Splenic Infarct Workup

  • Author: Manish Parikh, MD; Chief Editor: John Geibel, MD, DSc, MA   more...
 
Updated: Apr 4, 2012
 

Laboratory Studies

  • No specific diagnostic laboratory studies for splenic infarction exist, although an elevated white blood cell count is not infrequent.
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Imaging Studies

  • A CT scan, performed with intravenous, nonionic contrast, is the current diagnostic modality of choice. Prior to the CT scan era, diagnosis of splenic infarct was made most commonly at laparotomy for intra-abdominal catastrophe or on postmortem examination.
  • Magnetic resonance imaging (MRI), preferably performed with intravenous gadolinium contrast, is another useful modality that clearly identifies infarcted splenic parenchyma. Contrast-enhanced MRI and multidetector CT scanning allow 3-dimensional reconstructions in any plane (coronal, sagittal, or axial) to better visualize the classic appearance of wedge-shaped infarctions within the spleen.
  • Due to the dual blood supply of the spleen, contrast-enhanced studies should be performed during a delayed phase so that the normal early archiform pattern of arterial splenic enhancement does not mask lesions or create pseudolesions. Contrast studies should be performed during an appropriate delay (for patients with good cardiac reserve, 50 seconds is an acceptable scan delay) when most spleens will be in the uniform phase of enhancement.[20] These postcontrast scans clearly depict the classic segmental, wedge-shaped, low-attenuation defect (Figure 3).[21] Less frequently, the entire spleen may be infarcted, leaving only a rim of contrast-enhancing capsule.[22]
  • Other modes of diagnosis include radioisotope scans and ultrasonographic evaluation of the spleen.
  • Angiography is indicated when a vascular lesion is suspected as the etiologic cause, as in cases of arterial embolization, or when it is necessary to manage segmental bleeding by embolization.
  • Ultrasonographic imaging is useful in cases in which the splenic parenchyma can be visualized.[23] Significant amounts of luminal bowel gas, as well as morbid obesity, render this modality less useful. In a retrospective study of 49 episodes of acute splenic infarction, Antopolsky et al found ultrasonographic scanning to be diagnostically useful in only 18% of patients.[1]
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Histologic Findings

Pathologic examination of the resected spleen may provide information regarding the pathogenesis of the infarct (eg, evidence of septic or atheromatous emboli or the presence of an infectious etiology).

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Contributor Information and Disclosures
Author

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, and Society of American Gastrointestinal and Endoscopic Surgeons

Disclosure: Nothing to disclose.

Coauthor(s)

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, and Society of Critical Care Medicine

Disclosure: Nothing to disclose.

Specialty Editor Board

Lewis J Kaplan, MD, FACS, FCCM, FCCP  Director, SICU and Surgical Critical Care Fellowship, Associate Professor, Department of Surgery, Section of Trauma, Surgical Critical Care, and Surgical Emergencies, Yale University School of Medicine

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, and Surgical Infection Society

Disclosure: Nothing to disclose.

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

Disclosure: Medscape Salary Employment

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: American College of Surgeons, American Medical Association, American Medical Women's Association, American Society for Artificial Internal Organs, American Society of Transplant Surgeons, American Society of Transplantation, Association for Academic Surgery, Association of Women Surgeons, International College of Surgeons, International Liver Transplantation Society, New York Academy of Sciences, Pennsylvania Medical Society, Philadelphia County Medical Society, Society of Critical Care Medicine, and Transplantation Society

Disclosure: Nothing to disclose.

Paolo Zamboni, MD  Professor of Surgery, Chief of Day Surgery Unit, Chair of Vascular Diseases Center, University of Ferrara, Italy

Paolo Zamboni, MD is a member of the following medical societies: American Venous Forum and New York Academy of Sciences

Disclosure: Nothing to disclose.

Chief Editor

John Geibel, MD, DSc, 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

John Geibel, MD, DSc, 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, and Society for Surgery of the Alimentary Tract

Disclosure: AMGEN Royalty Consulting; ARdelyx Ownership interest Board membership

Additional Contributors

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.

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

  2. Edinburgh Med J. 1905;36.

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

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

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

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

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

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

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  14. 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. Feb 2005;61(2):343-5. [Medline].

  15. 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. Summer 1991;13(2):168-71. [Medline].

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

  19. 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. Sep 1993;35(3):430-6. [Medline].

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

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

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

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

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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).
 
 
 
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