Splenic infarction

Splenic infarction is a result of ischaemia to the spleen, and in many cases requires no treatment. However, identification of the cause of infarction is essential.  

Splenic infarcts can occur due to a number processes, involving either arterial supply, the spleen itself and the venous drainage. As such there is no one affected demographic; rather the demographics will represent the underlying cause.

Patients with a splenic infarction may present with left upper quadrant pain. Some may have constitutional symptoms such as fevers and chills while others may even have diffuse abdominal pain 5,9. Due to the location of the spleen, tucked under the left hemidiaphragm, referred pain to the left shoulder is also a feature 9

It should be noted that ~40% (range 30-50%) of patients with splenic infarction are asymptomatic 9

Aetiology

The majority of patients with splenic infarcts have one of the following two aetiologies: 

Other aetiological factors include 1-2:

The appearance of splenic infarction depends on the timing of imaging and the size of the infarct. Although once established both ultrasound and CT are sensitive to the diagnosis, in the hyperacute setting CT with contrast is the modality of choice if the diagnosis is suspected 9

Morphologically the typical infarct is of a pyramidal wedge of affected splenic tissue with the apex pointing towards the hilum, and the base on the splenic capsule. 

As the infarct matures, the wedge of infarcted tissue can undergo one or three processes which will dictate imaging features:

  1. resolution: no imaging findings
  2. contraction/scarring
  3. liquefaction
Ultrasound

Typically infarcts are hypoechoic compared to the rest of the spleen, although acutely they can be isoechoic and hard to identify. Sonographic features of acute splenic infarcts regarding shape can vary and include 5,9:

  • wedge-shaped (classic)
  • round 
  • irregularly
  • smooth (uncommon)

During contrast enhanced ultrasound, the infarcted area remains hypo-intense throughout all phases of the study 10

As the infarct matures, if it undergoes contraction and scarring it will appear as a hyperechoic region with retraction of the capsule 9. If liquefaction occurs, the area may be rounded and anechoic (splenic pseudocyst).

CT

CT is often considered the imaging investigation of choice, ideally performed during the portal venous phase, to avoid confusing heterogeneous enhancement normally seen during arterial phase 2,7,9. Imaging features may vary with the stage of the infarct. 

In the hyperacute phase, CT may show areas of mottled increased attenuation, representing areas of a haemorrhagic infarction. 

There are various classical and non-classical patterns of established splenic infarcts on CT, which include 3,9:

  • peripheral, wedge-shaped hypo-enhancing region: typical
  • multiple, heterogeneous areas of patchy enhancement
  • global splenic infarction, entire spleen is hypo-enhancing, e.g. in splenic torsion
  • infarction of a splenunculus 9

In the chronic phase, infarcts may disappear completely, but more commonly, they may reveal progressive volume loss caused by fibrotic contraction of the infarct, with hypertrophy of the surrounding normal spleen 7,9. Alternatively, if the infarct liquefies, a cystic lesion may be left with fluid density centrally 9

Initial management usually consists of hydration, analgesics, and frequent monitoring, with the resolution of symptoms in 7-to-14 days. Splenectomy was performed for persistent symptoms or complications.

Complications

Some complications are encountered, more frequently in patients with an embolic aetiology. These include:

Often, when imaging appearances are typical, there is little differential diagnosis. When less typical, or when imaging is sub-optimal, alternative diagnoses should be entertained, including 9:


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Article Information

rID: 17378
Section: Pathology
Synonyms or Alternate Spellings:
  • Splenic infarct
  • Splenic infarcts
  • Infarction of the spleen
  • Splenic infarctions

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    Case 12: complicated by abscess formation
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    Case 13: from infective endocarditis (US and CT)
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    Case 14 : case of Plasmodium vivax
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    Case 15: splenic artery compression by tumour
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    Case 16: with splenomegaly/myelofibrosis
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