Subarachnoid haemorrhage
Written by Sophie Robinson
Last Reviewed: September 2019
Review Due: September 2020
DEFINITION
'a subarachnoid headache (SAH) is bleeding into the subarachnoid space of the brain, located between arachnoid and pia mater meningeal layers'
AETIOLOGY1-4
Majority of SAH are caused by traumatic injuries
Spontaneous non-traumatic SAH are caused by
Rupture of saccular aneurysms in 80%
The remaining 20% are classed as non-aneurysmal perimesencephalic SAH which can result due to
Arteriovenous malformation which is an abnormal connection between arteries and veins
Arterial dissections
Use of anticoagulants
No defined cause
Vasculitis
Risk factors for spontaneous SAH
Female sex
Smoking – approximately 40% of SAH cases can be attributed to cigarette
smoking
Hypertension
Alcohol abuse
Close relatives have a 3-5 fold increased risk of SAH
Bleeding disorders
Autosomal dominant polycystic kidney disease
Connective tissue disorders (Ehlers-Danlos syndrome)
SIGNS AND SYMPTOMS2,5
Signs
Neck stiffness
Terson’s syndrome – retinal, subhyaloid or vitreous bleeds
Focal neurology at initial presentation can indicate site of aneurysm ie such as surgical IIIrd nerve palsy which can be due to compression of the posterior communicating artery by the aneurysm
Symptoms
Sudden onset headache:
Typically located in occipital region
Can be described as “being hit over the head with a baseball bat” or “thunderclap”5=
Reaches maximum intensity within seconds
Sentinel headache can occur a couple of weeks before onset of SAH:
Potentially due to a small warning leak from the offending aneurysm
Affects around 10-43% of patients
Nausea and vomiting
Photophobia
Collapse
Reduced conscious level
Seizures
Coma
Differential diagnosis for thunderclap headache
Trauma
SAH
Arterial dissection
Bacterial meningitis
Cerebral venous sinus thrombosis
Intracerebral haemorrhage
PATHOPHYSIOLOGY1-4,6,8
Structural abnormalities as a result of inflammatory processes will be acquired in the intimal and medial layers of cerebral vessels leading to the formation of cerebral aneurysms over a gradual period of time.
Berry aneurysms commonly form at junctions/bifurcations between the major cerebral vessels due to greater haemodynamic stress and turbulence1.
These include the bifurcation of the middle cerebral artery, junction of the anterior communicating with anterior cerebral artery, junction of posterior communicating with the internal carotid. Up to 19% of patients will be found to have multiple aneurysms.
The risk of aneurysm rupture will depend on its size, location, presence of symptoms, presence of multiple aneurysms, and the ethnicity of a patient, smoking history, hypertension, alcohol use and whether previous aneurysms have ruptured.
When the aneurysm ruptures blood, still under the force of arterial pressure, will be forced into the subarachnoid space until intracranial pressure equalises at the rupture site causing the bleeding to cease1.
This dramatic increase in intracranial pressure in conjunction with the damage the blood does directly to brain tissue and cerebral vasculature, elicits the signs, symptoms and complications of SAH.
The World Federation of Neurological Surgeons Grading Scale uses the GCS and includes the presence of focal neurological deficits, determined by motor deficit, to grade SAH severity.

Investigations
laboratory2-4
Full Blood Count
To help guide any blood transfusion needs
Crossmatch
Blood typing for transfusion
U&Es
May show hyponatraemia due to salt wasting
Glucose
Coagulation Screen
May show elevated INR, prolonged PTT
CRP
Serum troponin
Can be elevated in up to 30% of cases during the first 24 hours in the absence of coronary artery disease2
imaging
Non-contrast CT
Will detect >90% of SAH within the 1st 24 hours
Sensitivity decreases with time after the first 24 hours
Acute blood will appear hyperdense (white) on CT
The Fisher Scale can be used to predict cerebral vasospasm and clinical outcome after SAH dependent on the pattern of blood on initial CT
bedside
12-lead ECG
Approximately half of patients have an abnormal ECG on admission2
Arrhythmias
Prolonged QTc
ST-segment/T wave abnormalities
LP
If history is suggestive of SAH but the CT is initially negative
Ensure there is no contraindication for LP
Performed after 12 hours of headache onset to detect presence of xanthochromia in CSF (breakdown products of bilirubin)
Remains a sensitive test for identifying SAH for up to 2 weeks
treatment2-4,9,10
initial management
Refer to neurosurgery immediately
MDT input including neurosurgeons, neuroradiological interventionalists, intensivists
Admitted to intensive care unit once stabilised, ideally neurological or neurosurgical ICU
Intensive continuous monitoring including repeat neurological examinations and measures of GCS, BP, temperature, respiratory rate and heart rate
Initial stabilisation
Maintain cerebral perfusion pressure through adequate hydration
Stop antihypertensive medication unless HTN is extreme:
Systolic BP should be kept below 180mmHg until coiling or clipping of ruptured aneurysm to reduce risk for rebleeding
Fluid resuscitated with 2.5-3.0L of isotonic saline
Anti-embolic stockings as thromboprophylaxis – use of low-molecular weight heparins can increase the risk of intracranial bleeding
Analgesia
Nimodipine (calcium antagonist) to reduce vasospasm risk which has been shown to improve mortality and morbidity after SAH in a Cochrane review
adjuncts
Most surgeons will operate on patients who have a good neurological status during the first 72 hours to prevent rebleeding
There are two surgical options to secure the aneurysm: endovascular coiling and endovascular clipping
Coiling
Coiling typically preferred where possible due to better long-term outcome, but does have an increased risk of rebleeding as found by the International Subarachnoid Haemorrhage Trial (ISAT)
Coiling involves using platinum coils inserted into the aneurysm using a micro-catheter around which blood clots will form around the platinum coil and which will seal off the aneurysm and reduce pressure on the outer wall
About 1 in 5 people who have coiling procedure need further treatment
Coiling is typically a less invasive procedure and patients will usually leave the hospital sooner after the operation
Clipping
Clipping will involve exposing the aneurysm with a craniotomy and closing the base of the aneurysm with a clip
Open surgical clipping may be favoured in cases that also require clot evacuation or decompressive surgery
complications2,10
Rebleeding
Commonest cause of death
Occurs in 22% at 1 month after SAH
Risk factors for rebleeding include size of aneurysm and systemic hypertension
Cerebral ischaemia due to vasospasm
Delayed, focal or diffuse narrowing of large vessels in the circle of Willis due to the presence of blood in the subarachnoid space
Can result in permanent CNS deficit
Pathophysiology poorly understood, believed to result from delayed and reversible vasculopathy, impaired autoregulatory function and hypovolaemia, resulting in global or regional reduction of cerebral perfusion eventually leading to ischaemia
Develops between days 4 and 14 after SAH and can be seen via angiography in up to 70% of cases
Commonest cause of morbidity
Treated prophylactically with nimodipine
Hydrocephalus
Occurs in 15-20% of patients during first 72 hours2
Patient will present with signs of raised intra-cranial pressure including vomiting, impaired eye movements, reduced GCS, headache, vomiting
Can require placement of ventricular drain (commonly ventriculo-peritoneal drain) if it does not alleviate spontaneously
Hyponatraemia
Seizures
Antiepileptic treatment administered in patients with clinically apparent seizures
No evidence supporting the use of prophylactic antiepileptic drugs
Cardiac abnormalities
Arrhythmias
Non-specific ECG changes
Pulmonary oedema
prognosis1-3
Influenced by multiple non-modifiable factors and factors that are under the influence of therapeutic interventions and clinical management
Old age, level of responsiveness on admission and volume of subarachnoid blood are some of the most importance determinants for outcome following a SAH
Mortality rate of approximately 60% within 6 months
Mortality is slightly greater in black patients and women
Significant morbidity with around 50% of patients unable to return to work post-
SAH due to cognitive impairment
EPIDEMIOLOGY1
Affects approximately 7000 patients per year in the UK
The average age of onset is between 50 and 55 years
SAH accounts for about 5% of all strokes
REFERENCES
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Lawton MT, Vates GE. Subarachnoid Haemorrhage. New England Journal of Medicine. 2017; 377: 257-266, doi: 10.1056/NEJMcp1605827
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Keyrouz S. Subarachnoid Haemorrhage. BMJ Best Practice. 2018.
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Steiner T, Juvela S, Unterberg A, Jung C, Forsting M, Rinkel G. European Stroke Organisation
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Guidelines for the Management of Intracranial Aneurysms and Subarachnoid Haemorrhage. Cerebrovascular Diseases. 2013; 35(2): 93-112
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Longmore M, Wilkinson IB, Baldwin A, Wallin E. Subarachnoid haemorrhage. Oxford Handbook of Clinical Medicine, 9th edition. 2014.
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NHS. Brain aneurysm. NHS. 2018.
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Rosen DS, Macdonald RL. Subarachnoid Haemorrhage Grading Scales. Neurocritical Care. 2005; 2(2): 110-118
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Hunt WE, Hess RM. Surgical risk as related to time of intervention in the repair of intracranial aneurysms. J Neurosurg. 1968; 28(1): 14-20
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Report of World Federation of Neurological Surgeons committee on a universal subarachnoid haemorrhage grading scale. J Neurosurg 1988; 68: 985-986
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Molyneux AJ, Kerr RS, Yu LM, Sneade M, Yarnold JA, Sandercock P. International subarachnoid aneurysm trial (ISAT) of neurosurgical clipping versus endovascular coiling in 2143 patients with ruptured intracranial aneurysms: a randomised comparison of effects on survival, dependency, seizures, rebleeding, subgroups, and aneurysm occlusion. Lancet. 2005; 366(9488): 809-17