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General Surgery > Abdomen
Splenic Infarct
Article Last Updated: Feb 2, 2006
AUTHOR AND EDITOR INFORMATION
Section 1 of 12  
Author: Amber A Guth, MD, FACS, Associate Professor, Department of Surgery, New York University Clinical Cancer Center, New York University School of Medicine
Amber A Guth is a member of the following medical societies: Alpha Omega Alpha, American College of Surgeons, Association for Academic Surgery, Phi Beta Kappa, Society for Surgery of the Alimentary Tract, and Society of Critical Care Medicine
Coauthor(s):
H Leon Pachter, MD, FACS, Interim Chairman, Director of Division of Shock and Trauma, Professor, Department of Surgery, New York University Medical Center
Editors: 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; Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine; Amy L Friedman, MD, Professor of Surgery, Director of Transplantation, State University of New York Upstate Medical University College of Medicine, Syracuse; Paolo Zamboni, MD, Professor of Surgery, Chief of Day Surgery Unit, Chair of Vascular Diseases Center, University of Ferrara, Italy; John Geibel, MD, DSc, MA, Professor, Department of Surgery, Section of Gastrointestinal Medicine and Department of Cellular and Molecular Physiology, Yale University School of Medicine; Director of Surgical Research, Department of Surgery, Yale-New Haven Hospital
Author and Editor Disclosure
Synonyms and related keywords:
splenic infarction, spleen, segmental splenic infarct, global splenic infarct, splenic hemorrhage, splenic rupture, splenic abscess, splenic pseudocyst
Splenic infarct is a rare form of pathology. The infarct may be segmental or global, involving the entire organ. It is the result of arterial or venous compromise, and it is associated with a heterogeneous group of diseases. Surgery is indicated only in the presence of complications such as hemorrhage, rupture, abscess, or pseudocyst.
History of the Procedure
Due to the increasing use of abdominal imaging, splenic abscess, which formerly was recognized only at the time of laparotomy or pathologic examination of the resected spleen, is now being diagnosed with increasing frequency. This has led to the realization that an uncomplicated splenic infarct without associated infection and/or abscess can be treated nonoperatively.
Frequency
Splenic infarct is associated most commonly with hematologic disorders. The propensity for splenic infarction in sickle hemoglobinopathies is well known. The mechanism of splenic infarction in sickle cell disease is attributed to crystallization of the abnormal hemoglobin during periods of hypoxia or acidosis. The rigid erythrocyte leads to rouleaux formation and occlusion of the splenic circulation. In homozygous sickle cell disease, multiple infarcts during childhood commonly result in a scarred, contracted, auto-infarcted spleen by adulthood. Exposure to low oxygen tension, such as unpressurized airplane travel, or vigorous activity, such as skiing in high altitude locations, also can precipitate sickling and splenic infarction in individuals heterozygous for the sickle trait. Many of these altitude-related episodes can be safely treated with supportive care rather than with splenectomy (Sheikha, 2005).
Although splenic infarct rates of 50% and 72% have been reported in chronic myelogenous leukemia and myelofibrosis respectively, few large series describing this entity exist. In 1998, Nores reported 59 cases treated over a 30-year period at the University of California, Los Angeles (UCLA) and Cedars-Sinai Medical Center. In 1986, Jaroch identified 75 patients through clinical or autopsy reports at the Cleveland Clinic and found only an additional 77 cases in the literature. Most of the current literature consists of case reports.
Systemic embolization also can result in splenic infarct. It occurs most commonly in the setting of a left atrial or ventricular mural thrombus formed as the result of acute myocardial infarction. While autopsy series report a 9% incidence of splenic infarction in early deaths following an acute myocardial infarction, clinical series report a much lower incidence of splenic embolization, probably reflecting the silent clinical course of many splenic infarcts.
Another mechanical cause of splenic infarct can be due to the injection of gastric varices in the setting of portal hypertension and gastric variceal bleeding.
Splenic infarct has also been reported in association with postpartum toxic shock syndrome (Torda, 2005).
Etiology
- Hematologic disorders - Malignant
- Leukemia
- Lymphoma (ie, Hodgkin, non-Hodgkin)
- Myelofibrosis
- Hematologic disorders - Benign
- Hypercoagulable states - protein C or protein S deficiency, oral contraceptives, lupus anticoagulant
- Erythropoietin therapy
- Idiopathic venous thrombosis
- Polycythemia vera
- Sickle hemoglobinopathies
- Embolic disorders
- Endocarditis
- Atrial fibrillation
- Prosthetic mitral valve
- Paradoxical emboli from right heart
- Left ventricular mural thrombus following myocardial infarct
- Infected thoracic aortic graft
- HIV-associated mycobacterial infections
- Vascular disorders
- Autoimmune/collagen vascular disease
- Trauma
- Blunt trauma
- Torsion of the wandering spleen
- Left heart catheterization via femoral artery approach
- Sclerotherapy of bleeding gastric varices
- Pitressin infusion
- Embolization for splenic bleeding
- Operative etiologies
- Pancreatectomy
- Liver transplant
- Miscellaneous etiologies
- Splenic vein thrombosis
- Pancreatitis
- Amyloidosis
- Sarcoidosis
- Pancreatic cancer
- Adult respiratory distress syndrome (ARDS)
- Postpartum toxic shock syndrome
Pathophysiology
- In diseases such as chronic myeloid leukemia that result in massive splenomegaly secondary to the malignant infiltrative process, segmental infarcts are considered the result of outstripping the available blood supply.
- Splenic vein thrombosis, most commonly the result of pancreatitis or surgery, can result in venous infarction.
- Unusual causes of splenic infarction include malaria, pancreatitis, cocaine use, and splenic infarction occurring as a late complication of liver transplantation.
- The authors have treated one case of global splenic infarction in a person with multiple blunt trauma injuries who required hepatic packing as part of a damage control procedure. At the initial exploration, the spleen was intact, perfused, and viable. The patient subsequently required reoperation for release of an intra-abdominal compartment syndrome. Follow-up CT scans after the second operation revealed global splenic infarction that was attributed to occlusion of splenic venous outflow due to the severe intra-abdominal hypertension and resultant impedance of venous return from the visceral circulation.
- An anatomic variant that renders the spleen more susceptible to global infarction is that of the wandering spleen. The spleen is attached by a long vascular pedicle, without the usual fixating ligaments, to the diaphragm, colon, left kidney, and lateral abdominal wall. This allows torsion of the freely mobile spleen around its vascular pedicle, occluding the blood supply and leading to infarction. The treatment is surgical fixation of the spleen (ie, splenopexy), allowing preservation of the spleen if it has not infarcted as a result of occlusion of the splenic hilum. Techniques include suturing the spleen to the surrounding structures, wrapping it in omentum or mesh prior to suture fixation, or placing it in a surgically created retroperitoneal pouch.
Clinical
- The clinical spectrum varies from asymptomatic infarction discovered incidentally on radiologic or postmortem studies or at laparotomy for another indication to hemorrhagic shock secondary to massive subcapsular hemorrhage with free rupture into the peritoneal cavity.
- Approximately one third of splenic infarcts are clinically occult.
- The most common presenting symptom is left upper quadrant abdominal pain.
- Additional symptoms include fever and chills, nausea and vomiting, pleuritic chest pain, and left shoulder pain (Kehr sign).
- Septic thromboemboli can result in splenic abscesses, which present with sepsis and left upper abdominal pain.
The indications that warrant surgical intervention include sepsis, abscess, hemorrhage, or pseudocyst formation. Pseudocysts usually are the result of prior trauma, with organization and liquefaction of the resultant hematoma, surrounded by a fibrous pseudocapsule. Pseudocysts can be managed by local excision with preservation of the remaining normal splenic parenchyma.
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 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.
Overall, 52 of the 152 patients described in the Cleveland Clinic series underwent splenectomy for complications of splenic infarct.
As with all nonmalignant splenic disorders, splenic preservation is of great interest.
The arterial supply to the spleen consists of the splenic artery (a branch of the celiac axis) and the short gastric arteries (branches of the left gastroepiploic artery), which supply the upper pole of the spleen. Even with occlusion of the main splenic artery, collateral flow from the short gastric arteries often may preserve some or all of the splenic parenchyma.
Within the spleen, the arterial supply is segmental. Occlusion of these secondary branches results in the classic wedge-shaped infarct. Most commonly, these infarcts contract and fibrose over time, as demonstrated by the sickle hemoglobinopathies in which repeated episodes of infarction ultimately result in auto-infarction of the spleen.
- Asymptomatic infarct without complication does not require surgical intervention.
- Overall, most splenic infarcts do not require surgical intervention.
Lab Studies
- No diagnostic laboratory studies for splenic infarction exist, although an elevated white blood cell count is not infrequent.
Imaging Studies
- Computerized tomography scan is the current diagnostic modality of choice. Prior to the CT era, diagnosis of splenic infarct was made most commonly at laparotomy for intra-abdominal catastrophe or on postmortem examination.
- Contrast studies clearly depict the classic segmental wedge-shaped, low-attenuation defect. Less frequently, the entire spleen may be infarcted, leaving only a rim of contrast-enhancing capsule.
- Other modes of diagnosis include radioisotope scans and ultrasound evaluation of the spleen.
- Angiography is indicated when a vascular lesion is suspected as the etiologic cause, as in cases of arterial embolization, or to manage segmental bleeding by embolization.
- Bedside ultrasound imaging is useful in cases where the splenic parenchyma can be visualized. Significant amounts of luminal bowel gas, as well as morbid obesity, render this modality less useful.
- Magnetic resonance imaging is another useful modality that clearly identifies infarcted splenic parenchyma. Magnetic resonance images may be reconstructed easily in 3 dimensions (as can spiral CT scan images) if the images are obtained using gadolinium contrast.
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.
Medical therapy
Surgery is indicated only in the presence of complications. Otherwise, the infarcted spleen can be left in situ, and the patient is observed. Due to 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 in these patients.
The principal mainstay of medical therapy is analgesia with either narcotics or nonsteroidal anti-inflammatory agents.
Surgical therapy
- For an infarcted spleen with any of the above-mentioned complications, splenectomy is required.
- Because of the small but real risk of fatal overwhelming postsplenectomy sepsis, 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.
- Complications such as bleeding or pseudocyst formation also may be amenable to splenic salvage using techniques of partial splenectomy.
- While 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 using traditional open techniques or laparoscopic techniques.
- Perisplenic inflammation and dense adhesions can make splenectomy difficult. Another choice is to perform preoperative splenic artery embolization, which purposely infarcts the remaining spleen and minimizes blood loss that 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.
Preoperative details
- The choice of preoperative antibiotics should be guided by the patient's clinical status and associated comorbidities.
- Appropriate preoperative hydration is essential in anticipation of potential blood loss.
- A specimen for type and screen also should be obtained. Intraoperative scavenging of shed blood (ie, cell saver) is dangerous if the splenectomy is being performed for splenic abscess due to the risk of bacterial contamination of the reclaimed blood.
Intraoperative details
- The choice of incision (ie, midline laparotomy versus upper abdominal transverse incision) is determined by the underlying pathology and surgeon preference.
- Use of postoperative drainage again depends on the operative findings, including the presence of a frank abscess, and proximity of the dissection to the pancreatic tail. The authors' preference is for closed suction drainage to be placed in the splenic bed, and the timing of removal depends on the quantity and character of drainage. Note that the routine use of drainage of the splenic bed in the absence of extrasplenic abscess or pancreatic injury has been associated with an increased risk of local infection.
- The authors' current preference for deep venous thrombosis (DVT) prophylaxis is the use of sequentially inflating antiembolism boots to be applied prior to laparotomy.
- If concern exists regarding possible impingement upon the gastric wall during short gastric vessel division, a nasogastric tube may be left in place.
- Due to the intense inflammatory response that accompanies splenic infarct with abscess, the dissection can be extremely difficult, and a laparoscopic approach has not been described.
Postoperative details
- Following splenectomy or global infarct, administer pneumococcal vaccine (Pneumovax).
- Immunize children against Haemophilus also.
- Postoperative thrombocytosis occurs frequently. Antiplatelet therapy is initiated for platelet counts greater than 1 million/mm3. However, antiplatelet therapy also is controversial in this circumstance, and benefit has not been demonstrated with a randomized, prospective, controlled trial.
Follow-up
Follow-up is directed by the underlying cause for the infarction or abscess rather than the absence of the spleen.
- Hemorrhage: Hemorrhage can follow splenectomy due to the intense perisplenic inflammation.
- Splenic bed and/or subphrenic abscess: Abscess is not an uncommon complication. The first line of treatment is radiologic-guided percutaneous drainage.
- Pancreatic fistula: Because of the intimate association of the pancreatic tail and splenic hilum, pancreatic injury can occur, especially in the setting of intense inflammation and/or abscess. The majority of these resolve with nonoperative management, which includes wide drainage, use of a somatostatin analog to decrease exocrine pancreatic function, and either total parenteral nutrition (TPN) or enteral alimentation distal to the ligament of Treitz.
- Gastric fistula: Due to the intense inflammatory reaction that can accompany splenic abscess, the dissection of the spleen from the greater curve 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.
- Overwhelming postsplenectomy sepsis: As discussed above, the incidence is unknown. The overall postoperative sepsis rate is high because splenectomy often is undertaken for treatment of splenic abscess. The rate of sepsis is due to the cause for the abscess rather than the splenectomy.
The prognosis varies with the underlying disease process responsible for splenic infarction. Splenectomies for infarction of massively enlarged spleens that accompany hematologic malignancies have reported mortality rates as high as 35%. At the other end of the spectrum, many infarcts are clinically occult, with no significant long-term sequelae.
Asplenic individuals have an increased lifetime risk for developing overwhelming postsplenectomy sepsis, with the highest rate in the pediatric age group. Patients should be counseled to seek medical attention for even seemingly minor infections because these can progress to fatal septicemia within hours.
These considerations have proven to be the impetus for splenic preservation.
As laparoscopic techniques become more advanced, some of these surgical problems certainly will be amenable to laparoscopic splenectomy or partial splenectomy.
Intragastric ultrasound also may prove promising in the identification of splenic pathology.
Again, great interest is focused on extending the safe indications for splenic preservation.
| Media file 1:
Splenic infarct. CT 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 splenic parenchyma (white area along medial aspect of spleen). |
 |  View Full Size Image | |
Media type: CT
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| Media file 2:
Splenic infarct. Selective splenic arteriogram showing extravasation of contrast from the splenic artery at the splenic hilum prior to angioembolization (see Media file 3). |
 | View Full Size Image | |
Media type: Image
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| Media file 3:
CT scan of the spleen 5 days after angioembolization of bleeding splenic artery showing partial splenic infarct demonstrated by lack of IV contrast enhancement of lower pole of spleen. The patient experienced no adverse sequelae and has fared well since his discharge to home 5 days after the embolization (see Media file 2). |
 | View Full Size Image | |
Media type: CT
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Splenic Infarct excerpt Article Last Updated: Feb 2, 2006
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