Chapter 8
Stroke
HOW TO . . . Assess for inattention
HOW TO . . . Manage swallow after stroke
HOW TO . . . Estimate prognosis after stroke
HOW TO . . . Protect your patient from another stroke
Definition and classification
Definition
Stroke is the sudden onset of a focal neurological deficit, lasting >24h or leading to death, caused by a vascular pathology.
• Infarction: emboli, in situ thrombosis, or low flow
• Haemorrhage: spontaneous (not associated with trauma). Excludes subdural and extradural haematomas but includes spontaneous subarachnoid haemorrhage
Transient ischaemic attacks (TIAs) are focal neurological deficits (including monocular visual loss) due to inadequate blood supply that last <24h (in reality, most TIAs last just minutes).
Infarction and TIAs have the same pathogenesis, and the distinction is likely to become less helpful with time. Both stroke and TIA need urgent treatment, as it is impossible to distinguish TIA from stroke in the first few minutes and hours. Waiting to see if the focal neurology resolves causes neuronal loss at a rate of 1.9 million per minute. It is useful to think of a spectrum of disease severity from TIA to fatal stroke where early intervention to save brain tissue has parallels with approaches to myocardial salvage in coronary syndromes.
Stroke burden
• Incidence of first stroke is about 200 per 100 000 per year
• Prevalence is around 5–12 per 1000 population, depending on the age of the sample
• It is a disease of older people (over two-thirds of cases occur in the over 65s; <15% occur in under 45s)
• Globally it is the second most common cause of death
• In England and Wales, it accounts for 12% of all deaths and is the most common cause of severe disability among community dwellers
Classification
Various methods including:
• Pathogenesis—large vessel, small vessel, cardioembolic (AF or LV mural thrombus), valve disease, infective endocarditis, non-atheromatous arterial disease (vasculitis, dissection), blood disorders
• Vessel affected—anterior circulation (mainly middle cerebral artery (MCA)), lacunar (deep small subcortical vessels), posterior circulation (vertebral and basilar arteries)
Classification systems include:
• Bamford’s classification—clinical features to define likely stroke territory. Used in major trials and gives prognostic information about each group (see Table 8.1)
• TOAST classification—for subtypes of ischaemic stroke: large artery atherosclerosis, cardioembolism, small vessel occlusion, stroke of other determined aetiology, stroke of other undetermined aetiology
Table 8.1 Bamford classification
Predisposing factors
Fixed
• Age: stroke risk ↑ with age (this is the strongest risk factor)
• Ethnicity: higher risk in people of African and South Asian origin than those of European origin. Probably due to ↑ obesity, hypertension, and diabetes
• Family history: positive family history ↑ risk. Not simple inheritance—complex genetic/environmental interaction
• Previous stroke/TIA: risk of recurrence is about 10–16% in the first year, highest in the acute phase
• Other vascular disease: presence of any atheromatous disease (coronary, peripheral arterial, etc.) ↑ risk of stroke
Modifiable by lifestyle change
• Smoking: causal and dose related. Risk diminishes 5 years after quitting
• Alcohol: heavy drinking is a risk factor
• Obesity: ↑ risk of all vascular events in obesity—confounded by ↑ in other risk factors (hypertension, diabetes), but probably weak independent factor, especially central obesity
• Physical inactivity: ↑ stroke in less active—again confounded by presence of other risk factors in the inactive
• Diet: healthy eaters have lower risk but may have healthier lifestyles in general. Low-salt, high-fruit and vegetable, high-fish, and antioxidant diets are likely to be protective, but trials have failed to show an effect from dietary interventions
• Oestrogens: the oral contraceptive confers a slightly ↑ risk of stroke and should be avoided in the presence of other risk factors. Post-menopausal hormone replacement therapy (HRT) has been shown to ↑ risk of ischaemic stroke, but not TIA or haemorrhagic stroke
Medically modifiable
• Hypertension: clear association between ↑ BP and ↑ stroke risk across all population groups. Risk doubles with each 5–7mmHg ↑ in diastolic BP. Also ↑ with isolated systolic hypertension
• AF: risk of stroke significantly ↑ in AF (see 
‘Atrial fibrillation’, p. 274)
• Diabetes: risk factor independent of hypertension
• High cholesterol: weaker risk factor than in heart disease—likely due to diversity of stroke aetiologies
• Carotid stenosis: risk ↑ with ↑ stenosis and with the occurrence of symptoms attributable to the stenosis
• Other comorbidity: ↑ risk in some conditions such as obstructive sleep apnoea, sickle-cell anaemia, blood diseases causing hyperviscosity and vasculitides
Acute assessment
A medical emergency increasingly recognized by the general public (helped by UK public health initiatives such as the FAST campaign). Prompt assessment and treatment improves outcomes.
History
• Is it a focal neurological deficit?
• Did it come on ‘at a stroke’ or is there a hint of progression (simple stroke may worsen over several days, but think of alternative diagnoses, e.g. tumour)
• Is there headache or drowsiness? (haemorrhage more likely)
• Was there a fall or other head trauma?
► Think subdural and request an urgent scan.
• What are the vascular risk factors?
• What was the premorbid state?
• What are the comorbidities? (↑ chance of poor outcome)
• Where do they live, and with whom? Who are the significant family members?
Examination
• GCS (see ‘Appendix’, ‘Glasgow coma scale’, p. 710). A standardized measure to assess neurological deterioration. Unconsciousness or deteriorating GCS suggests haemorrhage, a large infarct with oedema, or a brainstem event.
• National Institutes of Health 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 areas: consciousness, orientation, obeying commands, gaze, visual fields, facial weakness, motor function in the arm and leg, limb ataxia, sensory, language, dysarthria, and inattention.
General examination
• General inspection (head trauma, signs of fitting—incontinence or tongue biting, frailty/general condition, skin, hydration)
• Temperature (especially after a long lie)
• Cardiovascular examination (pulse rate and rhythm, BP, cardiac examination for source of cardiac emboli, carotid bruits)
• Respiratory examination (aspiration pneumonia or pre-existing respiratory conditions)
• Abdominal examination (palpable bladder)
• Neurological examination (may need to be adapted if patient drowsy):
• Cranial nerves: especially visual fields and visual inattention (if difficulty with compliance, test blink response to threat, and look for a gaze preference which may occur with hemianopia or neglect); assess swallow (see ‘HOW TO . . . Manage swallow after stroke’, p. 187)
• Limbs: tone (may be diminished acutely), any weakness (grade power for later comparison). Is the distribution pyramidal—arm flexors stronger than extensors, leg extensors stronger than flexors? If weakness subtle, assess for pyramidal/pronator drift and fine movements of both hands—(dominant should be better), coordination (limited if power is diminished), sensation (gross testing by touching both sides with eyes closed), also sensory inattention, reflexes (initially may be absent, then become brisker with time). Plantars extensor on affected side
• Gait: assess in less severe stroke—is it safe? If not safe, can the patient sit unaided?
• Speech: dysarthria (trouble enunciating because of, e.g. facial weakness or posterior circulation stroke) or dysphasia (cortical disruption of speech—may be receptive and/or expressive):
— Receptive dysphasia is an inability to understand language—test with one-stage commands—‘close your eyes’ and progress to more complex tasks ‘put your left hand on your right ear’. Do not do the action yourself or the patient will copy you—a test of mimicry, rather than dysphasia. If comprehension intact, reassure the patient that you know they can understand but are having difficulty finding the right words
— Expressive dysphasia—problems producing speech. May be fluent (lots of words that make no sense) or non-fluent (unrecognizable words). Nominal dysphasia is part of an expressive dysphasia and is tested by asking the patient to name increasingly rare objects, e.g. watch, hand, second hand)
HOW TO . . . Assess for inattention
Occurs with parietal cortex damage where there are errors in awareness of self—the patient’s ‘automatic pilot’ has gone wrong.
In extreme cases (neglect), the patient will not recognize their own arm and only wash half of their body. Lesser degrees (inattention) are more common and complicate the rehabilitation process, as the patient must constantly be reminded of the existence of the affected side. Can affect vision or the whole of one side of the body—most commonly non-dominant hemispheric (i.e. right hemisphere, left inattention).
To test:
1. Establish that sensory input is present bilaterally, i.e. 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 fingers in both sides of the visual field) 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 during rehabilitation, often noted by therapists.
Investigations
(See Table 8.2.)
Table 8.2 The rationale for investigations in acute stroke
Acute management
Guidelines for acute care are published by the Royal College of Physicians (
http://www.rcplondon.ac.uk). See also NICE Stroke guidelines (2014). Overall care should occur on an acute stroke unit.
Diagnosis
Diagnosis should be made clinically (including assessment of the likely cerebral area affected) and reviewed by a clinician with expertise in stroke. CT scan should be performed unless there is good clinical reason for not doing so (e.g. dying patient for terminal care)
Medical interventions
• Thrombolysis with, e.g. tissue plasminogen activator (tPA) should be given promptly where indicated (see ‘Thrombolysis’, p. 190)
• Intra-arterial clot retrieval has evidence of benefit (up to 6h of onset) where expertise exists either in combination with thrombolysis or where thrombolysis is contraindicated
• Aspirin (300mg) should be given as soon as possible after the onset of stroke symptoms if haemorrhage is excluded (can be given nasogastrically (NG) or per rectum (PR)) and not a potential hemicraniectomy case
• BP—debate about the optimal BP in the acute phase—high BP is harmful long term but may be required to provide perfusion pressure with altered cerebral autoregulation acutely—trials ongoing. Guidelines advise that BP should not be lowered acutely in general, but existing antihypertensives continued
• Oxygen supplementation should be given to hypoxic patients only
• Hydration should be maintained to ensure normovolaemia and biochemical normality, and monitored closely
• Glucose should be measured and, if >11mmol/L, controlled using iv variable-dose insulin
• Pyrexia should be lowered with treatment of the underlying cause, fan, paracetamol, and sponging. High temperatures are associated with poorer outcomes, but the causal nature of this association is unknown
• DVT prevention is done with early mobilization. Compression stockings should not be used and the timing of low-dose low-molecular-weight heparin depends on individual risk/benefit analysis. Intermittent pneumatic compression devices are safe and effective in early disabling stroke.
• Neurosurgical opinion should be sought for hydrocephalus, posterior fossa haemorrhages/large infarcts, large haemorrhages with midline shift, and large MCA infarcts with malignant MCA syndrome
• Seizures should be treated (see ‘Epilepsy and stroke’, p. 165)
Multidisciplinary acute input
Protocols should be developed for early management (<24h), including monitoring consciousness level, assessing swallow (not gag), risk assessment for pressure sores, nutritional status, cognitive impairment, bowel and bladder care (avoiding catheterization if possible), and moving and handling requirements. Early SALT assessment should be done for all with swallow or language difficulties; early mobilization with a PT having expertise in stroke rehabilitation.
HOW TO . . . Manage swallow after stroke
Aspiration of saliva or food is one of the most common complications of stroke and a major cause of morbidity and mortality. Patients who are drowsy and dysarthric and those with dysphasia are most at risk of aspiration.
Assessment—ideally all patients should have their swallow assessed promptly by a professional with specific stroke dysphagia training. If the patient is low risk and you wish to do a bedside assessment:
1. Sit the patient upright, and listen to the chest to establish baseline
2. Ask the patient to cough, and note the strength and effectiveness
3. Give the patient a teaspoon of water, and ask them not to swallow
4. Look for leakage of water from the closed mouth
5. Ask the patient to swallow the water
6. Check for prompt, coordinated swallow with elevation of the tracheal cartilage
7. Watch for signs of aspiration—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 (slowly) or a small amount of yogurt
9. Ask the patient to say name/address, and listen for a ‘wet’ voice
Management—if the patient is high risk, there are concerns during the bedside test, or if there are problems encountered during feeding:
1. Make the patient ‘nil by mouth’
2. Provide alternative means of hydration at once with an iv infusion or an NGT
3. Refer for early SALT assessment, to stratify the impairment and make a plan for safe oral intake, reviewing at regular intervals
4. Early nutrition by NGT improves outcomes and allows medication to be given, in addition to feeding. Looped/bridle NGTs are much less likely to be dislodged but are harder to insert. Consider insertion on the inattentive side if recurrent NGT removal is a problem
Medium/longer-term management—if the patient continues to have swallowing problems, then a PEG or a radiologically inserted gastrostomy (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.
► It is important to understand that artificial feeding by any method does not prevent aspiration and, in some cases, can aggravate it. see ‘The ethics of clinically assisted feeding’, pp. 358–359, for discussion of the ethics of feeding.
Stroke units
Definition
Geographically defined unit staffed by a coordinated MDT with expertise in stroke. The gold standard is to admit stroke patients directly and continue care through to discharge—known as a comprehensive stroke unit. Some units deal with the emergency management (including thrombolysis and hemicraniectomy) and are termed Hyperacute Stroke Units (HASU). Others provide ongoing acute care or deal with the post-acute rehabilitation phase only. Regions may organize a ‘hub and spoke’ model where a single HASU admits all stroke patients for the first 72h of care, transferring rapidly to other local units. There is evidence for stroke-specific early supported discharge schemes reducing death or dependency as part of the overall pathway.
Benefits
Stroke units, when compared with general ward care, result in lower rates of death, dependency, and institutional care, without lengthening hospital stay. The number needed to treat in a stroke unit to prevent one death or dependency is 18.
Rationale
The majority of improvement seems to occur in the first 4 weeks, and the mechanism is unclear.
Key components of stroke units include:
• Meticulous attention to physiological homeostasis
• Attention to prevention of complications (such as thromboembolic disease and pressure sores)
• Interest, expertise, and motivation of staff
HOW TO . . . Estimate prognosis after stroke
After first-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 include:
The risk of recurrent stroke among survivors is 10–16% at 1 year, thereafter falling to about 4–5% per annum. The risk is higher with ↑ number of risk factors. Risk can also be estimated using the Bamford classification (see ‘Stroke’, ‘Definition and classification’, p. 179)
Recovery is usually slow, and a clear time frame established early on in the disease with the patient and relatives is helpful. Recovery is most rapid in the first 3 months, and this tends to be ‘front-loaded’, so the most dramatic improvements occur in the early weeks. Recovery then tends to slow but may continue for years.
► Each patient is different—recovery may be delayed by infections, depression, etc., and this time frame should be a guide only.
The risk of not returning to independence varies with stroke type. Overall, about 20–30% of survivors are dependent at a year, and 40–50% are independent.
Further reading
Stroke Unit Trialists’ Collaboration. Organised inpatient (stroke unit) care for stroke. Cochrane Database Syst Rev 2013; 9: CD000197. http://www.cochrane.org/reviews/en/ab000197.html.
Thrombolysis
Rationale
In acute ischaemic stroke, an artery becomes occluded by a thrombus in situ or an embolus, and blood supply is compromised. Death of surrounding brain tissue results in deficits in function associated with that part of the brain. Early recanalization of the vessel by lysing the thrombus may limit the extent of brain injury.
Risks
Treatment with thrombolysis leads to an excess in death due to intracranial haemorrhage (a fivefold ↑, compared with placebo).
Benefits
Despite early excess of deaths due to haemorrhage, treatment with thrombolysis leads to 44 fewer dead or dependent patients per 1000 treated with recombinant tPA (r-tPA) within 6h, and 126 fewer dead or dependent patients per 1000 treated with r-tPA within 3h.
Imaging
This must be done prior to giving thrombolysis to exclude haemorrhage. Perfusion- and diffusion-weighted MR scans may give more information than CT. All need to be interpreted by someone with the appropriate experience prior to thrombolysis. Plain axial CT remains the mainstay of imaging prior to thrombolysis.
Use
Thrombolysis is recommended in centres with sufficient expertise in stroke and with facilities to deal with complications. In these centres, treatment is considered in all patients with definite ischaemic stroke who present within 4.5h of the onset of symptoms. Where this expertise does not exist, the service may still be provided via telemedicine links with stroke ‘hubs’.
Exclusion criteria
There is a very long list of exclusions, but the following are the most common reasons to withhold treatment:
• Previous haemorrhage or active bleeding site
• Caution with very severe stroke
• Uncontrolled hypertension (>180/110mmHg)
Intra-arterial therapies
Rationale
Ischaemic stroke patients may present where there is a bleeding risk to systemic thrombolysis, and more localized therapy is safer. This can either be localized intra-arterial tPA or, more commonly, clot retrieval. This has been proven to be superior to iv thrombolysis alone and is now being offered in more and more centres. In the UK, this service is provided by interventional neuroradiologists, but elsewhere trained cardiologists or stroke physicians are taking the lead.
Ongoing management
Should involve all of the MDT.
Dieticians
Calculate food and fluid requirements for each individual patient; adapt the diet for specific needs (e.g. diabetic, weight loss); develop regimens for NG or PEG feeds; advise on provision of modified diets for stages of swallow recovery (thickened, pureed, 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); ongoing bowel and bladder management; ongoing skin care; facilitate practice of skills acquired in therapy; promote functional independence; first point of call for relatives.
Occupational therapist
Optimize functional ability (usually begin with upper limb work, coordinating with the PT); specific assessments of certain tasks (washing and dressing, kitchen safety, occupational tasks, etc.) as recovery continues; adaptation to 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 where needed.
Pharmacists
Review charts; promote safe prescribing.
Physiotherapists
Assess muscle tone, movement, and mobility; maximize functional independence by education and exercise; monitor respiratory function; initial bed mobility, then work on sitting balance, then transfers, and finally standing and stepping; help prevent complications such as shoulder pain, contractures, and immobility-associated problems (pressure sores, DVT/PE).
Psychologists
Assess the psychological impact of stroke on the patient and family; allow the patient to talk about the impact of the illness; monitor for depression and other mood disorder, highlighting the need for medication; document cognitive impairment; assist in retraining where neglect is prominent.
Social workers
Psychosocial assessment of the patient and family; support with financial matters (accessing pension, arranging power of attorney (POA), financing placement, etc.); advice and support for the patient and family on accommodation needs, especially finding a care home placement; link to community services (care package, community rehabilitation, day centres, etc.)
Speech and language therapists
Assess swallow and establish plan for safe oral intake; reassess, and plan nutritional route during recovery; language screening (dysarthria, dysphasia, and dyspraxia) with intervention to improve deficits.
HOW TO . . . Protect your patient from another stroke
Ensure that the following are addressed:
• Lifestyle issues—smoking, diet, and exercise
• Current advice is aspirin 300mg for 2 weeks, followed by clopidogrel 75mg thereafter. Adding clopidogrel to aspirin ↑ antiplatelet activity but has been shown to ↑ the risk of cerebral haemorrhage, but may be considered for monotherapy failure
• Lower BP—choice of agent debated. The important thing is just to lower the BP. If there are no contraindications, lowering BP per se is likely to be beneficial, but aim for <130/85
• Lower cholesterol—the Heart Protection Study clarified benefit post-stroke, including in older patients. The cut-off for treatment in this trial was 3.5
• Anticoagulation for AF—(see ‘Atrial fibrillation’, p. 274). In infarction, likely to be safe to start warfarin/DOAC after 2 weeks. With haemorrhage, judge each case individually. Haemorrhage due to thrombolysis is not a reason to withhold anticoagulation. In 1° haemorrhage, anticoagulation may never be justified
• Carotid endarterectomy—>70% symptomatic stenosis carries a stroke risk of about 15% per year and is an indication for endarterectomy where there is good recovery and the patient is fit for surgery (which can be done with local anaesthesia). Perform early for greater benefit See also ‘Vascular secondary prevention’, p. 310.
Complications
Contractures
Longer-term complication (see ‘Contractures’, p. 487).
Faecal incontinence
May be due to immobility, cognitive problems, or neurological impairment. Regulate bowel habit, where possible, with high-fibre diet and good fluid intake, and toilet regularly. If all else fails, then deliberately constipating the patient with codeine and using regular enemas can work. see ‘Faecal incontinence: management’, p. 546.
Infection
Commonly chest or urine. Think of it early if a patient becomes drowsy or confused or appears to deteriorate neurologically. Prompt screening for sepsis and treatment with antibiotics, oxygen, and hydration are indicated in the majority of patients in the acute phase (stroke outcome very unclear initially) but may be withheld in a more established stroke where the prognosis can be assessed more confidently as dismal (decision made with the family).
Muscle spasm
Very common on the affected side. Arthritic joints are exacerbated by spasm, and antispasmodics may need to be used, alongside analgesia, for effective pain relief. Try baclofen or tizanidine. ↑ the dose slowly after a few days, if needed, but watch out for drowsiness and loss of tone in the affected side that can hinder therapy. Resistant spasm may benefit from a course of botulinum toxin injections.
Pain
Commonly shoulder pain in a paralysed arm. Usually multifactorial, e.g. joint subluxation (treat with PT to strengthen muscles and arm support) interacting with muscle spasm and shoulder arthritis. Central post-stroke pain tends to affect all of the affected side and can be treated with neuromodulators (e.g. gabapentin)
Pressure sores
Are avoidable with good care; however, pressure damage may occur before admission but manifest only later (see ‘Pressure sores’, pp. 504–505).
Psychological problems
Low mood is extremely common post-stroke (at 4 months, 25% will be depressed, and over half of these remain depressed at a year). This is unrelated to the stroke type but is associated with a worse outcome (perhaps because of lower motivation in therapy). It should be actively sought (the screening question ‘Do you think you are depressed?’ is quick and effective; it may also be noticed by nurses, therapists, or family; tools such as the GDS can also be used but may be confounded by dysphasia). Treatment is with psychosocial support and antidepressants (e.g. citalopram). Anxiety is also very common and often responds to explanation and empowerment.
Post-stroke cognitive impairment is common (up to 80% prevalence). Delirium associated with acute stroke may improve, but cognitive deficits are often permanent (either fixed deficits or more global functioning).
Non-dominant hemisphere syndromes
Usually MCA strokes of the right hemisphere where language is crudely preserved, but there are issues with fluency, semantics, and interpretation of language (a kind of acquired neglect dyslexia). Deficits in assimilating information to make sense of reality can cause complex issues with insight and empathy and disease denial.
Thromboembolism
Very common post-stroke. Ensure well hydrated. Mobilize early. Intermittent pneumatic compression devices should be used in the acute phase. Low-dose low-molecular-weight heparin is used after the acute stage (when risk of haemorrhage into the brain diminishes). Have a low threshold for investigating a leg that becomes swollen or painful. Ensure careful VTE risk assessment is documented at each stage.
HOW TO . . . Manage urinary incontinence after stroke
This is very common, more so after severe stroke. It does, however, improve over time, and a flexible approach is required to ensure that a patient does not get catheterized and remains so.
• Initially, try to manage with pads and regular toileting
• If the skin starts to break down, or if the burden on carers is heavy, then a catheter can be inserted for a limited time span
• Once mobility improves, try removing the catheter—ensure this is seen by all as a positive and exciting step back towards independence, as it can cause considerable anxiety
• If this fails, check for, and treat, UTI and then try again
• If this fails, then replace the catheter and use bladder-stabilizing agents for about 2 weeks (e.g. tolterodine) before removing it again
• If all this fails, consider sheath catheter devices or bottles (with non-return valves for use in bed) in men; commodes next to the bed for women
► The need for a permanent catheter post-stroke should be reviewed regularly, as the condition is likely to improve (see ‘Urinary incontinence: causes’, pp. 534–535.
Longer-term issues
Return to the community
Best coordinated by the stroke MDT. Early supported discharge may be useful if the patient can transfer and there is a specialist community stroke team available. Later discharges are planned by the team, usually after careful assessment of needs (home alterations, care packages, etc.). The GP should be alerted to continue medical monitoring, in particular optimizing 2° prevention. Community teams (district nurses, community rehabilitation teams, home carers, etc.) should be aware of the patient’s needs (continence, diabetic monitoring, ongoing therapy needs, etc.) and ideally be involved in the discharge planning. The patient and family should have adequate information and training, as well as a contact point in case of problems (stroke coordinators often take this role). Voluntary agencies (e.g. the Stroke Association) are helpful, and the patient should be informed about them.
Driving regulations with cerebrovascular disease
• TIA/stroke with full neurological recovery—1 month off driving
• Recurrent TIAs—3 months off driving following last TIA
• Stroke with residual neurological deficit after 1 month—the patient must notify the DVLA, and the decision is made on a case-by-case basis, with evidence from medical reports
• Hemianopia, inattention, and impaired cognition are definite markers of lack of fitness to drive (can be decided by a GP or hospital physician). Subtle visual deficits need formal perimetry testing
• Dysphasia is harder—cognitive state is difficult to assess, and associated impairments (such as problems reading street signs or misinterpreting the environment) are not readily identified out of context
• Pure limb weakness can often be safely managed with car adaptation. If there are any doubts and the patient wishes to drive, then they should be seen in a driving assessment centre (the patient will have to pay)
• Stroke with seizure—this is treated as a provoked seizure. May be <1 year ban, depending on circumstances
See https://www.gov.uk/guidance/assessing-fitness-to-drive-a-guide-for-medical-professionals.
Follow-up
Some follow-up should be offered to all stroke survivors. The intensity and duration of inpatient care can contrast sharply with home. The realities of living with disability begin to sink in, and many questions and anxieties arise. Even minor strokes or TIAs require a further point of contact, as they will have been committed to lifelong medication and will need monitoring of risk factors. In addition, stroke recovery continues (albeit at a slower pace) for years and management plans made at discharge may need to be adapted.
The Stroke Association
Helpline: 0303 303 3100. http://www.stroke.org.uk.
Checklist for follow-up
(Usually 1–4 months after discharge)
Secondary prevention
Check drugs, BP, diabetic control, and cardiac rhythm.
Continence
• Are there continence problems?
• If a catheter is in situ, has mobility improved to a point at which trial removal can be done?
• If the patient was discharged on bladder-stabilizing drugs and has remained continent, can these be tailed off?
Nutrition
• Is nutrition adequate? (If not, refer to a dietician.)
• If a PEG tube is in place, is it still required?
• Does the patient warrant another assessment of swallowing (by SALT) to allow oral nutrition to begin?
Communication and speech
• Is there a need for a SALT review?
Mood
• Do they need referral to a psychologist or (rarely) a psychiatrist?
• If discharged on an antidepressant, can it be discontinued?
Physical progress
• Is there ongoing physical therapy?
• If not, is there continued improvement? If there has been deterioration, then refer back for assessment for further therapy (Royal College of Physicians’ guidelines)
Contractures
• Are there any contractures developing? (If so, refer to PT.)
Muscle spasms
• Have these developed or lessened since discharge?
• Review need for antispasmodic medication—titrate down if no longer required
Pain
• Commonly in shoulder, or post-stroke pain
• Has this developed or lessened?
Daily living
• Are there any issues in managing day to day?
• Is all the necessary equipment in place? (And is it still needed, e.g. a commode can be returned when the patient is able to mobilize to the toilet alone?)
• Is there anything that they would like to be able to do that they cannot? (e.g. read a book, take a bath)
• Would a further review by a therapist be helpful?
• Do they wish to drive? (see ‘Longer-term issues’, p. 196)
Support
• Are they in contact with a community stroke coordinator (if available)?
Transient ischaemic attack clinics
Rapid outpatient assessment of TIA and minor stroke, to establish diagnosis, commence 2° prevention, and lower risk of subsequent event.
How fast?
This depends on how high a risk the patient is. Use the ABCD2 score (see Table 8.3), and if the score is ≥4, the patient should be seen within 24h—in some services, these patients are admitted to hospital, but larger centres may provide 7-day/week outpatient services. Patients who have recurrent symptoms within a week or those in AF on anticoagulation should also be seen urgently. Those at lower risk should be seen within 7 days.
Currently, early antiplatelet agents, antihypertensives, and statin use have been shown to substantially reduce the chances of stroke at 1 week. Anticoagulation for patients with AF and early endarterectomy are also known to be beneficial for a subset of patients.
Function
• Confirm diagnosis—very variable, but up to half of referrals to a TIA clinic are non-stroke. Main alternatives are migraine, epilepsy, cardiac dysrhythmias, orthostatic hypotension, or rarely brain tumour
• Arrange investigations—to aid diagnosis (e.g. CT brain) or investigate risk factors (e.g. FBC, ESR, HbA1c, cholesterol, ECG, carotid Doppler, 24h tape, and echocardiogram)
• Modify risk factors—(see ‘HOW TO . . . Protect your patient from another stroke’, p. 193) set targets for BP and glucose control; advise about antiplatelet agents (there is significant regional variation in the therapy chosen, including aspirin with modified-release dipyridamole, or aspirin with clopidogrel for 1 month and then clopidogrel alone) and anticoagulation in AF; advise about statin use; refer for carotid endarterectomy urgently; advise about smoking cessation
• Education—of patients, relatives, and 1° care doctors. Discuss stroke disease and its modification, time frame for recovery, psychological aspects of stroke, and driving restrictions
Structure
Varies enormously. Ideally would have:
• Stroke specialist nurse—can take history, including standardized risk factor analysis, measure BP, provide education (leaflets, individual action plans), and coordinate investigations and follow-up. Role can be extended into the community—point of access for patients
• Time for explanation—many patients will feel overwhelmed by the amount of information they are being given. The specialist nurse can be very helpful in clarifying things, and information leaflets allow the information to be revisited at home. There are often several new tablets, or even suggesting surgery for a patient who feels well. Comprehension is vital for concordance
• Rapid access to investigations—particularly carotid Doppler and CT scanning. Many clinics run a ‘one-stop’ service where all assessments, investigations, and conclusions are completed at a single visit
• Prompt communication to GP—advice about risk reduction must be relayed promptly to the GP for maximum benefit. Ideally same day
Table 8.3 The ABCD2 score for TIA
| Score | |||
| A | Age | ≥60 | 1 |
| B | BP | ≥140/90mmHg | 2 |
| C | Clinical features | Unilateral weakness | 2 |
| Speech disturbance without weakness | 1 | ||
| D1 | Duration | ≥60min | 2 |
| 10–59min | 1 | ||
| <10min | 0 | ||
| D2 | Diabetes | Diabetes | 1 |
ABCD2 score—risk of stroke at 2 days: 0–3—1%; 4–5—4%; 6–7—8%.
Further reading
Johnson SC, Rothwell PM, Nguyen-Huynh MN, et al. Validation and refinement of scores to predict very early stroke risk after transient ischemic attack. Lancet 2007; 369: 238–92.