The critical care management of poor-grade subarachnoid haemorrhage

Abstract

Aneurysmal subarachnoid haemorrhage is a neurological syndrome with complex systemic complications. The rupture of an intracranial aneurysm leads to the acute extravasation of arterial blood under high pressure into the subarachnoid space and often into the brain parenchyma and ventricles. The haemorrhage triggers a cascade of complex events, which ultimately can result in early brain injury, delayed cerebral ischaemia, and systemic complications. Although patients with poor-grade subarachnoid haemorrhage (World Federation of Neurosurgical Societies 4 and 5) are at higher risk of early brain injury, delayed cerebral ischaemia, and systemic complications, the early and aggressive treatment of this patient population has decreased overall mortality from more than 50% to 35% in the last four decades. These management strategies include (1) transfer to a high-volume centre, (2) neurological and systemic support in a dedicated neurological intensive care unit, (3) early aneurysm repair, (4) use of multimodal neuromonitoring, (5) control of intracranial pressure and the optimisation of cerebral oxygen delivery, (6) prevention and treatment of medical complications, and (7) prevention, monitoring, and aggressive treatment of delayed cerebral ischaemia. The aim of this article is to provide a summary of critical care management strategies applied to the subarachnoid haemorrhage population, especially for patients in poor neurological condition, on the basis of the modern concepts of early brain injury and delayed cerebral ischaemia.

Fig. 1

Early pathophysiology of subarachnoid haemorrhage. Acute haemorrhage from an aneurysm can physically damage the brain and lead to acute transient global ischaemia. Transient global ischaemia secondary to increased intracranial pressure can also trigger sympathetic nervous system activation, leading to systemic complications. The contribution of each process to the pathophysiology is unknown, but transient global ischaemia and subarachnoid blood result in early brain injury, characterised by microcirculation constriction, microthrombosis, disruption of the blood–brain barrier, cytotoxic and vasogenic cerebral oedema, and neuronal and endothelial cell death. CBF cerebral blood flow, CPP cerebral perfusion pressure, ECG electrocardiographic, ET-1 endothelin-1, ICH intracranial haemorrhage, ICP intracranial pressure, MMP-9 matrix metalloproteinase-9, NO nitric oxide, TNF-R1 tumour necrosis factor receptor 1. First published in Nature Reviews Neurology [98]

Fig. 2

Pathophysiological processes in delayed cortical ischaemia. Key processes include angiographic vasospasm, microcirculatory constriction and formation of microthrombi, and waves of cortical spreading ischaemia, all of which can contribute to cerebral infarction. Delayed effects of the early brain injury such as neuronal and endothelial cell apoptosis, and systemic complications, can also occur. CPP cerebral perfusion pressure, ICP intracranial pressure, NO nitric oxide, SAH subarachnoid haemorrhage, TRP transient receptor potential. First published in Nature Reviews Neurology [98]

Fig. 3

Summary of a possible approach for the management of subarachnoid haemorrhage patients in poor neurological condition. ARDS acute respiratory distress syndrome, BP blood pressure, CPP cerebral perfusion pressure, CSF cerebrospinal fluid, CTA/CTP computed tomography angiography/computed tomography perfusion, DCI delayed cerebral ischaemia, DSA doxyl stearic acid, ECG electrocardiogram, GCS Glasgow Coma Scale, Hgb haemoglobin, HOB head of bed, ICH intracerebral haemorrhage, ICP intracranial pressure, IPC intermittent pneumatic compression, iv intravenously, IVH intraventricular haemorrhage, MAP mean arterial pressure, MRI/MRA magnetic resonance imaging/magnetic resonance angiography, NeuroICU neurointensive care unit, NIHSS National Institutes of Health Stroke Scale/Score, PaCO ₂ arterial partial pressure of carbon dioxide, SaO ₂ arterial oxygen saturation, SBP systolic blood pressure, SIADH syndrome of inappropriate secretion of antidiuretic hormone, SPECT single-photon emission computed tomography, T temperature, VTE venous thromboembolism, WFNS World Federation of Neurosurgical Societies

Fig. 4

Approach to low brain tissue oxygen. Consider the combined used of P_tiO₂ and microdialysis catheter to detect non-hypoxic patterns of cellular dysfunction [97]. According to the manufacturer, an equilibrium time as long as 2 hours may be necessary before P_tiO₂ readings are stable, because of the presence of the tip surrounding microhaemorrhages. Sensor damage may also occur during insertion. Increase inspired fraction of oxygen (FiO₂) to 100 %. If P_tiO₂ increases, it confirms good catheter function. Oxygen challenge to assess tissue oxygen reactivity. FiO₂ is increased from baseline to 100 % for 5 minutes to evaluate the function and responsiveness of the brain tissue oxygen probe. A positive response happens when P_tiO₂ levels increase in response to higher FiO₂. A negative response (lack of P_tiO₂ response to higher FiO₂) suggests probe or system malfunction. Another possibility if there is a negative response is that the probe placement is in a contused or infarcted area. Follow-up computed tomography might be necessary in this situation to ensure appropriate probe position. Mean arterial pressure (MAP) challenge to assess cerebral autoregulation. MAP is increased by 10 mm Hg. Patients with impaired autoregulation demonstrated an elevation in ICP with increased MAP. When the autoregulation is intact, no change or a drop in ICP levels follows the elevation in blood pressure. Another way to assess cerebral autoregulation is the evaluation of the index of P_tiO₂ pressure reactivity. When autoregulation is intact, P_tiO₂ is relatively unaffected by changes in CPP, so the index of P_tiO₂ pressure reactivity is near zero [170]. The threshold haemoglobin (Hgb) of 9 mg/dl to indicate blood transfusion was based on a previously published P_tiO₂ study [171]. CPP cerebral perfusion pressure, CSF cerebrospinal fluid, CT computed tomography, ICP intracranial pressure, PaCO ₂ arterial partial pressure of carbon dioxide, PaO ₂ partial pressure of oxygen in arterial blood, P _ti O ₂ brain tissue oxygen pressure, RASS Richmond Agitation-Sedation Scale, SAH subarachnoid haemorrhage, SBP systolic blood pressure