Stroke

Ischemic Stroke (80%)

Thrombotic/intrinsic vessel disease originates in the brain's vasculature. Causes include:

• atherosclerosis
• small vessel disease
• vasculitis
• vasospasm
• arterial dissection
• compression
• fibromuscular
• hypercoagulable state (oral contracepives, HRT)
• cerebral venous thrombosis

Embolic disease originates at remote sites. Causes include:

• cardiac wall thrombi (common): myocardial infarct, valvular disease, and atrial fibrillation important predisposing factors
• arterial thromboemboli, particulary from atherosclerotic plaques within the carotid arteries
• septic material
• air
• fat
• tumour
• paradoxical

Lacunar strokes (LACS) are usually due to intracerebral small vessel disease. They are clinically recognizable, with pure motor hemiplegia, pure sensory stroke, or ataxic hemiparesis. They also have the best functional outcomes of all stroke types.

Hemorrhagic Stroke

Intracerebral hemorrhage is responsible for 15% of stroke. Causes and risk factors include:

• hypertension
• trauma
• bleeding conditions (hereitary/acquired thrombophilia)
• amyloid angiopathy
• illicit drug use (ie cocaine)
• vascular malformation
• vasculitis
• hemorrhagic transformation of an infarct or tumour
• rupture of a mycotic aneurysm
• medications: anticoagulants, thrombolytics

Subarachnoid hemorrhage (SAH) is responsible for 5% of stroke. Younger age of onset is common, with women >men. Causes and risk factors include:

• aneurysm rupture
• vascular malformation
• bleeding conditions (hereitary/acquired thrombophilia)
• trauma
• amyloid angiopathy
• illicit drug use (cocaine)

Risk factors for all types of stroke include:

• hypertension (60% of the population attributable risk)
  • lowering 2 mmHg reduces risk by 10
• smoking (2x risk of infarction; 3x risk of subarachnoid hemorrhage)
• diabetes
• hyperlipidemia
• low exercise
• low cholesterol appears associated with increased intracerebral hemorrhage
• heavy drinking (increases risk 2.5x)
• obesity
• oral contraceptives or post-menopausal hormone treatment

Risk factors explain perhaps 60% of attributable risk for stroke, leaving the other 40% currently unaccounted for. A proportion of these may be genetic.

Global cerebral ischemia occurs when there is a generalized drop in perfusion such as can occur in cardiac arrest, shock, or severe hypotension. Focal cerebral ischemia follows reduction in blood flow to a given area due to large vessel disease, such as thrombosis or embolus, or due to small vessel disease such as vasculitis.

CNS cells show a hierarchy of susceptibility to ischemia, with neurons being the most sensitive. Glial cells are also vulnerable. Differences in blood flow and metabolic needs results in selective vulnerability of different populations following global events.

Thrombotic Stroke

The distinction between TIAs and stroke is arbitrary, as permanent tissue damage can be shown on MRI in at least 25% of patients with TIAs (Kidwell et al, 1999).

Large vessel stroke is most commonly due to atherothrombosis. These can be found at the bifurcation or siphon portion of the common carotid artery, middle cerebral artery stem, intracranial vertebral arteries, or origin of vertebral arteries.

Small vessel stroke, aka lacunar stroke, is most commonly due to lipohyalinotic occlusion following hypertension or occasionally atheroma. They occur in the penetrating branches of the anterior, middle, or posterior cerebral/basilar arteries.

Cardioaortic Embolic Stroke

Cardiac sources include atrial fibrillation, LV/LA thrombus, rheumatic valve disease, artificial valves, bacterial endocarditis, or atrial myxoma.

Ischemic penumbra

The ischemic penumbra is the structurally intact, but functionally impaired, tissue surrounding the area of infarct. It is the target of intervention, as its restoration can aid recovery. Molecular events begin with energy depletion, disruption of ion homeostasis, release of glutamate, calcium channel dysfunction, release of free radicals, membrane disruption, inflammatory changes, and apoptosis and necrosis (Dirnagl, Iadecola, and Moskowitz, 1999).

Hemorrhagic Stroke

The most common mechanism for hemorrhage is small-vessel disease causing lipohyalinotic aneurysms that rupture. About 2/3 of patients with primary cerebral hemorrhage have hypertension (Thrift, Donnan, and McNeil, 1995). Other causes include arteriovenous malformations, cerebral amyloid angiopathy, or infarction with secondary hemorrhage.

Most subarachnoid hemorrhage is caused by rupture of saccular aneurysms within the subarachnoid space

History

Assess, as specifically as possible, time of onset of s

Common signs of stroke include:

• weakness
• trouble speaking
• vision problems
• dizziness
• headache

It is important to discover how the patient was beforehand, to tease out causes.

What else is wrong? Assess the patient's prior level of function.

SAH often presents with the "worst headache ever", neck stiffness, nausea, and vomiting. However, mild SAH is frequently misdiagnosed.

Physical Exam

Vital (ABC's) are critical

Localization of the lesion, with attending signs and symptoms,

Neurological exam

• pay attention to visual and

pure motor hemiplegia, pure sensory stroke, ataxic hemiparesis

Lab Investigations

CBC, lytes, ur, sCr

• blood glucose: Hypoglycemia and hyperglycemia are the most common stroke mimics

Diagnostic Imaging

ECG to rule out arrhythmia or acute coronary syndromes.

Immediate imaging is necessary to rule in or out a hemorrhage.

• subdura

While unenhanced CT has been the primary imaging modality for years, MRI is likely the better of the two.

The ischemic penumbra is visible in some patients up to 24 hour after stroke by MRI. Perfusion-weighted imaging can be used to show areas of ischemia and can be compared with the ischemic core, visible by diffusion-weighted imaging.

left MCA infarct causing expressive aphasia

Carotid doppler shows flow velocity and areas of turbulence. A 50% stenosis will give a flow of 130 cm/s, while a 75% stenosis correlates with 230 cm/s.

Health Promotion and Primary Prevention

Hypertension control is top priority in preventing stroke. Lifestyle modifcation is accordingly very important: quit smoking, eat healthy, exercise, and reduce stress.

Small amounts of alcohol decreases risk.

Medication prevention includes lipid-lowering agents, anti-platelet therapy (81 mg ASA), and antithrombotic therapy (warfarin) for atrial fibrillation. However, warfarin is used in only 54% of patients with AF in Canada due to confusion about benefit and perceived risk of complication (Kapral et al, 2005).

For patients with atrial fibrillation unable or unwilling to take warfarin, both aspirin and clopidogrel appear helpful (ACTIVE investigators, 2009).

Pre-Hospital and Emergency Care

Stroke is a medical emergency that requires urgent hospital admission.

Do CT within 45 minutes to rule out hemorrhage and begin fibrinolytics if appropriate (heparin, warfarin, aspirin, tPA). tPA must be used within three hours.

Thrombolysis

Recombinant tissue plasminogen activator (tPA) is one of the most biologically effective treatments for acute ischemic stroke. 2008 Guidelines require treatment within 4.5 hours of stroke onset (Wardlaw et al, 2009), though

This short time window means that only 6/1000 patients benefit with treatment (Gilligan et al, 2005). tPA is effective at improving function, but not at reducing mortality (Hacke et al, 2004) hypertension, very severe neurological deficits, severe hyperglycemia, and possibly with early CT ischemic changes.

The major adverse effect is intracerebral hemorrhage, seen in 6-7% of cases. Increased risk is seen in with increased age.

Give bolus and then drip. Stop if: neurological deterioration, severe headache.

Inclusion criteria:

• acute ischemic stroke in agen >18
• 1h <stroke duration <4.5 hrs
• deficit that is disabling, or measurable on the NIHSS
• no ICH on CT or MRI
• informed consent (usually family)

Exclusion critiera:

• time of onset >4.5 hrs
• ICH on CT or MRI
• symptoms suggestive of SAH
• CT or MRI signs of acute hemispheric infarction involving over 1/3 MCA territory
• history of ICH
• stoke, serious head injury, or spinal trauma within prev 3 months
• seizure at onset
• recent major surgery
• SBP > 185 or CPB > 110mmHg
• elevated INR or PTT
• plt <100 x 109/L
• hypo, hyperglycemia
• any other condition which could increase risk of hemorrhage

Do not give ASA, clopidogrel, or heparin for 24 hours.

Blood Pressure Management

Labetalol 10-20 mg IV over 1-2 minutes

repeat q10 to a total dose of 300 mg

Other options: nicardapine

ICH: neurosurgery should always be consulted.

Largely supportive

Correct coagulopathy if present

Establish goals of care

Acute Stroke Care and Early Rehabilitation

Initial stroke recovery involves resolution of cerebral edema, ionic fluxes, and inflammatory processes.

There is conclusive evidence that organized inpatient care, such as is received on an interdisciplinary stroke care unit (SCU), decreases morbidity and mortality (Phillips, Eskes, and Gubitz, 2002). A core set of performance indicators exists and

Management of patients within a SCU reduces mortality and improves function by about 20% (Langhorne et al, 1993).

Stroke units bring together staff and patients into a single ward, usually at little additional cost. Immediate entry into a stroke unit helps prevent or reduce complications, such as aspiration or dehydration. Benefits depend on coordinated care of a multidisciplinary team, with integration of nursing, staff expertise, close involvement of caregivers, and education for staff, patients, and caregivers. Improved blood pressure control, early mobilization, and general adherence to best practice are all also important (Langhorne and Pollock, 2002; Cadilhac et al, 2004).

It appears SCU management has the potential to prevent death or disability for about 50 patients for every 1000 strokes, compared with 6 per 1000 for tPA and four per 1000 for aspirin (Gilligan et al, 2005).

The acute stroke team plays a substantial role in survival and recovery. An interdisciplinary team should come up with care plan within 48 hours and then begin its implementation. Members of the team include: food and nutrition services, neurology, neuropsychology, nursing, occupational therapy, pharmacy, physiotherapy, rehabilitation medicine, social work, speech-language pathology, spiritual care, team coordinator.

Physiotherapy is highly valued by patients and is effective (Pollock et al, 2007). The strongest evidence supports task-oriented exercise training aimed at improving balance and gait (Van Peppen et al, 2004). The intensity of therapy is important, with increases in time spent showing small but significant improvements. However, what appears to be more effective is the organization and coordination of care delivery by all health care providers involved.

Language impairments are common, an speach and language terapy is common, but understudied.

Cognitive impairment, especially memory deficits, spatial neglect, attention deficits, and mood disturbance are common and should be assessed.

Early rehabilitation, occurring within the first few months following stroke, uses neuroplasticity to recruit and reorganize neighbouring neural networks. At the same time, adaptation and coping strategies are used, based on educational and psychological practice.

Aneurysms can be clipped or coiled.

subarachnoid hemorrhage - prevent re-bleeding; nimodipine to decrease secondary vasospasm.

Acute Blood Pressure Management

Blood pressure control is critical post-stroke, and target blood pressure is 140/90 mmHg. Randomized controlled trials have not been defined, but the best combination appears to be a diuretic and and ACE inhibitor.

Long-Term Rehabilitation

Long-term rehabilitation is a mixture of therapeutic and problem-solving approaches to limit and adapt to the impact of stroke's brain damage on daily life.

Discharge from hospital is primarily determined by level of support at a patient's home. It does not necessarily signify maximum recovery has occurred, and accordingly, 'transfer of care' is perhaps a more apt description which highlights the need for continuing contact with rehab services (Young and Forster, 2007).

Population studes have shown the time to reach best functional performance for mild, moderate, and severe strokes to be 8, 13, and 17 weeks, respectively, though of course times can vary considerably for individual patients (Jorgensen et al, 1995).

Strokes cause sigificant needs for care, with up to 74% of patients requiring help with ADLs. It is important to equip and support caregivers in the community, and practical training programmes decrease burden, anxiety, and depression among caregivers while reducing costs (Patel et al, 2004).

Transferring care to the home earlier rather than later, and providing follow-up specialist services, reduces death or dependency and prevents deterioration (Young and Forster, 2007).

Family doctors play an important role in stroke prevention, education, early detection, and long-term treatment. Their interactions with the stroke team can provide valuable information for all members of the health care team, especially as transfer of care is underway.

Secondary Prevention

Early post-stroke VTE prophykaxis includes:

• early mobilization
• adequate hydration
• compression stockings
• optimized antiplatelet use: ASA or heparin
• anticoagulation for higher risk patients

Carotid Endarterectomy should be done within 2 weeks after an ipsilateral carotid sichemic stroke. Carotid stenting is an option for those who cannot go through endarterectomy.

Lower cholesterol, thin blood, and give anti thrombotics

• avoid combination ASA and clopidogrel

Early Events

Clinical outcomes depend on disease severity. In mild cases, a transient postischemic confusion state can be followed by complete recovery. In other cases, even with mild global ischemia, severe, irreversible damage can result.

About 1/4 of patients worsen during the first 24-48 hours.

A third of patients with hemorrhagic stroke can have rapid expansion of the hematoma within a few hours.

Mortality

About 1/4 of patients with stroke die within a month, about 1/3 by 6 months, and 1/2 by one year (Hankey et al, 2000). The outcomes are even worse for hemorrhagic stroke, with one-month survival around 50%. The major cause of early death is neurological deterioration, with complications such as aspiration or infection important as well. Later deaths are commonly cardiac or complications of stroke.

Anterior circulation syndromes have a poorer prognosis than other types, with lacunar syndromes having the best outcomes.

The best predictors of recovery at 3 months are initial neurological deficit and age. Other factors include high blood glucose, body temperature, and previous stroke.

Complications

With focal cerebrovascular disease, outcomes depend on the area of brain affected, and can evolve over time, with a degree of slow improvement occurring over months.

Neurologic complications include:

• cerebral edema
• seizures
• hemorrhagic transformation of infarct
• neurological deficits: sensory, motor, blindness, aphasia, other.

A stroke is not simply a brain disease. It affects the whole person and the family. Non-neurological complications include:

• MI
• arrhythmia
• aspiration/pneumonia
• DVT/PE
• malnutrition
• pressure sores
• orthopedic complications
• contractures
• depression, both in survivors and caregivers

Common problems include social isolation, restricted participation in leisure activities, delayed return to work, anxiety, and depression (Young and Forster, 2007). Common information needs include:

• causes and risk factors of stroke
• availablity of local services and support groups
• financial advice
• guidance on driving and transport
• medication and secondary prevention
• understanding of the care plan
• advice on returning to work and participation in leisure activities
• discussion of sexual issues

There are a number of excellent patient and family resources on stroke:

• The Heart and Stroke Foundation of Canada
• American Stroke Association
• Medline Plus: Stroke

Recurrence

Risk of recurrence can be guided by the ABCD₂ score.

A score of 4 or more justifies urgent evaluation, treatment, or observation, as 30-day stroke risk can be 5-15% (Johnston et al, 2007).

Diffusion-weighted MRI or MRA can identify occluded vessels and increased risk of recurrence.