Splenic Infarct 

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.

Recent studies

In a 10-year retrospective study, Antopolsky et al examined clinical presentations in 49 episodes of acute splenic infarction. The most common symptom was either abdominal or left flank pain (80% of episodes), while the most common sign was upper left quadrant tenderness (35% of episodes). In 16.6% of patients, splenic infarction was the presenting symptom of an underlying disease. No inhospital mortality or serious complications occurred in the cohort.^[1]

One of the earliest descriptions of splenic infarct was made in Germany in 1896, after a splenic infarction was seen microscopically following splenectomy for endocarditis (presumably due to septic emboli).^[2]

Frequency

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 and colleagues^[3] 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 and coauthors^[4] 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 increased radiologic imaging of patients (with subsequent increased incidental detection of splenic infarcts)^[5]
• The current standard of nonoperative management of blunt splenic injuries
• The increased use of angiographic embolization for vascular splenic injuries (as shown in the images below)^[6] 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).

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.^[3] The etiologies of splenic infarct are as follows:

• Malignant hematologic disorders

  • Leukemia
  • Lymphoma (ie, Hodgkin, non-Hodgkin)
  • Myelofibrosis
• Benign hematologic disorders

  • Hypercoagulable states - Protein C or protein S deficiency, oral contraceptives, lupus anticoagulant
  • Erythropoietin therapy
  • Idiopathic venous thrombosis
  • Polycythemia vera
  • Sickle hemoglobinopathies^[7]
• Embolic disorders

  • Endocarditis
  • Atrial fibrillation
  • Prosthetic mitral valve
  • Paradoxical emboli from right heart
  • Left ventricular mural thrombus following myocardial infarct
  • Infected thoracic aortic graft
  • Human immunodeficiency virus (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^{[8, 9]}

  • Pancreatectomy
  • Liver transplant
• Miscellaneous etiologies

  • Splenic vein thrombosis
  • Pancreatitis
  • Amyloidosis
  • Sarcoidosis
  • Pancreatic cancer
  • Adult respiratory distress syndrome (ARDS)
  • Postpartum toxic shock syndrome

• 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.^{[7, 10]} 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. In individuals who are heterozygous for the sickle trait, exposure to low-oxygen tension, such as that which occurs during unpressurized airplane travel, or vigorous activity, such as skiing in high-altitude locations, can precipitate sickling and splenic infarction by the above-described mechanism.^[11] 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.
• Thromboembolic events are another frequent cause of splenic infarcts.^[12] Splenic embolization may result from a variety of cardiovascular conditions, including a left atrial or ventricular mural thrombus that formed as a result of acute myocardial infarction or atrial fibrillation, or that developed from complications of cardiac catheterization or bacterial endocarditis. A report on 108 patients with left-sided endocarditis undergoing valvular surgery revealed a 19% incidence of splenic infarction; in almost half of the study's patients with infarction, the diagnosis was made incidentally on a computed tomography (CT) scan.^[13]
• Another mechanical cause of splenic infarct can be the injection of gastric varices in the setting of portal hypertension and gastric variceal bleeding.^[14]
• Hypercoagulable states can cause splenic infarction. For instance, hereditary protein C deficiency has been reported to cause splenic infarction.^[15] Acquired hypercoagulable states include myeloproliferative disorders, lupus anticoagulant, and erythropoietin therapy.
• Splenic infarct has also been reported in association with postpartum toxic shock syndrome.^[16]
• Splenic vein thrombosis, most commonly the result of pancreatitis or surgery, can result in venous infarction.
• Unusual causes of splenic infarction include malaria,^[17] pancreatitis, and cocaine use; it can also occur, uncommonly, as a late complication of liver transplantation.
• The authors have treated 1 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, which was 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.^[18] 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 clinical spectrum varies from asymptomatic infarction (discovered incidentally on radiologic or postmortem studies, or at laparoscopy or 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 (up to 70%). Additional symptoms include fever and chills, nausea and vomiting, pleuritic chest pain, and left shoulder pain (Kehr sign).
• Septic thromboemboli may result in splenic abscesses, which present with sepsis and left upper abdominal pain.
• In the series from UCLA, most of the patients with thromboembolic infarction were symptomatic; 70% of patients with emboli were febrile, and 86% of individuals with thrombosis had abdominal pain.^[3]

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 UCLA series revealed that patients with hematologic conditions were typically explored for complications of those conditions (69%), especially patients with nonmalignant conditions (90%), while patients with hematologic malignancies often (47%) underwent surgery for acute symptoms.^[3] Complications of splenic infarction were a frequent indication (60%) for operation in patients with septic emboli.^[3]

Pseudocysts usually are the result of prior trauma, with organization and liquefaction of the resultant hematoma, surrounded by a fibrous pseudocapsule. Small, asymptomatic pseudocysts (< 4cm) usually regress with time, whereas larger splenic cysts (>5 cm) require treatment because the risk of rupture can be as high as 25%.^[19]

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.

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).^[7]

• Asymptomatic infarct without complication does not require surgical intervention.
• Overall, most splenic infarcts do not require surgical intervention.