Subarachnoid Haemorrhage

Subarachnoid haemorrhage (SAH) is usually the result of bleeding from an aneurysm in the Circle of Willis, most often from a berry aneurysm. They are called berry aneurysms because of their shape. They were once thought to be congenital but there is now evidence that they are acquired, increase in incidence with age and that most do not rupture.¹

• Subarachnoid haemorrhage affects 6 to 12 people per 100,000 of the population per year and constitutes about 6% of first strokes.
• Approximately 85% of patients bleed from intracranial arterial aneurysms, 10% from a non-aneurysmal peri-mesencephalic haemorrhage and 5% from other vascular abnormalities including arteriovenous malformation.²
• Subarachnoid haemorrhage (SAH) represents a mere 5% of cases of stroke but it is relatively far more important as it tends to affect younger people of whom about half die in that episode.
• Half are under 55 years old.³
• 10 to 15% fail to reach hospital.

Risk Factors

• The bigger the aneurysm, the more likely it is to bleed. However, as about 90% of aneurysms are small, the majority that bleed are less than 1cm in diameter.⁴
• Hypertension
• Smoking
• Excessive alcohol intake.

The last 3 each roughly double the risk and these modifiable risk factors account for around two thirds of SAH.⁵

• Although no single gene has been isolated, genetic factors also play a part and account for around 10%.⁶
• Patients with a positive family tend to have their first SAH at a younger age.
• They are also more likely to have large and multiple aneurysms.

However, as this group accounts for only 10%, most patients with large or multiple aneurysms are sporadic rather than familial.

Berry aneurysms are found in 10% of patients with autosomal dominant adult polycystic kidney disease but they represent only 1% of cases of SAH.

The most characteristic feature is a sudden headache. This may last a few seconds or even a fraction of a second.⁷ The patient may even look round and accuse someone of hitting him on the back of the head. In general practice, it may be the only symptom in a third of patients.⁸ Of patients who present in general practice with a sudden headache, around 10% have subarachnoid haemorrhage.⁸

• The headache is often diffuse.
• The dominant feature is the severity rather than the suddenness of the headache, often being described as the most severe ever experienced.
• It usually lasts a week or two.

Other features include:

• Vomiting may occur but this does not distinguish it from other causes of headache including thunderclap headache without haemorrhage.
• Seizures occur in only about 7% but when they do, they are highly suggestive of a haemorrhage.

Examination

• On admission to hospital two thirds have a depressed level of consciousness of whom half are in coma but beware - SAH patients have been known to walk into the surgery complaining of sudden onset of headache.
• Neck stiffness may occur due to meningeal irritation by the blood but it is not invariable.
• Ophthalmoscopy will show intraocular haemorrhages in around 15% and especially those with depressed level of consciousness.
• There may be focal neurological signs, suggestive of a stroke. Complete or partial palsy of the oculomotor nerve is well recognised, especially with rupture of aneurysms of the internal carotid artery at the origin of the posterior communicating artery.
• Hypertension is a risk factor for the condition but a marked rise in blood pressure may occur as a reflex following haemorrhage.

• Other causes of stroke
• Meningitis
• Trauma
• Thunderclap headache.

Thunderclap headache is an idiopathic condition. Headache is intense but benign but it can resemble the headache of SAH. Onset is acute, possibly within 30 seconds, and CT or even angiography may be required to rule out SAH. The angiogram may be normal or show focal cerebral vasoconstriction. Most patients with thunderclap headache never have a second episode, nor are they at higher risk for haemorrhage. However, the term thunderclap headache is often used to describe the headache that is associated with SAH.

• Arterial blood gases may show hypoxia.
• An ECG may show changes. If these are wrongly interpreted as acute myocardial infarction and thrombolysis is given, the result is disastrous.
• Patients should have a CT scan at the earliest opportunity if subarachnoid haemorrhage is suspected. This should be undertaken immediately if the patient has an impaired level of consciousness and within 12 hours in all patients.⁹ On the first day, extravasated blood is present in more than 95% of patients, but this figure falls markedly over the next few days. The location of the haematoma usually gives a good indication of the site of the ruptured aneurysm. CT is the imaging technique of choice and the Royal College of Physicians advises against the use of MRI in preference to CT for initial diagnosis.
• If the CT scan is negative or equivocal lumbar puncture should be undertaken 12 or more hours after onset.⁹ A small number of patients with a negative CT scan will prove to have had a SAH on lumbar puncture.
  Samples can be spun down and a yellow tinge is almost diagnostic of SAH. Spectrophotometry should be used to permit detection of small amounts of xanthochromia. Microscopy and culture is important as meningitis can have a sudden onset. Samples should be protected from light as it breaks down bilirubin.
  
  It is important to wait at least 6 hours, if not 12 hours after the onset of the headache before attempting this to give time for blood or metabolic products of blood to reach the CSF in the spinal column. It is very easy to hit a vein during the procedure and this will produce a bloody tap. It is usual to take 3 bottles of fluid and the dictum is that it it was a bloody tap the concentration of the blood will diminish from the first to the third bottle. This is unreliable but the presence of bilirubin in the fluid does suggest that blood has been in the CSF and is being broken down.⁴ Pressure of the CSF must be recorded.
  
  
• When a diagnosis of subarachnoid haemorrhage has been made, CT angiography should be performed at the earliest possible opportunity. This may even be before the patient has left the scanning suite when the initial diagnosis was made.

Initial management of subarachnoid haemorrhage aims to prevent further bleeding and to reduce the rate of secondary complications such as cerebral ischaemia or hydrocephalus.

• By and large, drugs have not been shown to be beneficial with the exception of the calcium antagonists as they help to reduce spasm and cerebral ischaemia. This is supported by a Cochrane review and nimodipine is the drug of choice.¹⁰
• Blood pressure should not be reduced at the time unless the mean blood pressure is above 130mmHg or there is evidence of damage to end organs such as kidneys.⁴
• Prevention of further bleeding is important and a matter of priority. This will mean referral to a neurosurgeon and probably transfer to that unit.
• General nursing care of the stroke patient, who may well be unconscious, is very important to prevent further complications. The Glasgow Coma Scale score is used.

The Royal College of Physicians makes a number of recommendations.⁹ The capital letters in parentheses represent the level of evidence. For further information about the interpreatation of this, see different levels of evidence or the explanation in table 1.1 on page 6 of the document (page 26 of the pdf).

Early Management

Once the diagnosis is confirmed:

• Oral nimodipine 60 mg four-hourly should be given, unless there are specific contraindications (A)
• Anti-fibrinolytic agents (A) and steroids (D) should not be given
• General supportive measures to ensure adequate hydration and oxygenation should be instituted and should include adequate analgesia, eg codeine phosphate (D)
• All patients, irrespective of age or clinical grade, should be discussed with a neurosurgeon immediately (D)
• Transfer of patients to the neurosciences centre for further specialist management should be on the same day, and in accordance with local protocol (B)
• Imaging of cerebral vessels should be undertaken at the neurosciences centre (B).
• A ruptured aneurysm should be treated by endovascular or surgical obliteration as determined by the neurovascular team (A)
• All patients should be monitored for the development of treatable complications, especially hydrocephalus, cerebral ischaemia, electrolyte imbalance and hypotension (D).

Further Management

• Any patient with residual impairment after investigation and treatment should be referred to an appropriate specialist rehabilitation service (B)
• All surviving patients should be advised on secondary prevention, especially on treatment for hypertension and the need to stop smoking (A)
• Patients with a strong family history (one other affected first degree relative and/or with a history of polycystic kidney disease) should be advised that their family may be at greater risk of subarachnoid haemorrhage and a referral made to a neurovascular specialist for up-to-date information and advice (B).

The most imminent danger is further bleeding and so the aim is occlusion of the aneurysm. Endovascular obliteration by means of platinum spirals (coiling) is the preferred mode of treatment,¹¹ but some patients require a direct neurosurgical approach with surgical clipping of the aneurysm.

• In about 3%, cardiac arrest occurs at the onset but of those successfully resuscitated, about half can leave hospital to an independent existence.
• A delayed complication is cerebral ischaemia. The risk is reduced with oral nimodipine and probably by maintaining circulatory volume. The peak time for occurence is 5 to 14 days after the haemorrhage.
• Hydrocephalus might cause gradual obtundation in the first few hours or days. It can be treated by lumbar puncture or ventricular drainage, depending on the site of obstruction.
• Abnormalities of biochemistry are common and need appropriate management in intensive care.
• 5% or more of patients develop epilepsy after discharge.
• After occlusion of the anterior communicating artery in particular, around 30% develop anosmia.

A sudden deterioration in level of consciousness within the first few hours suggests further bleeding.

Improvement tends to occur between 4 and 18 months after the event but even those who have independent living often have some cognitive defect. Younger patients do better.
In a survey of 610 patients who were interviewed a mean of 8.9 years after SAH, there was marked morbidity.¹²

• Of the employed patients, 26% stopped working and 24% worked shorter hours or had a position with less responsibility
• On average, patients returned to work 9.4 months after discharge (range, 0-96 months)
• Related problems caused divorce in 7%
• There were changes in personality in 59%, with the most common being increased irritability (37%) or emotionality (29%)
• Patients with SAH had a statistically significant higher mean depression score than the control population. Approximately 10% of the patients had a Hospital Anxiety and Depression Scale score in the range of a probable depressive or anxious state
• Only 25% reported a complete recovery without psychosocial or neurological problems

As hypertension, smoking and excessive alcohol consumption are risk factors, individuals need to address such issues.

The question of management of aneurysms falls into 3 groups.

• Patients may be found to have incidental aneurysms.
• Patients with subarachnoid haemorrhage might have one or more unruptured aneurysms.
• There is the question of screening for aneurysms in patients who survive an episode of subarachnoid haemorrhage, and in first-degree relatives of patients with subarachnoid haemorrhage.

The management of incidental findings will depend upon many aspects. The risk of rupture increases with age but so does morbidity of the procedure and younger people stand to gain more years. It is a difficult decision and family history and patient wishes must be considered.

Those who have already had a SAH are usually offered treatment although if it is small or difficult to reach it may be left alone.

The results of screening first degree relatives of patients for aneurysms are not promising and few apparently dangerous lesions are found. Even routine screening of people with adult polycystic kidney disease is not recommended.