Splenic infarction refers to occlusion of the splenic vascular supply, leading to parenchymal ischemia and subsequent tissue necrosis. The infarct may be segmental, or it may be global, involving the entire organ. It is the result of arterial or venous compromise and is associated with a heterogeneous group of diseases.
Splenic infarction alone is not an indication for surgery. However, nonoperative management warrants close follow-up, and surgery is indicated for persistent symptoms or in the presence of complications such as hemorrhage, rupture, abscess, or persistent pseudocyst.
As laparoscopic techniques become more advanced, many of the surgical problems associated with splenic infarction certainly will prove amenable to laparoscopic splenectomy or partial splenectomy. There is great interest regarding the extension of the safe indications for splenic preservation. As technologies evolve, laparoscopic splenic preservation may become the future standard of care for segmental infarcts.
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 autoinfarction of the spleen). 
Infiltrative hematologic diseases cause congestion of the splenic circulation by abnormal cells. For instance, the mechanism of splenic infarction in sickle cell disease is attributed to crystallization of the abnormal hemoglobin during periods of hypoxia or acidosis. [1, 2] 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, autoinfarcted spleen by adulthood. In individuals who are heterozygous for sickle trait, exposure to low-oxygen tension (eg, during unpressurized airplane travel) or vigorous activity (eg, skiing in high-altitude locations) can precipitate sickling and splenic infarction by the above-described mechanism.  In myelofibrosis, the splenic parenchyma is infiltrated by extramedullary hematopoiesis, causing congestion of the splenic circulation.
In malignant hematologic diseases (eg, chronic myeloid leukemia), increased splenic oxygen requirements secondary to an increased splenic mass, coupled with a decreased oxygen-carrying capacity secondary to the anemia of hypersplenism, lead to infarction.
Thromboembolism is another common cause of splenic infarcts.  Splenic embolization may result from various cardiovascular conditions, including a left atrial or ventricular mural thrombus that formed as a result of acute myocardial infarction or atrial fibrillation or developed from complications of cardiac catheterization or bacterial endocarditis. A report on 108 patients with left-side endocarditis undergoing valvular surgery revealed a 19% incidence of splenic infarction; in almost half of the patients with infarction, the diagnosis was made incidentally on computed tomography (CT). 
Another mechanical cause of splenic infarct can be the injection of gastric varices in the setting of portal hypertension and gastric variceal bleeding. 
Hypercoagulable states can cause splenic infarction. For instance, hereditary protein C deficiency has been reported to cause splenic infarction.  Acquired hypercoagulable states include myeloproliferative disorders, lupus anticoagulant, and erythropoietin therapy.
Splenic infarct has also been reported in association with postpartum toxic shock syndrome. 
Splenic vein thrombosis, most commonly the result of pancreatitis or surgery, can result in venous infarction.
Unusual causes of splenic infarction include malaria,  pancreatitis, and cocaine use; it can also occur, uncommonly, as a late complication of liver transplantation.
The authors have treated one case of global splenic infarction in a person with multiple blunt injuries who required hepatic packing as part of a damage-control procedure. At 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 after the second operation revealed global splenic infarction, attributed to an occlusion of splenic venous outflow due to severe intra-abdominal hypertension and the 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.
There are numerous etiologies of splenic infarct. The vast majority (88%), however, are either infiltrative hematologic diseases that cause congestion of the splenic circulation by abnormal cells, or thromboembolic conditions that produce obstruction of larger vessels.  The etiologies of splenic infarct may be categorized as follows:
Autoimmune/collagen vascular disease
Trauma - Blunt trauma, torsion of the wandering spleen, left-heart catheterization via femoral artery approach, sclerotherapy of bleeding gastric varices, vasopressin infusion, embolization for splenic bleeding
Often a clinically silent condition, splenic infarct is associated most commonly with hematologic disorders. 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 et al  reported 59 cases treated over a 30-year period at the University of California, Los Angeles (UCLA) and at the Cedars-Sinai Medical Center. In 1986, Jaroch et al  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 only.
The frequency of visualized splenic infarcts may be rising because of the following factors:
The prognosis for splenic infarction varies according to the underlying disease process responsible for the infarct. Splenectomies for infarction of massively enlarged spleens accompanying hematologic malignancies reportedly are associated with mortalities 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 (OPSS), with the highest rate in the pediatric age group. Patients should be counseled to seek medical attention even for seemingly minor infections, because these can progress to fatal bloodstream infection within hours.
These considerations have proved to be the impetus for splenic preservation.