Download to read offline
![References
1. Kumar & Clark's Clinical Medicine 9th edition
2. Global burden of disease 2018: www.cdc.gov.org
3. Definition of stroke: American Heart Associtaion/American Stroke Association (AHA/ASA) 2010
4. Akinyemi 2021: Stroke in Africa: Profile, Progress, Prospects and Priorities.
5. KW Wahab 2008: Burden of Stroke in Nigeria.
6. B. Ekeh 2015: Stroke Mortality and its Predictors in a Nigerian Teaching Hospital.
7. Boon et al: Davidson's Principles and Practice of Medicine 20th edition -
www.studentconsult.com
8. Longo DL, et al.: Harrison's Principles of Internal Medicine, 18th edition
9. Schwartz DT. Emergency Radiology:Case Studies. McGraw Hill; 2008. pp. 501â522. [Google
Scholar]
10. Stroke Imaging: https://emedicine.medscape.com/article/338385-
overview?icd=login_success_email_match_norm
11. David S. Liebeskind and Joanna M. Wardlaw: Acute-on-Chronic Stroke ; Mar 2021;
https://doi.org/10.1161/STROKEAHA.121.033449Stroke. 2021;52:1486â1489](https://image.slidesharecdn.com/stroke-230325071353-36c3d1fa/75/STROKE-55-2048.jpg)
More Related Content
STROKE
- 1. STROKE Presentation by Ogechi GraceOkoli MBBS V University of Jos, Nigeria.
- 2. OUTLINE ⢠Introduction ⢠Definitionof terms ⢠Epidemiology ⢠Classification ⢠Aetiology ⢠Pathophysiology ⢠Management ⢠Prognosis ⢠Prevention ⢠Conclusion
- 3. INTRODUCTION ⢠Also knownas cerebrovascular accidents (CVA) ⢠Too much blood? Or too little blood? Or both? ⢠A medical emergency! ⢠A leading cause of morbidity and mortality.
- 4. DEFINITION OF TERMS â˘Stroke: a sudden focal neurological deficit of vascular origin lasting >24 hours, or resulting in death. ⢠Transient Ischaemic Attack (TIA): when the neurologic deficit lasts <24 hours. ⢠Stroke in evolution: when the focal neurologic deficit worsens after patient first presents. ⢠Completed stroke: when focal neurologic deficits persists but does not progress. ⢠Stroke in the young: stroke occurring in individuals <45 years of age.
- 5. DEFINITION OF TERMS(contd.) Current concepts in the definition include the following: ⢠24 hours time frame is now outdated: confusing and misleading; does not not suggest emergency; does not take into cognizance the use of thrombolytics. ⢠TIA is not benign as -10-20% develop stroke within 90 days. - 50% in 24-48 hours
- 6. DEFINITION OF TERMS(contd.) ⢠Currently defined by Stroke Council of AHA/ASA (2013) as ⢠Stroke: FND of vascular origin with objective evidence of infarction irrespective of duration of clinical symptoms. ⢠TIA: no objective evidence of acute infraction in the affected region of the brain, spinal cord or retina.
- 7. EPIDEMIOLOGY ⢠leading causeof death and disability ⢠1 in 4 adults will have a stroke in their lifetime ⢠1 in 4 of stroke survivors will have another within 5 years. ⢠2nd leading cause of death globally- 5.5 million deaths annually. ⢠3rd common cause of death in developed countries after heart failure and cancers. ⢠Africa- annual incidence of 316 cases per 100,000 person-years. ⢠3-year fatality rate in Africa >80% ⢠Nigeria- prevalence is 1.14 per 1000; 30-day case fatality rate is 40% ⢠JUTH- frequent cause of neurological admissions; 35% mortality rate, 76.2% within 1st week
- 8. EPIDEMIOLOGY ⢠Sex: commonerin males with 3:2 ⢠Age: ⢠affects all ages including children ⢠risk increases with age especially >64 years (75% of all cases) ⢠commoner in the 6th and 7th decades ⢠Race: blacks
- 9. CLASSIFICATION Based on mechanism, 1.Ischaemic stroke (85%) a. Large vessel stroke b. Small vessel stroke c. Cardio-embolic stroke d. Unclassified/Cryptogenic 2. Haemorrhagic stroke (10%) a. Intracerebral b. Subarachnoid 3. Others (5%)
- 10.
- 11. CLASSIFICATION (contd.) Based onclinical picture, 1. TIA 2. Completed stroke 3. Stroke in evolution
- 12. AETIOLOGY ⢠Risk factorsfor stroke are: 1. Modifiable and 2. Non-modifiable
- 13. RISK FACTORS (contd.) Non-modifiablerisk factors ⢠Increasing age: 75% in people >64years ⢠Sex: M>F, M=F(post-menopausal) ⢠Race: afrocarribean > asian > caucasian ⢠Family history of TIA & stroke ⢠Previous vascular event eg MI, stroke, or peripheral embolism
- 14. RISK FACTORS (contd.) Modifiablerisk factors ⢠Uncontrolled hypertension ⢠Cardiogenic: atrial fibrillation, valvular heart disease, DVT ⢠DM ⢠Hyperlipidaemia ⢠Obesity ⢠Haematologic: polycythaemia, SCDx, ⢠Lifestyle: sedentary, cigarette smoking, alcohol consumption ⢠Infections: HIV, syphillis, ⢠Pregnancy ⢠Drugs: oral contraceptive pills; IV drug abuse eg cocaine, heroin ⢠Malignancy: leukemia ⢠Others
- 15. RISK FACTORS (contd.) Specificrisk factors for haemorrhagic stroke ⢠Bleeding disorders eg haemophilia; CLD ⢠Prolonged anticoagulant and antiplatelet use ⢠Pre-existing cerebral aneurysm ⢠Vascular malformation ⢠Trauma
- 16. Causes of strokein the young ⢠Hereditary: CADASIL, CARASIL, MELAS, AVM, SCDx, thrombophilia, homocystinuria, moya-moya, collagen disorders ⢠Acquired: Infections (HIV, syphilis), vasculitis, SLE, drug abuse, trauma
- 17. Pathophysiology of Stroke Cerebralblood flow ⢠Brain: 1350g, 2% of total body weight ⢠Normal CBF = 50-65 ml/100g of brain tissue/minute ⢠CBF for the entire brain = 750-900 ml/min, i.e. 15% of the cardiac output. ⢠As CBF reduces, esp <30 ml/100g/min, dysfunction of brain tissue begins. ⢠CBF <18ml/100g/min, penumbric brain tissue formation is seen. ⢠CBF <10ml/100g/min, irreversible damage
- 18. Pathophysiology of Stroke â˘Cerebral perfusion pressure (CPP) ⢠CPP = MAP - ICP ⢠Hence, CPP is dependent on MAP and autoregulation ⢠Autoregulation by -Collateral supply -Vasodilation -Increased O2 extraction ⢠Further reduction in perfusion results in -Ischaemia -Infarction
- 19. Pathophysiology of IschaemicStroke ⢠Origin of emboli
- 20. Pathophysiology: Cellular level Occlusion Hypoxia Depletionof ATP Depolarization of membranes Influx of Ca+ and glutamates Neuronal damage
- 21. Pathophysiology of IschaemicStroke Ischaemia Infarction Cellular edema Ionic/Interstitial edema Vasogenic edema Necrosis
- 22. Pathophysiology of IschaemicStroke ⢠Haemorrhagic transformation -Due to reperfusion of damaged vascular endothelium -Seen in 5% of ischaemic stroke -May be haematoma or petechial bleeds -May be associated with neurologic decline
- 23. Pathophysiology of Haemorrhagicstroke Intracerebral haemorrhage ⢠Spontaneous rupture of small, deep penetrating arteries ⢠common sites: basal ganglia, thalamus, crebellum, pons. ⢠Entry of blood into the parenchyma causes cessation of function ⢠Associated rim of cerebral edema Subarachnoid haemorrhage ⢠Rupture of cerebral arteries into SA space
- 24.
- 25.
- 27. Management ⢠It isa medical emergency ⢠multidisciplinary ⢠Stroke unit: reduces mortality by 20% ⢠Principles of management include: a. Resuscitation b. Treat precipitating factor(s) that will worsen the stroke. c. Employ specific measures to treat ischaemic stroke. d. Management of complications & secondary prevention of stroke. e. Rehabilitation
- 28. Management: History ⢠Age â˘Sex ⢠handedness of the patient? - right or left hemispheric stroke ⢠Sudden neurologic deficit- collapse, weakness, speech deficit or blindness. ⢠Antecedent history of headache (thunderclap), vomiting, fainting - ?haemorrhagic ⢠location of the lesion -ACA: contralateral hemiparesis more in LL mutism, incontinence, disinhibition, gait apraxia -MCA: contralateral hemiparesis, more in the face and UL, than in LL -PCA: cortical blindness, impaired memory ⢠-SCDx, RVS, syphillis etc.
- 29. Management: History ⢠Historysuggestive of a risk factor -previous TIA -family history -hypertension, DM, dyslipidaemia -alcohol, cigarette -heart disease: chest pain, shoulder tip pain, palpitation, dyspnea, cough etc ⢠Complications ⢠Care ⢠other parts of history
- 30. Management: Physical Examination â˘CNS exam: GCS, swallow test, cn7 palsy, ⢠MSK ⢠CVS ⢠Resp
- 31. Differential Diagnoses ofStroke ⢠Subdural haematoma from trauma ⢠Cerebral abscess : fever, long progression ⢠Tumours: long progression ⢠Hypoglycemia: autonomic symptoms ⢠Hemiplegic migraine: resolves in <1 hour ⢠Todd's paralysis: with seizures ⢠Infections: TB, cryptococcosis, toxoplasmosis ⢠Meningitis ⢠Hysterical conversion
- 32. Making a diagnosis â˘a clinical diagnosis ⢠type of stroke is confirmed by imaging ⢠must contain -anatomical site of lesion -location of clinical manifestation -possible cause/precipitant eg. Left hemispheric stroke with right-sided hemiplegia 20 long standing hypertension
- 33. Investigations To support diagnosis,and to find out cause ⢠Imaging -MRI: gold standard -Brain CT scan: hyperdense (haemorrhagic), hypodense (ischaemic) -Vascular imaging (doppler): large or small vessel -Echo: valvular heart disease, mural thrombus
- 34. Fig 1: NCCTdemonstrates cortical and subcortical hypodensity involving the right mid to anterior temporal lobe.
- 35. Fig. 2: Axialnon-contrast CT scan of the brain demonstrates 2 areas of intracerebral hemorrhage in the right lentiform nucleus with surrounding edema and effacement of the adjacent cortical sulci and right sylvian fissure. Mass effect is present upon the frontal horn of the right lateral ventricle with intraventricular extension of hemorrhage.
- 36. Fig 3: Thenon-contrast CT (left image) demonstrates diffuse, high-density subarachnoid hemorrhage in the basilar cisterns and both Sylvian fissures. Diffuse loss of gray-white differentiation is present. Right image is Fluid- attenuated inversion recovery (FLAIR) MRI which is more sensitive for SAH
- 37. ⢠3 mainstages are used to describe the CT manifestations of stroke: -Acute (less than 24 hours), -Subacute (24 hours to 5 days) and -Chronic (weeks).
- 39. Investigations ⢠Blood -FBC: thrombocytopenia(haemorrhagic), -cytosis (ischaemic) -FBG/RBG: DM -Hb electrophoresis: SCDx -Lipid profile: dyslipidaemia -E/U/Cr -Clotting profile -ESR -Protein C, S; anti-thrombin III; anti-phospholipid antibodies ⢠Lumbar puncture: haemorrhagic tap, xanthochromia ⢠Kidney scan ⢠Retroviral screening
- 40. Difference btw haemorrhagicand ischaemic stroke Variant Haemorrhagic stroke Ischaemic stroke Preceeding activity + - Preceeding headache + - Convulsion + - LOC + - TIA - + BP at presentation +++ ++ CSF appearance Xanthochromia; haemorrhagic tap clear
- 41. Treatment Time is Brain!!! â˘lost with each hour of stroke -120 million neurones -830 billion synapses -714 kilometer of myelinated fibres
- 42. Resuscitation ⢠Airway: suction,intubation, tracheostomy ⢠Breathing: give O2 if SPO2 <95% ⢠Circulation: hypertonic fluid (N/S), mannitol (+/- frusemide cover) ⢠Position at 30o: cerebral edema, aspiration
- 43. Treat precipitating factorsthat can worsen symptoms- 5H's ⢠Hypo- / hyperglycemia: increases umbra ⢠Hypo- / hypertension: reduce only when MAP >145mmHg; or SBP =/> 220mmHg or DBP =/> 120mmHg Target is SBP </= 145 mmHg ⢠Hypoxia ⢠Hypovolemia ⢠Hyperthermia
- 44. Specific Treatment forIschaemic stroke ⢠Tissue plasminogen activator (TPA) if patient presents within 5 hours of stroke ⢠Antiplatelet eg low dose aspirin (150-250mg) if patient presents after 5 hours ⢠Antioxidants eg vit C, vit E ⢠Statins eg simvastatin
- 45. Other recommendations inmanagement ⢠Cholesterol lowering with atorvastatin or simvastatin ⢠Lifestyle modifications ⢠Endovascular interventions: angioplasty, stenting, mechanical clot disruption, clot extraction (mechanical embolus removal in cerebral embolism)
- 46. Management of complicationsand 2o prevention of stroke Acute/Early Complications ⢠Hyperglycemia ⢠Hyperthermia ⢠Seizures ⢠Cerebral edema ⢠Hydrocephalus
- 47. Chronic/Late Complications ⢠Contractures â˘Bed sores ⢠DVT ⢠UTI ⢠Pneumonia ⢠Dementia ⢠Psychosis
- 48.
- 49. Prevention 1. Lifestyle modification 2.Lower BP 3. Lower cholesterol levels 4. Surgery i.e. endarterectomy
- 50. Rehabilitation ⢠Physiotherapy ⢠Speechtherapy ⢠Occupational therapy ⢠Nutritional therapy
- 51. Prognosis Poor prognostic factorsinclude: ⢠Accompanying fever ⢠Low GCS ⢠Hypotension ⢠Low O2 saturation ⢠Hyperglycemia ⢠Total anterior circulation stroke- 55% mortality ⢠Pontine haemorrhage
- 52. Conclusion ⢠Stroke isa leading cause of death and disability ⢠Early recognition, classification and institution of treatment is key to reducing mortality and morbidity ⢠It is better prevented than treated.
- 53.
- 54.
- 55. References 1. Kumar &Clark's Clinical Medicine 9th edition 2. Global burden of disease 2018: www.cdc.gov.org 3. Definition of stroke: American Heart Associtaion/American Stroke Association (AHA/ASA) 2010 4. Akinyemi 2021: Stroke in Africa: Profile, Progress, Prospects and Priorities. 5. KW Wahab 2008: Burden of Stroke in Nigeria. 6. B. Ekeh 2015: Stroke Mortality and its Predictors in a Nigerian Teaching Hospital. 7. Boon et al: Davidson's Principles and Practice of Medicine 20th edition - www.studentconsult.com 8. Longo DL, et al.: Harrison's Principles of Internal Medicine, 18th edition 9. Schwartz DT. Emergency Radiology:Case Studies. McGraw Hill; 2008. pp. 501â522. [Google Scholar] 10. Stroke Imaging: https://emedicine.medscape.com/article/338385- overview?icd=login_success_email_match_norm 11. David S. Liebeskind and Joanna M. Wardlaw: Acute-on-Chronic Stroke ; Mar 2021; https://doi.org/10.1161/STROKEAHA.121.033449Stroke. 2021;52:1486â1489
Editor's Notes
- #10Â Large vessel- thrombotic occlusion : extra- or intracranial Small vessel- occlusion of branches of ant or middle or perforating arteries supplying white matter. They are end arteries and cause lacunar infarct <3cm Cardioembolic: from a cardiac arteries
- #35Â This 60-year-old female underwent NCCT after an episode of left upper extremity weakness. NCCT demonstrates cortical and subcortical hypodensity involving the right mid to anterior temporal lobe.
- #38Â Acute stroke represents cytotoxic edema, and the changes can be subtle but are significant. Also termed âearly ischemic changes âand were formerly termed âhyper-acuteâ. It is intracellular edema and causes loss of the normal gray matter/white matter interface (differentiation) and effacement of the cortical sulci. A thrombus in the proximal middle cerebral artery (MCA) is sometimes seen in the acute phase and appears as hyperattenuation. A subacute stroke represents vasogenic edema, with greater mass effect, hypoattenuation and well-defined margins. Mass effect and risk of herniation is greatest at this stage. Chronic strokes have loss of brain tissue and are hypoattenuating.