Page 486 - ACCCN's Critical Care Nursing

Neurological Alterations and Management 463

and haemorrhagic stroke. Smoking is the strongest risk by uncontrolled hypertension. Secondary intracerebral
factor for aneurysmal SAH. Atrial fibrillation, endocardi- haemorrhage is associated with arteriovenous malforma-
tis and medications containing supplemental oestrogen tions (AVMs), intracranial aneurysms, or certain medica-
are risk factors for embolic stroke. Seizures develop in tions (e.g. anticoagulants and amphetamines). Symptoms
approximately 10% of cases, usually appearing in the first are produced when an aneurysm or arteriovenous mal-
24 hours and more likely to be focal than generalised. formation (AVM) enlarges and presses on nearby cranial
Most patients with aphasia will have a cerebral infarction nerves or brain tissue or, more dramatically, when a
in the distribution of the left middle cerebral artery. 87 blood vessel, aneurysm or AVM ruptures, causing intra-
cerebral or subarachnoid haemorrhage. When an aneu-
Ischaemic Stroke rysm ruptures, arterial pressure forces blood into the
subarachnoid space between the arachnoid mater and
Ischemic stroke compromises blood flow and energy
supply to the brain, which triggers mechanisms that lead the surface of the brain. Free blood then travels through
to cell death. Infarction occurs rapidly in the region of the fissures into the basal cisterns and across the surface
most severe ischaemia (termed ischaemic penumbra) of the brain. When clotted, this blood can interfere with
and expands at the expense of the surrounding hypoxic the circulation and reabsorption of cerebrospinal fluid
tissue, from the centre to the periphery. Therapeutic strat- (CSF), potentially causing obstructive hydrocephalus and
egies in acute ischaemic stroke are based on the concept raised intracranial pressure. The commonest cause is a
of arresting the transition of the penumbral region into leaking aneurysm in the area of the circle of Willis or a
infarction, thereby limiting ultimate infarct size and congenital AVM of the brain. Blood in the subarachnoid
improving neurological and functional outcome. Isch- space is a powerful meningeal irritant, and it is this irrita-
aemic stroke can be further categorised as middle cerebral tion that causes most of the initial signs and symptoms
artery occlusion, acute basilar occlusion, and cerebellar of SAH.
infarcts. 88 In intracerebral haemorrhage the bleeding is usually arte-
rial and occurs most commonly in the cerebral lobes,
The management of an ischaemic stroke comprises four
primary goals: restoration of cerebral blood flow (reper- basal ganglia, thalamus, brainstem (mostly the pons) and
fusion), prevention of recurrent thrombosis, neuropro- cerebellum. Occasionally, the bleeding ruptures the wall
tection, and supportive care. The timing of each element of the lateral ventricle and causes intraventricular haem-
89
of clinical management needs to be implemented in a orrhage, which is often fatal.
decisive manner. Refer to Table 17.4 for classification and Normal brain metabolism is disrupted by the brain being
treatment strategies and to Online resources for specific exposed to blood. The sudden entry of blood into the
ischaemic stroke protocols. subarachnoid space or brain parenchyma results in a rise
in ICP, which then leads to compression and ischaemia
Haemorrhagic Stroke resulting from the reduced perfusion pressure and vaso-
spasm that often accompany intracerebral and subarach-
Haemorrhagic strokes are caused by bleeding into the noid haemorrhage. Depending on the severity, clinical
89
brain tissue, the ventricles or the subarachnoid space. findings include severe headache, nuchal rigidity, photo-
Primary intracerebral haemorrhage from a spontaneous phobia, nausea and vomiting, hypertension, ECG
rupture of small vessels accounts for approximately changes, pyrexia, cranial nerve deficits, visual changes,
80% of haemorrhagic strokes and is primarily caused sensory or motor deficits, fixed and dilated pupils, sei-
zures, herniation and sudden death.
The Factor Seven for Acute Hemorrhagic Stroke (FAST)
multicentre international clinical trial recently reported
that haemostatic therapy with recombinant activated
TABLE 17.4 Classification and type of ischaemic stroke factor VII (rFVIIa) reduced growth of the haematoma but
and treatment options did not improve survival or functional outcome after
intracerebral haemorrhage. 90
Classification Treatment options
Middle cerebral Intravenous or intra-arterial tissue
artery occlusion plasminogen activator (tPA). Subarachnoid Haemorrhage
Exclusion criteria: >3 hours elapsed from
stroke onset and widespread early Admission to ICU is indicated for subarachnoid haem-
infarct changes on CT scan. orrhage Hunt-Hess SAH severity Scale III (see Table
Tolerate autoprotective hypertension for 17.5) and greater to manage systemic complications,
perfusion of the ischaemic penumbra. recognise and treat clinical deterioration, investigate the
Acute basilar Anticoagulation with intravenous heparin. cause of the haemorrhage and to treat any underlying
occlusion Thrombolysis up to 12 hours after onset. aneurysm or arteriovenous malformation. Resuscitation
Cerebellar infarcts May be difficult to recognise because of is directed towards maintaining cerebral perfusion pres-
the slow evolution of brainstem and sure by ensuring adequate arterial blood pressure (often
cerebellar signs. with the use of inotropes to produce relative hyperten-
Aspirin, antihypertensives and sion although reactive hypertension is often present),
conventional cerebral oedema strategies.
ensuring a relatively high circulating blood volume