18d - Stroke.pptx pathophysiology, mgt, complications,

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1. MANAGEMENT OF ACUTE STROKE

2. OUTLINE Introduction Epidemiology Pathogenesis Pathophysiology Risk factors Clinical features Diagnosis Differential diagnosis Investigations Treatment Prophylaxis and prevention Complication prognosis conclusion

3. I ntroduction Stroke is defined as a rapidly developing clinical sign of focal or global neurological deficit lasting ≥ 24 hours or leading to death with no apparent cause other than vascular origin. Acute stroke can be defined as recent , sudden onset of persistent neurological deficit lasting ≥ 24 hours or leading to death with no cause other than vascular origin.

4. EPIDEMIOLOGY A stud by Komolafe et al showed that stoke accounted for 2.9% of all medical admissions A recent epidemiological study by Danesi et al, in Lagos reported a higher prevalence of 1.14 per 1000 compared to the previous community ratio of 58/100,000 – 400/100,000 with an annual mortality of 70/ 100,ooo In Africa, stroke accounts for 0.9-4% of hospital admissions and 2.8-4.5% of total deaths The prevalence rate in the west was 600/100,000 population and 900/100,ooo in Asia in early ‘80s

5. EPIDEMIOLOGY CONT… Incidence rate rises exponentially with increasing age, with a hundred fold increase in rate from 3/100,000 in the 3 rd and 4 th decades to almost 300/100,000 in the 8 th and the 9 th decades. There is gradual decline in the over all stroke death rates in many industrialized countries, however it still remains the 3 rd leading cause of death in U.S.A Among stroke survivors 30% requires assistance with activities of daily living, 20% require assistance with ambulation and 16% institutional care.

6. PATHOGENESIS Two major mechanisms are responsible for ischemia in acute stroke: thromboembolism and hemodynamic failure(systemic hypotension or low cardiac failure) Embolism: common sources, the heart and large arteries. Other rare sources of emboli are air, fat, cholesterol, bacteria, tumor cells, and particulate matter from injected drugs Cardioembolism: atrial fibrillation, sustained atrial flutter, sick sinus syndrome , left atrial appendage thrombus, left atrial myxoma etc Artery – to – artery embolism: embolic material is composed of clot, platelet aggregates or plaque debris that usually breaks off from atherosclerotic plaques, large vessel atherosclerosis.

7. PATHOPHYSIOLOGY Development of permanent neurologic sequelae is a time dependent process. Permanent neurological deficit occur if mean cerebral blood flow (CBF) fell below 30% of normal. The ischemic core represents tissue that is irreversibly damaged The ischemic penumbra presents tissue that is functionally impaired but structurally intact, potentially salvageable. The ischemic penumbra has a short life span, being rapidly incorporated into the core within hours of the ictus , 3-6hrs. Salvaging this tissue by restoring its flow to non ischemic levels is the aim of acute stroke therapy The final neuropathologic common denominator in stroke is ischemia of neurons. Two sequential processes occur Vascular/ hematological Abnormality of cellular chemistry that produces necrosis of neurons, glias and other supportive cells

8. PATHOPHYSIOLOGY CONT… Cascade of complex biochemical events occurs seconds to minutes after cerebral ischemia Cerebral ischemia is caused by reduced blood supply to microcirculation. Loss of aerobic glycolysis Intracellular accumulation of sodium and calcium ions Release of excitotoxic neurotransmmitters Elevation of lactate level with lactate level with local acidosis Free radical production and cell swelling Over activation of lipases and proteases Cell death

9. PATHOPHYSIOLOGY CONT… Complete interruption of CBF causes:- Suppression of electrical activity within 12-15 secs Inhibition of synaptic excitability of cortical neurons after 2-4mins Inhibition of electrical excitability after 4-6mins Normal CBF at rest in normal adult brain is approximately 50-55ml/100g per minute and cerebral metabolic rate of oxygen is 165mmol/100g per minute When blood flow decrease to 18ml/100g per minute brain reaches a thresh hold for electric failure( they have potential for recovery). Thresh hold of membrane failure occurs when CBF decreases to 8ml/100g per minute and cell death can results. These two thresh holds mark the upper and lower blood flow limits of ischemic penumbra.

10. RISK FACTORS The risk factors can either be modifiable or non modifiable. Modifiable risk factors Hypertension Diabetes mellitus Heart diseases e. g mitral stenosis , atrial fibrillation, subacute infective endocarditis, dilated cardiomyop etc TIA Hypercoagulable states Hyperviscosity states/ polycythemia Sickle cell anemia Dyslipidemias Cigarete smoking, heavy alcohol intake, drug abuse Homocystinemia Low social class

11. RISK FACTORS CONT… Obesity Lack of exercise Infections- HIV, Syphilis, TB meningitis Drugs – cocain , amphetamine Migrain Amyloid angiopathy

12. RISK FACTORS CONT… Non modifiable age Gender Race/ethnicity Family history Genetics ( MELAS, CADASIL etc)

13. Clinical features Depends on the pathology, and location/ extend of the lesion. Based on pathology Features of acute hemorrhagic stroke Usually during peak of activity Loss of consciousness usually present Severe throbbing head Convulsions Vomiting Hypertension meningism

14. Clinical features cont… Features of acute ischemic stroke Usually occurs at rest History suggestive of past transient ischemic attack e.g aphasia, hemiparesis , hemisensory loss, hemianopic visual loss, dysarthria , dysphagia etc General features include; Sudden difficulty in walking Sudden dizziness and loss of balance or coordination Sudden numbness or weakness of face, arm or leg, especially on one side of the body etc

15. Clinical features cont… Based on location Acute cortical stroke Aphasia Dysarthria Differential limb weakness (UL>LL) Lateralising sign e.g hemianospia , Broca’s / wernicke aphasia

16. Clinical features cont… Subcortical stroke Dense hemiplegia Tremor Hemiparesis Brain stem stroke Contralateral hemiparesis or hemiplegia Cranial nerve palsy, dysarthria , dizziness, diploplia and respiratory or cardiovascular instability.

17. D iagnosis The diagnosis of acute stroke can be made on simple history and examination- FAST : F ace- sudden weakness of the face. A rm- sudden weakness of one or both arms. S peech- difficulty speaking or slurred speech. T ime- the sooner treatment is started the better.

18. Differential diagnosis Space occupying lesions e.g Cerebral tumour Subdural hematoma Brain abscess Todd’s paralysis Hypoglycemia Hemiplegic Migrain Encephalitis

19. I nvestigations The purpose for investigations are: To confirm the clinical diagnosis and distinguish between hemorrhage and thrombo -embolic infarct. To look for underlying causes and to direct therapy To exclude other causes e.g tumour

20. Investigations To confirm diagnosis Non contrast CT scan of the head; is the single most important investigation in stroke. Used to differentiate ischemic from hemorrhagic stroke. Ischemic stroke has hypodense lesions where as hemorrhagic stroke have hyperdense lesion, perilesional edema; area of hypodensity surrounding the lesion. Swell sign; scattered hypodense points within the lesion ( it indicates on going bleeding) Other features include midline shift to contralateral side, obliteration of gyri and sulci (cerebral edema), obliteration of ventricular outline ( i.e ipsilaterally )

21. Investigations cont…. Draw backs of CT is that it can show hemorrhage immediately but cerebral infarction is often not detected Magnetic R esonance Imaging (MRI). Shows changes early in infarction and a later MRI shows the full extent of the damaged area or penumbra. Diffused – weighted MRI (DWM). Can detect cerebral infarction immediately but is as accurate as CT for the detection of hemorrhage

22. Investigations cont… General investigations Full blood Count and differentials to rule out infections Lumbar puncture; to rule out subarachnoid hemorrhage ECHO; to rule out cardio-embolic source Serum E, U/ Cr; detect electrolyte imbalance and renal compromise Random Blood Sugar; glucose status, and need for insulin ( RBS> 12mmol/L) Lipid profile Coagulation profile; PT/PTTK Veneral Disease Research Laboratory (VDRL)

23. T reatment Aim is to salvage the penumbra. Treatment is divided into three; Within six hours ( hyper acute treatment) Admit patient to multi disciplinary stroke unit Resuscitate Nurse at 30 degree head up. Airway: confirm patency and monitor Give high flow oxygen Secure IV access and give intra venous fluid ( Use Normal saline). 1L 8hrly for up-to 1-2wks ( to increase MAP to compensate increased ICP thereby maintaining cerebral perfusion pressure)

24. Treatment cont… Decompress the cranial cavity by giving IV mannitol 1.2g/kg in 500ml fluid or 250-500ml of 20% given 8hrly for 48hrs. Low dose IV furosemide (40mg) may be given Thrombolytics ; if patient present within 3-4hrs of acute ischemic stroke. Patient must meet eligibilty of thrombolysis in acute ischemic stroke which include; Age ≥ 18yrs Clinical diagnosis of acute ischemic stroke Assessed by experienced team Measurable neurological deficit CT or MRI consistent with acute ischemic stroke Timing of onset well established

25. Treatment cont… Statins ; plague stabilising BP control; it should not be lowered except when there are certain indications, which include; Persistent systolic pressure of > 220mmhg Persistent diastolic pressure of >120mmhg Persistent MAP> 145mmhg Presence of hypertensive emergencies e.g dissecting aortic aneurysms, preeclapsia / eclapmsia

26. Treatment cont… 6hrs-2wks (acute treatment) Patient still on admission Continue IV fluids Start Physiotherapy Prevent aspiration pneumonitis by passing Naso -gastric-tube. If fever is present, give paracetamol and abort seizures if present by giving anticonvulsants Give insulin if RBS is > 12mmol/L Give antioxidants; Vit E 300mg and Vit C 100mg tds ( mob free radicals) DVT prophylaxis; compression stockings, low dose aspirin( contraindicated in hemorrhagic stroke) Prevent bed sores by 2hourly turning or use of water bag Pass urethral catheter if incontinence is present Identify underlying cause and treat appropriately Surgery e.g multiple bore holes/brain flaps to decrease ICP ( only indicated when massive edema, drug not working, and worsening levels of consciousness

27. Treatment cont… > 2 weeks ( sub acute treatment) Occupation rehabilitation monitor patient for discharge Give outpatient appointment Counsel the patient on how to prevent stroke

28. Prophylactic measures ( long term treatment) and prevention Antiplatelet therapy Long term soluble aspirin ( 75mg daily). Reduces substantially the incidence of further infarction following thromboembolic stroke. Combined aspirin 75mg daily and clopidrogrel 75mg daily provide optimal prophylaxis against further thromboembolic stroke. Good BP control Good glycemic control

29. Complications of acute stroke Acute complications Aspiration pneumonitis Post stroke seizures Cerebral edema Dehydration Electrolyte imbalance Sub acute complications Infection; from NGT insertion, catheter, IV line. DVT Bedsores, hyperglycemia, hyperthemia , PEM

30. Complications cont… Chronic complications depression Dementia Loss of job Epilepsy Muscle wasting ( from disuse atrophy) contractures

31. P rognosis About 25% die within 2yrs of acute stroke and nearly 10% within the first month. Early mortality is higher following intracranial hemorrhage than thromboembolic infarction. Poor outcome is likely when there is coma, a defect in conjugate gaze and hemiplegia. Gradual improvement usually follows stroke, although late residual deficits are typically substantial. One third of survivors return to independent mobility and one third have disability concerning institutional care.

32. summary Acute stroke is a medical emergency which requires immediate and multidisciplinary approach. Presentation depends on the pathology( i.e hemorrhagic or ischemic mechanisms) and location of the lesion in the brain. It is associated with various risk factors which may be modifiable or non modifiable Prompt identification and treatment is associated with better prognosis .Gradual improvement usually follows stroke, although late residual effects are usually substantial

33. R eferences Kumar and Clark’s Clinical Medicine 8 th Edition . A compendium of Clinical Medicine by A.O Falase , O.O. Akinkugbe . The guide Medicine Common stuffs in medicine MBBS 6 Stroke lecture slides