Septic-embolic encephalitis

Last revised by Ian Bickle on 11 Jul 2020

Septic-embolic encephalitis, also known as septic-embolic brain abscess, refers to a focal or diffuse brain infection, ischemic and hemorrhagic damages following infective thromboembolism from any part of the body. It is usually caused by bacterial infections from endocarditis

Septic-embolic encephalitis must be differentiated from sepsis-associated encephalopathy, which is a clinical syndrome related to diffuse brain dysfunction in the context of sepsis without overt central nervous system (CNS) infection 5.

In most series, CNS involvement during the course of infective endocarditis occurs in ~30% (range 20-40%) of cases 2

Ischemic stroke is the most common mode of presentation of patients with septic-embolic encephalitis 1. Symptoms can vary from headache to unconsciousness, the most common are 1,3

Some etiological agents can get in the CNS carried by arterial blood from multiple systemic infectious foci 1-4

  • left-sided cardiac infections (i.e. aortic and mitral valve endocarditis)
  • pulmonary infections
  • infections in other body sites that can get the arterial circulation by an arteriovenous shunt

There are three main pathogenic mechanisms of brain damage 4:

  • occlusion of cerebral arteries by septic and thrombotic emboli (e.g. arising from heart valve vegetations): it can result in focal ischemia, cerebral hemorrhage, or both
  • meninges, brain parenchyma, or vascular walls infection by septic emboli or bacteremia; numerous microabscesses can be seen and occasionally they coalesce to form space-occupying macroabscesses
  • toxic and immune-mediated injury
  • Staphylococcus aureus (most common)
  • Streptococcus viridans
  • fungal infection

In almost 90% of cases of septic-embolic encephalitis findings occur in the distribution of middle cerebral artery (MCA) (due to favored anatomy), and rarely in the posterior circulation 1

MRI is superior to CT in depicting the different stages of septic-embolic encephalitis evolution.

Hypodense areas of ischemic infarction along with hyperdense hemorrhagic areas may be spotted in the anterior circulation territories. Contrast-enhanced images are essential to evaluate abscess formation. 

Local arteritis can promote mycotic aneurysm formation and vascular rupture.

Prompt administration of empiric antibiotics until the results of culture are available is vital. In cases that emboli continue to form despite antimicrobial treatment, surgical heart valve replacement may be necessary. 

Mycotic aneurysm: many regress spontaneously under clinical treatment, however, persistent aneurysms may need surgical or endovascular treatment 4.

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