Theme: Cerebral vascular diseases of the Brain and Spinal cord.
Hemorrhagic
strokes (subarachnoid hemorrhage, intracerebral hematoma (or apoplectic stroke)
and ventricular hemorrhage).
Etiology and pathogenesis,
clinical characteristics, diagnosis and treatment of strokes
Strokes
Definition
In broadest sense, the World Health Organization
has defined stroke as “rapidly developing clinical signs of focal (at times
global) disturbance of cerebral function, lasting more than 24 hours or leading
to death with no apparent cause other then that of vascular origin”.
Knowledge of cerebrovascular arterial anatomy and the brain regions
supplied by the arteries is useful in determining which vessels are involved in
acute stroke. Atypical patterns that do not conform to a vascular distribution
may indicate another diagnosis, such as venous infarction.
The cerebral hemispheres are supplied by 3 paired major arteries: the
anterior, middle, and posterior cerebral arteries. The anterior and middle
cerebral arteries are responsible for the anterior circulation and arise from
the supraclinoid internal carotid arteries. The posterior cerebral arteries
arise from the basilar artery and form the posterior circulation, which also
supplies the thalami, brainstem, and cerebellum. The angiograms in the images
below demonstrate some portions of the circulation involved in hemorrhagic
strokes.
Frontal view
of a cerebral angiogram with selective injection of the left internal carotid artery illustrates the anterior circulation.
The anterior cerebral artery consists of the A1 segment proximal to the
anterior communicating artery with the A2 segment distal to it. The middle
cerebral artery can be divided into 4 segments: the M1 (horizontal segment)
extends to the limen insulae and gives off lateral lenticulostriate branches,
the M2 (insular segment), M3 (opercular branches), and M4 (distal cortical
branches on the lateral hemispheric convexities).
Lateral view of a cerebral angiogram illustrates the branches
of the anterior cerebral artery (ACA) and sylvian triangle. The pericallosal
artery has been described as arising distal to the anterior communicating
artery or distal to the origin of the callosomarginal branch of the ACA. The
segmental anatomy of the ACA has been described as follows: (1) the A1 segment
extends from the internal carotid artery (ICA) bifurcation to the anterior
communicating artery, (2) A2 extends to the junction of the rostrum and genu of
the corpus callosum, (3) A3 extends into the bend of the genu of the corpus
callosum, and (4) A4 and A5 extend posteriorly above the callosal body and
superior portion of the splenium. The sylvian triangle overlies the opercular
branches of the middle cerebral artery, with the apex representing the sylvian
point.
Frontal projection from a right vertebral artery angiogram
illustrates the posterior circulation. The vertebral arteries join to form the
basilar artery. The posterior inferior cerebellar arteries (PICA) arise from
the distal vertebral arteries. The anterior inferior cerebellar arteries (AICA)
arise from the proximal basilar artery. The superior cerebellar arteries (SCA)
arise distally from the basilar artery before its bifurcation into the
posterior cerebral arteries.
Epidemiology
Epidemiology
Occurrence in the United States
Each year in the United States,
approximately 795,000 people experience new or recurrent stroke. Of these,
approximately 610,000 represent initial attacks, and 185,000 represent
recurrent strokes. Epidemiologic studies indicate that approximately 87% of strokes
in the United States are ischemic, 10% are secondary to intracerebral
hemorrhage, and another 3% may be secondary to subarachnoid hemorrhage.
A 2010 retrospective review from a stroke
center found that 40.9% of the 757 patients in the study had suffered
hemorrhagic strokes. The researchers speculate that improved
availability and implementation of computed tomography (CT) scanning may have unmasked
a previous underestimation of the actual percentage of hemorrhagic strokes, or
increased use of antiplatelet agents and warfarin may have led to a higher
incidence of hemorrhage. Alternatively, this higher rate may represent referral
bias of patients with intracerebral hemorrhages to medical centers with
neurosurgical capabilities.
The incidence of stroke varies with age,
sex, ethnicity, and socioeconomic status. For example, American Heart
Association (AHA) researchers found that rates of intracerebral hemorrhage are
higher in Mexican Americans, Latin Americans, blacks, Native Americans,
Japanese people, and Chinese people than they are in whites.[5]
Flaherty et al found that excess risk of
intracranial hemorrhage in African Americans is largely attributable to higher
hemorrhage rates in young and middle-aged persons, particularly for deep
cerebral and brainstem locations. Hypertension is the predominant risk factor.
International occurrence
According to the World Health Organization
(WHO), 15 million people suffer stroke worldwide each year. Of these, 5 million
die and another 5 million are left permanently disabled.
The global incidence of stroke has at
least a modest variation from nation to nation, suggesting the importance of
genetics and environmental factors, such as disparities in access to health
care in developing countries. The age-adjusted incidence of total strokes per
1000 person-years for people 55 years or older has been reported in the range
of 4.2 to 6.5. The highest incidences have been reported in Russia, Ukraine,
and Japan.
In a prospective, population-based
registry study from Italy, the crude annual incidence rate of intracerebral
hemorrhage was 36.9 per 100,000 population. When standardized to the 2006
European population, the rate was 32.9 per 100,000 population; standardized to
the world population, the rate was 15.9 per 100,000 population.
Overall, the incidence of acute stroke has
demonstrated a constant decline over the past several decades, most notably
during the 1970s-1990s, although in recent years the rate trend has begun to
plateau. However, the increased survival among stroke victims will place an
increased demand on health-care systems globally.
Stroke subtypes also vary greatly in
different parts of the world and between different races. For example, the
proportion of hemorrhagic strokes may be higher in certain populations, such as
the Chinese population, in which it has been reported to be up to 39.4%, and
the Japanese, in which it is reportedly up to 38.7%.
Prognosis
The prognosis in patients with hemorrhagic stroke
varies depending on the severity of stroke and the location and the size of the
hemorrhage. Lower Glasgow Coma Scale (GCS) scores are associated with poorer
prognosis and higher mortality rates. A larger volume of blood at presentation
is also associated with a poorer prognosis. Growth of the hematoma volume is
associated with a poorer functional outcome and increased mortality rate.
The intracerebral hemorrhage score is the most
commonly used instrument for predicting outcome in hemorrhagic stroke. The
score is calculated as follows:
·
GCS
score 3-4: 2 points
·
GCS
score 5-12: 1 point
·
GCS
score 13-15: 0 points
·
Age ≥80
years: Yes, 1 point; no, 0 points
·
Infratentorial
origin: Yes, 1 point; no, 0 points
·
Intracerebral
hemorrhage volume ≥30 cm3: 1 point
·
Intracerebral
hemorrhage volume < 30 cm3: 0 points
·
Intraventricular
hemorrhage: Yes, 1 point; no, 0 points
In a study by Hemphill et al, all patients with an
Intracerebral Hemorrhage Score of 0 survived, and all of those with a score of
5 died; 30-day mortality increased steadily with the Score.
Other prognostic factors include the following:
·
Nonaneurysmal
perimesencephalic stroke has a less severe clinical course and, in general, a
better prognosis
·
The
presence of blood in the ventricles is associated with a higher mortality rate;
in one study, the presence of intraventricular blood at presentation was
associated with a mortality increase of more than 2-fold
·
Patients
with oral anticoagulation-associated intracerebral hemorrhage have higher
mortality rates and poorer functional outcomes
In studies, withdrawal of medical support or issuance
of Do Not Resuscitate (DNR) orders within the first day of hospitalization
predict poor outcome independent of clinical factors. Because limiting care may
adversely impact outcome, American Heart Association/American Stroke
Association (AHA/ASA) guidelines suggest that new DNR orders should probably be
postponed until at least the second full day of hospitalization. Patients with
DNRs should be given all other medical and surgical treatment, unless the DNR
explicitly says otherwise.
Classification of stroke Stroke is classified by the pathology of the
underlying focal
brain injury into either
infarction or hemorrhage. Infarction is much more common than hemorrhage. The
proportion between them is 4:1 (80 % to 20%).
Hemorrhagic stroke means hemorrhage.
According to the localization of
hemorrhage it is divided into such groups:
1. Intracerebral (when the
hemorrhage is into the substance or parenchyma of the brain)
2. Membrane
a) subarachnoid (when the
bleeding originates in the subarachnoid spaces surrounding the brain)
b) epidural and subdural
(traumatic)
3. Combined
a) subarachnoid – parenchymatous
b) parenchymatous– subarachnoid
c) parenchymatous–ventricular
d) ventricular
Etiology
The most common causes of
hemorrhage are:
1. Hypertension
2. Symptomatic arterial hypertension
(at kidney diseases, systemic vessel processes)
3. Inborn arterial and arterial –
venous malformations
4. Blood diseases (leucosis,
polycythemia)
5. Cerebral atherosclerosis
6. Intoxications, such as uremia,
sepsis
The etiologies of stroke are varied, but
they can be broadly categorized into ischemic or hemorrhagic. Approximately
80-87% of strokes are from ischemic infarction caused by thrombotic or embolic
cerebrovascular occlusion. Intracerebral hemorrhages account for most of the
remainder of strokes, with a smaller number resulting from aneurysmal
subarachnoid hemorrhage.
In
20-40% of patients with ischemic infarction, hemorrhagic transformation may
occur within 1 week after ictus.
Differentiating between the different
types of stroke is an essential part of the initial workup of patients with
stroke, as the subsequent management of each disorder will be vastly different.
Risk factors
The risk of hemorrhagic stroke is
increased with the following factors:
·
Advanced age
·
Hypertension (up to 60% of cases)
·
Previous history of stroke
·
Alcohol abuse
·
Use of illicit drugs (eg, cocaine, other sympathomimetic drugs)
Causes of hemorrhagic stroke include the
following[8, 9, 11, 12, 13] :
·
Hypertension
·
Cerebral amyloidosis
·
Coagulopathies
·
Anticoagulant therapy
·
Thrombolytic therapy for acute myocardial infarction (MI) or acute ischemic
stroke (can cause iatrogenic hemorrhagic transformation)
·
Arteriovenous malformation (AVM), aneurysms, and
other vascular malformations (venous and cavernous angiomas)
·
Vasculitis
·
Intracranial neoplasm
Amyloidosis
Cerebral amyloidosis affects people who
are elderly and may cause up to 10% of intracerebral hemorrhages. Rarely,
cerebral amyloid angiopathy can be caused by mutations in the amyloid precursor
protein and is inherited in an autosomal dominant fashion.
Coagulopathies
Coagulopathies may be acquired or
inherited. Liver disease can result in a bleeding diathesis. Inherited
disorders of coagulation such as factor VII, VIII, IX, X, and XIII deficiency
can predispose to excessive bleeding, and intracranial hemorrhage has been seen
in all of these disorders.
Anticoagulant therapy
Anticoagulant therapy is especially likely
to increase hemorrhage risk in patients who metabolize warfarin inefficiently.
Warfarin metabolism is influenced by polymorphism in the CYP2C9 genes.
Three known variants have been described.CYP2C9*1 is the normal
variant and is associated with typical response to dosage of warfarin.
Variations *2 and *3 are relatively common polymorphisms that reduce the
efficiency of warfarin metabolism.[14]
Atrioventricular malformations
Numerous genetic causes may predispose to
AVMs in the brain, although AVMs are generally sporadic. Polymorphisms in
the IL6 gene increase susceptibility to a number of disorders,
including AVM. Hereditary hemorrhagic telangiectasia (HHT), previously known as
Osler-Weber-Rendu syndrome, is an autosomal dominant disorder that causes
dysplasia of the vasculature. HHT is caused by mutations inENG, ACVRL1,
or SMAD4 genes. Mutations in SMAD4 are also
associated with juvenile polyposis, so this must be considered when obtaining
the patient’s history.
HHT is most frequently diagnosed when
patients present with telangiectasias on the skin and mucosa or with chronic
epistaxis from AVMs in the nasal mucosa. Additionally, HHT can result in AVMs
in any organ system or vascular bed. AVM in the gastrointestinal tract, lungs,
and brain are the most worrisome, and their detection is the mainstay of
surveillance for this disease.
Hypertension
The most common etiology of primary
hemorrhagic stroke (intracerebral hemorrhage) is hypertension. At least two
thirds of patients with primary intraparenchymal hemorrhage are reported to
have preexisting or newly diagnosed hypertension. Hypertensive small-vessel
disease results from tiny lipohyalinotic aneurysms that subsequently rupture
and result in intraparenchymal hemorrhage. Typical locations include the basal
ganglia, thalami, cerebellum, and pons.
Aneurysms and subarachnoid hemorrhage
The most common cause of atraumatic
hemorrhage into the subarachnoid space is rupture of an intracranial aneurysm.
Aneurysms are focal dilatations of arteries, with the most frequently
encountered intracranial type being the berry (saccular) aneurysm. Aneurysms
may less commonly be related to altered hemodynamics associated with AVMs, collagen
vascular disease, polycystic kidney disease, septic emboli, and neoplasms.
Nonaneurysmal perimesencephalic
subarachnoid hemorrhage may also be seen. This phenomenon is thought to arise
from capillary or venous rupture. It has a less severe clinical course and, in
general, a better prognosis.
Berry aneurysms are most often isolated
lesions whose formation results from a combination of hemodynamic stresses and
acquired or congenital weakness in the vessel wall. Saccular aneurysms typically
occur at vascular bifurcations, with more than 90% occurring in the anterior
circulation. Common sites include the following:
·
The junction of the anterior communicating arteries and anterior cerebral
arteries—most commonly, the middle cerebral artery (MCA) bifurcation
·
The supraclinoid internal carotid artery at the origin of the posterior
communicating artery
·
The bifurcation of the internal carotid artery (ICA)
Genetic causes of aneurysms
Intracranial aneurysms may result from
genetic disorders. Although rare, several families have been described that
have a predisposition—inherited in an autosomal dominant fashion—to
intracranial berry aneurysms. A number of genes, all categorized as ANIB genes,
are associated with this predisposition. Presently,ANIB1 through ANIB11 are
known.
Autosomal dominant polycystic kidney
disease (ADPKD) is another cause of intracranial aneurysm. Families with ADPKD
tend to show phenotypic similarity with regard to intracranial hemorrhage or
asymptomatic berry aneurysms.
Loeys-Dietz syndrome (LDS) consists of
craniofacial abnormalities, craniosynostosis, marked arterial tortuosity, and
aneurysms and is inherited in an autosomal dominant manner. Although
intracranial aneurysms occur in LDS of all types, saccular intracranial aneurysms
are a prominent feature of LDS type IC, which is caused by mutations in
the SMAD3 gene.
Ehlers-Danlos syndrome is a group of
inherited disorders of the connective tissue that feature hyperextensibility of
the joints and changes to the skin, including poor wound healing, fragility,
and hyperextensibility. However, Ehlers-Danlos vascular type (type IV) also is
known to cause spontaneous rupture of hollow viscera and large arteries,
including arteries in the intracranial circulation.
Patients with Ehlers-Danlos syndrome may
also have mild facial findings, including lobeless ears, a thin upper lip, and
a thin, sharp nose. The distal fingers may appear prematurely aged (acrogeria).
In the absence of a suggestive family history, it is difficult to separate
Ehlers-Danlos vascular type from other forms of Ehlers-Danlos. Ehlers-Danlos
vascular type is caused by mutations in the COL3A1 gene; it is
inherited in an autosomal dominant manner.
Hemorrhagic transformation of ischemic
stroke
Hemorrhagic transformation represents the
conversion of a bland infarction into an area of hemorrhage. Proposed
mechanisms for hemorrhagic transformation include reperfusion of ischemically
injured tissue, either from recanalization of an occluded vessel or from
collateral blood supply to the ischemic territory or disruption of the
blood-brain barrier. With disruption of the blood-brain barrier, red blood
cells extravasate from the weakened capillary bed, producing petechial
hemorrhage or frank intraparenchymal hematoma.
Hemorrhagic transformation of an ischemic
infarct occurs within 2-14 days postictus, usually within the first week. It is
more commonly seen following cardioembolic strokes and is more likely with
larger infarct size. Hemorrhagic transformation is also more likely following
administration of tissue plasminogen activator (tPA) in patients whose
noncontrast computed tomography (CT) scans demonstrate areas of hypodensity. See the image below.
Noncontrast computed tomography scan
(left) obtained in a 75-year-old man who was admitted for stroke demonstrates a
large right middle cerebral artery distribution infarction with linear areas of
developing hemorrhage. These become more confluent on day 2 of hospitalization
(middle image), with increased mass effect and midline shift. There is massive
hemorrhagic transformation by day 6 (right), with increased leftward midline
shift and subfalcine herniation. Obstructive hydrocephalus is also noted, with
dilatation of the lateral ventricles, likely due to compression of the foramen
of Monroe. Intraventricular hemorrhage is also noted layering in the left
occipital horn. Larger infarctions are more likely to undergo hemorrhagic
transformation and are one contraindication to thrombolytic therapy.
Pathogenesis
Hemorrhage results from
rupture of the vessel anywhere within the cranial cavity or diapedesis in case
of increased penetrance of vessel’s wall. Rupture of the vessel is much more
common and takes about 80 % of all stroke cases while diapedesis occurs only in
20 % of cases.
Hypertension has been
implicated as the main cause of hemorrhage. Hypertension is the cause of a
weakening in the walls of arterioles and the formation of micro aneurysms.
Among elderly nonhypertensive patients with recurrent hemorrhages, amyloidal
angiopathy has been implicated as an important cause. Others causes include
arterial-venous malformations, aneurysms, bleeding disorders or
anticoagulation, trauma, tumors, cavernous angiomas and drug abuse.
Pathomorphology
In case of hemorrhagic stroke
we distinguish hematoma – like hemorrhage and transudation – like hemorrhage.
Pathophysiology
In intracerebral hemorrhage, bleeding
occurs directly into the brain parenchyma. The usual mechanism is thought to be
leakage from small intracerebral arteries damaged by chronic hypertension.
Other mechanisms include bleeding diatheses, iatrogenic anticoagulation,
cerebral amyloidosis, and cocaine abuse.
Intracerebral hemorrhage has a
predilection for certain sites in the brain, including the thalamus, putamen,
cerebellum, and brainstem. In addition to the area of the brain injured by the
hemorrhage, the surrounding brain can be damaged by pressure produced by the
mass effect of the hematoma. A general increase in intracranial pressure may occur.
According to the localization
there are:
1. Lateral hemorrhage (they are
located laterally compared with the internal capsule. They take about 40 % of
all hemorrhages).
2. Medial hemorrhage (they are
located medially compared with the internal scapula and take about 10 % of all
hemorrhages).
3. Combined hemorrhages (they
take the whole region of basal nuclei: subcortical nuclei, thalamus, and
internal capsule. They take about 16 % of all hemorrhages).
4. Cerebellar hemorrhages (6 – 10
%)
5. Brain stem hemorrhages (5 %).
Primary ventricular
hemorrhages are very rare. In case of large hemorrhage brain edema is
developed. The last is associated with dislocation of brain stem which is the
main cause of patients’ death.
The main cause of death is rupture into the
ventricular system and brain stem hemorrhage with lesion of main vital centers.
Clinical picture There are three main periods
of stroke:
1.
Acute (up to 3 – 4 months)
2.
Renewal (up to 1 year)
3.
Residual
Acute period is divided into such stages:
1. Precursors
2. Apoplectic stroke
3. Focal signs
Usually hemorrhage has rapid
development in day time during physical or emotional stress. The patients are
usually young. And they have risk – factors in anamnesis. Precursors are very
rare.
Two main groups of symptoms
are typical for hemorrhage – general cerebral and focal. Typically general
cerebral symptoms prevail over focal ones in case of hemorrhage.
General cerebral symptoms mean severe headache,
vomiting, consciousness disorders.
While examining patients with
consciousness disorders we should pay attention to the possibility of contact
with patient, his ability to follow commands, to say what has happened with
him, to orient in the space and time and so on.
Sometimes sopor occurs at the beginning of hemorrhage, which can develop in
coma in a few hours.
Coma is characterized by deep
consciousness disorder, disturbance of breathing and heart activity. The
patient doesn’t respond to stimuli.
At atonic coma all
reflexes are lost, blood pressure is decreased and there is breathing
disturbance.
In case of coma development
response to stimuli is absent, eyes are closed, mouth is opened, face is red,
lips are cyanotic, neck vessels are pulsing, there is breathing disturbance,
skin is cold, pulse is strained and slow, blood pressure is increased,
temperature increases in 24 hours. Patient is lying on his back. All muscles
are relaxed. Pupils are changed (there can be anizokoria, cross – eyes,
sometimes gaze paresis can be observed).Mouth angle is a little bit lower. On
the opposite side hemiplegia is often observed: the arm is falling down like
bine, there is hypotonia of muscles, reflexes are low, and Babinski sign is
often observed too.
Sometimes meningeal signs, vomiting
and dysphagia are observed too. Retention of urine or involuntary urination can
also occur. In case of cortex irritation epileptic attacks can be developed.
Large hemisphere hemorrhage is often complicated by secondary brain stem
syndrome. It manifests as progressive breathing disorders, disturbance of heart
activity, consciousness, eye movements, changes of muscle tonus (hormetonia),
autonomic disorders (sweating, tachycardia, hyperthermia).
Brain stem hemorrhage is associated with tetraparesis,
alternating syndromes, eye movement disorders, nystagmus, gorge disorders,
cerebellar syndromes. 
Pons hemorrhage manifests as ptosis, gaze
paresis, increased muscular tone (hormetonia).
Cerebellar hemorrhage usually starts with
dizziness, severe headache in occipital lobe, vomiting. Eye movement disorders,
ptosis, Gervig – Mazhandi syndrome, Parino syndrome are observed. It is also
associated with cerebellar symptoms, such as nystagmus, dysartria, hypotonia,
and ataxia. Paresis of extremities is not common.
The most common complication
of intracerebral hemorrhage is rupture into the ventricle system. This
is usually associated with worsening of patient’s state, hyperthermia,
breathing disorders, and hormetonia. Hormetonia manifests as changes of muscle
tone in extremities, when hypotonia is changed into hypertonia in a few seconds
or minutes.
At right hemisphere hemorrhage involuntary movements in
nonparalysed extremities are observed and they are called parakinesis.
On the side of lesion
there is anizokoria, Bechterev phenomena, painful trigeminal and occipital
points, automatic movements, gaze paralysis, Kerning sign.
On the opposite side –
positive Bare’s sign, mouth angle is located lower than normally.
foot is turned outside, pathological signs,
;
hypotonia, hyporeflexia
Physical
Examination
The assessment in patients with possible
hemorrhagic stroke includes vital signs; a general physical examination that
focuses on the head, heart, lungs, abdomen, and extremities; and a thorough but
expeditious neurologic examination. However, intracerebral hemorrhage may be
clinically indistinguishable from ischemic stroke. (Though stroke is less
common in children, the clinical presentation is similar.)
Hypertension (particularly systolic blood
pressure [BP] greater than 220 mm Hg) is commonly a prominent finding in
hemorrhagic stroke. Higher initial BP is associated with early neurologic
deterioration, as is fever.
An acute onset of neurologic deficit, altered
level of consciousness/mental status, or coma is more common with hemorrhagic
stroke than with ischemic stroke. Often, this is caused by increased
intracranial pressure. Meningismus may result from blood in the subarachnoid
space.
Examination results can be quantified
using various scoring systems. These include the Glasgow Coma Scale (GCS), the
Intracerebral Hemorrhage Score (which incorporates the GCS; see Prognosis), and
the National Institutes of Health Stroke
Scale.
Focal neurologic deficits
The type of deficit depends upon the area
of brain involved. If the dominant hemisphere (usually the left) is involved, a
syndrome consisting of the following may result:
·
Right hemiparesis
·
Right hemisensory loss
·
Left gaze preference
·
Right visual field cut
·
Aphasia
·
Neglect (atypical)
If the nondominant (usually the right)
hemisphere is involved, a syndrome consisting of the following may result:
·
Left hemiparesis
·
Left hemisensory loss
·
Right gaze preference
·
Left visual field cut
Nondominant hemisphere syndrome may also
result in neglect when the patient has left-sided hemi-inattention and ignores
the left side.
If the cerebellum is involved, the patient
is at high risk for herniation and brainstem compression. Herniation may cause
a rapid decrease in the level of consciousness and may result in apnea or
death.
Specific brain sites and associated
deficits involved in hemorrhagic stroke include the following:
·
Putamen - Contralateral hemiparesis, contralateral sensory loss, contralateral conjugate gaze paresis, homonymous hemianopia, aphasia,
neglect, or apraxia
·
Thalamus - Contralateral sensory loss, contralateral hemiparesis, gaze
paresis, homonymous hemianopia, miosis, aphasia, or confusion
·
Lobar - Contralateral hemiparesis or sensory loss, contralateral conjugate
gaze paresis, homonymous hemianopia, abulia, aphasia, neglect, or apraxia
·
Caudate nucleus - Contralateral hemiparesis, contralateral conjugate gaze
paresis, or confusion
·
Brainstem - Quadriparesis, facial weakness, decreased level of
consciousness, gaze paresis, ocular bobbing, miosis, or autonomic instability
·
Cerebellum – Ipsilateral ataxia, facial weakness, sensory loss; gaze
paresis, skew deviation, miosis, or decreased level of consciousness
Other signs of cerebellar or brainstem
involvement include the following:
·
Gait or limb ataxia
·
Vertigo or tinnitus
·
Nausea and vomiting
·
Hemiparesis or quadriparesis
·
Hemisensory loss or sensory loss of all 4 limbs
·
Eye movement abnormalities resulting in diplopia or nystagmus
·
Oropharyngeal weakness or dysphagia
·
Crossed signs (ipsilateral face and contralateral body)
Many other stroke syndromes are associated
with intracerebral hemorrhage, ranging from mild headache to neurologic
devastation. At times, a cerebral hemorrhage may present as a new-onset
seizure.
NIH STROKE SCALE The
NINDS t-PA Stroke Trial No. ___ ___-___ ___ ___-___ ___ ___
FORM 5 Pt. Date of Birth
___ ___/___ ___/___ ___
1 of 4 Hospital
________________________(___ ___-___ ___)
Date of Exam ___ ___/___
___/___ ___
Interval: 1[ ] Baseline
2[ ] 2 hours post treatment 3[ ] 24 hours post onset of symptoms ±20 minutes 4[
] 7-10 days
5[ ] 3 months 6[ ] Other
________________________________(___ ___)
Rev 3/24/93
Time: ___ ___:___ ___ 1[
]am 2[ ]pm
Administer stroke scale
items in the order listed. Record performance in each category after each
subscale exam. Do not go
back and change scores.
Follow directions provided for each exam technique. Scores should reflect what
the patient does, not
what the clinician
thinks the patient can do. The clinician should record answers while
administering the exam and work quickly.
Except where indicated,
the patient should not be coached (i.e., repeated requests to patient to make a
special effort).
IF ANY ITEM IS LEFT
UNTESTED, A DETAILED EXPLANATION MUST BE CLEARLY WRITTEN ON THE FORM. ALL
UNTESTED ITEMS WILL BE
REVIEWED BY THE MEDICAL MONITOR, AND DISCUSSED WITH THE EXAMINER BY
TELEPHONE.
Instructions Scale
Definition Score
1a. Level of
Consciousness: The investigator must choose a
response, even if a full
evaluation is prevented by such obstacles as an
endotracheal tube,
language barrier, orotracheal trauma/bandages. A
3 is scored only if the
patient makes no movement (other than reflexive
posturing) in response
to noxious stimulation.
0 = Alert; keenly responsive.
1 = Not alert, but arousable by minor
stimulation to obey,
answer, or respond.
2 = Not alert, requires repeated stimulation
to attend, or is
obtunded and requires
strong or painful stimulation to
make movements (not
stereotyped).
3 = Responds only with reflex motor or
autonomic effects or
totally unresponsive,
flaccid, areflexic.
______
1b. LOC Questions: The
patient is asked the month and his/her age.
The answer must be correct - there is no
partial credit for being close.
Aphasic and stuporous
patients who do not comprehend the questions
will score 2. Patients
unable to speak because of endotracheal
intubation, orotracheal
trauma, severe dysarthria from any cause,
language barrier or any
other problem not secondary to aphasia are
given a 1. It is
important that only the initial answer be graded and that
the examiner not
"help" the patient with verbal or non-verbal cues.
0 = Answers both questions correctly.
1 = Answers one question correctly.
2 = Answers neither question correctly.
______
1c. LOC Commands: The
patient is asked to open and close the
eyes and then to grip
and release the non-paretic hand. Substitute
another one step command
if the hands cannot be used. Credit is
given if an unequivocal
attempt is made but not completed due to
weakness. If the patient
does not respond to command, the task
should be demonstrated
to them (pantomime) and score the result (i.e.,
follows none, one or two
commands). Patients with trauma,
amputation, or other
physical impediments should be given suitable
one-step commands. Only
the first attempt is scored.
0 = Performs both tasks correctly
1 = Performs one task correctly
2 = Performs neither task correctly ______
2. Best Gaze: Only
horizontal eye movements will be tested.
Voluntary or reflexive
(oculocephalic) eye movements will be scored but
caloric testing is not
done. If the patient has a conjugate deviation of
the eyes that can be
overcome by voluntary or reflexive activity, the
score will be 1. If a
patient has an isolated peripheral nerve paresis
(CN III, IV or VI) score
a 1. Gaze is testable in all aphasic patients.
Patients with ocular
trauma, bandages, pre-existing blindness or other
disorder of visual
acuity or fields should be tested with reflexive
movements and a choice
made by the investigator. Establishing eye
contact and then moving
about the patient from side to side will
occasionally clarify the
presence of a partial gaze palsy.
0 = Normal
1 = Partial gaze palsy. This score is given
when gaze is
abnormal in one or both
eyes, but where forced
deviation or total gaze
paresis are not present.
2 = Forced deviation, or total gaze paresis
not overcome by the
oculocephalic maneuver.
______ NIH STROKE SCALE
The NINDS t-PA Stroke Trial No. ___ ___-___ ___ ___-___ ___ ___
FORM 5 Pt. Date of Birth
___ ___/___ ___/___ ___
2 of 4 Hospital
________________________(___ ___-___ ___)
Date of Exam ___ ___/___
___/___ ___
Interval: 1[ ] Baseline
2[ ] 2 hours post treatment 3[ ] 24 hours post onset of symptoms ±20 minutes 4[
] 7-10 days
5[ ] 3 months 6[ ] Other
________________________________(___ ___)
Rev 3/24/93
3. Visual: Visual fields
(upper and lower quadrants) are tested by
confrontation, using
finger counting or visual threat as appropriate.
Patient must be
encouraged, but if they look at the side of the moving
fingers appropriately,
this can be scored as normal. If there is unilateral
blindness or
enucleation, visual fields in the remaining eye are scored.
Score 1 only if a
clear-cut asymmetry, including quadrantanopia is
found. If patient is
blind from any cause score 3. Double simultaneous
stimulation is performed
at this point. If there is extinction patient
receives a 1 and the
results are used to answer question 11.
0 = No visual loss
1 = Partial hemianopia
2 = Complete hemianopia
3 = Bilateral hemianopia (blind including
cortical blindness)
______
4. Facial Palsy: Ask, or
use pantomime to encourage the patient to
show teeth or raise
eyebrows and close eyes. Score symmetry of
grimace in response to
noxious stimuli in the poorly responsive or noncomprehending patient. If facial
trauma/bandages, orotracheal tube,
tape or other physical
barrier obscures the face, these should be
removed to the extent
possible.
0 = Normal symmetrical movement
1 = Minor paralysis (flattened nasolabial
fold, asymmetry on
smiling)
2 = Partial paralysis (total or near total
paralysis of lower face)
3 = Complete paralysis of one or both sides
(absence of facial
movement in the upper
and lower face) ______
5 & 6. Motor Arm and
Leg: The limb is placed in the appropriate position: extend the arms (palms
down) 90 degrees (if sitting) or 45
degrees (if supine) and
the leg 30 degrees (always tested supine). Drift
is scored if the arm
falls before 10 seconds or the leg before 5 seconds.
The aphasic patient is encouraged using
urgency in the voice and
pantomime but not
noxious stimulation. Each limb is tested in turn,
beginning with the
non-paretic arm. Only in the case of amputation or
joint fusion at the
shoulder or hip may the score be "9" and the
examiner must clearly
write the explanation for scoring as a "9".
0 = No drift, limb holds 90 (or 45) degrees
for full 10 seconds.
1 = Drift, Limb holds 90 (or 45) degrees, but
drifts down before
full 10 seconds; does
not hit bed or other support.
2 = Some effort against gravity, limb cannot
get to or maintain
(if cued) 90 (or 45)
degrees, drifts down to bed, but has
some effort against
gravity.
3 = No effort against gravity, limb falls.
4 = No movement
9 = Amputation, joint fusion explain:
______________________
5a. Left Arm
5b. Right Arm ______
______
0 = No drift, leg holds 30 degrees position
for full 5 seconds.
1 = Drift, leg falls by the end of the 5
second period but does
not hit bed.
2 = Some effort against gravity; leg falls to
bed by 5 seconds,
but has some effort
against gravity.
3 = No effort against gravity, leg falls to
bed immediately.
4 = No movement
9 = Amputation, joint fusion
explain:_________________
6a. Left Leg
6b. Right Leg ______
______ NIH STROKE SCALE
The NINDS t-PA Stroke Trial No. ___ ___-___ ___ ___-___ ___ ___
FORM 5 Pt. Date of Birth
___ ___/___ ___/___ ___
3 of 4 Hospital
________________________(___ ___-___ ___)
Date of Exam ___ ___/___
___/___ ___
Interval: 1[ ] Baseline
2[ ] 2 hours post treatment 3[ ] 24 hours post onset of symptoms ±20 minutes 4[
] 7-10 days
5[ ] 3 months 6[ ] Other
________________________________(___ ___)
Rev 3/24/93
7. Limb Ataxia: This
item is aimed at finding evidence of a unilateral
cerebellar lesion. Test
with eyes open. In case of visual defect, insure
testing is done in
intact visual field. The finger-nose-finger and heelshin tests are performed on
both sides, and ataxia is scored only if
present out of
proportion to weakness. Ataxia is absent in the patient
who cannot understand or
is paralyzed. Only in the case of amputation
or joint fusion may the
item be scored "9", and the examiner must
clearly write the
explanation for not scoring. In case of blindness test by
touching nose from
extended arm position.
0 = Absent
1 = Present in one limb
2 = Present in two limbs
If present, is ataxia in
Right arm 1 = Yes 2 = No
9 = amputation or joint fusion,
explain ___________________
Left arm 1 = Yes 2 = No
9 = amputation or joint fusion,
explain ___________________
Right leg 1 = Yes 2 = No
9 = amputation or joint fusion,
explain ___________________
Left leg 1 = Yes 2 = No
9 = amputation or joint fusion,
explain ___________________
8. Sensory: Sensation or grimace to pin prick when tested, or
withdrawal from noxious stimulus in the obtunded or aphasic patient.
Only sensory loss attributed to stroke is scored as abnormal and the
examiner should test as many body areas [arms (not hands), legs,
trunk, face] as needed to accurately check for hemisensory loss. A
score of 2, "severe or total," should only be given when a
severe or total
loss of sensation can be clearly demonstrated. Stuporous and aphasic
patients will therefore probably score 1 or 0. The patient with brain
stem stroke who has bilateral loss of sensation is scored 2. If the
patient does not respond and is quadriplegic score 2. Patients in coma
(item 1a=3) are arbitrarily given a 2 on this item.
0 = Normal; no sensory loss.
1 = Mild to moderate sensory loss;
patient feels pinprick is less
sharp or is dull on the affected side; or there is a loss of
superficial pain with pinprick but patient is aware he/she
is being touched.
2 = Severe to total sensory loss;
patient is not aware of being
touched in the face, arm, and leg.
______
9. Best Language: A great deal of information about comprehension
will be obtained during the preceding sections of the examination. The
patient is asked to describe what is happening in the attached picture,
to name the items on the attached naming sheet, and to read from the
attached list of sentences. Comprehension is judged from responses
here as well as to all of the commands in the preceding general
neurological exam. If visual loss interferes with the tests, ask the
patient to identify objects placed in the hand, repeat, and produce
speech. The intubated patient should be asked to write. The patient in
coma (question 1a=3) will arbitrarily score 3 on this item. The examiner
must choose a score in the patient with stupor or limited cooperation
but a score of 3 should be used only if the patient is mute and follows
no one step commands.
0 = No aphasia, normal
1 = Mild to moderate aphasia; some
obvious loss of fluency or
facility of comprehension, without significant limitation on
ideas expressed or form of expression. Reduction of
speech and/or comprehension, however, makes
conversation about provided material difficult or
impossible. For example in conversation about provided
materials examiner can identify picture or naming card
from patient's response.
2 = Severe aphasia; all
communication is through fragmentary
expression; great need for inference, questioning, and guessing
by the listener. Range of information that can be exchanged is
limited; listener carries burden of communication. Examiner
cannot identify materials provided from patient response.
3 = Mute, global aphasia; no
usable speech or auditory
comprehension.
______
10. Dysarthria: If patient is thought to be normal an adequate sample
of speech must be obtained by asking patient to read or repeat words
from the attached list. If the patient has severe aphasia, the clarity of
articulation of spontaneous speech can be rated. Only if the patient is
intubated or has other physical barrier to producing speech, may the
item be scored "9", and the examiner must clearly write an
explanation
for not scoring. Do not tell the patient why he/she is being tested.
0 = Normal
1 = Mild to moderate; patient
slurs at least some words and, at
worst, can be understood with some difficulty.
2 = Severe; patient's speech is so
slurred as to be unintelligible
in the absence of or out of proportion to any dysphasia,
or is mute/anarthric.
9 = Intubated or other physical
barrier,
explain______________________________
NIH STROKE SCALE The NINDS t-PA Stroke Trial No. ___ ___-___ ___ ___-___
___ ___
FORM 5 Pt. Date of Birth ___ ___/___ ___/___ ___
4 of 4 Hospital ________________________(___ ___-___ ___)
Date of Exam ___ ___/___ ___/___ ___
Interval: 1[ ] Baseline 2[ ] 2 hours post treatment 3[ ] 24 hours post
onset of symptoms ±20 minutes 4[ ] 7-10 days
5[ ] 3 months 6[ ] Other
________________________________(___ ___)
Rev 3/24/93
11. Extinction and Inattention (formerly Neglect): Sufficient
information to identify neglect may be obtained during the prior testing.
If the patient has a severe visual loss preventing visual double
simultaneous stimulation, and the cutaneous stimuli are normal, the score is
normal. If the patient has aphasia but does appear to attend to both sides, the
score is normal. The presence of visual spatial neglect or anosagnosia may also
be taken as evidence of abnormality. Since the abnormality is scored only if
present, the item is never untestable.
0 = No abnormality.
1 = Visual, tactile, auditory,
spatial, or personal inattention or extinction to bilateral simultaneous
stimulation in one of the sensory modalities.
2 = Profound hemi-inattention or
hemi-inattention to more than one modality. Does not recognize own hand or
orients to only one side of space. ______
Additional item, not a part of the NIH Stroke Scale score.
A. Distal Motor Function: The patient's hand is held up at the forearm by
the examiner and patient is asked to extend his/her fingers as much as
possible. If the patient can't or doesn't extend the fingers the examiner
places the fingers in full extension and observes for any flexion movement for
5 seconds. The patient's first attempts only are graded. Repetition of the
instructions or of the testing is prohibited.
0 = Normal (No flexion after 5
seconds)
1 = At least some extension after
5 seconds, but not fully extended.
Any movement of the fingers which is not command is not scored.
2 = No voluntary extension after 5
seconds. Movements of the fingers at another time are not scored.
a. Left Arm
b. Right Arm
12. _____________________________________ (___ ___ ___)
Person
Administering Scale
Code
The run of the disease
The patients with brain
hemorrhage are in very severe state. 70 % to 95 % of them died. About 40 % - 45
% of them die during the first day, the rest of them - live 3 or 5 days.
The main cause of death is compression of brain
stem as a result of brain edema and rupture into ventricular system associated
with disorders of vital centers.
In case of good prognosis the
patients usually recover from coma, then reflexes appear, general cerebral
symptoms regress, the patients start to gorge, then they start to move,
sensation and speech renew also.
Diagnostics
In case of rapid development
of all symptoms with loss of consciousness, high blood pressure and presence of
focal symptoms there is no problem with putting diagnosis. But when the
hemorrhage starts gradually without loss of consciousness, then it is much more
difficult to put a diagnosis. In this case instrumental and laboratory
examination has a great meaning.
In blood usually
leucocytosis, related lymphopenia, hyperglycemia (up to 8 – 10 mmole/l) is
observed.
In liquor which is
flowing out under high pressure during lumbar puncture a great number of
erythrocytes are found.
1. normal, 2. subarachnoid
haemorrhage, 3. intracerebral haematoma, 4. serous meningitis
2. On eye
fundus – retinal hemorrhages, hypertonic angioretinopathy and Salus
symptoms are observed.
At echoencephaloscopy there is dislocation of
middle structures on 6 –7 sm to the healthy side.
By means of angiography we can find out
aneurysm, dislocation of blood vessels, to find out zone “without vessels “.
EEG
CT and MRI find out hyperdensive focuses.
Mixed
parenchimatous-ventricular haemorrhage Epidural haematoma
Subdural haematoma
Diagnostic
Considerations
Intracerebral hemorrhage may be clinically
indistinguishable from ischemic stroke, and a thorough history and physical
examination are important. An acute onset of neurologic deficit, altered level
of consciousness/mental status, or coma is more common with hemorrhagic stroke
than with ischemic stroke. A history of trauma, even if minor, may be
important, as extracranial arterial dissections can result in ischemic stroke.
Seizures are more common in hemorrhagic
stroke than in ischemic stroke and occur in up to 28% of hemorrhagic strokes,
generally at the onset of the intracerebral hemorrhage or within the first 24
hours. Postictal (Todd) paralysis and hyperosmolality should also be
considered.
Other problems to consider are as follows:
·
Hyponatremia or hypernatremia
·
Migraine headache
·
Hyperosmolar hyperglycemic nonketotic coma
Differential diagnosis
1. Infarction of brain
(thrombembolic)
2. Epistatus
3. Uremic coma
4. Diabetic coma
5. Traumatic hemorrhage
6. Brain tumor with inside
hemorrhage.
Approach Considerations
Laboratory tests should include a complete blood
count, a metabolic panel, and—particularly in patients taking
anticoagulants—coagulation studies (ie, prothrombin time or international
normalized ratio [INR] and an activated partial thromboplastin time).[28]
Brain imaging is a crucial step in the evaluation of
suspected hemorrhagic stroke and must be obtained on an emergent basis. Brain
imaging aids diagnosing hemorrhage, and it may identify complications such as
intraventricular hemorrhage, brain edema, or hydrocephalus. Either noncontrast
computed tomography (NCCT) scanning or magnetic resonance imaging (MRI) is the
modality of choice.
Computed tomography (CT)-scan studies can also be
performed in patients who are unable to tolerate a magnetic resonance
examination or who have contraindications to MRI, including pacemakers,
aneurysm clips, or other ferromagnetic materials in their bodies. Additionally,
CT-scan examination is more easily accessible for patients who require special
equipment for life support. See the image below.
Noncontrast computed tomography scan of the brain (left)
demonstrates an acute hemorrhage in the left gangliocapsular region, with
surrounding white matter hypodensity consistent with vasogenic edema.
T2-weighted axial magnetic resonance imaging scan (middle image) again
demonstrates the hemorrhage, with surrounding high-signal edema. The coronal
gradient-echo image (right) demonstrates susceptibility related to the
hematoma, with markedly low signal adjacent the left caudate head.
Gradient-echo images are highly sensitive for blood products.
CT angiography and contrast-enhanced CT scanning may
be considered for helping identify patients at risk for hematoma expansion.
Extravasation of contrast within the hematoma indicates high risk.
When clinical or radiologic findings suggest an
underlying structural lesion, useful techniques include CT angiography, CT
venography, contrast-enhanced CT scanning, contrast-enhanced MRI, magnetic
resonance angiography (MRA), or magnetic resonance venography.[28]
Conventional angiography is the gold standard in
evaluating for cerebrovascular disease and for providing less-invasive
endovascular interventions. This modality can be performed to clarify equivocal
findings or to confirm and treat disease seen on MRA, CTA, transcranial
Doppler, or neck ultrasonograms. However, Zhu et al found that in patients with
spontaneous intracranial hemorrhage, angiographic yield was significantly lower
in patients older than 45 years and those who had preexisting hypertension.[29]
Although the traditional approach to excluding
underlying vascular abnormalities in patients with spontaneous intracerebral
hemorrhage is to use digital subtraction angiography (DSA) in the acute and
subacute phases, Wong et al found that MRA was able to detect most structural
vascular abnormalities in the subacute phase in most patients. Consequently,
they recommend MRA as the screening test.
Subarachnoid hemorrhage (SH)
Etiology The most common cause of SH is
aneurysm rupture. The other causes include
hypertension, atherosclerosis, blood diseases, rheumatism, brain tumors, and
uremia and so on. The rupture risk – factors are physical or
emotional stress, changes of blood pressure, alcohol usage.
According to Samoiylov
(1990) there are 8 kind of etiologic factors of subarachnoid hemorrhage:
1. Aneurysmatic (50 – 62 %) –
aneurysm rupture.
2. Hypertensive (at hypertension)
3. Atherosclerotic (15 %)
4. Traumatic (5 – 6 %)
5. Infectious – toxic (8.5 %)
6. Blastomatose (at tumors)
7. Pathohemic (at blood diseases)
8. Cryptogenic (4 – 4.8 %)
Table 9-2
Signs and symptoms of aneurysms according to site of origin
|
Origin of aneurysm |
Structure involved |
Signs and symptoms |
|
Internal carotid, cavernous portion |
Compression of cranial nerves III, IV, VI;
compression of ophthalmic division of cranial nerve V; compression of
pituitary; rupture into cavernous sinus producing an AV fistula |
Mydriasis, diplopia, ptosis,
trigeminal neuralgia,
atypical facial pain, hypopituitarism, noise
in the head |
|
Internal carotid, supraclinoid portion |
Compression of optic nerve, compression of
optic chiasm, compression of cranial
nerve III |
Visual failure, optic atrophy, visual field
defects, mydriasis, diplopia, ptosis |
|
Ophthalmic artery |
Compression of optic nerve, compression of
pituitary |
Visual failure, optic atrophy, hypopituitarism |
|
Middle cerebral artery |
Irritation of the cortex |
Usually causes few signs and symptoms before rupture,
partial seizures |
|
Anterior cerebral artery |
Compression of optic chiasm, compression of olfactory tract |
Visual field defects, unilateral anosmia |
|
Posterior communicating artery |
Compression of cranial nerve III, compression of
cranial nerve VI |
Mydriasis, diplopia, ptosis |
|
Posterior cerebral artery |
Compression of the midbrain |
Usually causes few signs and symptoms before
rupture, hydrocephalus, stupor,
akinetic mutism |
|
Basilar artery |
Compression of cranial nerve V, compression of
cranial nerve VII, compression of midbrain |
Trigeminal neuralgia, atypical facial
pain, facial paralysis, hydrocephalus |
|
Vertebral artery |
Compression of cranial nerves K, X,
compression of brainstem |
Paralysis of the palate, pharynx, dysphonia, dysphagia, vertigo, ataxia, vomiting |
Clinical features
The development of the disease is rapid,
without precursors. Although some of patients have symptoms of aneurysm:
headache in frontal lobe, paresis of CN (Oculomotor N is often damaged).
The first signs of SH are severe headache
or feeling of hot liquid flowing in the brain. At the beginning this pain is
local (in the region of occipital lobe) than it becomes more diffuse. Later
pains in neck, back appear, sometimes they irradiate in legs. Simultaneously
with headache vomiting and nausea occur. Besides these symptoms there are often
general cerebral symptoms, such as short loss of consciousness,
psychomotor excitement, seizures.
In a few hours or the next day meningeal
syndrome occur. It manifests as rigidity of occipital muscles, symptoms of
Kernig, Brudzinski, and general hyperesthesia. Significant focal neurologic
symptoms are not common. Only in case of basal hemorrhage CNs suffers (that is
the reason of ptosis, cross – eye, dyplopia, paresis of mimic muscles).
That’s why lesion of CNs is typical for basal aneurysm
rupture.
In acute stage of hemorrhage a lot of patients have focal symptoms:
paresis of extremities, sensory and speech disorders. Usually it can be
explained by associated brain hemorrhage, arterial spasm and as a result local
ischemia. Spasm is usually developed on the 3rd – 4 th day and lasts till 3rd –
4 th week.
On the second or third day almost all patients with SH have increased
temperature to 37.5 – 38°. Leucocytosis is also
observed. In liquor fresh blood is found out.
In severe cases significant
disorders of heart – vascular system and breathing are observed.
The most common clinical scoring systems for
grading aneurysmal subarachnoid hemorrhage are the Hunt and Hess grading scheme
and the World Federation of Neurosurgeons (WFNS) grading scheme, which
incorporates the Glasgow Coma Scale. The Fisher Scale incorporates findings
from noncontrast computed tomography (NCCT) scans.
The main complications of SH are:
1. Arterial vasospasm
occurs in approximately 30 percent of cases of SAH and has a peak incidence
6 to 8 days postbleed. However, it can occur from 4 to 12 days after aneurysm rupture. Once vasospasm develops, it can persist for several days to several
weeks.
Patients with a large volume of blood in the
basal cisterns carry the highest risk of spasm.18 Blood in the sylvian fissure indicates intermediate risk.19
About 12 percent of patients with extensive vasospasm will develop permanent neurological deficits or die.
The pathogenesis of
vasospasm is obscure. It probably related
to the presence of oxyhemoglobin in the subarachnoid blood clot, leading to the release
of cytokines that stimulate release of
endothelia, an agent known to cause vasospasm. Increased
concentrations of endothelia have been demonstrated in plasma and cerebrospinal fluid (CSF) after SAH.
An alternative hypothesis proposes that the
presence of blood in the subarachnoid space
leads to inflammation and the release of platelet activating factor from
inflammatory cells, platelets, and vascular endothelium,
resulting in contraction of the muscle in cerebral arterial walls and vasospasm.
2. Rebleeding
following ruptured aneurysm is
maximum in the first 24 h with a cumulative risk of about 20 percent in the
next 14 days. Rebleeding results in death in about 60 percent of affected
cases.
3. Intracerebral
hematoma can produce a contralateral homonymous hemianopia and hemiparesis.
4. A subdural
hematoma may result from rupture of an aneurysm
into the subdural space.
5. Acute hydrocephalus
is the result of occlusion of the subarachnoid
space by breakdown products of red blood cell disintegration and the
ensuing inflammatory response. Hydrocephalus occurs
in more than 50 percent of cases of SAH within 30 days of the hemorrhage but
can occur quickly within a period of several hours following SAH. Ventricular
peritoneal shunting may be required in those who show delayed neurological
deterioration and persistent ventricular enlargement.
6. Cardiac
arrhythmias and in some cases cardiac injury with pulmonary edema presumably
the result of cerebral or brainstem injury
are recognized complications of SAH.
7. Inappropriate secretion of antidiuretic hormone
may occur in severe SAH or as a postoperative complication. Some patients
develop hyponatremia due to inhibition of
renal tubular sodium absorption rather than inappropriate secretion of antidiuretic hormone.
8. Pulmonary and urinary tract infections,
dehydration, electrolyte disturbances, and the development of decubiti are
not unusual in comatosed patients.
9. Epilepsy develops in 9 percent
of patients who survive SAH, occurring within 4 weeks after the hemorrhage in
the majority of cases.
Diagnostic Procedures
1. Computed tomography
(CT) scanning is the
procedure of choice in the diagnosis of SAH and will confirm the diagnosis in 85
percent of cases, if this study is performed within 48 h of bleeding. A CT scan
will reveal blood in the basal cisterns in most patients with SAH (Fig. 9-3),
and the extent of an intracerebral hematoma, cerebral
infarction, cerebral edema, and acute hydrocephalus
are readily demonstrated. Intraventricular
and intracerebral bleeding and hydrocephalus have adverse effects on survival.
Localized thick or diffuse collections of subarachnoid
blood in the basal cisterns are associated with a high risk of vasospasm and a poorer prognosis.28 Aneurysms are occasionally seen in an enhanced
CT scan.
Subarachnoid haemorrhage in posterior cranial fosse. Subarachnoid
haemorrhage in anterior cranial fosse.
2. Magnetic resonance imaging (MRI) scanning
has no advantage in the diagnosis in the early stages of SAH. However, MRI may
detect the site of blood clot when it is no longer detectable by CT and is
useful in detecting the probable source of hemorrhage in cases with multiple aneurysms. Magnetic resonance angiography should always be performed in cases
of SAH when cerebral angiography fails to
demonstrate an aneurysm and is regarded
as the superior technique when compared to digital subtraction angiography in some centers.
3. Lumbar
puncture reveals a bloody CSF under increased pressure. The supernatant
fluid is xanthochromic within 6 h of
SAH. There is a polymorphonuclear pleocytosis
within 24 h, and later, appearance of mononuclear
cells. Red blood cells usually disappear from the CSF by 5 days; their
persistence indicates that further hemorrhage has occurred. Xanthochromia usually lasts for about 28 days.
An estimate of the date of onset of SAH can be made by measuring the presence
of oxyhemoglobin and bilirubin in the xanthochromic fluid by CSF spectrophotometry.
Oxyhemoglobin appears at the onset of SAH and gradually disappears. Bilirubin appears after 2 or 3 days and
increases in amount as oxyhemoglobin decreases.
Recurrent hemorrhage is associated with a late rise in the presence of oxyhemoglobin. Lumbar puncture continues to
have an important role in the diagnosis of SAH.
4. Skull x-rays occasionally show the presence
of calcification in the wall of an aneurysm. Erosion
of the lateral wall of the sella or
anterior clinoid processes may occur. Pineal shift occurs in the presence of a
large hematoma. An ophthalmic aneurysm can cause enlargement of the optic
foramen.
5. Fourvessel arteriography with multiple views to demonstrate the origin of each of the major
intracranial arteries should be performed
as early as possible in all cases of SAH (Fig. 9-5). The objective of this
study is the demonstration of the origin of the aneurysm
to define the neck of the aneurysm, and
to detect the presence of multiple aneurysms (Fig.
9-6), or demonstrate the presence or absence of vasospasm.
The complication rate of arteriography performed
by an experienced neuroradiologist, using
modern techniques, is less than 1 percent. Rebleeding from a ruptured aneurysm during arteriography
is rare, occurring in less than 3 percent of cases. The risk of
rebleeding is significantly higher during the first 6 h after the initial
event.32 Consequently, it is prudent to delay arteriography for at least 6 h after the
initial hemorrhage.
6. CT angiography. High-quality CT angiography provides adequate depiction of aneurysms in 90 percent of cases allowing
surgery to be performed on the basis of CT angiography
alone.
7. Transcranial Doppler
ultrasound monitoring is a useful procedure in the detection of vasospasm leading to delayed ischemic neurological deficits complicating
SAH.
Prognosis Usually is not good. As during
the 2nd – 4th weeks recurrent hemorrhage can occur which can cause patient’s
death.
Thus we usually put the diagnosis of SH in case of:
1. Stroke – like development with
general cerebral and meningeal symptoms and absence of significant focal
neurologic deficit.
2. The presence of blood in
liquor (bleeding liquor during first day and yellow liquor on 3rd – 5th day)
3. Retinal hemorrhages are on eye
fundus
Differential
diagnosis:
1. Meningitis
2. Acute food toxic infection
3. Infectious diseases
Lumbar puncture, CT, MRI, US
helps to put diagnosis; angiography helps to find localization and sizes of
aneurysm.
Differential treatment of haemorrhage:
The main directions of
treatment are:
1. To lower increased blood
pressure
2. To liquidate brain edema and
lower intracranial pressure
3. To increase coagulative
properties of blood and decrease penetrance of vessels’ wall
4. To prevent and treat cerebral
vessels spasm
5. To normalize vital and
autonomic functions and prevent complications
6. To treat hypoxia and brain
metabolism disorders
1. To lower increased blood
pressure
Clofelini, b-aqdrenoblockers (anaprilini,
obzidani, inderali), Calcium antagonists (nifidipini, adalat) IACE (capoten,
enalapril, renarapril) are used.
At too high blood pressure ganglioblockers are used:
-
Pentamini 5% 1.0
-
Benzohexonium 2.5 % 1 ml
-
Arfonad 5 ml 5 % i/v in physiologic solution
Blood Pressure Control
No controlled studies have defined optimum
BP levels for patients with acute hemorrhagic stroke, but greatly elevated BP
is thought to lead to rebleeding and hematoma expansion. Stroke may result in
loss of cerebral autoregulation of cerebral perfusion pressure.
Suggested agents for use in the acute
setting are beta blockers (eg, labetalol) and angiotensin-converting enzyme
inhibitors (ACEIs) (eg, enalapril). For more refractory hypertension, agents
such as nicardipine and hydralazine are used. Avoid nitroprusside because it
may raise intracranial pressure.
The 2010 AHA/ASA guidelines acknowledge
that evidence for the efficacy of managing BP in hemorrhagic stroke is
currently incomplete. With that caveat, the AHA/ASA recommendations for
treating elevated BP are as follows[28] :
·
If systolic BP is over 200 mm Hg or mean arterial pressure (MAP) is over
150 mm Hg, then consider aggressive reduction of BP with continuous IV infusion;
check BP every 5 minutes
·
If systolic BP is over 180 mm Hg or MAP is over 130 mm Hg and intracranial
pressure may be elevated, then consider monitoring intracranial pressure and
reducing BP using intermittent or continuous intravenous medications, while
maintaining a cerebral perfusion pressure of 60 mm Hg or higher
·
If systolic BP is over 180 or MAP is over 130 mm Hg and there is no
evidence of elevated intracranial pressure, then consider modest reduction of
BP (target MAP of 110 mm Hg or target BP of 160/90 mm Hg) using intermittent or
continuous intravenous medications to control it, and perform clinical
reexamination of the patient every 15 minutes
·
In patients presenting with a systolic BP of 150 to 220 mm Hg, acute
lowering of systolic BP to 140 mm Hg is probably safe
For patients with aneurysmal subarachnoid
hemorrhage, the 2012 AHA/ASA guidelines recommend lowering BP below 160 mmHg
acutely to reduce rebleeding.
The ongoing Antihypertensive Treatment in Acute Cerebral Hemorrhage-II (ATACH-II) phase 3 randomized
clinical trial is designed to determine whether the likelihood of death or
disability at 3 months after spontaneous supratentorial intracerebral
hemorrhage is lower when systolic BP has been reduced to 180 mm Hg or below or
to 140 mm Hg or below. In ATACH-II, intravenous nicardipine is started within 3
hours of stroke onset and continued for the next 24 hours.
2. To liquidate brain edema and lower
intracranial pressure
Intracranial Pressure
Control
Elevated intracranial pressure may result
from the hematoma itself, from surrounding edema, or from both. The frequency
of increased intracranial pressure in patients with intracerebral hemorrhage is
not known.
Elevate the head of the bed to 30°. This
improves jugular venous outflow and lowers intracranial pressure. The head
should be midline and not turned to the side. Provide analgesia and sedation as
needed. Antacids are used to prevent gastric ulcers associated with
intracerebral hemorrhage.
More aggressive therapies, such as osmotic
therapy (ie, mannitol, hypertonic saline), barbiturate anesthesia, and
neuromuscular blockage, generally require concomitant monitoring of
intracranial pressure and BP with an intracranial pressure monitor to maintain
adequate cerebral perfusion pressure of greater than 70 mm Hg. A randomized,
controlled study of mannitol in intracerebral hemorrhage failed to demonstrate
any difference in disability or death at 3 months.[33]
Hyperventilation (partial pressure of
carbon dioxide [PaCO2] of 25 to 30-35 mm Hg) is not recommended,
because its effect is transient, it decreases cerebral blood flow, and it may
result in rebound elevated intracranial pressure.[2] Glucocorticoids are not effective and
result in higher rates of complications with poorer outcomes.
3. To increase coagulative
properties of blood and decrease penetrance of vessels’ wall
a) CaCl2 10 – 20 ml 10 % i/v
Vicasoli 1 – 2 ml 1 % i/v
ascorbinic acid 2 – 5 ml 5 –
10 % solution I/m
b) Antifibrinolytics:
EAKA 100 ml 5 % solution 1–2
times per day I/v by drops during 5 – 7 days. Then we use it orally –
c) At decompensated fibrinolysis we use
Trasiloli 20 – 30 000 U i/v by drops in 250 ml of
physiologic solution
Hordox 5 000 U i/v by drops every other day
d) to normalize microcirculation we use:
dicinoni 2 ml 12.5 % solution 2 – 3 times per day during 10 days, then 2
tablets (
Ascorutini, rutamini (1 ml i/m 1 – 2 times per day)
4. To prevent and treat cerebral
vessels spasm:
Antagonists of Calcium are used:
Nimotop is introduced I / v 15 mg per
kg per day during 5 – 6 hours. On the 5th – 7 th day it is used
orally 60 mg every 4 hours during 7 – 10 days.
5. To normalize vital and autonomic functions
and prevent complications
6. To treat hypoxia and brain metabolism disorders.
The same measures as in
nondifferential treatment are used.
7. Symptomatic treatment.
At severe headache
·
baralhini 5 mli/ v
·
combination of analgini ( 4 ml 50 % solution ) with 1
ml 1 % dimedroli and novocaini 5 ml 0.5 % solution
·
promedoli are used.
At vomiting
·
haloperidoli 1 – 2 ml 0.5 % solution
·
droperidoli 1 ml 0.25 % solution are used
At seizures
·
sibazoni 2 – 4 ml 0.5 % solution,
·
natrii oxybutiras 10 ml 20 % solution i/v are used
Surgical treatment is used at lateral or lobar
hemorrhages less the 100 ml.
At subarachnoid hemorrhages surgical treatment is recommended during first
48 hours or on the second week.
Invasive Therapy
A potential treatment for hemorrhagic stroke is
surgical evacuation of the hematoma. However, the role of surgical treatment
for supratentorial intracranial hemorrhage remains controversial. Outcomes in
published studies are conflicting. The
international multicenter Trial in Intracerebral Haemorrhage (STICH), which
compared early surgery with initial conservative treatment, failed to
demonstrate a surgery-related benefit.[43]
In contrast, a meta-analysis of trials for surgical
treatment of spontaneous supratentorial intracerebral hemorrhage found evidence
for improved outcome with surgery if any of the following applied[44] :
·
Surgery
undertaken within 8 hours of ictus
·
Volume
of the hematoma 20-50 mL
·
Glasgow
coma score 9-12
·
Patient
age 50-69 years
In addition, evidence suggests that a subset of
patients with lobar hematoma but no intraventricular hemorrhage may benefit
from intervention.[45] A study
in this group of patients (STICH II) has been completed, but results are still
pending.[46]
In patients with cerebellar hemorrhage, surgical
intervention has been shown to improve outcome if the hematoma is greater than
3 cm in diameter. It can be lifesaving in the prevention of brainstem
compression.
Endovascular treatment of aneurysms
Endovascular therapy using coil embolization, as an
alternative to surgical clipping, has been increasingly employed in recent
years with great success (see the following images), although controversy still
exists over which treatment is ultimately superior.
A cerebral angiogram was performed in a 57-year-old
man with a family history of subarachnoid hemorrhage and who was found on
previous imaging to have a left distal internal carotid artery (ICA) aneurysm.
The lateral projection from this angiogram demonstrates a narrow-necked
aneurysm arising off the posterior aspect of the distal supraclinoid left ICA,
with an additional nipplelike projection off the inferior aspect of the dome of
the aneurysm. There is also a mild, lobulated dilatation of the cavernous left
ICA.
Follow-up cerebral angiogram after coil embolization
in a 57-year-old man with a left distal internal carotid artery aneurysm.
Multiple coils were placed with sequential occlusion of the aneurysm, including
the nipple at its inferior aspect. A small amount of residual filling is noted
at the proximal neck of the aneurysm, which may thrombose over time.
The International Subarachnoid Aneurysm Trial (ISAT)
of neurosurgical clipping versus endovascular coiling reported that independent
survival was higher at 1 year with endovascular coiling and that the survival
benefit continued for at least 7 years.[47] This
randomized, multicenter, international trial included 2143 patients. The
investigators also noted that the risk of late rebleeding was small in both
groups but higher in the endovascular coiling group, reconfirming the higher
long-term anatomic cure rate of surgery.[47, 48]
More recently, the Barrow Ruptured Aneurysm Trial
(BRAT), which included 358 patients, demonstrated superior functional outcome
at 1 year with endovascular coil embolization than with microsurgical clipping
for acutely ruptured intracerebral aneurysm. Further, in contrast to the ISAT
results, no patient in the endovascular embolization group suffered a recurrent
hemorrhage.[49] Outcomes
at 3-year follow-up of the BRAT patients continued to favor coil embolization,
though the difference no longer reached statistical significance.[50]
Endovascular treatment of aneurysms may be favored
over surgical clipping under the following circumstances[51] :
·
The
aneurysm is in a location that is difficult to access surgically, such as the
cavernous internal carotid artery (ICA) or the basilar terminus
·
The
aneurysm is small-necked and located in the posterior fossa
·
The
patient is elderly
·
The
patient has a poor clinical grade
The following factors militate against endovascular
treatment:
·
Wide-based
aneurysms or those without an identifiable neck
·
Aneurysms
with a vessel extending off the aneurysm dome
·
Severely
atherosclerotic or tortuous vessels that limit the endovascular approach
Although vasospasm may be treated with intra-arterial
pharmaceutical agents, such as verapamil or nicardipine, balloon angioplasty
can be used for opening larger vessels (see the images below). The combination
of the 2 treatments appears to provide safe and long-lasting therapy for
severe, clinically significant vasospasm.[52]
Frontal view from a cerebral angiogram in a
41-year-man who presented 7 days earlier with subarachnoid hemorrhage from a
ruptured anterior communicating artery (ACA) aneurysm (which was treated with surgical
clipping). There is significant narrowing of the proximal left ACA, left M1
segment, and left supraclinoid internal carotid artery, indicating vasospasm.
Angiographic view in a 41-year-man who presented 7 days
earlier with subarachnoid hemorrhage from a ruptured anterior communicating
artery (ACA) aneurysm (which was treated with surgical clipping). Superimposed
road map image demonstrates placement of a wire across the left M1 segment and
balloon angioplasty. The left proximal ACA and supraclinoid internal carotid
artery (ICA) were also angioplastied, and intra-arterial verapamil was
administered. Follow-up image on the right after treatment demonstrates
resolution of the left M1 segment and distal ICA, which are now widely patent.
Residual narrowing is seen in the left proximal ACA.
Ventriculostomy
Placement of an intraventricular catheter for
cerebrospinal fluid drainage (ie, ventriculostomy) is often used in the setting
of obstructive hydrocephalus, which is a common complication of thalamic
hemorrhage with third-ventricle compression and of cerebellar hemorrhage with
fourth-ventricle compression. Ventriculostomies are associated with a risk of
infection, including bacterial meningitis.
In renewal period we prescribe
·
cerebrolizini 5 ml 2 – 3 times per day
·
piracetami 10 ml 20 % solution
·
instenoni 2 ml
·
actovegini 2 ml twice a day
Prevention of Hemorrhagic Stroke
Antihypertensives
The 2010
AHA/ASA guidelines for spontaneous ICH recommend that after acute intracerebral
hemorrhage, patients without medical contraindications should have BP well
controlled, especially for hemorrhage in typical hypertensive vasculopathy
locations. In
addition, the guidelines strongly recommend maintenance of BP below 140/90 mm
Hg to prevent a first stroke. In patients with hypertension plus either
diabetes or renal disease, the treatment goal is BP below 130/80 mm Hg.
BP-lowering
medications include thiazide diuretics, calcium channel blockers,
angiotensin-converting enzyme inhibitors (ACEIs), and angiotensin receptor
blockers (ARBs). For patients with diabetes, the use of ACEIs and ARBs to treat
hypertension is a class I-A recommendation (strongest and best-documented),
according to the 2011 AHA/ASA primary prevention guidelines. Beta blockers are
considered second-line agents given their inferiority in preventing vascular
events, despite producing similar reductions in BP. (Adverse effects of ACEIs
include cough [10%], which is less common with ARBs.)
Although
statin therapy is recommended for primary prevention of ischemic stroke (class
I-A recommendation), especially
if other risk factors are present, some studies have found an increased risk of
intracerebral hemorrhage with statin use. However, a meta-analysis of 31
randomized, controlled trials of statin therapy found that active statin
therapy was not associated with a significant increase in intracerebral
hemorrhage.[54]
In the Heart
Outcomes Prevention Evaluation (HOPE) study, the addition of the ACEI ramipril
to all other medical therapy, including antiplatelet agents, reduced the
relative risk of stroke, death, and myocardial infarction by 32% compared with
placebo. Only
40% of the efficacy of ramipril could be attributed to its BP-lowering effects.
Other postulated mechanisms included endothelial protection.
Whether the
beneficial effect of ramipril represents a class effect of ACEIs or whether it
is a property unique to ramipril is unclear.
In the
Perindopril Protection Against Recurrent Stroke Study (PROGRESS), a regimen
based on perindopril, an ACEI, was superior to placebo. Although
this drug alone was not superior to placebo, the combination of perindopril
with indapamide (a thiazide diuretic) substantially reduced the recurrence of
stroke. Much of the effect in reducing stroke recurrence was attributable to
the lowering of BP, in contrast to findings for ramipril from the HOPE study.
The
Antihypertensive and Lipid-Lowering Treatment to Prevent Heart Attack Trial
(ALLHAT) showed slight superiority of chlorthalidone (a thiazide diuretic) over
lisinopril (an ACEI) in terms of stroke occurrence.
The Losartan
Intervention for Endpoint Reduction in Hypertension Study (LIFE) demonstrated
that an ARB (losartan) was superior to a beta blocker (atenolol) in reducing
the occurrence of stroke.
The
Morbidity and Mortality after Stroke, Eprosartan Compared With Nitrendipine for
Secondary Prevention (MOSES) study found that the ARB eprosartan was superior
to the calcium channel blocker nitrendipine in the secondary prevention of
stroke and transient ischemic attack (TIA). This
was true despite comparable BP reductions. The absolute annual difference in
stroke and TIA risk was approximately 4%. The study was relatively small, and
most events were TIAs.
Lifestyle interventions
Smoking
cessation, a low-fat diet (eg, Dietary Approaches to Stop Hypertension [DASH]
or Mediterranean diets), weight loss, and regular exercise should be encouraged
as strongly as pharmacologic treatment. Written prescriptions for exercise and
medications for smoking cessation (ie, nicotine patch, bupropion, varenicline)
increase the likelihood of success with these interventions.
Reducing
sodium intake and increasing consumption of foods high in potassium to reduce
BP may also help in primary prevention. High
alcohol intake should be reduced, as drinking more than 30 drinks per month has
been tied to increased risk of intracerebral hemorrhage.
Exercise
A Finnish
study showed that the likelihood of stroke in men with the lowest degree of
physical fitness (maximal oxygen uptake [VO2max] < 25.2
mL/kg/min) was more than 3 times greater than in men with the highest degree of
physical fitness (VO2max >35.3 mL/kg/min). level
of physical fitness was a more powerful risk factor than low-density
lipoprotein cholesterol level, body mass index, and smoking, and it was nearly
comparable to hypertension as a risk factor.
The 2011
AHA/ASA guidelines for the primary prevention of stroke, which address
hemorrhagic and ischemic stroke, emphasize exercise and other lifestyle
modifications. The guidelines endorse the 2008 Physical Activity Guidelines for Americans,
which include a recommendation of at least 150 minutes per week of
moderate-intensity aerobic physical activity.