Diagnosis and management of subarachnoid haemorrhage

Abstract

Aneurysmal subarachnoid haemorrhage (aSAH) presents a challenge to clinicians because of its multisystem effects. Advancements in computed tomography (CT), endovascular treatments, and neurocritical care have contributed to declining mortality rates. The critical care of aSAH prioritises cerebral perfusion, early aneurysm securement, and the prevention of secondary brain injury and systemic complications. Early interventions to mitigate cardiopulmonary complications, dyselectrolytemia and treatment of culprit aneurysm require a multidisciplinary approach. Standardised neurological assessments, transcranial doppler (TCD), and advanced imaging, along with hypertensive and invasive therapies, are vital in reducing delayed cerebral ischemia and poor outcomes. Health care disparities, particularly in the resource allocation for SAH treatment, affect outcomes significantly, with telemedicine and novel technologies proposed to address this health inequalities. This article underscores the necessity for comprehensive multidisciplinary care and the urgent need for large-scale studies to validate standardised treatment protocols for improved SAH outcomes.

Fig. 1. Computerised tomography (CT) of the brain and CT Angiography of subarachnoid and intraventricular haemorrhage.

A Computerised tomography scan showing subarachnoid and intraventricular haemorrhage; B Culprit aneurysm shown on 3D rendering from CT angiography, treated with an external ventricular drain; C Closer view of unruptured aneurysm.

Fig. 2. An approach to the management of aneurysmal subarachnoid haemorrhage.

NCCT non-contrast CT, CTA CT angiography, DSA digital subtraction angiography, MRI magnetic resonance imaging, MRA magnetic resonance angiography, ABCDE airway breathing circulation disability exposure, GCS Glasgow coma scale, SBP systolic blood pressure, MAP mean arterial blood pressure, ICP intracranial pressure, EVD external ventricular drain, Hb haemoglobin, ECG electrocardiogram, DCI delayed cerebral ischaemia, CPP cerebral perfusion pressure, TCD transcranial doppler, TCCD transcranial colour doppler, EEG elecroencephalogramPtiO₂-brain tissue oxygenation, CMD cerebral microdialysis, CBF cerebral blood flow, ARDS acute respiratory distress syndrome, IAP intraabdominal pressure, DVT deep vein thrombosis, HAI hospital-acquired infection, LOC loss of consciousness. Created with Biorender.com.

Fig. 3. Pathophysiology of aSAH.

The time ranges at bottom depict approximate/presumed periods when the various processes occur. CSF cerebrospinal fluid, CBF cerebral blood flow, CBV cerebral blood volume, ICP intracranial pressure, Oxy-Hb oxyhaemoglobin, EDHF endothelial derived hyperpolarising factor, ET-1 endothelin 1, FasL Fas ligand, AIF apoptosis inducing factor, IL-6 interleukin 6, NO nitric oxide, PAF platelet-activating factor, PGI2 prostacyclin, TNFR tumour necrosis factor receptor, vWF von Willebrand factor, DCI delayed cerebral ischaemia, BBB blood brain barrier.