Neurologie AVC (Partea II)

5/19/2018 Neurologie AVC (Partea II)

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A cerebral hemorrhage can take several forms:

Intracerebral hemorrhages. This is bleeding inside the brain.The symptoms and prognosis of an intracerebral bleedvary depending on the size and location of the bleed.

Subarachnoid hemorrhages. This is bleeding between thebrain and the membranes that cover the brain.

Subdural hemorrhages. This is bleeding between the layers

of the brain's covering the meninges!.

"pidural hemorrhages. This is bleeding between the skull andthe covering of the brain.

INTRACRANIAL HEMORRHAGE


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#ausesThere are several causes of bleeding inside the skull$ including:

%ead in&uries. or people under the age of ()$ this is the mostcommon cause of hemorrhage inside the skull. In the elderly$subdural hematoma after relatively minor head in&ury is notuncommon.

Arteriovenous malformation A*+!. This is an anatomical abnormalityin the arteries or veins in or around the brain. Such an abnormalitymay be present from birth$ but it is only detected if symptomsdevelop. Symptoms resulting from bleeding of an A*+ vary$depending on size and location.

Aneurysm. This is a weakening in a blood vessel wall that swells. Thethin walls of an aneurysm can burst and cause bleeding into thesubarachnoid space and the brain$ leading to hemorrhagic stroke.

%ypertension. ,oorly controlled hypertension over a long period oftime can weaken blood vessel walls



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Primary (Hypertensive) Intracerebral Hemorra!e

This is the common$ well-known spontaneous brainhemorrhage. It is due predominantly to chronichypertension and degenerative changes in cerebralarteries. In recent decades$ with increased awareness ofthe need to control blood pressure$ the proportion of casesattributable to hypertension has been greatly reduced/more than one-third such hemorrhages are innormotensives$ and the hemorrhages more often than

previously arise in locations that are not typical forhypertension. 0evertheless$ the hypertensive cerebralhemorrhage serves as a paradigm for understanding andmanaging all the other types.



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Most Common "ites an# "o$rces o% IntracerebralHemorra!e.

Intracerebralemorra!esmost commonlyinvolve cerebral

lobes& ori!inatin!%rom'

penetratin!cortical branceso% te anterior&mi##le& or

posterior cerebralarteries (A)

basal !an!lia&ori!inatin! %romascen#in!lentic$lostriatebrances o% te

mi##le cerebralartery ()

te talam$s&

ori!inatin! %romascen#in!talmo!enic$latebrances o% teposterior cerebralartery(C)

te pons& ori!inatin!

%rom parame#ian brances o% te basilar artery(*)

an# tecerebell$m&ori!inatin! %rompenetratin!brances o% teposterior

in%erior& anteriorin%erior& ors$perior cerebellararteries(E)+


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The bleeding occurswithin brain tissue$

and rupture ofarteries lying in thesubarachnoid spaceis practically unknownapart from aneurysm.The e1travasationforms a roughlycircular or oval massthat disrupts thetissue and grows involume as thebleeding continues.


An unenhanced #T scan showing the typical picture of a massive primaryhypertensive! hemorrhage in the basal ganglia. The third ventricle and opposite

lateral ventricle are compressed and displaced by the e1panding mass 23 h after

onset of stro,e!.


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Pato!enesis The nature of thehypertensive vascular lesion thatleads to arterial rupture is not fully

known$ but in the few cases studiedby serial sections$ the hemorrhageappeared to arise from an arterialwall altered by the effects ofhypertension$ i.e.$ the change

referred to in a preceding sectionas segmental lipohyalinosis andthe false aneurysmmicroaneurysm! of #harcot-4ouchard. 5oss 5ussell has

affirmed the relationship of theseaneurysms to hypertension andhypertensive hemorrhage$ andtheir fre6uent localization onpenetrating small arteries andarterioles of the basal ganglia$thalamus$ pons$ and subcortical



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Clinical Pict$re 7f all the cerebrovascular diseases$

brain hemorrhage is the most dramatic and fromancient times has been surrounded by an aura ofmystery and inevitability. It has been given its ownname$ apople1y. The prototype is an obese$plethoric$ hypertensive male who$ while sane andsound$ falls senseless to the ground - impervious toshouts$ shaking$ and pinching - breathes stertorously$and dies in a few hours. A massive blood clot escapesfrom the brain as it is removed postmortem. 8ith

smaller hemorrhages$ the clinical picture conformsmore closely to the usual temporal profile of a stro,e$i.e.$ an abrupt onset of symptoms that evolvegradually and steadily over minutes$ hours$ or a day

or two$ depending on the size of the ruptured arteryand the speed of bleeding.



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Laboratory -in#in!s+ Among laboratory methods for thediagnosis of intracerebral hemorrhage$ the #T scan

occupies the foremost position. This procedure has provedtotally reliable in the detection of hemorrhages that are 2.)cm or more in diameter. Smaller pontine hemorrhages arevisualized with less certainty. The #T scan is particularly

useful in the diagnosis of brain hemorrhages that do notspill blood into the #S and were heretofore clinicallyunrecognizable. At the same time$ coe1istinghydrocephalus$ tumor$ cerebral swelling$ and displacementof the intracranial contents are readily appreciated. +5I is

particularly useful for demonstrating brainstemhemorrhages and residual hemorrhages$ which remainvisible long after they can no longer be seen by the #Tscan after 9 to ( weeks!. %emosiderin and iron pigment

have their own characteristic appearances$ as describedearlier.



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Treatment+ The general medical management of the

comatose patient with intracerebral hemorrhage is thesame as that of patients with ischemic or embolicinfarction. The management of patients with largeintracerebral hemorrhages and coma includes themaintenance of ade6uate ventilation$ use of controlledhyperventilation to a ,#73 of 3( to ) mm%g$ monitoringof intracranial pressure and its control by the use oftissue-dehydrating agents such as mannitol osmolalitykept at 3;( to )( mosmol


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Treatment 5apid reduction in blood pressure$ in the hope of

reducing further bleeding$ is not recommended$ since itrisks compromising cerebral perfusion in cases of raisedintracranial pressure. 7n the other hand$ sustained meanblood pressures of greater than 22) mm%g maye1aggerate cerebral edema and risk further bleeding. It isat appro1imately this level of acute hypertension that theuse of beta-blocking esmolol$ labetalol!$ or angiotensin-converting enzyme inhibitory drugs is recommended.

>iuretics are helpful in combination with any of the

antihypertensive medications. +ore rapidly acting andtitratable agents such as nitroprusside may be used ine1treme situations$ recognizing that they may further raiseintracranial pressure.



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Treatment Surgical removal of the clot in the acute

stage$ either by evacuation or aspiration$ mayoccasionally be lifesaving$ and we have referrednumerous patients$ in whom hemispheral hemorrhageswere more than cm in diameter and whose clinicalstate was deteriorating$ for surgical treatment. The mostsuccessful surgical results have been in patients withlobar or putaminal hemorrhages. Although selectedpatients may be saved from progression to brain death$the underlying focal neurologic deficit is not altered.

+oreover$ even this degree of success re6uires thatoperation be carried out before or very soon after comasupervenes. 7nce the patient becomes deeplycomatose$ with dilated fi1ed pupils$ the chances of

recovery are negligible.



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Al!oritm %or te Mana!ement o% Intracerebral Hemorra!e+


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This is the fourth mostfre6uent

cerebrovasculardisorder - followingatherothrombosis$embolism$ and primaryintracerebralhemorrhage. Saccular

aneurysms are alsocalled berryaneurysms$ as theytake the form of small$thin-walled blistersprotruding from arteries

of the circle of 8illis orits ma&or branches.Their rupture causes aflooding of thesubarachnoid space byblood under highpressure. As a rule$ the


"pontaneo$s "$baracnoi# Hemorra!e (R$pt$re# "acc$lar Ane$rysm)

The principal sites of saccular aneurysms.Appro1imately ;) percent of aneurysms are

on the anterior half of the circle of 8illis.


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Clinical Pict$re ,rior to rupture$ saccular aneurysms are usually

asymptomatic. "1ceptionally$ if sufficiently large to compress pain-sensitive structures$ they may cause localized cranial pain. 8ith acavernous or anterolaterally situated aneurysm on the first part of themiddle cerebral artery$ the pain may be localized to the orbit. Ananeurysm on the posterior-inferior or anterior-inferior cerebellar artery

may cause unilateral occipital or cervical pain. The presence of a partialoculomotor palsy with dilated pupil may be indicative of an aneurysm ofthe posterior communicating-internal carotid &unction rarely posteriorcommunicating-posterior cerebral &unction!. 7ccasionally$ largeaneurysms &ust anterior to the cavernous sinus may compress the optic

nerves or chiasm$ third nerve$ hypothalamus$ or pituitary gland. In thecavernous sinus they may compress the third$ fourth$ or si1th nerves$ orthe ophthalmic division of the fifth nerve. A monocular visual field defectmay also develop with a supraclinoid aneurysm near the anterior andmiddle cerebral bifurcation or the ophthalmic-carotid bifurcation.




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In summary, the clinical sequence of sudden severe headache, collapse, relativepreservation of consciousness with a paucity of lateralizing signs, and neckstiffness is diagnostic of subarachnoid hemorrhage due to a ruptured saccularaneurysm.Almost all patients are hypertensive for one or several days following the bleed$but preceding hypertension is not more common than in the general population.=evels of 3)) mm%g systolic are seen occasionally &ust after rupture but usuallythe pressure is elevated only moderately and fluctuates with the degree of headpain. Spontaneous intracranial bleeding with normal blood pressure shouldalways suggest ruptured aneurysm or arteriovenous malformation$ a bleedingdiathesis$ and$ rarely$ hemorrhage into a cerebral tumor. 0uchal rigidity is usuallypresent but occasionally absent$ and the main complaint of pain may be referableto the interscapular region or even the low back rather than to the head.

"1amination of the fundi fre6uently reveals smooth-surfaced$ sharply outlinedcollections of blood that cover the retinal vessels?the so-called preretinal orsubhyaloid hemorrhages/ 5oth spots are seen occasionally. 4ilateral 4abinskisigns are found in the first few days following rupture. ever to ;@# may be seenin the first week. 5arely$ escaping blood enters the subdural space and producesa hematoma$ evacuation of which may be lifesaving.


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Laboratory -in#in!s A #T scan will detectblood locally or diffusely in the subarachnoidspaces or within the brain or ventricularsystem. This should be the initial investigativeprocedure$ since it confirms a subarachnoidhemorrhage in more than ;( percent of cases.The blood may appear as a subtle shadowalong the tentorium$ difficult to distinguish fromthe veins in this area$ or in the sylvian orad&acent fissures. A large localized collection ofsubarachnoid blood may indicate the locationof the aneurysm and the region of subse6uentvasospasm as already noted. 8hen two or

more aneurysms are visualized byarteriography$ the #T scan may identify the onethat had ruptured by the clot that surrounds it.Also$ a coe1istent hydrocephalus will bedemonstrable. If the #T scan documentssubarachnoid blood with certainty$ a spinal tap

is not necessary.

4lood fills the subarachnoidspace over the cerebralhemispheres as well asentering the sulci and

interhemispheric fissure.


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Laboratory -in#in!s In all other cases a lumbar puncture should beundertaken when the clinical features suggest a subarachnoid hemorrhage.sually the #S is grossly bloody$ with 54# counts up to 2 million per cubicmillimeter or even higher. 8ith a relatively mild hemorrhage$ there may beonly a few thousand cells. It is unlikely that an aneurysm can rupture entirelyinto brain tissue without some leakage of blood into the subarachnoid fluid$so that the diagnosis of ruptured saccular aneurysm by lumbar puncture!cannot be confirmed unless blood is present in the #S. sually deep1anthochromia is found after centrifugation if several hours have elapsed.#arotid and vertebral angiography is the only certain means ofdemonstrating an aneurysm and does so in some B( percent of patients inwhom the correct diagnosis of spontaneous subarachnoid hemorrhage ismade on clinical grounds. +5I and +5A detect most aneurysms of the basal

vessels but are as yet of insufficient sensitivity to replace conventionalangiography.


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Treatment This is influenced by the neurologic and general medical state ofthe patient as well as by the location and morphology of the aneurysm.Ideally$ all patients should have the aneurysmal sac surgically obliterated$but the mortality is high if the patient is stuporous or comatose grade I* or*$ see below!. 4efore deciding on a course of action$ it has been useful toassess the patient with reference to the widely employed scale introduced by4otterell and by %unt and %ess$ as follows:

Crade I. Asymptomatic or with slight headache and stiff neck

Crade II. +oderate to severe headache and nuchal rigidity but no focal orlateralizing neurologic signs

Crade III. >rowsiness$ confusion$ and mild focal deficitCrade I*. ,ersistent stupor or semicoma$ early decerebrate rigidity andvegetative disturbances

Crade *. >eep coma and decerebrate rigidity.


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Treatment The general medical management in the acute

stage includes the following$ in all or part: bed rest$ fluidadministration to maintain above-normal circulating volumeand venous pressure$ use of elastic stockings and stoolsofteners/ administration of propranolol$ intravenousnitroprusside$ or other medication - to reduce greatly elevatedblood pressure and then maintain systolic blood pressure at2() mm%g or less/ and pain-relieving medication forheadache this alone will often reduce the hypertension!. Theprevention of systemic venous thrombosis is critical$ usually

through the use of cyclically inflated whole leg compressionboots. The use of anticonvulsants is controversial/ manyneurosurgeons administer them early$ with a view ofpreventing a seizure-induced risk of rebleeding. 8e have

generally avoided them unless a seizure has occurred.


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Treatment #alcium channel blockers are being used e1tensively to reducethe incidence of stro,efrom vasospasm. 0imodipine$ D) mg administeredorally every 9 h$ is currently favored. Although calcium channel blockers donot alter the incidence of angiographically demonstrated vasospasm$ theyhave reduced the number of strokes in each of five randomized studies.,atients with stupor or coma who have massive hydrocephalus often benefitfrom decompression of the ventricular system. This is accomplished initiallyby e1ternal drainage and may re6uire permanent shunting if thehydrocephalus returns. The risk of infection of the e1ternal shunt tubing ishigh if it is left in place for much more than days.The timing of surgery for grade III patients is still controversial$ but if theirgeneral medical condition allows$ they probably also benefit from the sameaggressive approach. In grade I* patients$ the outcome is generally dismal$

no matter what course is taken$ but we have usually avoided early operation.The insertion of ventricular drains into both frontal horns has occasionallyraised a patient with severe hydrocephalus to a better grade and promptedearly operation. In the hands of e1perienced anesthesiologists andcerebrovascular surgeons using microdissection$ the operative mortality$even in grades III and I* patients$ has now been reduced to 3 to percent.


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Treatment

The timing of surgery for grade III patients is stillcontroversial$ but if their general medical condition allows$they probably also benefit from the same aggressiveapproach. In grade I* patients$ the outcome is generallydismal$ no matter what course is taken$ but we have usuallyavoided early operation. The insertion of ventricular drainsinto both frontal horns has occasionally raised a patient withsevere hydrocephalus to a better grade and prompted earlyoperation. In the hands of e1perienced anesthesiologists

and cerebrovascular surgeons using microdissection$ theoperative mortality$ even in grades III and I* patients$ hasnow been reduced to 3 to percent.


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Treatment

The timing of surgery for grade III patients is stillcontroversial$ but if their general medical condition allows$they probably also benefit from the same aggressiveapproach. In grade I* patients$ the outcome is generallydismal$ no matter what course is taken$ but we have usuallyavoided early operation. The insertion of ventricular drainsinto both frontal horns has occasionally raised a patient withsevere hydrocephalus to a better grade and prompted earlyoperation. In the hands of e1perienced anesthesiologists

and cerebrovascular surgeons using microdissection$ theoperative mortality$ even in grades III and I* patients$ hasnow been reduced to 3 to percent.


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Trombosis o% Cerebral .eins an# .eno$s "in$ses

Thrombosis of the venous sinuses$ particularly of the superiorsagittal or lateral sinus$ usually develops in relation to

infections of the ear and paranasal sinuses or to one of thehypercoagulable states.7cclusion of cortical veins that are tributaries of the duralsinuses takes the form of an venous infarctive stro,e.>iagnosis is difficult e1cept in certain clinical settings knownto favor the occurrence of venous thrombosis$ such as thetaking of birth control pills or postpartum and postoperativestates. Anticoagulant therapy beginning with heparin forseveral days$ followed by warfarin$ combined with antibiotics

if the venous occlusion is inflammatory$ has been lifesaving insome cases but the overall mortality rate remains high at 2)to 3) percent$ in part due to large hemorrhagic venousinfarctions. The trial by "inhaupl and colleagues$ however$

has settled the 6uestion in favor of aggressiveanticoagulation.


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Trombosis o% Cerebral .eins an# .eno$s "in$ses

A! Sagittal T2 8I showshyperintense signal inthrombosed superior

longitudinal sinus. 4!A1ial T3 8I showsfrontal bilateral venousinfarcts with hypointensecentral area and

peripheral hyperintensityassociated withperilesional edema. #!

A1ial postgadolinium T28I shows hyperintensity

in the superiorlongitudinal sinus andcortical veins.%emorrhagic infarct withperilesional edema in theleft frontal lobe is seen.

Thrombophlebitis of thesuperior longitudinal sinusand bilateral hemorrhagic

infarct. 32-year-oldwoman with headache$bilateral hemiparesis$ andstupor.


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*I--ERENTIATION O- .A"C/LAR *I"EA"E -ROM OTHER NE/ROLOGICILLNE""E"

The diagnosis of a vascular lesion rests essentially on

recognition of the stro,esyndrome/ without evidence of thisthe diagnosis must always be in doubt. The three criteria bywhich the stro,eis identified should be reemphasized: 2!the temporal profile of the clinical syndrome$ 3! evidence offocal brain disease$ and ! the clinical setting. >efinition of

the temporal profile re6uires a clear history of thepremonitory phenomena$ the mode of onset$ and theevolution of the neurologic disturbance in relation to thepatient's medical status. If these data are lacking$ the stro,e

profile may still be determined by e1tending the period ofobservation for a few days or weeks$ thus invoking theclinical rule that the physician's best diagnostic tool is asecond and third e1amination. An inade6uate history is themost fre6uent cause of diagnostic error.

Pro%ila0ia primar1 (2) E f it t d l d id FG!


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Pro%ila0ia primar1 (2) En conformitate cu gradul de evidenFG!ScopulH prevenirea primului eveniment vascular

Cauze genetice ale AVC ischemicH Jn cazurile pacienFilor cu patologii genetice ce au determinat A*#ul poate fi necesarG

consultaFia geneticianului

H >atele privitor la screening-ul genetic ca profila1ie primarG a A*# sunt insuficiente

Hipertensiunea arterialH Screening-ul sistematic pentru hipertensiunea arterialG cel puFin fiecare 3 ani la adulFi Ki

mai frecvent la vErstnici! Ki managementul adecvat$ inclusiv dieta alimentarG$ modificareastilului de viaFG Ki tratament farmacologic sunt recomandate.

TabagismulH AbFinerea de la tabagism Ki sistarea fumatului la fumGtorii actuali sunt recomandateH "vitarea tabagismului pasiv ca mGsurG de profila1ie a A*#trebuie luatG En consideraFieH tilizarea produselor nicotinice Ki a medicamentelor perorale pentru combaterea

tabagismului trebuie luatG En consideraFie

Diabetul zaharatH TA necesitG strict control atEt En diabet tip 2 cEt Ki tip 3 nivelul recomandat L2)


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Pro%ila0ia primar1 (3)

Fibrilaia atrialH ,acienFilor cu A Ki patologie valvularG cardiacG En special cu proteze de valve! sunt

recomandate anticoagulanteleH

Tratamentul antitrombotic este recomandat pentru profila1ia A*# la pacienFii cu A non-valvularG bazat pe evaluarea riscului absolut$ riscului hemoragiilor Ki accesul pacientului lamonitoring calificat anticoagulant

H 8arfarina I05 3$)-$)! este recomandatG pacienFilor cu risc Enalt M9N risc anual de A*#!Ki pacienFilor cu risc moderat En baza preferinFelor pacientului! cu A care nu aucontraindicaFii clinic semnificative la anticoagulante orale

Alte cauze cardiace

H 8arfarina poate fi administratG pacienFilor cu infarct miocardic cu supradenivelarea S-T KidisfuncFia ventricularG stEngG cu tulburGri regionale e1tinse de motricitate ale miocardului

H 8arfarina poate fi administratG pacienFilor cu disfuncFie severG a ventriculului stEng cu saufGrG insuficienFG cardiacG congestivG

DislipidemiaH ,acienFilor hipertensivi cu risc Enalt$ chiar la valorile normale ale =>=$ este recomandat

tratamentul cu statine Ki modificarea regimului de viaFGH Tratamentul sugerat pentru pacienFii cu valori Enalte de colesterol Ki =>= include scGdereamasei ponderale$ sporirea activitGFii fizice$ sistarea tabagismului$ Ki niacinG sau gemfibrozil

H #u toate cG datele studiilor controlate lipsesc$ la pacienFii cu niveluri ma&orate delipoproteine este recomandatG administrarea niacinei pEnG la 3 mg


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Stenoza carotidian asimptomaticH ,acienFii cu stenozG carotidianG asimptomaticG vor fi evaluaFi pentru depistarea altor factori

de risc Ki tratamentul adecvat al acestora.H

Se recomandG administrarea acidului acetilsalicilic En toate cazurile cu e1cepFia celoraunde este contraindicatGH "ndarterectomia carotidianG profilacticG este recomandatG pacienFilor cu grad sever de

stenozG constatatG. Se va efectua En centrele En care rata mortalitGFii dupG "# nudepGKeKte N

H Selectarea pacienFilor se face En concordanFG cu starea comorbidG Ki pronosticul de viaFGH Angioplastia carotidianG stentul! este alternativG rezonabilG pentru pacienFii cu risc Enalt la

tratament chirurgicalH =uEnd En consideraFie rezultatele periprocedurale Ki la interval de 2 an$ rGmEne neclar care

metodG trebuie efectuatG: endarterectomia sau angioplastia Infecii

H >atele privind recomandarea antibioticoterapiei ca mGsurG de profila1ie a A*# ischemic Enbaza rezultatelor seropozitive pentru un agent patogen sau a combinaFiei de patogeninecesita stratificare minuFioasG.

Terapia hormonal postmenopauzalH ,entru profila1ia primarG a A*# nu este recomandatG terapia hormonalG postmenopauzalG

estrogeni O


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Pro%ila0ia primar1 (5) egimul alimentar !i nutriia

H ,ersoanelor cu hipertensiune arterialG este recomandat scGderea aportului de sodiu Ki sporireaaportului de potasiu pentru scGderea TA

H >ieta recomandatG este bogatG En fructe$ legume$ grGsimi nesaturate Ki limitatG En grGsimi saturate

Acti"itatea fizicH Sporirea activitGFii fizice este asociatG cu scGderea riscului de A*# ischemicH "1erciFii fizice zilnice de intensitate moderatG

#bezitateaH 7bezitatea este definitG prin indice de masG corporalG M )kgacG pacientul este identificat cu probleme de adicFie$ se recomandG tratament specializat

Anticoncepionale oraleH 5iscul de A*# ischemic la administrarea anticoncepFionalelor orale cu doze hormonale mici la femeile

fGrG factori de risc adiFionali$ este &osH 0u sunt recomandate femeilor cu factori de risc adiFionali de e1. tabagism$ evenimente trombembolice

anterioare!H emeile care utilizeazG anticoncepFionale orale Ki au factori de risc adiFionali vor fi tratate agresiv En

vederea combaterii factorilor de risc



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Pro%ila0ia primar1 (6) Tulburri de respiraie $n somn %sforit& (Poate fi una din cauze a unei hipertensiuni rebele)

H "valuarea simptomele de sleepapnoesomnolenFa pe parcursul zilei$ sforGit! Ki Endreptarea pentruconsultaFie la specialist pentru investigaFii.

'igrena

H >atele privind tratamentul specific ce ar reduce riscul de A*# ischemic la femeile cu migrenG$ inclusivmigrena cu aurG$ sunt inconcludente

HiperhomocisteinemiaH aportul zilnic de folaFi 9)) Pg


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Pro%ila0ia primar1 (7)Concl$8ii

Toate persoanele trebuie evaluate Envederea factorilor de risc

ToFi factorii de risc modificabili trebuietrataFi insistent


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Pro%ila0iasec$n#ar1 (2)

ScopulH prevenirea evenimentelor vasculare repetate

Direciile prioritare in profila(ia secundar)H #ontrolul TAH #ontrolul diabetului zaharatH #ori&area dislipidemiei

H Sistarea tabagismuluiH =imitarea consumului de alcoolH 5educerea masei corporaleiureticeO


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Pro%ila0iasec$n#ar1 (3) Hipertensiunea arterial

H Sunt recomandate antihipertensive dupG perioada hiperacutG. #ifrele FintG nu sunt clardefinite$ dar TA normalG este L 23)= L2)) mg


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Pro%ila0iasec$n#ar1(4)

Concluziile pentru pacienii cu patologie cerebro"ascular

H ScGderea nivelului de colesterol cu 2mmol


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Pro%ila0ia sec$n#ar1 (5)

TabagismulH Tuturor pacienFilor cu A*# ischemic sau AIT En anamnezG ce fumeazG se va recomanda

sistarea tabagismului

Consumul de alcoolH Tuturor pacienFilor cu A*# ischemic sau AIT En a anamnezG ce fac abuz de alcool se va

recomanda sistarea consumului de alcool.

,ndarterectomia carotidianH Stenoza carotidianG ipsilateralG severG Q)N-;)N!$ "# este recomandatG

H Stenoza carotidianG ipsilateralG moderatG ()N-D;N! "# este recomandatG En referinFGde vErstG$ se1$ comorbiditGFi Ki severitatea simptomelorH Stenoza L()N nu este indicatG "#

Angioplastia carotidianH A,# este recomandatGH Stenoza MQ)N dificilG pentru intervenFie chirurgicalG

H #ondiFii medicale ce cresc riscul intervenFiei chirurgicale$ sau En cazurile de stenozG saurestenozG dupG "#

H A,# are rata de mortalitate de 9-DN



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Pro%ila0ia sec$n#ar1 (6) Fibrilaie atrial

,acienFilor cu A*# ischemic sau AIT cu fibrilaFie atrialG persitentG sau paro1ismalGeste recomandatG 8arfarina En calitate de anticoagulant nivel I05 FintG 3$( variazG

Entre 3$) Ki $)! ,acienFilor care nu pot administra anticoagulante orale le este recomandatG AA#

3(mg #ombinaFia AA# cu clopidogrelul necesitG vigilenFG En administrare$ deoarece sporeKte

riscul hemoragiilor la pacienFii cu A*# sau AIT> ,acienFilor alergici la AA# este recomandat clopidogrelul



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Pro%ila0iasec$n#ar1(7)

Recoman#1ri c$ nivel #e evi#en91 A

H Tratament antihipertensivH #ontrolul glicemiei pentru a reduce complicaFiile microvasculareH Statine pentru a reduce =>= la L3$D mmol


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Con#$ita pacient$l$i !namnezaecomandri pentru culegerea anamnesticului

,roblema A*#-ului trebuie pe larg mediatizatG cu scopul ca orice persoanG sG recunoascG simptomele dedebut Ki sG apeleze serviciul de urgenFG.

Aceste simptome sunt: SenzaFia bruscG de slGbiciune sau amorFealG En regiunea feFei$ braF$ picior$ En special lateralizatG pe o

parte a corpului #onfuzie subitG$ tulburGri de vorbire Ki EnFelegere >eteriorarea subitG a vederii la unul sau ambii ochi >ificultate subitG de deplasare$ verti&$ tulburGri de coordonare Ki balansare #efalee subitG severG fGrG cauzG evidentG "1amenul medical primar va fi direcFionat pentru depistarea factorilor de risc a patologiei aterosclerotice

sau cardiace$ inclusiv hipertensiunea arterialG$ diabet zaharat$ tabagism$ colesterolemie EnaltG$ bypass

coronarian sau fibrilaFie atrialG. A*# trebuie suspectat la orice pacient cu deficit neurologic acut sau alterarea nivelului de conKtienFG. Simptomele caracteristice pentru A*# includ: %emiplegia sau hemipareza acutG %emianopsie completG sau parFialG >izartrie sau afazie Ata1ie$ verti&$ sau nistagm ScGderea bruscG a nivelului de conKtienFG.

=a pacienFii tineri colectarea anamnesticului va fi direcFionatG spre evidenFierea traumei recente$coagulopatiilor$ utilizarea drogurilor En special cocainG!$ migrenei$ sau anticoncepFionalelor orale.

Stabilirea timpului de debut este crucialG pentru iniFierea terapiei trombolitice. >acG pacientul se trezeKte cusimptome$ atunci timpul de debut va fi considerat momentul cEnd pacientul pentru ultima datG a fost vGzutfGrG simptome.

=a pacienFii candidaFi pentru terapia tromboliticG$ se va Endeplini ancheta de evaluare cu criterii de includere.

Con#$ita pacient$l$i : "anifest#rile clinice


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Con#$ita pacient$l$i: "anifest#rile clinice

Semnelema.ore ale AVC Simptome cu dereglare de con!tien'de la stare confuzionalG$ obnubilare superficialG pEnG la

comG/H $ot#% &valuarea pacientului 'n com# se va efectua conform scalei lasgow

Simptome senziti"e)> parestezii unilaterale ale membrelor$> parestezii faciale asociate cu parestezii unilaterale ale membrelor/

Simptome motorii)> deficitul motor de tip piramidal preponderent unilateral/

Simptome "izuale:> hemianopsie macularG/

Simptome de dereglri de limba.:>

afazie motorie$ senzorialG$ amnesticG sau mi1tG/ Simptome cerebeloase)> ata1ie> tulburGri de coordonare/

Simptome pro"ocate de lezarea trunchiului cerebral:> diplopie$> disfonie$> disfagie$

> dizartrie$> verti&/ Alte simptome:

> crize paro1istice epileptice$> tulburGri sfincteriene$> tulburGri psihice$> etc.

Con#$ita pacient$l$i : Investigaii paraclinice (*)


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Con#$ita pacient$l$i: Investigaii paraclinice (*)

Investi!a9ii #e laborator +emograma desf#urat#%

H ,oatedepista aKa cauze de A*# ischemic policitemia$ trombocitoza$ trombocitopenia$leucemia! sau a patologiei concomitente de e1.: anemia!.

-iochimia sanguin#%H ace diagnosticul diferenFial cu stGri ce mimeazG A*# ischemic de e1.: hipoglicemia$

hiponatriemia! sau a&utG En confirmarea patologiei concomitente de e1.: diabet$ insuficienFGrenalG!.

oagulograma%H ,oate depista coagulopatia. "ste utilG En special pentru decizia asupra iniFierii tratamentului

cu trombolitice sau anticoagulante.

-iomarcherii cardiaci%H ImportanFi din cauza asocierei frecvente a patologiei cerebrale vasculare cu patologia

coronarianG. AdiFional cEteva studii sugereazG corelarea Entre nivelul crescut al enzimelorcardiace Ki pronosticul nefavorabil En A*# ischemic.

/creeningul to0icologic%H Se efectueazG doar la ,acienFii cu anamnestic compromis

Con#$ita pacient$l$i : Investigaii paraclinice (1)


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Con#$ita pacient$l$i Investigaii paraclinice (1)Investi!a9ii ima!istice

CT cerebral nati" %fr contrast&H #T cerebral nativ urgent este obligatoriuR pentru diferenFierea A*#-ului ischemic de cel

hemoragic Ki aprecierea distribuFiei anatomice. #T cerebral nativ En combinaFie cu #Tangiografie Ki #T de perfuzie posedG grad sporit de sensibilitate comparativ cu oricare dintehnicile menFionate utilizate desinestGtGtor.

H #T cerebral H reprezintG momentul cheie En evaluarea A*# H ului$ astfel are loc tria&ul pentruterapia tromboliticG.

H #T cerebral e1clude alte procese cu risc vital: hematoame$ neoplasme$ abcese.H +odificGrile tabloului #T En cursul evolutiv al A*#: Sensibilitate ma1imG dupG 39 ore de la debut

A*# ischemic/ >upG D H 23 ore se vizualizeazG imagistic edemul perifocal prin zona dehipodensitate. ,rimele ore de la debut H prezenFa unei arii masive hipodense induce dubiiprivind corectitudinea datelor anamnestice timpul de debut! .,rezenFa precoce a zonei deinfarct En tabloul imagistic coreleazG cu pronostic nefavorabil.

,(amen ultrasonograficH "1amen duple1 al carotidelor: se efectueazG En caz de suspecFie a stenozei sau ocluziei de

carotidG.H >oppler transcranial: util pentru estimarea porFiunilor pro1imale vasculare$ inclusiv al A#+$

porFiunii intracraniene al a.carotide interna Ki artera vertebro H bazilarG.H "chocardiografia: se efectueazG En caz de suspiciu al embolismului cardiogenic.

"chocardiografia transesofagianG H utilG En depistarea disecFiei de aortG toracalG Ki trombilor Enatriul stEng En caz de fibrilaFie atrialG. In"estigare prin ezonan 'agnetic cerebral

H Are sensibilitate mai EnaltG comparativ cu #T nativ En depistarea infarctelor precoce dupG debut.H 0u este sensibil En depistarea precoce a hemoragiilor

Con#$ita pacient$l$i : Investigaii paraclinice (2)


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Con#$ita pacient$l$i Investigaii paraclinice (2)

Alte investi!a9ii

,lectrocardiograma

H "ste indicatG la toFi ,acienFii cu A*# acut$ deoarece D)N dinembolii cardiogenici sunt asociaFi cu fibrilaFie atrialG sau infarctacut de miocard.

H nele ghiduri de conduitG recomandG monitorizarea cardiacGcontinuG la toFi ,acienFii$ deoarece 9N din ,acienFi au aritmii cu

risc vital Ki N infarct de miocard concomitent.

AngiografiaH Se efectueazG la pacienFii cu A*# ischemiccu suspiciu la

patologie vascularG ocluzivG displazie fibromuscularG$ vasculitG!sau disecFii arteriale

*ia!nostic$l #i%eren9ial conform problemelor clinice)


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! 9 p )

'igrena) Simptomele neurologice En cadrul migrenei au debut mai lent$ gradual Ki dezvoltaremai lentG.

Crize comiiale) #rizele convulsive de regulG reprezintG fenomene pozitive miKcGri En

e1tremitate! decEt pierderea funcFiei neurologice slGbiciune sau pareza e1tremitGFii!$simptomele En perioada postictalG pot mima A*# ischemic tulburGri ale vorbirii$ confuziepostictalG$ parezG postictalG Ki alte simptome vizuale sau senzitive!

Sincope/ Amnezia tranzitorie global) Se caracterizeazG prin instalarea bruscG atulburGrilor de memorie antero Ki retrogradG fGrG simptome neurologice de focar.

0atologii ale sitemului ner"os periferic)+ononeuropatiile Ki radiculopatiile pot fi

diferenFiate prin distribuFia simptomelor Ki prezenFa sindromului algic En caz de radiculopatie.,aralizia 4ell$ neurita vestibularG Ki neuropatiile craniene pot mima A*# ischemic Ki necesitGe1aminare minuFioasG

Alte procese de "olum intracraniene %tumori+ abcese&) >ebutul Ki evoluFia autendinFG gradualG

1eurozele)de tipul an1ietGFii Ki atacurilor de panicG trebuie evaluate En unele cazuri

Tulburri metabolice)%ipoglicemia este cea mai frecventG tulburare metabolicG cemimeazG A*#. ,acientul cu anamnestic de diabet sau patologie hepaticG trebuie e1aminatpentru hipoglicemie

Hemoragie intracerebral)%emoragia intracerebralG se dezvoltG de regulG la ,acienFiihipertensivi cronici$ primul semn deseori este cefaleea severG.


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*ia!nostic$l #i%ere9ial al A.C iscemicsubtipuri de A*#! 2!

EmbolicU "mbolii: origine cardiac sau arterial

Sursele cardiace)H fibrilaFia atrialGH infarct de miocard recentH proteze valvulareH valvulopatiile

H endocarditeleH trombi muraliH cardiomiopatia dilatativGH foramen ovale persistent

Surse arteriale)

H emboli aterotromboticiH emboli colesterolici

Clinica) debut subit$ neuroimagistic pot fi depistate infarcte anterioare En cEteva teritoriivasculare sau emboli calcificaFi.

*ia!nostic$l #i%ere9ial al A.C iscemic subtipuri de A*#! 3!


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*ia!nostic$l #i%ere9ial al A.C iscemic subtipuri de A*#! 3!

Trombotic Include A*# de vas mare sau de vas mic lacunar!

#rigine) ocluzie in situ al leziunilor aterosclerotice$ En arterele carotide$ vertebro-bazilare sau

cerebrale$ de regulG pro1imal ramurilor ma&ore. =ezarea endoteliului duce la activareasubendoteliului$ activarea trombocitelor$ activarea cascadei de agregare$ inhibarea fibrinolizei Ki stazasanguinG

A.C trombotice de regulG sunt cauzate de ruperea plGcilor aterosclerotice. =a ,acienFii cuaterosclerozG generalizatG$ pot fi cauzate de ateroscleroza vaselor intracraniene

La Pacien9ii tineri' stGri de hipercoagulare sindrom antifosfolipidic$ deficienFa ,roteinei #/ deficienFa proteinei S!

anemia drepanocitarG displazia fibromuscularG disecFiile arteriale Ki vasoconstricFia cauzatG de abuz de substanFe to1ice

Lac$nar 5eprezintG 3)N din toate A*# ischemice #rigini)7cluzia ramurilor penetrante a arterei cerebrale media$ arterelor lenticulo-striate$ ramurilor

penetrante ale cercului 8illis$ ramuri penetrante ale arterei bazilare Ki


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THE EN*

;/E"TION"

Neurologie AVC (Partea II)

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Transcript of Neurologie AVC (Partea II)