How to examine a stroke patient Skin -Xanthelasma Rash (arteritis, splinter haemorrhages, livedo reticularis) Colour and temperature change (limb ischaemia/deep venous thrombosis) Eyes -Arcus senilis Diabetic changes Hypertensive changes Retinal emboli Abdomen - Palpable bladder (urinary retention) Locomotor -Injuries sustained during collapse with stroke

Cardiovascular system - rhythm (atrial fibrillation) BP (hypertension, hypotension) JVP (heart failure, hypovolaemia) Murmurs (sources of embolism) Peripheral pulses and bruits (generalised arteriopathy) Respiratory system Signs of pulmonary edema Signs of respiratory infection

Cerebral infarct Cardiac embolism-- Echocardiography (including transoesophageal) Premature atherosclerosis --Serum lipids Arterial dissection MRI   Angiography Thrombophilia --Protein C, protein S   Antithrombin III   Factor V Leiden, prothrombin Homocystinuria --Urinary amino acids   Methionine loading test Antiphospholipid antibody syndrome --Anticardiolipin antibodies/lupus anticoagulant SLE-- Antinuclear antibodies Vasculitis --ESR   CRP   Antineutrophil cytoplasmic antibody (ANCA) CADASIL-- (cerebral autosomal dominant arteriopathy with subcortical infarcts and leucoencephalopathy) MRI brainGenetic analysisSkin biopsy

Mitochondrial cytopathy-- Serum lactate   White cell mitochondrial DNA   Muscle biopsy   Mitochondrial molecular genetics Fabry's disease --Alpha-galactosidase levels in blood

Neurovascular syphilis --Syphilis serology

neurological deficits worsening during the first few hours or days after their onset .

1-extension of infarction..2- hemorrhage into it3-or the development of edema with consequent mass effect.

It is important to distinguish such patients from those who are deteriorating as a result of complications such as hypoxia ,

sepsis, epileptic seizures or metabolic abnormalities .Patients with cerebellar hematomas or infarcts with mass effect

may develop obstructive hydrocephalus .Some patients with large hematomas or infarction with massive edema in the cerebral hemispheres may benefit from anti-edema agents, such as mannitol or artificial ventilation, and surgical decompression.

BRAIN ATTACKmnemonic

B-blood pressure. Don’t treat acutely(unless >200/120)R-Respiration.KeepO2 saturation>95%.A- Airway management.I-IV saline-Keep hydration.N-normoglycemia-Avoid dextroseA-Aspirin-As soon as hemorrhage exclude by CT.T-Tempture.keep<37C and treat pyrexia.

T-TEDS(compressive stocking) to prevent DVT.A-assess water swallow testC-CT scan as soon as possibleK-Keep 30 head –up tilt.

Airway Check that the patient can protect his/her airway and swallow without evidence of aspiration Perform a swallow screen and keep patient nil by mouth if swallowing unsafe Breathing Check that the patient is breathing adequately; check oxygen saturation and give oxygen if saturation < 95% Circulation Check peripheral perfusion, pulse and blood pressure adequate and treat with fluid replacement, anti-arrhythmics and inotropic drugs as appropriate Hydration Screen for signs of dehydration and give fluids parenterally or by nasogastric tube if necessary Nutrition Assess nutritional status and provide nutritional supplements if necessary ,if dysphagia persists for a day or two, start feeding via a nasogastric tube

Blood pressure Unless there is heart failure or renal failure, evidence of hypertensive encephalopathy or aortic dissection, do not lower the blood pressure in the first week since cerebral perfusion may decrease. Blood pressure often returns towards the patient's normal level within the first few days Blood glucose Check blood glucose and treat with insulin when levels are ≥ 11.1 mmol/L (200 mg/dL) (via infusion or glucose/potassium/insulin (GKI)). Monitor closely to avoid hypoglycemia Temperature Check for pyrexia and investigate and treat underlying cause Give antipyretics since raised brain temperature may increase infarct volume Pressure areas Check pressure areas and introduce measures to reduce the risk of bed sores,treat infection ,maintain nutrition ,Provide a pressure-relieving mattress ,turn immobile patients regularly Incontinence Check for constipation and urinary retention and treat appropriately ,avoid urinary catheterisation unless the patient is in acute urinary retention or incontinence is threatening

Thrombolysis in acute ischemic stroke

‘. The maximum benefit appears to be when thrombolysis is given within

4.5 hours of onset. Treating 1000 patients within 3 hours prevents about 60 patients from being dead or dependent at 3 months.

Risk of haemorrhage In the absence of contraindications, aspirin (300 mg daily) should be started immediately after an ischemic stroke unless rt-PA has been given, in which case it should be withheld for at least 24 hours. Aspirin reduces the risk of early recurrence and has a small but clinically worthwhile effect on long-term outcome .it may be given by rectal suppository or by nasogastric tube in dysphagic.

{ aspirin started within 48 hours of onset improves long-term outcome. Treating 1000 patients for 2 weeks prevents 13 being dead or dependent by 6 months}

Anticoagulation with heparin has been widely used to treat acute ischaemic stroke in the past. it should not be used in the routine management of acute stroke .

1-recent myocardial infarction, 2 -arterial dissection

3 -progressing strokes.

Intracranial hemorrhage must be excluded on brain imaging before considering anticoagulation .

Complication Prevention Treatment Chest infection -Nurse semi-erect,a void aspiration (nil by mouth, nasogastric tube, possible gastrectomy) Antibiotics, Physiotherapy

Epileptic seizures Maintain cerebral oxygenation, Avoid metabolic disturbance ,Anticonvulsants Deep venous thrombosis/pulmonary embolism -Maintain hydration, Early mobilization,Anti-embolism stockings, Heparin (for high-risk patients only) Anticoagulation (exclude hemorrhagic stroke first)

Painful shoulder -Avoid traction injury, Shoulder/arm supports, Physiotherapy PhysiotherapyLocal corticosteroid injections Pressure sores Frequent turning, Monitor pressure areas, Avoid urinary damage to skin ,Nursing care, Pressure-relieving mattress Urinary infection -Avoid catheterisation if possible, Use penile sheathConstipation Appropriate aperients and diet Appropriate aperients Depression and anxiety Maintain positive attitude and provide information Antidepressants

2nd prevention

The average risk of a further stroke is 5-10% within the first week of a stroke or TIA, perhaps 15% in the first year and 5% per year thereafter.

Blood pressure lowering in secondary prevention of stroke. Lowering blood pressure even in the 'normal range' reduces the risk of recurrent stroke, myocardial infarction and vascular deaths in patients who have suffered a stroke .Antiplatelet drugs in secondary prevention of ischaemic stroke.

In patients with ischaemic stroke, aspirin, clopidogrel or a combination of aspirin and dipyridamole reduces the risk of recurrent stroke, myocardial infarction and

vascular deaths . Statins in secondary prevention of ischaemic stroke.

In patients with ischaemic stroke, statins reduce the risk of recurrent stroke, myocardial infarction and vascular deaths .

Anticoagulants in secondary prevention of ischemic stroke 'There is no net benefit to be gained in the routine use of anticoagulants after acute stroke except in the presence of at AF.

Cerebral venous disease

Thrombosis of the cerebral veins and venous sinuses is less common than arterial thrombosis but has been recognised with increasing frequency over recent years .

Cerebral venous sinus occlusion causes raised intracranial pressure and patchy ischaemia, which is often haemorrhagic .

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Causes of cerebral venous thrombosis

Predisposing systemic causes Dehydration Pregnancy Behçet's diseaseThrombophilia Hypotension Oral contraceptive use

Local causes: Paranasal sinusitis Meningitis, subdural empyema Penetrating head and eye wounds Facial skin infection Otitis media, mastoiditis Skull fracture

Cavernous sinus thrombosis: Proptosis, Ptosis, headache, external and internal ophthalmoplegia, papilloedema, reduced sensation in trigeminal first division.Often bilateral, patient ill and febrile .Superior sagittal sinus thrombosis: Headache, papilloedema, seizures .Clinical features may resemble idiopathic intracranial hypertension .

May involve veins of both hemispheres, causing advancing motor and sensory focal deficits.

Transverse sinus thrombosis: Hemiparesis, seizures, papilloedema may spread to jugular foramen and involve cranial nerves

•Anticoagulation is usually beneficial, even in the presence of venous haemorrhage .

•In selected patients, the use of endovascular thrombolysis has been advocated.

Management of underlying causes and complications

Causes of intracerebral haemorrhage and associated risk factors

Complex small vessel disease with disruption of vessel wall- Age ,Hypertension  , Low cholesterol

Amyloid angiopathy -Familial (rare)   Age

Impaired blood clotting -Anticoagulant therapy   Blood dyscrasia ,  Thrombolytic therapy

Vascular anomaly -Arteriovenous malformation   Cavernous haemangioma

Substance misuse -Alcohol   Amphetamines   Cocaine

Primary intracerebral haemorrhage

Arteriovenous malformation (AVM) --MRI/angiography– Drug misuse Drug screen (amphetamine, cocaine) Coagulopathy --Prothrombin time (PT) and activated partial thromboplastin time (APTT)   Platelet count

Subarachnoid haemorrhage Saccular ('berry') aneurysm --MRI/angiography AVM-- MRI/angiography Vertebral dissection --MRI/angiography

Most common loci of ICH and signs

1-putamin(40%)-contralateral hemiparesis and hemisensory loss, pupil normal and conjugate gaze paresis to opposite side

2-thalamus(20%)-contralateral sensory loss greater than motor, small poorly reactive, eye down and in, upgaze paralysis

3-lobar(15%)

4-caudate(8%) –contralateral hemiparesis, some times ipsilateral horner

5-pons(8%)-quadraparesis,small,reactive pupil, ocular bobbing

6-cerebellum-ipsilateral ataxia

1/8Thunderclap headache

About 1 patient in 8 with a sudden severe headache has SAH and, in view of this, all patients with this presentation require investigation to exclude a subarachnoid hemorrhage.

Subarachnoid hemorrhage typically presents with a sudden, severe 'thunderclap' headache (often occipital) which lasts for hours or even days, often accompanied by vomiting.

Physical exertion, straining and sexual excitement are common antecedents .

There may be loss of consciousness at the onset, so subarachnoid haemorrhage should be considered if a patient is found comatose .

On examination the patient is usually distressed and irritable, with photophobia. There may be neck stiffness due to subarachnoid blood but this may take some hours to develop.

Focal hemisphere signs such as hemiparesis or aphasia may be present at onset if there is an associated intracerebral hematoma.

A third nerve palsy may be present due to local pressure from an aneurysm of the posterior communicating artery, though this is rare.

Fundoscopy may reveal a subhyaloid hemorrhage, which represents blood tracking along the subarachnoid space around the optic nerve.

SAH

Subarachnoid hemorrhage (SAH) is less common than other types of stroke and affects about 6/100 000 of the population.

Women are affected more commonly than men and the condition usually presents before the age of 65 .

The immediate mortality of aneurysmal subarachnoid hemorrhage is about 30% and survivors have a recurrence, or rebleed, rate of about 40% in the first 4 weeks and 3% annually thereafter

85 of SAH are caused by saccular or 'berry' aneurysms arising from the bifurcation of cerebral arteries, particularly in the region of the circle of Willis. There is an increased risk in first-degree relatives of those with saccular aneurysms, and an increased risk of SAH in patients with polycystic kidney disease and congenital connective tissue defects such as Ehlers-Danlos syndrome.

In about 10% of cases, SAH are non-aneurysmal haemorrhages (so-called peri-mesencephalic haemorrhages), which have a very characteristic appearance on CT and a benign outcome in terms of mortality and recurrence .

Some 5% of SAH are due to arteriovenous malformations and vertebral artery dissection

The diagnosis of SAH can be made by CT, negative result does not exclude the diagnosis since small of blood in the subarachnoid space cannot be detected by.Lumbar puncture should be performed after 12 hours from symptom onset, if possible.

If either of these tests is positive, cerebral angiography is required to determine the optimal approach to prevent recurrent bleeding .

Complication and prognosis

• 30% immediate mortality.• 40% recurrence or bleeding in the 1st 4 weeks.Complications:1-recrrence 2-intraparenchmal extension3-arterial vasospasm4- acute or sub acute hydrocephalus5-seizures6-inappropriate secretion of ADH