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Hypertensive Intracerebral Hemmorrhage

Hypertensive Intracerebral Hemmorrhage. Gerry Dunlap, MS3 Fall 2005. Patient Presentation. May have onset after exertion or intense emotional activity More often during routine activity May occur during trauma

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Hypertensive Intracerebral Hemmorrhage

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  1. Hypertensive Intracerebral Hemmorrhage Gerry Dunlap, MS3 Fall 2005

  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. 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. 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. Signs/ Symptoms • Neurological signs present depend on location of hemorrhage

  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. Cerebellar Inability to walk Vomiting Headache, possibly referred to neck or shoulder Neck Stiffness Gaze palsy Facial weakness Location

  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. 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. 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. 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. 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. 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. 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. 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. 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. 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. 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. 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. 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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