|
Stroke is
is the 3rd largest cause of death in developed countries. It is estimated
that 21 per 1000 patients per year experience a first stroke, two thirds
of whom require medical intervention. It is defined as the rapid
development of focal or global disturbance of cerebral function, lasting
more than 24 hours or leading to death with no apparent cause other than
a vascular origin (WHO, 1973). A transient ischemic attack
(TIA) is an acute cerebral dysfunction resulting from vascular problem,
which recovers within 24 hours.
Cerebral venous
occlusion resulting in venous infarcts constitutes about 1% of the
strokes .
It is discussed elsewhere.
Risk factors:
Older age group have shown a definite
increased risk as compared to those below 50 years of age.
Men are more at risk than women, probably
due to increased association of smoking and their
lifestyle.
Hypertensives (BP >160/95) have three
times overall increase in incidence of stroke. Diastolic as well as
systolic pressures are important. Isolated systolic hypertension and
unstable hypertension have been shown to increase the risk.
Myocardial infarction, typically transmural and
anterior in location, there is an increased risk of an embolic stroke.
Silent infarction is associated with 17% stroke rate over 10 years.
Atrial fibrillation, particularly if associated
with rheumatic valvular lesion, increases the risk by a factor of
6, more so in the aged.
History of TIA has been shown to increase
the risk by about 16.5% in the first year after a TIA.
Lipid levels have not shown any direct
correlation with the risk of stroke; but low cholesterol level has been
associated with cerebral hemorrhage in the Japanese.
Diabetics have double the risk.
Blacks and Orientals have shown
increased risk due to the above endogenous factors.
Obesity, Smoking, Contraceptives
(mainly in over the age of 35 years, whether they are current or
former users, increase the risk by about 5 times), Excessive alcohol
use, and lack of physical activity have all been shown as risk
factors.
Etiology:
In Hypotension (BP<60mmHg), the cerebral
auto regulation fails with selective infarction in watershed zones
between major vessels initially. Due to selective vulnerability, globus
pallidus is affected. The age of the patient, duration of ischemia and
other factors decide the outcome.
Emboli from the left side of the heart and the
origin of internal carotid are one of the commonest causes. Mitral
valvular lesions and congenital heart defects are prone for vegetations
which may be carried as emboli. These emboli are usually multiple
and loge at the junction between the cortex and the white matter. The
infarcts are usually less than 2 cm in diameter and are pale (white
infarct) to start with. They may become hemorrhagic (red infarct).
Thrombotic infarcts classically occur
in elderly diabetics. Extreme narrowing of the basilar and middle
cerebral arteries due to atheroma is the cause. They are white
infarcts to start with and may become hemorrhagic.
Lacunar infarcts are due to primary arterial
disease of the penetrating branches. They are less than 15mm in size.
Rarer causes include trauma to the
carotid/vertebral arteries, collagen diseases, moyamoya disease,
fibromuscular dysplasia, vasospastic conditions (SAH, migraine etc), and
the conditions which alter the rheological properties if the blood such
as , polycythemia, leukemia etc.
Pathophysiology:
When the brain is rendered ischemic, the electrical activity
disappears in 10-20 seconds; sodium-potassium pump fails within 30
seconds; glucose level drops rapidly; there is intracellular water and
sodium influx, causing edema in 3 minutes. In
5-10minutes, intracellular lactate levels have risen fivefold and
cellular glucose is exhausted. To this point the changes are reversible.
Prolonged ischemia causes progressive and irreversible
cellular death and edema worsens. Acute strokes may be classified into two
general types: ischemic and hemorrhagic. About 6% of all strokes are due
to subarchnoid
hemorrhage, either due to vasospasm (ischemic) or intraparenchymal
hemorrhage (hemorrhagic) or both.
Approximately
80% of strokes are ischemic. Bland infarction is
characterized by bland widespread leukocyte infiltration and macrophage
invasion, with only scattered red cells being found. Hemorrhagic
transformation occurs regularly in the natural evolution of acute
embolic stroke. Transformation of a bland embolic infarct to hemorrhagic
infarction is rare in the first 6 hours. Approximately 20% of
patients with cardioembolic stroke have hemorrhagic transformation in the
infarcted zone, usually occurring within 48 hours. The pathogenesis
appears to relate to reperfusion of bleeding from recanalized but
ischemically injured vessels by the natural, dynamic dissolution of
thrombi. Reperfusion into the ischemically injured vessels can therefore
result in varying degrees of blood extravasation through the damaged
blood-brain barrier. Investigators from Japan examined the brains of
14 patients who died from herniation of the brain after cardioembolic
stroke with persistent occlusion of the internal carotid-middle arterial
axis and speculated that the blood pressure rises might explain
hemorrhagic infarction in many cases. It is suggested that hyperglycemia
and restoration of blood flow to ischemic territories were strong risk
factors for hemorrhaic infarct conversion. .ost hemorrhagic
transformations are asymptomatic, and it is not uncommon to detect this
on CT patients who are stable or improving.
20%
of strokes are hemorrhagic stroke which is due to hemorrhagic
transformation of ischemic infarct in 15% of cases; in 10%, it is
"spontaneous" intraparenchymal
hematoma.. Hemorrhagic infarction may vary from patchy
petechial bleeding to more confluent hemorrhages, representing multifocal
extravasation of blood from capillaries or venules. An intraparanchymal
hemorrhage occurs when a diseased artery within the brain ruptures,
flooding the surrounding brain tissue with blood. The major risk
factor for intraparenchymal hemorrhage is hypertension. Most signs
and symptoms associated with intracerebral hemorrhage are caused by the
compression of brain structures and blood vessels. There are certain
features on CT that help characterize these two types. On CT, hemorrhagic
infarction appears as a discontinuous heterogeneous mixture of high and
low densities occurring within the vascular territory of the
infarct. In contrast, intraparenchymal hemorrhage appears as a
discrete, homogeneous collection of blood that often exerts mass effect
and may extend beyond the original infarct boundaries or even into the
ventricles.
Some
degree of mass effect due to brain swelling is associated in acute stroke.
It ranges from very insignificant as in lacunar infarcts to a massive
swelling due to multrilocular infarcts with increase in intracranial
pressure (ICP), brain shift, and uncal or cingulated herniation. Increase
in ICP and subsequent reduced cerebral perfusion pressure (CPP) aggravate
ischemia. In addition, CSF flow is disturbed due to brain shifts,
compounding brain ischemia.
In
early ischemia, there is intracellular swelling due to derangement
of Na+/K+ pump in the glial membrane and cell metabolism resulting in Na+
and H2O accumulation resulting in cytotoxic edema. Recent animal
studies have shown that cytotoxic edema reliably occurs in acute CVI and
precedes the onset of vasogenic edema. The blood brain barrier (BBB) is
not disturbed. The CSF formation is not increased. Both the white and the
grey matter are involved. The chemical potential of the plasma
increases and water enters the brain due abnormal gradient. The BBB is
intact. The CSF formation is increased. Both intra and extracellular compartments
are affected.
Within
few hours, the BBB is disrupted, and there is increased cell
permeability. The extracellular space is enlarged; there is abnormal
diffusion of nutrients with consequent acidosis, hypoxia, and
inflammatory changes. Polymorphs intensively accumulate in the regions of
cerebral infarction; this accumulation correlated with the severity of
the brain tissue damage and poor neurological outcome. There is a
new evidence for an association between increased serum level of immune
complexes and the clinical course of cerebral ischemia. Endogenous
substances such as, histamine, bradykinin, excitary aminoacids,
arachdonic acid, superoxide, hydrogen, and hydroxyl radicals are released
and vasogenic edema is superimposed.Cytotoxic and vasogenic edema
is maximal by 24 to 72 hours after the ischemic event. Superoxide
dismutase is one of the major free radical scavenging systems that
might play a role in both degenerative and acute diseases of the central
nervous system; its activity is serum is reduced in acute stroke. Free
calcium is released from its source by a variety of messenger
systems. Selective neuronal vulnerability is calcium related.
Intracellular accumulation of calcium is accompanied by a loss of free
intracellular Mg++, which may directly relate to the extent of
cellular damage, which contributes to secondary injury. Infarction is
related to free radicals and acidosis, and the vascular lesions in stroke
are the result of inflammatory reactions involving calcium, free
radicals, and lipid mediators. Lactic acidosis due to lactic acid
accumulation and increased pCO2 can denature the proteins and alter the
activities of ph dependent enzymes. Lactate enhances brain edema. This
edema aggravates the mass effect which in turn aggravates the ischemia.
The “3rd day edema’ is a well known entity, and the critical time lasts
until the 5th day in the majority, unless there is another ischemic event
later.
The changes are similar in the region (penumbra)
surrounding the area of complete ischemia.
In the normal brain there is coupling of cerebral blood flow
(CBF) to cerebral metabolic rates (CMRO2 & CMRglu). A local decrease
in CBF (misery perfusion) may be associated with normal CMRO2 by
increasing oxygen extraction from the blood. When this compensation
fails, CMRO2 falls due to oligaemia. Luxury perfusion represents a
further uncoupling and CBF exceeds CMRO2, as seen usually after weeks as
a contrast enhancing ring in CT, presumably due to anastomatic
collaterals. Occasionally there may be an area of contralateral
cerebellar or transcallosal homotopic hypoperfusion (diachisis) with
large infarcts.
After a prolonged period of ischemia, restoration of CBF may
still be associated with cell death-delayed neuronal death.
different neurons show differential susceptibility to this phenomenon,
being greatest in the hippocampus followed by cerebral cortex, striatum,
septum and medial geniculate bodies.
Clinical features:
Sudden, unheralded onset of full neurological deficit within
few minutes to hours suggest a stroke. Associated altered sensorium is
common. Typically the cerebral infarction is painless, although about 25%
complain of mild headache. Absence of neck stiffness rule out SAH. Pain over
the carotids radiating to the mastoid (carotodynia) is uncommon;
its presence suggests extracranial carotid artery disease and carotid
dissection.
The neurological deficit is
determined by the site of occlusion.
|
ACA
contralateral hemiplegia and hemisensory loss
(leg > arm and face)
with or without urinary incontinence
“primitive reflexes” e.g. grasp, snout,
palmomental
MCA
contralateral hemiplegia and hemisensory loss
(face and arm > leg)
contralateral homonymous hemianopsia,
gaze deviation away from hemiplegic side
Dominant: (Gerstmann syndrome):
aphasia (expressive / receptive)
agraphia, acalculia, L/R confusion, finger
agnosia
Non-dominant:
neglect of contralateral limbs
anosagnosia, asomatognosia, dressing apraxia
ICA
combinations of ACA + MCA
“watershed” infarcts ('man in a barrel')
ipsilateral Horner’s
monocular blindness / amaurosis fugax
PCA
contralateral homonymous hemianopsia
sparing macular vision (also supplied by MCA)
“Anton syndrome” if bilateral
Proximal occlusion of PCA (Weber syndrome):
ipsilateral IIIrd nerve palsy + contralateral
hemiparesis
|
Lateral Medullary (Wallenburg syndrome)
(occlusion of PICA or VA)
cerebellar signs (dysarthria, ispilateral limb
ataxia)
brain
stem signs (vertigo, nystagmus, nausea/vomiting)
ipsilateral Horner’s
ipsilateral pain / temp. sensory loss of face
contralateral pain/temp. sensory loss of limbs
and trunk
ipsilateral pharyngeal and laryngeal paralysis
Medial Medullary (Dejerine's) (rare)
(occlusion of paramedian br. of vert. or
basilar)
contralateral hemiplegia
ipsilateral tongue weakness/atrophy
contralateral proprioception / vibration loss
Basilar Artery (locked-in-syndrome)
quadriplegia
lower cranial nerve paralysis
(mute, facial/tongue paralysis, aphagia)
With
or without
preservation of upper cranial
nerves (vertical eye movements)
preservation of consciousness
Lacunar
Occlusion of deep penetrating arteries
e.g. lenticulostriates, thalamostriates,
perforators of basilar
Types (occluded artery; localization):
1. Pure motor (lenticulostriate art.; post. limb
Int.Capsule)
2. Pure sensory (thalamogeniculate art.; VPL)
3. Dysarthria/clumsy hand (perf. br. of basilar;
dorsal pons)
4. Ataxic hemiparesis (perf. br. of basilar;
ventral pons but also ant. limb Int.Capsule)
Clinical:
- Hypertension, DM
- Cortical function is preserved.
- In 1 and 2 generally face, arm, and leg are
equally involved.
|
Without retinal changes, diagnosis of hypertensive
encephalopathy should not be made. Transient hypertension is common in
any acute cerebral pathology.
|
Neuroimaging:
CT:
In general hypodense area is seen in 24-48 hours after a
stroke; in larger infarcts it may be shown within few hours.
Occasionally thrombosis in a feeding artery may be seen as an
hyperdense area.Area of edema is not proportionate to the pathology
initially and involves grey and white matter Initially there may not be
any contrast enhancement. 1-2 weeks later, there may be patchy
areas of enhancement due to attempts at reperfusion.
|
|
|
MRI:
|
MRI-Bifrontal infarct
|
|
The changes are
seen within few hours in T2 sequences. Gadolinium enhancement in the
parenchyma does not occur until a week. Loss of flow void in the major
arteries may be only after few minutes of the ictus. MRAngiography may
reveal a stenosis and /or thrombosed artery.
Doppler study and angiography
may be obtained if an acute surgical or endovascularprocedure is
contemplated.
|
|
|
Management:
|
CT-Corona
radiata infarct
|
|
The management
is MEDICAL.
The aim is to mitigate against further ischemia; to
prevent further stroke; and to rehabilitate the patient.
Initial approach:
Pre-CT Protocol. If a patient presents with
the sudden onset of neurologic dysfunction referable to the brain,
the immediate steps to take include:
|
|
|
- maintain
airway, assess breathing, and elevate head of bed 30 degrees
|
CT-Frontal infarct
|
|
- place oxygen
2-4 liters/minute via nasal cannula
- obtain vital signs (and place intravenous catheter of
normal saline)
- obtain Complete blood count, coagulation profile, and
biochemistry chemistry panel (with glucose finger stick if possible)
- obtain ECG and chest X-ray
|
|
|
- obtain patient
weight
|
CT-Lacunar infarct
|
|
- obtain
historical data (especially for potential contraindications for
thrombolysis)
- perform NIH Stroke Scale
- if patient comatose - perform Glasgow
Coma Scale
- stabilize neck and obtain cervical spine X rays when
trauma is suspected
|
|
|
- in all
patients, obtain urgent CT of brain.
|
MRA-basilar artery stenosis.
|
Thrombolytic Therapy for Acute Ischemic Stroke
Thrombolysis, the lysis of a cerebral arterial clot with
tissue plasminogen activator (tPA) within hours of symptom onset in
ischemic stroke, is approved for treatment of acute ischemic stroke since
1996. Intravenous r-TPA (0.9 mg/kg, maximum 90 mg) with 10% of the dose
given as a bolus followed by an infusion lasting 60 minutes is
recommended treatment within 3 hours of onset of ischemic stroke. Two
other agents, pro-urokinase (intra-arterial administration directly into
M1 or M2 arterial thrombus) and intravenous ancrod, a fibrinogen-lowering
agent derived from the venom of the Malayan pit viper, have shown
therapeutic benefit, and may be available for acute ischemic stroke
therapy in the future. A drawback to these therapies is a relatively
short time window from symptom onset to treatment (up to 3 hours for tPA
and ancrod and up to 6 hours for pro-urokinase). Study to determine if a
lower dose of tPA might lower the risk of hemorrhagic complications and
possible extension of the hyperacute treatment window beyond 3 hours by
use of neuroprotective drugs may have significant bearing on the outcome.
Inclusion Criteria:
Ischemic stroke with a clearly defined symptom onset
No evidence of intracranial blood on brain CT scan. If CT
demonstrates early changes of a recent major infarction such as sulcal
effacement, mass effect, edema, or possible hemorrhage, thrombolytic
therapy should be avoided.
180 minutes or less from the time of symptom onset to
initiation of IV t-PA
Measurable neurologic deficit such as hemiplegia
Exclusion Criteria:
History of intracranial hemorrhage
Stroke or serious head trauma within 3 months
Major surgery within 14 days
GI or GU tract hemorrhage within 21 days
Received anticoagulants within 48 hours
Time of onset of stroke not known or stroke noticed on
awakening
Rapidly improving or minor stroke symptoms such as ataxia
alone, sensory loss alone, dysarthria alone, or minimal weakness
NIH stroke scale >22
Suspected subarachnoid hemorrhage despite a normal CT scan
Seizure at the onset of stroke
Systolic BP > 185 mm Hg or Diastolic BP > 110 mm Hg at
the time of treatment initiation
Aggressive BP treatment, i.e., continuous IV infusion of an
anti-hypertensive to achieve above goal
Arterial puncture at a noncompressible site within 7 days
Elevated PTT, PT > 15 seconds, INR >1.7, platelet
count < 100,000, glucose < 50 or > 400
Recent myocardial infarction.
Concerns and Controversies About TPA:
1. Occlusive thrombi should first be identified
2. Conditions that may masquerade as stroke (e.g.,
complicated migraine, seizure, functional deficits) are difficult to
distinguish quickly from stroke based on clinical exam and head CT
3. Occlusions of main-stem and divisional MCA and basilar
artery respond better to intraarterial thrombolytic treatment, whereas
intravenous therapy is better for branch MCA occlusions; ICA occlusions
do not respond to intravenous therapy
4. Brain hemorrhage developed in 20% of ECASS and 6.4% in
NINDS trial. Most bleeding occurs within the first 24 hours after
administration of thrombolytic medication. If a patient neurologically
deteriorates reassessment of the patient’s airway and hemodynamics
followed by an emergent head computerized tomographic (CT) scan are required. If the t-PA is still infusing it should
be stopped and coagulation studies (PT, PTT, and fibrinogen) sent. If the
head CT reveals an intracranial hemorrhage, then transfusion of 6-8 units
cryoprecipitate or fresh frozen plasma (FFP) with fibrinogen is
recommended and should be continued until any coagulopathy is corrected.
At present, the role of surgical evacuation of intracranial hemorrhages
after thrombolytic therapy is not defined. Because the use of
thrombolytic drugs carries the real risk of major bleeding, emergent
ancillary care and the facilities to handle bleeding complications must
be readily available.
5. Rapid applications of noninvasive vascular imaging tests
(e.g., MRI, MRA, CUS, TCD, CT angiography) should be employed to define
cerebrovascular status
6. Immediate intravenous tPA use opts for time and ignores
specificity (i.e., treatment of lesions that will not respond)
7. Hazard risk is high (12% absolute chance of excellent
outcome but 3% risk of death due to ICH)
Neuroimaging Strategies that may improve outcome of
thrombolysis:
MRI technology has better resolution, provides more
information and efficiently, and may accelerate appropriate selection of
patients for acute ischemic stroke intervention. Diffusion weighted
imaging (DWI) and perfusion imaging (PI) have become available for
clinical use. DWI is very sensitive to acute brain ischemia and detects
increased signal intensity which indicates reduced apparent diffusion
coefficient (ADC) or regions of limited water diffusion. DWI may be able
to distinguish cytotoxic from vasogenic edema, and characteristic changes
may help to determine the age of stroke lesion. Fast image acquisition is
necessary as the technique is sensitive to movement artifacts. PI
captures cerebral blood flow at the capillary level. PI has high spatial
resolution, minimal invasiveness and can be integrated with other MRI
techniques on a single machine. DWI/PI mismatch may be a sign of
reversible infarction and a predictor of viability of acute stroke
intervention and may expand the 3- hour window. PI requires about 10
minutes of scan time to complete. Overall, DWI and PI seem to allow for
earlier detection and characterization of ischemic stroke than is
possible by other practical means.
Some also advocate TCD pre-and post-thrombolytic therapy to
assess patency of the intracranial circulation. Before using MRI for
thrombolysis this technology must be able to detect acute hemorrhage.
Another MRI application is bolus-tracking, perfusion-weighted MRI. This
technique reflects brain hemodynamics and is performed by rapid
intravenous bolus of gadolinium. Regions with very low blood flow do not
receive much gadolinium and perfusion brain maps are generated that
reflect this effect. CT angiography, another technique that requires
rapid infusion of intravenous contrast, can identify regions of
hypoperfusion distal to vascular occlusion. By this method CT perfusion
maps may be developed with little additional time added (5 minutes) to
the noncontrast CT.
Blood Pressure Management after thrombolysis in Acute
Stroke:
Consensus on the exact management of hypertension in acute
ischemic stroke does not exist, but guidelines are available from the
American Heart Association. Sublingual use of nifedipine is discouraged
because of the potential of adverse experiences, including neurologic
worsening, secondary to excessive lowering of the blood pressure. Simple
maneuvers such as elevation of the head of the bed may help control
hypertension by increasing cerebral venous drainage and, in patients with
CHF will ease dyspnea and anxiety. The approval of rt-PA for acute ischemic
stroke greatly complicates management of blood pressure. Once clot
dissolution occurs, the ischemic region, which may contain damaged
vasculature, is re-exposed to systemic pressure. A hyperperfusion
syndrome with brain hemorrhage and swelling is a known complication of
untreated hypertension after revascularization procedures such as carotid
endarterectomy. All thrombolytic agents impair the clotting system which
further compounds the problem of brain hemorrhage. Hypertension is also a
risk factor for brain hemorrhage in patients undergoing thrombolysis for
cardiac ischemia. It is preferable to avoid thrombolysis in patients
whose blood pressure is greater than 185 mm Hg systolic or 110 mmHg
diastolic or in those patients who require aggressive treatment of blood
pressure to reach these limits. In addition, elevated arterial blood
pressure should be closely monitored and treated during the first 24
hours in those who undergo thrombolytic therapy. Thus, treatment of
elevated blood pressure in acute ischemic stroke in the setting of
thrombolytic therapy differs from guidelines for ischemic stroke patients
in general. Agents which are easily titrated are preferred because
uncontrolled, prolonged hypotension is less likely and their action can
be halted quickly in the case of neurologic worsening. Intravenous
labetalol is often useful except in patients with asthma, acute
congestive heart failure, or AV conduction block. Intravenous enalapril,
and especially nitroprusside , can be carefully titrated to a specific
blood pressure goal.
Neuroprotection:
Neuroprotection may increase the therapeutic window for
thrombolysis. Some neuroprotective agents work during acute ischemia to
limit injury to the penumbra neurons, while others act during
reperfusion. Although clinical trials have failed to reveal overall
treatment benefit, there is reason to believe that researchers will find
an efficacious agent. Drugs that have been tried so far include
Glutamate Antagonists: Selective NMDA/ AMPA
receptor or broad spectrum antagonists such as gamma D-glutamyl glycine
dextrorphan, dizocilpine, remacemide, eliprodil and YM90K.
Calcium Channel Antagonists: Nimodipine,,
SNXlll and lifarizine.
Sodium Channel Antagonists: Riluzole
and fosphenytoin
Glycine Antagonists: GV 150526
Free Radical Scavengers: 21-aminosteroids
(eg. tirilazad), super-oxide dismutase and phenylbutyl nitrone (PBN).
Gangliosides: GM 1 ganglioside
Membrane Stabilizers: Citicholine
Anti-inflammatory Agents: Anti-lCAM and Anti
CD-11 antibody.
Magnesium sulphate
In the future, optimal therapy may be achieved by combining
neuroprotective agents with complementary mechanisms. Because these drugs
most likely will not display adverse effects in patients with hemorrhagic
stroke, ambulance crews could begin administering this stroke cocktail in
the field. Upon arrival at the hospital, the patient would undergo
imaging studies of the head, and assessment for potential administration
of a medical or mechanical thrombolytic would take place.
Other measures:
In addition to the general and the neuroprotective measures,
Warfarin is indicated in cardiogenic
emboli and perhaps, in stroke in evolution.
Platelet modifying agents such as, aspirin,
have a role particularly in men.
New guidelines:
(The American
Heart Association/American Stroke Association, April 19, 2007)
- During initial evaluation, the single most important
point in the patient's history is the time of symptom onset.
Patients with acute stroke symptoms should receive testing for blood
glucose, coagulation times, and complete blood count with platelets,
along with 12-lead electrocardiogram and serum cardiac enzymes.
However, chest radiography may be withheld if there are no signs of
pulmonary or cardiac disease. The evaluation of the patient should
be concluded within 60 minutes of arrival in the emergency
department.
- CT remains the most common imaging modality for
the evaluation of acute stroke, and, besides hemorrhage, there is no
CT finding that is specific enough to preclude treatment with
recombinant TPA (rtPA). MRI also is acceptable in the evaluation of
acute stroke.
- Patients' blood pressure may decline
spontaneously in the first 24 hours after stroke. Patients who are
candidates for TPA (rtPA) should have their
systolic blood pressure lowered to at least 185 mm Hg and their
diastolic blood pressure lowered to at least 110 mm Hg. Consensus
opinions state that patients with persistent elevations in systolic
blood pressure higher than 220 mm Hg or diastolic blood pressure
higher than 120 mm Hg should receive antihypertension therapy.
- Hyperglycemia in the range of 140 to 185 mg/dL in
the stroke patient should prompt consideration of insulin therapy.
- Hyperbaric oxygen should not be used in the acute
stroke patient except in cases of air embolus.
- TPA (rtPA) is the treatment of choice for
thrombolysis in acute stroke. Treatment with streptokinase is not
recommended, and reteplase, urokinase, and other thrombolytic agents
should not be used outside of the setting of a clinical trial.
- Intra-arterial thrombolysis may be used for
patients with occlusions of the middle cerebral artery who can be
treated within 6 hours of symptom onset.
- Urgent anticoagulation generally is not
recommended in lieu of intravenous thrombolysis and should be
withheld in patients with moderate or severe stroke because of an
increased risk for intracranial hemorrhage.
- Aspirin therapy at a dose of 325 mg may be
initiated within 24 to 48 hours after stroke onset. Based on current
evidence, the authors recommend against the routine use of
clopidogrel following stroke.
- During hospitalization, stroke patients should
receive a swallowing evaluation as well as prophylaxis against deep
venous thrombosis with heparin or low-molecular-weight heparin.
Surgery:
Surgery has very few indications in acute infarct. It may be
indicated in a posterior fossa infarct (to drain the associated dilated
ventricles and occasionally, in evacuation of the infarcted cerebellum).
Emergency revascularization procedures such as,
endarterectomy in selected patients, are being reported
increasingly of late.
Endovascular procedures such as,
angioplasty, thrombectomy, intraarterial papaverine, are being
experimented.
Rehabilitation:
The final step of therapy would be participation in a
state-of-the-art rehabilitation program.
A multidisciplinary approach is of paramount importance.
Provision of dedicated physiotherapy, speech therapy, and occupational
therapy have been formalized in many centers.
|
