Ebook Oh''s intensive care manual (8/E): Part 2
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Ebook Oh''s intensive care manual (8/E): Part 2
■■ ______________________________________________________51Acute cerebrovascular complicationsThearina de BeerCerebrovascular disease is common and it Ebook Oh''s intensive care manual (8/E): Part 2ts acute manifestation - stroke - produces considerable morbidity and mortality. Stroke is defined as an acute focal neurological deficit caused by cerebrovascular disease, which lasts for more than 24 hours or causes death before 24 hours. Transient ischaemic attack (TIA) also causes focal neurolog Ebook Oh''s intensive care manual (8/E): Part 2y, but this resolves within 24 hours. Stroke is the fourth largest cause of death in the United Kingdom, the second largest worldwide and is the mostEbook Oh''s intensive care manual (8/E): Part 2
common cause of physical disability in adults.1 Stroke can be categorised as ischaemic or haemorrhagic (Table 51.1).The main risk factors are increasi■■ ______________________________________________________51Acute cerebrovascular complicationsThearina de BeerCerebrovascular disease is common and it Ebook Oh''s intensive care manual (8/E): Part 2matocrit.PROGNOSIS IN ACUTECEREBROVASCULAR DISEASE________________________Mortality after stroke averages 30% within a month, with more patients dying after subarachnoid haemorrhage (SAH) or intracerebral haemorrhage than after cerebral infarction, although survival to 1 year is slightly better in t Ebook Oh''s intensive care manual (8/E): Part 2he haemorrhagic group. In all types of stroke, about 30% of survivors remain disabled to the point of being dependent on others. Risk of stroke increaEbook Oh''s intensive care manual (8/E): Part 2
ses with age and doubles even.' decade over the age of 55? Thus stroke is often accompanied by significant age-related medical co-morbidity. In the pa■■ ______________________________________________________51Acute cerebrovascular complicationsThearina de BeerCerebrovascular disease is common and it Ebook Oh''s intensive care manual (8/E): Part 2stroke becomes a self-fulfilling prophecy. The challenge for intensivists is to identify those patients who are most likely to survive, and not to offer aggressive therapy to those who are not. Stroke should be regarded as a medical emergency. Patients should initially be treated in a stroke unit as Ebook Oh''s intensive care manual (8/E): Part 2 there IS good evidence of reduction in both mortality and dependency compared with those treated in a general ward. The UK National Institute for HeaEbook Oh''s intensive care manual (8/E): Part 2
lth and Clinical Excellence (NICE) has published guidelines aimed at ensuring early diagnosis and aggressive therapy.-'CEREBRAL INFARCTIONInfarction o■■ ______________________________________________________51Acute cerebrovascular complicationsThearina de BeerCerebrovascular disease is common and it Ebook Oh''s intensive care manual (8/E): Part 2on with inadequate collateral circulation. It may occur due to cerebral thrombosis or embolism.AETIOLOGY AND PATHOLOGYCEREBRAL THROMBOSISAtherosclerosis is the major cause of major arterial occlusion and most often produces symptoms if it occurs at the bifurcation of the carotid artery or the caroti Ebook Oh''s intensive care manual (8/E): Part 2d syphon Progressive plaque formation causes narrowing and forms a nidus for platelet aggregation and thrombus formation. Ulceration and rupture of thEbook Oh''s intensive care manual (8/E): Part 2
e plaque exposes its thrombogenic lipid core, activating the clotting cascade. Hypertension and diabetes mel-litus are common causes of smaller arteri■■ ______________________________________________________51Acute cerebrovascular complicationsThearina de BeerCerebrovascular disease is common and it Ebook Oh''s intensive care manual (8/E): Part 2ost-traumatic) or carotid occlusion by strangulation or systemic hypotension after cardiac arrest. Cerebral venous thrombosis, responsible for less than 1% of strokes, may occur in hyper-coagulable states, such as dehydration, polycythaemia, thrombocythaemia, some oral contraceptive pills, protein c Ebook Oh''s intensive care manual (8/E): Part 2 or s deficiency, or antithrombin III deficiency or vessel occlusion by tumour or abscess. Cerebral infarction may also result from sustained systemicEbook Oh''s intensive care manual (8/E): Part 2
hypotension from any cause, particularly if associated with hypoxaemia.CEREBRAL EMBOLISMEmbolism commonly occurs from thrombus or platelet aggregatio■■ ______________________________________________________51Acute cerebrovascular complicationsThearina de BeerCerebrovascular disease is common and it Ebook Oh''s intensive care manual (8/E): Part 2is very likely in the presence of atrial fibrillation, left-sided valvular disease, recent myocardial infarction, chronic atrial enlargement or ventricular aneurysm. TheABSTRACT_________________________________________Stroke, whether it is ischaemic or haemorrhagic, is an acute medical emergency, an Ebook Oh''s intensive care manual (8/E): Part 2d great strides have been made in its treatment in the last 10 years. It still remains a high-ranking cause of death worldwide, but outcomes have imprEbook Oh''s intensive care manual (8/E): Part 2
oved with the newer treatments. When a stroke is suspected, a computed tomography scan of the brain needs to be performed within an hour of presentati■■ ______________________________________________________51Acute cerebrovascular complicationsThearina de BeerCerebrovascular disease is common and it Ebook Oh''s intensive care manual (8/E): Part 2 support. Subarachnoid haemorrhage patients should be in a neurosurgical centre with access to interventional neuroradiologists. With rehabilitation, the stroke survivors can make a significant recovery.KEYWORDSStrokeischaemic stroke haemorrhagic stroke intracerebral haemorrhage intracerebral bleed Ebook Oh''s intensive care manual (8/E): Part 2subarachnoid haemorrhage endovascular coiling mechanical thrombectomy652Acute cerebrovoscular complicationsTable 51.1 Classification of strokeISCHAEMIEbook Oh''s intensive care manual (8/E): Part 2
C STROKE CAN BE DIVIDED INTO FIVE TYPES:HAEMORRHAGIC STROKE CAN BE DIVIDED INTO TWO TYPES:1Large-artery atherosclerosis 2.Cardioembolism 3.Small-vesse■■ ______________________________________________________51Acute cerebrovascular complicationsThearina de BeerCerebrovascular disease is common and it Ebook Oh''s intensive care manual (8/E): Part 2H)presence of a patent foramen ovale or septal defects allows paradoxical embolism to occur. Iatrogenic air embolism may occur during cardiopulmonary bypass, cardiac catheterisation or cerebral angiography. Embolisation may also occur as a complication of attempted coil embolisation of cerebral aneu Ebook Oh''s intensive care manual (8/E): Part 2rysms or arteriovenous malformations (AVMs) after SAH.CLINICAL PRESENTATION_____________________________In cerebral thrombosis, there is initially noEbook Oh''s intensive care manual (8/E): Part 2
loss of consciousness or headache, and the initial neurological deficit develops over several hours. Cerebral embolism may be characterised by sudden ■■ ______________________________________________________51Acute cerebrovascular complicationsThearina de BeerCerebrovascular disease is common and it Ebook Oh''s intensive care manual (8/E): Part 2 event.Where infarction occurs in a limited arterial territory the clinical signs are often characteristic. The commonest site involves the middle cerebral artery, which classically produces acute contralateral brachiofacial hemiparesis with sensory or motor deficits, depending on the precise area o Ebook Oh''s intensive care manual (8/E): Part 2f infarction. Infarction of the middle cerebral territory leads to a dense contralateral hemiplegia, contralateral facial paralysis, contralateral hemEbook Oh''s intensive care manual (8/E): Part 2
ianopia and ipsilateral eye deviation. Dominant left-hemisphere lesions result in language difficulties from aphasia, dysphasia, dysgraphia and dyscal■■ ______________________________________________________51Acute cerebrovascular complicationsThearina de BeerCerebrovascular disease is common and it Ebook Oh''s intensive care manual (8/E): Part 2 side. In strokes involving the posterior fossa, the precise pattern of symptoms depends on the arterial territories involved and the presence or absence of collaterals. The onset of symptoms, such as gait disturbance, headache, nausea, vomiting and loss of consciousness, may be very rapid. Venous t Ebook Oh''s intensive care manual (8/E): Part 2hrombosis may occur, particularly in the cerebral veins, sagittal or transverse dural sinuses, causing headache, seizures, focal neurology and loss ofEbook Oh''s intensive care manual (8/E): Part 2
consciousness. Other cognitive effects of stroke include memory impairment, anxiety, depression. emotional lability, aprosody and spatial impairment.■■ ______________________________________________________51Acute cerebrovascular complicationsThearina de BeerCerebrovascular disease is common and it Ebook Oh''s intensive care manual (8/E): Part 2ome. The precise clinical presentation depends on the size of the infarcted area and its position in the brain. Vascular lesions, such as carotid dissection, can present with ipsilateral Horner syndrome with facial pain, a painful Horner's from local stellate ganglion damage or if there is significa Ebook Oh''s intensive care manual (8/E): Part 2nt ischaemia from impaired flow or emboli, then with contralateral signs consistent with infarction.3INVESTIGATIONS_______________________________A fuEbook Oh''s intensive care manual (8/E): Part 2
ll history and examination of the patient will produce a differential diagnosis that will require specific investigations. The aim is to make the diag■■ ______________________________________________________51Acute cerebrovascular complicationsThearina de BeerCerebrovascular disease is common and it Ebook Oh''s intensive care manual (8/E): Part 2xtension of the lesion or complications occurring.BLOOD TESTSA blood glucose test should be done to exclude diabetes and rule out hypoglycaemia as a cause for symptoms. A full blood count should be taken to look for polycythaemia. infection or thrombocythaemia. A raised erythrocyte sedimentation rat Ebook Oh''s intensive care manual (8/E): Part 2e or C-reactive protein level may indicate vasculitis, infection or carcinoma. warranting further appropriate investigations. Cardiac enzymes and tropEbook Oh''s intensive care manual (8/E): Part 2
onin should be taken after an electrocardiogram (ECG). Urea and electrolytes, as well as creatinine and liver function tests, should be taken to ruleGọi ngay
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