR, Elkowitz A. Traumatic cysts of the spleen--the role of cystectomy and splenic preservation: experience with seven consecutive patients. J Trauma. 1993 Sep. 35(3):430-6. [Medline].

  23. Cavazos S, Ratzer ER, Fenoglio ME. Laparoscopic management of the wandering spleen. J Laparoendosc Adv Surg Tech A. 2004 Aug. 14(4):227-9. [Medline].

  24. Matsushima H, Kuroki T, Adachi T, Kitasato A, Hirabaru M, Hidaka M, et al. Laparoscopic spleen-preserving distal pancreatectomy with and without splenic vessel preservation: The role of the Warshaw procedure. Pancreatology. 2014 Sep 30. [Medline].

  25. De Greef E, Hoffman I, Topal B, et al. Partial laparoscopic splenectomy for splenic abscess because of Salmonella infection: a case report. J Pediatr Surg. 2008 May. 43(5):E35-8. [Medline].

  26. Héry G, Becmeur F, Méfat L, et al. Laparoscopic partial splenectomy: indications and results of a multicenter retrospective study. Surg Endosc. 2008 Jan. 22(1):45-9. [Medline].

Splenic infarct. Computed tomography scan of a 51-year-old man following a motor vehicle accident. American Association for the Surgery of Trauma (AAST) grade III splenic injury, with active extravasation of contrast from the splenic parenchyma (the white area along the medial aspect of the spleen).
Splenic infarct. Selective splenic arteriogram showing extravasation of contrast from the splenic artery at the splenic hilum prior to angioembolization (same patient as in the above image).
Computed tomography scan of the spleen 5 days after angioembolization of a bleeding splenic artery, showing partial splenic infarct (demonstrated by a lack of IV contrast enhancement of the lower pole of spleen). The patient experienced no adverse sequelae and fared well following his discharge to home 5 days after the embolization (same patient as in the above images).
All material on this website is protected by copyright, Copyright © 1994-2016 by WebMD LLC. This website also contains material copyrighted by 3rd parties.