Splenic infarct

Principles

• Most infarcts occur for a reason - either embolic or because of a prothrombotic state - and the cause needs to be found
  • Older patients - cardioembolic/atherosclerotic
  • Younger patients - APS, haematological disorders, infections
• Most patients get anticoagulation
• Intervention is reserved for complications - abscess, haemorrhage

Risk factors

• 72% had a comorbidity a/w splenic infarction

Aetiology

Embolus (62.5% in one case series)

• • Cardiogenic
    • AF
    • AMI
    • Iatrogenic - after a cardiac procedure
    • Infective endocarditis
    • Valvular
      • Mitral valve disease/replacement
      • Aortic valve replacement
  • Aortic
  • Paradoxical

Thrombosis

• • Infection-associated - pancreatic abscess, sepsis, malaria
  • Autoimmune disease - lupus, APS
  • Haematological disease - myeloproliferative disorder, myelodysplastic syndrome, sickle cell disease
    • Most common cause in patients under 40
    • CML especially associated with splenic infarcts
  • Cryptogenic - actually unusual
  • Splenic vein/PV thrombosis
  • Trauma
  • Atherosclerosis

Presentation

• Pain 85%
  • LUQ pain 50%
• WCC elevated 30%

Complications

• Can transform into abscess
• Haemorrhagic necrosis - unlikely
• Persistent pain longer than 2/52 could be an indication for splenectomy

Investigation

• CT - arterial phase to look for proximal sources of emboli, and perhaps PV phase to assess for local anatomy/complications etc. Remember to look for emboli to other organs, including limbs.
• ECG
• Echo?
• Holter?
• BCs
• Haematology workup: JAK2/APS

Management

• Anticoagulation if there is a prothrombotic state, cardioembolic source, malignancy, thrombophilia, or a truly cryptogenic infarct
• Anticoagulation not used in sickle cell disease
• If sepsis/fever, treat initially for splenic abscess
• If can't find source, needs thrombophilia panel, echo, Holter, etc