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(BQ) Part 2 book Oh''s intensive care manual has contents: Neurological disorders, endocrine disorders, endocrine disorders, infections and immune disorders, severe and multiple trauma, environmental injuries, pharmacologic considerations, metabolic homeostasis,.... and other contents.
51 Acute cerebrovascular complications Thearina de Beer Cerebrovascular disease is common and its 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 neurology, 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 most common cause of physical disability in adults.1 Stroke can be categorised as ischaemic or haemorrhagic (Table 51.1) The main risk factors are increasing age, hypertension, ischaemic heart disease, atrial fibrillation, smoking, diabetes, obesity, some oral contraceptives and raised cholesterol or haematocrit PROGNOSIS IN ACUTE CEREBROVASCULAR 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 year is slightly better in the haemorrhagic group In all types of stroke, about 30% of survivors remain disabled to the point of being dependent on others Risk of stroke increases with age and doubles every decade over the age of 55.1 Thus stroke is often accompanied by significant age-related medical co-morbidity In the past, this may have been partially responsible for a relatively non-aggressive approach to the treatment of stroke patients, so the gloomy prognosis of stroke 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 there is good evidence of reduction in both mortality and dependency compared with those treated in a general ward The UK National Institute for Health and Clinical Excellence (NICE) has published guidelines aimed at ensuring early diagnosis and aggressive therapy.2 CEREBRAL INFARCTION Infarction of cerebral tissue (ischaemic stroke) occurs as a result of inadequate perfusion from occlusion of cerebral blood vessels (large or small) in association with inadequate collateral circulation It may occur due to cerebral thrombosis or embolism AETIOLOGY AND PATHOLOGY CEREBRAL THROMBOSIS Atherosclerosis 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 carotid syphon Progressive plaque formation causes narrowing and forms a nidus for platelet aggregation and thrombus formation Ulceration and rupture of the plaque exposes its thrombogenic lipid core, activating the clotting cascade Hypertension and diabetes mellitus are common causes of smaller arterial thrombosis Rarer causes of thrombosis include any disease resulting in vasculitis, vertebral or carotid artery dissection (either spontaneous or post-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 hypercoagulable states, such as dehydration, polycythaemia, thrombocythaemia, some oral contraceptive pills, protein C or S deficiency, or antithrombin III deficiency or vessel occlusion by tumour or abscess Cerebral infarction may also result from sustained systemic hypotension from any cause, particularly if associated with hypoxaemia CEREBRAL EMBOLISM Embolism commonly occurs from thrombus or platelet aggregations overlying arterial atherosclerotic plaques, but 30% of cerebral emboli will arise from thrombus in the left atrium or ventricle of the heart This is very likely in the presence of atrial fibrillation, left-sided valvular disease, recent myocardial infarction, chronic atrial enlargement or ventricular aneurysm The Abstract and keywords 651.e1 ABSTRACT KEYWORDS Stroke, whether it is ischaemic or haemorrhagic, is an acute medical emergency, and 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 improved with the newer treatments When a stroke is suspected, a computed tomography scan of the brain needs to be performed within an hour of presentation, and what type of stroke it is will determine further management Stroke patients should be treated in hyperacute stroke centres with neurosurgical 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 Stroke ischaemic stroke haemorrhagic stroke intracerebral haemorrhage intracerebral bleed subarachnoid haemorrhage endovascular coiling mechanical thrombectomy 652 Acute cerebrovascular complications Table 51.1 Classification of stroke ISCHAEMIC STROKE CAN BE DIVIDED INTO FIVE TYPES: HAEMORRHAGIC STROKE CAN BE DIVIDED INTO TWO TYPES: Large-artery atherosclerosis Cardioembolism Small-vessel occlusion Stroke of other determined aetiologies Stroke of undetermined aetiology Intracerebral haemorrhage (ICH) Subarachnoid haemorrhage (SAH) 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 aneurysms or arteriovenous malformations (AVMs) after SAH CLINICAL PRESENTATION In cerebral thrombosis, there is initially no loss of consciousness or headache, and the initial neurological deficit develops over several hours Cerebral embolism may be characterised by sudden onset and rapid development of complete neurological deficit No single clinical sign or symptom can reliably distinguish a thrombotic from an embolic 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 of infarction Infarction of the middle cerebral territory leads to a dense contralateral hemiplegia, contralateral facial paralysis, contralateral hemianopia and ipsilateral eye deviation Dominant left-hemisphere lesions result in language difficulties from aphasia, dysphasia, dysgraphia and dyscalculia Non-dominant right hemispheric lesions cause the patient to neglect the left side, and failure to communicate with anyone approaching from that 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 thrombosis may occur, particularly in the cerebral veins, sagittal or transverse dural sinuses, causing headache, seizures, focal neurology and loss of consciousness Other cognitive effects of stroke include memory impairment, anxiety, depression, emotional lability, aprosody and spatial impairment Bilateral brainstem infarction after basilar artery thrombosis may produce deep coma and tetraparesis Pontine stroke may produce the ‘locked-in’ syndrome 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 significant ischaemia from impaired flow or emboli, then with contralateral signs consistent with infarction.3 INVESTIGATIONS A full history and examination of the patient will produce a differential diagnosis that will require specific investigations The aim is to make the diagnosis, establish the nature, size and position of the pathology, so that correct treatment can target the effects of the primary injury, and prevent extension of the lesion or complications occurring BLOOD TESTS A 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 rate or C-reactive protein level may indicate vasculitis, infection or carcinoma, warranting further appropriate investigations Cardiac enzymes and troponin should be taken after an electrocardiogram (ECG) Urea and electrolytes, as well as creatinine and liver function tests, should be taken to rule out a metabolic component A coagulation screen should also be taken together with serum cholesterol, triglyceride and syphilis serology Specific investigation for thrombophilia due to protein C, protein S, Leiden factor V and antithrombin III abnormalities should be undertaken in patients with venous thrombosis or patients with otherwise unexplained cerebral infarction or TIA A pregnancy test should be performed on females under the age of 55 ELECTROCARDIOGRAPHY This may demonstrate atrial fibrillation, other arrhythmia or recent myocardial infarct ECHOCARDIOGRAPHY Either transthoracic or transoesophageal echocardiography (TOE) may demonstrate mural or atrial appendage thrombus as a source of embolism TOE is more effective in detecting patent foramen ovale, aortic arteriosclerosis or dissection Base the decision to perform echocardiography on history, ECG or physical findings.2 IMAGING New guidelines suggest a computed tomography (CT) brain scan within hour of presentation with Cerebral embolism a suspected stroke These techniques are used to distinguish infarction from haemorrhage Tumour, abscess or subdural haematoma may also produce the symptoms and signs of stroke Early scanning is vital if interventional treatment, such as thrombolysis, thrombectomy, anticoagulation, antiplatelet therapy or surgery, is planned The CT scan may be normal or show only minor loss of grey/white matter differentiation in the first 24 hours after ischaemic stroke, but haemorrhage is seen as areas of increased attenuation within minutes After a couple of weeks, the CT appearances of an infarct or haemorrhage become very similar and it may be impossible to distinguish them if CT is delayed beyond this time CT angiography (CTA) will often demonstrate vascular abnormalities and vasospasm but multimodal magnetic resonance imaging (MRI), a combination of diffusion and perfusion-weighted MRI and magnetic resonance angiography (MRA), is much more sensitive in demonstrating small areas of ischaemia Timing from the onset of symptoms and the exclusion of intracranial haemorrhage (ICH) determines the suitability and benefit of thrombolysis.4 Where cerebral infarction has occurred as a result of venous thrombosis, the best imaging technique is MRA Any patient with a stroke or TIA in the internal carotid artery territory should have duplex Doppler ultrasonography, which may demonstrate stenosis, occlusion or dissection of the internal carotid Where trauma is an aetiological factor reconstruction CT bone window views are required to demonstrate any site of fracture-associated vascular injury MANAGEMENT There is strong evidence that admission to a specialised stroke care unit as soon as possible after the occurrence of a stroke provides a cost-effective reduction in long-term brain damage and disability.2 In general, only those patients with a compromised airway due to a depressed level of consciousness or life-threatening cardiorespiratory disturbances require admission to medical or neurosurgical intensive care units (ICUs) In either case, attention to basic resuscitation, involving stabilisation of airway, breathing and circulation, is self-evident AIRWAY AND BREATHING Patients with Glasgow Coma Scores (GCS) of or less, or those with absent gag or defects of swallowing (both of which may occur at higher GCS), will require intubation to preserve their airway and to prevent aspiration Where this requirement is likely to be prolonged, early tracheostomy should be considered Adequate oxygenation and ventilation should be confirmed by arterial blood gas analysis, and supplemental oxygen prescribed if there is any evidence of hypoxia If hypercarbia occurs then ventilatory support to achieve 653 normocarbia is necessary to prevent exacerbation of cerebral oedema A multicentre international study demonstrated that ICU mortality was 37% and hospital mortality was 45% for ventilated stroke patients; it also demonstrated a longer ventilation time and higher tracheostomy rate than non-neurological patients.5 CIRCULATORY SUPPORT A large number of stroke patients will have raised blood pressure (BP) on admission, presumably as an attempt by the vasomotor centre to improve cerebral perfusion Hypertensive patients may have impaired autoregulation and regional cerebral perfusion may be very dependent on BP The patient’s clinical condition and neurological status should determine treatment rather than an arbitrary level of BP Current recommendations are that emergency administration of antihypertensive agents should be withheld unless the systolic pressure is >220 mm Hg or the diastolic pressure is >120 mm Hg Aggressive lowering of BP is not without risk and may result in the progression of ischaemic stroke, so reduction should be monitored closely (not exceeding 15% of normal BP).6 It would seem reasonable on physiological grounds to avoid drugs that cause cerebral vasodilatation in that they may aggravate cerebral oedema, although there is no hard evidence for this Cardiac output should be maintained and any underlying cardiac pathology, such as failure, infarction and atrial fibrillation, treated appropriately METABOLIC SUPPORT Both hypo- and hyperglycaemia have been shown to worsen prognosis after acute stroke; therefore blood sugar levels should be maintained in the normal range (145 mL within 14 hours and >82 mL within hours of onset Electroencephalography (EEG) and tissue cerebral tissue oxygenation have been used to predict cerebral oedema; intracranial pressure (ICP) monitoring has not been proven to change the outcome Craniectomy has to be large enough to extend past the margins of the infarct This seems to be well tolerated even after thrombolysis There is no difference in outcome whether dominant or non-dominant hemispheres are involved The patients who survive after craniectomy have moderate to severe disability and may have a high incidence of psychological complications A recent study has shown benefit in this procedure for patients over 60 years.11 Whether this is acceptable to patients has not been studied.12 Other forms of surgical intervention proven to be effective in making more intracranial space and reducing ICP are drainage of secondary hydrocephalus by extraventricular drain (EVD) insertion or evacuation Intracerebral haemorrhage 655 of haemorrhage into infarcted areas, resulting in new compressive symptoms This is especially useful in the posterior fossa where the room for expansion of mass lesions is limited by its anatomy COMPLICATIONS Local complications include cerebral oedema, haemorrhage into infarcted areas or secondary hydrocephalus General complications include bronchopneumonia, aspiration pneumonia, deep-vein thrombosis, urinary tract infections, pressure sores, contractures and depression Stroke patients who are ventilated seem particularly susceptible to ventilator-acquired pneumonia.13 A team approach of specialist nursing, physiotherapists, occupational and speech and language therapists is best able to avoid these complications SPONTANEOUS INTRACRANIAL HAEMORRHAGE Spontaneous ICH producing stroke may occur from either intracerebral haemorrhage (10%) or SAH (5%) INTRACEREBRAL HAEMORRHAGE The incidence of intracerebral haemorrhage is about 9/100,000 of the population, mostly in the age range of 40–70 years, with an equal incidence in males and females Figure 51.2 Devastating intracerebral haemorrhage AETIOLOGY AND PATHOLOGY CLINICAL PRESENTATION The commonest cause is the effect of chronic systemic hypertension This results in degeneration of the walls of vessels or microaneurysms, by the process of lipohyalinosis, and these microaneurysms then suddenly rupture This may also occur in malignant tumour neovasculature, vasculitis, mycotic aneurysms, amyloidosis, sarcoidosis, malignant hypertension, primary haemorrhagic disorders and over-anticoagulation Occasionally, cerebral aneurysms or AVMs may cause intracerebral haemorrhage without SAH Where intracerebral haemorrhage occurs in young patients, the most likely cause is an underlying vascular abnormality In some areas, this is also associated with the abuse of drugs with sympathomimetic activity, such as cocaine The rupture of microaneurysms tends to occur at the bifurcation of small perforating arteries Common sites of haemorrhage are the putamen (55%), cerebral cortex (15%), thalamus (10%), pons (10%) and cerebellum (10%) Haemorrhage is usually due to the rupture of a single vessel, and the size of the haemorrhage is influenced by the anatomical resistance of the site into which it occurs The effect of the haemorrhage is determined by the area of brain tissue that it destroys Cortical haemorrhages tend to be larger than pontine bleeds (Fig 51.2), but the latter are much more Usually, there are no prodromal symptoms, and a sudden onset of focal neurology or depressed level of consciousness occurs Headache and neck stiffness will occur in conscious patients if there is subarachnoid extension by haemorrhage into the ventricles Where intraventricular extension occurs there may be a progressive fall in GCS as secondary hydrocephalus occurs, and this may be accompanied by ocular palsies, resulting in ‘sunset eyes’ Early deterioration is common in the first few hours after haemorrhagic stroke and more than 20% of patients will drop their GCS by two or more points between the initial onset of symptoms and arrival in the emergency department.14 As with ischaemic stroke, focal neurology is determined by which area of the brain is involved The only way to differentiate absolutely between ischaemic, intracerebral and SAH is by appropriate imaging The symptoms relate to tissue destruction, compression and raised ICP, which, if progressive, will result in brainstem ischaemia and death destructive owing to the anatomical density of neural tracts and nuclei INVESTIGATIONS The general investigations are essentially those listed previously for ischaemic stroke, since it is difficult 656 Acute cerebrovascular complications to distinguish between the two in the early stages Patients undergoing treatment with oral anticoagulants, particularly warfarin in atrial fibrillation, mean that anticoagulant-associated ICH is increasing in frequency and a full coagulation screen is essential.14 CT and/or MRI should be performed at the earliest opportunity The early deterioration seen in ICH relates to active bleeding and repeat imaging after hours of symptom onset often shows significant enlargement of the initial haematoma CTA/MRA or venography is very important to determine the cause of the haemorrhage such as AVM, aneurysm or tumour neovasculature Lumbar puncture may be performed to exclude infection if mycotic aneurysm is suspected, but only after CT has excluded raised ICP or noncommunicating hydrocephalus MANAGEMENT The general management principles are identical to those for ischaemic stroke There is, of course, no place for anticoagulation or thrombolysis, and reversal of any coagulation defect, either primary or secondary to therapeutic anticoagulation, must be undertaken as a matter of urgency A full coagulation screen must be performed and the administration of vitamin K, fresh frozen plasma, cryoprecipitate, etc., directed by the results Where emergency decompressive surgery is indicated, warfarin-induced coagulopathy should be corrected using prothrombin complex concentrate (Beriplex or Octaplex) Intraventricular extension occurs in around 45% of cases and the insertion of an EVD may increase the conscious level, particularly in the presence of secondary hydrocephalus The EVD level should be set so that the cerebrospinal fluid (CSF) drains at around 10 mm Hg The normal production of CSF should produce an hourly output and a sudden fall in output to zero should alert staff to the possibility that the drain has blocked This is particularly likely if the CSF is heavily blood-stained The meniscus of the CSF within the drain tubing should be examined for transmitted vascular pulsation or the level of the drain temporally lowered by a few centimetres to see if drainage occurs If the drain is blocked, secondary hydrocephalus will recur Because of the risk of introducing infection and causing ventriculitis, the drain must be unblocked in a sterile manner by the neurosurgeons Blood in the CSF acts as a pyrogen, but the patient’s high temperature should never be ascribed to this alone, and regular blood cultures and CSF samples are required as part of sepsis surveillance Operative decompression of the haematoma should be undertaken only in neurosurgical centres, and safe transfer must be assured if this is considered The administration of mannitol prior to transfer should be discussed with the neurosurgical unit There is some evidence that patients with supratentorial intracerebral haemorrhage less than 1 cm from the cortical surface benefitted from surgery within 96 hours, although this finding did not reach statistical significance 15 Current recommendations of the American Heart Association/American Stroke Association (AHA/ ASA) are: ‘Patients with cerebellar hemorrhage who are deteriorating neurologically or who have brainstem compression and/or hydrocephalus from ventricular obstruction should undergo surgical removal of the hemorrhage as soon as possible’.14 The management of hypertension following spontaneous intracerebral haemorrhage may be difficult as too high a BP may provoke further bleeding, whereas too low a BP may result in ischaemia Current recommendations of the AHA/ASA are: ‘ICH patients presenting with SBP between 150 and 220 mm Hg and without contraindication to acute BP treatment, acute lowering of SBP to 140 mm Hg is safe and can be effective for improving functional outcome’.14 This should be done for days.2 The adoption of these guidelines may have significant resource implications regarding access to ICU beds to provide the required levels of monitoring There is no place for steroids, and hyperventilation to PaCO of 30 mm Hg (4 kPa) or less to control raised ICP will have detrimental effects on cerebral blood flow in other areas of the brain SUBARACHNOID HAEMORRHAGE SAH refers to bleeding that occurs principally into the subarachnoid space and not into the brain parenchyma The incidence of SAH is around 6/100,000; the apparent decrease, compared with earlier studies, is due to more frequent use of CT scanning, which allows exclusion of other types of haemorrhage Risk factors are the same as for stroke, but SAH patients are usually younger, peaking in the sixth decade, with a femaleto-male ratio of 1.24 : 1 The only modifiable risk factors for SAH are smoking, heavy drinking, the use of sympathomimetics (e.g cocaine) and hypertension, which increase the risk odds ratio by or Overall mortality is 50%, of which 15% die before reaching hospital, with up to 30% of survivors having residual deficitproducing dependency High-volume centres (>60 cases per year) have shown a much improved outcome over that of low-volume centres (160 150 90 Apnoea 51–70 >70 Apnoea (mm Hg) 200–300 65 Unequal or dilated Fixed and dilated 1.5 times control >3.5 3.0–3.5 6.5–7.5 7.5 7.0–8.0 12.0–15.0 15.0 40–60 250–400 400 32 Points (kPa) 17.3–21.3 7.3–8.7 >21.3 5.3–7.2 26.7 6.7–8.5 14.6 (kPa) 26.6–39.9 8.7 2 6 2 6 4 4 5 5 10 1 5 2 6 4 8 3 Infants: 0–1 year of age Paediatric risk of mortality (PRISM) score = (systolic blood pressure points) + (diastolic blood pressure points) + (heart rate points) + (respiratory rate points) + (oxygenation points) + (Glasgow Coma Score points) + (pupillary reaction points) + (coagulation points) + (bilirubin points) + (potassium points) + (calcium points) + (glucose points) + (bicarbonate points) 1382 Appendix III SEPSIS-RELATED ORGAN FAILURE ASSESSMENT SCORE Easy to calculate, describes the sequence of complications in a critically ill patient rather than predicting outcome Organ system Measure Respiration Coagulation Liver Cardiovascular Central nervous system Renal Pa O2 : Fi O2 ratio Platelet count Serum bilirubin Hypotension Glasgow Coma Score Serum creatinine or urine output Measure Finding Pa O2 : Fi O2 ratio (mm Hg) ≥400 300–399 200–299 100–199 0.1 µg/kg/min 15 13–14 10–12 6–9 3–5 Serum creatinine 5.0 mg/dL Urine output