Stroke management

Stroke
• A stroke, or cerebrovascular accident, is defined as
abrupt onset of a neurologic deficit that is attributable
to a focal vascular cause.
• Causes of stroke
• `Ischaemic stroke (85 %)
• Embolic stroke (75% of ischemic stroke)
• Thrombotic stroke (25 % of ischemic stroke)
• Hemorrhagic stroke (15%)
DDs
• Syncope
• Hypoglycaemia
• Migraine (with or without headache)
• Focal seizures ,Todd's paresis (weakness after epileptic seizure)
• Demyelination ,
• Encephalitis
Ischemic stroke
• Thrombotic: Thrombosis at the site of ruptured mural plaque
leads to artery-to-artery embolism or vessel occlusion.
• Large-artery stenosis: Major cerebral arteries are involved
• Small-vessel disease: Small penetrating arterial branches
supply the deep brain parenchyma are involved
• Cardio-embolic: The heart is a common source of embolic
material. Atrial fibrillation (and other arrhythmias) leading to
thrombosis in a dilated left atrium is the most common
cause.
• Hypoperfusion: Severe hypotension, such as in cardiac arrest,
may lead to border-zone infarction in the watershed areas
Embolic stroke
• Emboli may either be of cardiac(most common cause) or
arterial origin.
• Cardiac sources include atrial fibrillation (Mitral Stenosis /
regurgitation), acute myocardial infarctions, prosthetic valves,
endocarditis, mural thrombi, dilated cardiomyopathy, or
patent foramen ovale.
• Arterial sources are atheroembolic or cholesterol emboli that
develop in the arch of the aorta and in the extracranial
arteries (ie, carotid and vertebral arteries).
• Embolic strokes tend to have a sudden onset, and
neuroimaging may demonstrate previous infarcts in several
vascular territories.
Haemorrhagic stroke
• Causes of ICH and SAH
• ICH Causes -
• Hypertension is the most common cause (80%).It is due to rupture
of small perforating arteries.
• AV Malformation, Bleeding disorders,
• Platelet disorders, Autoimmune diseases
• SAH Causes –
• Aneurysm rupture is most common cause (50%),
• AV Malformation, Bleeding disorders, Trauma
ICH causes
Common sites of ICH Common sites of Aneurisms#
Putamen (Most Anterior circulation
common site, Anterior communicating artery
putamen is with in At the bifurcation of MCA*
basal ganglia) from ICA*
Thalamus Origin of PCA*
Caudate nucleus from ICA*
Pons Posterior circulation
At the apex of basilar artery
At the Origin of PICA*
and superior cerebellar arteries from basilar artery
*MCA –Middle cerebral artery, *PCA –Posterior cerebral artery,*ICA –Internal carotid artery
*PICA–Posterior inferior cerebellar artery
Clinical features according to involved artery
Carotid territory( Ipsilateral(same side) mono-ocular blindness
Anterior circulation Contralateral (Opposite side)Hemiparesis and facial
strokes) weakness
Hemianesthesia
Aphasia,
Seizures
Reduced carotid pulsation with bruit
Vertebrobasilar Sudden fall (drop attacks)
territory(Posterior Ataxia, Dysarthria, Vertigo, Tinnitus,
circulation strokes) Diplopia, Nystagmus
Difficulty in swallowingLMN facial weakness,
Horner’s Syndrome*
Clinical features of haemorrhagic stroke
• Sudden,severe headache(thunderclap headache), Vomiting, Seizures,
Papilloedema, loss of consciousness
• Neck stiffness in SAH and intra ventricular extension
• Blood in CSF study
• H/o 2nd,3rd ,4th ,5th Cranial nerve involvement due to
• compression by the aneurysms before it ruptures.
• Prognosis - In general, supratentorial hematomas with volumes <30
mL have good prognosis; 30–60 mL,have intermediate prognosis; and
>60 mL, poor prognosis.
• Extension into the ventricular system, location within the posterior
fossa, depressed level of consciousness at initial presentation and
advanced age have a worse prognosis.
Basic investigations
• Electrolyte disorders, hyperglycemia, hypoglycemia, and uremia should be ruled out.
• Hypoglycemia is the most common abnormality that produces stroke like symptoms.
• Post-stroke hyperglycemia may be a stress response to the stroke, but it can also contribute to brain damage.
• Hyperglycemia predisposes to brain hemorrhage in patients receiving tPA, and may even increase the risk of
intracerebral bleed in persons not receiving tPA.
• Complete blood count: CBC provides information regarding hemoglobin, hematocrit ( anemia, polycythemia
or sickle cell disease), thrombocytopenia and thrombocytosis and possible infections(WBC count).
• Prothrombin time (PT) and activated partial thromboplastin time (aPTT) tests: Many patients with acute
stroke may be on anticoagulants ( heparin or warfarin). Treatment decisions, like tpA use, require
coagulation status.
• Additional laboratory tests - Toxicology screen (if history is not available or CT/ MRI does not correlate with
clinical features), fasting lipid profile, ESR, pregnancy test.
• In suspected hypercoagulable states - protein C, protein S, antithrombin III, Factor V Leiden, antinuclear
antibody (ANA), VDRL and homocysteine., anticardiolipin antibody etc..
• Lumbar puncture (LP): LP is required to rule out meningitis or subarachnoid hemorrhage (SAH) when the CT
scan is negative but the clinical suspicion is high.
Imaging
• CT SCAN: Noncontrast CT can detect hemorrhages, and they also identify
extraparenchymal bleed.
• CT Scans obtained in < 6 (may be up to 24–48) hours of an ischemic infarction
generally show no abnormality.
• CT may also fail to show small ischemic strokes in the posterior fossa because of
bone artifact; small infarcts on the cortical surface may also be missed.
• MRI - MRI can detect the extent and location of infarction in all areas of the brain,
including the posterior fossa and cortical surface. It also identifies intracranial
hemorrhage and other abnormalities but is less sensitive than CT for detecting
acute blood.
• Digital subtraction angiography (DSA) to detect vascular lesions, including
occlusions, stenoses, dissections, and aneurysms.
• Carotid doppler scanning to detect carotid stenoses.
• Echo cardiography, ECG in cardiac embolism
Blood sugar management
• Administer intravenous glucose / Insulin (avoid
hypoglycemia / hyperglycemia)
• Serum glucose should be kept between 140 and 180
mg/dL are recommended with insulin infusion if
necessary.
Controll of BP in ischemic stroke - Maintain CPP
• BP control for thrombolysis: Before lytic therapy,
antihypertensives should be started with target
Systolic BP≤185 mmHg and diastolic BP≤110 mmHg.
• The blood pressure should be <180/105 mmHg for at
least 24 hours after intravenous tPA treatment.
• Labetalol 10 mg IV every 10 minutes (consider
doubling dose - i.e. 20 mg, 40 mg, 80 mg) to
maximum total dose of 150 mg. Start maintenance
infusion, 2 mg per minute
• Current recommendations are to lower MAP <130
In haemorrhagic stroke BP controll
• For patients with acute bleed with SBP 150 to 220 mmHg,
acute lowering of SBP to 140 mmHg is recommended
• For patients with acute bleed with SBP >220 mmHg,
aggressive reduction of blood pressure with a continuous
intravenous infusion of antihypertensive medication to SBP
of 140 to 160 mmHg is a reasonable target.
• For patients with MAP >150 mmHg, also consider aggressive
reduction of BP with continuous IV infusion of
antihypertensive to lower MAP<130 mmHg.
• IV Labetalol - 5 to 20 mg every 15 minutes ,then infusion 2
mg per minute (maximum 300 mg/day)
Nimodepin in SAH
• T. Nimodipine 60 mg 4th hourly – to reduce vasospasm in SAH
• Delayed cerebral ischemia as a result of cerebral vasospasm is the
most common cause of death and disability after aneurysmal
subarachnoid hemorrhage (SAH). It leads to death or permanent
neurologic deficits in over 17-40% of SAH patients
Administration of IV Tissue Plasminogen Activator
(t - PA)
• Door-to-needle time of <60 minutes is the target time for
thrombolysis initiation.
• Do a noncontrast head CT within 20 minutes to rule out IC bleed
• Administer 0.9 mg/kg intravenously (maximum 90 mg) IV as 10% of
total dose by bolus in 1-2 minutes, followed by remainder of total
dose over 1 h
tPA
Indication
Age >18 years
Clinical diagnosis of Ischemic stroke
Onset of symptoms <4.5 h
If the exact time of stroke onset is not
known, onset may be defined as the last
time the patient was known to be normal
Non-contrast CT scan showing no
hemorrhage or edema of >⅓ of the
MCA territory
BP: blood pressure; HCT, hematocrit; INR, international normalized ratio; MCA, middle cerebral artery; PTT,
partial thromboplastin time.
Contraindication
Sustained BP >185/110 despite treatment
Platelets <100,000;
HCT <25%
Blood glucose <50 or >400 mg/dL
Use of heparin within 48 h and prolonged APTT /
PT-INR
Rapidly improving symptoms
Prior stroke or head injury within 3 months;
prior intracranial hemorrhage
Major surgery in preceding 14 days
Gastrointestinal bleeding in preceding 21 days ,
Recent myocardial infarction Coma or stupor
Raised ICP management
• Make sure the head of bed is raised to 30 degrees
• Be sure that the ICP elevation is not associated with tracheal suctioning or other noxious stimulus.
• Hyperventilation causes a rapid lowering of ICP by inducing cerebral vasoconstriction. A
PaCO2 goal of >30 to 35 mmHg is suggested. However, the effect of hyperventilation on ICP only
lasts for a few hours.
• Mannitol Initial bolus of 0.5 to 1 g/kg, Followed by repeated infusions of 0.25 to 0.5 g/kg as
needed, generally every four to twelve hours with monitoring of serum osmolality. The goal of
therapy is to achieve plasma hyperosmolality (300 to 310 mosmol/kg) to force water to exit the
brain,higher doses can cause reversible acute renal failure
• Hypertonic saline (3% saline) is also an effective hyperosmolar agent for the control of elevated
ICP. Give 3% saline as an infusion to maintain serum sodium levels of 145 to 155 mEq/L.
• If ICP is not responsive to sodium infusion, consider a sedative agent, such as propofol 1-3 mg/kg.
Administration of propofol may be associated with circulatory depression that should be
corrected with IV fluids or a vasopressor infusion to maintain CPP goal. Propofol may be
continued as an infusion 200 mcg/kg/min.