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Hypertensive Intracerebral Hemmorrhage

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Hypertensive Intracerebral Hemmorrhage

  1. 1. Hypertensive Intracerebral Hemmorrhage Gerry Dunlap, MS3 Fall 2005
  2. 2. Patient Presentation • May have onset after exertion or intense emotional activity • More often during routine activity • May occur during trauma • As opposed to embolism and subarachnoid, symptoms progress to peak gradually over several hours, instead of appearing at maximal intensity
  3. 3. Patient Presentation • ½ of patients present with headache and vomiting • Additional symptoms such as decrease in LOC may occur if hematoma progresses in size • Seizures in 7 to 9%, more often in lobar hemorrhages than cerebellar or deep hemorrhages • May progress to stupor and coma if the bleed is severe enough
  4. 4. Pathogenesis • Hemorrhages occur in the territory of penetrator arteries branching off major intracerebral arteries • Small arteries are more susceptible to effects of systemic hypertension- abrupt change in caliber from larger vessels to smaller • Current theory of hemorrhage similar to pathogenesis in larger systemic vessels: chronic HTN- intimal hyperplasia with hyalinosis- focal necrosis- vessel wall ruptures – More massive hemorrhage may occur if clotting cascade unable to compensate for the damage
  5. 5. Signs/ Symptoms • Neurological signs present depend on location of hemorrhage
  6. 6. Location • Putaminal- 50-60% Hemiplegia hemisensory loss homonymous hemianopsia gaze palsy Stupor coma p: Putamen c: Caudate ic: Insular Cortex al: Ant limb Int Capsule pl: Post limb Int Capsule t: Thalamus hem: Hemorrhage cav: Post drainage cavity
  7. 7. Location • Cerebellar – Inability to walk – Vomiting – Headache, possibly referred to neck or shoulder – Neck Stiffness – Gaze palsy – Facial weakness
  8. 8. Location • Thalamic – Hemiparesis – Hemisensory loss – Aphasia – Neglect (nondominant hemisphere) – “wrong way eyes”- eyes deviate toward the hemiparesis, as opposed to hemispheric injury 13 year old boy, acute right sided HA Numbness on L side of body and face no motor deficit Hemorrhage in R posterodorsal thalamus involving pulvinar nucleus
  9. 9. Location • Lobar – Most often in parietal and occipital lobes – Occipital lobes present with contralateral homonymous hemianopsia – High incidence of seizures – Frontal region- contralateral plegia or paresis of the leg with arm sparing
  10. 10. Location • Pontine – deep coma within minutes of the hemorrhage, due to disruption of the reticular activating system – Total paralysis – Pinpoint pupils Pontine hemorrhage in R pons anterior to fourth ventricle, near facial nerve nuclei
  11. 11. Differential Diagnosis • Based on risk factors- severely hypertensive patient with a typical bleed can be assumed to have ICH • History of recent trauma • Underlying bleeding disorder • Iatrogenic anticoagulant therapy • Neoplastic bleeding • Drug abuse, ie cocaine- more likely with underlying AVM
  12. 12. Differential • Amyloid Angiopathy – Usually lobar, occasionally cerebellar – Posterior portions of brain, including parietal and occipital lobes – May have multiple hemorrhages – Typically older than 65
  13. 13. Differential • Intracerebral Arteriovenous Malformation • 0.14% estimated incidence in US population (1/5 to 1/7 of incidence of intracranial aneurysms) • Annual risk of an ICH is 2-3%, with mortality of 10%, increasing with subsequent bleeds • May be present as part of neurocutaneous symndrome; ie Sturge-Weber or Rendu- Osler-Weber Images from: MyPacs.com
  14. 14. Treatment • ICP control – Maintaining Cerebral Perfusion Pressure (CPP) above 60 mmHg – CPP=MAP-ICP – Goal: To reduce mass effect and hydrocephalus, yet maintain perfusion pressure – Can reduce increased ICP by IV mannitol (1g/kg bolus with .25 to .5 g/kg q 6hr) – Also with barbiturate anesthesia, hyperventilation (provides temporary lowering effect)
  15. 15. Treatment • Ventricular drain or shunt may be required to obtain ICP control • Blood pressure control is challenging- maintaining sufficient CPP while preventing extension of hemorrhage by increased MAP • Maintain systolic between 140 to 160 mmHg
  16. 16. Treatment • Surgery- indications vary depending on site of bleed – Cerebellar hemorrhages need to be decompressed if greater than 3 cm – Supratentorial ICH hematoma evacuation more controversial • 1997 meta-analysis had insufficient data to draw conclusions of risk/ benefit of surgery • Now considered to treat refractory increases in ICP in a per patient basis – Patients with decreased LOC (obtundation- stupor) – Also supportive of surgery- recent onset, ongoing deterioration, involvement of nondominant hemisphere, accessible hematoma location
  17. 17. Imaging- CT vs. MRI • HEME study- Hemorrhage and Early MRI Evaluation • MRI was much more accurate at detecting hemorrhage than CT – Study was stopped early due to clear superiority of MRI over CT • High concordance of the two imaging modalities with acute hemorrhage • MRI more sensitive (49 patients of 200) at detecting chronic hemorrhage or microbleeds – However, MRI does not pick up subarachnoid hemorrhages as well, so CT remains the imaging most often performed upon admission into the hospital
  18. 18. Imaging • MRI findings depend on the age of the bleed • Degradation of hemoglobin in the hemorrhage provides different blood products (deoxyhemoglobin, methemoglobin) with different signal enhancement on MRI • Variable presentation of Hyperacute (1-6 hours) subacute, chronic and microbleeds
  19. 19. Summary • Presents as an escalating neurological insult, submaximal at onset • Signs depend on cerebral location • Treatment includes medical and surgical approaches to limit extent of ongoing hemorrhage while maintaining CPP • CT in the acute setting to allow for possibility of visualizing subarachnoid hemorrhage, otherwise MRI is more sensitive for diagnosis
  20. 20. References • UptoDate.com- Hypertensive intracerebral hemorrhage • Kidwell CS, Chalela JA, Saver JL, et al; “comparison of MRI and CT for detection of acute intracerebral hemorrhage,” JAMA, October 2004;292(15):1823 • Cotran, Kumar, Collins; Robbins Pathologic Basis of Disease 6th ed., page 1310-14 • Goetz; Textbook of Clinical Neurology 2nd ed., page 410-20 • Images: – MyPacs.com- various images for ICH – Sherman SC; “pontine hemorrhage presenting as an isolated facial nerve palsy,” Ann Emerg Med, Jul 2005, 46(1): 64-6 – Mijovic-Prelec D, Bentley P, Caviness VS; “selective rotation of egocentric spatial representation following right putaminal hemorrhage,” Neuropsychologia; 2004; 42(13):1827-37 – Kirollos RW, Tyagi AK, Ross SA, et al.; “management of spontaneous cerebellar hematomas: a prospective treatment protocol,” Neurosurgery; Dec 2001; 49(6):1378-86 – Wester K, Irvine DRF, Hugdahl K; “auditory laterality and attentional deficits after thalamic haemorrhage,” Journal of Neurology; Aug 2001; 248(8):676-83

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