Subarachnoid haemorrhage (SAH) is bleeding in the subarachnoid space between the arachnoid and pia mater meningeal layers.
SAH can be a life-threatening emergency and it is estimated that 10-15% of patients die before they reach hospital.
SAH can be divided into traumatic or spontaneous
Trauma is the most common cause of SAH. There is usually evidence of trauma in the clinical history (e.g. road traffic accident). An isolated SAH in the setting of mild traumatic brain injury usually has a good prognosis. Subarachnoid haemorrhage in the context of severe traumatic brain injury is usually associated with other forms of injury such as intracerebral haemorrhage or extradural haemorrhage.
The most common causes of a spontaneous SAH are:
The primary risk factors associated with a spontaneous SAH are smoking and hypertension.
Risk factors for spontaneous SAH can be divided into modifiable and non-modifiable.
The brain is encased in three meningeal layers: the dura, arachnoid and pia mater.
Three components of neuroanatomy are critical understand SAH:
The brain is encased in three meningeal layers, which are the dura, arachnoid and pia mater (outside to inside). The pia mater is adherent to the surface of the brain and spinal cord. The subarachnoid space is found between the arachnoid and pia mater. There are multiple bloods vessels that run in this space including the circle of Willis.
The circle of Willis is an arterial polygon and is the main arterial blood supply to the brain. It connects the anterior and posterior cerebral circulation, which arise from the carotid and vertebrobasilar systems, respectively.
Circle of Willis
Saccular or berry aneurysms are usually located at the branching points of major blood vessels. The maximum haemodynamic stress in a vessel is seen at these points. Saccular aneurysms tend to occur in the anterior communicating artery (30-40%), posterior communicating artery (25%) and middle cerebral artery (20%). Approximately 10% of aneurysms occur at basilar tip or the bifurcation.
Aneurysms occur all along the anterior and posterior circulation.
Patient classically complain of a 'thunderclap' or sudden-onset headache.
Spontaneous SAH is associated with a sudden-onset or 'thunderclap' headache. This describes a severe headache that reaches maximum intensity within seconds (‘the worst headache of my life’).
Headache may be associated with photophobia (difficulty tolerating light) and neck stiffness. Collectively, these three features are known as meningism.
Both Kernig’s and Brudzinski’s are classical signs of meningeal irritation. May be seen in bacterial meningitis or subarachnoid haemorrhage. However, absence of these signs does not exclude these diagnoses.
A subarachnoid haemorrhage or enlarging cerebral aneurysm may be associated with a third nerve palsy.
The third cranial nerve is known as the oculomotor nerve. It has important motor function to the pupil, eyelid and extraocular muscles. A third nerve palsy can occur anywhere along its path from nucleus to orbital apex.
An isolated acute third nerve palsy is concerning for an enlarging aneurysm with risk of rupture and requires urgent assessment. The patient may complain of double vision and the eye will appear 'down and out' with ptosis (drooping eyelid), pupillary dilatation (if pupil involved) and loss of the light reflex (if pupil involved).
The presence or absence of pupillary involvement helps to determine the aetiology. This is because parasympathetic motor fibres associated with the pupillary light reflex are situated superficially within the nerve. Therefore, compressive lesions (e.g. aneurysms) will affect fibres leading to pupillary dilatation and loss of light reflex. On the other hand, vascular lesions (e.g. ischaemia, diabetes mellitus) tend to affect the inner fibres preferentially. This 'spares' the superficial parasympathetic fibres leading to pupillary sparing.
For more information see Third nerve palsy notes.
Diagnosis of spontaneous SAH is suspected clinically and then confirmed on imaging or cerebrospinal fluid analysis.
SAH should be suspected in any patient with a sudden or rapid onset severe headache, which is classical of SAH. These patients require urgent assessment and computed tomography (CT) of the head.
A plain CT Head is required to check for the presence of acute blood in the subarachnoid space. If performed within six hours of onset of symptoms (ictus), it has a sensitivity of 98.7% and specificity of 99.9% for detecting a subarachnoid haemorrhage. Additional imaging is required following diagnosis (discussed below).
CT head showing subarachnoid haemorrhage
This high sensitivity and specificity declines over time. The sensitivity is only 58% at day 5. If CT is performed > 6 hours from symptom onset, then a lumbar puncture is required to exclude the diagnosis.
If a CT is performed within 6 hours of symptom onset and does not show a SAH, the risk of aneurysmal SAH is < 1%. A meta-analysis in 2016 showed that the risk of 'missed SAH' was < 1.5 in 1000 patients with SAH if no lumbar puncture was completed in patients meeting the following criteria:
Therefore, the need for lumbar puncture should be a risk/benefit decision based on history, neurological status, and local pathways in patients presenting and being scanned within 6 hours. Current NICE guidelines published in November 2022 (NG228) advise that a lumbar puncture does not routinely need to be completed in this scenario.
If a CT Head does not show any evidence of SAH then a lumbar puncture (LP) is required.
A LP is used to collect and assess the cerebrospinal fluid (CSF) for evidence of SAH. This is particularly important for patients presenting > 6 hours from onset.
Typically, haemoglobin and bilirubin are not found in CSF but after a SAH, red blood cells lyse and release oxyhaemoglobin which is converted to bilirubin. Oxyhaemoglobin on its own suggests a recent bleed or a traumatic lumbar puncture but the presence of both oxyhaemoglobin and bilirubin is suggestive of SAH. The LP should be delayed by 12 hours from symptom onset to improve the sensitivity of detecting red blood cell breakdown products (e.g. xanthochromia/bilirubin)
Four factors are important when completing a LP for SAH:
Once SAH has been established, angiography is needed to determine if there is any underlying vascular lesion. This involves a contrast scan called a CT Angiogram (intracranial). This helps to determine if there is any underlying aneurysm or arteriovenous malformation. Some aneurysms may go undetected on a CT angiogram, especially if the quality is poor.
The gold standard is digital subtraction angiogram (DSA). This is an invasive procedure which requires an arterial puncture (femoral or radial) and insertion of a guidewire and contrast. This procedure is both diagnostic and therapeutic as aneurysms can be investigated but also secured to prevent a re-bleed using coils and other various interventional devices.
It is very important to distinguish unruptured intracranial aneurysms (UIA) from aSAH.
UIA and aSAH are two separate entities (UIA ≠ aSAH). With the increasing use of imaging, more and more incidental aneurysms are being detected. Spontaneous SAH due to a ruptured aneurysm is a clinical emergency, whereas UIA are managed in a multi-disciplinary neurovascular setting and in outpatient clinics. There are scoring systems available to help manage UIAs including PHASES and ISUIA.
Patients with a suspected SAH require urgent observations, bloods, imaging +/- lumbar puncture.
NOTE: Cushing's reflex is a physiological response to raised intracranial pressure, which causes hypertension, bradycardia and irregular respirations (Cushing's triad). It is a late sign and suggests impending brainstem herniation.
In the acute setting, additional bloods such as CRP may be performed if the differential for a headache includes an infective cause such as meningitis.
Discussed further in diagnosis.
Discussed further in diagnosis.
Subarachnoid haemorrhage is a medical emergency that requires urgent management.
The management of SAH has several key elements.
Whilst the initial investigative work-up and management happens under emergency or medical care, spontaneous aSAH is managed under neurosurgery.
Patients with a SAH can present fully alert or conscious or in a coma. This is assessed using the Glasgow Coma Score (from 3 to 15) and determines the grading (see under clinical scores). A systematic ABCDE is utilised in emergency settings. If the patient has a low GCS (below 8) they will require airway management. Otherwise, they are investigated with appropriate imaging or lumbar puncture as needed.
A patient presenting with a suspected aSAH should be monitored closely with neuro-observations.
As there is always a risk of re-rupture, patients should be given analgesia, anti-emetics to prevent Valsalva whilst vomiting. Intravenous fluids are commenced with strict input/output monitoring. As patients require close monitoring they are transferred to neurosurgery to a level 1 bed or high dependency bed (HDU).
Patients are given nimodipine 60mg every 4 hours for 21 days from ictus of symptoms. It is incorrectly stated this reduces the risk of cerebral vasospasm. This is partially the case as the trial this is derived from demonstrated more favourable outcomes and reduced incidence of vasospasm in the group that received nimodipine compared to the control.
Most importantly, they require a prompt CT angiogram. If there is indeed an aneurysm, they will be transferred to the neurosurgical team for further management
If the patient presents with a low GCS in the setting of SAH, they may have developed a neurosurgical emergency known as hydrocephalus (accumulation of CSF in the ventricular system) which can be diagnosed on a CT Head. Other causes of low GCS may occur including seizures.
After initial resuscitation and airway management, the presence of hydrocephalus may require insertion of an external ventricular drain (EVD). This is a form of CSF diversion and helps to reduce intracranial pressure. This does not drain the blood from a SAH nor is that the purpose of this procedure. It is intended to manage hydrocephalus
If an aneurysm is detected, it needs to be secured to prevent a further bleed. This is a complex decision made under the neurosurgical team but can be done under interventional radiology during a DSA.
The two principle methods include:
Either method will secure the aneurysm and minimise the risk of further bleeds. Coiling is more commonly utilised.
SAH are associated with several complications including rebleeding and vasospasm.
If an aneurysm has been identified, it is prone to re-bleeding until it is secure. This requires coiling or clipping.
There is a risk of cerebral vasospasm in SAH as the blood load can irritate the arterial vasculature prompting a spasm which may cause strokes.
Vasospasm is a major complication from day 3-7 post ictus. Patients receive nimodipine for 21 days from ictus to reduce poor outcomes.
Early or late hydrocephalus may develop post SAH which requires CSF diversion via an EVD or a lumbar drain.
Several scores associated with SAH, including the modified World Federation of Neurological Societies (mWFNS) and modified fisher.
This score is used for grading the severity of an aneurysmal SAH and the modified Fisher for the risk of vasospasm associated with SAH.
The mWFNS is based on the Glasgow Coma Score (3-15) of the patient on presentation with an aSAH. This score is linked to likely outcomes of the patient using the Glasgow Outcome Scale (GOS) and modified Rankin Scale (mRS).
For example, a patient with a proven SAH on CT Head who is GCS E4V4M6 (14) would be classed as mWFNS Grade 2. Please note, some older resources refer to the original WFNS grading system from 1988 which mentions neurological deficit and this is now considered outdated. The most recent version uses only GCS.
This score is used to assess the risk of vasospasm associated with SAH.
The modified Fisher scale is used to determine the risk of vasospasm based on the findings on imaging. In any bleed, vasospasm can occur due to contact between blood products and the lining of the arterial wall. This can result in strokes and delayed ischaemia. The amount and degree of blood load can determine the risk of vasospasm.
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