Etiology and pathogenesis
The development of parenchymal infarction can follow several scenarios, depending on which vascular bed is affected or what systemic disease acts as the trigger.
Arterial infarcts (Splenic Arterial Infarcts) are most commonly the result of arterial embolization (arterial emboli). Other causes include atheroma (atheroma), acute pancreatitis, various coagulopathies, and iatrogenic interventions, such as post-embolization status of the hepatic artery. If septic emboli are the cause, the pathogenesis is complicated by a localized infectious process.
Venous infarcts (Splenic Venous Infarcts) usually occur in the setting of splenic vein occlusion or portal venous hypertension. Specific granulomatous infections, such as tuberculosis or histoplasmosis, can also lead to their development.
In addition, ischemic changes are typical for conditions accompanied by:
- Massive sequestration of red blood cells (sickle cell anemia is a classic example).
- Storage disorders (storage disorders).
- Infiltrative involvement of the parenchyma (e.g., in leukemias).
Morphology of arterial and venous lesions
An arterial infarct typically presents with a classic morphological pattern: well-demarcated wedge-shaped lesions (wedge-shaped lesions) are visualized in the periphery of the organ. The involvement is often multifocal. For instance, a large infarct may be located in the upper pole of the spleen, while smaller foci reside in the lower pole. If the infarct is of septic origin, multiple small hypodense foci—microabscesses—are revealed in the parenchyma alongside the wedge-shaped zones.
The basis of a venous infarct in portal hypertension is often small focal hemorrhages. Over time, they organize and transform into so-called Gandy-Gamna bodies (Gandy-Gamna bodies). Due to hemosiderin accumulation, they exhibit a very specific radiological appearance:
- On ultrasound, they are defined as multiple foci with increased echogenicity.
- On CT, they are often poorly visualized and only become noticeable when markedly hypodense or calcified.
- On MRI, they are best seen on T1-weighted and T2-weighted images as areas of low signal. On chemical-shift gradient-echo (gradient-echo) sequences in-phase (in-phase), they demonstrate a pronounced blooming or enlargement effect (blooming effect). This is due to a significant magnetic susceptibility effect (susceptibility effect) resulting from a longer echo time compared to opposed-phase images.
Stages of infarction: ultrasound and CT
The radiological appearance of a splenic infarct depends on the age of the process. Several stages are distinguished:
- Hyperacute stage (Day 1): The margins of the lesion are not yet formed. Ultrasound shows hypoechoic zones with indistinct borders. Unenhanced CT reveals poorly defined areas of decreased density. If the infarct is hemorrhagic, the CT pattern will be heterogeneous due to areas of high density (fresh blood).
- Acute (2–4 days) and subacute (4–8 days) stages: The lesion acquires a typical wedge shape with clear boundaries. On ultrasound, it appears hypoechoic without a cystic structure. Contrast-enhanced CT reveals an area of low density that does not enhance with contrast media.
- Resolution stage (2–4 weeks): Necrotic zones begin to decrease in size. Parenchymal density on unenhanced and contrast-enhanced CT may gradually return to normal values.
- Long-term sequelae: The lesion may resolve completely. In other cases, residual splenic contour deformation develops, the affected zone undergoes calcification, or it transforms into an acquired pseudocyst (devoid of an epithelial lining).
Complications
Although many infarcts may resolve conservatively, they carry a risk of life-threatening conditions. The main complications include:
- Infection: Secondary infection can develop in the ischemic zone with the formation of a post-infarction splenic abscess. On CT, it will appear as a large hypodense lesion.
- Splenic rupture: In extensive necrosis, the organ capsule may fail, leading to hemoperitoneum and requiring emergency surgical intervention (splenectomy).
Briefly: answers to topical questions
What is the clinical presentation and main symptoms of a splenic infarct?
The clinical presentation of a splenic infarct is characterized by pain and signs of inflammation, although small lesions are often mild or asymptomatic. The main symptoms include:
- Acute pain — localized in the left upper quadrant, often radiating to the left shoulder and left scapula (Kehr's sign), intensified by breathing and movement.
- Dyspeptic disorders — nausea, vomiting, abdominal bloating.
- Fever — low-grade or high-grade fever as a reaction to necrosis.
- Physical findings — tenderness on palpation, abdominal muscle guarding, left-sided pleural or peritoneal friction rub, splenomegaly may be present.
What laboratory changes are characteristic of a splenic infarct?
Laboratory changes in a splenic infarct reflect tissue necrosis and systemic inflammation. The following abnormalities are characteristic:
- Leukocytosis — occurs as a reaction to tissue necrosis.
- Elevated LDH — a marker of tissue necrosis (the LDH-3 isoenzyme is present in the spleen).
- Inflammatory markers — with massive involvement, acute-phase reactive changes are observed.
Additionally, changes associated with the underlying disease that caused the infarct may be detected (e.g., specific red blood cell morphology in sickle cell anemia or markers of myeloproliferative disorders).
How to differentiate a splenic infarct from an abscess and a tumor on CT?
Differential diagnosis on contrast-enhanced CT is based on the evaluation of shape, density, and enhancement pattern.
| Sign | Splenic Infarct | Splenic abscess | Tumor (lymphoma) |
|---|---|---|---|
| Shape and contours | Peripheral, well-defined wedge-shaped lesions (wedge-shaped lesions) | Large or multiple small low-density lesions | Focal deposits; visualized at a diameter greater than 1 cm |
| Density | Low density | Decreased density | Decreased density |
| Contrast enhancement | No contrast enhancement (no enhancement) | Not detailed in the sources | Not detailed in the sources |
Additionally, infarction may be complicated by the formation of a post-infarction abscess, which appears as a large low-density lesion.
What is the management strategy for uncomplicated splenic infarction?
In uncomplicated splenic infarction, conservative management is the treatment of choice. The main therapeutic areas include:
- Symptomatic treatment — adequate pain control.
- Dynamic monitoring — regular ultrasound or CT follow-up of the lesion.
- Etiotropic therapy — treatment of the underlying condition that caused the thromboembolism.
- Anticoagulant therapy — prescribed for confirmed cardioembolic or thrombophilic origin.
Splenectomy is used for complications, including rupture with hemorrhage and abscess formation, as well as in cases of unclear diagnosis or recurrent infarctions with pronounced clinical symptoms.
MRI differences: Arterial infarction is a WEDGE (wedge-shaped lesion, high signal on T2-WI). Venous infarction is BLOOMING (hemosiderin deposition in Gandy-Gamna bodies produces a "blooming/blurring" effect due to magnetic susceptibility).
Class and exam questions
What does a typical arterial infarction look like on contrast-enhanced CT?
In the acute and subacute stages, it appears as a peripheral, well-defined wedge-shaped low-density lesion that shows no contrast enhancement.
What indicates the septic nature of an arterial embolism?
In septic embolism, in addition to classical wedge-shaped zones of necrosis, multiple small hypodense lesions—microabscesses—are visualized within the splenic parenchyma.
What are Gandy-Gamna bodies and in what pathology do they occur?
These are multiple small organized hemorrhages in the parenchyma that occur against the background of portal venous hypertension and venous infarctions. They contain hemosiderin.
Which method best detects Gandy-Gamna bodies?
MRI using gradient echo sequences (in-phase images), where they produce low-signal foci with a "blooming" effect due to iron magnetic susceptibility.
What else to study on this topic
- Splenic abscesses (bacterial, fungal, and tuberculous)
- Splenic trauma and evaluation of hemoperitoneum (FAST protocol)
- Cystic lesions: true congenital cysts and acquired pseudocysts
- Benign and malignant splenic neoplasms
- Polysplenia syndrome and its association with developmental defects (Kartagener syndrome)
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