Improving diagnosis of atraumatic splenic lesions, part I: nonneoplastic lesions

    Improving diagnosis of atraumatic splenic lesions, part I: Non-neoplastic lesions Zina J. Ricci, Sarah K. Oh, Victoria Chernyak, Milana Flusberg, Alla M. Rozenblit, Bindu Kaul, Marjorie W. Stein, Fernanda A. Mazzariol PII: DOI: Reference:

S0899-7071(16)00020-6 doi: 10.1016/j.clinimag.2016.01.012 JCT 7994

To appear in:

Journal of Clinical Imaging

Received date: Revised date: Accepted date:

9 November 2015 16 January 2016 26 January 2016

Please cite this article as: Ricci Zina J., Oh Sarah K., Chernyak Victoria, Flusberg Milana, Rozenblit Alla M., Kaul Bindu, Stein Marjorie W., Mazzariol Fernanda A., Improving diagnosis of atraumatic splenic lesions, part I: Non-neoplastic lesions, Journal of Clinical Imaging (2016), doi: 10.1016/j.clinimag.2016.01.012

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Improving Diagnosis of Atraumatic Splenic Lesions, Part I: Nonneoplastic Lesions

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Authors: Zina J Ricci, MD (corresponding author) Department of Diagnostic Radiology Montefiore Medical Center of the Albert Einstein School of Medicine 111 E 210th Street Bronx, NY 10467 Phone: 718-920-4396 Fax: 718-325-2037 [email protected]

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Sarah K Oh, MD Department of Diagnostic Radiology Montefiore Medical Center of the Albert Einstein School of Medicine 111 E 210th Street Bronx, NY 10467 [email protected]

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Victoria Chernyak, MD, MS Department of Diagnostic Radiology Montefiore Medical Center of the Albert Einstein School of Medicine 111 E 210th Street Bronx, NY 10467 [email protected] Milana Flusberg, MD Department of Diagnostic Radiology Montefiore Medical Center of the Albert Einstein School of Medicine 111 E 210th Street Bronx, NY 10467 [email protected] Alla M Rozenblit, MD Department of Diagnostic Radiology Montefiore Medical Center of the Albert Einstein School of Medicine 111 E 210th Street Bronx, NY 10467 [email protected] Bindu Kaul, MD Department of Diagnostic Radiology Jack D. Weiler Hospital of the Albert Einstein School of Medicine

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1825 Eastchester Rd Bronx, NY 10461 [email protected]

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Marjorie W Stein, MD Department of Diagnostic Radiology Montefiore Medical Center of the Albert Einstein School of Medicine 111 E 210th Street Bronx, NY 10467 [email protected]

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Fernanda A Mazzariol, MD Department of Diagnostic Radiology Montefiore Medical Center of the Albert Einstein School of Medicine 111 E 210th Street Bronx, NY 10467 [email protected]

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Grants: none

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Received Certificate of Merit Focal Splenic Lesions: CT and MR Imaging Pearls. Electronic educational exhibit for American Roentgen Ray Society Annual Meeting 2013

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Abstract: Focal atraumatic splenic lesions often pose a diagnostic challenge on cross sectional imaging. They can be categorized based on etiology as non-neoplastic (reviewed in Part I), benign neoplastic and malignant neoplastic lesions. Lesions can also be characterized based on prevalence as common, uncommon and rare. Familiarity with pertinent clinical parameters, etiology, pathology, prevalence and ancillary features such as splenomegaly, concomitant hepatic involvement, and extrasplenic findings, in addition to knowledge of imaging spectra of these lesions can improve diagnostic confidence. Since the non-neoplastic lesions are usually easily recognized, it is critical that the radiologist identifies them avoiding unnecessary work up.

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Introduction: Radiologists not uncommonly encounter focal atraumatic

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splenic lesions on imaging and are faced with the challenge of determining their significance. This is especially difficult because focal splenic lesions

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often lack a classic appearance (1). The radiologist needs to decide

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whether such lesions can be left alone because they are definitively benign, require further imaging workup or surveillance because they are

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indeterminate in nature, or whether they are frankly malignant mandating

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more rapid attention and management. This review divides focal splenic lesions into three etiologic categories (Table 1) that will be presented in a

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three-part series aimed to improve radiologic diagnosis and management

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(2-10). Non-neoplastic lesions will be discussed in this paper (Part 1),

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benign neoplastic lesions (including non-neoplastic mass-like lesions) will be discussed in Part II and malignant neoplastic lesions will be discussed in Part III. We further subdivided focal splenic lesions into common, uncommon and rare lesions (Table 3) based on our radiologic observations and review of the literature (2-12). In general, non-neoplastic splenic lesions are usually easily recognizable on imaging, cause little diagnostic confusion, and comprise the majority of commonly encountered focal splenic lesions. Based on the

ACCEPTED MANUSCRIPT Incidental Findings Committee II’s guidelines in the American College of Radiology White Paper (2013), classic benign asymptomatic lesions

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require no follow-up imaging (1). The etiologies of non-neoplastic focal splenic lesions are further subdivided in Table 2 (2,9,12). In Part I, we will

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review pertinent clinical correlates, etiology, pathology, prevalence and

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ancillary imaging findings in conjunction with key CT and MRI imaging features of non-neoplastic focal splenic lesions. It is our belief that

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diagnostic accuracy is dramatically improved when the radiologist

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incorporates knowledge of all these factors together. A brief overview of the management of these lesions will also be included.

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I. Vascular Etiology

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Infarct: Splenic infarcts are common, often found incidentally, and

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patients can be asymptomatic or present with sudden left upper quadrant pain that worsens on deep inspiration (13). Splenic infarction can be due to arterial

or

venous

obstruction.

Arterial

obstruction

is

due

to

thromboembolic disease and occurs most commonly with endocarditis or atrial fibrillation. Intrasplenic sinusoidal venous thrombosis is usually due to splenomegaly and occurs most commonly from infiltrative hematologic disease such as leukemia or lymphoma (2). Venous infarcts are more common in patients younger than 40 years of age, while arterial infarcts

ACCEPTED MANUSCRIPT are more common in those older than 40 years of age. Less common causes of infarcts include: splenic artery embolization, splenic vascular

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disease, torsion, collagen vascular disease, trauma, postoperative state, pancreatic disease (pancreatitis or malignancy) and portal hypertension

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(14). Splenic rupture is a rare complication of splenic infarction, with

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associations including bacterial endocarditis, splenic abscess, recent cardiac surgery, and anticoagulant therapy (15). Infarcts with subcapsular

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blood have been reported on ultrasound in cases complicated by splenic

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rupture (16). Management of splenic infarction consists of treating the underlying hematologic or cardiac disorder.

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Splenic infarcts are classically peripheral, wedge-shaped defects

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with their apices pointed at the splenic hilum, although they can also be

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linear (17) or rounded. They are often multiple and occasionally global. Their borders may be smooth or jagged. They occasionally mimic cysts due to liquefactive necrosis (2) or exhibit a peripheral “rim sign” on post contrast examination due to preserved capsular blood flow (Fig 1) (17). Their appearance on enhanced CT varies with their age: hyperacute infarcts are vague heterogeneous hypoenhancing defects, acute to subacute infarcts become progressively better defined hypodense defects and healed infarcts regress most often or from an atrophic notch (12). On MRI, the

ACCEPTED MANUSCRIPT signal of infarcts varies with their age and degree of hemorrhage (17). Acute hemorrhagic infarcts may be hyperintense on T1-weighted images

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(18), subacute infarcts may be hypointense on T1-weighted images and hyperintense on T2- weighted images mimicking cysts (Fig 2) (2), and

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healed infarcts may be hypointense on T1 and T2-weighted images.

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Infarcts are most conspicuous on delayed contrast-enhanced images (18). Sickle Cell Disease: In Sickle Cell Disease, most prevalent in African

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Americans, the spleen is the earliest and most common organ to be

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affected, typically enlarging in the first decade of life and variably shrinking later on due to autosplenectomy (19), with focal splenic nodules

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relatively common and requiring not treatment (20). The spleen size can be

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normal, variably shrunken or even enlarged in Sickle Cell Disease. Some

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older patients, typically heterozygotes, suffer splenic sequestration crisis with hemorrhage in an enlarged spleen (21), hypersplenism, massive splenic infarction (>50% involvement), or rarely splenic abscess caused by Salmonella (19). Rounded intrasplenic spared nodules vary in size, are usually multiple, and are seen in a variably sized shrunken spleen. They are hypodense in a background of a calcified spleen on CT (Fig 3), have normal splenic signal in a background of hypointense spleen on MRI and

ACCEPTED MANUSCRIPT exhibit uptake of Tc-99m sulfur colloid (20). Extrasplenic findings in sickle cell anemia include hemosiderosis, cholelithiasis, cardiomegaly and

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skeletal infarcts. II. Infectious Etiology

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Macroabscess: Symptoms of splenic abscess are usually nonspecific

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including fever, abdominal pain and leukocytosis (22). Infective endocarditis is the most common predisposing condition (23), with others

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including diabetes mellitus, intravenous drug use with endocarditis, and

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immunocompromised states such as HIV infection, organ transplant, steroid therapy and chemotherapy especially for leukemia (22).

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Percutaneous imaging-guided drainage and intravenous antibiotics are the

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treatment of choice. Multiple, complex collections usually require

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splenectomy (24). Splenic

abscess,

a

localized

purulent

collection

lacking

encapsulation (2), is usually due to hematogenous spread of infection to the spleen but can also occur due to superinfection of an infarct (Fig 4) or contiguous spread of infection from adjacent organs (22). Most splenic macroabscesses are bacterial in etiology, with Staphylococcus aureus or Streptococcus commonly seen (25). Outside of North America, meliodosis and less commonly, brucellosis are well known causes of hepatosplenic

ACCEPTED MANUSCRIPT abscesses (26,27). On CT, bacterial abscess typically appears as a solitary smooth or

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irregular bordered, unilocular or multilocular, hypodense collection. It occasionally has an enhancing rim and infrequently has intracavitary gas

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(2,25). Infiltration of the perisplenic fat is often seen (Fig 5). Perisplenic

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or subcapsular fluid due to abscess rupture may be seen (2). Splenic meliodomas are usually multiple, smaller than 3 cm abscesses with or

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without septations. Concomitant liver abscesses vary in appearance but

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multiple, peripherally located symmetric internal locules (“CT necklace sign”) within a hepatic abscess is highly suggestive of meliodosis (27).

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Splenic brucelloma is usually solitary and more common in the liver than

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the spleen. It appears as an irregular-bordered hypodense mass with thin or

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thick enhancing trabeculations separating hypodense solid or cystic areas. Unique compact chunky central or marginal calcification (“snowflake appearance”) is pathognomonic. Contrast-enhanced CT best reveals the hypodense abscess cavity underlying the dense calcification (26). On MRI, macroabscesses typically match fluid signal and lack enhancement. Minimal peripheral enhancement may be seen if a capsule develops (3). Microabscesses: Symptoms of splenic microabscesses are non-specific with fever the most common. Patients are often neutropenic.

An

ACCEPTED MANUSCRIPT immunocompromised state is the major risk factor, most frequently occurring in leukemic patients undergoing chemotherapy, AIDS patients,

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organ transplant recipients and those on chronic steroids (12). Splenic microabscesses are most often due to fungal infection, most

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frequently Candida albicans, and less commonly Aspergillus fumigatus

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and Cryptococcus neoformans, or due to hematogeneous spread of Mycobacterium tuberculosis from pulmonary infection (12). In Cat Scratch

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Disease, infection with Bartonella henselae, causes small hepatosplenic

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abscesses, and is more common in children than adults (28). Pneumocystis carinii and Histoplasma capsulatum are uncommon causes of splenic

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granulomas (29).

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microabscesses, that are typically only revealed later on as calcified

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Microabscesses are multiple small (5-10 mm and usually less than 2 cm) rounded lesions best seen on post

contrast

exam. Mild

hepatosplenomegaly and small hepatic lesions are commonly present (Fig 6). On CT, lesions are usually hypodense. When a central hyperdense focus is seen in the lesion center, termed a “wheel-within-a-wheel” pattern, it indicates necrotic hyphae and is specific to a fungal origin. In Cat Scratch Disease, splenic microabscesses are uncommonly isolated to the spleen and most often have concomitant hepatic abscesses (28). Although

ACCEPTED MANUSCRIPT many microabscesses heal with calcification or completely regress, they can remain indefinitely as hypoattenuated lesions based on our

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observation. On MRI, fungal lesions are hyperintense foci on T2-weighted images typically lacking enhancement (2,18), although peripheral

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enhancement can also occur (30). Tuberculous lesions have more variable

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signal based on their disease phase. They are usually hypointense on T1 and T2-weighted images thought due to free radicals, fibrosis,

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granulomatous tissue or calcification and usually have peripheral

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enhancement due to granulation tissue with central caseation necrosis (31). Extrasplenic findings include hypodense abdominal lymphadenopathy,

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thickening (12).

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hyperdense ascites, nodular peritoneal thickening and ileocecal wall

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Calcified Splenic Granulomas: Calcified splenic granulomas are a common incidental finding due to splenic microabscesses healed with calcification. Prior pulmonary tuberculosis or histoplasmosis infections are the two most common causes (29). Pneumocystis carinii and brucellosis are less common causes (29,32,33). Calcified

granulomas

appear

as

a

variable

number

of

pathognomonic stippled punctate splenic calcifications usually in a normal sized spleen on CT scan. The larger and more numerous the splenic

ACCEPTED MANUSCRIPT calcifications are, the more likely the etiology is histoplasmosis than tuberculosis (33) and the presence of more than five splenic calcifications

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is almost always due to histoplasmosis, as tuberculous splenic calcified granulomas tend to be sparser in number (Fig 7) (34). Concomitant

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hepatopulmonary calcified granulomas and calcified hilar and mediastinal

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lymph nodes will often be seen with prior histoplasmosis or tuberculosis. Calcifications from healed PCP can be punctate or ring-like and often

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infiltrate the spleen (29,32). They can also be accompanied by punctate

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calcifications in the liver, kidneys, abdominal lymph nodes and adrenal glands due to multiorgan PCP infection (12,29). Hepatosplenic brucellosis

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causes larger pathognomonic chunky calcifications (35). On MRI, calcified

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splenic granulomas are best seen on GRE T1-weighted images with a long

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echo time due to blooming artifact (3). Hydatid Cyst: Splenic hydatid cysts are rare with a reported prevalence of 0.9 to 8%. The spleen is the third most common location of hydatid disease after the liver and lung. In Mediterranean countries, Africa, South America, the Middle East, Australia and New Zealand, humans are usually infected by eating eggs from the tapeworm, Echinococcus granulosis, in contaminated food or from contact with dogs. The eggs invade the intestinal mucosa, ascend the portal vein and deposit in the liver. Splenic

ACCEPTED MANUSCRIPT involvement is due to hematogenous spread or intraperitoneal spread from liver cyst rupture. Patients are asymptomatic or have left upper quadrant

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pain, splenomegaly and fever. Eosinophilia is common (36). Serologic testing has 90-100% sensitivity for multiorgan cysts (37). Since cyst

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rupture can cause anaphylactic shock, treatment is total or partial

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splenectomy combined with antihelminthic medication (36). Hydatid cysts have three layers (pericyst, endocyst and ectocyst), are

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usually solitary and can be intrasplenic or perisplenic, deforming the

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splenic contour due to intraperitoneal seeding (36). Imaging features parallel parasitic development. Early on, type I cysts are unilocular

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containing hydatid sand (debris due to freed scolices). The pericyst is

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hyperdense on non-contrast CT exam, calcified in half of cases,

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hypointense on T1 and T2-weighted images and enhances. Internal septa variably enhance (38). “Completely liquid” type I cysts indistinguishable from simple cysts are rare (39). Later on, type II cysts contain internal septa, daughter cysts and collapsed membranes (Fig 8). Daughter cysts form in the mother cyst periphery (“cartwheel” appearance”) and are less dense than the mother cyst on CT and more hyperintense than the mother cyst on T2-weighted images. The mother cyst is heterogeneously hypointense on T1-weighted images and heterogeneously hyperintense on

ACCEPTED MANUSCRIPT T2-weighted images in the majority of cases. Collapsed membranes (intracystic detached laminated membranes from the pericyst) are

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hyperdense on CT and hypointense on T2-weighted images. MRI better depicts the wrinkled inner cyst lining due to incompletely detached

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membranes than CT. The “snake sign” refers to the serpentine arrangement

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of the collapsed membranes. Longer standing type III cysts contain totally calcified dead content (36,38). Concomitant hepatic cysts are typically

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present, as solitary isolated splenic cysts are extremely rare (36).

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III. Cystic Lesions

True Cysts and Pseudocysts: Splenic true cysts and pseudocysts are

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relatively common incidental asymptomatic lesions that may only cause

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symptoms when large enough to cause mass effect.

Abdominal pain may

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occur as a result of rapid increase in cyst size, superinfection, or rupture (39). These cysts require no treatment. True cysts, also known as congenital, epidermoid, or epithelial cysts (39), are developmental in origin and have an inner endothelial lining postulated to represent infolding of the peritoneal mesothelium or collections of peritoneal mesothelial cells trapped within the splenic sulci. True cysts have a thin imperceptible wall and may have trabeculations and septations (4), reported in 86% of true cysts and 17% of false cysts (12).

ACCEPTED MANUSCRIPT False cysts, also known as pseudocysts, are acquired lesions that have a thick fibrous wall and lack an endothelial lining. Pseudocysts tend to be

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smaller than true cysts, have a thicker “fibrous” wall, are more likely to contain internal hemorrhage or debris (2) and often have wall calcification,

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reported in 50% of false cysts and 14% of true cysts (Fig 9). They may

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develop as a result of prior trauma, infection, pancreatitis or infarction (12). The majority (80%) of splenic cysts are pseudocysts (4).

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True cysts and pseudocysts are usually round and unilocular and

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indistinguishable from one another on imaging. Both are hypodense on CT, of water attenuation. Peripheral “eggshell” wall calcification is more

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commonly seen in pseudocysts than in true cysts. Both typically match

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fluid signal on MRI (Fig 10). Variable signal on T1- weighted images is

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due to internal hemorrhage or debris, which occurs more commonly in pseudocysts. Both types lack enhancement on post contrast exam, but true cysts can have enhancing internal trabeculae (2). Lymphangioma: Splenic lymphangiomas are relatively uncommon lesions typically found in children and less commonly in adults, predilecting females (40). Although usually asymptomatic, they can cause symptoms of left upper quadrant pain, nausea and abdominal distention when large. Hemorrhage, consumptive coagulopathy, hypersplenism,

ACCEPTED MANUSCRIPT portal hypertension and rupture are reported with large lesions (5,41). Although slow growth is typical, rare cases of rapid growth are reported

Trenaunay-Weber

Syndrome

(42).

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(40). Splenic lymphangiomas are uncommon in patients with KlippelAlthough

rare,

splenic

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lymphangiomatosis can be isolated or a feature of generalized

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angiomatosis (42,43). Splenectomy is reserved for symptomatic lesions (5).

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Believed congenital in origin, lymphangiomas are due to

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lymphangiectasis and consist of flattened endothelial-lined spaces filled with proteinacious material with thick fibrous internal trabeculae and

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walls. They arise from the splenic capsule or trabeculae where lymphatic

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tissue is prominent. Three histologic forms are capillary, cavernous or

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cystic, with cystic the most common (5). Splenic lymphangiomas have three morphologies: solitary cystic mass, multiple cystic masses or diffuse masses enlarging the spleen (lymphangiomatosis) (5). Lesions are well defined, contain multiple internal cysts separated by thin septa that often abut the capsule (44) and range in size from a few millimeters to much larger sizes. When multiple splenc lesions are present, the lesions vary in size (5). On CT, lymphangiomas are hypodense microcystic structures with innumerable fine thin septa that may

ACCEPTED MANUSCRIPT contain curvilinear mural or septal calcification. On MRI, they match fluid signal, but can also be hyperintense on T1-weighted images due to

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eosinophilic proteinaceous or hemorrhagic content. Thin internal fibrous septa are hypointense on T2-weighted images and enhance on post contrast

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CT or MRI (Fig 11) (44). Lymphangiomatosis appears as innumerable

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lesions of varying size replacing and typically enlarging the spleen that have features of lymphangiomas when large or cause mottled enhancement when

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small and infiltrative, rendering them indistinguishable from malignancy.

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MRI may resolve those with classic features (43). A small subset of lymphangiomas appears solid. Some are rich in

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dilated blood sinuses in their red pulp that exhibit diffuse mottled arterial

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phase enhancement with progressive delayed enhancement and have

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nonenhancing lymphatic cystic spaces (45). Others are stromal-rich simulating hemangiomas. They are hypointense on T1-weighted images and inhomogeneously hyperintense on T2-weighted images, exhibiting peripheral arterial phase enhancement with progressive diffuse delayed enhancement (46). IV. Miscellaneous Lesions Gamna Gandy Bodies: Gamna Gandy bodies are asymptomatic siderotic splenic nodules most commonly seen in patients with portal hypertension.

ACCEPTED MANUSCRIPT Reported in 9 to 12% of patients with portal hypertension, they can occur in

other

conditions,

including

sickle

cell

anemia,

acquired

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hemochromatosis, paroxysmal nocturnal hemoglobinuria (PNH), leukemia, lymphoma, and angiosarcoma. Gamna Gandy bodies are due to

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intrasplenic foci of hemorrhage and necrosis caused by congestive

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splenomegaly and contain hemosiderin, calcium and fibrous tissue (8). Nodules measure less than 1 cm in size and are usually innumerable.

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They are inconspicuous on nonenhanced CT unless they contain enough

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calcification to be hyperdense (47). They are hypointense on all MRI sequences, being most conspicuous on T2*-weighted images and in-phase

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gradient-recalled echo (GRE) images due to blooming artifact and on post

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contrast T1-weighted images (Fig 12). They lack enhancement (18) and are Extrasplenic

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indistinguishable from calcified granulomas on MRI. findings include cirrhosis, splenomegaly, varices, and ascites.

Summary: When a focal atraumatic splenic lesion is encountered, it is important for the radiologist to recognize the non-neoplastic lesions because they are benign “leave alone” entities that should not lead to unnecessary

imaging

surveillance,

further

workup

or

surgical

management. The radiologic diagnosis of non-neoplastic focal splenic lesions is usually easy to make. When correlation with clinical parameters,

ACCEPTED MANUSCRIPT lesions prevalence and ancillary imaging findings is made, radiologic

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non-neoplastic focal lesions are presented in Table 4.

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diagnostic confidence can be improved. The latter salient features of the

Consideration of lesion prevalence when analyzing focal splenic

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lesions is helpful as the majority of focal splenic lesions are benign, and

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the majority of common focal splenic lesions are non-neoplastic in origin, with the exception of hemangiomas and hematolymphoid malignancy.

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Hemangiomas usually have a suggestive enhancement pattern and

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hematolymphoid malignancy is usually associated with splenomegaly. The most common incidental non-neoplastic splenic lesions are infarct and

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calcified granuloma. The most common focal splenic cystic lesion is a

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pseudocyst or true cyst.

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The observation of splenomegaly or coincidental hepatic lesions is a useful radiologic tool but plays less of a role in evaluation of nonneoplastic focal splenic lesions than it does with neoplastic lesions. Most non-neoplastic focal splenic lesions are seen in the absence of splenomegaly with the exception of microabscesses and Gamna Gandy bodies. Infarcts are seen in either normal sized or enlarged spleens. Similarly, most non-neoplastic focal splenic lesions do not have accompanying hepatic lesions with the exception of hydatid cysts,

ACCEPTED MANUSCRIPT microabscesses and calcified granulomas. Non-neoplastic focal splenic lesions typically require no

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management with the exception of infarcts and abscesses. Patients with splenic infarcts usually require hematologic or cardiac management to

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search for an underlying cause. Patients with splenic macroabscess require

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intravenous antibiotics and percutaneous image guided drainage, with splenectomy reserved for the minority of cases that fail catheter drainage

antifungal

therapy.

Patients

with

hydatid

cysts

require

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require

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(24). Imunocompromised patients with splenic microabscesses most often

antihelminthic therapy and resection or splenectomy. Pseudocysts, true

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cysts and lymphangiomas have virtually no clinical significance, unless

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they are large enough to cause symptoms of mass effect. Lymphangiomas

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can show slow growth that should not be considered a sign of malignancy. Focal splenic nodules in a patient with sickle cell disease should not be confused with a neoplastic process as they represent noninfarcted spared splenic tissue. Calcified granulomas most commonly reflect prior histoplasmosis or tuberculous infection. Finally, Gamna Gandy bodies have clinical relevance, as they indicate portal hypertension in cirrhotic patients.

ACCEPTED MANUSCRIPT Acknowledgements: We thank Dawn Tucker for her assistance in reference acquisition References

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1. Heller MT, Harisinghani M, Neitlich JD, Yeghiayan P, Berland LL. Managing incidental

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findings on abdominal and pelvic CT and MRI, part 3: white paper of the ACR incidental findings committee II on splenic and nodal findings. JACR 2013; (10) 833-839. masses of the spleen: radiologic-

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2. Urrutia M, Mergo PJ, Ros LH, Torres GM, Ros PR. Cystic

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pathologic correlation. Radiographics 1996;(16)107-129.

3. Elsayes KM, Narra VR, Mukundan G, Lewis JS, Menias CO, Heiken JP. MR Imaging of the

4. Freeman JL.

MA

Spleen: Spectrum of Abnormalities. Radiographics 2005; (25) 967-982. Jafri SZH, Roberts JL, Mezwa DG, Shirkhoda A.

CT of Congenital and

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Acquired Abnormalities of the Spleen. Radiographics 1993; (13) 597-610.

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5. Abbott RM, Levy AD, Aguilera NS, Gorospe L, Thompson WM. From the archives of the AFIP: Primary vascular neoplasms of the spleen: radiologic-pathologic correlation.

CE

Radiographics 2004; (24) 1137-1163.

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6. Ferrozzi F, Bova D, Draghi F, Garlaschi G. CT findings in primary vascular tumors of the spleen. AJR 1996; (166) 1097-1101. 7. Zeeb, LM, Johnson JM, Madsen MS, Keating DP. Sclerosing angiomatoid nodular transformation. AJR 2009;192(5):W236-8. 8. Bhatt S, Simon R, Dogra VS. Gamna-Gandy bodies. J Ultrasound Med 2006; (25) 1625-1629.

ACCEPTED MANUSCRIPT 9. Thipphavong S, Duigenan S, Schindera ST, Gee MS, Philips S. Nonneoplastic, benign and malignant splenic diseases: cross-sectional imaging findings and rare disease entities. AJR

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2014; (203) 315-322. 10. Zhang ML, Wu N, Huang W, Lv N (2013). Imaging findings of primary splenic lymphoma: a

8(11):e80264.doi:10.1372/journal.pone.0080264.

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review of 17 cases in which diagnosis was made at splenectomy. PloS ONE

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11. Kim SH, Han JK, Lee KH, et al. Abdominal Amyloidosis: spectrum of radiological findings.

MA

Clinical Radiology 2003; (58) 610-620.

12. Rabushka L, Kawashima A, Fishman EK. Imaging of the spleen: CT with supplemental MR

ED

examination. Radiographics 1994;(14) 307-332.

13. Balcar I, Seltzer S, Davis S, Geller S. CT patterns of splenic infarction: a clinical and

PT

experimental study. Radiology 1984; (151) 723-729.

1986;(100) 743-750.

CE

14. Jaroch MT, Broughan, TA, Hermann RE. The natural history of splenic infarction. Surgery

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15. Dimitrakakis G, Von Oppell U, Zilidis G, Srivastava A. Splenic rupture complicating aortic valve replacement for bacterial endocarditis. Interactive Cardiovascular and Thoracic Surgery 2008; (7):138-140 16. Goerg C, Schwerk WB. Splenic infarction: sonographic patterns, diagnosis, follow-up and complications. Radiology 199; 174:803-807 17. Ito K, Mitchell DG, Fujita T, et al. MR imaging of acquired abnormalities of the spleen. AJR 1997;(168) 697-702. 18. Luna A, Ribes R, Caro P, Luna L, Aumente E, Ros PR. MRI of focal splenic lesions without and with dynamic gadolinium enhancement. AJR 2006;(186)1533-1547.

ACCEPTED MANUSCRIPT 19. Al-Salem AH. Splenic complications of sickle cell anemia and the role of splenectomy. ISRN Hematology 2011;2011:864257. Doi:10.5402/2011/864257.

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20. Levin TL. Berdon WE, Haller JO, Ruzal-Shapiro C, Hurlet-Jenson A. Intrasplenic masses of

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“preserved” functioning splenic tissue in sickle cell disease: correlation of imaging findings (CT, ultrasound, MRI, and nuclear scintigraphy). Pediatr Radiol 1996; (26) 646-649.

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21. Roshkow JE, Sanders LM. Acute splenic sequestration crisis in two adults with sickle cell

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disease: US, CT and MR imaging findings. Radiology 1990;(177) 723-725. 22. Joazlina ZY, Wastie ML, Ariffin N. Computed tomography of focal splenic lesions in

MA

patients presenting with fever. Singapore Med J 2006; (47) 37-41. 23. Wang CC, Lee CH, Chan CY, Chen HW. Splenic infarction and abscess complicating infective

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endocarditis. Am J Emerg Med 2009; (27) 1021.e3-5.

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24. Thanos L, Dailiana T, Papaioannou G, et al. Percutaneous CT-guided drainage of splenic abscess. AJR 2002; (179) 629-632.

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25. Drevelengas A. The spleen in infectious disorders. JBR-BTR 2000; (83) 208-210. Hepatosplenic brucelloma: clinical

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26. Carazo ER, Parra FM, Jemenez Villares MP, et al.

presentation and imaging features in six cases. Abdominal Imaging 2005;(30) 291-296. 27. Apisarnthanarak P, Thairatananon A, Muangsomboon K, Lu DSK, Munday LM, Apisarnthanarak A. Computed tomography characteristics of hepatic and splenic abscesses associated with meliodosis: a 7-year study. J of Medical Imaging and Radiation Oncology 2011; (55) 176-182. 28. Rappaport D, Cumming WA, Ros PR. Disseminated hepatic and splenic lesions in cat-scratch disease: imaging features. AJR 1991;(156) 1227-1228.

ACCEPTED MANUSCRIPT 29. Radin DR, Baker EL, Klatt EC, et al. Visceral and nocal calcification in patients with AIDSRelated Pneumocystis carinii infection. AJR 1990: (154) 27-31.

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30. Moore NJE, Leef JL, Pang, Y. Systemic Candidiasis. Radiographics 2003; (23): 1287-1290.

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31. De Backer AI, Vanhoenacker FM, Mortele KJ, et al. MRI features of focal splenic lesions in patients with disseminated tuberculosis. AJR 2006; (186) 1097-1102.

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AIDS: CT findings. Radiology 1990; (174) 157-160.

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32. Lubat E, Megibow AJ, Balthazar EJ, et al. Extrapulmonary Pneumocystis carinii infection in

33. Gurney JW, Conces DJ, Jr. Pulmonary histoplasmosis. Radiology 1996; (199) 297-306.

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34. Okudaira M, Straub M, Schwarz J. The etiology of discrete splenic and hepatic calcifications in an endemic area of histoplasmosis. N Engl J Med 1955; (252) 887-891.

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35. Ariza J, Pigrau C, Canas C, et al. Current understanding and management of chronic

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hepatosplenic suppurative brucellosis. Clinical Infectious Diseases 2001; (32) 1024-33. 36. Pedrosa I, Saiz A, Arrazola J, Ferreiros J, Pedrosa CS. Hydatid disease: radiologic and

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pathologic features and complications. Radiographics 2000; (20) 795-817.

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37. Brunetti E, Kern P, Vuitton DA. Expert consensus for the diagnosis and treatment of cystic and alveolar echinococcosis in humans. Acta Trop. 2010;114(1):1-16. 38. Marrone G, Crino F, Caruso S, et al. Multidisciplinary imaging of liver hydatidosis. World J Gastroenterol 2012;(18) 1438-1447. 39. Dachman AH, Ros PR, Murari PJ, Olmsted WW, Lichtenstein JE. Nonparasitic Splenic Cysts: A Report of 52 Cases with Radiologic-Pathologic Correlation. AJR 1986; (147) 537-542. 40. Verghese BG, Kashinath SK, Kanth RR. Lymphangioma of the spleen-a rare tumor rarely seen in an adult: a case report and comprehensive literature review. Euroasian J of Hepato-Gastroenterl 2013; (3) 64-69.

ACCEPTED MANUSCRIPT 41. Komatsuda T, Ishida H, Konno K, et al. Splenic lymphangioma: US and CT diagnosis and clinical manifestations. Abdom Imaging 1999; (24) 414-417.

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42. Montes M, Ciudad MJ, Mendea C. Cystic lymphangioma of the spleen in a patient with

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Klippel-Trenanunay-Weber syndrom: MRI findings. Radiologia 2007; (49) 355-7. 43. Yang DH, Goo HW. Generalized lymphangiomatosis: radiologic findings in three pediatric

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patients. Korean J Radiol 2006; (7) 287-291.

MRI correlation. Eur Radiol 2001; (11) 1187-1190.

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44. Bezzi M, Spinelli A, Pierleoni M, Andreoli G. Cystic lymphaniogma of the spleen: US-CT-

World J Gastroenterol 2013; (19) 781-783.

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45. Yang F, Chen WX. Splenic lymphangioma that manifested as a solid-cystic mass: a case report.

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46. Chang WC, Liou CH, Kao HW, Hsu CC, Chen CY, Yu CY. Solitary lymphangioma of the

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spleen: dynamic MR findings with pathological correlation. The British J of Radiology 2007; (80) e4-e6.

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47. Selcuk D, Kemirel K, Kantarci F, Mihmanli I, Ogut G. Gamna-Gandy bodies: a sign of portal

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hypertension. Turk J Gastroenerol 2005; (16) 150-152.

ACCEPTED MANUSCRIPT Legends:

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Figure 1: 48-year-old male with cirrhosis and splenomegaly who

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underwent splenic artery embolization with Onyx to treat

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pancytopenia of hypersplenism. (a) Enhanced CT in late portal

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phase one-day post embolization shows splenomegaly with geographic wedged shaped areas of hypoenhancment (black

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asterisk) consistent with acute infarcts and intervening spared

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enhancing parenchyma. Branching intrasplenic foci of high

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attenuation (black arrow) correlates with intraarterial embolization

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material. (b) Enhanced CT 6 months later, performed for persistent cytopenia, shows retracting hypoenhancing splenic

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necrosis (black asterisk) with associated capsular retraction and rim enhancement (black arrow) Intraarterial embolization material is retained.

Figure 2: 48-year-old female with pancreatitis and multiple splenic infarcts. Coronal T2-weighted MRI shows three sharply defined hyperintense foci, one wedge-shaped (long white arrow),

ACCEPTED MANUSCRIPT one linear (white arrowhead) and one rounded (short white arrow).

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All are hypointense on T1 (not shown) except the rounded one that

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was hyperintense indicating hemorrhagic content, and all were

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nonehancing (not shown).

Figure 3: 23-year-old female with Sickle Cell Disease with spared

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splenic nodules and autosplenectomy. Axial enhanced-CT image

innumerable

hypodense

nodules

(black

arrow).

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sized

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shows a slightly shrunken densely calcified spleen with varying

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Hepatomegaly is present (white asterisk).

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Figure 4: 49-year-old male with bacterial endocarditis status post aortic valve replacement with left upper quadrant pain, fever and elevated WBC count. (a) Nonenhanced CT image shows multiple band like areas of splenic hypoattenuation (black arrow) consistent with infarcts. (b) A more caudad image shows a larger bulging focus of splenic hypoattenuation (black asterisk) with perisplenic stranding inferiorly (white arrow). Patient underwent percutaneous

ACCEPTED MANUSCRIPT drainage revealing purulent hemorrhagic content with bacterial

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growth due infarct superinfection.

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Figure 5: 66-year-old female with pancreatic carcinoma with fever

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and abdominal pain due to superinfection of a globally infarcted spleen. Axial-enhanced CT image demonstrates a globally

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infarcted bulbous spleen (white asterisk) due to malignant

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occlusion of the splenic artery and vein by pancreatic mass (white

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arrow). Perisplenic fat stranding (black arrowhead) and malignant

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periceliac and periportal lymphadenopathy (black asterisk) are present. Patient was treated with percutaneous drainage and

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intravenous antibiotics.

Figure 6: 14-year-old with Cat Scratch disease. (a) Enhanced-CT image shows multiple subcentimeter hypodense nodular foci (black arrow) in a mildly enlarged spleen. (b) A more cephalic image shows concomitant hepatic abscesses (black arrowhead).

ACCEPTED MANUSCRIPT Figure 7: 69-year-old man with a history of tuberculosis and

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calcified splenic granulomas. Nonenhanced-CT image shows (a) a

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few punctate splenic calcifications (white arrowhead) in a normal

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sized spleen. Calcified right inferior hilar lymph nodes and a right

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lower lobe calcified granuloma are not shown.

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Figure 8: 19-year-old Albanian female with disseminated

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echinococcal cysts for planned surgical resection. Axial-enhanced

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CT image shows a large splenic cyst involving the hilum (white

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asterisk), a partially calcified hepatic cyst (white arrowhead) and a gastrohepatic ligament cyst (long white arrow). Cysts have

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enhancing walls and enhancing septa (short black arrow) due to endocyst

invagination.

An

additional

subdiaphgragmatic

perisplenic cyst indenting the spleen is not shown. Splenectomy revealed splenic hydatid cysts containing protoscolices.

Figure 9: 57-year-old female with incidental splenic cystic lesion on imaging. Axial-enhanced CT image shows a well-defined cystic

ACCEPTED MANUSCRIPT lesion with heavy rim calcification (white arrow). Although this

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can be a true cyst or pseudocyst, it is more likely to represent

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pseudocyst given prominent rim calcification and unlikely to

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represent hydatid cyst in the absence of expected travel history or

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additional hepatic cysts.

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Figure 10: 76-year-old female with two incidental splenic cysts

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consistent with true cysts or pseudocysts on imaging. (a) On

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nonenhanced-CT the cysts are hypodense (white arrow) lacking

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calcification with the smaller one not included. Note splenic artery calcification (black arrow). (b) T2-weighted MRI shows the cysts

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to be hyperintense (white arrows). (c) Contrast-enhanced MRI shows lack of enhancement of the cysts. Both cysts were mildly hypointense on T1-weighted images (not shown).

Figure

11:

72-year-old

female

with

incidental

splenic

lymphangioma on imaging. (a) Coronal enhanced CT image shows a well-defined cystic lesion abutting the capsule with fine

ACCEPTED MANUSCRIPT enhancing septa (black arrow). (b) Coronal T2-weighted MRI

(c) Axial contrast-enhanced

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hypointense septae (white arrow).

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shows the lesion to be hyperintense (white asterisk) with thin

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GRE T1-weighted image in late hepatic venous phase shows

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enhancement of multiple smooth septa (white arrow) that were similarly avidly enhancing on arterial and portal venous phase (not

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shown).

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Figure 12: 57-year-old male status post liver transplant for

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cirrhosis with splenic Gamna Gandy bodies on MRI. Innumerable punctate hypointense foci (white arrow) are most conspicuous on

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(a) GRE-in-phase image and less conspicuous on (b) GRE-out-ofphase images. T1-weighted and T2-weighted images (not shown) show bland splenomegaly. Note TIPS in the right lobe (white arrowhead) and surgical clip (black arrow).

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ACCEPTED MANUSCRIPT Table 1: Etiology of Focal Splenic Lesions

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III. Malignant Neoplastic Lesions Systemic Lymphoma Primary Splenic Lymphoma Leukemia Chloroma Hemangioendothelioma Hemangiopericytoma Angiosarcoma Parenchymal Metastases Surface Metastases Extraosseous Multiple Myeloma

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Infarct Sickle cell disease Macroabscess Microabscesses Calcified granuloma (histoplasmosis, TB, PCP, Brucellosis) Hydatid cyst Pseudocyst True cyst Lymphangioma Gamna Gandy bodies

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Non-neoplastic Lesions

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I.

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II. Benign Neoplastic (including nonneoplastic mass-like lesions)

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Hemangioma Hamartoma Sclerosing Angiomatoid Nodular Transformation (SANT) Littoral cell angioma Extramedullary hematopoiesis (EMH) Inflammatory pseudotumor Angiomyolipoma Peliosis Sarcoidosis Gaucher’s Disease Amyloidosis

ACCEPTED MANUSCRIPT

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Table 2: Etiology of Non-Neoplastic Focal Splenic Lesions

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I. Vascular Infarct Sickle cell disease

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II. Infectious

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III. Cystic Lesions

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Macroabscess Microabscesses Calcified granuloma (histoplasmosis, TB, PCP, Brucellosis) Hydatid cyst

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Pseudocyst True cyst Lymphangioma IV. Miscellaneous

Gamna Gandy bodies

ACCEPTED MANUSCRIPT Table 3: Prevalence of Focal Splenic Lesions 1. Common Lesions

2. Rare Lesions

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2. Uncommon Lesions

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Lymphangioma Hamartoma Parenchymal metastases Surface metastases Sarcoidosis

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Littoral cell angioma Sclerosing Angiomatoid Nodular Transformation (SANT) Peliosis Extramedullary hematopoiesis (EMH) Primary Splenic Lymphoma Hemangioendothelioma Hemangiopericytoma Angiosarcoma Chloroma Hydatid cyst Gaucher’s Disease Inflammatory pseudotumor Hemangiomatosis Lymphangiomatosis Amyloidosis Extraosseous Multiple Myeloma Angiomyolipoma

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Calcified granulomas Infarct Sickle cell disease Gamna Gandy bodies Pseudocyst True cyst Macroabscess Microabscesses Hemangioma Systemic Lymphoma Leukemia

ACCEPTED MANUSCRIPT Table 4. Non-neoplastic Focal Splenic Lesions - Summary of Clinical Correlates and Imaging Findings Clinical Correlate

Splenome galy

Hepatic Involvemen t

Extrasplenic Imaging Clues

Infarct

 Associated with hematologic disorder (leukemia, lymphoma) or cardiac disease (endocarditis, atrial fibrillation)  Incidental finding in adults  African American  Sequestration uncommon in adults

Yes with hematologi c disease

No

 Other solid or hollow viscera infarcts in thromboem bolic disease

No (exception - adults with acute sequestrati on crisis)

Yes (hemosidero sis)

 Secondary hemosidero sis  Cardiomeg aly  Cholelithia sis or prior cholecystec tomy  Skeletal infarcts

No

 Concomita nt liver abscesses with meliodoma s (CT necklace sign) and brucelloma s (snowflake calcificatio n)

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Sickle Cell Disease

Macroabsce  Nonspecific ss fever, pain, leukocytosis  1/3 triad of fever, LUQ pain and tender mass  Most often seen with infective endocarditis  Also in diabetes, intravenous drug abuse, and immunocompro

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Ima ging App eara nce  Single or multiple  Wedge-shaped, linear or round  Hypoenhancement  + Rim sign

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Lesion

 Shrunken calcified spleen  Focal spared nodules in calcified or dark signal spleen  Hyperdense spleen (hemosiderosis)  Splenomegaly with infarcts (single, multiple or massive); can be hemorrhagic  Acute sequestration crisis: splenomegaly and heterogeneous attenuation on CT; MRI: heterogenous T1WI hypointense / hyperintense; T2WI hyperintense foci with dark rim due to hemorrhage  Solitary unilocular or multilocular hypodense collection on CT  Fluid signal collection on MRI  Only occasional rim enhancement  Uncommon diagnostic intracavitary gas  Perisplenic fat infiltration common  Perisplenic or subcapsular fluid due to rupture

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 Mild splenomegaly  Multiple small hypoenhancing lesions w/o rim enhancement (except TB + rim enhancement)  “Wheel-within-awheel” pattern (fungal)

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No

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Hydatid Cyst

 + Low attenuation abdominal lymphaden opathy, hyperdense ascites, nodular peritoneal thickening and ileocecal wall thickening in TB Yes  Calcified (calcified hepatic and granulomas pulmonary in granulomas histoplasmo and sis or TB) calcified hilar, mediastinal or lymph nodes (histoplasm osis or TB)  Calcified granulomas in liver, kidneys, abdominal lymph nodes, adrenals (PCP) Yes  May see (additional additional hepatic cyst) intraperitone al cysts Yes (microabsce sses)

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 Asymptomatic  + history of TB, Histoplasmosis (endemic major river valleys of central USA), or PCP (AIDS patients)

Yes

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Calcified granulomas

mised states  + Fever and neutropenia  Immunocompr omised  Risks: IV, organ transplant, diabetes mellitus, steroid or chemotherapy treatment

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Microabsce sses

 Travel history in endemic areas (Mediterra nean countries, Africa, S America, Middle East, Australia, New Zealand)

No

 Represent 80% of splenic cysts

No

No

 Absent

 CT: Variable number of punctate splenic calcifications (poorly seen on MRI)  Larger lesions and more than 5 lesions favors histoplasmos is over TB

 Perisplenic due to intraperitoneal seeding  Isolated splenic cyst: rare  C-: hyperdense wall or calcified (50%) wall  T1WI and T2WI dark rim (pericyst)  Daughter cysts and collapsed membranes  Snake sign /wrinkled internal lining better seen on MRI than CT  Indistinguishable from true cyst

ACCEPTED MANUSCRIPT

No

No

Lymphangi oma

 Rare splenic lesions in KlippelTrenaunnayWeber syndrome

No

No

Gamna Gandy Bodies

 In portal HTN  Other: sickle cell anemia, acquired hemochromatos is, PNH, leukemia, lymphoma and angiosarcoma

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 Less common cause of splenic cyst  Endothelial lining  Congenital

 Absent

 Absent

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True cyst

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 Smaller size, thicker wall, and more likely to have internal debris/hemorrhage than true cyst  Wall calcification more common than in true cysts  Indistinguishable from pseudocyst  Imperceptible wall and more commonly has trabeculations and septations than pseudocyst  3 Forms: solitary (most common), multiple, and diffuse infiltrative nodular (splenomegaly)  Lobulated cystic lesion with thin enhancing wall and septa  Wall and septa may have curvilinear calcification  Can be T1 high SI due to blood/protein  T2WI dark septa: due to fibrous connective tissue  Innumerable <1 cm nodules  Splenomegaly frequently  CT: not apparent (maybe faintly hyperdense on CCT)  MRI: T1WI and T2WI hypointense w/o enhancement  Best seen on T2*weighted, GRE inphase – blooming in long TE sequence due to iron content

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 Thick fibrous wall  Due to prior trauma, infection, infarction or pancreatitis

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Yes (cirrhosis)

 Cirrhosis, varices, splenomega ly, ascites