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Cerebral aneurysm and aneurysmal subarachnoid haemorrhage NS740 Bowles E (2014) Cerebral aneurysm and aneurysmal subarachnoid haemorrhage. Nursing Standard. 28, 34, 52-59. Date of submission: December 17 2013; date of acceptance: February 11 2014.

Aims and intended learning outcomes

Abstract A cerebral aneurysm is a weak or thin spot on a blood vessel in the brain that swells and fills with blood. Rupture of a cerebral aneurysm, known as aneurysmal subarachnoid haemorrhage, is a medical emergency and   is associated with increased mortality. This article explores the anatomy and physiology of the brain and blood vessels. Current research and guidelines are used to highlight risk factors for cerebral aneurysms and their rupture and to discuss best practice for treating both. The article provides information on the management and complications of the condition, alongside nursing considerations, long-term care, discharge   and rehabilitation.

Author Emma Bowles Staff nurse, Neuro Intensive Care Unit, Derriford Hospital, Plymouth. Correspondence to: [email protected]

Keywords Cerebral aneurysm, cerebrovascular system and disorders, rehabilitation, subarachnoid haemorrhage

Review All articles are subject to external double-blind peer review and checked for plagiarism using automated software.

Online Guidelines on writing for publication are available at www.nursing-standard.co.uk. For related articles visit the archive and search using the keywords above.

This article aims to increase the reader’s knowledge of cerebral aneurysms. It provides an overview of the relevant anatomy and physiology, as well as the aetiology of cerebral aneurysms. It also explores the management and treatment of unruptured and ruptured cerebral aneurysms. After reading this article and completing the time out activities you should be able to: Describe  the cerebral circulation. Identify  signs and symptoms of cerebral aneurysm and cerebral aneurysm rupture. Discuss  surgical and endovascular treatment options for unruptured and ruptured cerebral aneurysms, and the advantages and disadvantages of these options. Consider  the nursing demands and priorities for patients with unruptured and ruptured cerebral aneurysms.

Introduction Cerebral aneurysms affect about 3.6-6.0% of the population worldwide (Wardlaw and White 2000). Rupture of cerebral aneurysms, also known as aneurysmal subarachnoid haemorrhage (aSAH), is a significant cause of mortality and morbidity worldwide. It affects approximately six to 12 people per 100,000 of the population worldwide each year. About 10-15% of those with aSAH will die before reaching hospital and 25% will die within 24 hours of the bleed, with overall survival rates estimated at 50% (Royal College of Physicians (RCP) 2012). Although overall trends show that survival rates are increasing, the incidence of aSAH appears to be largely unchanged (Connolly et al 2012). With an increasing

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Cerebral blood flow originates from the arch of the aorta (Figure 1). The blood supply flows through the subclavian and common carotid arteries before reaching the brain through two pairs of vessels: the internal carotid arteries and the vertebral arteries. The internal carotid artery reaches the surface of the brain lateral to the point at which the optic nerves cross (the optic chiasma). It then separates into its terminal branches: the anterior and the middle cerebral arteries (Figure 1). Together, these arteries supply the frontal, parietal and temporal lobes of the brain, including structures such as the primary motor and sensory cortices, and the auditory cortex. The vertebral arteries ascend through the vertebrae and enter the cranial cavity through the foramen magnum. They run along the medulla and join at the junction with the pons to form the basilar artery. The basilar artery extends along the length of the pons and terminates when it branches off into a pair of posterior cerebral arteries. Together, the vertebral and basilar arteries supply blood to the brainstem, cerebellum and occipital lobes (Crossman and Neary 2005, Barker and Cicchetti 2012). The circle of Willis sits at the base of the brain and surrounds the optic chiasma (Figure 2). It is formed from the posterior and anterior circulation, which are joined by the anterior communicating artery and a pair of posterior communicating arteries. Its circular structure ensures that cerebral blood supply can continue

Intracranial aneurysms Aetiology and risk factors

An aneurysm is a localised swelling or dilation of an artery caused by weakening of the arterial wall (Marcovitch 2010). In the cerebral

1 Revise the major structures of the brain and their involvement in motor and sensory function.

FIGURE 1 Cerebral blood supply Middle cerebral artery

Anterior cerebral artery

Posterior cerebral  artery Basilar artery External  carotid artery

Internal carotid artery Vertebral artery

Common carotid artery

Aorta PETER LAMB

Cerebral blood supply

should one of the contributing arteries become narrowed or occluded (Crossman and Neary 2005, Barker and Cicchetti 2012).

FIGURE 2 Circle of Willis (cerebral arterial circle) Anterior  communicating  artery

Right anterior  cerebral artery Right internal  carotid artery

Left middle  cerebral artery

Right posterior  communicating  artery Basilar  artery

Right posterior  cerebral artery Spinal cord

Left vertebral  artery

PETER LAMB

number of people surviving aSAH, but potentially being left with physical and cognitive deficits, there is a significant financial burden on the NHS and on community and rehabilitation services to meet the potential long-term care needs of these patients (RCP 2012). The NHS has had to change to meet these increasing demands. With recognition that expert, evidence-based care will produce the best outcomes for patients, 27 specialist neurological and neuroscience centres have been created in England, Wales and Northern Ireland (National Confidential Enquiry into Patient Outcome and Death (NCEPOD) 2013). Guidelines on managing patients with aSAH, based on the best available research, have been published by the RCP (2012) and the American Heart Association and American Stroke Association (Connolly et al 2012). These guidelines have been used by some centres to develop treatment algorithms to standardise care for patients. Complete time out activity 1

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CPD cerebrovascular disorders vascular system, aneurysms usually occur at the joins and on the large arteries that make up or branch off from the circle of Willis (Hickey 2009). The exact pathophysiological reasons for aneurysm formation are largely unclear, although risk factors have been identified (Table 1). It has been suggested that there is a possible link with the structure of the arteries, in particular the vessel walls, which are thinner compared with arteries of the same size elsewhere in the body (Greenberg 2010). Complete time out activity 2

Presentation and diagnosis

The majority of aneurysms are small (less than 7mm in diameter) and are unlikely to rupture (Juvela et al 2000). Most patients with cerebral aneurysms remain asymptomatic until the time of rupture (Hickey 2009). Patients experiencing symptoms such as those listed in Box 1, should receive urgent care because symptoms may be indicative of sudden growth in the aneurysm, which may suggest imminent rupture (Lindsay et al 2010). Unruptured cerebral aneurysms are usually diagnosed following radiological imaging. This may be via a computed tomography (CT) or magnetic resonance imaging (MRI) scan, or angiography. Imaging may have been performed as part of investigations into neurological symptoms, or investigations in patients with a familial history of aSAH. Some unruptured aneurysms are diagnosed when patients present with aSAH, with about one quarter of patients identified as having additional unruptured aneurysms on their admission CT scan (Lindsay et al 2010).

Management of unruptured aneurysms and risk factors for aneurysm rupture

Research shows that definitive treatment of an unruptured aneurysm is largely beneficial for patients (Wiebers et al 2003). However, treatment is invasive, usually involving surgery or an endovascular procedure, and has associated risks. Treatment decisions are mainly dictated by the characteristics of the patient, in particular age and co-morbidities, and the aneurysm itself, and will be made in full discussion with the patient. Certain modifiable risk factors exist. Hypertension should be treated and patients should be advised to refrain from excessive alcohol consumption and smoking. Smoking has been found to double the risk of rupture (Lindsay et al 2010). Although weight is not a risk factor, a healthy diet should generally be encouraged, particularly since research has demonstrated a link between a diet high in vegetables and a decreased risk of aSAH (Connolly et al 2012).

BOX 1 Symptoms associated with unruptured cerebral aneurysm Upper eyelid droop (ptosis). Dilated pupil. An inability to move one eye in certain directions or gaze becomes misaligned. Generalised or localised headache. Pain above and behind the eyes. Neck pain. Upper back pain. Nausea and vomiting. (Adapted from Hickey 2009)

TABLE 1 Risk factors for cerebral aneurysm Modifiable risks

Non-modifiable risks

Hypertension. Female gender. Smoking. Age 40-60 years. High alcohol consumption. Family history of cerebral aneurysm or aneurysmal subarachnoid haemorrhage. Congenital predisposition.

Associated conditions Atherosclerosis. Embolus. Infection. Trauma. Autosomal polycystic kidney disease. Fibromuscular dysplasia. Arteriovenous malformations, including moyamoya disease. Connective tissue disorders, such as Ehlers-Danlos syndrome and Marfan’s syndrome. Bacterial endocarditis. Coarctation of the aorta. Osler-Weber-Rendu syndrome.

(Adapted from Greenberg 2010, Woodward and Mestecky 2011, Hussain et al 2013)

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Aneurysmal subarachnoid haemorrhage Presentation and diagnosis

Signs and symptoms of aSAH depend largely on the severity of the bleed and the site of the aneurysm rupture (Box 2). Some patients present with subtle symptoms, for example severe headache and no other neurological symptoms, while others may be misdiagnosed as having a cardiac event with headache being overlooked (NCEPOD 2013). Delayed diagnosis or misdiagnosis will lead to delayed treatment, putting patients at further risk (NCEPOD 2013). Generally, patients present following an acute onset of severe headache. Research highlights that the presence of acute, sudden-onset headache is indicative of some underlying pathology, which may require urgent management (Ferguson 2009). Current guidance recommends that such patients should undergo further investigations (Ferguson 2009). A non-contrast CT scan of the head is the first-line investigation. CT scans have high sensitivity (close to 100%) for diagnosing aSAH within the first three days of the bleed (Ferguson 2009). Negative CT scans should be followed 12 hours later by a lumbar puncture to look for yellowing of the cerebrospinal fluid (xanthochromia), which is present following aSAH (Ferguson 2009, Connolly et al 2012, RCP 2012). If aSAH is diagnosed, the next step is to locate the aneurysm and visualise its shape. This will help guide decisions about how to treat the aneurysm. Cerebral digital subtraction angiography is commonly used for this purpose. CT angiography (CT head with contrast medium to visualise the cerebral arteries) is another option, but it is not clear whether this scan is sensitive enough to identify very small aneurysms of less than 3mm (Connolly et al 2012). Complete time out activity 3

Nursing care before treatment

The nursing management of patients in the acute stage of aSAH may be associated with several challenges, and many factors will need to be considered. Using the ABCDE approach to assessment may be helpful (Box 3). There is the potential for complications such as those listed in Table 2 to develop before the ruptured aneurysm can be treated. Rebleeding, in particular, is associated with an increased risk of mortality and morbidity (Connolly et al 2012). It is important that patients with aSAH are observed closely; they may require invasive monitoring such as intra-arterial blood pressure monitoring. Central venous access may also be necessary to administer certain vasoactive infusions. These factors may necessitate admission of the patient to a high dependency unit. Nurses caring for patients following aSAH should be confident and competent in assessing neurological status using a recognised scale such as the Glasgow Coma Scale (GCS) (Teasdale and Jennett 1974), as well as assessing pupil size and reaction to light, and limb strength or power. It is important to identify and report any subtle changes in neurological status because these could be early indicators that complications are developing. Nurses should also be competent and confident in managing external ventricular drains (EVD), as highlighted in Table 3, should hydrocephalus develop. Given the life-threatening nature of the condition, it is important that patients have access to experienced neurosurgical staff, and appropriate diagnostic and treatment interventions. The RCP (2012) advise that an early referral be made to a specialist neurosurgery or neuroscience centre. Arrangements for patient transfer may then be made if the centre agrees to take over care delivery. Complete time out activity 4

2 What resources are available in your area of practice for educating patients on smoking cessation, control of hypertension and alcohol misuse? To help you we have put together the following online bundles with articles free to read until April 30. See rcnpublishing.com/r/ smoking-cessation rcnpublishing.com/r/ hypertension rcnpublishing.com/r/ alcohol You might like to write a short presentation on current guidance for colleagues.

BOX 2

Treatment

3 A patient has been admitted to your clinical area with suspected aSAH. The patient’s score on the Glasgow Coma Scale is E3 (eye), V4 (verbal), M6 (motor), pupils are equal and reacting to light and there are no limb deficits. Using a systematic ABCDE approach to patient assessment, highlight potential concerns and any interventions necessary.

Symptoms associated with aneurysmal subarachnoid haemorrhage

The aim of treatment for both ruptured and unruptured aneurysms is the same: occlude the aneurysm from the circulation to prevent rebleeding. To minimise the risk of rebleeding, it is recommended that treatment should take place within 48 hours of the initial bleed (RCP 2012). Aneurysm occlusion is achieved in two ways: Surgical  clipping – this is performed under general anaesthesia and via open craniotomy. The aneurysm is located and a spring-loaded microclip is secured around the neck of the aneurysm. No further blood can enter the aneurysm from the artery and rebleeding is

4 Identify your nearest specialist neurosurgery or neuroscience centre. What should you consider if you were planning to transfer a patient? You may want to discuss this list of considerations with a more experienced colleague and note his or her suggestions.

Sudden onset of acute headache. Loss of consciousness. Seizures. Focal neurological deficits such as limb weakness or cranial nerve palsy. Symptoms of meningeal irritation such as nausea and vomiting, photophobia and neck   pain or stiffness. Hypertension. Ocular haemorrhage. (Adapted from Hickey 2009)

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CPD cerebrovascular disorders prevented (Hickey 2009, Lindsay et al 2010). Endovascular  coiling – this is a less invasive procedure. It can be performed under general or moderate anaesthesia. The aneurysm is located by angiography, usually by using the femoral artery. A catheter then feeds metal coils into the aneurysm. The coils are detached from the delivery wire by an electrical charge (Guglielmi et al 1991). This charge attracts blood components and causes thrombus formation around the coils, which occludes the artery (Hickey 2009). The International Subarachnoid Aneurysm Trial is the only large, randomised, multicentre trial to compare these two treatment methods (Molyneux et al 2005). Their findings are valuable to neurosurgical and radiological teams in deciding which treatment option is in the patient’s best interest. The trial found that patients treated endovascularly had better mortality and morbidity rates. This is despite the fact that complete occlusion rates were lower and incidence of rebleeding was higher in this group (Molyneux et al 2005). As a result,

endovascular coiling has become the treatment of choice and by 2011 in England, Wales and Northern Ireland, 80% of aSAH cases were being treated endovascularly (NCEPOD 2013). Guidelines support this and suggest that where both treatment options are feasible, endovascular coiling should be considered (Connolly et al 2012).

Nursing care Following treatment of ruptured and unruptured aneurysms, patients will require close monitoring for risk of deterioration and any side effects associated with general anaesthesia. Post-operative care will include regular respiratory, cardiovascular and neurological assessment (GCS score, pupil reaction and limb strength or power), symptom management and adequate hydration. Surgical wounds need to be assessed regularly for signs of excessive leakage and infection. Patients may also have a wound drain, and any output will need to be monitored and recorded (Woodward and Mestecky 2011).

BOX 3 ABCDE approach to assessment of patients with aneurysmal subarachnoid haemorrhage (A) Airway Look for signs of airway obstruction, such as paradoxical chest and abdominal movements and cyanosis. (B) Breathing Look for signs of respiratory distress, including use of accessory muscles, abdominal breathing, central cyanosis, noisy breathing (secretions, wheeze). Count the respiratory rate. Identify if there is a history of respiratory conditions such as asthma or chronic obstructive pulmonary disease (COPD). (C) Circulation Ensure close monitoring of cardiovascular status. Cardiac arrhythmias can occur following aneurysmal subarachnoid haemorrhage and a 12-lead electrocardiograph may be indicated. Hypertension can also occur and this may need to be controlled with titratable antihypertensives. Guidelines suggest a target systolic blood pressure of 160mmHg or seizure may increase risk. Risk exists until aneurysm is definitively treated.

Sudden and severe deterioration of the patient. Sudden severe headache. Drop in GCS score. Nausea and vomiting. New focal deficits. If EVD is in situ, there may be a sudden large output with fresh blood present. Cardiovascular changes.

Usually more severe than the initial bleed, approximately 70% of patients who rebleed will die. Medical emergency which   may necessitate resuscitation. Nursing management focuses on prevention. Important to avoid hypertension (systolic BP >160mmHg). Early treatment of aneurysm is the most effective means of preventing rebleeding.

(Adapted from Bear et al 2001, Hickey 2009, Woodward and Mestecky 2011, Connolly et al 2012)

TABLE 3 Nursing considerations for the management of external ventricular drains Action Maintain an occlusive dry dressing around the insertion site. Monitor the insertion site for signs of infection and/or cerebrospinal fluid (CSF) leak. Maintain the integrity, safety and sterility of the system, particularly when repositioning the patient. Check regularly that the drain remains at the appropriate height, particularly following repositioning of the patient. Monitor and document the quantity of drainage – frequency of these observations will be dictated locally, but are usually performed hourly – as well as the colour (in particular the presence of blood) and clarity of drainage (opaqueness not caused by the presence of blood might indicate presence of infection).

Rationale Prevents the introduction of infection. Prevents the introduction of infection. Prevents the introduction of infection. Prevents over or under drainage of CSF and therefore reduces the risk of brain herniation. Prevents over or under drainage to ensure any changes are reported early, for example the presence of new fresh blood or large volumes of drainage. Provides data on the disease process. Provides valuable information to help medical teams make treatment decisions such as whether or not to raise the height of or remove external ventricular drains.

(Adapted from Hickey 2009)

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CPD cerebrovascular disorders major cause of death and disability following aSAH (Connolly et al 2012). Complete time out activity 5

Ongoing care Around 50% of patients who survive aSAH are left with some form of physical or cognitive deficit (Connolly et al 2012, RCP 2012) (Box 4). These impairments may improve with specialist input. However, even if good recovery is made in terms of physical and cognitive

deficits, patients may still experience problems with attention, concentration and memory. It is estimated that only one third of patients return to the job they had before the aSAH (NCEPOD 2013). Early referral to rehabilitation services when necessary, will assist ongoing care and encourage collaboration between professionals to provide patient-centred care. Nurses play a vital role in reinforcing any education from physical exercises to strategies to assist speech. They are also well placed to provide

TABLE 4 Complications following treatment of ruptured and unruptured aneurysms Complication Delayed seizures. Risk factors include: Middle cerebral artery. Associated intracerebral haematoma. Rebleeding. Infarction. Poor neurological status on admission. Hypertension.

Reason A symptom rather than a disease. Affected areas of the brain cause neurones to fire inappropriately.

Treatment Long-term antiepileptics, for example sodium valproate and levetiracetam.

Chronic hydrocephalus

Hydrocephalus occurs when blood from the bleed remains in the cerebrospinal fluid (CSF) or blocks reabsorption. This leads to increased volume in the ventricular system, causing raised intracranial pressure. Persistent hydrocephalus requires a longer term form of CSF drainage.

Permanent diversion of CSF through an internalised ventricular shunt. Post-operative assessment of signs of shunt failure leading to untreated hydrocephalus. This may be seen as a drop in the patient’s Glasgow Coma Scale (GCS) score. It is important to monitor for signs of infection, such as fever.

Hyponatraemia

This occurs when the bleed affects the limbic system in the brain and hormone production. This can cause either the syndrome of inappropriate antidiuretic hormone secretion (low sodium as a result of excessive dilution of the blood) or cerebral salt wasting (kidneys fail to conserve sodium, causing hypovolaemia).

Cautious correction with an intravenous (IV) hypertonic fluid solution and/or fludrocortisone. Avoid rapid rise in serum sodium levels as this can cause nerve demyelination.

Anaemia

Associated with blood loss from haemorrhage.

Close monitoring of haemoglobin levels to detect anaemia. The patient may require transfusion of packed red blood cells. Ensure oxygen delivery to the brain is not compromised.

Vasospasm – can occur in up to 60% of patients. The risk peaks 7-10 days post bleed and does not persist past 21 days. Symptoms include limb weakness, arm drift and drop in GCS score. (Arm drift – the inability to keep arms raised with palms facing backwards while the eyes are closed. The arm ‘drifts’ to the side, which may indicate vasospasm.)

Narrowing of the cerebral arteries

Administer nimodipine 60mg orally every four hours (this has a vasodilatory effect so it may be necessary to consider spreading out the dose if it lowers blood pressure. IV fluids may be necessary to maintain a normal circulating volume. Ensure induced hypertension to maintain adequate cerebral perfusion – limits will be set locally. IV titratable vasopressors may be required.

(Adapted from Connolly et al 2012)

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encouragement, and emotional and practical support to patients and relatives or carers. Discharge planning should start early to allow adequate opportunity for discussion with family and carers, as well as for any necessary equipment to be ordered and adaptations to take place. Consistent, accurate information should be given to patients, relatives and carers

BOX 4 Deficits following aneurysmal subarachnoid haemorrhage Physical deficits Hemiplegia. Hemiparesis. Incontinence (urinary and faecal). Seizures. Poor co-ordination. Swallowing deficits. Fatigue. Cognitive deficits Difficulty processing language (receptive dysphasia). Difficulty with speech or expressing oneself using language (expressive dysphasia). Disorientation. Difficulty maintaining concentration. (Adapted from Connolly et al 2012, National Confidential Enquiry into Patient Outcome and Death 2013)

and where possible, specialist nurse input should be obtained. Complete time out activity 6

Conclusion The majority of cerebral aneurysms are small, unsymptomatic and unlikely to rupture. However, aSAH is a life-threatening condition, which can leave patients with profound physical and cognitive deficits. Modifiable risk factors include smoking, hypertension and excessive alcohol intake. Healthcare professionals have an important role, through public health education, in reducing the incidence of aSAH. Management of a ruptured aneurysm is complex and healthcare professionals need to be aware of guidance that standardises care and ensures the best evidence-based treatment is given to patients. Deterioration in a patient’s condition can occur suddenly and nurses need to be able to detect subtle symptoms that may indicate aSAH. Because patients with aSAH may experience physical or cognitive deficits, nurses need to be able to offer support and ensure referral for rehabilitation NS Complete time out activity 7

5 Reflect on the psychological, social and financial effects of aSAH for patients, families and carers. List possible concerns and identify agencies in your area that might be able to offer support and assistance. 6 Discuss the rehabilitation process for patients following aSAH and the practice of splinting limbs with a physiotherapist. 7 Now that you have completed the article, you might like to write a practice profile. Guidelines to help you are on page 62.

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Greenberg MS (Ed) (2010) Handbook of Neurosurgery. Seventh edition. Thieme, New York NY. Guglielmi G, Viñuela F, Sepetka I, Marcellari V (1991) Electothrombosis of saccular aneurysm via endovascular approach. Part 1: electrochemical basis, technique, and experimental results. Journal of Neurosurgery. 75, 1, 1-7. Hickey JV (2009) The Clinical Practice of Neurological and Neurosurgical Nursing. Sixth edition. Lippincott Williams & Wilkins, Philadelphia PA. Hussain I, Duffis EJ, Gandhi CD,   Prestigiacomo CJ (2013)   Genome-wide association studies of intracranial aneurysms: an update. Stroke. 44, 9, 2670-2675. Juvela S, Porras M, Poussa K (2000) Natural history of unruptured intracranial aneurysms: probability of and risk factors for aneurysm rupture. Journal of Neurosurgery. 93, 3, 379-387.

Lindsay KW, Bone I, Fuller G (2010) Neurology and Neurosurgery Illustrated. Fifth edition. Churchill Livingstone/Elsevier, Edinburgh. Marcovitch H (Ed) (2010) Black’s Medical Dictionary. 42nd edition.   A & C Black, London. Molyneux AJ, Kerr RSC, Yu LM   et al (2005) 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. The Lancet. 366, 9488, 809-817. National Confidential Enquiry into Patient Outcome and Death (2013) Managing the Flow? A Review of the Care Received by Patients who were Diagnosed with an Aneurysmal Subarachnoid Haemorrhage. www.ncepod.org. uk/2013sah.htm (Last accessed: April 4 2014.)

Resuscitation Council (UK) (2011) Immediate Life Support. Third edition. RCUK, London. Royal College of Physicians (2012) National Clinical Guideline for Stroke. tinyurl.com/d89efaq (Last accessed: March 31 2014.) Teasdale G, Jennett B (1974) Assessment of coma and impaired consciousness. A practical scale. The Lancet. 2, 7872, 81-84. Wardlaw JM, White PM (2000) The detection and management of unruptured intracranial aneurysms. Brain. 123, Pt2, 205-221. Wiebers DO, Whisnant JP, Huston J et al (2003) Unruptured intracranial aneurysms: natural history, clinical outcome, and risks of surgical and endovascular treatment. The Lancet. 362, 9378, 103-110. Woodward S, Mestecky A-M (Eds) (2011) Neuroscience Nursing: Evidence-Based Practice.   Wiley-Blackwell, Oxford.

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Cerebral aneurysm and aneurysmal subarachnoid haemorrhage.

A cerebral aneurysm is a weak or thin spot on a blood vessel in the brain that swells and fills with blood. Rupture of a cerebral aneurysm, known as a...
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