1. Hemorrhagic Stroke Dr. Grant Stotts Director, Ottawa Stroke Program

2.  Review Hemorrhagic Stroke  Subarachnoid Hemorrhage (SAH)  Intracerebral Hemorrhage (ICH)  Objectives to be addressed sequentially  Objectives emphasize SAH Outline Unit III - Hemorrhagic Stroke - Stotts

3. ①4830 Discuss the epidemiology and etiology of cerebral aneurysms. ② 4831 List the common anatomic sites of aneurysmal formation. ③ 4832 Describe the common clinical manifestations of a) a sentinel bleed and b) an aneurysmal rupture and c) compression from giant unruptured aneurysms. ④ 4833 Describe the investigation and management principles of patients with suspected subarachnoid hemorrhage (SAH). ⑤ 4834 Discuss potential complications of SAH, including vasospasm and hydrocephalus. ⑥ 4835 Discuss how hemorrhagic stroke differs from ischemic stroke in its clinical and radiologic presentation. ⑦ 4836 List the most common causes and manifestations of subarachnoid and intracerebral hemorrhage. 7 Objectives

4. Discuss the epidemiology and etiology of cerebral aneurysms. Objective 4830 Unit III - Hemorrhagic Stroke - Stotts

5. Aneurysms: Background Intracranial aneurysms occur in 1 to 5% of the population – Autopsy studies – 50 – 80% do not rupture More common in: – Adults – Women Associated factors: – Hypertension – Smoking – Excessive EtOH use Familial forms are less common (10%) Strong association with polycystic kidney disease

6. 1. Location at Artery Bifurcations 2. Defect in Arterial Wall: Tunica Media 2 Major Factors in Aneurysm Formation Unit III - Hemorrhagic Stroke - Stotts

7.  More likely to rupture if  Larger (> 7 mm)  Growth with time Aneurysm Rupture Risk Unit III - Hemorrhagic Stroke - Stotts

8. Causes of Subarachnoid Hemorrhage Majority due to trauma Spontaneous SAH – Aneurysm 85% Clinically one of the most important presentations to recognize Mortality rate: 30-40% Most survivors are disabled – Other: cocaine, vasculitis, coagulopathy

9. List the common anatomic sites of aneurysmal formation. Objective 4831 Unit III - Hemorrhagic Stroke - Stotts

10. Pathology Aneurysms tend to occur at artery bifurcations NEJM 2006;355:928-39.

11. Bifurcations around the Circle of Willis Cerebral Aneurysm Locations Unit III - Hemorrhagic Stroke - Stotts

12.  Cerebral arteries follow subarachnoid space  Subarachnoid space is continuous through the brain and spine  Therefore, a lumbar puncture can test for blood products even if the hemorrhage was intracranial Aneurysm Location: Subarachnoid Space Unit III - Hemorrhagic Stroke - Stotts

13. Describe the common clinical manifestations of : b) an aneurysmal rupture a)a sentinel bleed c) compression from giant unruptured aneurysms. Objective 4832 Change in order Unit III - Hemorrhagic Stroke - Stotts

14. b) Subarachnoid Hemorrhage: Clinical Manifestations Thunderclap Headache – Maximal at onset Predominant clinical feature – Severe in intensity (10 out of 10)

15.  Clinical Presentation  Acute, thunderclap, headache  Acute loss of consciousness  Nausea, vomiting  Seizure  Clinical deficits may occur if pressure is high enough to injure surrounding tissue Aneurysmal Rupture Unit III - Hemorrhagic Stroke - Stotts

16.  Sentinal = Minor bleed  Likely represents minor hemorrhage with rapid thrombus formation within the aneurysm  Occurs in ~ 20% of SAH cases  80% will not have clinical warning  Rebleed rate: 50% in 1 week  Clinical recognition allows for time window to detect aneurysms  Symptoms similar to SAH with thunderclap headache a) Sentinel Bleed Unit III - Hemorrhagic Stroke - Stotts

17. c) Compression from Giant Aneurysms Unit III - Hemorrhagic Stroke - Stotts What is the deficit? Which CN nerve raises the eyelid? Which CN lowers the eyelid?

18.  Cranial nerve deficits  CN III palsy from Posterior Communicating Artery aneurysm most common  Headache  Seizure c) Compression from Giant Aneurysms Unit III - Hemorrhagic Stroke - Stotts

19. Describe the investigation and management principles of patients with suspected subarachnoid hemorrhage (SAH). Objective 4833 Unit III - Hemorrhagic Stroke - Stotts

20.  CT Head  95% sensitivity o Most sensitive if done < 12 hours  Lumbar Puncture if:  CT is negative and  History is suggestive of SAH  Must wait 6 hours after headache onset to do LP Initial Investigations for Subarachnoid Hemorrhage Unit III - Hemorrhagic Stroke - Stotts

21. Lumbar Puncture Hemorrhagic Stroke – Dr. Stotts

22. Unit III - Hemorrhagic Stroke - Stotts Important Aspects About the Lumbar Puncture RBC count is tested in the first and last CSF tube collected – In SAH, the RBC count will be similar between the 2 tubes – Traumatic LP: venous blood enters needle before subarachnoid space is entered Cell count will drop by the last tube as it is diluted by CSF SAH: First Tube RBC = Last Tube RBC Traumatic Tap: First Tube RBC > Last Tube RBC

23. Unit III - Hemorrhagic Stroke - Stotts Important Aspects About the Lumbar Puncture You should wait approximately 6 hours after headache onset before the LP is performed – Xanthochromia is a yellowish discoloration due to bilirubin from hemoglobin breakdown – Takes 3 - 6 hours to develop – Helpful if RBC count is low in the case of a sentinel bleed where there is no active bleeding Xanthochromia

24. Unit III - Hemorrhagic Stroke - Stotts Imaging Aneurysms When a SAH is detected, the next step is to determine if there is a cerebral aneurysm. Non-invasive imaging: used first – CT Angiogram – MR Angiogram Invasive imaging may be necessary – Catheter cerebral angiogram CT Angiogram

25. Unit III - Hemorrhagic Stroke - Stotts Cerebral Aneurysm Treatment Surgical Clipping Historically the most common way to treat cerebral aneurysms Endovascular Coiling Generally considered first-line treatment for the majority of aneurysms NEJM 2006;355:928-39.

26. Unit III - Hemorrhagic Stroke - Stotts Aneurysm Coiling Catheter usually inserted into the femoral artery Angiograms can be performed to see position of catheter during the procedure Detachable coils are inserted into the aneurysm until it is filled Coils are thrombogenic Patients are followed by MR scanning to evaluate possibility of regrowth Avoids craniotomy NEJM 2006;355:928-39.

27. Unit III - Hemorrhagic Stroke - Stotts Aneurysm Coiling Images before and after endovascular coiling Courtesty: Dr. C. Lum Neuroradiology, Ottawa Hospital

28. Discuss potential complications of SAH, including vasospasm and hydrocephalus. Objective 4834 Unit III - Hemorrhagic Stroke - Stotts

29.  Immediate (May require management in ER)  Decreased Level of Consciousness  Airway Protection  Cardiac Effects o Arrhythmia  Seizure  Delayed  Rebleeding (coil or clip)  Hydrocephalus  Vasospasm Complications of SAH Unit III - Hemorrhagic Stroke - Stotts

30.  Hydrocephalus  Blood obstructs CSF outflow pathways (arachnoid villi)  CSF accumulates and expands, increasing intracranial pressure SAH Complications: Hydrocephalus Unit III - Hemorrhagic Stroke - Stotts

31.  Vasospasm  Uncertain cause, components of blood breakdown suspected  Severe vasospasm can lead to ischemia (stroke)  Usually 3 - 7 days after onset Delayed Complications of SAH Unit III - Hemorrhagic Stroke - Stotts

32. Discuss how hemorrhagic stroke differs from ischemic stroke in its clinical and radiologic presentation. Objective 4835 Unit III - Hemorrhagic Stroke - Stotts

33. Intracerebral Hemorrhage

34.  Acute onset neurological deficit  Deficit depends on location of bleed – same as ischemic stroke  Contralateral hemiparesis/sensory loss and visual field deficits are common with hemispheric ICH  Ataxia can develop with cerebellar hemorrhage  Brainstem deficits can occur with ICH in the brainstem or by secondary compression  Often:  Headache  Vomiting  Progressive deterioration in level of consciousness and/or worsening deficits Presentation of Intracerebral Hemorrhage Unit III - Hemorrhagic Stroke - Stotts

35.  Clinically, a stroke is more likely hemorrhagic if:  Rapid deterioration in level of consciousness  Headache +/- Vomiting  History of trauma  However:  Imaging is necessary to verify  Usually CT scan Clinical Differentiation of Ischemic and Hemorrhagic Stroke

36. Unit III - Hemorrhagic Stroke - Stotts Radiologic Differentiation of Ischemic and Hemorrhagic Stroke Computed tomography (CT) is the most widely used imaging modality to determine acute stroke type Hemorrhagic Stroke – Blood (acutely) is more dense than brain tissue Will appear bright on CT immediately Ischemic stroke – Initially CT Head may be normal – With tissue death there is (cytotoxic) edema involving cellular swelling – This leads to a decrease in tissue density – May take hours to develop Hemorrhage Ischemic

37. Intracerebral Hemorrhage: Management Limit progression of hematoma – Reverse anticoagulation if taking warfarin – Control blood pressure Investigate for underlying cause of hemorrhage – Vascular malformations CT or MR Angiogram often done initially – Other causes can be investigated if this testing is negative Initial CT Images 3 Hours Later Courtesy: Dr. D. Dowlatshahi

38. Unit III - Hemorrhagic Stroke - Stotts CT Imaging of Cerebral Blood Vessels CT Head CT Angiogram AVM

39. Unit III - Hemorrhagic Stroke - Stotts Further Arteriovenous Malformation (AVM) Images From the Same Patient CT Angiogram Angiogram Images demonstrate abnormal network of vessels between (middle cerebral) artery and veins without intervening capillaries.

40. List the most common causes and manifestations of subarachnoid and intracerebral hemorrhage. Objective 4836 Unit III - Hemorrhagic Stroke - Stotts

41. Causes of Intracerebral Hemorrhage 1. Subcortical  Hypertension most common cause 2. Lobar  Involving major lobes of the brain  Hemorrhage extends out to the cortex  Examples: o Amyloid angiopathy o Anticoagulant-associated hemorrhage o Coagulopathy-associated hemorrhage Unit III - Hemorrhagic Stroke - Stotts Subcortical Lobar Location of bleed generally is associated with etiology.

42. Subcortical Hemorrhage Major Cause Hypertension leads to formation of microaneurysms in small, penetrating arteries – Lenticulostriate vessels, branches usually from middle cerebral artery, degenerate with prolonged hypertension – Note these same vessels are responsible for lacunar ischemic infarcts as the vessels can also develop hypertrophy with prolonged hypertension – These vessels are too small to be seen on any available imaging. The CIBA Collection of Medical Illustrations volume I, Nervous System Part II, Neurologic and Neuromuscular Disorders. Frank H. Netter. Pg. 59

43. Lobar Hemorrhage Major Etiologies: – Bleed into tumor – Bleed after ischemic infarct – Warfarin use or coagulopathy – Amyloid angiopathy Bleed after ischemic infarct

44. Amyloid Angiopathy: Connection to Alzheimer’s Disease (Not on objectives list) Amyloid Precursor Protein is cleaved into 2 predominant fragments – Soluble fragment (Aβ40) deposits in muscular layers of cerebral arteries and capillaries Vessels become fragile and spontaneously rupture Major cause of bleeding in the elderly – Insoluble fragment (Aβ42) deposits lead to amyloid plaque which is one of the major pathological findings in Alzheimer’s Disease – These conditions can overlap but may also occur independently Stroke 2009;40;2601-2606.

45. Conclusions Recognize the presentation of subarachnoid hemorrhage – Thunderclap headache Management of suspected subarachnoid hemorrhage – CT and LP Intracerebral hemorrhage – Subcortical: Hypertension – Cortical: Amyloid angiopathy Management of intracerebral hemorrhage – Control blood pressure to prevent hematoma expansion – Investigate for underlying vascular cause