This paper will discuss the case study relating to the patient, Mrs Amelia Middleton, and answer a series of questions relating to the pathophysiology of stroke, nursing care of the patient, and response to pharmacological issues with her treatment
Farrell & Dempsey (2014b) define the pathophysiological characteristics of an ischaemic stroke as being the disruption to cerebral blood supply due to an obstruction in a blood vessel (p. 1649). This disruption can be described as an ischaemic cascade, which commences with a fall in cerebral blood flow to less than 25mL/100g/min (p. 1649). When this occurs, neurons are unable to maintain aerobic respiration, causing a decrease in adenosine triphosphate (ATP) production. To combat this, mitochondria switch to anaerobic respiration, which produces large amounts of lactic acid, causes changes in cellular pH levels, anaerobic respiration is less efficient, and neurons are not capable of producing sufficient ATP to fuel the depolarisation processes (Farrell & Dempsey, 2014b, p. 1649; Craft, Gordon, & Tiziani, 2011). With the loss of ATP production, the active transport across the cell membrane ceases, leading to the destruction of the cell membrane, releasing more calcium and glutamate, vasoconstriction and generation of free radicals. As the cascade continues, intracellular pressures increase, causing oedema (Craft, et al., 2011, p. 192). This oedema reaches it maximum after about 72 hour, and slowly subsides over the following two weeks.
There are four types of haemorrhagic stroke, namely – intracerebral, intracranial cerebral aneurysm, arteriovenous malformations, and subarachnoid haemorrhage, all with varying pathophysiology (Farrell & Dempsey, 2014b, p. 1661). The most common type is the intracerebral haemorrhage, which is mostly found in patients with hypertension and cerebral atheroschlerosis. Certain types of arterial pathology, brain tumour, and the use of medications may also cause intracerebral haemorrhage (Farrell & Dempsey, 2014b). Bleeding related to the condition is most commonly arterial and normally occurs in the putamen and adjacent internal capsule, cerebral lobes, basal ganglia, thalamus, cerebellum and brain stem (Farrell & Dempsey, 2014b).
Intracranial aneurism is dilation of the walls of a cerebral artery developing because of weakness in the arterial wall (Farrell & Dempsey, 2014b). Presumed causes of aneurysms are weakness in arterial walls, congenital abnormalities, hypertensive vascular disease, head trauma, infection, or advancing age. Aneurysms can occur in any area of the brain but commonly occur at the circle of Willis arteries. Arteries affected by aneurysms are the internal carotid artery, anterior cerebral artery, anterior communicating artery, posterior communicating artery, posterior cerebral artery and middle cerebral artery (Farrell & Dempsey, 2014b).
Arteriovenous malformations are caused by abnormalities in embryonic development or are the result of trauma. It is the formation of a mass of arteries and veins without a capillary bed, whose absence, leads to dilation of arteries and veins with eventual rupture. This type of haemorrhage is common in younger people (Farrell & Dempsey, 2014b).
Subarachnoid haemorrhage may occur because of arteriovenous malformation, intracranial aneurysm, trauma or hypertension. Most common causes are leaking aneurysms in the area of the circle of Willis or a congenital arteriovenous malformation of the brain (Farrell & Dempsey, 2014b).
Both ischaemic and haemorrhagic stroke have modifiable and non-modifiable precipitating factors. Modifiable factors are those that can be changed and include: