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1 Approximately 70-80% of all strokes are ischemic and 20-30% are hemorrhagic Hemorrhagic stroke is defined as an acute neurologic injury resulting from bleeding in the brain There are two distinct types of hemorrhagic stroke: intracerebral hemorrhage (ICH) and subarachnoid hemorrhage (SAH).

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3 SAH accounts for 3-5% of all strokes. Classically the patient experiences the worst headache of his or her life. One in 5 patients report a less severe headache in the hours or days preceding the event. The event may be accompanied by focal neurologic signs, nausea/vomiting, loss of consciousness, seizure.

4 The most common cause of spontaneous SAH is the rupture of a cerebral aneurysm, accounting for about 85% of SAHs. Aneurysms tend to occur at the branch points of cerebral vessels. The 30-day mortality is in the range of 33 to 45%.

5 Cerebral aneurysms are present in about 2% of the population Overall the annual risk of rupture is about 0.7% Rupture risk is related to aneurysm size and location. The risk of rupture increases significantly for aneurysms greater than 7 mm in diameter and for those arising from the posterior communicating arteries or posterior circulation.

6 80-85% of aneurysms are located in the anterior circulation, commonly at the origins of the posterior or anterior communicating arteries or the middle cerebral artery bifurcation. Posterior circulation aneurysms most often occur at the basilar tip or posterior-inferior cerebellar artery origin.

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8 The factors that strongly influence outcome after SAH can be divided into patient factors, aneurysm factors and institutional factors. Of the patient factors, by far the most important determinant is the deleterious effect of acute SAH on the brain documented by the worst Hunt and Hess Grade.

9 Hunt and Hess Grade Grade 1: Asymptomatic or mild headache and slight nuchal rigidity Grade 2: Moderate to severe headache, stiff neck, no neurologic deficit except cranial nerve palsy Grade 3: Drowsy or confused, mild focal neurologic deficit Grade 4: Stupor, moderate or severe hemiparesis Grade 5: Deep coma, decerebrate posturing

10 Other patient factors include age and medical comorbidities, such as hypertension, atrial fibrillation, congestive heart failure, coronary heart disease, and renal disease. Vasospasm severity, re-hemorrhage, and acute hydrocephalus are also significantly related to outcome. Aneurysm factors include size and location in the posterior circulation.

11 Institutional factors include the availability of endovascular services and the volume of SAH patients treated. With aggressive management of SAH including emergency ventricular drain placement, ultraearly aneurysm repair, multidisciplionary medical care involving intensivists, and endovascular therapies for vasospasm such as selective infusion of intraarterial vasodilators and balloon angioplasty approximately half of Hunt and Hess grade V survivors had cognitive deficits only slightly reduced compared with the normative population mean.

12 Patients with a good cognitive outcome after a severe SAH were significantly younger (median age 46 versus 52 years), had more years of education (13 versus 9 years) and had smaller cerebral ventricular scores.

13 The mainstay of SAH diagnosis is the noncontrast head CT. In the 12 hours after SAH, the sensitivity of CT for SAH is 98% to 100%, declining to 93% after 24 hours and to 57% to 85% after 6 days. Because the diagnostic sensitivity of CT scanning is not 100%, a lumbar puncture should be performed if the clinical presentation is suspicious for a SAH.

14 Cerebral angiography is currently the standard for diagnosing cerebral aneurysm as the cause of SAH

15 The selection of surgery versus coiling depends on several factors including: Aneurysm location Presence of a large hematoma Aneurysm size Aneurysm neck size Patient co-morbidities

16 Intracerebral Hemorrhage (ICH) causes 10-15% of first-ever strokes, with a 30-day mortality rate of 35% to 52%; half of the deaths occur in the first two days. 20% of ICH patients are independent at 6 months.

17 Causes of ICH Cerebral aneurysms Cerebral arteriovenous malformations Cavernous malformations Moya-moya disease Vasculitis Hypertension Amyloid angiopathy Anticoagulants/ antiplatelet agents Recreational drugs Post-infarction Blood dyscrasias Idiopathic *Brain tumors *Unrecognized trauma

18 Hospital admissions for ICH have increased by 18% over the last ten years Increases in the number of elderly people Lack of adequate blood pressure control Increasing use of anticoagulants and antiplatelet agents

19 Rapid recognition and diagnosis of ICH are essential because of its frequently rapid progression during the first several hours. The classic presentation includes the onset of a focal neurologic deficit, which progresses over minutes to hours. This smooth progression of a focal deficit over a few hours is uncommon in ischemic stroke and rare in SAH.

20 Initial CT 2 45 later

21 Brain imaging is a crucial part of the emergent evaluation. CT and MRI have equal ability to identify the presence of acute ICH, its size and location. Indications for cerebral angiography include SAH, abnormal calcifications, obvious vascular abnormalities and isolated intraventricular hemorrhage (IVH).

22 Hypertensive vasculopathy is the most common cause of ICH. The underlying mechanism is related to the effects of systemic blood pressure on small penetrating arteries that arise from major intracranial vessels. In response to hypertension, these small vessels can develop intimal hyperplasia, intimal hyalinization and medial degeneration, which predispose them to focal necrosis and rupture.

23 The classic location of hypertensive hemorrhages reflects the territories supplied by these small perforators, with 60-65% in the putamen and internal capsule, 15-25% in the thalamus and 5-10% in the pons.

24 Cerebral amyloid angiopathy (CAA) is another common cause of ICH. Strongly associated with age, rarely seen in patients under 60 years and progressively increases in incidence after the age of 65. CAA is characterized by the deposition of amyloid beta-peptide in the small and medium-sized vessels of the cortex with relative sparing of vessels in the basal ganglia, white matter, and posterior fossa. Affected vessels undergo fibrinoid degeneration, necrosis and microaneurysm formation.

25 CAA-related hemorrhages tend to occur in the cortex causing lobar hemorrhages more often in the temporal and occipital lobes.

26 Treatment of ICH The observation that substantial ongoing bleeding occurred in patients with ICH and was linked to neurological deterioration led to interest in the control of blood pressure and the use of activated factor VII.

27 Guidelines for the Management of Blood Pressure MAP <110 or SBP<160 and >90 for the first hours if no ICP monitor present Keep CPP >70 if ICP monitor present

28 Ongoing trials have reported that aggressive reduction of blood pressure to less than 140 mm Hg probably decreases the rate of hematoma enlargement without increasing adverse events. However, because the effect on clinical outcome has not been fully assessed, the more conservative BP targets should be followed. Caution is advised about lowering blood pressure too aggressively without concomitant management of CPP.

29 Management of ICP in ICH The European Stroke Initiative (EUSI) guidelines recommend monitoring of intracranial pressure for patients who need mechanical ventilation. Both the American Stroke Association (ASA) and EUSI recommend selective use of mannitol, hypertensive saline and short-term hyperventilation to maintain the CPP>70.

30 With increasing use of warfarin, oral anticoagulation (OAC) associated ICH represents an increasing proportion (up to 17%) of ICH cases and carries a very high mortality (up to 67%). No matter what the indication for warfarin, the benefits of initial reversal after ICH always outweigh the risks of stopping OAC.

31 Warfarin doubles ICH mortality Warfarin increases risk of hematoma expansion (OR 6.22) Hematoma expansion occurs over more prolonged time course

32 Reversal of Anticoagulation An INR of 1.4 in any ICH patient should be considered life-threatening. Guidelines from US, UK and Australia recommend Prothrombin complex concentrate (PCC) Vitamin K Fresh Frozen Plasma

33 Vitamin K promotes endogenous clotting factor synthesis but takes 6h to have an effect. PCC has several advantages over FFP including no need for thawing or compatibility testing, smaller volumes and higher factor IX levels. Although FVIIa can rapidly correct the INR, it does not replenish all of the vitamin K-dependent factors and therefore, may not restore thrombin generation as well as PCC.

34 Seizures after ICH Incidence is between 4.6% and 8.2%. The routine use of anti-epileptics is not recommended because of uncertainties about their efficacy and outcomes. Subclinical seizures occur is up to 30% of patients after ICH. Continuous EEG monitoring should be considered in ICH patients with a decreased level of consciousness that is out of proportion to the amount of brain injury.

35 Venous Thromboembolism Prophylaxis Symptomatic and asymptomatic deep vein thrombosis occurs in 3.7% and 40% of ICH patients respectively. All patients with reduced mobility should have SCDs. Low molecular weight heparin should be introduced 1-4 days after the onset of ICH, once cessation of bleeding has been demonstrated.

36 Management of Blood Glucose Maintain euglycemia as with other critically ill patients (<140 or 150 mg/dl?) Avoid large swings in blood glucose

37 Neurosurgery Surgical Trial in Intracerebral Hemorrhage (STICH) randomized 1033 patients with supratentorial ICH to surgery within 72 h or to conservative management and demonstrated no outcome benefit from surgery. STITCH II is investigating the outcome of surgery for lobar hematomas <1 cm from the surface or the brain in patients without IVH. Several minimally invasive surgery trials which combine stereotactic guidance of catheters combined with thrombolytic enhanced hematoma evacuation are ongoing.

38 Recommendation for Surgical Approaches Patients with Cerebellar hemorrhage >3cm who are deteriorating neurologically or who have brain stem compression should have surgical removal of the clot.

39 For patients with lobar clots within 1 cm of the surface, evacuation of supratentorial ICH by standard craniotomy should be considered.

40 Ventricular drainage should be considered in all stuporous or comatose patients with intraventricular hemorrhage and acute hydrocephalus.

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42 Prognosis of ICH 60% of patients with an ICH Score of 0, 50% with an ICH score of 1, 15% with an ICH score of 2, 10% with an ICH score of 3 have a modified Rankin score (mrs) of 1 or 2 at 12 months.

43 In summary, the prevention of clot expansion is the best way of improving outcomes from ICH. The most effective way of preventing ICH is blood pressure control and avoiding over anticoagulation. THANK YOU