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

  1. Lawton MT, Vates GE. Subarachnoid Haemorrhage. New England Journal of Medicine. 2017; 377: 257-266, doi: 10.1056/NEJMcp1605827

  2. Keyrouz S. Subarachnoid Haemorrhage. BMJ Best Practice. 2018. 

  3. Steiner T, Juvela S, Unterberg A, Jung C, Forsting M, Rinkel G. European Stroke Organisation 

  4. Guidelines for the Management of Intracranial Aneurysms and Subarachnoid Haemorrhage. Cerebrovascular Diseases. 2013; 35(2): 93-112 

  5. Longmore M, Wilkinson IB, Baldwin A, Wallin E. Subarachnoid haemorrhage. Oxford Handbook of Clinical Medicine, 9th edition. 2014. 

  6. NHS. Brain aneurysm. NHS. 2018.

  7. Rosen DS, Macdonald RL. Subarachnoid Haemorrhage Grading Scales. Neurocritical Care. 2005; 2(2): 110-118

  8. 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

  9. Report of World Federation of Neurological Surgeons committee on a universal subarachnoid haemorrhage grading scale. J Neurosurg 1988; 68: 985-986

  10. 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

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