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Diagnostic Ultrasound - Abdomen and Pelvis

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Splenic Infarct<br />

Diagnoses: Spleen<br />

– Emboli to small intraparenchymal arteries → small<br />

infarcts, often multiple, may be asymptomatic<br />

– Emboli to splenic artery/major branches → large or<br />

massive infarcts, acute symptoms<br />

– Cardioembolic: Myocardial infarction, atrial fibrillation<br />

– Atheroembolic: Aorta, celiac artery<br />

– Emboli from aneurysm: Aortic, celiac, SA<br />

○ Infarction due to severe splenomegaly<br />

– Chronic myelogenous leukemia, myelofibrosis<br />

(extramedullary hematopoiesis), lymphoma,<br />

hemoglobinopathies, infections (EBV, CMV, malaria)<br />

– Infiltrative disorders → splenomegaly <strong>and</strong> increased<br />

oxygen requirement; congestion from intrasplenic<br />

microcirculatory obstruction <strong>and</strong> possibly anemia;<br />

result: Ischemia that may become critical → infarction<br />

– Hemoglobinopathies → splenomegaly/increased<br />

oxygen dem<strong>and</strong> <strong>and</strong> direct microcirculatory<br />

obstruction (e.g., sickle cell crisis)<br />

○ Infarction due to splenic artery occlusion<br />

– Atherosclerosis, vasculitis, fibromuscular dysplasia,<br />

complication of liver transplantation/other surgery,<br />

torsion (w<strong>and</strong>ering spleen)<br />

○ Infarction due to SVT or parenchymal small vessel<br />

thrombosis<br />

– Pancreatitis-related SVT<br />

□ Chronic pancreatitis: 10-40% SV thromboses<br />

□ Associated with pseudocysts: (1) edema, cellular<br />

infiltration, fibroinflammatory reaction in vein wall;<br />

(2) direct compression of SV<br />

□ Acute pancreatitis: Less frequent cause than<br />

chronic pancreatitis<br />

– Other etiologies: Hypercoagulable states, direct<br />

neoplastic invasion/compression (usually pancreatic<br />

carcinoma), portal vein thrombosis > SV extension,<br />

abdominal sepsis (SV thrombophlebitis), blunt trauma,<br />

complication of variceal sclerotherapy or surgery<br />

Gross Pathologic & Surgical Features<br />

• Infarction<br />

○ Necrosis/hemorrhage within splenic parenchyma;<br />

possibly splenic pseudocyst chronically<br />

Microscopic Features<br />

• Bright b<strong>and</strong> sign thought to reflect preserved fibrous<br />

trabeculae surrounded by intervening coagulative necrosis<br />

• Infarction may be accompanied by microscopic features of<br />

an underlying infiltrative disorder<br />

CLINICAL ISSUES<br />

Presentation<br />

• Most common signs/symptoms<br />

○ Often asymptomatic, found incidentally by imaging<br />

– Only ~ 10% of infarcts are recognized clinically<br />

– Asymptomatic infarcts are small but may be<br />

sequential <strong>and</strong> multiple<br />

○ Left upper quadrant abdominal pain;<br />

nausea/vomiting/malaise<br />

○ Splenomegaly, due to congestion, inflammation,<br />

hemorrhage, or underlying disorder<br />

○ If related to chronic SV thrombosis, may see secondary<br />

signs related to varices (such as upper GI bleeding)<br />

Demographics<br />

• Age<br />

○ Related to underlying disorders<br />

• Gender<br />

○ Related to underlying disorders<br />

• Epidemiology<br />

○ Governed by underlying disorders<br />

Natural History & Prognosis<br />

• Small infarcts → parenchymal scarring<br />

○ Multiple infarcts may reduce splenic function<br />

• Large infarcts<br />

○ Resorption of necrotic tissue/hematoma → scar<br />

○ Encapsulation of necrotic tissue/hematoma →<br />

pseudocyst<br />

○ Splenic abscess: Potential complication especially when<br />

infarct caused by septic embolization<br />

○ Splenic rupture<br />

• Acute SA or SV thrombosis<br />

○ May cause infarction <strong>and</strong> associated pathology, but<br />

collateralization may prevent this outcome<br />

• Chronic SV thrombosis<br />

○ Possible gastroesophageal hemorrhage, depending on<br />

route of major collaterals<br />

○ Can be recurrent, intractable, life threatening<br />

Treatment<br />

• Infarction: Treatment governed by size<br />

○ Small: Self-limiting, no treatment<br />

○ Large: Observation or splenectomy; rupture risk with<br />

massive infarcts<br />

• SA or SV thrombosis: Treatment governed by extent of<br />

infarction <strong>and</strong> gastroesophageal hemorrhage<br />

○ Gastroesophageal hemorrhage: Endoscopic<br />

sclerotherapy, splenectomy if recurrent/intractable<br />

DIAGNOSTIC CHECKLIST<br />

Image Interpretation Pearls<br />

• Classic appearance of acute splenic infarct: Hypoechoic,<br />

peripheral, wedge shaped, <strong>and</strong> avascular<br />

○ Non-classic: Rounded or peripheral b<strong>and</strong> morphology;<br />

global infarction; hyperechoic<br />

○ Bright b<strong>and</strong> sign<br />

• Chronic infarction: Atrophic, scarred spleen,± calcification<br />

• Associated findings: Splenomegaly, SV occlusion (with large<br />

perisplenic varices), SA thrombosis<br />

SELECTED REFERENCES<br />

1. Llewellyn ME et al: The sonographic "bright b<strong>and</strong> sign" of splenic infarction. J<br />

<strong>Ultrasound</strong> Med. 33(6):929-38, 2014<br />

2. Mackenzie DC et al: Identification of splenic infarction by emergency<br />

department ultrasound. J Emerg Med. 44(2):450-2, 2013<br />

3. Benter T et al: Sonography of the spleen. J <strong>Ultrasound</strong> Med. 30(9):1281-93,<br />

2011<br />

4. Kamaya A et al: Multiple lesions of the spleen: differential diagnosis of cystic<br />

<strong>and</strong> solid lesions. Semin <strong>Ultrasound</strong> CT MR. 27(5):389-403, 2006<br />

5. Madoff DC et al: Splenic arterial interventions: anatomy, indications,<br />

technical considerations, <strong>and</strong> potential complications. Radiographics. 25<br />

Suppl 1:S191-211, 2005<br />

6. Goerg C et al: Splenic infarction: sonographic patterns, diagnosis, follow-up,<br />

<strong>and</strong> complications. Radiology. 174(3 Pt 1):803-7, 1990<br />

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