Section 5.3: Splenic Pathology

Introduction to Splenic Pathology

The spleen is the largest organ of the reticuloendothelial system, responsible for filtering blood, recycling iron, and producing immune responses. Due to its highly vascular nature, the spleen is susceptible to systemic, infectious, vascular, and traumatic pathologies. Understanding the sonographic appearance of these conditions, particularly the progression of traumatic hematomas, is crucial for both clinical practice and registry examinations.

Splenomegaly

Splenomegaly is defined as the abnormal enlargement of the spleen. In the average adult, the normal spleen measures between 8 and 12 cm in longitudinal length. A splenic length of greater than 12 to 13 cm is the primary diagnostic criterion for splenomegaly. Sonographers must measure the spleen from its upper pole to its lower pole at the hilum in the coronal plane, ensuring the diaphragm is visualized to avoid underestimation.

Causes of Splenomegaly

Splenomegaly is rarely a primary disease; rather, it is a manifestation of an underlying systemic condition. The causes can be categorized as follows:

1. Portal Hypertension: The most common cause of splenomegaly in Western societies, typically secondary to liver cirrhosis. Increased pressure in the portal system causes venous congestion in the splenic vein, leading to splenic enlargement. Splenic varices and a dilated splenic vein (>10 mm) at the hilum are common concurrent findings.
2. Hematologic Malignancies: Leukemia and lymphoma cause massive splenomegaly due to the infiltration of neoplastic cells into the splenic red and white pulp.
3. Infections: Acute infections, particularly infectious mononucleosis (Epstein-Barr virus), malaria, and endocarditis, lead to lymphoid hyperplasia and splenic congestion.
4. Storage Diseases: Conditions like Gaucher's disease or amyloidosis cause the accumulation of abnormal metabolic products in splenic tissues.

Splenic Infarction

A splenic infarction occurs when there is an occlusion of the main splenic artery or one of its segmental branches. This tissue ischemia is commonly caused by emboli originating from the heart (e.g., in patients with bacterial endocarditis, atrial fibrillation, or prosthetic valves), vasculitis, or hematologic disorders such as leukemia and sickle cell anemia (where sickled red blood cells clog the splenic microvasculature, leading to auto-splenectomy over time).

On ultrasound, an acute splenic infarct classically presents as a wedge-shaped, hypoechoic peripheral lesion. The base of the wedge points toward the outer splenic capsule, while the apex points toward the splenic hilum. In the acute phase, the infarct is hypoechoic because of edema and necrosis. Over time, as the necrotic tissue undergoes liquefaction, fibrosis, and scarring, the infarct changes sonographically: it becomes hyperechoic and echogenic, shrinks in size, and causes a retraction of the splenic capsule, resulting in localized volume loss.

Splenic Abscess

Splenic abscesses are uncommon but carry a high mortality rate if untreated. They are typically the result of hematogenous spread of infection from endocarditis, septicemia, intravenous drug abuse, or direct extension from adjacent abdominal infections.

Sonographically, a splenic abscess appears as a complex cystic or solid mass with irregular, thickened walls. The internal contents are typically hypoechoic or anechoic but often contain septations and low-level internal echoes representing purulent debris. A highly specific finding is the presence of gas bubbles within the collection. These gas bubbles appear as hyperechoic foci that produce dirty shadowing or comet-tail (ring-down) artifacts, helping differentiate an abscess from a simple or post-traumatic cyst.

Splenic Cysts

Splenic cysts are categorized as primary (true) or secondary (false) based on the presence of an epithelial lining:

• Primary (True) Cysts: These possess an epithelial lining and are usually congenital in origin (epidermoid cysts). On ultrasound, they present as round, thin-walled, completely anechoic masses with posterior acoustic enhancement. They may occasionally contain internal trabeculations or marginal calcifications. Parasitic cysts (caused by Echinococcus granulosus / hydatid disease) are another type of true cyst, presenting with a classic 'daughter cyst' or 'cyst-within-a-cyst' appearance, along with hydatid sand and wall calcifications.
• Secondary (False) Cysts: These lack an epithelial lining and are typically the chronic sequelae of prior splenic trauma, hemorrhage, or infection. As a subcapsular or intraparenchymal hematoma resolves, it liquefies into a serous fluid collection. On ultrasound, secondary cysts have thicker, more irregular walls than primary cysts and frequently demonstrate internal debris, cholesterol crystals, and mural calcification.

Splenic Rupture and Hematoma

The spleen is the organ most frequently injured in blunt abdominal trauma. Splenic rupture can also occur spontaneously in organs weakened by infections (such as infectious mononucleosis) or malignancies. During trauma triage, the Focused Assessment with Sonography for Trauma (FAST) exam is utilized to screen for free fluid (hemoperitoneum) in the peritoneal spaces, including the splenorenal recess and Morrison's pouch.

Splenic hematomas are classified into two main types based on their relationship to the splenic capsule:

1. Subcapsular Hematoma: The capsule remains intact, and the blood collection is confined beneath it. Sonographically, this appears as a crescent-shaped fluid collection that conforms to the outer contour of the spleen, compressing and indenting the underlying splenic parenchyma.
2. Intraparenchymal Hematoma: The blood collection is located entirely within the splenic parenchyma, presenting as a focal mass-like lesion.

Crucially, the sonographic appearance of splenic blood collections evolves dynamically over time as the clot forms, retracts, and liquefies. Understanding these progressive changes is vital to avoid diagnostic errors: