Professional Documents
Culture Documents
Gavriliuc
Department of
Neurology,
AVC
Medical and
Pharmaceutical
Nicolae Testemitsanu
State University,
Republic of Moldova
EPILEPSIA
FACULTATEA STOMATOLOGIE, CICLUL NEUROSTOMATOLOGIE
FIZIOPATOLOGIA COMEI
PRINCIPALELE CAUZE CARE PRODUC COMA:
1. O leziune a trunchiului
cerebral sau tulburri
metabolice ce lezeaz sau
deprim Sistemul Reticular
Activator (SRA).
2. O leziune emisferic
bilateral sau o inhibiie a
activitii emisferelor.
1+2
Scala Glasgow
15
14 - 13
12 - 9
8-4
3
Informaia epidemiologic
Accidentul vascular cerebral reprezint a treia cauz de
mortalitate dup afeciunile cardiace i boala neoplazic
i prima cauz n rndul bolilor neurologice.
Incidena anual i mortalitatea prin AVC au sczut
considerabil (pe plan mondial) n ultimii ani, acest lucru
datorndu-se unui bun control al factorilor de risc.
Republica Moldova se afl printre primele tari ale Europei
la capitolul mortalitii prin boli cerebro-vasculare.
Rata mortalitii pacienilor cu AVC n lume constituind
8% pentru pacienii ce au benifeciat de tratament n
unitile de STROKE i 27% - 33% pentru cei care nu a
fost posibil internarea n unitile specializate.
Factorii de risc
Nemodificabili
Vrsta
Rasa
Sexul
Greutatea ponderal mic la natere
Anamnestic familial de AVC sau AIT
Factorii de risc modificabili, bine documentai
Hipertensiune arterial
Tabagism
Diabet zaharat
Patologia carotidian
Fibrilaie atrial
Anemia falciform
Dislipidemia
Stilul alimentar
Obezitatea
Inactivitatea fizic
Terapia hormonal postmenopauzal
BOLILE CEREBRO-VASCULARE
Etiologia alteraiilor arterelor i venelor rezultnd n
anormaliti cerebrale
1. Tromboza aterosclerotic.
2. Spasme de arter cerebral (atac ischemic cerebral
tranzitoriu).
3. Embolia.
4. Hemoragia hipertensiv.
5. Anevrismul sacular sau malformaia arterio-venoas cu sau
fr ruptur.
6. Arterita
a. Sifilisul meningovascular, arterita secundar ca
consecin a meningitei piogenice sau tuberculoase, infecii rare
(tifos, schistosomiasis, malarie, micoze, etc.)
b. Bolile esutului conjunctiv (poliarterita nodoas, lupus
erythematosus), arterita necrotizant, arterita Wegener, arterita
temporal, boala Takayasu, granulomatoza sau arterita cu celule
gigante a aortei, angiita arterelor cerebrale.
1. Tromboza
aterosclerotic.
BOLILE CEREBRO-VASCULARE
Etiologia alteraiilor arterelor i venelor rezultnd n
anormaliti cerebrale
1. Tromboza aterosclerotic.
2. Spasme de arter cerebral (atac ischemic cerebral
tranzitoriu).
3. Embolia.
4. Hemoragia hipertensiv.
5. Anevrismul sacular sau malformaia arterio-venoas cu sau
fr ruptur.
6. Arterita
a. Sifilisul meningovascular, arterita secundar ca
consecin a meningitei piogenice sau tuberculoase, infecii rare
(tifos, schistosomiasis, malarie, micoze, etc.)
b. Bolile esutului conjunctiv (poliarterita nodoas, lupus
erythematosus), arterita necrotizant, arterita Wegener, arterita
temporal, boala Takayasu, granulomatoza sau arterita cu celule
gigante a aortei, angiita arterelor cerebrale.
BOLILE CEREBRO-VASCULARE
Etiologia alteraiilor arterelor i venelor rezultnd n
anormaliti cerebrale
1. Tromboza aterosclerotic.
2. Spasme de arter cerebral (atac ischemic cerebral
tranzitoriu).
3. Embolia.
4. Hemoragia hipertensiv.
5. Anevrismul sacular sau malformaia arterio-venoas cu sau
fr ruptur.
6. Arterita
a. Sifilisul meningovascular, arterita secundar ca
consecin a meningitei piogenice sau tuberculoase, infecii rare
(tifos, schistosomiasis, malarie, micoze, etc.)
b. Bolile esutului conjunctiv (poliarterita nodoas, lupus
erythematosus), arterita necrotizant, arterita Wegener, arterita
temporal, boala Takayasu, granulomatoza sau arterita cu celule
gigante a aortei, angiita arterelor cerebrale.
3. Embolia.
BOLILE CEREBRO-VASCULARE
Etiologia alteraiilor arterelor i venelor rezultnd n
anormaliti cerebrale
1. Tromboza aterosclerotic.
2. Spasme de arter cerebral (atac ischemic cerebral
tranzitoriu).
3. Embolia.
4. Hemoragia hipertensiv.
5. Anevrismul sacular sau malformaia arterio-venoas cu sau
fr ruptur.
6. Arterita
a. Sifilisul meningovascular, arterita secundar ca
consecin a meningitei piogenice sau tuberculoase, infecii rare
(tifos, schistosomiasis, malarie, micoze, etc.)
b. Bolile esutului conjunctiv (poliarterita nodoas, lupus
erythematosus), arterita necrotizant, arterita Wegener, arterita
temporal, boala Takayasu, granulomatoza sau arterita cu celule
gigante a aortei, angiita arterelor cerebrale.
4. Hemoragia hipertensiv.
BOLILE CEREBRO-VASCULARE
Etiologia alteraiilor arterelor i venelor rezultnd n
anormaliti cerebrale
1. Tromboza aterosclerotic.
2. Spasme de arter cerebral (atac ischemic cerebral
tranzitoriu).
3. Embolia.
4. Hemoragia hipertensiv.
5. Anevrismul sacular sau malformaia arterio-venoas
cu sau fr ruptur.
6. Arterita
a. Sifilisul meningovascular, arterita secundar ca
consecin a meningitei piogenice sau tuberculoase, infecii rare
(tifos, schistosomiasis, malarie, micoze, etc.)
b. Bolile esutului conjunctiv (poliarterita nodoas, lupus
erythematosus), arterita necrotizant, arterita Wegener, arterita
temporal, boala Takayasu, granulomatoza sau arterita cu celule
gigante a aortei, angiita arterelor cerebrale.
BOLILE CEREBRO-VASCULARE
Etiologia alteraiilor arterelor i venelor rezultnd n
anormaliti cerebrale
1. Tromboza aterosclerotic.
2. Spasme de arter cerebral (atac ischemic cerebral
tranzitoriu).
3. Embolia.
4. Hemoragia hipertensiv.
5. Anevrismul sacular sau malformaia arterio-venoas cu sau
fr ruptur.
6. Arterita
a. Sifilisul meningovascular, arterita secundar ca
consecin a meningitei piogenice sau tuberculoase, infecii rare
(tifos, schistosomiasis, malarie, micoze, etc.)
b. Bolile esutului conjunctiv (poliarterita nodoas, lupus
erythematosus), arterita necrotizant, arterita Wegener, arterita
temporal, boala Takayasu, granulomatoza sau arterita cu celule
gigante a aortei, angiita arterelor cerebrale.
6. Arterita
a. Sifilisul
meningovascular,
arterita secundar
ca consecin a
meningitei
piogenice sau
tuberculoase,
infecii rare (tifos,
shistosomiasis,
malarie, micoze,
etc.).
BOLILE CEREBROVASCULARE
Etiologia alteraiilor arterelor i venelor rezultnd n
anormaliti cerebrale
7. Tromboflebita cerebral: secundar otogen, infeciei
sinusurilor paranazale, a feei, etc.; n cadrul meiningitei i
empiemului subdural; stri de slbire general a organismului,
postpartum, postoperativ, insuficien cardiac, sau de cauz
nedeterminat.
8. Boli hematologice: utilizare de anticoagulante i trombolitice,
policitemia, talassemia, purpura trombocitopenic trombotic,
trombocitopeniile, angioendotelioza neoplastic, etc.
9. Traumatismul i disecia arterei carotide i bazilare.
10. Angiopatia amiloid.
11. Anevrismul disecant al aortei.
12. Complicaiile arteriografiei.
7. Tromboflebita
cerebral secundar
otogen, infeciei
sinusurilor paranazale,
a feei, etc.; n cadrul
meningitei i
empiemului subdural;
stri de slbire
general a
organismului,
postpartum,
postoperativ,
insuficien cardiac,
sau de cauz
nedeterminat.
Tromboflebita sinusului
longitudinal superior cu
infarct hemorrhagic
bilateral. Femeie n vrst
de 21 ani cu cefalee,
tetraparez, i stupoare.
BOLILE CEREBROVASCULARE
Etiologia alteraiilor arterelor i venelor rezultnd n
anormaliti cerebrale
7. Tromboflebita cerebral: secundar otogen, infeciei
sinusurilor paranazale, a feei, etc.; n cadrul meiningitei i
empiemului subdural; stri de slbire general a organismului,
postpartum, postoperativ, insuficien cardiac, sau de cauz
nedeterminat.
8. Boli hematologice: utilizare de anticoagulante i
trombolitice, policitemia, talassemia, purpura
trombocitopenic trombotic, trombocitopeniile,
angioendotelioza neoplastic, etc.
9. Traumatismul i disecia arterei carotide i bazilare.
10. Angiopatia amiloid.
11. Anevrismul disecant al aortei.
12. Complicaiile arteriografiei.
BOLILE CEREBROVASCULARE
Etiologia alteraiilor arterelor i venelor rezultnd n
anormaliti cerebrale
7. Tromboflebita cerebral: secundar otogen, infeciei
sinusurilor paranazale, a feei, etc.; n cadrul meiningitei i
empiemului subdural; stri de slbire general a organismului,
postpartum, postoperativ, insuficien cardiac, sau de cauz
nedeterminat.
8. Boli hematologice: utilizare de anticoagulante i trombolitice,
policitemia, talassemia, purpura trombocitopenic trombotic,
trombocitopeniile, angioendotelioza neoplastic, etc.
9. Traumatismul i disecia arterei carotide i bazilare.
10. Angiopatia amiloid.
11. Anevrismul disecant al aortei.
12. Complicaiile arteriografiei.
9. Traumatismul i
disecia arterei
carotide i bazilare.
BOLILE CEREBROVASCULARE
Etiologia alteraiilor arterelor i venelor rezultnd n
anormaliti cerebrale
7. Tromboflebita cerebral: secundar otogen, infeciei
sinusurilor paranazale, a feei, etc.; n cadrul meiningitei i
empiemului subdural; stri de slbire general a organismului,
postpartum, postoperativ, insuficien cardiac, sau de cauz
nedeterminat.
8. Boli hematologice: utilizare de anticoagulante i trombolitice,
policitemia, talassemia, purpura trombocitopenic trombotic,
trombocitopeniile, angioendotelioza neoplastic, etc.
9. Traumatismul i disecia arterei carotide i bazilare.
10. Angiopatia amiloid.
11. Anevrismul disecant al aortei.
12. Complicaiile arteriografiei.
BOLILE CEREBROVASCULARE
Etiologia alteraiilor arterelor i venelor rezultnd n
anormaliti cerebrale
7. Tromboflebita cerebral: secundar otogen, infeciei
sinusurilor paranazale, a feei, etc.; n cadrul meiningitei i
empiemului subdural; stri de slbire general a organismului,
postpartum, postoperativ, insuficien cardiac, sau de cauz
nedeterminat.
8. Boli hematologice: utilizare de anticoagulante i trombolitice,
policitemia, talassemia, purpura trombocitopenic trombotic,
trombocitopeniile, angioendotelioza neoplastic, etc.
9. Traumatismul i disecia arterei carotide i bazilare.
10. Angiopatia amiloid.
11. Anevrismul disecant al aortei.
12. Complicaiile arteriografiei.
BOLILE CEREBROVASCULARE
Etiologia alteraiilor arterelor i venelor rezultnd n
anormaliti cerebrale
7. Tromboflebita cerebral: secundar otogen, infeciei
sinusurilor paranazale, a feei, etc.; n cadrul meiningitei i
empiemului subdural; stri de slbire general a organismului,
postpartum, postoperativ, insuficien cardiac, sau de cauz
nedeterminat.
8. Boli hematologice: utilizare de anticoagulante i trombolitice,
policitemia, talassemia, purpura trombocitopenic trombotic,
trombocitopeniile, angioendotelioza neoplastic, etc.
9. Traumatismul i disecia arterei carotide i bazilare.
10. Angiopatia amiloid.
11. Anevrismul disecant al aortei.
12. Complicaiile arteriografiei.
BOLILE CEREBROVASCULARE
Etiologia alteraiilor arterelor i venelor rezultnd n
anormaliti cerebrale
7. Tromboflebita cerebral: secundar otogen, infeciei
sinusurilor paranazale, a feei, etc.; n cadrul meiningitei i
empiemului subdural; stri de slbire general a organismului,
postpartum, postoperativ, insuficien cardiac, sau de cauz
nedeterminat.
8. Boli hematologice: utilizare de anticoagulante i trombolitice,
policitemia, talassemia, purpura trombocitopenic trombotic,
trombocitopeniile, angioendotelioza neoplastic, etc.
9. Traumatismul i disecia arterei carotide i bazilare.
10. Angiopatia amiloid.
11. Anevrismul disecant al aortei.
12. Complicaiile arteriografiei.
12.
Complicaiile
arteriografiei.
BOLILE CEREBROVASCULARE
13. Migrena
cu deficit
neurologic
persistent.
BOLILE CEREBROVASCULARE
14. Angajri
(hernii) cerebrale
supratentoriale
i subtentoriale,
n gaura rupt
posterioar.
BOLILE CEREBROVASCULARE
Etiologia alteraiilor arterelor i venelor rezultnd n
anormaliti cerebrale
13. Migrena cu deficit neurologic persistent.
14. Angajri (hernii) cerebrale supratentoriale i subtentoriale,
n gaura rupt posterioar.
15. Cauze mixte: displazia fibromuscular cu disecare
local de carotid, arter cerebral medie, or arter
vertebral, bazilar; iradiere cu raye X, infarct cerebral
n teritoriu a. Cerebrale medii n cadrul traumatismului
cranio-cerebral nchis, compresie prin anevrism sacular
fr ruptur, complicaii de utilizare a contraceptivelor
orale.
16. Cauze nedeterminate ale vrstei copilreti i adultului
tnr: boala moyamoya; ocluzia arterial multipl progresiv
(Taveras).
BOLILE CEREBROVASCULARE
Etiologia alteraiilor arterelor i venelor rezultnd n
anormaliti cerebrale
13. Migrena cu deficit neurologic persistent.
14. Angajri (hernii) cerebrale supratentoriale i subtentoriale,
n gaura rupt posterioar.
15. Cauze mixte: displazia fibromuscular cu disecare local de
carotid, arter cerebral medie, or arter vertebral, bazilar;
iradiere cu raze X, infarct cerebral n teritoriu a. Cerebrale
medii n cadrul traumatismului cranio-cerebral nchis,
compresie prin anevrism sacular fr ruptur, complicaii de
utilizare a contraceptivelor orale.
16. Cauze nedeterminate ale vrstei copilreti i
adultului tnr: boala moyamoya; ocluzia arterial
multipl progresiv (Taveras).
CEREBROVASCULAR DISEASES
CEREBROVASCULAR DISEASES
Circle of Willis
At the base of the brain, the
carotid and vertebrobasilar
arteries form a circle of
communicating arteries
known as the circle of Willis.
From this circle other arteries -the anterior cerebral artery
(ACA), the middle cerebral
artery (MCA), the posterior
cerebral artery (PCA) - arise
and travel to all parts of the
brain.
Because the carotid and
vertebrobasilar arteries form
a circle, if one of the main
arteries is occluded, the
distal smaller arteries that it
supplies can receive blood
from the other arteries
(collateral circulation).
CEREBROVASCULAR DISEASES
More than any other organ, the brain
depends from minute to minute on an
adequate supply of oxygenated blood.
Constancy of the cerebral circulation is
assured by a series of baroreceptors
and vasomotor reflexes under the
control of centers in the lower
brainstem.
Brain tissue deprived of blood undergoes
ischemic necrosis or infarction (also
referred to as a zone of softening or
encephalomalacia). Obstruction of an
artery by thrombus or embolus is the
usual cause of focal ischemic damage,
but failure of the circulation and
hypotension from cardiac
decompensation or shock, if severe and
prolonged, can produce focal as well as
diffuse ischemic changes.
CEREBROVASCULAR DISEASES
Ischemic cascade
Free radicals, arachidonic acid, and nitric oxide are generated
by this process, leading to further neuronal damage. Within
hours to days after a stroke, specific genes are activated,
leading to the formation of cytokines and other factors that
in turn cause further inflammation and microcirculatory
compromise. Ultimately, the ischemic penumbra is
consumed by these progressive insults, coalescing with the
infarcted core, often within hours of the onset of the stroke.
The central goal of therapy in acute ischemic stroke is to
preserve the ischemic penumbra. This can be
accomplished by limiting the severity of ischemic injury (ie,
neuronal protection) or reducing the duration of ischemia
(ie, restoring blood flow to the compromised area).
day
20
50
SCOPUL TRATAMENTULUI
PACIENTULUI CU ICTUS
CEREBRAL:
1. PACIENTULUI I SE OFER O
ANS OPTIMAL DE
SUPRAVIEUIRE.
2. REDUCEREA LA MINIMUM A
CONSECINELOR ICTUSULUI
PENTRU BOLNAV I PENTRU
PERSOANELE CARE NGRIJESC
DE EL.
COMPARTIMENTELE TRATAMENTULUI
ACCIDENTULUI VASCULAR
CEREBRAL:
1. Tratamentul nedifereniat n perioada
acut.
2. Tratamentul conservator difereniat i
tratamentul neurochirurgical n
perioada acut.
3. Reabilitarea.
4. ngrijirea de lung durat.
the thalamus,
originating from
ascending
thalmogeniculate
branches of the
posterior cerebral
artery (C);
penetrating
cortical branches
of the anterior,
middle, or
posterior cerebral
arteries (A);
and the
cerebellum,
originating from
penetrating
branches of the
posterior
inferior, anterior
inferior, or
superior cerebellar
arteries (E).
basal ganglia,
originating from
ascending
lenticulostriate
branches of the
middle cerebral
artery (B);
INTRACRANIAL HEMORRHAGE
The bleeding occurs
within brain tissue,
and rupture of
arteries lying in the
subarachnoid space
is practically unknown
apart from aneurysm.
The extravasation
forms a roughly
circular or oval mass
that disrupts the
tissue and grows in
volume as the
bleeding continues.
INTRACRANIAL HEMORRHAGE
INTRACRANIAL HEMORRHAGE
INTRACRANIAL HEMORRHAGE
INTRACRANIAL HEMORRHAGE
INTRACRANIAL HEMORRHAGE
INTRACRANIAL HEMORRHAGE
INTRACRANIAL HEMORRHAGE
Spontaneous Subarachnoid Hemorrhage (Ruptured Saccular Aneurysm)
INTRACRANIAL HEMORRHAGE
Spontaneous Subarachnoid Hemorrhage (Ruptured Saccular Aneurysm)
In summary, the clinical sequence of sudden severe headache, collapse, relative
preservation of consciousness with a paucity of lateralizing signs, and neck
stiffness is diagnostic of subarachnoid hemorrhage due to a ruptured saccular
aneurysm.
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.
Levels of 200 mmHg systolic are seen occasionally just after rupture but usually
the pressure is elevated only moderately and fluctuates with the degree of head
pain. Spontaneous intracranial bleeding with normal blood pressure should
always suggest ruptured aneurysm or arteriovenous malformation, a bleeding
diathesis, and, rarely, hemorrhage into a cerebral tumor. Nuchal rigidity is usually
present but occasionally absent, and the main complaint of pain may be referable
to the interscapular region or even the low back rather than to the head.
Examination of the fundi frequently reveals smooth-surfaced, sharply outlined
collections of blood that cover the retinal vesselsthe so-called preretinal or
subhyaloid hemorrhages; Roth spots are seen occasionally. Bilateral Babinski
signs are found in the first few days following rupture. Fever to 39C may be seen
in the first week. Rarely, escaping blood enters the subdural space and produces
a hematoma, evacuation of which may be lifesaving.
INTRACRANIAL HEMORRHAGE
Spontaneous Subarachnoid Hemorrhage (Ruptured Saccular Aneurysm)
Laboratory Findings A CT scan will detect
blood locally or diffusely in the subarachnoid
spaces or within the brain or ventricular
system. This should be the initial investigative
procedure, since it confirms a subarachnoid
hemorrhage in more than 95 percent of cases.
The blood may appear as a subtle shadow
along the tentorium, difficult to distinguish from
the veins in this area, or in the sylvian or
adjacent fissures. A large localized collection of
subarachnoid blood may indicate the location
of the aneurysm and the region of subsequent
vasospasm as already noted. When two or
more aneurysms are visualized by
arteriography, the CT scan may identify the one
that had ruptured by the clot that surrounds it.
Also, a coexistent hydrocephalus will be
demonstrable. If the CT scan documents
subarachnoid blood with certainty, a spinal tap
is not necessary.
INTRACRANIAL HEMORRHAGE
Spontaneous Subarachnoid Hemorrhage (Ruptured Saccular Aneurysm)
Laboratory Findings In all other cases a lumbar puncture should be
undertaken when the clinical features suggest a subarachnoid hemorrhage.
Usually the CSF is grossly bloody, with RBC counts up to 1 million per cubic
millimeter or even higher. With a relatively mild hemorrhage, there may be
only a few thousand cells. It is unlikely that an aneurysm can rupture entirely
into 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 CSF. Usually deep
xanthochromia is found after centrifugation if several hours have elapsed.
Carotid and vertebral angiography is the only certain means of
demonstrating an aneurysm and does so in some 85 percent of patients in
whom the correct diagnosis of spontaneous subarachnoid hemorrhage is
made on clinical grounds. MRI and MRA detect most aneurysms of the basal
vessels but are as yet of insufficient sensitivity to replace conventional
angiography.
INTRACRANIAL HEMORRHAGE
Spontaneous Subarachnoid Hemorrhage (Ruptured Saccular Aneurysm)
Treatment This is influenced by the neurologic and general medical state of
the 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 IV or
V, see below). Before deciding on a course of action, it has been useful to
assess the patient with reference to the widely employed scale introduced by
Botterell and by Hunt and Hess, as follows:
Grade I. Asymptomatic or with slight headache and stiff neck
Grade II. Moderate to severe headache and nuchal rigidity but no focal or
lateralizing neurologic signs
Grade III. Drowsiness, confusion, and mild focal deficit
Grade IV. Persistent stupor or semicoma, early decerebrate rigidity and
vegetative disturbances
Grade V. Deep coma and decerebrate rigidity.
INTRACRANIAL HEMORRHAGE
Spontaneous Subarachnoid Hemorrhage (Ruptured Saccular Aneurysm)
INTRACRANIAL HEMORRHAGE
Spontaneous Subarachnoid Hemorrhage (Ruptured Saccular Aneurysm)
Treatment Calcium channel blockers are being used extensively to reduce
the incidence of stroke from vasospasm. Nimodipine, 60 mg administered
orally every 4 h, is currently favored. Although calcium channel blockers do
not alter the incidence of angiographically demonstrated vasospasm, they
have reduced the number of strokes in each of five randomized studies.
Patients with stupor or coma who have massive hydrocephalus often benefit
from decompression of the ventricular system. This is accomplished initially
by external drainage and may require permanent shunting if the
hydrocephalus returns. The risk of infection of the external shunt tubing is
high if it is left in place for much more than 3 days.
The timing of surgery for grade III patients is still controversial, but if their
general medical condition allows, they probably also benefit from the same
aggressive approach. In grade IV 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 occasionally
raised a patient with severe hydrocephalus to a better grade and prompted
early operation. In the hands of experienced anesthesiologists and
cerebrovascular surgeons using microdissection, the operative mortality,
even in grades III and IV patients, has now been reduced to 2 to 3 percent.
INTRACRANIAL HEMORRHAGE
Spontaneous Subarachnoid Hemorrhage (Ruptured Saccular Aneurysm)
Treatment
The timing of surgery for grade III patients is still
controversial, but if their general medical condition allows,
they probably also benefit from the same aggressive
approach. In grade IV 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 occasionally raised a patient with
severe hydrocephalus to a better grade and prompted early
operation. In the hands of experienced anesthesiologists
and cerebrovascular surgeons using microdissection, the
operative mortality, even in grades III and IV patients, has
now been reduced to 2 to 3 percent.
INTRACRANIAL HEMORRHAGE
Spontaneous Subarachnoid Hemorrhage (Ruptured Saccular Aneurysm)
Treatment
The timing of surgery for grade III patients is still
controversial, but if their general medical condition allows,
they probably also benefit from the same aggressive
approach. In grade IV 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 occasionally raised a patient with
severe hydrocephalus to a better grade and prompted early
operation. In the hands of experienced anesthesiologists
and cerebrovascular surgeons using microdissection, the
operative mortality, even in grades III and IV patients, has
now been reduced to 2 to 3 percent.
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.
I. ( ).
1.
2. (
).
3. .
II.
1..
2. .
3. .
4. -.
5. .
- (
)
I.
II.
III.
IV.
.
.
.
.
I.
II. .
III. - .
Encefalita herpetic
Investigaii complementare.
THE END
QUESTIONS ???