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Intracranial Hemorrhage

Intracranial Hemorrhage. Presentation by: Dr. Ebrahim asheghi. ICH by numbers. Result of a rupture of blood vessel in the brain Accounts for 10-15% of all cerebrovascular accidents 2 million strokes every year worldwide Rise of admissions in the past 10 years by 18%

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Intracranial Hemorrhage

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  1. Intracranial Hemorrhage Presentation by: Dr. Ebrahimasheghi

  2. ICH by numbers • Result of a rupture of blood vessel in the brain • Accounts for 10-15% of all cerebrovascular accidents • 2 million strokes every year worldwide • Rise of admissions in the past 10 years by 18% • Prognosis is poor: estimated mortality • 30% at 7 days • 60% at 1 year • 82% at 10 years • >90% at 16 years

  3. Outline • Intracranial hemorrhage • Mechanism and pathophysiology • Clinical features • Management principles

  4. Mechanisms of ICH • Hypertension • Vascular malformations • Intracranial tumors • Bleeding diathesis, anticoagulation, fibrinolysis • Cerebral amyloid angiopathy • Granulomatous angiitis & vasculitides • Sympathomimetic agents (amphetamine, cocaine) • Hemorrhagic infarction • Trauma

  5. Clinical features • Features of intracranial hypertension • Headache, vomiting, decreased LOC • Correlated with hematoma size and prognosis • Progressive over time • Seizures in lobar ICH • Focal neurological deficits depending on the location of ICH

  6. POP QUIZ When are patients most likely to suffer from primary ICH? • Midnight (excessive partying…) • 8 AM (don’t want to go to work) • Noon (excessive hunger) • 5 PM (too much excitement from ending work)

  7. POP QUIZ When are patients most likely to suffer from primary ICH? • Midnight (excessive partying…) • 8 AM (don’t want to go to work) • Noon (excessive hunger) • 5 PM (too much excitement from ending work)

  8. Hypertension and ICH • Most important risk factor (>70% of 1ry ICH) • Bifurcation of small penetrating arteries (50–700 μm diameter) • Atherosclerosis • Lipid deposition, layering of platelet and fibrin aggregates, breakage of elastic lamina, atrophy and fragmentation of smooth muscle, dissections, and granular or vesicular cellular degeneration • Charcot and Bouchard aneurysm • Fibrinoid necrosis of the subendothelium  focal dilatations  rupture of microaneurysm

  9. N Engl J Med 2001;344(19):1450–1460

  10. Lobar hemorrhage 25% • Penetrating cortical branches of ACA, MCA, & PCA • Peripheral location  lower frequency of coma • Lower mortality • Better functional outcome N Engl J Med 2001;344(19):1450–1460

  11. Basal ganglia 35-40% • Ascending lenticulostriate branches of MCA • Wide spectrum of severity extending to coma and decerebrate rigidity • Ventricular extension carries very poor prognosis N Engl J Med 2001;344(19):1450–1460

  12. Thalamus 10-15% • Ascending thalamogeniculate branches of PCA • Abrupt hydrocephalus from aqueductal obstruction from intraventricular clot • Responds to ventriculostomy N Engl J Med 2001;344(19):1450–1460

  13. Pons 5% • Paramedian branches of the basilar artery • Bilateral carries very poor prognosis (coma, quadriplegia, decerebrate posturing, horizontal ophthalmoplegia, pinpoint reactive pupils) N Engl J Med 2001;344(19):1450–1460

  14. Cerebellum 5-10% • Penetrating branches of the PICA, AICA, SCA • Abrupt onset vertigo, h/a, n/v, inability to walk in absence of weakness • Ipsilateral ataxia, horizontal gaze palsy, peripheral facial palsy • Unpredictable deterioration to coma N Engl J Med 2001;344(19):1450–1460

  15. Vascular malformations • Aneurysms, AVM, cavernous angiomas • Younger, female patients, familial history • Imaging may show concurrent SAH • Dx by MRI and cerebral angiography • Usually supratentorial, lobar ICH • Cavernous angioma: on MRI (T2) central nidus of irregular bright signal mixed with mottled hypointensity, surrounded by peripheral hypointense ring

  16. Vascular malformations

  17. Intracranial tumour • Accounts for 10% of cases • GBM or metastases (melanoma, bronchogenic carcinoma, renal cell carcinoma) • Suggestive features: • Papilledema • Atypical location (e.g. corpus callosum) • Disproportionate amount of surrounding edema • Multiple sites simultaneously • Non-contrast CT: ring of high-density hemorrhage with low-density center • Contrast CT/MRI: presence of enhancing nodules

  18. Management principles • A-B-C: Airway support • Decreased level of consciousness • Bulbar muscle dysfunction • Blood pressure control • Acute hemostatic treatment • Anticoagulation reversal • Intracranial pressure control • Monitoring • Neurological and cardiovascular deterioration greatest in the 24hours following symptom onset

  19. Blood pressure & ICH • BP is elevated on admission even in patients who have no history of hypertension • MAP > 120mmHg in over 2/3 of patients • Precipitant of the hemorrhage? • Reflection of chronic hypertension? • Attempt to maintain CPP? • Sympathetic activation 2ry to pain & anxiety? • Tends to return to baseline 7-10 days post ICH

  20. Acute management of BP Cerebral autoregulatory curve CPP = MAP – ICP

  21. PROs  BP associated with poor outcome  risk of hematoma enlargement  edema formation Systemic damage (e.g. ongoing cardiac ischemia) CONs Chronic HTN shifts cerebral autoregulatory curve to the right  ICP may require  BP to maintain CPP Previously thought to induce ischemic damage to the at risk penumbra Acute management of BP

  22. Edema & ischemic penumbra? • Up to 75% increase in volume in the first 24 hours • Peaks around 5 to 6 days and lasts up to 14 days • Early large edema relative to hematoma is a predictor of poor outcome • Hibernation phase • Mitochondrial dysfunction causing hypometabolism • Regional hypoperfusion 2ry hypometabolism • Usually not severe enough to cause ischemia • Global cerebral ischemia • Very elevated ICP and low cerebral perfusion pressure

  23. Acute management of BP • Baseline blood pressure • Age • Presumed cause of hemorrhage (ruptured aneurysm or AVM?) • Elevated intracranial pressure • How fast should BP be lowered? • Rapidly lowering MAP by  15% does not lower CBF • Reductions of 20% can affect CBF • Current guidelines suggest a reduction of ≤ 20% in the first 24 hrs • Which agents should be used? • Short and rapidly acting IV antihypertensive • Labetalol, hydralazine, esmolol, nicardipine, enalapril • Sodium nitroprusside and nitroglycerin should be used with caution d/t vasodilation and potential effect on ICP

  24. Acute management of BP • ASA Guidelines 2007 (Class IIb, Level C) • sBP>200 mmHg or MAP>150 mmHg • Aggressive BP control with IV infusion and BP monitoring q5minutes • sBP>180 mmHg or MAP>130 mmHg WITH elevated ICP • Consider monitoring ICP • Intermittent bolus or continuous infusion to aim for CPP > 60-80 mmHg • sBP>180 mmHg or MAP>130 mm Hg WITHOUT elevated ICP • Consider modest BP reduction of blood pressure with intermittent bolus or continuous infusion • Aim for MAP of 110 mmHg or BP of 160/90 mmHg

  25. Hematoma expansion • Hematoma enlargement • >70% have hematoma enlargement w/in 3 hrs of symptom onset; 1/3 clinically significant • Most occur within 3 hrs, can be up to 12 hrs • Independent predictor of worse outcome &  mortality

  26. Hematoma expansion Journal of the Neurological Sciences 261 (2007) 99–107

  27. Recombinant Factor VIIa • Factor VIIa has locally action at sites of tissue injury and vascular-wall disruption by binding tissue factor & generating thrombin and activating platelets • Recombinant FVIIa directly activates fX on the surface of activated plts resulting in acceleration of coagulation • Factor Seven for Acute Hemorrhagic Stroke (FAST) trial, N Engl J Med 2008;358:2127-37 • 841 patients, within 4 hours of onset of stroke • Placebo vs. 20 μg/kg vs. 80 μg/kg of rFVIIa • 1ry end point: 90-day functional outcome or death

  28. Recombinant Factor VIIa • Significant reduction in growth of hematoma volume in the 80 μg/kg group • No significant difference in functional outcome and mortality • Venous thromboembolic events were similar in all three groups • Arterial thromboembolic events were significantly more frequent in the 80 μg/kg group

  29. ABC of hematoma size • Broderick, JP et al. Stroke 1993;24:987-993 • 1.26 million subjects from Greater Cincinnati

  30. ABC of hematoma size • Bedside ABC/2 method for hemorrhage volume in cm3 1. Identify the CT slice with the largest area of hemorrhage 2. Measure the largest diameter of the hemorrhage on this slice (A) 3. Measure the largest diameter 90° to (A) on the same slice (B) 4. Approximate number of 10-mm slices on which the ICH was seen was calculated (C) • If area > 75% compared to where the hemorrhage was largest, the slice was considered 1 hemorrhage slice • If area 25% to 75%, the slice was considered 1/2 a slice • If area < 25%, the slice was not considered a slice • A, B, and C were then multiplied and the product divided by 2

  31. CT-A “Spot Sign” • Focal area of enhancement within the hematoma on CTA have been shown to be: • Independent predictor of hematoma expansion • Associated with longer median hospital stay • Independent of time to presentation • Sensitivity 91%, specificity 89%, NPV 96%

  32. CT-A “Spot Sign” • Recent proposal of a “Spot Sign” definition (Can J Neurol Sci 2009;36:456-461) • Serpiginous and/or spot-like appearance • Within the margin of the parenchymal hematoma without connection to an outside vessel • >1.5mm diameter in maximal axial dimention • >Double the HU density compared to background hematoma (>150 HU) • Multiple or single in number • Comparison to unenhanced CT for mimickers • Calcifications (tumour, choroid, infectious, etc)

  33. Anticoagulation associated ICH • Warfarin is a Vit K antagonist • Inhibits biosynthesis of factors II, VII, IX, X • Maximum effect is 48 hrs after administration • Incidence of ICH is 0.3-0.6% per year in patients on chronic warfarin anticoagulation • Risk factors • Age, chronic hypertension, CAA, leukoaraiosis • Elevation of INR (doubled risk for 0.5  above 4.5!) • INR correlated with hematoma expansion and prognosis

  34. Anticoagulation associated ICH • Goal of treatment: fully reverse INR to normal range • High dose Vitamin K 10-20 mg IV slow infusion • Effect takes 12-24hrs • Helps achieving sustained reversal of INR • Fresh frozen plasma 15cc/kg  4U • Volume overload, insufficient factor IX • ABO compatibility, thawing, infusion time (30hrs) • Prothrombin Complex Concentrates (PCC, Octaplex) • Combination of II, VII, IX, X, variable protein C and S • Dosage dependant on initial INR • Smaller volume, correct INR as fast as 30 min

  35. Anticoagulation associated ICH • ICH associated with IV heparin • Rapidly normalize activated partial thromboplastin time • Protamine sulfate 1 mg per 100 U heparin, adjusted for time since last heparin dose • 30-60 min: 0.5 to 0.75 mg per 100U heparin • 60-120 min: 0.375 to 0.5 mg per 100 U heparin • >120min: 0.25 to 0.375 mg per 100 U heparin • Slow IV injection (<5 mg/min, max dose 50 mg) • Beware of systemic hypotension

  36. AAICH – restarting anticoagulation • 1% recurrent ICH in initial 3 mths post ICH • Risk estimated to double with anticoagulation Stroke. 2007;38:2001-2023

  37. Miscellaneous • Venous thromboembolism prophylaxis • Intermittent pneumatic compression • Heparin SQ prophylaxis (3-4 d if no bleeding) • IVC filter (proximal venous thrombosis) • Hyperglycemia • Associated with poor outcome and  mortality • Marker of outcome or contributor? • Hyperpyrexia • Associated with poor outcome and neuro deterioration • Septic workup, treat with antipyretics or cooling devices • Often central in origin

  38. Thank you

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