Cerebral Hemorrhage By Arlyn M. Valencia, M.D. Associate Professor, University Of Nevada School Of Medicine

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Discussion of Spontaneous Cerebral Hemorrhages

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Cerebral Hemorrhage By Arlyn M. Valencia, M.D. Associate Professor, University Of Nevada School Of Medicine

  1. 1. CEREBROVASCULAR ACCIDENT OR ―BRAIN ATTACK‖ Third leading cause of death   750, 000 cases/year  Leading cause of significant disability  Cost: $40 billion/year
  2. 2. Types of Stroke Ischemic, 80%  - thrombosis, 50% (small & large-vessel) - embolism, 30%  Hemorrhagic, 20% - intracerebral (HTN as risk) - subarachnoid (aneurysm)
  3. 3. CEREBRAL HEMORRHAGE HEMORRHAGIC STROKE   PRIMARY INTRACEREBRAL HEMORRHAGE  SUBARACHNOID HEMORRHAGE  HEMORRHAGE FROM CEREBRAL AMYLOID ANGIOPATHY
  4. 4. CEREBRAL HEMORRHAGE HEMORRHAGIC STROKE   PRIMARY INTRACEREBRAL HEMORRHAGE  SUBARACHNOID HEMORRHAGE  HEMORRHAGE FROM CEREBRAL AMYLOID ANGIOPATHY
  5. 5. HEMORRHAGIC STROKE The transformation of a bland infarct into a  hemorrhagic infarct is a common occurrence (highest in autopsy studies)  ―The concept of migratory embolus‖
  6. 6. Right Middle Cerebral Artery Territory Infarct
  7. 7. Risk Factors For Hemorrhagic Transformation of a Bland Infarct Advanced age   Embolization as etiology  High systolic BP  CT shows mass effect  Larger territory strokes  Anticoagulation  History of coagulopathy
  8. 8. HEMORRHAGIC INFARCT
  9. 9. CEREBRAL HEMORRHAGE HEMORRHAGIC STROKE   PRIMARY INTRACEREBRAL HEMORRHAGE  SUBARACHNOID HEMORRHAGE  HEMORRHAGE FROM CEREBRAL AMYLOID ANGIOPATHY
  10. 10. RISK FACTORS FOR ICH Advancing age   HTN (autopsy studies on patients with ICH showed high incidence of LVH; PROGRESS – Perindopril Protection Against Recurrent Stroke Study:76% relative risk reduction of ICH in comparison to placebo  Cigarette smoking  alcoholism
  11. 11. PRIMARY INTRACEREBRAL HEMORRHAGE Five most common sites:  putamen: 35 % - 50% subcortical white matter 30% thalamus: 10%-15% pons 5%-12% cerebellar white matter <5%
  12. 12. THE ANTERIOR CIRCULATION
  13. 13. Most ICH originate from the rupture of  small deep penetrating arteries (50 to 200 um); most common: lenticulostriates  Same arteries are recognized to be occluded in lacunar infarcts (process: fibrinoid necrosis or lipohyalinosis)
  14. 14. Massive Right Putaminal Hemorrhage
  15. 15. Subcortical White Matter ICH
  16. 16. Pontine Hemorrhage
  17. 17. Thalamic Hemorrhage
  18. 18. Right Cerebellar Hemorrhage
  19. 19. CEREBRAL HEMORRHAGE HEMORRHAGIC STROKE   PRIMARY INTRACEREBRAL HEMORRHAGE  SUBARACHNOID HEMORRHAGE  HEMORRHAGE FROM CEREBRAL AMYLOID ANGIOPATHY
  20. 20. SUBARACHNOID HEMORRHAGE Accounts for 5-10% of all strokes   Incidence has not declined in 30 years  80% due to rupture of intracranial saccular aneurysm  30-day mortality rate 50%  Most deaths occur within one week
  21. 21. RUPTURED ANEURYSM SITES: International Cooperative Study On The Timing Of Aneurysm Study Anterior communicating artery (ACom)  34%  ICA 30%  MCA 22%  Basilar tip, PICA, basilar trunk branches— 7.6%
  22. 22. CAUSES OF SUDDEN DEATH IN SAH Large intraparenchymal hematoma   Destruction of brain tissue  Acute hydrocephalus  Increased intracranial pressure  Cardiac arrhythmias, MI, PE and respiratory failure
  23. 23. LEADING CAUSES OF DEATH ON HOSPITALIZED PATIENTS Sequelae of initial hemorrhage   Recurrent aneurysmal  Vasospasm leading to ischemic stroke  Severe medical complications
  24. 24. CEREBRAL HEMORRHAGE HEMORRHAGIC STROKE   PRIMARY INTRACEREBRAL HEMORRHAGE  SUBARACHNOID HEMORRHAGE  HEMORRHAGE FROM CEREBRAL AMYLOID ANGIOPATHY
  25. 25. CEREBRAL AMYLOID ANGIOPATHY Amyloid deposition in the cerebral vessels  sufficient to cause symptomatic vascular dysfunction  Vessel rupture and spontaneous ICH untreatable and unpreventable  Prevalence of CAA: 2.3% age 65-74; 8% age 75-84 ;12.1% 85 and older
  26. 26. HEMORRHAGE SECONDARY TO CEREBRAL AMYLOID ANGIOPATHY (CAA) Most common cause of lobar  hemorrhages in non-hypertensive individuals  Elderly patients  Evidence of small microbleeds in MRI  Long-term recurrence increased
  27. 27. RISK FACTORS FOR CAA LOBAR HEMORRHAGE Advanced age   APOE epsilon2 or epsilon4  Alzheimer’s disease
  28. 28. RISK FACTORS FOR NON-CAA ICH Family history of ICH   Frequent use of alcohol  Previous ischemic stroke  Low serum cholesterol level
  29. 29. ICH: EVALUATION AND WORK-UP: History and PE  Computed Tomography (CT) scan of the head  12-lead EKG, chest X-ray  Complete blood count, PT, PTT  Chemistries (sodium, phosphate, glucose  abnormalities may mimic stroke) Urine and serum toxicology (drugs and alcohol) 
  30. 30. Other Neuroimaging Techniques & Ancillary Tests Magnetic Resonance Imaging (MRI)  Diffusion Weighted Imaging (DWI), Magnetic Resonance Angiography (MRA)  Ultrasound (Carotid Duplex, Transcranial Doppler, 2-D echo)  Conventional Angiography
  31. 31. SUBACUTE INTRACEREBRAL HEMORRHAGE
  32. 32. Under special circumstances, the following tests may be required: Cervical spine x-ray   Arterial blood gas  Lumbar puncture  Electroencephalogram (EEG)
  33. 33. Glasgow Coma Scale 1 2 3 4 5 6 Opens eyes in Opens eyes in Does not open Opens eyes Eyes response to response to N/A N/A eyes spontaneously painful stimuli voice Utters Oriented, Makes no Incomprehensibl Confused, Verbal inappropriate converses N/A sounds e sounds disoriented words normally Abnormal Flexion / Makes no Extension to Localizes Obeys Motor flexion to painful Withdrawal to movements painful stimuli painful stimuli Commands stimuli painful stimuli
  34. 34. Overview of ICH Management ICH has frequent early, ongoing bleeding and progressive deterioration, severe clinical deficits and subsequent high mortality and morbidity rates Good general supportive management (airways,  oxygenation, circulation, glucose level, fever, DVT prophylaxis) Slowing or stopping initial bleeding  Blood removal from parenchyma or ventricles  Management of complications of blood in the rain  (increased ICP, decreased CPP)
  35. 35. CASE SPECIFIC MANAGEMENT Correctible/controllable causes of  hemorrhage (e.g. warfarin)  Clipping of aneurysm
  36. 36. Herniation Early clinical signs: mental status change,  pupillary dilatation, vomiting  Late clinical signs: ocular paresis, decerebrate rigidity, coma and death
  37. 37. TREATMENT OF BRAIN SWELLING Cerebral perfusion pressure =MAP-ICP Fluid Restriction (1200 ml /day/m2)  Controlled hyperventilation: 25 mm Hg  Mannitol, 0.25 mg/kg IV over 20 minutes; repeat PRN,  serum osmolality maintained in the range of 300- 320mOsm/l Barbiturate coma, with ICP monitoring (subrachnoid bolt,  IV catheter or Camino catheter): maintain CPP greate than 50 mmHg; pentobarbtial serum level of 2-4 mg/dl Drainage of CSF (ventriculostomy)  Lobectomy 
  38. 38. Before Intraven- tricular TPA After
  39. 39. INTRAVENTRICULAR HEMORRHAGE 
  40. 40. Intracerebral hemorrhage has frequent early, ongoing bleeding and progressive deterioration, severe clinical deficits and subsequent high mortality and morbidity rates.
  41. 41. THANK YOU!

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