CHAPTER 15 Stroke (cerebrovascular accident)
INTRODUCTION
This chapter discusses stroke incidence, signs and symptoms, pre-hospital care, diagnosis, types, acute care and rehabilitation issues that may arise during the trajectory of care. Two case studies will also be presented to demonstrate care priorities for two very different types of stroke.
THE INCIDENCE OF STROKE
In Australia, there are between 40,000 and 48,000 acute stroke presentations each year, of which approximately 9000 result in death, accounting for nearly 7% of all deaths in Australia (Begg et al, 2007). Globally, there are about 5.5 million acute stroke presentations each year and stroke is the third leading cause of death in the developed world (World Health Organization & Center for Disease Control, 2004). In 2003, it was estimated that over 346,700 Australians experienced a stroke at some time during their lives, with 146,400 suffering from some form of disability as a direct result (Australian Institute of Health and Welfare, 2006). The cost of stroke and other cerebrovascular diseases amounted to $896 million in 2000–01 (1.8% of total health system expenditure), of which aged care homes accounted for 50% and hospitals 40% (National Health Priority Action Council (NHPAC), 2006). In New Zealand, stroke accounts about 9% of all deaths per year (Ministry of Health, 1999).
RISK FACTORS AND PRIMARY PREVENTION
SOCIAL FACTORS
Potential risk factors or vulnerability towards conditions can be avoidable but, due to personal circumstances, may be extremely difficult to overcome and can be seen as (personally) unmodifiable. Social determinants have been and will continue to be used to determine an individual’s predisposition to conditions such as stroke. Numerous factors associated with the socially disadvantaged such as level of education, informed health decisions and access to healthcare all contribute to overall risk (Scanlon & Lee, 2007).
AGE (THE ELDERLY)
With advancing age also comes the increased risk of debilitating conditions such as stroke. The relative risk of stroke doubles with each decade from about 45 to 55 years (Goldstein et al, 2006; Sauerbeck, 2006). The incidence of mortality and ongoing severity morbidity associated with stroke also increases with age.
ETHNICITY
There is evidence that racial background is associated with predisposition or vulnerability towards developing certain conditions. In the United States, those of African-American or Hispanic descent (Sauerbeck, 2006) are more likely to suffer a stroke than the general population. In Australia, Aboriginal and Torres Strait Islander peoples are more than twice as likely to suffer a stroke than the general population (Australian Institute of Health and Welfare & National Heart Foundation of Australia, 2004). This may also be related to modifiable determinants of health compounding these risks.
HEREDITY
Positive family history of conditions has been well established as an indicator for risk. Through ongoing genetic research numerous genes have been identified as known risk factors for both ischaemic and haemorrhagic stroke (Markus & Alberts, 2006). Unfortunately, the availability of genetic testing and awareness of this particular risk are not widespread. Education is required about the positive outcomes of pre-emptive screening and possible modifiable risk factors.
SEX
Gender differences are common for most cardiovascular conditions. Men are approximately 1.3 times more likely than women to have a stroke (Goldstein et al, 2006). The reason for this may be related to the failure of many men to have regular check-ups or act on early warning signs and symptoms of conditions such as stroke (Scanlon & Lee, 2007). Again, this determinant may be related to modifiable (behavioural) determinants of stroke.
TRANSIENT ISCHAEMIC ATTACK
A transient ischaemic attack (TIA) mimics stroke symptoms and is sometimes called a ‘mini stroke’. The symptoms last less than 24 hours and spontaneously resolve. If left untreated, however, a transient ischaemic attack can further develop into embolic stroke. The causes of TIAs are predominantly clots or embolisms that can originate from atherosclerotic plaque or thrombosis from elsewhere in the body. TIA must be actively and aggressively treated because of this increased risk of stroke (Sacco, 2004; Sacco et al, 2006), which is as high as 20% after one month but is at its highest within the first 72 hours after the initial TIA (Intercollegiate Stroke Working Party, 2004).
HIGH BLOOD PRESSURE
There are numerous complications that occur as a result of hypertension, none more serious than the associated vascular changes such as loss of smooth motor function. These changes can weaken (thus rupture) or degrade (through constant vasoconstriction to maintain the hypertensive state) the cerebral vasculature to such an extent that stroke is inevitable. Lowering BP is an effective method for reducing the risk of stroke and subsequent stroke (Bath & Sprigg, 2006; Woo et al, 2004).
HIGH BLOOD CHOLESTEROL
Hypercholesterolaemia is of particular concern due to changes to the vascular system, including profound changes that take place in the cerebral vascular system. Its direct effects on the cerebral vascular system and stroke, however, are currently widely debated as to whether there is a correlation (Donnan & Davis, 2004; Feigin et al, 2005; Piechowski-Jowiak & Bogousslavsky, 2004; Thrift, 2004). Regardless of this, the indirect effects can be attributed to the damage caused to the arteries supplying the heart, causing cardiac dysfunction, which may in turn lead to ischaemic stroke through embolisation.
CAROTID STENOSIS
The increased incidence of clot formation (and thus thrombosis and embolism) associated with stenosis of the carotid arteries also increases the potential for stroke (Altaf et al, 2007; Hankey, 2006). This stenosis may also be attributed to the atherosclerotic changes associated with hypercholesterolaemia, as mentioned previously, leading to emboli lodging in usually the middle cerebral artery.
ATRIAL FIBRILLATION
This heart condition has a tendency to produce emboli secondary to turbulence in the atria. These in turn are ‘flicked off’ towards the path of least resistance (aorta—carotid arteries—cerebral arterial circulation) until they can travel no further, lodging in an arterial vessel and causing stroke. Those suffering with atrial fibrillation have an increased risk of more severe stroke (Rastas et al., 2007). Patients with this condition require anti-coagulation to decrease this very real complication.
DIABETES
Elevated blood glucose levels are found in at least 30% of all stroke victims admitted to hospital (Sacco et al, 2006). Apart from the well-documented effects that diabetes has on all vital functions of the body, its effects on the vascular system in particular not only substantially increase the risk of stroke but also complicate patient outcomes. If left untreated hyperglycaemia can further complicate recovery, as it is linked to associated brain oedema as well as infarct expansion within 24 hours of initial stroke (Baird et al, 2003). Oedema related to the infarcted brain tissue expands within the limited space of the cranial vault and causes adjacent brain cells also to become damaged and even temporarily or permanently cease functioning.
TOBACCO SMOKING
Tobacco smoking is a well-known risk factor for all cardiovascular disease, including stroke (Scanlon, 2006). Nicotine, apart from being highly addictive, is also a known poison. Tobacco smoking’s effects can thus cause a rise in blood pressure, increase in heart rate and vasoconstriction of all arteries. Each of these on its own could cause stroke; together the likelihood is increased.
ALCOHOL CONSUMPTION
Evidence for the relationship between alcohol use and stroke can be seen as conflicting as the effects of alcohol can be both beneficial and detrimental. The anticoagulation effect of moderate alcohol use is beneficial for ischaemic stroke, lessening the potential for clot or thrombosis formation (Goldstein et al, 2006). However, the overall risk increases exponentially with heavy alcohol use (Reynolds et al, 2003), as the increased anticoagulation effect of alcohol use also increases the risk of haemorrhagic stroke.
OBESITY
There are clear links between obesity and any number of chronic conditions, and stroke is no different. The risk of ischaemic stroke, in particular stroke caused by atherosclerosis, is increased by 10 to 20% with obesity (Chen et al, 2006). Obesity puts the individual at risk of hypertension and diabetes, both known risk factors of stroke, and further increases their potential. Studies have also shown that regular exercise can also reduce the chance of stroke (Hu et al, 2005).
OTHER FACTORS
Hormone replacement therapy and the contraceptive pill are associated with an increase stroke incidence. However, they are not seen as priorities in assessing and preventing stroke (Goldstein et al, 2006).
PRE-HOSPITAL CARE
Of paramount importance for stroke survival is appropriate and timely pre-admission or hospital care. Worldwide, guidelines support this rapid response to presenting symptoms in order to achieve better patient outcomes (Adams et al, 2007; Intercollegiate Stroke Working Party, 2004; National Stroke Foundation, 2007; Scottish Intercollegiate Guidelines Network, 2006). Symptoms associated with stroke should never be ignored, as any delay in diagnosis and treatment can further exacerbate the sufferer’s condition and lead to preventable complications, including death.
SIGNS AND SYMPTOMS OF STROKE
Stroke symptoms typically last more than 24 hours or result in the death of the sufferer (not to be confused with TIAs, which last less than 24 hours). The National Stroke Foundation has developed a public media campaign to increase awareness around stroke and what to do. The campaign (National Stroke Foundation, 2006) is aimed at presenting the symptoms of stroke simply, allowing for assessment that could be performed by anyone, thus increasing the likelihood of rapid assessment and appropriate treatment. The campaign is based on the acronym FAST:
DIAGNOSIS
Once clinical signs and symptoms of stroke are present the sufferer has a very limited amount of time to receive treatment to obtain maximum benefit. This time frame has been conservatively estimated at two hours (Zweifler, 2003). On presenting to the emergency department, rapid assessment and diagnosis should be performed to rule out all possibilities. Signs and symptoms of stroke do mimic other possible life threatening conditions and differential diagnosis to stroke can include but is not limited to traumatic brain injury, migraine, hypoglycaemia, seizure, brain tumoar and systemic infection. The first and most definitive diagnostic test is the computed tomography (CT) scan. A CT scan can at least differentiate very quickly between ischaemia and hemorrhagic stroke, as well as other possible diagnoses such as brain tumour or trauma. Haemorrhagic strokes often have telltale signs of acute blood characterised white appearance or hyperdense regions anywhere within the cerebrospinal fluid pathways (the ventricles, guri and sculi etc), whereas ischaemic stroke areas of infarction may appear dark or hypodense within normal structures of the brain (Wardlaw et al, 2004). Sometimes, however, ischaemic stroke may not be evident on a CT scan for up to 48 hours after initial symptoms are present (Frizzell, 2005). At this point treatment for stroke diverges. If a CT scan rules out haemorrhagic stroke or other differential diagnosis then appropriate treatment is commenced. If it confirms haemorrhagic stroke then further investigation is necessary to determine the source of the bleed. This is usually performed by angiography, which can be done by CT scan or magnetic resonance imaging (MRI) scans but most commonly is done with fluoroscopy digital subtraction. Angiography of the cerebral arteries allows visualisation of abnormalities such as aneurysms or arterio venous malformations.