Subarachnoid haemorrhage (SAH) describes bleeding into the subarachnoid space of the brain, which is located between the arachnoid and pia mater meningeal layers. These meningeal layers cover the brain and have a protective effect against intracerebral infections. Arachnoid villi are present in the arachnoid mater, which continuously absorb cerebrospinal fluid (CSF) circulating around the central nervous system (CNS).
SAH is a devastating and life-threatening condition, which damages the brain through hypoxia, increased intracranial pressure (ICP) as well as through direct cranial injury. If left untreated, it can lead to permanent neurological disabilities, coma and death. Death rates from the initial SAH are reported to range between 40-60%. 1
SAH can be associated with a traumatic injury or be spontaneous.
The majority of SAH are caused by traumatic injuries, such as road traffic accidents (RTAs), however, in this article, we will focus predominantly on spontaneous SAH.
It is important to note that, for spontaneous SAH, most intracranial aneurysms remain asymptomatic until they rupture and cause a haemorrhage. Outlined below are the common clinical features of SAH.
General clinical features
Sudden onset severe headache, reaching maximum intensity within seconds (often referred to as a “thunderclap headache”)
Nausea and vomiting
Other clinical features
Reduced conscious level:
Loss of consciousness can occur secondary to raised intracranial pressure
Occurs secondary to meningeal irritation
The inability to extend the knee due to pain when the patient is supine and the hip and knee are flexed to 90º.
A positive Kernig’s sign is caused by irritation of motor nerve roots passing through inflamed meninges as they are under tension.
Kernig’s sign is however unreliable and is only a test of non-specific meningeal irritation, meaning that other pathology such as bacterial or viral meningitis can also cause a positive result.
Full history and examination
A full history and examination are essential in narrowing the differential diagnosis.
If the patient is too unwell to give a complete history, you may need to gain a collateral history from relatives, friends or other witnesses.
Coagulation studies (useful to know prior to lumbar puncture or surgery)
Urgent CT imaging
Plain CT head scan – this is to look for evidence of blood in the subarachnoid space or hydrocephalus
CT angiogram – this highlights the arterial vessels of the brain using contrast, which can sometimes allow identification of an aneurysm
This is only necessary if SAH is suspected but the CT scan is clear and does not show any evidence of raised intracranial pressure (risk of brainstem coning).
A lumbar puncture needs to be performed at least 12 hours after the onset of symptoms, for the result to be reliable.
Visual inspection and chemical analysis of the CSF is done to identify xanthochromia. This is when the CSF has become stained yellow due to the infiltration of blood from the haemorrhage.
Analysis can reveal an increase in pigments, such as bilirubin and oxyhaemoglobin, resulting from haemolysis of red blood cells.
Both traumatic and spontaneous SAH types are a medical emergency, requiring prompt treatment and stabilisation.
Initially, a thorough ABCDE assessment should be performed, with urgent problems identified and managed appropriately to stabilise the patient.
The airway should be assessed to ensure it is patent. Patients with a reduced level of consciousness, as can be the case in SAH, are at risk of occluding their airway and may require intervention (e.g. oropharyngeal airway or intubation).
Respiratory rate and oxygen saturations
Auscultation of the lung fields
Patients may be hypoxic secondary to an occludedairway or early aspirationpneumonia
Blood pressure and pulse should be recorded
IV fluids may need to be administered to maintain an adequate blood pressure
Patients may require electrolytereplacement (hyponatraemia common in SAH)
Calcium channel blockers (e.g nimodipine) must be given to reduce cerebral artery spasm, to reduce secondary cerebral ischaemia and further neurological deterioration.
The patient’s Glasgow Coma Scale (GCS) should be assessed and if below 8, anaesthetic input may be required to manage the airway.
Invasive intracranial pressure monitoring may be required if the patient’s GCS deteriorates.
A thorough assessment of the patient’s entire body should be performed to recognise secondary injuries (either due to primary trauma or secondary collapse).
All SAH cases should be discussed urgently with a local neurosurgical team. In selected cases, surgery is undertaken to manage the cause of the bleed or to manage intracranial pressure (e.g. ventricular drain).
There are a variety of ways in which the SAH, or its consequences, can be managed surgically:
Obliteration of the ruptured aneurysm: this can be done via clipping, insertion of a fine wire coil or other endovascular treatments.
Balloon angioplasty if the patient develops cerebral vasospasm.
Ventricular drainage for cases with secondary hydrocephalus.
This depends on the cause and severity of SAH in addition to the presence of other injuries or co-morbidities.
However, it is important to note that approximately 50% of patients die immediately, or soon after the haemorrhage.
The patient’s whole clinical presentation in addition to their GCS score and neurological deficit, are important in assessing prognosis. Scales, such as the Hunt and Hess or WFNS classification, as also helpful in determining the prognostic outcome.
Due to blood pooling in the ventricular system, the normal drainage mechanism of for CSF is lost, resulting in a build-up of CSF within the ventricular system.
This causes a progressive rise in the intracranial pressure, ultimately leading to a deteriorating GCS and ultimately death if left untreated.
Obstructive hydrocephalus can be diagnosed on a CT scan, as the ventricles appear enlarged (ventriculomegaly).
A ventricular drain is often inserted, to provide a route of draining for the CSF, in an attempt to maintain a viable intracranial pressure.
This is a serious complication of SAH and a poor prognostic feature
Cerebral arteries vasoconstrict, reducing blood supply to the cerebral tissue distal to the area of vasospasm, leading to secondary brain ischaemia.
Calcium-channel blockers such as Nimodipine have been shown to reduce the degree of vasospasm.
Re-bleeding of aneurysms
This is a devastating complication and is a leading cause of mortality from cerebral aneurysms.
Long-term neurological deficits can occur secondary to direct (e.g. haemorrhage) or indirect (raised ICP and vasospasm) damage to cerebral tissue.
Hull York Medical Student
Mr Konstantinos Lilimpakis
Neurosurgical Clinical Fellow
Kopitnik, T.; Samson, D. Management of subarachnoid emergency. Journal of Neurology, Neurosurgery, and Psychiatry. 1993. 56: 947-959. Available online at https://jnnp.bmj.com/content/jnnp/56/9/947.full.pdf. Accessed 01/10/2018.
Kumar and Clarke: Anne Ballinger, Anne Ballinger, Parveen J. Kumar, Michael L. Clark Pages: 899 Size: 19.4 MB Format: PDF Publisher: Saunders Published: 29 September, 2011 p700-800
Image of meningeal layers. By SVG by Mysid, original by SEER Development Team, Jmarchn [CC BY-SA 3.0 ], via Wikimedia Commons
Brain Aneurysm Foundation. Risk factors. Published online in 2018. Available online at https://www.bafound.org/about-brain-aneurysms/risk-factors/ Accessed 30/09/2018.