Stroke (cerebrovascular accident CVA) MUDr Petra Reková doc. MUDr Jiří Bauer, CSc

Transkript

1 1 Stroke (cerebrovascular accident CVA) MUDr Petra Reková doc. MUDr Jiří Bauer, CSc

2 2 Stroke - definition Rapidly developing clinical signs of focal and sometimes general disruption of brain function of central origin. i.e. clinical, laboratory or basic neuroimaging examination doesn t indicate other than vascular cause of neurological deficit

3 3 Stroke - causes Disturbance in blood supply to certain brain area or to the whole brain (ischemic cerebrovascular accident - icva) 80-85% Bleeding into the brain tissue (intracerebral hemorrhage) or to subarachnoid space (subarachnoid hemorrhage - SAH) 15-20% icva ICH SAH

4 4 Stroke - epidemiology Incidence: 300/ inhabitants of Czech republic per year, age-dependent disease Mortality: the second most common cause of total mortality lethal cases per year in CR icva 1/3 of affected people die within 12 months ICH 2/3 of patients die within 6 months SAH 1/2 of patients die within 3 months Disability

5 Ischemic cerebrovascular accidents (icva) 5

6 6 icva etiopathogenesis 1/5 Normal condition: perfusion ml/100g of brain tissue/min.

7 7 icva etiopathogenesis 2/5 Oligemia: perfusion ml/100g of brain tissue/min. compensatory dilatation of arterioles, enhanced extraction of oxygen and glucose in brain capillaries clinically asymptomatic Syndrome of emergency perfusion: perfusion ml/100 g of brain tissue/min. compensatory dilatation of arterioles, enhanced extraction of oxygen and glucose in brain capillaries, aerobic metabolism is continually replaced by anaerobic metabolism clinically asymptomatic

8 8 icva - etiopathogenesis 3/5 Ischemic penumbra: perfusion less than 20 ml/100g but more than ml/100g of brain tissue/min compensatory mechanisms are not sufficient disruption of neuronal functions development of clinical symptomatology, damage still reversible Cerebral infarction: perfusion less than ml/100g of brain tissue/min compensatory mechanisms fail both functional and structural disruption of neurons development of necrosis clinical symptomatology is persistent, damage irreversible

9 9 icva - etiopathogenesis 4/5 normal condition oligemia syndrome of emergency perfusion ischemic penumbra cerebral infarction

10 10 icmp - etiopathogenesis 5/5 Regional: failure of cerebral perfusion in the territory of affected artery thrombosis embolism Global: failure of cerebral perfusion in the whole brain (cardiac arrest, cardiac failure, global hypoxia)

11 11 icva - classification 1/4 Classification of icva according to time course transient ischemic attack (TIA) reversible ischemic neurological deficit (RIND) completed stroke progressing stroke

12 12 icva - classification 2/4 Classification of icva according to localization of affected artery: anterior circulation carotid territory posterior circulation vertebrobasilar territory

13 13 icva - classification 3/4 Classification of icmp according to the cause: disease of large blood vessels (macroangiopathy) 40-50% of icva magistral cerebropetal arteries; atherothrombotic process disease of small vessels (microangiopathy) 20% of icva small perforating arteries arising from the circle of Willis and from major stems of cerebral arteries; lipohyalinosis, fibrinoid necrosis, atherosclerosis

14 14 icva - classification 4/4 Classification of icva according to the cause: cardioembolic stroke 20% of icva embolism from the heart heart diseases accompanied by formation of thrombi in the left atrium or ventricle; defects of cardial septum with paradoxical embolism other specified causes of stroke 5% of icva disorders of blood coagulation, migrainous infarction other non-specified causes of stroke 5-15% of icva

15 15 icva clinical picture 1/5 Clinical picture variable localization, extent, quickness of ischemia onset, compensatory mechanisms, general condition of affected individual

16 16 icva clinical picture 2/5 A: regional ischemic lesions 1. Carotid territory: the first most common symptom: contralateral hemiparesis with more pronounced disability of upper limb speech disorder if dominant hemisphere is affected neglect syndrome if nondominant hemisphere is affected middle cerebral artery

17 17 icva clinical picture 3/5 Contralateral hemiparesis with more pronounced disability of lower limb, without speech disorder anterior cerebral artery. Multiple focal lesions of cortico-subcortical areas multiinfarct dementia.

18 18 icva clinical picture 4/5 A: regional ischemic lesions 2. Vertebrobasilar territory: supratentorial contralateral homonymous hemianopsia with preserved central vision; cortical blindness (bilateral lesion) posterior cerebral artery

19 19 icmp clinical picture 4/5 infratentorial alternating hemipareses dissociated sensory disturbances vestibular syndrome oculomotor dysfunctions dysarthria disturbances in swallowing, hoarseness, hiccup, locked-in syndrome (severe global movement dysfunction with preserved vigilance and sensitivity) basilar artery

20 20 icva clinical picture 5/5 B: global hypoxic-ischemic brain injury less severe damage combination of symptoms from various arterial territories severe damage disturbed consciousness; with prolonged duration apalic syndrome arrest of brain circulation for 5 and more minutes cerebral death

21 21 icva - diagnosis 1/8 1. Medical history 2. Clinical picture differential diagnosis: tumors, abscesses, Todd s paresis after epileptic seizure, migraine with aura, hypoglycemia, myasthenia gravis (brainstem lesions) 3. Urgent laboratory examination biochemistry, complete blood count, coagulation parameters 4. Imaging techniques

22 22 icmp - diagnosis 2/8 Imaging techniques computer tomography CT) method of choice Acute stage Acute stage: often negative (important to search early signs of ischemia) Acute and subacute stage: altered density (hypodensity) in the ischemic region, cerebral edema After 24 hours Chronic stage: hypodensity in the region of past ischemia

23 23 icva - diagnosis 3/8 Imaging techniques CT visualization of vascular bed CT angiography

24 24 icva - diagnosis 4/8 Imaging techniques CT evaluation of cerebral perfusion - perfusion CT enables discrimination between infarction and penumbra

25 25 icva - diagnosis 5/8 Imaging techniques magnetic resonance (magnetic resonance imaging, MRI) - evaluation of perfusion and diffusion disturbances discrimination between infarction and penumbra zone resonance angiography (MRA) visualisation of brain vessels without necessity of contrast agent MRI detects ischemic lesion sooner and more precisely than CT X availiability, high time and financial demands, contraindications

26 26 icva - diagnosis 6/8 Imaging techniques digital subtraction angiography (DSA) computer processing of angiographic findings, morphological assessment of vascular bed with demonstration of stenoses, occlusions, aneurysms and other vascular anomalies The most precise visualization of vascular bed x invasive

27 27 icva - diagnosis 7/8 Imaging techniques Sonography (extracranial cerebropetal arteries, intracranial cerebral arteries major stems) Detection of stenoses, occlusions, dissected arteries, character and extent of atherosclerotic damage Special ultrasonographic techniques (microembolization, cerebrovascular reserve, rightto-left shunt)

28 28 icva - diagnosis 8/8 Imaging techniques echocardiography transthoracic, transesophageal: evaluation of anatomical, functional and hemodynamic conditions in the heart and ascending aorta

29 29 icva - therapy 1/11 Emergent condition treatment as soon as possible (the sooner treatment begun, the better the results), stroke centre, stroke team, individualization of treatment 1. Total intensive early therapy including psychotherapy, rehabilitation, logopedic support 2. Recanalization 3. Treatment and prevention of secondary brain damage 4. Surgical interventions 5. Early prevention 6. Therapeutic hypothermia experimental method

30 30 icva - therapy 2/11 1. Total intensive therapy stabilization of vital functions prevention of complications (particularly prevention of bronchopneumonia, pulmonary embolism, deep vein thrombosis, decubitus ulcers) ensuring sufficient cerebral perfusion in early stages of stroke (tolerance of BP values 220/120 mmhg) treatment of hyperpyrexia, hyperglycemia, reactive depression care of the gastrointestinal system (nutrition, stability of internal environment) intensive rehabilitation logopedic support psychotherapy

31 31 icva - therapy 3/11 2. Recanalization: aim to restore arterial blood flow as fast as possible carotid territory - to 4,5 hours after occurence of first symptoms basilar artery no limitation (as soon as possible)

32 32 icva - therapy 4/11 2. Recanalization A: thrombolytic therapy tissue plasminogen activator (rtpa, alteplase, Actilyse) intravenously, intraarterially, in a combined manner 30% without deficit or with mild functional disability potentiation with help of ultrasound application sonothrombolysis zevní komorová drenáž

33 33 icva - therapy 5/11 2. Recanalization B: intervention procedures percutaneous transluminal angioplasty stents mechanical extraction of blood clot thrombectomy with use of aspiration techniques up to 8 hours from the first symptoms of stroke X available only in highly specialized centres

34 34 icva - therapy 6/11 2. Recanalization C: surgical interventions emergency carotid artery desobliteration

35 35 icva - therapy 7/11 3. Treatment and prevention of secondary injury of CNS slowdown of further development and suppression of progression of ischemic brain damage neuroprotective therapy (studies) antioedematic therapy drainage position of body, sedation, osmotherapy, decompressive craniectomy

36 36 icva - therapy 8/11 4. Surgical procedures decompressive craniectomy emergent carotid artery desobliteration cerebellar ischemia (craniectomy, resection of infarcted tissue, external ventricular drainage)

37 37 icva therapy 9/11 Primary prevention complex of measures aiming at minimalization of infarction risk A: elimination of modifiable risk factors arterial hypertension heart disease with high potential of embolism diabetes mellitus hyperlipidemia stenosing processes in cerebropetal arteries lifestyle regimen (no smoking, moderate consumption of alcohol, weight reduction, adequate amount of physical activity)

38 38 icva - therapy 10/11 Secondary prevention complex of measures aiming at reduction of risk of stroke recurrence A: elimination of risk factors, suppresion of development of endothelial dysfunction, lifestyle regimen B: antiplatelet therapy in all patients, except from patients with high risk of cardioembolism acetylsalicylic acid, combination of acetylsalicylic acid with slow-release dipyridamol, clopidogrel C: anticoagulation therapy atrial fibrillations, conditions after myocardial infarction with evidence for blood clots in left-sided heart compartments, artificial valves warfarin

39 39 icva - therapy 11/11 D: surgical and endovascular interventions carotid endarterectomy (considered in case of stenosis of more than 50%) percutaneous transluminal angioplasty, stent various reconstruction procedures

40 Hemorrhagic strokes (intracranial hemorrhage - ICH) 40

41 41 ICH - etiopathogenesis 1/3 rupture of vascular wall in some of cerebral vessels rarely of venous origin

42 42 ICH etiopathogenesis 2/3 1. Anatomical abnormalities: local damage to vascular wall (atherosclerosis, lipohyalinosis, fibrinoid necrosis) lower resistance to intraarterial pressure small aneurysms deposition of amyloid into the vascular wall vascular anomalies (arteriovenous malformations, cavernous angiomas, venous angiomas) ischemic lesion of vascular wall hemorrhagic transformation of infarction focus

43 43 ICH etiopathogenesis 3/3 2. Hemodynamic abnormalities: long-term or short-term increase in blood pressure 3. Disorders of blood coagulation diseases (hemophilia) rather rare iatrogenic genesis consequence of anticoagulation or thrombolytic therapy, rarely of antiplatelet medication

44 44 ICH - klasifikace 1. Typical hemorrhage: central regions of cerebral hemispheres, less frequently brainstem or cerebellum 80% hypertension 2. Atypical (lobar, globose) hemorrhages: more superficially subcortical location 20% rupture of vascular anomaly, amyloid angiopathy in higher age

45 45 ICH clinical picture 1/2 Clinical picture variable cause, location, size, quickness of ICH generation, compensatory mechanisms, overall condition of an affected individual Typical hemorrhages: combination of focal symptoms with intracranial hypertension, common fast progression to comatous state unfavorable prognosis, high mortality Lobar hemorrhages: focal symptomatology in the foreground, focal epileptic seizure at the beginning in 1/3 of patients more favourable prognosis

46 46 ICH clinical picture 2/2 Cerebellar hemorrhage: sudden headache, nausea, vomiting, gait and balance disorders with development of homolateral neocerebellar and vestibular symptomatology serious clinical condition (!) Brainstem hemorrhage: brainstem symptomatology according to localization of bleeding mostly life-limiting prognosis

47 47 ICH diagnosis 1/3 1. Medical history 2. Clinical picture differential diagnosis: tumors, abscesses, Todd s paresis after epileptic seizure, migraine with aura, hypoglycemia, myasthenia gravis (brainstem lesions) 3. Urgent laboratory examination biochemistry, complete blood count, coagulation parameters 4. Imaging techniques

48 48 ICH diagnosis 2/3 Imaging technigues computer tomography (CT examination) acute stage: visualization of hemorrhage immediately after its outburst Magnetic resonance - detects well degradation products of hemoglobin enables recognition of age of hemorrhagic focus. As a novel function, MR allows to detect acute bleeding as well.

49 49 ICH - diagnosis 3/3 Imaging techniques CT angiography diagnostics of aneurysms, arteriovenous malformations and other vascular anomalies rezonance angiography (MRA) technique of choice in diagnostics of anomalies with low blood flow (cavernomas) X difficulties with availability, more time-demanding in comparison to CT, more financially demanding, several contraindications

50 50 ICH therapy 1/4 Emergent condition stroke centre, stroke team, individualization of therapy 1. Total intensive early therapy including psychotherapy, rehabilitation and logopedic care 2. Suppression of hemorrhage progression 3. Treatment and prevention of secondary brain damage

51 51 ICH therapy 2/4 1. total intensive care stabilization of vital functions, prevention of complications, ensuring sufficient cerebral perfusion, therapy of hyperpyrexia, hyperglycemia, care of the gastrointestinal systém, nutrition, stability of internal environment, prevention of deep vein thrombosis, prevention of decubitus ulcers, treatment of reactive depression rehabilitation psychotherapy logopedic support

52 52 ICH therapy 3/4 2. suppression of hemorrhage progression progression of bleeding approximately in 1/3 of patients (particularly in association with anticoagulation treatment, coagulopathy) Lowering of mean arterial pressure under 130 mm Hg (hypertensive patients) under 105 mm Hg (normotensive patients) Acceleration of blood coagulum formation administration of plasmatic coagulation factors (frosen plasm) concentrate of plasmatic factors II, VII, IX, X (Prothromplex) always with vitamin K

53 53 ICH therapy 4/4 3. Treatment and prevention of secondary brain damage pressure of hematoma toxicity of degradation products development of brain oedema surgical removal of hematoma (only specific situations cerebellar hemorrhage, lobar hemorrhage) antioedematic therapy

54 54 ICH - prevention Prevention treatment of hypertension lifestyle regimen no smoking, no drugs of abuse, moderate consumption of alcohol controls of anticoagulation treatment

55 Subarachnoidal hemorrhage (SAH) 55

56 56 SAH - definition Intrusion of blood into leptomeningeal space, i.e. space between pia mater and arachnoid mater. Bleeding not only into external CSF space (i.e. basal cisterns, brain sulci), but concomitantly with intracerebral and intraventricular hemorrhage as well (the latter sometimes separatedly). Subarachnoidal hemorrhage (SAH) 5% of all CVA.

57 57 SAH - etiopathogenesis rupture of aneurysm of arteries in the Circle of Willis bleeding from arteriovenous malformation bleeding from dural malformation traumatic SAH

58 58 SAH - aneurysms 1/2 Prevalence of aneurysms in the Circle of Willis and in arteries that arise from the circle - 1-5% of population. Higher prevalence in patients with polycystic kidney disease, Marfan syndrome, Ehler-Danlos syndrome; cases with familial incidence. Yearly risk of the first rupture 1-2%.

59 59 SAH - aneurysms 2/2 Localization Most frequently - anterior communicating artery Characteristics solitary, in 20-30% of cases multiplex, of variable size (mm - cm) various shapes (sacciform, fusiform, dissecting)

60 60 SAH clinical symptoms 1/3 Headache with typical sudden onset (within a second or several seconds), of cruel severity, in variable location Nausea, vomiting Meningeal syndrome upper meningeal syndrome develops within tens of minutes or several hours, lower meningeal syndrome develops longer, may be absent)

61 61 SAH clinical symptoms 2/3 Disturbances of consciousness quantitative (from somnolence to coma) qualitative (disorientation, agitation, aggressiveness, confusion) Pareses of cranial nerves of oculomotor nerve (aneurysma of posterior communicating artery), multiple (if basilar artery affected) Focal neurological symptoms in case of intracerebral propagation of SAH Acute lethal cases 5% of patients die before hospitalization

62 62 SAH clinical symptoms 3/3 Clinical picture scale for evaluation of SAH by Hunt and Hess Grade Clinical picture 0 Aneurysm that hasn t bled I. Mild headache, slight nuchal rigidity, without focal symptoms II. III. IV. Moderate to severe headache, nuchal rigidity, paresis of cranial nerve, with no other focal symptoms Disturbance of consciousness (somnolence, confusion), focal neurological symptoms Severe disturbance of consciousness (stupor, coma), hemiparesis V. Coma, decerebrate symptoms

63 63 SAH diagnosis 1/2 1. Medical history and clinical picture diff. dg. blockage of cervical spine, cervicocranial syndrome, coital headache, migraine, neuroinfection, acute psychosis, intoxication, primary thunderclap headache 2. Imaging and laboratory examination CT of brain within the first 24 hours - 95%-98% sensitivity (MRI of brain age of hemorrhage) Lumbar puncture and examination of cerebrospinal fluid (spectrophotometry!) to exclude false negativity

64 64 SAH - diagnosis 2/2 Imaging and laboratory examination Angiography (DSA, MRA, CTA) to identify the cause of SAH. Source of bleeding not demonstrated in 30% of SAH. Repeated angiography after 3-6 weeks = demonstration of source in other 10-20% of patients.

65 65 SAH - complications 1/2 Relapse of hemorrhage 20-30% of patients in the first 30 days mortality 60-70%, the first day 5%, 2nd-30th day: 1-2% / per day clinical picture: sudden loss of consciousness diagnostics: CT of brain therapy: urgent operation

66 66 SAH - complications 2/2 Vasospasms onset: 3rd-5th day, maximum 5th-14th day, subsiding within 2 4 weeks clinics: emotional flattening, bradypsychism, prefrontal symptoms, focal symptoms diagnostics: TCD, TCCS therapy: 3H (hypertension, hypervolemia, hemodilution), nimodipine Hydrocephalus acute obstructive CT of brain, external ventricular drainage hyporesorptive CT of brain, ventriculoperitoneal shunt

67 67 SAH - therapy 1/2 According to clinical condition (Hunt-Hess), findings from neuroimaging examination, character of bleeding source and its localization: 1. Conservative therapy 2. Surgical and endovascular interventions 3. Treatment of complications

68 68 SAH - therapy 1/2 1. Conservative therapy A: total intensive care (constipation, cough, stress - diet with crude fiber, laxatives, mucolytic medication, analgesics, anxiolytics, hypnotics) B: bed rest (optimal duration not known)

69 69 SAH - therapy 2/2 2. Surgical and endovascular interventions early - within 72 hours x delayed open (clipping) x endovascular (coiling) 3. Treatment of complications

70 70 Case report, questions

71 Case report, questions 68-year-old female patient transferred to hospital by ambulance on March 14th, 2011, at 5 p.m. Medical history: PMH: hypertension, diabetes mellitus (on a diet) Abuse: 15 cigarettes per day for 40 years HPI: on March 14, 2011, at 12.30, she felt sudden weakness of right upper limb while working in the garden. At the same time, she wasn t able to express what she wanted. She waited approximately 4 hours in hope that difficulties may disappear spontaneously. However, symptoms persisted, so she called an ambulance. 71

72 72 Case report, questions Objective findings: Neurological: central paresis of n.vii on the right, right-sided hemiparesis with more pronounced disability of right upper limb, mild phatic disorder. Somatic: BP 220/100, HR 90/min. regular. Obesity BMI 35, without any other abnormalities.

73 73 Case report, questions Questions: 1. Is this stroke? a) yes b) no c) can t be told for sure, not enough data

74 74 Case report, questions We will complete laboratory examination + imaging technique Questions: 2. Which imaging technique shall we use? a) urgent MR angiography of brain b) RTG of head c) urgent CT of brain

75 75 Case report, questions The result of imaging technique (on the right). Question: 3. Could it be stroke? a) yes, it is ischemic stroke b) yes, it is ICH c) it is probably SAH without finding on CT, it is necessary to perform LP

76 76 Case report, questions 5 hours passed from onset of symptoms to acquisition of all necessary tests (laboratory, clinical, imaging). Questions: 4. If there are no other contraindications, shall we use intravenous thrombolysis as treatment for this patient? a) yes, thrombolytic time window is 6,0 hours b) no, thrombolytic time window is 4,5 hours c) no, management of a patient was delayed by calling an ambulance

77 77 Case report, questions Time is brain!

78 78 References Kalita Z et al. Akutní cévní mozkové příhody. Praha: Jesenius Maxdorf Kalvach P et al. Mozkové ischemie a hemoragie. 3. vydání. Praha: Grada Publishing a.s BauerJ, Čéška R. Cévní mozkové příhody. V Čéška et al. Interna. Praha: Triton Warlow CP, Denis MS, van Gijn J, Hankey GL, Sandercoock PA, Bambord JM et al. Stroke, a practical guide to management. 2nd ed. Oxford: Blackwell Science The European Stroke Organisation (ESO) Executive Committee and the ESO Writing Committee. Guidelines for management of ischaemic stroke and transient ischaemic attack Cerebrovasc dis 2008; 25(5): Morgenstern LB, Hemphill JC jr, Anderson C, Becker K, Broderick JP, Connolly ES et al. Guidelines for the management of spontaneous intracerebral. hemorrhage. A guideline for helthcare professionals from the American Hearth Association/American Stroke Association. Stroke 2010;41(9):

79 79 Stroke (cerebrovascular accidents) THE END