Splenic Infarction

Published on 20/07/2015 by admin

Filed under Radiology

Last modified 22/04/2025

Print this page

rate 1 star rate 2 star rate 3 star rate 4 star rate 5 star
Your rating: none, Average: 0 (0 votes)

This article have been viewed 4493 times

 Diagnosis best made on portal venous phase images due to heterogeneous arterial phase enhancement

image Global infarction: Complete nonenhancement of spleen

– ± cortical rim sign: Preserved enhancement of peripheral rim of spleen in massive infarction
image Segmental infarction: Wedge-shaped or rounded low-attenuation area usually at periphery of spleen

– Can be multiple, especially when caused by emboli
• Chronic findings on CECT

image Most often results in scarring and volume loss
image Multiple repetitive infarcts in sickle cell disease can lead to small, calcified spleen (autoinfarcted spleen)
image Infarct can develop into splenic cyst
• MR findings: Low signal on T1WI, heterogeneous high signal on T2WI, and hypoenhancing on T1WI C+ images
• Complications (< 20% of patients)

image Perisplenic fluid/hematoma suggests splenic rupture
image Development of rim-enhancing fluid collection: Splenic abscess

TOP DIFFERENTIAL DIAGNOSES

• Splenic laceration
• Splenic cyst or abscess
• Heterogeneous arterial phase enhancement of spleen
• Splenic tumors

CLINICAL ISSUES

• Many different causes, but 2 most common are 

image Hematologic disease or hematologic malignancies (sickle cell, myelofibrosis, leukemia, etc.)
image Embolic conditions (septic emboli, cardiac emboli from atrial fibrillation, etc.)
• Most cases require no treatment, but rarely surgery or intervention for pain or complications
image
(Left) Axial CECT in a sickle cell patient demonstrates an enlarged spleen with multiple wedge-shaped acute splenic infarcts image. While sickle cell patients can develop a small, calcified autoinfarcted spleen, the spleen may be enlarged in the early stages of the disease.

image
(Right) Axial CECT demonstrates a large, global infarct of the spleen with only a tiny amount of enhancing splenic tissue image. Notice the peripheral enhancement (rim sign) image at the margins of the infarct as a result of preserved flow through capsular vessels.
image
(Left) Axial CECT in a 67-year-old man with a 10-year history of atrial fibrillation, now presenting with acute LUQ pain, demonstrates a peripheral, low-attenuation splenic infarct with straight margins image.

image
(Right) Axial CECT in the same patient identifies a left ventricular thrombus image as the source of the arterial embolus to the spleen. Embolic disease is likely the most common cause of splenic infarcts in older patients.

TERMINOLOGY

Definitions

• Global or segmental parenchymal splenic ischemia and necrosis caused by vascular occlusion

IMAGING

General Features

• Best diagnostic clue

image Peripheral, wedge-shaped, nonenhancing areas within splenic parenchyma on CECT in patients with LUQ pain
• Location

image Entire spleen may be infarcted or more commonly segmental areas
• Size

image Variable: Global or segmental
image Spleen may or may not demonstrate splenomegaly
• Morphology

image Most commonly wedge-shaped areas of nonenhancement when infarct is segmental

– Straight margins indicate vascular etiology (rather than a mass or fluid collection)
– May very rarely be rounded (atypical appearance)

Radiographic Findings

• Radiography

image May be associated with lower left lobe atelectasis and pleural effusion on chest x-ray

CT Findings

• NECT

image Infarcts may be difficult (or impossible) to visualize without intravenous contrast
image Areas of hemorrhagic transformation within infarcts appear hyperdense on NECT
• CECT

image Acute findings

– Diagnosis best made on portal venous phase images: Heterogeneous enhancement during arterial phase (due to differential enhancement of red and white pulp) makes identification of subtle infarcts difficult
– Global: Complete nonenhancement of spleen

image ± cortical rim sign: Preserved enhancement of peripheral rim of spleen in massive infarction due to preserved flow from capsular vessels
image Mottled higher density areas within infarcted spleen may represent either tiny islands of residual enhancing splenic tissue or hemorrhage
– Segmental: Wedge-shaped or rounded low-attenuation area usually at periphery of spleen

image Can be multiple, especially when caused by emboli
image In some instances, accessory spleens (splenules) may be infarcted
image Spleen may or may not be enlarged in acute phase
– Complications (< 20% of patients)

image Presence of fluid or hematoma surrounding spleen in setting of infarct suggests splenic rupture (most often in setting of large or global infarct)
image Development of discrete rim-enhancing fluid collection ± internal gas should raise concern for splenic abscess
image Chronic findings

– Infarcts should evolve over time, leaving areas of scarring and volume loss in spleen

image Sites of old infarcts may show calcification
image Remaining spleen may undergo compensatory hypertrophy
– Multiple repetitive infarcts in sickle cell disease can lead to a small, calcified spleen (autoinfarcted spleen)
– Infarct can develop into splenic cyst (secondary or acquired cyst)

MR Findings

• T1WI

image Low signal within area of infarct (can show high T1WI signal due to hemorrhagic infarct)
• T2WI

image Heterogeneous high signal within area of infarct
• T1WI C+

image Wedge-shaped area of hypoenhancement

Ultrasonographic Findings

• Grayscale ultrasound

image Wedge-shaped hypoechoic area(s) within periphery of spleen

– May rarely be rounded or irregularly shaped at center of spleen (atypical)
image Bright band sign: Highly echogenic linear bands in area of infarct may be specific sign of infarction
• Color Doppler

image Diminished or absent flow in areas of infarction

Angiographic Findings

• Conventional angiography: Main splenic artery occlusion or segmental emboli

Imaging Recommendations

• Best imaging tool

image Portal venous phase CECT
• Protocol advice

image  

DIFFERENTIAL DIAGNOSIS

Splenic Laceration

• Hypodense, wedge-shaped defect in spleen in patient with recent history of trauma
• Almost always high-attenuation hematoma adjacent to laceration ± large hemoperitoneum
• May have high-attenuation active arterial extravasation

Splenic Cyst

• Nonneoplastic cysts divided into primary “true” epithelial cysts and secondary “false” cysts (no epithelial lining)

image Primary cysts most often epidermoid cysts (10-25% of all splenic cysts), but can be parasitic (echinococcal)
image Secondary cysts result from prior infection, infarction, trauma, or hematoma
• Usually well-defined, rounded fluid attenuation cyst with variable internal complexity and peripheral calcification
• Can result from prior infarct, but much better defined, rounded, and water density

Splenic Abscess

• Complex intraparenchymal or perisplenic loculated fluid collection with peripheral enhancement, internal complexity/debris, and possible internal gas
• Unlike infarct, splenic abscess is a discrete, rounded fluid collection with adjacent fat stranding/inflammation

image May develop from evolution of prior infarct
• May appear as multiple small lesions (microabscesses) due to fungal infections in immunocompromised patients

Normal Heterogeneous Enhancement of Spleen in Arterial Phase

• Striated appearance of spleen in arterial phase (due to differential enhancement of red and white pulp) should not be confused with splenic infarcts

Splenic Tumors

• Primary or secondary neoplasms of spleen (whether benign or malignant) should appear focal and mass-like, with rounded borders (not wedge-shaped or linear)
• Lymphoma and some metastases (metastatic melanoma or mucinous neoplasms) may appear low density and hypoenhancing, resembling density of infarcts

PATHOLOGY

General Features

• Etiology

image Large variety of different causes resulting in occlusion of arterial/venous vasculature supplying spleen

– Hematologic disorders

image Sickle cell hemoglobinopathies: Risk of splenic infarct during high-altitude travel or airplane flight
image Myelofibrosis
image Hypercoagulable states
image Leukemia and lymphoma
image Any cause of hypersplenism/splenomegaly (including mononucleosis and infections)
– Thromboembolism

image Atrial fibrillation
image Aortic atherosclerotic disease with embolization to splenic artery
image Aortic valve emboli from subacute bacterial endocarditis
– Anatomic causes

image Splenic torsion (including torsion due to wandering spleen): Laxity or absence of splenic ligaments results in spleen “wandering” to ectopic locations, increasing incidence of torsion and infarction
– Miscellaneous

image Pancreatitis or pseudocysts
image Portal hypertension
image Any surgical procedure involving upper abdominal organs (particularly pancreatic tail, stomach, left adrenal gland)
image Collagen vascular disease
image Tumors (gastric, pancreatic, adrenal) involving splenic hilum and vessels
• Genetics
• Predisposition among some hematologic causes, such as sickle cell disease and sickle cell trait
• Liquefactive necrosis

Staging, Grading, & Classification

• Segmental

image Wedge-shaped or round segmental lesion
image Straight margins typical
• Global

image Entire spleen avascular
image May demonstrate cortical rim sign

Gross Pathologic & Surgical Features

• Acute infarction

image Hemorrhagic or bland necrosis
• Chronic infarction

image Fibrous scar
image Rarely calcification

Microscopic Features

• Coagulative necrosis, hemorrhage

CLINICAL ISSUES

Presentation

• Most common signs/symptoms

image Many patients can be asymptomatic (1/3 of patients)

– Most common with small splenic infarcts
image Most common symptoms: LUQ pain, fever, chills, malaise, nausea, vomiting
image May be associated with other infarcts (e.g., kidney and bowel) in patients with splenic infarcts due to emboli
• Lab data: Anemia (53%), leukocytosis (41%), elevated platelet count (7%)

Demographics

• Age

image 2-87 years (mean: 54)
• Gender

image M = F
• Epidemiology

image Many different causes, but 2 most common causes are

– Hematologic disease or hematologic malignancies: Sickle cell, myelofibrosis, leukemia, etc; most common causes in younger patients

image Probably caused by congestion and occlusion of splenic vessels by abnormal cells associated with hematologic disorder
image Most common cause of splenic infarcts overall
– Embolic conditions (septic emboli, cardiac emboli from atrial fibrillation, embolization of ulcerated atherosclerotic plaque); most common cause in older patients

Natural History & Prognosis

• Most cases require no treatment and symptoms cease naturally
• Rarely surgery or intervention for pain or complications

image Complications: Abscess, rupture, subcapsular hematoma, hemorrhage, pseudocyst formation

Treatment

• Asymptomatic: Supportive treatment (pain control with analgesics)
• Symptomatic: Splenectomy for intolerable/increasing pain or splenic rupture; image-guided drainage for splenic abscess formation

DIAGNOSTIC CHECKLIST

Consider

•  

Image Interpretation Pearls

• Wedge-shaped, peripheral area of nonenhancement on portal venous phase CECT
• Do not confuse normal striated enhancement pattern on arterial phase CECT for splenic infarct
image
(Left) Axial CECT in a young child with acute abdominal pain demonstrates a large, hypoenhancing mass image in the pelvis.

image
(Right) Coronal CECT in the same patient again shows the same mass image in the pelvis with fluid in the adjacent right pelvis image and no spleen noted in the abdomen. This mass was found at surgery to represent torsion and infarction of a “wandering” spleen. The spleen in such cases is found in ectopic locations due to laxity or absence of the splenic ligaments.
image
(Left) A large fluid collection image envelops small areas of normal splenic tissue image. This was found at surgery to represent a massively infarcted spleen with contained rupture, resulting in the fluid collection.

image
(Right) Patient status post embolization for hypersplenism shows severe splenomegaly with no enhancement except for a small portion of the medial spleen image. Massive acute infarction is often not desired in splenic embolotherapy, as patients can develop infections of infarcted tissue.
image
(Left) Sagittal ultrasound in a 48-year-old woman with myelodysplastic syndrome and a 1-week history of LUQ pain shows marked splenomegaly & a wedge-shaped hypoechoic area image in the lower pole of the spleen, consistent with infarction. The patient was placed on analgesics and recovered uneventfully.

image
(Right) Axial NECT in a 55-year-old woman presenting with a history of sickle cell anemia demonstrates a spleen that is very small, densely calcified image, and nonfunctional, sometimes termed “autosplenectomy.”
image
Axial CECT shows a thrombus in the aorta image and an extensive area of nonenhancement due to splenic infarction image. Note the left lobe hepatic infarction image.

image
Axial CECT at a more caudal level in the same patient reveals an additional finding of thrombus in the inferior vena cava image.
image
Axial CECT shows typical signs of acute infarction. Note the segmental foci of nonenhancing splenic tissue image. The absence of capsular retraction (volume loss) confirms the acute nature of the infarcts.
image
Axial CECT shows an acute segmental infarction in a patient having undergone a recent transplantation. Note the multiple segmental, wedge-shaped foci of nonenhancement within the spleen image.
image
Axial CECT performed soon after surgery shows an irregular wedge-shaped foci image of nonenhancing spleen, findings characteristic of acute infarction.
image
Axial CECT in the same patient repeated seven months later shows only small residual scars image as sequelae of infarcted tissue.
image
Axial CECT shows an acute infarction in a patient with an enlarged spleen due to mononucleosis. Most of the spleen is nonenhancing and infarcted, with only scattered islands of viable tissue image.
image
Axial CECT shows a global splenic infarction. Note the complete lack of enhancement of the splenic parenchyma image.
image
Axial CECT in a patient with a global splenic infarction demonstrates a peripheral “cortical rim” sign image.
image
Axial CECT in a patient with an acute splenic infarction demonstrates a peripheral wedge-shaped infarct image.
image
Axial CECT in a patient with a chronic splenic infarction demonstrates calcification image.
image
Axial CECT in a patient with splenic infarcts demonstrates multiple peripheral, wedge-shaped emboli image.
image
Axial CECT demonstrates a lack of enhancement in the upper pole of the spleen image.
image
Axial CECT shows segmental foci of nonenhancing splenic tissue image. The absence of capsular retraction (volume loss) confirms the acute nature of the infarcts.
image
Axial CECT demonstrates extensive large splenic infarcts image, appearing as wedge-shaped areas of nonenhancement.
image
Axial CECT in the same patient demonstrates a splenic artery aneurysm image thought to be the cause for the patient’s infarct (likely as a result of emboli from the aneurysm)

SELECTED REFERENCES

1. Gaetke-Udager, K, et al. Multimodality imaging of splenic lesions and the role of non-vascular, image-guided intervention. Abdom Imaging. 2014; 39(3):570–587.

 

Llewellyn, ME, et al. The sonographic “bright band sign” of splenic infarction. J Ultrasound Med. 2014; 33(6):929–938.

Lawrence, YR, et al. Splenic infarction: an update on William Osler’s observations. Isr Med Assoc J. 2010; 12(6):362–365.

Gorg, C, et al. Chronic recurring infarction of the spleen: sonographic patterns and complications. Ultraschall Med. 2003; 24(4):245–249.

Romero, JR, et al. Wandering spleen: a rare cause of abdominal pain. Pediatr Emerg Care. 2003; 19(6):412–414.

Sodhi, KS, et al. Torsion of a wandering spleen: acute abdominal presentation. J Emerg Med. 2003; 25(2):133–137.

Wilkinson, NW, et al. Splenic infarction following laparoscopic Nissen fundoplication: management strategies. JSLS. 2003; 7(4):359–365.

Hatipoglu, AR, et al. A rare cause of acute abdomen: splenic infarction. Hepatogastroenterology. 2001; 48(41):1333–1336.

Andrews, MW. Ultrasound of the spleen. World J Surg. 2000; 24(2):183–187.

Barzilai, M, et al. Noninfectious gas accumulation in an infarcted spleen. Dig Surg. 2000; 17(4):402–404.

Toth, PP, et al. Spontaneous splenic infarction secondary to diabetes-induced microvascular disease. Arch Fam Med. 2000; 9(2):195–197.

Nores, M, et al. The clinical spectrum of splenic infarction. Am Surg. 1998; 64:182–188.

Nores, M, et al. The clinical spectrum of splenic infarction. Am Surg. 1998; 64(2):182–188.

Argiris, A. Splenic and renal infarctions complicating atrial fibrillation. Mt Sinai J Med. 1997; 64(4–5):342–349.

Rypens, F, et al. Splenic parenchymal complications of pancreatitis: CT findings and natural history. J Comput Assist Tomogr. 1997; 21(1):89–93.

Beeson, MS. Splenic infarct presenting as acute abdominal pain in an older patient. J Emerg Med. 1996; 14(3):319–322.

Frippiat, F, et al. Splenic infarction: report of three cases of atherosclerotic embolization originating in the aorta and retrospective study of 64 cases. Acta Clin Belg. 1996; 51(6):395–402.

Collie, DA, et al. Case report: computed tomography features of complete splenic infarction, cavitation and spontaneous decompression complicating pancreatitis. Br J Radiol. 1995; 68(810):662–664.

Chin, JK, et al. Liver/spleen scintigraphy for diagnosis of splenic infarction in cirrhotic patients. Postgrad Med J. 1993; 69(815):715–717.

Valentine, RJ, et al. Splenic infarction after splenorenal arterial bypass. J Vasc Surg. 1993; 17(3):602–606.

Orringer, EP, et al. Case report: splenic infarction and acute splenic sequestration in adults with hemoglobin SC disease. Am J Med Sci. 1991; 302(6):374–379.

Goerg, C, et al. Splenic infarction: sonographic patterns, diagnosis, follow-up, and complications. Radiology. 1990; 174(3 Pt 1):803–807.

Ting, W, et al. Splenic septic emboli in endocarditis. Circulation. 1990; 82(5 Suppl):IV105–IV109.

Related posts:

Epithelioid Hemangioendothelioma Postoperative Pancreas Acute Pancreatitis and Complications Emphysematous Cholecystitis Cricopharyngeal Achalasia Boerhaave Syndrome