Splenic infarction

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Asiri Ediriwickrema, M.D., M.H.S. [2]

A splenic infarct occurs when the vascular supply for the spleen becomes occluded leading to tissue hypoxia and necrosis. It can be the result of either arterial or venous compromise, and it is associated with multiple of disease states. The most common etiologies include malignancy, hypercoagulable disorders, and embolic disorders.^[1][2] It is also common that splenic infarctions are the presenting signs of a previously unknown condition.^[3] Patients can be asymptomatic, however, most develop left upper quadrant abdominal pain. Splenic infarction is often diagnosed with computed tomography. Splenic infarcts can be managed medically, however, surgical intervention is indicated if the patient develops complications including hemorrhage, rupture, abscess, or pseudocyst.^[4]

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]

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.

• 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.

• 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 (i.e., 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.

A. Brief Descriptions：

• Nearly 99% of infarcts are caused by thromboembolic events, and almost all are the result of arterial occlusions.
• White infarcts are encountered with arterial occlusion and in solid tissues.

B. Gross Findings：

• Recent infarcts are hemorrhagic,whereas older, more fibrotic infarcts are pale yellow-gray.

C. Micro Findings：

• Necrotic area with homogenous pinkish appearance.
• Hematoidin crystals can be found in this section.
• Inflammatory cells seated on the margin of infarct area.

• Pathologic examination of the resected spleen may provide information regarding the pathogenesis of the infarct, e.g. evidence of septic or atheromatous emboli or the presence of an infectious etiology.

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  Inflammatory cells seated on the margin of infarct area

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  Inflammatory cells
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  Hemosiderin laden macrophages in the more fibrous areas (junction of infarction)

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  Multiple infarcts in a spleen greatly enlarged by malignant lymphoma. The multiple areas of infarction are well demarcated

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]

^{[1] [2] [3] [4] [5] [6] [7] [8]}

• Leukemia

• Lymphoma (i.e., Hodgkin lymphoma, Non-Hodgkin lymphoma)

• Myelofibrosis

• Hypercoagulable states

• Protein C deficiency

• Protein S deficiency

• Oral contraceptives

• Lupus anticoagulant

• Erythropoietin therapy

• Idiopathic venous thrombosis

• Polycythemia vera

• Sickle hemoglobinopathies

• 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

• SLE

• Kawasaki disease

• Wegener’s granulomatosis

• Polyarteritis nodosa

• 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

• Pancreatectomy

• Liver transplantation

• Meningococcaemia

• Kala-azar (visceral leishmaniasis)

• Infectious mononucleosis

• Clostridium perfringens

• Campylobacter fetus

• Salmonellosis

• Plasmodium vivax

• Plasmodium falciparum

• Leptospirosis

• Naratriptan
• Sumatriptan

• Splenic vein thrombosis

• Pancreatitis

• Amyloidosis

• Sarcoidosis

• Pancreatic cancer

• Adult respiratory distress syndrome (ARDS)

• Postpartum toxic shock syndrome

Splenic infarction can be induced for the treatment of such conditions as portal hypertension or splenic injury^[9]. It can also be used prior to splenectomy for the prevention of blood loss.

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Splenic infarction 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.

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]

• 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.

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