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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.
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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
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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.
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Without retinal changes, diagnosis of hypertensive
encephalopathy should not be made. Transient hypertension is common in
any acute cerebral pathology.
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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.
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MRI:
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MRI-Bifrontal infarct
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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.
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Management:
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CT-Corona radiata infarct
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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:
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- maintain
airway, assess breathing, and elevate head of bed 30 degrees
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CT-Frontal infarct
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- 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
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- obtain
patient weight
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CT-Lacunar infarct
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- 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
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- in all
patients, obtain urgent CT of brain.
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MRA-basilar artery stenosis.
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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.
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