Stroke care

The care of large numbers of patients with strokes is often seen as a chore with little reward; however a modicum of attention to detail and a bit of thought can turn this task into quite a rewarding aspect of the care of internal medicine patients.

Assessing the degree of disability.
Consciousness.

The Glasgow coma scale was not originally designed for use in stroke patients, and essays have been written on its poor performance in this situation, although there is some evidence that it can be used for prognostication. If you do use it, don’t just write down a single ‘ratio’ but rather describe what you did and what response you managed to elicit for each of the three sections.

Perspective – reliability of the Glasgow Coma Scale

For a long time the GCS was considered to be reliable based on the finding of substantial agreement between individual observers and the average or consensus readings for a group of observers. More recent work¹ has suggested that for inexperienced users there may be substantial consensus amongst themselves, but they can be consistently out by about one point when compared to more experienced observers.

Motor. A muscle by muscle grading of power is not necessary, but the opposite extreme, of simply grading the power in a limb, is too brief. Choose one or more muscle groups and test them formally so that you or somebody else can come back on another occasion and assess progress (or deterioration!) For instance, test hand grip, finger extension, and elbow flexion in the arm, and hip flexion and foot plantar and dorsiflexion in the leg.

Speech. Expressive aphasia is common. At the very least determine if this is present by suggesting non-verbal ways of permitting response – writing, blinking a ‘yes’, etc. You can open very important doors to communication for a frightened and isolated individual.

Eye opening. Usually straightforward, although often asymmetrical.

Perspective: Glasgow Coma Scale for prognostication.

Another study². used components of the Glasgow Coma Scale to prognosticate. They divided the group on a GCS score above or below 9 (using only the vocal and eye components) for those who were not dysphasic and a score of 4 on the eye component alone for those who were. A score of less than 9 (eye plus vocal) had a sensitivity of 74% for two week mortality (specificity 76%, LR+ 3.1, LR- 0.6.) For a score of less than 4 on eyes alone, sensitivity was 44%, specificity 87% and LR+ 3.4, with a LR- of 0.6.

Swallowing

At your very earliest convenience formally test swallowing – if a gag reflex is present, give 2 ml of water; if swallowed, give 5, then 10 ml. Only once you have personally watched this and ensured no aspiration occurred (coughing, choking or change of voice!), give the patient a cup with water. If this is tolerated, then the nursing staff can be allowed to feed the patient in the ward. Remember that you need to sit the patient up to do this – none of us are very good at swallowing lying flat. Water swallow tests have sensitivities of the order of 70% , but the evidence is pretty thin³ Coughing or choking, or a ‘wet’ or gurgly voice are the features to look out for – progressively increasing volumes up to 100 ml will probably improve sensitivity to about 90%, at the cost of specificity.

Perspective – who is likely to aspirate

The presence of an intact gag reflex is not a very reliable sign that a stroke patient is unlikely to aspirate (LR- 0.5) but the presence of an inability to swallow water when formally tested, is of value⁴ , with a LR+ of 5.6 (2.4 to 12.9) and an LR- of 0.2 (0.1 to 0.5.) If water swallowing is normal, then testing pharyngeal sensation in that group will increase sensitivity to 100%, but at the cost of testing many normal swallowers. (For every 100 persons with normal water swallowing, you will find only 14 who have abnormalities of pharyngeal sensation, but all of these are likely to aspirate.)

A practical conclusion from this is to give water first and then pop a spatula/orange stick into the pharynx of those passing the water test. However, if you feel rushed, it is safer to prescribe nasogastric feeding (because more than half of all stroke patients are likely to aspirate) and review later when you have a chance to assess the situation quietly and at your own pace. The clinical significance of aspiration detected on cineflouroscopy is, however, unclear

Continence.

A patient lying in a pool of urine on a stretcher is not necessarily incontinent – lack of a urinal or bedpan may have caused this in a patient well aware of bladder function, so ask the patient! If the patient is too obtunded to answer then he or she will need bladder care.

Therapies in acute stroke

All patients without severe headache or neck stiffness (signs suggestive of an intracerebral or subarachnoid bleed) or suspected aspirin allergy should be given aspirin 150 mg daily.

Leave the blood pressure alone initially unless there are associated hypertensive emergencies such as aortic dissection, hypertensive pulmonary oedema, or hypertensive encephalopathy⁵ Blood pressure should not be lowered abruptly – 15% drop in 24 hours maximum, and don’t interfere at all if less than 220 systolic and 120 diastolic.

The 2000 patient CATIS study⁶ has provided some support for this approach, showing substantially no difference in outcomes between those given treatment to lower systolic blood pressure by 10% to 25% within the first 24 hours of admission and those not treated. In both groups the systolic blood pressure dropped to less than 150 within 3 days.

DVT prophylaxis with heparin in patients with other risk factors is reasonable, but may be associated with an increased risk of intracerebral haemorrhage when used in full anticoagulation doses.⁷

Anticonvulsants are only indicated if a further seizure happens after the initial event, which is often described as a ‘fit’ by the relatives.

Corticosteroids, mannitol, mechanical hyperventilation and barbiturates are NOT indicated.

Warfarin is indicated if there is embolic potential such as atrial fibrillation or a mechanical heart valve.

Supplemental oxygen is indicated only for hypoxaemia, e.g. associated with aspiration or pneumonia. In a patient without evidence of desaturation, the presence of the mask can be frightening, can worsen aspiration risk, and is without benefit in terms of neuroprotection.⁸

Pay attention to glucose control in diabetics, remembering the caloric intake is a function of nursing care and is at times erratic. Meticulously tight glucose control has not been demonstrated to confer a survival or reduced disability advantage Gray CS, Hildreth AJ, Sandercock PA, et al. Glucose-potassium-insulin infusions in the management of post-stroke hyperglycaemia: the UK glucose insulin in stroke trial. Lancet Neurol. 2007;6:397-406..

Taking over impaired functions in stroke patients

Airway

Ensure that the patient can maintain an airway, and consider placing an oral airway or an endotracheal tube if appropriate. In a situation where nursing care is suboptimal (i.e. where regular endotracheal tube care may not happen) and where an elderly patient with multiple comorbidities is likely to have very poor prognosis, not intubating but simply counselling the family and providing palliative nursing care may be a more appropriate course.
Consider urinary catheterisation or Paul’s tubing.

Feeding and hydration.

Do not starve people with strokes. If in doubt about ability to swallow, insert a naso-gastric tube and give tap water 2 litres and 1 litre of prepared enteral feed from day 1; increase enteral feed proportion as tolerated, e.g. 2 litres of feed and 1 litre of water. Consider this order as part of the preliminary assessment; if it is not written down at that stage it is often forgotten.

Communication with stroke patients

Communicate with the family from the time of presentation about long term placement and the desirability of the patient being looked after at home from as early as possible.
Be inventive in communicating, right from the beginning, with the patient, who is lonely, isolated, scared and frustrated.

Stroke versus Transient Ischaemic Attack

The practical value of differentiating the two is to identify patients who are at low risk of another stroke in the next week or so, and who could reasonably safely be managed as outpatients.

Perspective – using the ABCD score to identify high short-term stroke risk.ABCD score

A study from Oxford⁹ is of some help in identifying patients with TIAs who are at high risk of developing a full stroke in the next week, and who should probably be admitted for further management.

	Feature	Score
A	Age > 60 years	1
	Age < 60 years	0
B	BP systolic >140 or diastolic >90	1
	BP both systolic < 140 and diastolic < 90	0
C	Clinical: unilateral weakness	2
	Clinical: speech change without weakness	1
D	Duration > 60 minutes	2
	Duration 10-59 minutes	1
	Duration < 10 minutes	0

The score for each component is then added up. A score of <4 is associated with a 7 day stroke risk of 0%, 4 with 2%, 5 with 16%, and if the score is 6 then there is a 36% chance of a stroke in the next seven days.
Perspective – is it actually a stroke?

Simple signs perform quite well. A review¹⁰ found that the LR+ for a stroke was 5.5 if any one or more of new facial paralysis, arm drift, or abnormal speech was present, and the LR- was 0.39 if none of these features was present.

Perspective – early neurological deterioration

Worsening neurological status within 5 days of admission may occur in one in five stroke patients, and is associated with a fourfold increase in hospital mortality (44% vs 10%)¹¹ Pay attention to simple things, such as fever, hyperglycaemia, dehydration and hypoxia.

Assigning a cause for a stroke

An elderly hypertensive patient with sudden onset neurological deficit with no prodrome has a very high likelihood of having suffered a vascular event for which there is no specific therapy other than attending to general risk factors (blood pressure reduction, diabetes control, use of aspirin).

With younger patients and more atypical features, the probability of finding another cause rises, and the logic then goes that such patients warrant extensive investigation even though the yield is often still rather low. The key issue, however, is finding fixable causes to prevent further deterioration, or identifying patients who appear to have a stroke but have suffered some other type of sudden neurological event.

The key screening test is a very adequate history, looking for type of onset, preceding headaches and background ethanol misuse. Examination should include a careful cardiovascular examination (BP, pulse rhythm, apex palpation, and auscultation for cardiac murmurs and carotid bruits).

Investigations appropriate in most stroke patients

• ECG
• Syphilis serology
• HIV serology
• U&E to help assess hydration
• FBC to exclude polycythaemia.
• CRP

Most other investigations should be directed by clinical findings.

• Echocardiography if clinical or ECG evidence suggestive of valvular heart disease or septal defect. (‘Routine’ transthoracic echos have a low yield, in terms of management changes, in the absence of any clinical or ECG abnormalities.)
• ANF (antinuclear factor) if there are features of arthritis or other lupus manifestations in a young person.
• Carotid Doppler ultrasound is appropriate in a patient with an audible bruit and good recovery after a stroke. Some would argue that all young patients with adequate recovery (and all patients with TIAs) warrant a Doppler, regardless of whether a bruit is audible.
• Screening for thrombophilias is a bit controversial in view of the cost and low pick-up rate. A reasonable compromise in a young person is to do a PTT, INR and a lupus anticoagulant. If these are all normal, the chance that you have missed a clinically important thrombophilic state is low.

Perspective – ethanol abuse and stroke.

Patients who abuse ethanol are more likely to have subdural haematomas because they (or their friends) bump their heads without them noticing. If in any doubt about the history, patients with background ethanol use should be considered for CT scan. However alcohol abuse itself is associated with an increased relative risk of stroke of 1.64 (CI 1.39-1.93) – infarct 1.69, bleed 2.18¹².

Determining the need for a CT an apparent stroke patient.

If there is a clear history of a sudden onset hemiplegic neurological event in an elderly patient, then very little will be gained by referring the patient for a scan. The essentials of management concern hydration, prevention of aspiration by positioning, and discussion of prognosis with the family.

The following patients should be considered for a CT scan

• All young (<40 years) patients with new onset hemiplegias or other focal neurological deficits of abrupt onset.
• All patients in whom there is lack of clarity about the circumstances surrounding the event – i.e., if there is a history of trauma, recent alcohol use, or when no useful history is available.
• Patients with abrupt onset cerebellar signs (any combination of vomiting, nystagmus, and the well-known motor signs) as they may have posterior fossa haemorrhage, which often responds well to surgical evacuation but which if untreated can lead to rapid and fatal coning.
• Patients with papilloedema or subhyaloid haemorrhages. (Possible subarachnoid haemorrhage.)
• Patients with a stiff neck or severe headache (possible subarachnoid haemorrhage or base of brain vasculitis secondary to meningitis).

The following will probably not benefit from scanning:

• Patients in whom no functional neurological recovery is likely – e.g. fixed dilated pupils, Cheyne-Stokes respiration, dense hemiplegia already present for many days when first seen. Remember that people with severe organo-phosphate poisoning may have fixed pupils and an abnormal sensorium.
• Patients with severe and untreatable intercurrent illnesses (e.g. terminal AIDS, metastatic cancer, end-stage chronic renal failure).
• Perhaps also not patients with an easily identifiable secondary cause for infarction – e.g. strongly positive serum syphilis serology

Reversible ‘strokes’

Events that may be classified as strokes (usually because of an inadequate history) include:

• Todd’s paralysis after a fit (usually reverses after a ‘magic’ 24 hours, but if the pattern is consistent (‘always weak on that side after a bad fit…’) and there is a trend to improvement then allow a longer period – perhaps up to 48 hours – before investigating further.
• Subdural with sudden expansion.
• Ongoing non-convulsive status epilepticus. Consider this particularly if the patient’s condition seems to wax and wane.
• Spinal pathology – check that the signs really are hemiplegic and not paraplegic!
• Conversion disorder.

Perspective – the magnitude of benefit from aspirin.

The Antiplatelet Trialist’s Collaboration¹³ Mean duration of treatment was 3 years. This demonstrated a 1.7% ARR in mortality (0.5 to 2.9%, placebo rate 13.3%, NNT 59) and a 2% reduction in non-fatal stroke (NNT 50 (95% CI 33 to 116.)

A subsequent Cochrane review¹⁴. added some more data, and expressed it differently:

For every 1000 patients treated with aspirin for 6 months, you would have 13 more patients alive and independent, (NNT 76) at a cost of 2 extra symptomatic intracranial bleeds. You would also prevent 7 recurrent strokes and one pulmonary embolus. (You would help 21 and harm 2, and treat 979 without any benefit to them.)

Timing of the benefit

A time course analysis¹⁵. has shown that most of this benefit accrues early, and those with minor strokes or TIAs are obviously more likely to benefit than those with already major events. For patients with a TIA or ischaemic stroke, the probability of another stoke is more than 35 per 100 person years without aspirin, and less than 15 with aspirin, for the first 6 weeks after then event, with much of this benefit accruing in the first two weeks. After 12 weeks, the control and the aspirin event rates are both about 5 per 100 person years. Give it early, and even consider stopping after 12 weeks if no other major indications (such as ischaemic heart disease) and side-effects have become an issue.

Anticoagulation in the acute phase (first 14 days after a stroke)

Outcomes[1]	Baseline risk	ARR	NNT
Outcome at 14 days after starting aspirin in acute stroke (Pooled CAST[2] + IST[3])
Composite of death or new stroke	9.1%	0.92%	110
Another stroke	2.3%	0.69%	146
No significant difference in mortality (ARR 0.46%, CI  0.9% to – 0.008%, p = 0.054) or CNS bleeds*
Patients who were inadvertently given aspirin after a haemorrhagic stroke
Another stroke	2.1%	1.9%	54
New CNS bleed	6.9%	-0.4% (NS)
There was also no significant difference in mortality
Heparin in acute stroke (IST)
Another stroke	3.8%	0.9%	112
New CNS bleed	0.4%	0.8% (increase)	125 (NNH)
No significant difference in mortality
Heparin in stroke with atrial fibrillation (IST)
Another stroke	4.9%	2.1%	48
New CNS bleed	0.4%	1.6% (increase)	59 (NNH)
Full dose versus prophylactic dose heparin in acute stroke (IST)
Death or another stroke	10.8%	1.7% (increase)	58 (NNH)
CNS bleed	0.7%	1.0% (increase)	97 (NNH)
There was no significant difference in the individual endpoints of death or recurrent stroke
Full dose heparin versus no heparin (IST)
Transfusion or extracranial bleed		1.6% (increase)	63 (NNH)
No difference in death or recurrent stroke
Prophylactic dose heparin versus no heparin (IST)
Death or recurrent stroke	10.8%	1.2%	84
Recurrent stroke		0.9%	112
CNS bleed		0.3% (increase)	334 (NNH)
No difference in transfusion or extracranial bleed

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[1] Cheng Z, Sandercock P, Pan H, et al. Indications for Early Aspirin Use in Acute Ischemic Stroke. Stroke. 2000;31:1240-1249.

[2] CAST (Chinese Acute Stroke Trial) Collaborative Group. CAST: randomised placebo-controlled trial of early aspirin use in 20 000 patients with acute ischaemic stroke. Lancet 1997; 349: 1641–49.

[3] International Stroke Trial Collaborative Group. The International Stroke Trial (IST): a randomised trial of aspirin, subcutaneous heparin, both, or neither among 19 435 patients with acute ischaemic stroke.Lancet 1997; 349: 1569–81.

A “CNS bleed” is the composite of a new intracerebral haemorrhage, or haemorrhagic transformation of a previous stroke. Figures shown in the table are mostly listed because the differences reached statistical significance (NS = not significant.) NNH = number needed to harm.

In summary, aspirin in the acute stage has a modest but worthwhile effect on mortality and stroke prevention, and this benefit still holds if the stroke was a bleed rather than an infarct. Heparin overall does as much harm as good; low-dose heparin is of modest benefit but causes increased CNS bleeds. Heparin in stroke with atrial fibrillation is neutral – significant benefit of 2.1% stroke recurrence is offset by a 1.6% increase in new CNS bleeds. Assuming new bleed and recurrent ischaemic stroke have similar clinical consequences, then for heparin in stroke with AF the ARR is 2.1-1.6% = 0.5%, or NNT of 200.

Perspectives – early management of hypertension in stroke patients

Everyone has an opinion on this, but unfortunately the evidence is rather scanty¹⁶.. A systematic review¹⁷ identified only five randomised trials addressing this issue, involving only 218 patients. Unsurprisingly, it showed that blood pressure treatment dropped the blood pressure (by about 10 mmHg systolic in the first 24 hours) but had no measurable effect on outcome. The source of the magic figure of 120 diastolic is obscure – it is widely quoted but weakly referenced.

Perspective – benefits from adequate hydration

A small prospective observational study¹⁸. of patients with stroke seen in a London hospital who were subjected to intensive investigation for thromboembolic disease (leg and chest MRI scans) reached some rather sobering conclusions.

Out of 102 patients recruited, 40.2% developed VTEs (venous thromboembolism) which were subclinical in 85%, and even more concerningly 10.8% had MRI evidence of pulmonary embolism at some stage during their hospital stay. The average patient was biochemically dehydrated by Day 9, having arrived euvolaemic. The odds ratio of developing a VTE was 2.8 for those with a urea of >7.5 mmol/l (probability 65%).

Perspective – enteral tube feeding.

The timing when enteral feeding starts has been shown to influence outcome. Avoiding tube feeding for the first week in dysphagic patients resulted in a 5.8% absolute increase in the risk of death The FOOD Trial Collaboration. Effect of timing and method of enteral tube feeding for dysphagic stroke patients (FOOD): a multicentre randomised controlled trial. Lancet 2005;365:764-72.; however, the reduction in case fatality in those fed early was associated with an increase in patients surviving but requiring long term institutional care. The use of early PEG feeding (percutaneous gastrostomy) was found by the same trial group to be associated with a small (1%) but statistically insignificant increase in the risk of death – there was certainly no survival advantage from the early use of a PEG.

Pseudobulbar palsy

The pons contains cranial nerve nuclei V and VII which are responsible for chewing and swallowing. Patients with bilateral cortical or internal capsule lesions, usually coming on at separate times, may develop difficulty swallowing because of lack of even unilateral innervation of these nuclei. In other words, while there is still supply from one side, the patient can still swallow, but when the second stroke, which may otherwise be relatively minor, takes out the second set of motor afferents to the nuclei, the patient suddenly develops a problem with swallowing without necessarily a major new limb motor weakness.

• It usually occurs in the setting of an individual with one or more documented previous strokes.
• There is sudden onset of dysphagia, with or without new lateralising signs.
• The patient has a relatively immobile face, and often drools saliva because of inability to swallow.
• Dysarthria may be present.
• The jaw jerk is brisk in about 70% of patients.Jaw jerk
• The gag reflex is often but not always absent (still present in about 30% of patients).
• A striking and somewhat disconcerting clue is the appearance of inappropriate crying or laughing, during which the previously still face moves freely¹⁹..

Management consists of early placement of a nasogastric tube, attention from a speech therapist if available, and then either placement of a gastrostomy, or lessons to the family in care of a nasogastric tube.

Routine care of stroke patients in hospital

Fever. The usual cause is aspiration pneumonia or a urinary tract infection. Look for these and treat them promptly, including the use of paracetamol. Treat the first infection while waiting for neurology to settle; thereafter in a patient with poor recovery discuss with family and seniors whether to treat subsequent infections.
Heparin 5000 units sc. 8 – 12 hourly may reduce DVT risk and is unlikely to cause haemorrhagic transformation; however the evidence of real benefit is scanty.
Severe hyperglycaemia may lead to worse cerebral damage and is worth treating. Be aware of the danger of precipitating hypoglycaemia in poorly attended patients.
Arrange physiotherapy from day 1, and maintain communication with the physiotherapists so that you don’t keep people in hospital longer than necessary, or discharge that one patient in whom the physiotherapists are making great progress… Conversely, the unconscious patient with a dense hemiplegia and little evidence of improving sensorium is unlikely to benefit much beyond nursing and family education about positioning and contracture prevention.
Nutrition and fluid balance is essential.

Perspective – nasogastric tube placement

Inserting a nasogastric tube can be difficult without patient co-operation. It may help to induce the swallowing reflex by inserting a small paediatric tube through the other nostril, and placing its tip in the oropharynx. Injecting small boluses of water (0.5-2 ml) through this tube may induce a swallowing reflex that will allow passage of the larger tube²⁰

A network analysis²¹ demonstrated that likelihood ratios for pH is dependent on the value chosen, but that if the key feature is testing that it is not in the lung, then the pH 5.5 cut-off is probably acceptable, and auscultation is useless:

Method	Likelihood ratio in stomach rather than lung	Likelihood ratio in stomach rather than oesophagus
pH <	Infinite	11
pH < 5.5	Infinite	1.37
pH <6	200	1
Auscultation epigastrium	1.3	0.5
Auscultation LUQ	1	2.2

Radiology as a confirmation has a couple of caveats: a tube below the diaphragm is not necessarily in the stomach (left lower lobe extends down on the PA and AP films) and deviation at the level of the carina is an important clue that the tube is in the lung rather than correctly positioned. A 2017 review of registrar’s ability to safely determine NGT position used the following criteria²²:

• “Does the tube follow the contours of the oesophagus and avoid those of the bronchi?

• Does the tube clearly bisect the carina?

• Does it cross the diaphragm in the midline?

• Is the tip clearly visible below the left hemi-diaphragm?”

In that study only 18% of responses correctly documented tube position using all four criteria. Another interesting way of confirming placement which saves on radiation exposure and is quick, but requires some training of operators, is abdominal ultrasound.²³ The 2017 Cochrane systematic review²⁴ points out that although studies look promising, we still lack evidence that ultrasound is validated as a stand-alone test after which NGT feeding is safe.

Dealing with neurogenic dysphagia.

The management of swallowing difficulties in patients with neurological disorders (usually strokes) is beyond the scope of this manual, and relies heavily on the services of a competent speech therapist and adequate technology to make an accurate swallowing diagnosis’, which basically means the facilities and time to perform cinefluoroscopy on stroke patients²⁵.

• If in doubt, use nasogastric tube feeding until the situation is clearer.
• Some patients who look as if they are going to have major swallowing difficulties seem to settle quite quickly, so it is worth re-evaluating the water swallow after a few days.
• It is quite difficult to swallow lying flat on your back and being feed from a poorly positioned spoon. Suggest elevation of the head of the bed.
• Thicker consistency food such as porridge may be easier to swallow than clear fluids.
• There are numerous tricks and manoeuvres which may aid swallowing – some are designed to re-train weak muscles and others are designed to facilitate the actual mechanics of swallowing. Examples:
• chin tuck posturingChin tuck posturing – tuck the chin in so that the food bolus sits anteriorly in the mouth, then lift the head, shift the bolus back and swallow in one movement.
• neck extension posturingNeck extension posturing – patients and relatives often try this intuitively – putting the head back to get gravity to assist in getting the food to the back of the throat. This is often not very successful in stroke patients (it may be of more value in motor neurone disease) as it may increase the propensity to aspirate.
• lingual sweepLingual sweep – conscious reminder to do what we all do normally – sweep tongue round all parts of mouth to clear residua after a swallow.
• cyclic ingestionCyclic ingestion – alternate liquid and solid mouthfuls.
• bolus placementBolus placement – place the food on the side of the tongue that is still working.
• adjustment of size of bolus and rate of feeding. Little bits are often easier to handle than big bits, as most feeders of small children know.
• Family members often have more time and interest than busy nurses, so get them involved early.

Rehabilitation and discharge.

Only in very affluent societies is there the opportunity for stroke patients to be managed long-term in special facilities. Many argue very cogently that this type of facility is inappropriate even if you can afford it, and that being with family is an integral part of the rehabilitative process. In less affluent societies it is usually the responsibility of family to take over care at discharge.

• Can the proposed chief caregiver cope? An elderly spouse who is also unwell may simply be unable to manage the burden. Mobilising the family resources, and even bringing in relatives from elsewhere may take some time, but in the end it is probably worth accepting an extra few days in hospital if it prevents the patient returning in a worse condition in a week or two. Similarly, ambitious plans to have the neighbour watch out during the day, and have a school-going child manage at night rarely work – you need to explain to relatives how rigorous the work involved really is.
• Have you optimised medication? Remember that getting BP control perfect in a supine patient, particularly by too vigorous use of diuretics, can lead to clinically significant postural hypotension once sitting or standing is eventually attempted, and this inability to sit may puzzle physiotherapists and doctors alike. You can always tighten up medication once the patient is up. The same applies to oral hypoglycaemics – a formerly mobile person may need less medication after a stroke, as access to food now becomes dependent on another person.
• Has in-hospital care plateaued? While the patient is still benefiting from physiotherapy, don’t abruptly discharge without first discussing with the physiotherapist.
• If speech therapy is available and needed, has the patient been assessed?
• Have you sorted out access to disability grants if appropriate?
• In the absence of basic physiotherapy, have you conveyed the essentials to the patient and caregiver? (Progressive targets – swallowing, training in one-handed dressing and bathing, practicing reaching for small objects placed in lap, walking with assistance²⁶
• Has care and training of the care-giver(s) been completed? A UK study²⁷. demonstrated that adequate training of the care giver not only improves quality of life for both patient and care giver, but makes economic sense²⁸, with duration of admission being reduced by an average of 12.4 days (95% CI 5.6-19.5).
• Advice on avoidance and management of pressure sores
• Advice on nutrition and management of nasogastric tube if present.
• Advice and a practical demonstration on how to change a patient in bed if needed, how to lift a patient, and how to get a patient in and out of a chair.
• Advice and practical demonstration of how to deal with problems of continence.
• Hands-on teaching about gait facilitation
• How to deal with communication issues if the stroke has affected speech.

Prognostication in stroke patients

Relatives and patients often ask about expected outcome. The reality is that in community based studies about half of patients will be either dead or dependent a year after a stroke. If patients are going to recover to independence, they generally do so within the first month. Patients with higher cerebral dysfunction and hemiplegia at presentation have a less than 5% chance of being independent a year later.

The definitions of stroke provided by the Oxfordshire Community Stroke Project are of some value in prognostication²⁹.:

1. Total anterior circulation infarct (TACI):
   1. Homonymous visual field defect AND
   2. Ipsilateral motor or sensory deficit (two of face, arm or leg) AND
   3. Higher cerebral dysfunction (dysphasia, visuospatial disorder, reduced consciousness)
2. Partial anterior circulation infarct (PACI):
   1. Two out of the three TACI components OR
   2. Higher cerebral dysfunction on its own OR
   3. Like a TACI but the ipsilateral motor/sensory signs are in only one of the three areas instead of two) 
3. Lacunar infarct (LACI):
   1. Pure motor stroke OR
   2. Pure sensory stroke OR
   3. Both OR
   4. Ataxic hemiparesis
4. Posterior circulation infarct (POCI):
   1. Ipsilateral cranial N palsy with contralateral motor or sensory limb signs OR
   2. Bilateral motor or sensory signs OR
   3. Abnormality of conjugate eye movement OR
   4. Homonymous visual field defect OR
   5. Cerebellar signs without ipsilateral long tract signs

For the whole series of 543 patients in this study, the mortality rate was 10% at 30 days and 23% at one year; the respective figures for TACI (92 patients) were 39% and 60%. The presence of a TACI predicted death or dependency at 30 days with a high specificity (99%) but modest sensitivity (33%, LR+ 22.2, LR- 0.7.) The performance was almost identical at one year, reflecting the fact that most of the mortality impact of a stroke happens within the first month.

Perspective – interobserver reliability of OCSP classification

A study³⁰. of 194 patients across four hospitals looked at the reliability of the above classification reached by a stoke physician or a neurology resident when compared to the gold standard of a ‘blinded stroke neurologist’ and found that kappa (a measure of agreement beyond chance) for TACS was 0.5, for PACS 0.37 and for LACS 0.63, reflecting that even this form of syndromic classification is still subject to clinical disagreement.

Of some concern, neuro-imaging studies showed that the anatomical diagnosis was wrong in 21% of patients, whether made by a general clinician or a stroke neurologist.

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1. Rowley G, Fielding K. Reliability and accuracy of the Glasgow Coma Scale with experienced and inexperienced users. Lancet. 1991;337:535-8 ↩

2. Weir J, Bradford AP, Lees KR. The prognostic value of the components of the Glasgow Coma ScaleGlasgow Coma Scale following acute stroke. QJM. 2003;96:67-74 ↩

3. Boaden E, Burnell J, Hives L, Dey P, Clegg A, Lyons MW, Lightbody CE, Hurley MA, Roddam H, McInnes E, Alexandrov A, Watkins CL. Screening for aspiration risk associated with dysphagia in acute stroke. Cochrane Database Syst Rev. 2021 Oct 18;10(10):CD012679. doi: 10.1002/14651858.CD012679.pub2. PMID: 34661279; PMCID: PMC8521523. ↩

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5. SAMA – Neurological Association of South Africa Stroke Working Group. Stroke therapy clinical guideline. S Afr Med J. 2003;90:276-305 ↩

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