Intracerebral microbleeds in sepsis: susceptibility-weighted MR imaging findings

Abstract

We present two patients with sepsis and intracerebral microbleeds. The first case is a nine years old girl who presented visual hallucinations, tremors in the limbs, and an episode of generalized tonic-clonic seizure in the 12 th day of an otherwise successfully treatment of a pulmonary sepsis. Brain magnetic resonance imaging (MRI) showed numerous small rounded foci of decreased signal intensity on susceptibility-weighted imaging (SWI) spread throughout the brain, predominantly in the corpus callosum (Fig 1), which had high signal intensity on the phase map of SWI, suggesting blood deposits. The remaining conventional MRI sequences were normal. The patient and her mother denied any history of head trauma. During hospitalization, platelets counts, partial thromboplastin time, prothrombin time, and international normalized ratio were always normal.The second patient is a 40 years old woman treating a septic shock of urinary origin for three weeks, who presented generalized tonic-clonic seizures. SWI showed linear low signal intensity on the cortex surface, mainly in frontal lobes, and multiple foci of low signal intensity on the subcortical white matter and cerebellum, which had high signal intensity on the phase images of SWI, suggesting areas of subarachnoid hemorrhages in the frontal lobes and microbleeds into the subcortical white matter and cerebellum (Fig 2). During hospitalization, D-dimer was normal. Although she had some altered values in platelets count (100,000/mm 3 , was the lower value), prothrombin time (worst INR value was 2.3), and partial thromboplastin time, due to sepsis, she did not developed disseminated intravascular coagulation.The typical imaging features of intracerebral microbleeds are small foci of decreased signal intensity on gradient-recalled echo T2* and/or SWI on MRI, usually without correspondence on others sequences 1 . Generally, microbleeds are related with hemorrhagic transformation of an ischemic stroke, recurrence of spontaneous intracerebral bleeding, cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy, cerebral amyloid angiopathy and trauma 1. There are few studies correlating intracerebral microbleeds with infective endocarditis 2 , but none with other causes of sepsis. -weighted imaging (A) and phase images of susceptibility-weighted imaging (B) show multiple foci of low signal intensity on genu and splenium of the corpus callosum and subcortical white matter on susceptibility-weighted imaging, with high signal intensity on the phase images of susceptibility-weighted imaging, suggesting blood deposits. FLAIR image (C) on the same position shows no abnormalities.

Cerebral Microbleeds: Imaging and Clinical Significance

“…A number of critical medical conditions are associated with occurrence of CMBs and should be considered as causal factors when CMBs are encountered in critically ill patients without previous neurologic conditions (Fig 9). These conditions include infective endocarditis (90) (with microbleeds in over 50% of patients) (91), extracorporeal membrane oxygenation (92), and sepsis (93). Although the exact mechanism through which microbleeds develop in these conditions is unknown, hypotheses range from pyogenic vasculitis or subacute microvascular inflammatory processes (94) to endothelial dysfunction and microemboli (93).…”

Astroglia in Sepsis Associated Encephalopathy

“…Atherosclerosis and hypertension related vessel damage impair autoregulation of brain blood circulation, which may rapidly decompensate in systemic inflammation and MODS. This is particularly evident in ischemic-reperfusional and hemorrhagic damage over the most vulnerable regions of the brain [193,194].…”

A murine model of inflammation-induced cerebral microbleeds

“…It is now well recognized that CMH are not only associated with cerebrovascular diseases including stroke, cerebral amyloid angiopathy (CAA), and cerebral hypertensive vasculopathy [1] but are also found in patients with sepsis [7], Parkinson’s disease [8], chronic obstructive pulmonary disease (COPD) [9], and traumatic brain injury (TBI) [10] and in normal aging adults [1]. One common feature of these entities is systemic inflammation [11], and recent human studies show a link between systemic inflammation and CMH pathogenesis.…”