A detailed Stroke lectures and it’s management

A detailed description on the management of stroke

1. Cerebrovascular diseases Stroke

2. Definitions Stroke is defined as rapidly developing clinical sign of focal or global neurologic deficit lasting ≥24 hours or leading to death with no apparent cause other than vascular origin Transient ischemic attacks (TIA) is neurologic deficit lasting less than 24hours

3. American heart association and American stroke association; defined central nervous system infarction as brain, spinal cord or retinal infarction based on pathological, imaging or other objective evidence of cerebral, spinal cord or retinal injury in a defined vascular distribution or clinical findings lasting for more than 24 hours or death and other etiologies excluded .

4. Intracerebral hemorrhage is defined as focal collection of blood within the brain parenchyma or ventricular system not cause by trauma. Sub arachnoid hemorrhage is defined as bleeding into the sub arachnoid space .

5. Epidemiology A study by Komolafe et al showed that stroke 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 prevalence ratio of 58/100,000 – 400/100,000 with an annual mortality of 70/100,000.

6. 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 900/100,000 in Asia in early ‘80s

7. Incidence rate rises exponentially with increasing age, with a hundred fold increase in rate from 3/100,000 in the 3 rd & 4 th decades to almost 300/100,000 in the 8 th and 9 th decades There is gradual decline in the overall stroke death rates in many industrialized countries, however it still remains the 3 rd leading cause of death in USA.

8. Among stroke survivors 30% require assistance with activities of daily living, 20% require assistance with ambulation and 16% institutional care .

9. Types In general usage, morbidity studies subdivide stroke into Subarachnoid hemorrhage Ischemic / thrombo -embolic (cerebral infarction) Intracerebral hemorrhage

10. Cerebral infarction - 70% Intracranial hemorrhage - 10-15% Subarachnoid hemorrhage- 5% Undetermined etiology - 10-15%

11. TOAST: trial of 10172 in acute stroke treatment classification denotes subtypes of ischemic stroke 1) Large artery atherosclerosis 2) Cardio-embolism 3) Small- vessel occlusion 4) Stroke of determined etiology 5) Stroke of undetermined etiology

12. Non modifiable Age Gender Race/ethnicity Family history Genetics

13. Risk factors cont Modifiable Low socioeconomic status Arterial hypertension Diabetes mellitus Dyslipidemia Heart disease, Cigarette Smoking Excessive alcohol intake 8. Aortic arch atheromatosis Modifiable 9 Body mass index 10 Low serum folate 11 Oral contraceptive use 12 Prior stroke 13 Increased fibrinogen 14 Elevated anticardiolipin antibodies 15 Elevated homocyst (e) ine

14. Pathophysiology Final neuropathologic common denominator in stroke is ischemia of the neurons Two sequential processes occur Vascular / hematological Abnormality of cellular chemistry that produce necrosis of neurons, glias and other supportive cells

15. Path physiology Cascade of complex biochemical events occurs seconds to minutes after cerebral ischemia. Cerebral ischemia is caused by reduced blood supply to microcirculation.

16. Energy metabolism Loss of aerobic glycolysis Intracellular accumulation of sodium and calcium ions Release of excitotoxic neurotransmitters Elevation of lactate level with local acidosis Free radical production and cell swelling Over activation of lipases and proteases CELL DEATH

17. Complete interruption of CBF causes Suppression of electrical activity within 12-15 seconds Inhibition of synaptic excitability of cortical neurons after 2-4minutes Inhibition of electrical excitability after 4-6minutes 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

18. When blood flow decrease to 18mL/100g per minute brain reaches a threshold for electric failure and have potential of recovery. Second level is threshold of membrane failure occurs when CBF decreases to 8mL/100g per minute and cell death can results.

19. These two thresholds mark the upper and lower blood flow limits of ischemic penumbra Pathological characteristics of Ischemic stroke depend on mechanism of stroke, size of obstruction and availability of collateral blood flow

20. Clinical features The focal/ global deficit is often abrupt in onset, In cerebrovascular diseases the symptoms, signs and severity of stroke vary and depend on the vascular territory affected and extent of the lesion.

21. Hemiparesis , hemiplegia , tetraparesis , tetraplegia dysphasia, dysarthria and unilateral or bilateral sensory loss can occur, disturbance of gaze or palsies of extra ocular muscles, dysphagia , dysarthria , dizziness, vertigo, hiccups, ataxia, Horner’s syndrome, vomiting, and respiratory arrest. Diminishing level of consciousness

22. Diagnosis History and clinical examination Investigations to confirm diagnosis and determine the stroke sub type Assessing the stroke severity Establish cause or risk factor Establish baseline data for monitoring improvement or deterioration

23. Establishing the diagnosis and determining the subtype are by Neuro -imaging CT scan Magnetic resonance imaging MRI The bedside assessment of pathologic stroke type based on clinical and laboratory data includes – World Health Organizations criteria, Siriraj Stroke Scale (SSS), Guy's Hospital stroke score (GHSS).

24. Siriraj score Variable C F Score Consciousness (X 2.5) Alert 0 Drowsy, stupor 1 Semi-coma , coma 2 Vomiting (X2) No 0 Yes 1 Headache within 2hrs (X2) No 0 Yes 1 Diastolic Blood pressure (X0.1) Atheroma markers (X3) DM, angina, IC None 0 one or more 1 Constant - 12

25. Assessing the stroke severity National Institutes of Health Stroke Scale (NIHSS), Canadian Neurological Scale (CNS), Middle Cerebral Artery Neurological Score (MCANS) Scandinavian Stroke Scale, Modified Rankin scale and European Stroke Scale

26. Establish cause or risk factor are ECG Blood pressure measurement Blood glucose Cholesterol (serum lipids) etc BCH and Immunological tests Establish baseline data for monitoring improvement or deterioration

27. Treatment Protect the ischemic brain from necrosis Treat the underlying disease Prevent and treat complications Rehabilitate the disabled

28. Restoration of blood supply Blood flow and nutrients before irreversible infarction Medical : rtPA , streptokinase Surgical: embolectomy, vascular reconstruction, thrombo-endartectomy

29. Protect neurons from adverse milieu created by biochemical changes Free radical scavengers: 21 Amino-steroid, Ascorbic acid and alpha tocopherol, tocotrienol Inhibitors of Excitatory amino acid, NMDA receptor blockers MK 801,

30. Treat the underlying disease Hypertension accounts for 80% of predisposing factor Indications for immediate treatment 1 Dissecting aortic aneurysm 2 Ischemic heart disease/ myocardial infarction 3 Acute pulmonary edema 4 Rapid decline in renal function These complication are usually found if the mean arterial blood pressure is > than 145

31. Prevent and treat complications Cerebral edema: Cytotoxic and intracelluar Slight head –up tilt 15-30 improves venous drainage and reduces edema Limiting fluid intake to 1.5L/day Hyper tonic / Hyper- osmolar agents creates an osmotic gradient; Mannitol, glycerol

32. Pulmonary embolism Sub-cutaneous heparin Hyperglycemia Treated with insulin Fever Antibiotics Dysphagia Nasogatric feeding is encourage Aspiration pneumonia Regular suctioning Contracture Physiotherapy

33. Prevention Removal of risk factor if identify Treat HTN, DM Discourage Smoking and Alcohol, Sedentary life style Encourage regular exercise Drugs Aspirin Clopidogrel Dipyridamole Warfarin Carotid end arterectomy Exchange blood transfusion in SCD

34. Subarachnoid Hemorrhage SAH accounts for about 3-5% of CVD in developed countries with annual incidence of 11/100,000 of the population at risk Mortality was about 25% in the first 24hr and after re-bleed and vasospasm, a further 25% mortality

35. Underlying Cause falls into four groups Vascular (aneurysm (57%) + Arterio - venous AVM 5%) Primary brain lesion (trauma, tumor and inflammation) Systemic disorders (hypertension and blood dyscrasias ) No cause is found in about 20%

36. Subarachnoid Hemorrhage Findings depends on 1. Amount and location of the hemorrhage

37. Clinical features of SAH Headache Neck stiffness Photophobia ± Focal neurological signs and loss of consciousness PCA ----3rd nerve palsy MCA ---- Hemiparesis with dysphagia ACA ----Ischemia paramedian vessels---- diencephalic damage

38. Grading Grade I- Asymptomatic or headache and neck stiffness only Grade II- Headache, neck stiffness and cranial nerve palsy (3 rd ) Grade III -Drowsy, confused, or mild neurologic deficit Grade IV – Stupor with hemi-paresis Grade V -Deep coma decerebrate rigidity or moribound

39. World federation of neurological surgeons Scale Grade 1: GCS 15; motor deficit absent Grade 11: GCS 13 or 14 motor deficit absent Grade 111:GCS 13 or 14 motor deficit present Grade 1V: GCS 7-12 motor deficit absent or present Grade V: GCS 3-6 motor deficit absent or present

40. Diagnosis Lumbar puncture Blood stained CSF CT Scan Blood in the basal cistern Intravenous Digital substraction Angiography Four vessel angiography

41. Treatment Definitive treatment Surgery for aneurysm Medical Nimodipine Pain relieve

42. Complications Re-Bleed Vasospasm Others Hematoma Hydrocephalus Epilepsy