mononeuropathy Drugs (eg isoniazid, nitrofurantoin, vincristine, amiodarone) \200 Paraproteinaemias and amyloid \200 Chronic in \202 ammatory demyelinating polyradiculoneuropathy (rare autoimmune motor neuropathy) PERIPHERAL NEUROPATHIES 173 Investigations \200 Always check B 12 , glucose, TFTs, serum and urine immunoglobulins, E SR and C-reactive protein (CRP) before labeling a neuropathy idiopathic Look carefully for an occult tumor (eg breast examination and CXR) \200 Family history \200 Nerve conduction studies will con \201 rm nerve damage and distinguish demyelination from axonal damage (which sometimes helps with differential diagnosis) but th ey are not always required in straightforward cases Further specialist tests include immunology, tumor markers, lumbar puncture, molecular genetics tests, and nerve biopsy Treatment The important thing is to identify reversible causes quickly but even treat- able causes rarely respond dramatically \200\224 the aim is usually prevention of further dete rioration. Chronic in \202 ammatory polyradiculoneuropathy is treated by steroids, plasma exchange and intravenous immunoglobulin but most other chronic neuropathies have no speci \201 c treatment. Supportive and symptomatic treatment (eg appropriate footwear, analgesia, environ- mental adaptation) is important. Guillain \200\223Barr syndrome This is an acute in \202 ammatory demyelinating polyneuropathy. \200 Causes ascending pa ralysis , weakness beginning in the feet and hands and migrating towards the trunk It can cause life-threatening complications, particularly if the respiratory muscles are af fected or if there is dysfunction of the autonomic nervous system The disease is usually triggered by an acute infection This is a medical emergency which re sponds to iv immunoglobulins or plasmapheresis. These patients can deteriorate rapidly and should be managed in conjunction with specialist neurology units. Even patients who look we ll should have their vital capacity measured daily to warn of impending respiratory failure . 2The main hurdle is recognizing the diagnosis. 174 CHAPTER 7 Neurology Subdural haematoma A condition which is much more common in old age because as the brain sh rinks the veins which lie between it and the skull are much more likely to get torn followi ng trauma (even minor injury). Older people are also more likely to have falls/head injurie s and are more commonly on predis- posing drugs (eg aspirin, warfarin). Other risk factors include alcoholism, epilepsy, and haemodialysis. Features 2Subdurals frequently present with very non-speci \201 c symptoms in a frail conf used patients. A high index of suspicion is required. \200 Subdurals can occur acutely (a nd present within hours of an accident) or more slowly as the classical \200\230chronic su bdural haematoma \200\231 although this distinction doesn \200\231t help guide management \200 A history of head injury occurs in only about half \200 Common features include dro wsiness and confusion (rarely \202 uctuant), postural instability, progressive focal neurology (eg hemiparesis, unequal pupils), headach e, blurred vision Rarely transient neurology (mimicking TIA) or parkinsonism can occur \200 Some patients a re asymptomatic and large collections can be incidental \201 ndings Examine for papilloedema, focal neurology, and long tract signs Diagnosis \200 CT head scan \200\224 look for crescent-shaped haematoma compressing sulci (hypodense/black is old blood, hyperdense/white indicates recent bleeding) and midlin e shift All patients who have new UMN signs with confusion and or drowsiness should be scanned It is harder to decide when to scan a confused patient without such signs \200\224 most ag ree it is reasonable to look for other causes of acute confusion before asking for a head s can as long as the patient is being observed for any change in neurological signs or consci ous level Have a lower threshold for scanning patients on aspirin or warfarin and for those who have evidence of falls, particularly facial bruising. MRI is slightly superior and useful when C T changes are subtle (an isodense phase occurs on CT in transition between hyperdense and h ypodense changes) or very small haematomas are suspected Management Decisions are usually made in conjunction with the local neurosurgical team (alt hough in practice only about 1/3 of patients will end up having surgery). Stop aspirin and reverse warfarin therapy if possible. Observation (with or without dexamet hasone to reduce intracerebral pressure) is frequently used in: \200 Asymptomatic patients \200 Those with small bleed s who are stable/improving \200 Those not \201 t for transfer/surgery SUBDURAL HAEMATOMA 175 When conservative management is adopted, record conscious level (GCS \200\224 see b Append ix, \200\230Glasgow Coma Scale \200\231, p.696) and any focal neurology at least daily or if there is any change. Any deterioration should prompt repeat CT scan and reconsideration of surgery. Burrhole surgery is not complex and is done under local anesthetic. Recovery after surgery can be dramatic. Complications include re-bleeding and seizures. Use symptoms (especially c onscious level) not CT appearance to decide on surgery. Mortality is around 10 % \200\224 highest with depressed conscious level and bilateral haematoma. Those left with residual ne urology should receive rehabilitation as in stroke. 176 CHAPTER 7 Neurology Sleep and insomnia With increasing age less sleep is needed (approximately 1hr less than yo ung adults), circadian rhythm is less marked and sleep becomes more fragmented with greater dif \201 culty getting to sleep. Deep (stage 3 and 4) sleep is reduced but dreaming sleep /REM (rapid eye movement) is preserved. Insomnia is a symptom which correlates poorly with observed actual sleep time (ie patients who complain of poor sleep may be observed by nurses/family to sleep well while those who s leep very little do not necessarily complain). It can be very distressing and is associated with increased morbidity and mortality. Around 25 % of elderly people have chronic insomni a \200\224 even higher rates with psychiatric and medical conditions. Insomnia is a partic ular problem in an unfamiliar noisy ward environment and doctors are often under considerab le pressure to prescribe sedatives. Treatment of insomnia First ensure that underlying causes are looked for and treated: \200 Pain at night \200\224 consider using analgesics with sedative side effects eg opiates Nocturnal urinary frequency, eg due to polyuria, peripheral oedema, prostatism Comorbidities, eg orthopnoea, oesophageal re \202 ux, Parkinson \200\231s disease \200 D epression/anxiety \200\224 very common and use of an antidepressant will improve sleep much better than a hypnotic Alcohol dependence \200 Drugs \200\224 corticosteroids, omeprazole, phenytoin, amiodaron e, sulfasalazine atorvastatin, ramipril, as well as psychiatric drugs, eg paroxetine, halop eridol, and chlorpromazine can cause insomnia. B -blockers and levodopa cause nightmares The following non-pharmacological interventions (sleep hygiene) can be tried \200 Reduce or stop daytime \200\230catnapping \200\231 \200 Avoid caffeine, heavy meals and alcohol in the evening (alcohol helps to fall asleep but reduces sleep quality) Use a bedtime routine \200 Ensure environment is dark, quiet, comfortable \200 Relaxati on and cognitive behavioral techniques can be useful \200 Try warm milky drinks \200 Ma nage expectations \200\224 older people will rarely sleep as much or well as younger people SLEEP AND INSOMNIA 177 Drugs \200 Benzodiazepines (eg temazepam 10mg) are licensed for short term (<4 weeks) management of insomnia and anxiety. They do work well when used correctly (see b \200\230HOW TO Use benzodiazepines for insomnia \200\231, p.177) The newer Z-drugs (eg zopiclone, zolpidem, and zaleplon) are only for insomnia. They have s horter half lives and fewer side effects (although zopiclone is still a cause of daytime dr owsiness). Overall they are probably slightly superior to benzodiazepines but the same caut ions about dependence apply Other hypnotics (eg chloral hydrate, chlomethiazole, antihistamines) can be toxic, especial ly in overdose and provide no major advantages \200 A new class of drugs that act on mela tonin pathways may be bene \201 cial but lacks a proven safety record in older people HOW TO Use benzodiazepines for insomnia Tolerance develops after only 4 weeks and benzodiazepines fail to produce a useful sedative effect, however, it only takes this long for dependence to occur. Dependence may be physic al (with rebound insomnia, anxiety or even delirium) and/or psychological (the patient beli eves they will not be able to sleep without tablets). The shorter the half-life the greater the withdrawal effects. Benzodiazepine use has been associated with increased falls, reduc ed functional status, road traf \201 c accidents, depression, and memory impairment. Although awareness of these problems have reduced the number of long-term benzodiazepine users, there is still over-prescribing. Prevention of dependence \200 Do not use benzodiazepines for mild or non-distressing inso mnia \200\224 try non-pharmacological measures \201 rst Never prescribe benzodiazepines for more than 4 weeks \200 Never prescribe benzodiazepine s medication at discharge from hospital All patients/carers should receive warnings about benzodiazepine side effects (especially d ependence) and the reason for limiting course length at the outset GPs should limit repeat prescriptions and audit their practice Treatment of dependence \200 Explain and motivate patient/carers \200 Gradual reduction regimen, eg diazepam by 2 \200\2232.5mg every 2 weeks \200 In dif \201 cult cases switc h to equivalent dose of diazepam \201 rst \200\224 long half-life produces milder withdrawal symptoms Continuing support \200 Occasionally acute withdrawal is undertaken by mistake (eg drug a ccidentally not prescribed for a couple of weeks during acute admission with fractured neck of femur). In these cases do not automatically re-start the benzodiazepines and do explain why to the patient or they will just re-start it when they return home 178 CHAPTER 7 Neurology Other sleep disorders Hypersomnolence This is excessive daytime sleepiness despite a normal night of sleep. Causes include brain disease (eg dementia, stroke), cardiopulmonary diseas e (eg cardiac failure, COPD), obstructive sleep apnoea, hypothy- roidism, narcolepsy, and s edative drugs. Restless legs syndrome A common (10 % older people) unpleasant sensation in limbs which inc reases with drowsiness and is eradicated by movement. Can be associ- ated with limb jerking during sleep with sleep disturbance. Both symptoms respond to benzodiazepines. Dopamine ag onists are also used with some success. Circadian rhythm disorders Jet lag is the best known but advanced sleep phase syndrome (sle epi- ness occurs too early in evening but there is early morning wakening) and delayed slee p phase (sleepiness comes too late at night) can occur without such a precipitant. Treat by gradually altering bedtime and bright light therapy when wakefulness desired. Sleep apnoea in older patients Obstructive sleep apnoea and central sleep apnoea are very c ommon in older patients and can contribute to daytime sleepiness, accidents and heart failu re. Unfortunately periods of apnoea are less likely to be symp- tomatic than in the young a nd where symptoms do exist they are often multifactorial so diagnosis and compliance with t herapy (non-invasive positive pressure ventilation) can be problematic. REM sleep behavior disorder Dream-enacting behavior during REM sleep, occurring because of a lack of muscle atonia that usually accompanies REM sleep. About half will go on to develo p neurological pathology, eg Parkinson \200\231s disease, Lewy body disease. Treatment with benzodiazepines may be successful. Further reading Harbison J . ( 2002 ). Sleep disorder in older people . Age Ageing 31 : 6 \200\223 9 . 179 Chapter 8 Stroke De \201 nition and classi \201 cation 180 Predisposing factors 182 Acute assessment 184 HOW TO Assess for inattention 185 Investigations 186 Acute management 188 HOW TO Manage swallow after stroke 189 Stroke units 190 HOW TO Estimate prognosis after stroke 191 Thrombolysis 192 Ongoing management 194 HOW TO Protect your patient from another stroke 195 Complications 196 HOW TO Manage urinary incontinence after stroke 197 Longer-term issues 198 Transient ischaemic attack clinics 200 180 CHAPTER 8 Stroke De \201 nition and classi \201 cation De \201 nition Stroke is the sudden onset of a foc al neurological de \201 cit, lasting more than 24hr or leading to death, caused by a vascu lar problem. \200 Infarction: emboli, in situ thrombosis or low \202 ow \200 Hemorrha ge: spontaneous (not associated with trauma). Excludes subdural and extradural haematomas, but includes spontaneous subarachnoid hemorrhage Use of the term cerebrovascular accident is now discouraged. Transient ischaemic attacks are focal neurological de \201 cits (including monocular visua l loss) due to inadequate blood supply that last <24hr (in reality, most TIAs last just min utes). Infarction and TIAs have the same pathogenesis, and the distinction is likely to become les s helpful with time. Both stroke and TIA need urgent treatment, and as it is impossible to distinguish TIA from stroke in the \201 rst few minutes and hours, the distinction become s less relevant. Waiting to see if the focal neurology resolves causes neuronal loss at a r ate of 1.9 million per minute. The term \200\230brain attack \200\231 is being used to des cribe the full spectrum of disease severity from TIA to fatal stroke, where early intervent ion to save brain tissue has parallels with approaches to myocardial salvage in coronary sy ndromes. Stroke burden \200 Incidence of \201 rst ever stroke is about 200 per 100 000 per year \200 Prevalence is around 5 \200\22312 per 1000 population, depending on the age of the sample It is a disease of older people (over 2/3rds of cases occur in the over 65s, less than 15 % occur in under 45s) Globaly it is the third most common cause of death (after coronary heart disease and all cancers) In England and Wales it accounts for 12 % of all deaths and is the commonest cause of sever e disability among community dwellers Classi \201 cation Various methods including; \200 Infarct or hemorrhage (also haemorrha gic infarcts) \200 Pathogenesis \200\224 large vessel, small vessel, cardioembolic (AF o r LV mural thrombus), valve disease, infective endocarditis, non-atheromatous arterial dise ase (vasculitis, dissection), blood disorders Vessel affected \200\224 anterior circulation (mainly middle cerebral artery), lacunar (deep small subcortical vessels), posterior circulation (vertebral and basilar arte ries) Bamford \200\231s classi \201 cation \200\224 clinical features to de \201 ne likely str oke territory. Used in major trials and gives prognostic information about each group (see Tabl e 8.1 ). DEFINITION AND CLASSIFICATION 181 Table 8.1 Bamford \200\231s classi \201 cation Total anterior circulation stroke (TACS) Features Hemiparesis and hemisensory loss Homonymous hemianopia Cortical dysfunction (dysphasia, vis io-spatial or perceptual problems) 85 % 15 % Occlusion of the internal carotid artery or pr oximal middle cerebral artery Emboli from heart, aortic arch or carotids, in situ thrombosi s Dead Dependent Independent Infarction (TACI) Hemorrhage Causes 60 % 35 % 5 % Prognosis at 1 year Partial anterior circulation stroke (PACS) Features Two of the three listed in this table above OR cortical dysfunction alone 85 % 15 % Occlusi on of the anterior or middle cerebral artery Dead Dependent Independent Infarction (PACI) Hemorrhage Causes Prognosis at 1 year 15 % 30 % 55 % Lacunar stroke (LACS) Features OR OR OR Hemiparesis Hemi-sensory loss Hemi-sensorimotor loss Ataxic hemiparesis (with NO cortical d ysfunction) 95 % 5 % Small perforating arteries microatheroma Hypertensive small vessel dis ease Dead Dependent Independent Infarction (LACI) Hemorrhage Causes 10 % 30 % 60 % Prognosis at 1 year Posterior circulation stroke (POCS) Features Brainstem symptoms and signs (diplopia, vertigo, ataxia, bilateral limb problems, hemianopi a, cortical blindness, etc.) 85 % 15 % Occlusion of vertebral, basilar or posterior cerebra l artery Emboli from heart, aortic arch or vertebrobasilar artery Dead Dependent Independen t Infarction (POCI) Hemorrhage Causes 20 % 20 % 60 % Prognosis at 1 year 182 CHAPTER 8 Stroke Predisposing factors Fixed \200 Age : stroke risk increases with age (this is the stronge st risk factor) \200 Sex : males > females \200 Ethnicity : higher risk in Blacks and A sians than Whites living in the West. Probably due to increased obesity, hypertension, and diabetes Family history : positive family history increases risk. Not simple inheritance \200\224 c omplex genetic/environmental interaction Previous stroke/TIA : risk of recurrence is about 10 \200\22316 % in the \201 rst year, highest in the acute phase Other vascular disease : presence of any atheromatous disease (coronary, peripheral arteria l etc) increases risk of stroke Modi \201 able by lifestyle change \200 Smoking : causal and dose related. Risk diminish es 5 years after quitting \200 Alcohol : Con \202 icting evidence with some studies sugg esting any alcohol consumption increases risk, while others suggest heavy drinking is a risk factor, but moder ate intake is protective Obesity : Increased risk of all vascular events in obesity \200\224 confounded by increase in other risk factors (hypertension, diabetes) but probably weak independent fa ctor, especially central obesity Physical inactivity : Increased stroke in less active \200\224 again confounded by presenc e of other risk factors in the inactive; to date limited evidence that increased activity l owers risk Diet : Healthy eaters have lower risk, but may have healthier lifestyles in general. Low sa lt, high fruit and vegetable, high \201 sh and antioxidant diets are likely to be protect ive, but trials have failed to show an effect from dietary interventions Oestrogens : the oral contraceptive confers a slightly increased risk of stroke and should be avoided in the presence of other risk factors. Postmenopausal hormone replacement therap y has been shown to increase risk of ischaemic stroke, but not TIA or haemorrhagic stroke Medically modi \201 able \200 Hypertension : clear association between increasing BP and increased stroke risk across all population groups. Risk doubles with each 5 \200\2237 mmH g increase in diastolic blood pressure. Also increases with systolic rises and even isolate d systolic hypertension AF : Risk of stroke signi \201 cantly increased in AF (see b \200\230Atrial \201 brillation \200\231, p.276) Diabetes : risk factor independent of hypertension \200 High cholesterol : weaker risk fa ctor than in heart disease \200\224 likely due to diversity of stroke aetiologies Carotid stenosis : risk increases with increasing stenosis and with the occurrence of symptoms attributable to the stenosis Other comorbidity : Increased risk in some conditions, such as sickle-cell anemia, blood diseases causing hyperviscosity and vasculitides This page intentionally left blank 184 CHAPTER 8 Stroke Acute assessment Due to the development of new acute treatments (eg thrombolysis and caroti d endarterectomy) the focus for modern stroke management in hospital has shifted towards ra pid and accurate diagnosis during the \201 rst few hours/days. History \200 Is it a focal neurological de \201 cit? \200 Did it come on \200\230at a stroke \200\231 or is there a hint of progression (simple stroke may worsen over several days, but think of alternative diagnoses, eg tumor) Is there headache or drowsiness? (hemorrhage more likely) \200 Was there a fall or other head trauma? 2 Think subdural and request urgent scan. \200 What are the vascular risk fa ctors? \200 What was the premorbid state? \200 What are the comorbidities? (Increases c hance of poor outcome) \200 What are the medications? (Call GP surgery if unknown) \200 Where do they live, and with whom? Who are the signi \201 cant family members? Examination \200 GCS (see b Appendix, \200\230Glasgow Coma Scale \200\231, p.696). A sta ndardized measure to assess neurological deterioration. Unconsciousness or deteriorating GC S suggests hemorrhage, large infarct with oedema or brainstem event. NIH Stroke Scale (NIHSS) . Clinical evaluation instrument with documented reliability and validity. Used to assess severity of initial stroke (when making a thrombolysis decision), outcome and degree of recovery in stroke. Grades the following a reas: consciousness, orientation, obeying commands, gaze, visual \201 elds, facial weakne ss, motor function in the arm and leg, limb ataxia, sensory, language, dysarthria and inatt ention. General examination \200 General inspection (head trauma, signs of \201 tting \200\224 incontinence or tongue biting, frailty, and general condition, eg skin) Temperature (especially after a long lie) \200 Cardiovascular examination (pulse rate and rhythm, blood pressure, cardiac examination for source of cardiac emboli, carotid bruits) Respiratory examination (aspiration pneumonia or pre-existing respiratory conditions) Abdominal examination (palpable bladder, organomegaly) \200 Neurological examination (may need to be adapted if patient drowsy) \200 Cranial nerves : especially visual \201 eld s and visual inattention (if dif \201 culty with compliance, test blink response to threat , and look for a gaze preference which may occur with hemianopia or neglect), assess swallo w (see b \200\230HOW TO Manage swallow after stroke \200\231, p.189) Limbs : tone (may be diminished acutely), any weakness (grade power for later comparison). Is the distribution pyramidal \200\224 arm \202 exors stron ger than extensors, leg extensors stronger than \202 exors? ACUTE ASSESSMENT 185 If weakness subtle, assess for pyramidal/pronator drift and \201 ne movements of both han ds \200\224 (dominant should be better), coordination (limited if power is diminished), se nsation (gross testing by touching both sides with eyes closed), also sensory inattention, re \202 exes (initially may be absent, then become brisker with time). Plantars extensor o n affected side Gait : assess in less severe stroke \200\224 is it safe? If not safe can the patient sit unaided? Speech : dysarthria (trouble enunciating because of, eg facial weakness or posterior circul ation stroke) or dysphasia (cortical disruption of speech \200\224 may be receptive and/or expressive): \200 Receptive dysphasia is an inability to understand language \200\224 t est with one-stage commands \200\224 \200\230close your eyes \200\231 and progress to more complex tasks \200\230put your left hand on your right ear \200\231. Don \200\231t do the action yourself or the patient will copy you \200\224 a test of mimicry rather than dysphasia. If comprehension intact, reassure the patient that you know they can understand, but are havi ng dif \201 culty \201 nding the right words Expressive dysphasia \200\224 problems producing speech. May be \202 uent (lots of words that make no sense), or non- \202 uent (unrecognizable words). Nominal dysphasia is part of an expressive dysphasia and is tested by asking the patient to name increasingly rare ob jects, eg watch, hand, second hand) HOW TO Assess for inattention Occurs with parietal cortex damage, where there are err ors in aware- ness of self \200\224 the patient \200\231s \200\230automatic pilot \200 \231 has gone wrong. In extreme cases, the patient will not recognize their own arm, and only wash half of their body. Lesser degrees are more common, and complicate the rehabilitation process, as the pa tient must constantly be reminded of the existence of the affected side. Can affect vision or whole of one side of body \200\224 most commonly non-dominant hemispheric (ie right hem isphere, left neglect) To test: 1. Establish that sensory input is present bilaterally, ie check that the patient can feel a touch to each hand individually and does not have a hemianopia (may be hard to establish where extreme gaze preference exists) 2. Provide two stimuli at once (touch both hands together, or move \201 ngers in both sides of the visual \201 eld) and see if the patient preferentially notices the sensory input on the good side. If so, there is inattention of the bad side Even if formal testing does not reveal inattention, sometimes it will become apparent durin g rehabilitation, often noted by therapists. 186 CHAPTER 8 Stroke Investigations (Table 8.2 ) Table 8.2 The rationale for investigations in acute stroke Test Rationale FBC Anemic or polycythaemic Elevated white count suggestive of sepsis High or low platelet count Urea and electrolytes Look for evidence of dehydration, and assess \202 uid replacement LFTs Baseline assessment Evidence of comorbidity CK Evidence of muscle breakdown (if prolonged lie on \202 oor) Glucose Diabetic \200\224 old or new diagnosis (elevated sugars initially may represent hyperglyca emic stress response) Hypoglycaemia 2 may mimic stroke Cholesterol Vascular risk factor ESR Elevation in vasculitis or sepsis (including endocarditis) CRP Any evidence of sepsis (eg aspiration pneumonia) Blood cultures Consider if sepsis or new heart murmur heard (endocarditis) Urinalysis Diabetic, vasculitis, urinary infection ECG Assess rhythm (look for AF) Evidence of IHD/MI or previous hypertension CXR Often useful screening test \200\224 look for any sign of aspiration, what is the heart si ze, etc. CT brain Guidelines advise scan within 24hr for all strokes, or sooner (<1hr) if: Thrombolysis candidate <GCS 13 or \202 uctuating neurology Severe headache at onset On warfarin - Papilloedema, neck stiffness or fever CT will distinguish stroke from non-stroke, eg tumor, identify whether bleed or an infarct, the likely cause of the event \200\224 carotid territory infarcts from stenosis, multiple infarcts from cardiac emboli Blood appears white in early CT; infarcts may not show acutely ( \201 rst few hours), deve lop into low-density areas after a few days INVESTIGATIONS 187 Table 8.2 (Contd.) Test Rationale Small infarcts may never be seen, and the diagnosis is made clinically or on MR scan 2A nor mal CT does not exclude a stroke Carotid Doppler Request in carotid territory events with good recovery where the patient is a candidate for endarterectomy Echocardiogram Consider where multiple (? cardio embolic) infarcts, in AF, after recent MI (looking for th rombus) or where there is a murmur 188 CHAPTER 8 Stroke Acute management Guidelines for acute care are published by the Royal College of Physicians ( M www.rcplondon.ac.uk ), see also National Stroke Strategy 2007 ( M www.dh.gov.uk ). Diagnosis Care should occur on an acute stroke unit. Diagnosis should be made clin- ically (including assessment of likely cerebral area affected) and reviewed by a clinician with ex pertise in stroke. CT scan should be performed unless there is good clinical reason for not doing so (eg dying patient for terminal care) Medical interventions \200 Thrombolysis with tissue plasminogen activator (tPA) should be given promptly where indicated (see b \200\230Thrombolysis \200\231, p.192) Aspirin (300mg) should be given as soon as possible after the onset of stroke symptoms if h emorrhage is excluded (can be given NG or PR) BP \200\224 debate about the optimal BP in the acute phase \200\224 high BP is harmful lo ng term, but may be required to provide perfusion pressure with altered cerebral auto regul ation acutely \200\224 trials ongoing. Guidelines advise that BP should not be lowered acu tely in general, but existing antihypertensives continued Oxygen supplementation should be given to hypoxic patients \200 Hydration should be maint ained to ensure euvolaemia and biochemical normality, and monitored closely Glucose should be measured and euglycaemia maintained \200\224 likely to improve recovery of ischaemic penumbral tissue Pyrexia should be lowered with treatment of the underlying cause, fan, paracetamol, and spo nging. High temperatures are associated with poorer outcomes, but the causal nature of this association is unknown DVT prevention is done with early mobilization. There now good evidence that compression stockings should not be used routinely and low dose low molecular weight heparin is contraindicated acutely due to increased bleeding Neurosurgical opinion should be sought for hydrocephalus, posterior fossa hemorrhages, larg e hemorrhages with midline shift and large middle cerebral artery (MCA) infarcts in patient s <60 (malignant MCA syndrome) Centrally acting drugs should be avoided (eg sedatives) \200 Seizures should be treated ( see b \200\230Epilepsy and stroke \200\231, p.167) Multidisciplinary acute input Protocols should be developed for early management, including moni- toring consciousness level, assessing swallow (not gag), risk assessment for pressur e sores, nutritional status, cognitive impairment, bowel and bladder care (avoiding cathete rization if possible), and moving and han- dling requirements. Early SALT assessment should be done for all with swallow or language dif \201 culties. Early mobilization with the ph ysiothera- pist having expertise in stroke rehabilitation. ACUTE MANAGEMENT 189 HOW TO Manage swallow after stroke Aspiration of saliva or food is one of the commone st complications of stroke and a major cause of morbidity and mortality. Patients who are d rowsy, dysarthric and those with a dysphasia are most at risk of aspiration. Assessment \200\224 Ideally all patients should have their swallow assessed promptly by a SALT or professional with speci \201 c stroke dysphagia training. If the patient is low ri sk and you wish to do a bedside assessment: 1. Sit the patient upright and listen to the ch est to establish baseline 2. Ask the patient to cough, and note the strength and effectiven ess 3. Give the patient a teaspoon of water, and ask them not to swallow 4. Look for leakag e of water from the closed mouth 5. Ask the patient to swallow the water 6. Check for promp t, coordinated swallow with elevation of the tracheal cartilage 7. Watch for signs of aspiration \200\224 coughing and spluttering. These may not occur for several minutes so do not leave immediately 8. If no problems then try a half-glass of water (drunk slowly) or a small amount of yogurt Management \200\224 If the patient is high risk, there are concerns during the bedside tes t or if there are problems encountered during feeding: 1. Make the patient to \200\230nil by mouth \200\231 2. Provide alternative means of hydration at once with an iv infusion, or nasogastric tube (NGT) 3. Refer for early SALT assessment, to stratify the impairment and make a plan for safe oral intake, reviewing at regular intervals 4. Nutrition will need to be considered if the swallow is not safe after a day or two (stud ies show no bene \201 t to feeding in very early stages). Passing a NGT allows medication to be given in addition to feeding, but it is uncomfortable and may become dislodged. In re cent years many centers are using looped/bridle NGTs, which are much less likely to be disl odged. Medium/longer-term management \200\224 if the patient continues to have swallowing problem s, then a PEG or radiologically inserted gastros- tomy (RIG) tube can be inserted. Patients on long-term feeding should be reviewed regularly as swallow can return many months later and oral feeding can gradually be introduced and sometimes tubes can be removed. 2It is imp ortant to understand that arti \201 cial feeding by any method does not prevent aspiration and in some cases can aggravate it. See b \200\230The ethics of clinically assisted feedi ng \200\231, p.360, for discussion of the ethics of feeding. 190 CHAPTER 8 Stroke Stroke units De \201 nition Geographically de \201 ned unit staffed by a coordinated MDT with expertise in stroke. The gold standard is to admit stroke patients directly and con- t inue care through to discharge \200\224 known as a comprehensive stroke unit. Some units d eal with acute admissions only, others with the post-acute rehabilitation phase only. There is evidence for stroke-speci \201 c early sup- ported discharge schemes reducing death or dependency. Bene \201 ts Stroke units when compared with general ward care result in lower rates of de ath, dependency, and institutional care, without lengthening hospital stay. The number need ed to treat in a stroke unit to prevent one death or dependency is 18. Rationale The majority of improvement seems to occur in the \201 rst 4 weeks, and the mec hanism is unclear. Key components of stroke units include: Meticulous attention to physiological homeostasis \200 Attention to prevention of complic ations (such as thromboembolic disease and pressure sores) Early mobilization \200 Coordinated MDT care \200 Interest, expertise, and motivation o f staff \200 The individual impact of each of these is unknown, but combined they confer signi \201 cant bene \201 ts to the stroke patient Further reading Stroke Unit Trialists Collaboration, Cochrane Review online : M www2.cochra ne.org/reviews/en/ ab000197.html. STROKE UNITS 191 HOW TO Estimate prognosis after stroke After \201 rst-ever stroke, death occurs in 12 % by a week, in 31 % at 1 year, and in 60 % at 5 years. Indicators of a poor prognosis i nclude: \200 Impaired consciousness \200 Gaze preference \200 Dense weakness \200 C ardiac comorbidity \200 Urinary incontinence \200 Pupillary abnormalities The risk of r ecurrent stroke among survivors is 10 \200\22316 % at 1 year, there- after falling to about 4 \200\2235 % per annum. The risk is higher with increasing number of risk factors. Recovery is usually slow, and a clear time-frame established early on in the disease with t he patient and the relatives is helpful. Recovery is most rapid in the \201 rst 3 months, and this tends to be \200\230front loaded \200\231 so the most dramatic improvements occu r in the early weeks. Recovery then tends to slow, but may continue for up to 2 years. 2Eac h patient is different \200\224 recovery may be delayed by infections, depression etc., an d this time-frame should be a guide only. The risk of not returning to independence varies with stroke type. Overall, about 20 \200 \22330 % of survivors are dependent at a year, and 40 \200\22350 % are independent. 192 CHAPTER 8 Stroke Thrombolysis Rationale In acute ischaemic stroke, an artery becomes occluded by thrombus in situ or embolus, and blood supply is compromised. Death of surrounding brain tissue result s in de \201 cits in function associated with that part of the brain. Early recanalization of the vessel by lysing thrombus may limit the extent of brain injury. The agent used is i v recombinant tPA (r-tPA). Risks Treatment with thrombolysis leads to an excess in death due to intracra- nial hemorrh age (a \201 vefold increase compared with placebo). Bene \201 ts Despite early excess of deaths due to hemorrhage, treatment with thrombolysis leads to 44 fewer dead or dependent patients per 1000 treated with r-tPA within 6hr, and 1 26 fewer dead or dependent patients per 1000 treated with r-tPA within 3hr. Imaging This should be done prior to giving thrombolysis to exclude hemorrhage. Perfusion- and diffusion-weighted MR scans may give more information than CT. CT perfusion is being us ed more frequently. All need to be inter- preted by someone with the appropriate experience prior to thrombolysis. Plain axial CT remains the mainstay of imaging prior to thrombolysi s. Use Thrombolysis is recommended in centers with suf \201 cient expertise in stroke, and wi th facilities to deal with complications. In these centers, iv r-tPA is considered in all p atients with de \201 nite ischaemic stroke who present within 3hr of the onset of symptoms . Where this expertise doesn \200\231t exist, the service may still be provided via telemed icine links with stroke \200\230hubs \200\231. Careful discussion with the patient and fam ily of risks and bene \201 ts is required. Exclusion criteria There is a very long list of exclusions but the following are the common est reasons to withhold treatment: \200 Previous hemorrhage or active bleeding site \200 Seizure at onset \200 Impaired coagulation \200 Caution with very severe stroke This page intentionally left blank 194 CHAPTER 8 Stroke Ongoing management Should involve all of the MDT: Dietician Calculate food and \202 uid requirements for each individual patient; adapt die t for speci \201 c needs (eg diabetic, weight loss); develop regimens for NG or PEG feeds; advise on provision of modi \201 ed diets for stages of swallow recovery (thickened, pure ed, etc.); review nutrition as recovery alters needs. Doctors Diagnosis; manage medical complications; establish therapies. Nurses Monitor patient continuously; assist with basic care (physiological and physical); o ngoing bowel and bladder management; ongoing skin care; facilitate practice of skills acqui red in therapy; promote functional inde- pendence; \201 rst point of call for relatives. Occupational therapist Optimize functional ability (usually begin with upper limb work, coo rdi- nating with the physiotherapist); speci \201 c assessments of certain tasks (washing and dressing, kitchen safety, occupational tasks, etc.) as recovery continues; adaptation t o home environment by a series of home visits, with and without the patient, and the supply of aids (rails, bed levers, toilet raises, bath boards, etc.), provision of wheelchairs wh ere needed. Pharmacist Review charts; promote safe prescribing. Physiotherapist Assess muscle tone, movement and mobility; maximize functional independ- en ce by education and exercise; monitor respiratory function; initial bed mobility, then work on sitting balance, then transfers and \201 nally standing and stepping; help prevent co mplications such as shoulder pain, contrac- tures and immobility associated problems (press ure sores, DVT/PE). Psychologist Assess psychological impact of stroke on patient and family; allow the patient to talk about the impact of the illness; monitor for depression and other mood disorder, h ighlighting the need for medication; document cognitive impairment; assist in retraining wh ere neglect is prominent. Social worker Psychosocial assessment of patient and family; support with \201 nancial ma tters (accessing pension, arranging power of attorney, \201 nancing place- ment etc.); ad vice and support for patient and family on accommodation needs, especially \201 nding a c are home placement; link to community services (care package, community rehabilitation, day centers, etc.) ONGOING MANAGEMENT 195