Spontaneous subarachnoid haemorrhage

Abstract

Subarachnoid haemorrhage (SAH) is the third most common subtype of stroke. Incidence has decreased over past decades, possibly in part related to lifestyle changes such as smoking cessation and management of hypertension. Approximately a quarter of patients with SAH die before hospital admission; overall outcomes are improved in those admitted to hospital, but with elevated risk of long-term neuropsychiatric sequelae such as depression. The disease continues to have a major public health impact as the mean age of onset is in the mid-fifties, leading to many years of reduced quality of life. The clinical presentation varies, but severe, sudden onset of headache is the most common symptom, variably associated with meningismus, transient or prolonged unconsciousness, and focal neurological deficits including cranial nerve palsies and paresis. Diagnosis is made by CT scan of the head possibly followed by lumbar puncture. Aneurysms are commonly the underlying vascular cause of spontaneous SAH and are diagnosed by angiography. Emergent therapeutic interventions are focused on decreasing the risk of rebleeding (ie, preventing hypertension and correcting coagulopathies) and, most crucially, early aneurysm treatment using coil embolisation or clipping. Management of the disease is best delivered in specialised intensive care units and high-volume centres by a multidisciplinary team. Increasingly, early brain injury presenting as global cerebral oedema is recognised as a potential treatment target but, currently, disease management is largely focused on addressing secondary complications such as hydrocephalus, delayed cerebral ischaemia related to microvascular dysfunction and large vessel vasospasm, and medical complications such as stunned myocardium and hospital acquired infections.

Figure 1:. Neuroimaging of patients with aneurysmal subarachnoid haemorrhage

Head CT demonstrating modified Fisher scores 1 (A, B), 2 (C, D), 3 (E, F), 4 (G, H), hydrocephalus (I, J), and intracerebral haemorrhage (K, L).

Figure 2:. Management approach for patients with aneurysmal subarachnoid haemorrhage

SAH=subarachnoid haemorrhage. BLS=basic life support. ACLS=advanced cardiac life support. ICP=intracranial pressure. MAP=mean arterial pressure. SBP=systolic blood pressure. DCI=delayed cerebral ischaemia. IIC=ictal-interictal continuum. IABP=intra-aortic balloon pump. EEG=electroencephalogram. *As per US guidelines (European guidelines recommend <180 mm Hg).

Figure 3:

Digital subtraction angiography of patient demonstrating right, multilobulated middle cerebral artery bifurcation aneurysm

Figure 4:. Patient with aneurysmal SAH and DCI diagnosed with multimodality monitoring and cognitive-motor dissociation

A 73-year-old woman who presented with severe headache and loss of consciousness. She was diagnosed with aneurysmal subarachnoid haemorrhage (SAH) (A, B; Hunt Hess 4, mFS 4) from an aneurysm at the right middle cerebral artery (CT angiography; C). Operative treatment failed at an outside hospital before she was transferred to a tertiary care centre. She arrived in deep coma with a coma recovery scale-revised score of 9 out of 23 that quickly deteriorated to 7. To support detection of delayed cerebral ischaemia (DCI), on post-bleed day 5 the decision was made to place a multimodality monitoring bundle into the left frontal lobe (placement on the right was impossible due to the previous craniotomy) including measurements for intracranial pressure (ICP), brain oxygenation (PbtO2), brain temperature, regional cerebral blood flow (rCBF), cerebral microdialysis (MD), and surface and intracortical electroencephalogram (EEG). Baseline EEG demonstrated a minor breach over the right hemisphere but otherwise symmetric EEG (K). On post-bleed day 10 she was diagnosed with DCI triggered by focal changes on surface EEG (L) and PbtO2, rCBF, cerebral glucose, pyruvate and rising lactate and lactate-pyruvate ratio (LPR) (M, first dotted line). On post-bleed day 13 she was diagnosed with cognitive motor dissociation using the motor command protocol while the coma recovery scale-revised remained unchanged at 7 (M, second dotted line). She was severely disabled at 3 months (Glasgow outcome scale-extended of 3) post-injury.