Diagnosis of cerebral vasospasm and risk of delayed cerebral ischemia related to aneurysmal subarachnoid haemorrhage: an overview of available tools

Abstract

In the first weeks following aneurysmal subarachnoid haemorrhage, cerebrovascular alterations may impact the outcome significantly. Diagnosis of cerebral vasospasm and detection of alterations at risk of delayed cerebral ischemia are key targets to be monitored in the post-acute phase. Available tools include clinical monitoring, as well as studies that can detect possible arterial narrowing, alterations of perfusion, metabolism and neurophysiology. Each technique is able to investigate possible vascular impairment and has different advantages and limits. All available techniques have been described. Among these, the most practical have been selected and compared for their peculiar characteristics. Based on this analysis, a flowchart to monitor these patients is finally proposed.

Serum soluble lectin‐like oxidized low‐density lipoprotein receptor‐1 as a biomarker of delayed cerebral ischemia after aneurysmal subarachnoid hemorrhage

“…WFNS scores, modified Fisher score, and Hunt‐Hess score are highly associated with hemorrhagic severity after aSAH and are usually recorded to predict occurrence of DCI. However, DCI is a complex process with underlying complicated pathophysiological mechanisms (Bacigaluppi et al, ; Carr et al, ; Foreman, ). As a consequence, some biomarkers have been fully investigated for their predictive ability for DCI in recent decades (Yang et al, ; Zhu et al, ).…”

“…After aSAH, cerebral vasospasm can induce the decreased cerebral blood flow, subsequently resulting in delayed cerebral ischemia (DCI), and finally leading to severe neurological deficit and even death (Burrell et al, ; Francoeur & Mayer, ; Geraghty & Testai, ). The accumulating evidence shows microvasculature, coagulation and fibrinolytic systems, cortical spreading depressions, and the immune system might participate in pathophysiological process of DCI (Bacigaluppi et al, ; Carr, Zuckerman, & Mocco, ; Foreman, ). However, the actual pathogenesis of DCI still warrants to be explored.…”

Elevated IL-6 and TNF-α Levels in Cerebrospinal Fluid of Subarachnoid Hemorrhage Patients

“…Of the 57 SAH patients, 10 patients were classified as neurological grade I, 25 as neurological grade II, 14 as neurological grade III, and 8 as neurological grade IVor V. Based on the presence of CVS, SAH patients were divided into two groups: CVS group (n=27) and non-CVS group (n=30). The diagnostic criteria for CVS were as follows: (1) symptom fluctuation or disease aggravation after treatment; (2) drowsiness or patient became progressively confused and entered into coma; (3) presence of focal signs; (4) increased intracranial pressure; (5) patients were confirmed as mild CVS (120~140 cm/s), moderate CVS (141~200 cm/s), and severe CVS (141~200 cm/s) based on the middle cerebral artery (MCA) blood flow measured by transcranial Doppler (TCD) ultrasonography, and the flow velocity ratio for MCA and internal carotid artery (ICA) was more than 3; and (6) rebleeding after SAH [24]. In addition, 65 healthy controls (35 males and 30 females; mean age 59.2±10.6 years, range 32 to 73 years; average BMI 20.5±3.1 kg/cm 2 ), without any history of steroids and immunosuppressive drugs, were enrolled as healthy group at the same medical center.…”

Non-invasive assessment of intracranial pressure

“…The authors calculated a pressure index from the EEG analysis in brain‐injured patients and detected a significant negative correlation between pressure index and ICP ( r = −0.849, P < 0.001). However, EEG is not an immediately available technique and thus may not be suited for the emergency setting , and this technique requires further validation before it can be applied in clinical practice.…”