Background

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.
Anatomy
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). [1]
Pathophysiology
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. [3] 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. [4] 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). [5]
Another mechanical cause of splenic infarct can be the injection of gastric
varices in the setting of portal hypertension and gastric variceal bleeding. [6]
Hypercoagulable states can cause splenic infarction. For instance, hereditary
protein C deficiency has been reported to cause splenic infarction. [7] Acquired
hypercoagulable states include myeloproliferative disorders, lupus
anticoagulant, and erythropoietin therapy.
Splenic infarct has also been reported in association with postpartum toxic
shock syndrome. [8]
Splenic vein thrombosis, most commonly the result of pancreatitis or surgery,
can result in venous infarction.
Unusual causes of splenic infarction include malaria, [9] 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. [10] 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.
Etiology
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. [11] The etiologies of splenic infarct may
be categorized 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 [1]
 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, vasopressin infusion, embolization for splenic bleeding
 Operative etiologies [12, 13] - Pancreatectomy, liver transplant
 Miscellaneous - Splenic vein
thrombosis, pancreatitis, amyloidosis, sarcoidosis,pancreatic cancer,
acute respiratory distress syndrome (ARDS), postpartumtoxic shock
syndrome
Epidemiology
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 [11] 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 [14] 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:
 Increased radiologic imaging of patients (with subsequent increased
incidental detection of splenic infarcts) [15]
 Current standard of nonoperative management of blunt splenic injuries
  Increased use of angiographic embolization for vascular splenic
injuries [16]
Prognosis
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.