VOL: 97, ISSUE: 34, PAGE NO: 36
Juliet Bostwick, MSc, RGN, is lecturer practitioner, Oxford Brookes University/Oxford Radcliffe Hospital NHS Trust
Mary Sneade, BA, RGN, RM, is assistant trial manager, Oxford Radcliffe Hospital NHS Trust
Subarachnoid haemorrhage - bleeding into the subarachnoid space around the brain - usually occurs after the rupture of a cerebral aneurysm and affects about 7,000 people a year in the UK (Hutchinson et al, 1998).
Of these, 25-30% die before they reach hospital. Of those who survive the initial bleed, 50% make a full recovery, 33% die within three months and 17% survive with a severe neurological deficit (Hickey, 1996). Some patients (10-15%) have multiple aneurysms and, in rare cases, the condition runs in families.
Subarachnoid haemorrhage can occur without warning and have a devastating effect on patients and their families. Why aneurysms develop is not known, but they may be caused by a form of degenerative vascular disease, with smoking a possible contributory factor (Bandolier, 1996).
The main causes of death or severe neurological deficit after subarachnoid haemorrhage are the effects of the initial bleed, aneurysmal rebleeding and cerebral ischaemia caused by arterial vasospasm. Cerebral ischaemia/infarction usually develops four to 10 days after the initial bleed, but can occur between 24 hours and several weeks later, or even after treatment of the aneurysm.
Blood supply to the brain
The brain receives about 750ml of blood every minute (Hickey, 1996), supplied by four major arteries - the two internal carotid and the two vertebral arteries that branch to form the anterior and posterior cerebral circulation respectively.
The main cerebral arteries are the anterior, middle and posterior cerebral arteries. The brain is totally dependent on its blood supply for the provision of glucose and oxygen for metabolism. A lack of oxygen to the brain for a period of two to five minutes can result in irreversible neuronal death.
Functionally, the anterior and posterior circulation usually remain separate, but they connect at the circle of Willis to provide a collateral circulation. Cerebral aneurysms usually occur at the bifurcations and branches within the circle of Willis (Fig 1).
Pathophysiology of aneurysms
Aneurysms were once thought to be congenital. However, it is now believed that defects of the internal elastic layer of the artery are more important in the formation of an aneurysm and are probably related to arteriosclerotic damage (Lindsay et al, 1999). Hypertension may also play a role: more than half of patients with a ruptured aneurysm have pre-existing evidence of raised blood pressure.
When an aneurysm ruptures, arterial blood is forced under high pressure into the subarachnoid space, spreading via the cerebrospinal fluid (CSF) pathways into the basal cisterns. Fibrin, platelets and fluid seal off the site of bleeding.
The blood clot that results from the initial bleed into the subarachnoid space can interfere with the absorption of CSF, causing hydrocephalus. Hydrocephalus is the abnormal build-up of CSF in the ventricles of the brain.
Meningism occurs as a result of irritation caused by the blood in the subarachnoid space. Meningism is a condition characterised by stiffness of the neck, headache and other symptoms that suggest meningococcal irritation, but without the actual inflammation of the meninges seen in meningitis.
Signs and symptoms
Most patients are asymptomatic until the haemorrhage, although some may exhibit warning signs, such as cranial nerve palsy or localised headache (from a leaking aneurysm), which are often ignored or attributed to another cause.
When the haemorrhage occurs, patients experience violent headaches which they often describe as the worst headache they have ever had. This usually makes them collapse. Subarachnoid haemorrhage must be considered as the cause of a sudden and unusual headache until proven otherwise.
Other symptoms may include temporary loss of consciousness, vomiting and photophobia as well as the onset of a focal neurological deficit. This arises because of damage in specific areas of the brain related to the cerebral vascular territory involved, such as hemiplegia (limb weakness) or dysphasia (speech disorder).
Patients are classified according to the World Federation of Neurological Surgeons scale, which is based on the Glasgow Coma Scale (Drake et al, 1988), as the severity of subarachnoid haemorrhage relates to a patient’s clinical state (Table 1). This scale has largely replaced the previously used Hunt and Hess grading scale (Hunt and Hess, 1968).
A computed tomography (CT) scan is the primary method of diagnosis and may help to identify the site of the aneurysm rupture as well as the presence of hydrocephalus.
A lumbar puncture will establish a diagnosis of subarachnoid haemorrhage. However, this should be avoided if an intracerebral clot is evident on the CT scan as it could cause the brain to shift downward, causing compression of the brain stem and death (Lindsay et al, 1999).
Removal of too large a volume of CSF may also cause rebleeding. In patients with suspected subarachnoid haemorrhage whose CT scan is normal, it is vital to perform a lumbar puncture to confirm diagnosis and rule out meningitis.
Angiography is usually carried out at the earliest convenience, depending on the patient’s clinical condition, to confirm the presence and location of any aneurysms (Fig 2). However, it must be noted that angiography fails to reveal the source of the bleed in 20% of cases (Lindsay et al, 1999) and repeat angiography may be required.
Pretreatment nursing management
The main aims of care before treatment are to minimise the risk of a potentially fatal recurrent bleed and treat the symptoms caused by the initial bleed. In untreated patients, 30% will bleed again within 28 days and 70% of these will die (Fulbrook et al, 1999).
Early detection of a deterioration in the patient’s neurological condition is essential for the prompt treatment of complications such as hydrocephalus or vasospasm. The latter occurs when, following subarachnoid haemorrhage, the arteries that lie in the subarachnoid space become surrounded by blood. Dead blood cells containing haemoglobin irritate the smooth muscles, which makes them contract.
The nurse can play an important role in influencing the patient’s outcome and reducing the risk of the patient developing a permanent neurological deficit, such as hemiplegia or dysphasia, as a consequence of vasospasm or ischaemia.
The patient’s neurological and vital signs, including oxygen saturation, should be monitored using the Glasgow Coma Scale (Shah, 1999; Teasdale and Jennett, 1974).
It is important to establish an initial baseline assessment of observations. These must subsequently be recorded at regular intervals, depending on the patient’s condition. It is recommended that this is done at least every four hours in the case of a patient with a WFNS grade I haemorrhage. Hydrocephalus may cause a dramatic deterioration in the patient’s Glasgow Coma Scale score.
After having a subarachnoid haemorrhage, patients often experience ongoing severe headache. Pain is well documented as a cause of raised intracranial pressure and it is important to make pain relief a priority for such patients (Hickey, 1996).
Regular administration of an analgesic such as codeine phosphate is recommended, either orally or intramuscularly. This has been shown to provide worthwhile additional pain relief when given with paracetamol (McQuay and Moore, 1998). Small doses of opiates or benzodiazepines can be given, but only with close observation in an intensive or high-dependency setting (Fulbrook et al, 1999).
The use of codeine in preference to morphine is common practice as it is generally believed to reduce the masking of neurological deterioration and respiratory depression. However, according to Herbert (2001), much of the evidence in support of this is anecdotal.
It is vital that patients do not become dehydrated as this increases haemoconcentration, which is in turn thought to increase the incidence of cerebral vasospasm (Hickey, 1996). The recommended intake of three litres in 24 hours may be achieved only if administered via intravenous infusion.
Electrolytes, particularly sodium levels, should be monitored, preferably on a daily basis. A low blood-sodium level (hyponatraemia) may develop in many patients as a result of excessive renal secretion of sodium (Lindsay et al, 1999).
The complications of hyponatraemia may include the onset of confusion, disorientation and seizures (Oh, 1995).
Mobility and environment
Patients should be nursed in bed to minimise the risk of rebleed, although some units allow them out of bed to use the commode. Most neurosurgical units, however, nurse patients flat, supported by one or two pillows, although there is some indication that a head elevation of 30° can promote venous drainage from the brain (Hickey, 1996).
The patient should be nursed in a quiet environment, with bright lighting avoided to minimise the effects of photophobia. While it is vital for patients to have contact with their relatives at this difficult time, it may be advisable to restrict the length of visits and the number of visitors.
It is vital for nurses to keep their knowledge and skills up to date to ensure that patients who have had a subarachnoid haemorrhage receive optimal care.
- Next week: Invasive management and potential complications.