Cerebral small blood vessel disease

Cerebral small blood vessel disease (in standard preoperative imaging reports) is independently associated with increased risk of CV death following carotid endarterectomy. This statement is produced by an article published in the European Journal of vascular and endovascular surgery2020.

1). What is cerebral small blood vessel disease?

Cerebral small vessel disease (CSVD) is composed of several diseases affecting the small arteries, arterioles, venules, and capillaries of the brain, and refers to several pathological processes and etiologies. Neuroimaging features of CSVD include recent small subcortical infarcts, lacunes, white matter hyperintensities, perivascular spaces, microbleeds, and brain atrophy. The main clinical manifestations of CSVD include stroke, cognitive decline, dementia, psychiatric disorders, abnormal gait, and urinary incontinence.

2). What are cerebral small blood vessels?

Cerebral small vessels comprise two components. First, the leptomeninges vasoganglion, which is derived from subarachnoid space covering, and the convex surface of the brain. Second, perforating arteries are derived from anterior, middle, posterior cerebral arteries that supply the subcortical parenchyma. The cerebral small vessels are crucial to the maintenance of adequate blood flow to the sub-surface brain structure. They include small arteries, arterioles, venules, and capillaries which are commonly sized at 50–400 µm.

3). What are the outcomes of cerebral small vessel disease (CSVD) of the brain?

Small vessel disease accounts for up to 25% of all ischemic strokes but also put patients at twice the risk for these conditions. In addition, CSVD is a leading cause of functional loss, disability and cognitive decline in the elderly.

4). What are the neuroimaging findings of CSVD?

Neuroimaging of CSVD primarily involves visualizing recent small subcortical infarcts, lacunar infarct, WMH, microbleeds, enlarged perivascular spaces, and brain atrophy.

5). What are lacunar infarcts?

Gattringer and colleagues recommended the new term ‘recent small subcortical infarct’ instead of the lacunar infarct.

Gattringer T, Eppinger S, Pinter D, Pirpamer L, Berghold A, Wunsch G, Ropele S, Wardlaw JM, Enzinger C, Fazekas F. Morphological MRI characteristics of recent small subcortical infarcts. Int J Stroke. 2015;10(7):1037–1043.

Lacunar stroke accounts for up to a quarter of all acute ischemic strokes. it is a small fluid-filled cavity that was thought to mark the healed stage of a small deep brain infarct. In neuroimaging, a lacuna is a round or ovoid, subcortical, fluid-filled cavity with a similar signal to cerebrospinal fluid (CSF). It measures between 3–15 mm in diameter, which is consistent with a previous acute small deep brain infarct or hemorrhage in the territory of one perforating arteriole. Lacunar infarcts are typically located in the basal ganglia, internal capsule, thalamus, corona radiata, centrum semiovale (CSO), and brainstem. Poirier and colleagues divided the lacunas into three subtypes based on the formation: Subtype I lacunas are secondary to old lacunar infarction; subtype II lacunas secondary to old hemorrhagic lesions; subtype Ⅲ lacunas are secondary to enlarged perivascular spaces. Herve and colleagues classified the lacunar lesions by three-dimensional MRI reconstruction, according to their shapes into four types: Slab, stick, multiple components, or ovoid/spheroid, then proposing that most of the lacunar infarcts (83%) were ovoid or spheroid. Infarct lesions manifest isolated, adjacent to or fused into white matter hyperintensity.

Moreau and colleagues found that lacunas almost always present at 90 days after acute lacunar infarction and appear as a central CSF-like hypointensity with or without a surrounding border of hyperintensity on FLAIR sequence but only CSF-like hypointensity and hyperintensity on T1-weighted and T2-weighted, respectively. Moreover, the sensitivity of FLAIR for cavitation was greatly lower than for T1-weighted sequences.

6). What is the effect of CSVD on people undergoing carotid endarterectomy?

The presence of SVD in pre-operative brain imaging reports can serve as a predictor for the three-year risk of cardiovascular death in symptomatic patients undergoing CEA but does not predict peri-operative or long term risk of stroke. Published: April 21, 2020DOI:https://doi.org/10.1016/j.ejvs.2020.02.004

Nephrogenic Systemic Fibrosis (NSF)

Vascular surgery patients with arterial problems generally require angiograms to evaluate the patency of the vascular lumen. There is always a concern about doing an angiogram ( CT angio or conventional angio) in those patients with decreased eGFR. Some times MRangiogram with gadolinium is recommended in. those patients. But that can result in nephrogenic systemic fibrosis (NSF).

Nephrogenic systemic fibrosis (NSF) incidence was found to be found to be 4.3 cases per thousand patient-years. When gadolinium is used in a patient there is 2.4% risk of nephrogenic systemic fibrosis. NSF is also known as nephrogenic fibrosing dermopathy. This was first described in 2006 in the Journal of American Society of nephrology by Marckmann P et al describing a case series of 13 patients. New contrast agents are introduced with the hope that they have a lesser risk of NSF. Gadobenate dimeglumine is one such newer agent. Clinically NSF looks like scleroderma and eosinophilic fasciitis but histologically it looks like scleromyxedema. Biopsy shows proliferation of dermal fibroblasts, dendritic cells, thickened collagen bundles,   increases elastic fibers and mucin deposition. Toll-Like Receptors (TLR) four and seven seems to play an important role in the development of NSF. 

Although NSF occurrence after exposure to newer GBCAs is very rare, the relatively scarce data among patients with acute kidney injury and those with risk factors for chronic kidney disease limit conclusions about safety in these populations (Joseph Lunyera 2020).