Epidemiologic features Incidence 10~20 cases per 100,000 Increases with age Men, especially older than 55 years old Blacks and Japanese Hypertension.

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Presentation transcript:

Epidemiologic features Incidence 10~20 cases per 100,000 Increases with age Men, especially older than 55 years old Blacks and Japanese Hypertension  the most important !

Cerebral Hemorrhage Up to 50%, 30 day mortality Little effective therapy

ICH – Worse Outcomes Than Ischemic Stroke 100% Independent 90% Dependent 80% 70% 60% 50% 40% Dead 30% ICH accounts for 10% to 15% of all strokes and is associated with the highest mortality and morbidity.1 The worldwide incidence of ICH ranges from 10 to 20 cases per 100,000 population.2 Between 35% and 52% of patients with ICH die within 1 month of symptom onset,3-5 and only 20% are functionally independent at 6 months.5 American Heart Association. Heart Disease and Stroke Statistics–2005 Update. Qureshi AI et al. N Engl J Med. 2001;344:1450-1460. Broderick JP et al. J Neurosurg. 1993;78:188-191. Anderson CS et al. J Neurol Neurosurg Psychiatry. 1994;57:936-940. Counsell C et al. Cerebrovasc Dis. 1995;5:26-34. 20% 10% 0% ICH Ischemic 1. American Heart Association. Heart Disease and Stroke Statistics-2005 Update; 2. Qureshi AI. et al. N Engl J Med. 2001;344:1450-1460; 3. Broderick JP. et al. Stroke. 1999;30:905-915; 4. Broderick JP. et al. N Engl J Med. 1992;326:733-736

These structures include the Thalamus Deep intracerebral hemorrhage is a type of stroke due to bleeding within the deep structures of the brain. These structures include the Thalamus Basal ganglia Pons Cerebellum.

Sites of Intracerebral Hemorrhage Quereshi et al. N Engl J Med. 2001;344:1450-60

Hypertensive Intracerebral Hem: Sites 55% 15 10 1. Putamen-Claustrum 2. Cerebral white matter 3. Thalamus 4. Pons 5. Cerebellum

Stroke Evolution Both ischemic stroke and hemorrhagic stroke are dynamic, evolving conditions Shown on serial imaging studies with CT, MRI and PET This changing pathophysiology results in increased lesion volume and worse outcome Therapies aimed at limiting stroke growth

Hematoma Growth Hematomas expand on serial CT 38% <24 hours Continued bleeding or rebleeding Adverse prognosis Silva et al. Stroke. 2005

Adverse Prognostic Factors Old age Large hematoma volume Hematoma growth & increase with time Low GCS Intraventricular bleeding or extension Infratentorial site

Hemorrhage and Volume Expect good recovery for small volume less than 10 ml Mortality 90% for comatose patients with large volume more than 60 ml

Hematoma Growth 3 hours

9 hours

6.5 hours after onset 2.0 hours after onset

Symptoms Change level of consciousness Apathetic Lethargy Sleepiness Stupor Coma & Unconsciousness *

Headache Nausea or vomiting Hemiplegia or hemiparesis Hemihypesthesia

Diagnosis CT scan infarction or hemorrhage Location and size of the hematoma Presence of ventricular extension Hydrocephalus

Diagnosis Conventional angiography for secondary cause of ICH ( AVM, aneurysm..) MRI, MRA  sensitivity ?

Diagnosis Complete blood count (CBC) & Platelet count Bleeding time Blood clotting tests (Prothrombin time or partial thromboplastin time) Liver function tests & Kidney function tests

Medical Management of Acute ICH

Management Evaluation & management Hyperventilation, Oxygen Head elevation 30 degree

ICH: Cerebral Edema Osmolar therapy High-dose 20% mannitol (1.4 g/kg) results in better ICP control and outcome than lower doses GUIDELINE: Mannitol 20% for patients with increased ICP or symptomatic mass effect Yu YL. et al. Stroke. 1992; 23:967 Cruz J. et al. Neurosurgery. 2002; 51:628

Management Mass effect & intracranial hypertension Hematoma, edema tissue, obstructive hydrocephalus herniation ! Use of hyperventilation and osmotic agent improved the long-term outcome

Management Intensive monitoring of neurologic & cardiovascular status Instability is highest during the first 24 hrs GCS, hourly BP

ICH: Cerebral Edema Dexamethasone No benefit on outcome, but complications (infections and hyperglycemia) are more common STANDARD: No Steroids! Poungvarin N. et al. N Engl J Med. 1987;316:1229 Tellz H. et al. Stroke. 1973;4(4):541-6

ICH: Blood Pressure Management Management of blood pressure Elevation of blood pressure  expansion of hematoma poor outcome !

May ameliorate local edema May limit early hematoma growth BP Reduction Potential benefits: May ameliorate local edema May limit early hematoma growth Potential risk: Aggravation of perilesional ischemia OPTION: Maintain MAP <130 mm Hg Aggressive option: MAP ≤105 mm Hg Broderick et al. Stroke. 1999;30:905

ICH: Blood Pressure Management BP Reduction: preferred IV agents Labetolol or esmolol (b blockers) Nicardipine (CCB) Fenoldopam (dopamine agonist) Best to avoid Nitroprusside Rose J. and Mayer SA. Neurocritical Care. 2004;1:287

ICH: Seizure Prophylaxis Seizure after ICH 10% have generalized tonic-clonic seizures OPTION: Prophylactic phenytoin for 7 days for patients with large (especially lobar) ICH at risk for increased ICP Passero S. et al. Epilepsia. 2002;43:1175

Seizures and recurrent hemorrhage Most seizure  within 24 hrs Anticonvulsants  discontinued after the first month if no seizure. Seizures more than 2 weeks  at risk of further seizure  long-term treatment.

Surgical Management of ICH

Ventricular Drainage Hydrocephalus is an independent predictor of poor outcome External drainage is associated with a 25% improved survival rate U. Of Michigan Stroke Program

Cerebellar Hematoma Can be approached with minor damage Decompression of brain stem Surgical  GCS less than 14, volume > 40 ml

Surgery U. Of Michigan Stroke Program

Goals of Surgery for ICH Prevent herniation Improve functional outcome U. Of Michigan Stroke Program

Prognosis The outlook depends on the size of the hematoma and the amount of brain swelling. Recovery may occur completely, or there may be some permanent loss of brain function. Death is possible, and may quickly occur despite prompt medical treatment. Medications, surgery, or other treatments may have severe side effects.

Complications Hydrocephalus Fluid build-up in the brai Loss of cognitive function & Vision loss Permanent neurological deficit Surgery complications

Subarachnoid Hemorrhage (SAH)

Causes of SAH Rupture of an existing aneurysm 85% anteriorly Especially the anterior communicating artery Aneurismal size often >7mm and Rupture of an AV malformation Trauma Tumor

Physical examination Third-nerve palsy: P-com Sixth-nerve palsy: post. Fossa Bilateral weakness in legs or abulia: A-com Nystagmus or ataxia: post. Fossa Aphasia, hemiparesis: MCA

subhyaloid hemorrhages

Lumbar puncture Hx,PE:(+), CT(-) Xanthochromia: hemoglobin--> oxyhemoglobin (reddish pink) bilirubin (yellow): 12 hr centrifuged--> spectrophotometry Sensitivity: (12hr~2wk)

Angiography Gold standard Sources: 80-85%

Initial Management Monitor closely for signs of raised ICP Intubated (if not already) Hyperventilated Mannitol Surgery (clips/coils/drains)

Neurologic complication Rebleeding Hydrocephalus Vasospasm/ Ischemia Seizures Cerebral edema