Intra Cerebral Hemorrhage

Intra Cerebral hemorihage * hemorrhage within brain parynchema. * afprimally 10-30% of all strokes * spontaneous (16 trauma) with matality 30-40% * 12-15 /100 600 - Etrology → Primary → HTN 80% i 3 Amyloid angiopathy Secondary → Vascular, Tumors, Inf, Ifammatery, Hematdogy, Drag - Risk Pactors raging * > 55 y - male HTN-A use of medication & Drugs - Previous CVA (23 x times) life style & stress - liver disens - anticoagulant medications - it affect small 8, medium size arteries → liponyalinesis (medial degeneration, fragmentation, necrosis) *micro anuresm (harcot - Bouchard amunesns) Causing ICH. * occlusion causes lacunar infarction * Clinical presentationg * Typically has an Acute oncet (minutes) = TIA like symptoms - Headach - Sudden once of Pecal neurological delicit - altered level of conscicusness 30% - Seizure. - Signs of 1 ICP (headach, nausia as vomiting , * Transient acute oncet with Rapid prognession * Rapidly or slowly progressive ancet (haunes) - specific symptoms depend on location of ICH out come Dependons age s neurolgial status of presendation CS 8 or less location of hemorrhage, size of Hematoma. Prognosis: - 30d mortality 44% mostly due te cerebral herniation - Rebleeding 2-6%, and higher in poorly controlled HTN Investigations: - lab → coagulation profile - IT scan (hyperdense leision) - CT angiogram → If yourg, sAH - MRI / MRA - Cerebral angiogram → if associated aneungsm or AVMS manegment. medical * Control BP 8 ICP * - Intubale if GCS <9 (prevent hypoxemia » hyper carbia) (shost period hyperventilation) - sedation Surgi can to for deterrating Loc A External ventricular Drain for intraventricular hemorrhage and hydrocephalus - ICP monitoring (should be < 20) (CP should be > 60) Graindtomy & Evacuation - lobar (temporal) - Cerebellar - other location medical & surgic therapy has Same autome. As 25% Deteriation from hemavema expansion in 24 h Novo seven (Recombinant activated Facter 7 ) (Rebleeding) Siren with in he limit Rebleding by 50%, Improve outcome. SE → Systemic Inrombosks Subarachnoid hemorchage * Bleeding into subarachnoid Stace (intracramal vessels between arachnoid & pia) - Peak age 55€60 , but 20% of cases under age 45 y. - Etidlogy: trauma MC * → Spontaneus: - Ruptured Anurysm 60% * = coagulapathtes - AV M 20% - HTN, atherescelerosis, tumors, int, bload dyscara - unknown 10%. IRF: HHTN, Pregnancy with eclampsia or AVM, OCP, substance abuse s smoking " (o% Anurysm? is Dilation of an artory that results from a weakening of inner muscular layer (intima) of blood vessel wall. Due to unknown Cause Cerebral Anarysm in 1% of population, peak at 5th decade Mc in female - unknoun but RF& HTN, smoking, Congenital, Polyaste Kidreans - natural History unruptured anangesm * Ruptured Anurgsm SAlt occure in 1-2% per year. - 4% in 24 h - 1% Perday fer 2 w - 50% at 4 - 6 m - Back to 1-21 per year clinical presentation s → = Death > ½ * Loc 8 neurological defiat > → headach (worse headach in therr life ) (sudden) N/V , photophobia breit Loc neck pain & rigidity → meningismus (Ve Kerning &, brudzinski) Crainal neuropathy (CN' 3,4) , occular hemarshague complications: Vasospasm, hydrocephalus, neurogenu pulmonaly elema, hyponadimia Diabètes insicides a Cardiac arihetumia, MI, CHF, Death Disabilites Investigations → Blood in cistren fissure of brain * CT Scan: Can show SAH 90% (Đ WH 201, ICH 20%, 5DH 2% hydiccephalus 15% , anungsm 5% Can be -ve in 10% * Lumbar functune) only in -ve CT 8s highly suspicion meningitis. → tve: Blood I rantrachromia (yellow) → Problem → Rebleeding Cerebral angrography gold standard for anungs *MRA - CTA.) Risk RIo 4% in fust day Conservative Prevent Rebleding, - R/0 15-20% in 2 w Yout - 02 s ventilation, 11P0, bed rest, elevale heud, Vitals monitors ECG, foley * Improve BP 8 hydiate → aim BP = 120-150 (No hypotension) "analgesics - Nimodifine (Cerebral Vosadialator, Improve CBF) - seizure prophylatic anurysm: Endovascular therapy s clpping of anurysm Prognoss: 50% mortality (within 1st 2-3 weeks) 30% Arteriovenous Malformation Cavernous Malformations Dural Fistulas Definition Tangle of abnormal vessels/ arteriovenous shunts, with no Benign vascular hamartome consisting of irregular sinusoidal Fistulas connecting dural arteries to dural veins or the dural sinus intervening capillary beds or brain parenchyma; usually congenital vascular channels located within the brain without intervening Frequently described to occur at the transverse and cavernous sinuses. neural tissue or associated large arteries/ veins Etiology Several genes now described (COM1, COM2, COM3) Hypothesized to be related to venous sinus thrombosis formation, Unknown true incidence and subsequent microvascular shunt formation within the dura between arteries and veins Epidemiology Prevalence -0.14%, M:F = 2:1, average age at diagnosis = 33 yr Prevalence of 0.1-0.2%, both sporadic and hereditary forms described Unknown true incidence 15-20% of patients with hereditary hemorrhagic telangiectasia Constitute 10-15% of all intracranial vascular abnormalities (Osler-Weber-Rendu syndrome) will have cerebral AVMs Clinical Features Hemorrhage (40-60%): small AVMs are more likely to bleed due to Seizures (60%), progressive neurological deficit (50%) Asymptomatic, pulsatile tinnitus if involving sigmoid or transverse sinuses, bruits, headache. direct high pressure AV connections hemorrhage (20%), H/A Carotid cavernous involvement classically produces proptosis, Seizures (50%): more common with larger AVMs Often an incidental finding chemosis, and bruits. Mass effect Hemorrhage risk less than AVM, usually minor bleeds Symptoms of SAH, SDH, or ICH Focal neurological signs secondary to ischemia (high flow → "steal phenomena") Localized headache, increased ICP Bruit (especially with dural AVMs) May be asymptomatic ("silent") Investigations MRI (flow-void), MRA 72WW MRI (non-enhancing) gradient echo sequencing (best for diagnosis) Non-enhanced CT to r/o hemorrhage Angiography (7% will also have one or more associated aneurysms) MRI; however, this does not demonstrate the arterial supply to the fistula Angiography remains the gold standard Treatment Decreases risk of future hemorrhage and seizure Surgical excision Approach is dependent on size, location and symptoms, and includes: Surgical excision is treatment of choice Only appropriate for asymptomatic lesions that are surgically accessible Conservative treatment (supratentorial lesions are less likely to bleed than infratentorial lesions) Neuroradiological endovascular interventions SRS (stereotactic radiosurgery) is preferred for small (<3 cm) or very deep lesions Radiation therapy Endovascular embolization (glue, balloon) can be curative (5%) or used as adjuvant to surgery or SRS in larger lesions Combination of the above Conservative (e.g. palliative embolization, seizure control if necessary) Prognosis 10% mortality, 30-50% morbidity (serious neurological deficit) per bleed 8.1% annual risk of hemorrhage 6.9% annual risk for non-hemorrhagic neurological deficit Risk of major bleed in untreated AVMs: 2-4% per year 10.4% mortality rate