Intracerebral hemorrhage (ICH) =Hemorrhagic stroke Non-traumatic intracerebral haemorrhage Spontaneous bleeding into the brain tissue ICH: CT HIGHLIGHTS ◼ ICH, although less common than ischemic stroke, is the major cause of stroke mortality and there is not yet a definitive therapy beyond supportive care. ◼ Early stabilization of acute ICH involves identifying and treating the cause(s) of decreased alertness, aggressively correcting blood pressure, and reversing any coagulopathy. ◼ Long-term management of ICH requires correctly identifying the underlying etiology and, when possible, correcting it. Causes Spontaneous intracerebral bleeds The second most common cause of stroke Accounting for 20% of hospital admissions for stroke High blood pressure raises the risk of spontaneous intracerebral hemorrhage by two to six times Other causes Head trauma • Penetrating head trauma • Depressed skull fractures • Acceleration-deceleration trauma Rupture of an aneurysm or arteriovenous malformation (AVM) Bleeding within a tumor A very small proportion is due to cerebral venous sinus thrombosis. Weakness, sensory disorder Contralaterally Blurred visoin Speech disorders Acute headache Vertigo, dizziness Signs and symptoms ICH 10-20% of strokes High blood pressure 72- 81% Reduction of DBP (5, 7,5, 10 mm Hg) results to reduction of ICH (34%, 46%, 56%) Treatment of systolic HT in elderly is connected with 36% reduction of ICH. Risk factors • TKS 160 mm Hg or TKD 110 mm Hg • RR 5.55 (95% CI 3.07 to 10.0) Study ARIC 15 792 pts • gender, smoking, drinking, BMI, waist cirkumference, diabetes Other risk possible factors • Smoking • Risk factor for lobar ICH only • Diabetes Swedish study 2006 Risk factors ◼ ASA ◼ Epistaxis ◼ Anticoagulation ◼ Warfarin / DOAC ◼ 2% of treated patiens ◼ Risk of bleeding 8- 11x Hypolipidemics ◼ Thrombolysis ◼ 6,4% Pathophysiology ◼ Chronic hypertension produces a small vessel vasculopathy characterized by lipohyalinosis, fibrinoid necrosis, and development of Charcot-Bouchard aneurysms, affecting penetrating arteries Localisation of ICH among pts with HBP ◼ 40- 50% Putamen ◼ 20% Lobar ◼ 15% Thalamus ◼ 8% Cerebellum ◼ 8% Pons ◼ 8% Nucleus caudatus ICH: CT Brain-stem haemorrhage A-V Malformation ICH: mortality and prognosis Overall mortality 25%- 50% • Size and localisation • thalamus, cerebellum, ponsworse prognosis • Level of consciousness • Coma at admission: 64% mortality Prognostic factors ICH: Indication for surgery ◼ Haematoma < 20 ml: good prognosis regardless of therapy. ◼ Haematoma > 60 ml: bad prognosis regardless of therapy. ◼ Surgical treatment ◼ Cerebellar ICH. ◼ Gradual decrease of the level of the consciousness (haematoma > 20 ml). Subarachnoideal haemorage SAH Incidence of aneurysmatic SAH 6/100 000/year Etiology 85% spontaneous bleeding from the ruptured aneurysma SAH: aneurysm A1 SAH- diagnosis ◼ Acute headache ◼ Instantaneous severe headache, development during 1 min. lasting at least 1 hour. History of unusually severe headache that started suddenly. ◼ Absence of the neck stiffness doesn’t exclude SAH ! ◼ Takes hours to develop and in some cases it is not present during whole course ◼ Loss of consciousness 50% pts. ◼ 40% headache and meningism only. ◼ SAH can be present in patient without ◼ Meningeal signs ◼ Focal signs and symptoms ◼ Loss of consciousness ◼ Should be SAH considered (and excluded) in all patients with acute (explosive) headache ? ◼ YES SAH- diagnosis ◼ Thunderclap headache only ◼ SAH 12% ◼ Risk of ruptured aneurysm 6%. ◼ CT+CSF negative ◼ SAH excluded and angiography not indicated ◼ Distribution of blood on CT scan can predict the absence of the aneurysm and vice versa CT imaging: metod of first choice ◼ 199 pts with the ruptured aneurysm- CT during first 12 h. negative only in 2 persons. ◼ During first 6 h. (0.2) ◼ Delayed examination – decreased sensitivity ◼ If CT negative, LP indicated ◼ Spinal tap should be postpone at least 12 h. (xanthochromia= hemoglobin degradation products) ◼ Discrimination of the artificial bleeding and hemorrhage due to SAH is visually not possible. ◼ The reliable method is spectrophotometry ◼ Test of three tubes doesn’t exclude SAH ◼ Finding of erytrophages confirms SAH ◼ 12 h. after bleeding is xanthochromia present in all cases and lasts 2 weeks. SAH: CT • Bleeding due to ruptured aneurysm85% • Non-aneurysmatic perimesencefalic bleeding10% • Other5% • Among newborn never found, very rare in childhood • Hereditary predisposition exists: pts with positive familial history are younger, have more frequently multiple aneurysms or aneurysms on ACM Aneurysm is not inborn How many people has aneurysm? All 2.7% 60 6.2% 40-60 3.7% Size of the aneurysm- annual risk of bleeding • 3-4% 10-25 mm • 0,5% and less  10 mm AcoA 41% ACI 31% ACM 18% Post. 10% Localisation of ruptured aneurysms Severity scale Hunt and Hess SAH: fusiform aneurysm SAH: aneurysm PICA SAH: aneurysm VB SAH: 3 aneurysms (MRA) Prognosis of aneurysmatic SAH 50% patients die 50% of the survivors have severe disability 8-17% die before admission to hospital Treatment Timing of treatment Risk of repeated bleeding 1. day 20% 1. m 40% from survivors 50% cummulative risk 4 w- 6 m gradual decrease from 1-2%/d to constant final 3%/y Treatment Diagnosis as soon as possible Fast localisation of the aneurysm(s) Clipping or coilling Coilling Main complications Acute hydrocephalus • Transient ventricular catheter • Permanent VP shunt Cerebral ischaemia • Vasospasms • Nimodipin (prevention) • 3H (therapy) AV malformation • AVM is usually congenital • Discovered by autopsy • During treatment of an unrelated disorder Abnormal connection between arteries and veins bypassing the capillary system • The annual detection of the symptomatic AVMs is approximately 1 per 100,000 / year (Netherlands, Minnesota) • The prevalence in adults was approximately 1,4% (autoptic study) How many of people affected with brain AVM are asymptomatic ??? Signs and symptoms Headache Seizures Pulsing noise in the head Focal signs • progressive weakness Bleeding AVM: clinical manifestation ◼ Bleeding (< 3 cm) 42% ◼ Annual risk of bleeding 2- 4% ◼ Bleeding ◼ 18% mortality ◼ 60% of survivors have no or minimal deficit ◼ Epileptic seazures (>3 cm) 25% ◼ Focal deficit (ischaemia) 10% Diagnostic work-up ◼ CT ◼ MR ◼ Angiography ◼ X rays (calcifications) Treatment ◼ Treatment depends on the location and size of the AVM and whether there is bleeding or not. ◼ Sudden bleeding ◼ Restoration of vital functions ◼ Anticonvulsant medications to control seizure ◼ Medications or procedures to relieve intracranial pressure ◼ Preventive treatment of as yet unruptured brain AVM ◼ Controversial results ◼ Several studies suggested favorable long-term outcome for unruptured AVM patients not undergoing intervention. Spetzler-Martin grade AVM size Adjacent eloquent cortex Draining veins Under 3 cm = 1 Non-eloquent = 0 Superficial only = 0 3–6 cm = 2 Eloquent = 1 Deep veins = 1 Over 6 cm = 3 Eloquent cortex = removed will result in loss of sensory processing or linguistic ability, minor paralysis, or paralysis. The risk of post-surgical neurological deficit (difficulty with language, motor weakness, vision loss) increases with increasing Spetzler-Martin grade AV malformation: DSA AV malformation: after operation AVM: treatment possibilities ◼ Resection ◼ Craniotomy ◼ Embolisation ◼ Radiologically guided catheter ◼ Radiation surgery ◼ Gamma knife The goal: Total occlusion of AVM Take home message High blood pressure is main risk factor for ICH Surgical therapy of ICH is controversial CT scan is diagnostic procedure of choice within firrst 12 hours with 98% of accuracy SAH: Gold standard is LP, should be postpone at least 12 hours Take home message 2 Sudden headache, SAH should be considered and excluded Non-ruptured aneurysm- risk of bleeding depends on size Silent AVM- therapy is controversial