Ischemic and hemorrhagic stroke

a case presentation followed a description of stroke, its main types and its management in emergency and indoor settings

1. Case Presentation Dr. Gauhar Mahmood Azeem House Officer, Medical Unit 4, Services Hospital Lahore.

2. Clinical History Biodata : A 75 year old female resident of Lahore presented to Medical Emergency Services Hospital on the 1 st of December 2014 with complaints of Presenting Complaints: Right sided body weakness 1 hour Inability to talk 1 hour

3. Clinical History History of present illness: Patient is a known hypertensive (25 years) and known patient of IHD (10 years) and was relatively well 2 hours back when while walking to the bathroom the patient fell suddenly and after receiving help could not talk or move the right arm or leg, there was also deviation of face to the left…

4. Clinical History History of present illness: …The weakness was sudden in onset, was not associated with fits, up rolling of eyes, tongue bite, or urination. The patient was previously mobile and has no history of preceding fever, there is no history of vomiting, headaches, or any such events before.

5. Clinical History Past History Hypertension 15 years Low ejection fraction 40% known for 6 months No history of diabetes, hepatitis, tuberculosis is there.

6. Clinical History Treatment History: Patient treated for an episode of shortness of breath 6 months back. Drug History: Patient taking Norvasc 5mg Ascard 75mg Loprin 75mg Drug compliance recently not good Patient not known allergic to any medication

7. Clinical History SocioEconomic History Higher Middle Class family. Owns own home. Occupational History Retired Professional banker.

8. Clinical History Family History Was positive for Hypertension, Diabetes and Ischemic Heart Disease.

9. Examination Vitals Pulse: 118/min rate and rhythm irregularly irregular Blood Pressure: 160/80 mmHg Respiratory Rate: 16/min Temperature: 98’F Blood Sugar Random: 249 mg/dl

10. Examination Central Nervous System Examination GCS: M6 V1 E4 11/15 Sensory loss not present. Right sided facial weakness, deviation to the left side. Patient has aphasia, dysphagia. Eye movement normal Power: Right Arm 0/5 Left Arm 5/5 Right Leg 0/5 Left Leg 5/5

11. Examination Tone Increased in Right arm and leg. Normal in left arm and leg. Reflexes Reflexes on the right side were exaggerated. Those on left side were normal. Planters Right Plantar was up going. Left Plantar down going.

12. Examination Respiratory System Air entry equal on both sides, mild bilateral inspiratory crepts . Gastrointestinal System Abdomen looks normal, no visceromegaly , no area of tenderness, percussion note resonant, no shifting dullness, bowel sounds present.

13. Examination Cardiovascular System Pulse Rate 118/min Pulse was irregularly irregular Mitral area 2 cm lateral to the mid- clavicular line. There was no abnormal heart sound appreciated and finding on auscultation was irregularly irregular rhythm.

14. Investigations CBC Hb 8.6 TLC 14.8 Hct 28 Platelets 351

15. Investigations LFT ALT 23 AST 19 RFT Creatinine 0.6 Serum Electrolytes Na+ 148 K+ 5.0 PT 15 APTT 35

16. Investigations UCE Pus Cells 3-6 Epithelial cells 1-2 Cardiac Enzymes CPK 99 LDH 382 CKMB 15

17. ECG

18. CT Brain No areas of abnormal attenuation seen on CT scan. Normal Senile atrophic changes seen. Calcified Choroid Plexus. (60 % of infarcts are seen within 3-6 hours and virtually all are seen in 24 hours)

19. Differential Diagnosis Ischemic Stroke Hemorrhagic Stroke (CT scan rules this out)

20. Diagnosis Ischemic Stroke most likely due to Embolus

21. Treatment Plan INJ N/S x 1000CC x IV x BD INJ HEPARIN 1cc x SC x OD Tab ATORVA x 40mg x PO x OD Tab HERBESSER x 30mg x PO x TDS ( diltiazem ) Tab LOPRIN 75mg x 2 x PO x OD INJ RISEK x 40mg x IV x OD Oxygen inhalation to keep saturation O2 to 94-96% Ted Stocking, Chest Physio , Limb Physio . Planned CXR, Echocardiography, Carotic Doppler, Fasting Lipid Profile.

22. STROKE

23. Definitions Stroke Clinical syndrome of rapid onset of focal deficits of brain function lasting more than 24 hours or leading to death Transient Ischemic attack (TIA) Clinical syndrome of rapid onset of focal deficits of brain function which resolves within 24 hours

24. Definitions Progressive Stroke A stroke in which the focal neurological deficits worsen with time Also called stroke in evolution Completed Stroke A stroke in which the focal neurological deficits persist and do not worsen with time

25. Types of Stroke Ischemic Hemorrhagic

26. Risk Factors Ischemic Stroke Nonmodifiable risk factors include the Age Race Sex Ethnicity History of migraine headaches [21] Fibromuscular dysplasia Heredity: Family history of stroke or transient ischemic attacks (TIAs)

27. Risk Factors Ischemic Stroke Modifiable Risk Factors Hypertension (the most important) Diabetes mellitus Cardiac disease: Atrial fibrillation, valvular disease, heart failure, mitral stenosis, structural anomalies allowing right-to-left shunting ( eg , patent foramen ovale ), and atrial and ventricular enlargement Hypercholesterolemia TIAs Carotid stenosis Hyperhomocystinemia Lifestyle issues: Excessive alcohol intake, tobacco use, illicit drug use, physical inactivity [24] Obesity Oral contraceptive use/postmenopausal hormone use Sickle cell disease

28. Risk Factors Hemorrhagic Stroke Advanced age Hypertension (up to 60% of cases) Previous history of stroke Alcohol abuse Use of illicit drugs ( eg , cocaine, other sympathomimetic drugs)

29. Middle Cerebral Artery

30. Anterior Cerebral Artery

31. Posterior Cerebral Artery

32. Ischemic Stroke 80% of strokes Arterial occlusion of an intracranial vessel leads to hypoperfusion of the brain region it supplies

33. Etiology Thrombotic Lacunar stroke Large vessel thrombosis Hypercoagulable disorders Systemic Hypoperfusion Venous Thrombosis Embolic Artery to artery Carotid bifurcation Aortic arch Cardioembolic Atrial fibrillation Myocardial infarction Mural thrombus Bacterial endocarditis Mitral stenosis Paradoxical embolus

34. Thrombotic Stroke Atherosclerosis is the most common pathology leading to thrombotic occlusion of blood vessels Hypercoagulable disorders – uncommon cause Antiphospholipid syndrome Sickle cell anemia Polycythemia vera Homocysteinemia Vasculitis : PAN, Wegener’s granulomatosis , giant cell arteritis

35. Thrombotic Stroke Lacunar stroke Accounts for 20% of all strokes Results from occlusion of small deep penetrating arteries of the brain Pathology: lipohyalinosis & microatheroma Thrombosis leads to small infarcts known as lacunes Clinically manifested as lacunar syndromes

36. Embolic Stroke Cardioembolic stroke Embolus from the heart gets lodged in intracranial vessels MCA most commonly affected Atrial fibrillation is the most common cause Others: MI, prosthetic valves, rheumatic heart disease Artery to artery embolism Thrombus formed on atherosclerotic plaques gets embolized to intracranial vessels Carotid bifurcation atherosclerosis is the most comon source Others: aortic arch, vertebral arteries etc.

37. Pathophysiology of Ischemic Stroke Blood supply to the brain is auto-regulated Blood flow If zero leads to death of brain tissue within 4-10min <16-18ml/100g tissue/min infarction within an hour Ischemia leads to development of an ischemic core and an ischemic penumbra

38. Ischemic Penumbra Tissue surrounding the core region of infarction which is ischemic but reversibly dysfunctional Maintained by collaterals Can be salvaged if re-perfused in time Primary goal of revascularization therapies

39. Hemorrhagic Stroke Two types Intracerebral hemorrhage(ICH) Subarachnoid hemorrhage(SAH) Higher mortality rates when compared to ischemic stroke

40. Intracerebral Haemorrhage Result of chronic hypertension Small arteries are damaged due to hypertension In advanced stages vessel wall is disrupted and leads to leakage Other causes: amyloid angiopathy , anticoagulant therapy, cavernous hemangioma , cocaine, amphetamines

41. Subarachnoid Haemorrhage Most common cause is rupture of saccular or Berry aneurysms Other causes include arteriovenous malformations, angiomas , mycotic aneurysmal rupture etc. Associated with extremely severe headache

42. Pathophysiology of haemorrhagic stroke Explosive entry of blood into the brain parenchyma structurally disrupts neurons White matter fibre tracts are split Immediate cessation of neuronal function Expanding hemorrhage can act as a mass lesion and cause further progression of neurological deficits Large hemorrhages can cause transtentorial coning and rapid death

43. Management

44. Management of Ischemic Stroke The central goal of therapy in acute ischemic stroke is to preserve tissue in the ischemic penumbra, where perfusion is decreased but sufficient to stave off infarction. ABC’s The goal for the emergent management of stroke is to assess the patient’s airway, breathing, and circulation (ABCs); stabilize the patient as necessary; and complete initial evaluation and assessment, including imaging and laboratory studies, within 60 minutes of patient arrival

45. Management of Ischemic Stroke Supplemental oxygen is recommended when the patient has a documented oxygen requirement ( ie , oxygen saturation < 95 %) In the small proportion of patients with stroke who are relatively hypotensive, administration of IV fluid, vasopressor therapy, or both may improve flow through critical stenosis Hypoglycemia or hyperglycemia needs to be identified and treated early in the evaluation .

46. Management of Ischemic Stroke Fibrinolytic Therapy With rtPA ( alteplase ) within 3-4.5 hours of symptoms onset. Patient must meet the inclusion criteria and not have a contraindication Antiplatelet Therapy AHA/ASA guidelines recommend giving aspirin, 325 mg orally, within 24-48 hours of ischemic stroke onset. The benefit of aspirin is modest but statistically significant and appears principally to involve the reduction of recurrent stroke

47. Management of Ischemic Stroke Threshold for Blood Pressure lowering Thresholds for antihypertensive treatment in acute ischemic stroke patients who are not fibrinolysis candidates, according to the 2013 ASA guidelines, are systolic blood pressure higher than 220 mm Hg or diastolic blood pressure above 120 mm Hg . In those patients, a reasonable goal is to lower blood pressure by 15% during the first 24 hours after onset of stroke. Care must be taken to not lower blood pressure too quickly or aggressively, since this could worsen perfusion in the penumbra.

48. Management of Ischemic Stroke Fever Control Antipyretics are indicated for febrile stroke patients, since hyperthermia accelerates ischemic neuronal injury. Substantial experimental evidence suggests that mild brain hypothermia is neuroprotective . Manage Cardiac Arrythmias eg in our case diltiazem was given to manage AF In Cerebral Edema IV Mannitol can be given Pass NG tube if indicated, pass foleys .

49. Management of Ischemic Stroke Secondary prevention of stroke Platelet antiaggregants Antihypertensives Statins Lifestyle interventions Management of other conditions that may be contributing, eg probable carotid endarterectomy for stenosis and anticoagulation in valvular problems or AF Prevent pressure sores, aspirations, contractures, DVT

50. Management of Haemorrhagic Stroke The treatment and management of patients with acute intracerebral hemorrhage depends on the cause and severity of the bleeding. Basic life support, as well as control of bleeding, seizures, blood pressure (BP), and intracranial pressure, are critical. ICH is a neurological emergency and initial management should be focused on assessing the patients airway, breathing capability, blood pressure and signs of increased intracranial pressure.

51. Management of Haemorrhagic Stroke The patient should be intubated based on risk of aspiration, impending ventilatory failure (PaO 2  < 60 mmHg or pCO 2  > 50 mmHg), and signs of increased intracranial pressure. Emergency measures for ICP control are appropriate for stuporous or comatose patients, or those who present acutely with clinical signs of brainstem herniation. The head should be elevated to 30 degrees, 1.0–1.5 g/kg of 20% mannitol should be given by a rapid infusion, and the patient should be hyperventilated to a pCO 2  of 30–35 mmHg.

52. Management of Hemorrhagic Stroke In patients presenting with a systolic BP of 150 to 220 mm Hg, acute lowering of systolic BP to 140 mm Hg is probably safe. Management of seizures if any Acute management of seizures entail administering intravenous lorazepam (0.05–0.10 mg/kg) followed by an intravenous loading dose of phenytoin or fosphenytoin (15–20 mg/kg), valproic acid (15–45 mg/kg), or phenobarbital (15–20 mg/kg).

53. Management of Hemorrhagic Stroke If hemorrhage is due to anticoagulation, give Vitamin K, FFP and PCC Fever should be treated aggressively because it is independently associated with a poor outcome Neurosurgical Consultation