Stroke and Subarachnoid

Haemorrhage
DR. AMIT KUMAR RAY
ASSISTANT PROFESSOR, DEPT. OF ANAESTHESIOLOGY
R.G.KAR MEDICAL COLLEGE, KOLKATA
Introduction

 Acute stroke (cerebral infarct or intracerebral hemorrhage) is the most frequent cause of
admission in neurocritical care units.
 Prompt attention and intervention may salvage some patients from this catastrophic
problem.
 Approximately 85% of all strokes are ischemic.
Acute Ischemic Stroke

 Stroke is a sudden loss of adequate perfusion to a segment of the brain causing

irreversible damage.
 Its presentation varies considerably and may be as subtle as minor sensory loss or as
impressive as the complete loss of motor function (except for eye movements) as seen in
the locked-in syndrome.
 Clinical diagnosis is usually possible if the onset history and pattern of deficits match a
typical stroke syndrome.
 Other pathologies that may mimic stroke include hypoglycemia, postictal “Todd’s
paralysis,” complicated migraine, and psychosomatic disorders.
Management

 Initiate resuscitation as per ABCD.

 Intubation is done routinely when the Glasgow coma scale (GCS) is less than or equal to 8,
when there is insufficient ventilation (PO 2 < 60 mmHg or PCO 2 > 50 mmHg), obvious
signs of pupillary asymmetry, and depressed consciousness that threatens the airway.
 General critical care management is similar to other ICU patients: maintain homeostasis of
acid–base physiology, oxygenation, euvolemia, euglycemia ( <150mg/dl), stress ulcer
protection etc.
 Variations include inhibiting fever (which has been shown to worsen outcome in stroke)
and avoiding the practice of permissive hypercapnia (due to potential elevation of
intracranial pressure).
 Aspirin (or another antiplatelet agent) should be given to ischemic stroke patients within
48 hours.
 But combining clopidogrel and aspirin has shown to be deleterious and therefore should
not be given unless there is another indication for the combination such as a coronary
stent.
 Heparin is no longer recommended for acute ischemic stroke.
 Anticoagulation for atrial fibrillation is indicated, but does not have to be started in the
setting of an acute stroke.
 Enoxaprin has been shown to be superior in preventing deep venous thrombosis and
should be given with in 24 hrs of stroke.
 Seizure prophylaxis is not indicated in ischemic stroke. However, suspicion of seizure
should be evaluated and treated if appropriate.
 For ischemic strokes <3 hours old( extended upto 4.5 hrs), intravenous thrombolysis
with tissue plasminogen activator (tPA) is the intervention of choice in selected
patients.
 The recombinant tissue plasminogen activator (rtPA) given at a dose of 0.9 mg/Kg up to a
maximum of 90 mg (10% of dose given as a bolus over 1 min and the remainder infused
over 1 h).
 Appropriate informed consent should be taken from the patient or surrogate.
Eligibility criteria for thrombolysis in acute stroke

 Inclusion criteria
 Clinical diagnosis of ischemic stroke
 With measurable neurological deficit consistent with ischemic stroke
 Within 3–4.5 h of onset of symptoms (if exact time of stroke onset is unclear, it is defined
as the time when the patient was last noted to be normal).
 Age > 18 yrs.
 No signs of ICH or advanced cerebral infarction like sulcal oedema, hemispheric swelling
in CT scan.
Exclusion criteria

History
 Stroke or head trauma within the prior 3 months
 Any prior history of intracranial hemorrhage
 Major surgery in the previous 14 days
 Gastrointestinal or genitourinary bleeding within the previous 21 days
 Myocardial infarction (MI) within the prior 3 months
 Arterial puncture at a noncompressible site within 7 days
 Lumbar puncture within 7 days
 Clinical
 Rapidly improving stroke symptoms, minor and isolated neurological signs
 Seizure at the onset of stroke with postictal residual neurological impairments
 Symptoms suggestive of subarachnoid haemorrhage, even if the CT scan is normal
 Clinical presentation consistent with acute MI or post-MI pericarditis
 Persistent SBP > 185 mmHg, DBP > 110 mmHg, or requiring aggressive therapy to control
BP
 Pregnancy or lactation
 Active bleeding or acute trauma (fracture)
Laboratory
 Platelets <100,000/mm 3
 Serum glucose <50 mg/dL (2.8 mmol/L) or >400 mg/dL (22.2 mmol/L)
 International normalized ratio >1.7 if the patient is on warfarin and increased activated
partial thromboplastin time if on heparin.
Maintain haemodynamics

 Stroke often causes reactive hypertension to perfuse the ischemic penumbra.

 High blood pressure should be tolerated up to 220/120mmHg unless there is evidence of
ongoing end-organ damage(acute myocardial infarction, dissecting aneurysms, heart
failure, renal failure).
 If the patient is to undergo thrombolysis, the patient’s blood pressure (BP) should be kept
below 185/110 mmHg prior to thrombolysis and for 24 h after.
 Intravenous (IV) labetalol is the drug of choice, preferably by IV infusion. Initial bolus
dose of 10 mg IV should be followed by infusion of 2–8 mg/min, or intermittent boluses
of 10 mg every half an hour. Maximum daily dose of IV labetalol is 300 mg/day.
 Nicardipine, ACE inhibitor or Hydralazine are other option.
 Nitrates are avoided because of their potential for venous dilatation and subsequent
intracranial pressure elevation.
Complication in the 1st week of stroke

 Three common complications to watch for include infarct expansion, infarct related
edema, and hemorrhagic transformation.
 Infarct expansion can be suspected if there is worsening of sensorium or appearance of
new neurological deficits.
 In such patients, hypertension should not be aggressively corrected; if necessary,
antihypertensive drugs should be withheld. A cautious trial of induced hypertension may
be tried. With an increase in mean arterial pressure (MAP), if the neurological deficits
improve, elevated MAP needs to be maintained.
Infarct related oedema

 Infarct-related edema usually starts at day 2 of stroke and lasts until day 7. Peak on 3rd to 5th
day.
 Pupillary asymmetry and deepening coma are clinical pointers to edema occurrence and
worsening. May lead to secondary infarction.
 It is treated with bolus therapy of 20% mannitol (1 g/Kg IV) given over 10–20 min repeated as
frequently as needed, or hypertonic saline( 3-5ml/kg over 10-20 min), head of bed elevation to
30° and avoiding jugular compression by keeping head midline.
 Surgical intervention – Decompressive hemicraniectomy.
 Infarct-related edema can be prevented by avoiding hypoxemia, hypoventilation, hypovolemia,
hypotonic solution, dehydration, seizures, and fluctuations in serum glucose levels.
Haemorrhagic transformation

 Hemorrhagic transformation is suspected clinically by a decrease in sensorium and

confirmed by a CT scan.
 It should be managed by withholding antiplatelets and anticoagulants.
Acute Haemorrhagic Stroke

 Step 1: Maintain A B C D protocol.

 Step 2: Reduce BP judiciously.
 If systolic blood pressure (SBP) is between 150-220 mmHg or MAP (SBP + 2 × DBP)/3 is
between 120 -150 mmHg, then consider reduction of SBP to around 140 mmHg and MAP
around 110 mmHg.
 IV labetalol is the drug of choice, preferably by IV infusion.
 Initial bolus dose of 10 mg IV followed by infusion of 2–8 mg/min, or intermittent boluses of
10 mg every half an hour. Maximum daily dose of
 IV labetalol is 300 mg/day.
 Monitor heart rate, and hold infusion if it is less than 60/min.
 Other agents that are recommended for treating hypertension in hemorrhagic stroke are
nicardipine, angiotensin-converting enzyme inhibitor, and hydralazine.
 Nitrates should be avoided because they tend to increase ICP.
 Step 3: Consider management of raised ICP. Raised ICP is expected to follow ICH and
is defined as ICP >20 mmHg for >3 min, with the therapeutic goal being decrease of ICP
to <20 mmHg or maintaining the cerebral perfusion pressure between 50 and 70 mmHg.
 Raised ICP is treated with bolus therapy of 20% mannitol (1g/kg) IV given over 10–20
minutes repeated as frequently as needed or hypertonic saline and head of bed elevation to
30°.
 Step 4: Cautious use of fresh frozen plasma (FFP), platelet transfusion, or aFVII
(activated factor VII).
 In addition to FFP, patients on oral anticoagulation should also receive vitamin K and
have further doses of oral anticoagulation withheld.
 Monitoring of PT, APTT.
 Step 5: Selected use of antiepileptics
 Step 6: Consider cerebral angiography in young , normotensive with no definite cause of
haemorrhage.
 Step 7: Consider surgical management in cerebellar haemorrhage and deteriorating,
brainstem haemorrhage, decompressive craniotomy in young individuals.
 Step 8: General care Deep vein thrombosis prophylaxis with mechanical compression
device should be started at the earliest in ICH and low molecular weight heparin or UFH
in cerebral infarct.
 Antiulcer prophylaxis should be started with H 2 blocker.
 Proper skin and eye care should be provided.
 Aspiration precaution should be taken.
 Proper nutrition should be provided.
 Bowel and bladder functions should be taken care of.
 Contractures should be prevented by supervised physiotherapy.
 Fever and glycemic control should be properly managed.
Subarachnoid Haemorrhage

 Subarachnoid hemorrhage (SAH) comprises bleeding into the subarachnoid space

(containing cerebrospinal fluid [CSF]) surrounding the brain and the spinal cord.
 The most common etiology of SAH is aneurysmal rupture.
 Other causes include trauma, vascular malformations, hemorrhagic infarctions and
hypertensive hemorrhages.
 Although SAH comprises 10% or less of all acute cerebrovascular events, it affects a
younger population and carries with it significant mortality (20% to 30% within 30 days)
and persistent neurologic morbidity.
Diagnosis

 Patients with SAH usually present with sudden severe headache that reaches maximum
intensity within seconds (i.e., “thunderclap headache”).
 This may be associated with syncope or persistent alteration in the level of consciousness.
Meningismus develops over a few hours.
 The diagnosis is confirmed by noncontrast computed tomography (CT) of the head that
has greater than 95% sensitivity if performed within 24 hours of symptom onset.
 Negative CT findings despite clinical suspicion should undergo lumbar puncture to
evaluate for red blood cells and xanthochromia (the yellow discoloration of centrifuged
CSF seen with blood breakdown).
Assess severity

The Hunt and Hess scale

 1. Asymtomatic or, mild headache, slight neck rigidity
 2. Moderate-to-severe headache, neck rigidity, no neurological deficit other than cranial
nerve palsy
 3. Drowsiness/confusion, mild focal neurological deficit
 4. Stupor, moderate-to-severe hemiparesis
 5. Coma, decerebrate posturing
World Federation of Neurosurgical Societies classification, mentioned as follows:
 1. Glasgow coma score (GCS) 15, motor deficit absent
 2. GCS 13 or 14, motor deficit absent
 3. GCS 13 or 14, motor deficit present
 4. GCS 7–12, motor deficit absent or present
 5. GCS 3–6, motor deficit absent or present
Management

 ABCD protocol.
 Strict bed rest is advisable to prevent rebleeding of the aneurysm. Stool softeners, cough
suppressants and a quiet environment are useful adjuncts.
 The risk of rebleeding is as high as 20% in the first 24 to 48 hours after SAH. Along with
ventricular arrhythmias, this is the most common cause of early death after SAH.
 Pain control should be achieved with titrated doses of opioids. Nonsteroidal anti-
inflammatory drugs should be avoided.
 Prior to definitive aneurysmal treatment, blood pressure should be aggressively controlled
to prevent further bleeding; mean arterial pressure (MAP) should be kept below 110 mm
Hg. Short-acting antihypertensives (e.g., labetalol, nicardipine) are preferred.
 Blood pressure can be liberalized after successful aneurysm treatment; higher blood
pressure postoperatively also promotes cerebral perfusion.
 Mannitol is best avoided as it has been reported to precipitate rebleeding presumably by
affecting transmural gradients across the aneurysm.
 Ten percent of patients (especially those with severe SAH and elevated cardiac enzyme
levels) will have stunned myocardium with wall motion abnormalities or globally
depressed systolic and/or diastolic function on acute echocardiography.
 This form of “stress induced cardiomyopathy” is reversible and often resolves within 1 to
2 weeks.
 Perform cerebral angiography to delineate the aneurysm.
 Take measures to prevent rebleeding by securing the aneurysm by microsurgical clipping
and endovascular coiling.
 Prevent, identify and manage vasospasm. Onset of vasospasm typically occurs on days
3–5, peaks on days 5–14, and resolves over 2–4 weeks.
 Diagnosis of vasospasm is made by clinical examination, presence of fresh infarct on CT
or by angiography or bedsideTranscranial Doppler studies ( high blood flow velocity ).
 Oral nimodipine—an oral calcium channel antagonist, 60 mg 4-hourly for 21 days—is
indicated to reduce poor outcome due to vasospasm.
 Symptomatic cerebral vasospasm can be managed with “triple-H therapy,” that is,
hypervolemia, induction of hypertension and hemodilution.
 Bolus 15 mL/kg of NS to induce mild hypervolemia. Raise MAP 15% above patient’s
baseline using vasopressors if necessary.
 Consider hemodynamic monitoring in patients with heart failure or pulmonary edema,
with goal of optimizing hemodynamics.
 Assess response to intervention.
 Prevent and treat seizures. Levetiracetam at a dose of 1000 mg twice daily is a
commonly used regimen.
 Manage hyponatremia.
 The reported incidence of hyponatremia after SAH ranges from 10% to 30% and may be an
independent risk factor for poor outcome.
 Fluid restriction is required in patients with hyponatremia due to the syndrome of inappropriate
antidiuretic hormone secretion. This can precipitate delayed ischemic deficits, and therefore, a
careful balance has to be maintained.
 Hyponatremia in many cases with SAH is due to the “cerebral salt-wasting syndrome.” This
state is associated with features of volume depletion differentiating it from syndrome of
inappropriate antidiuretic hormone (SIADH). Correction of hypovolemia with isotonic fluids is
indicated in such cases.
 Daily measurement of serum sodium and intake output chart is important.
 Manage neurogenic pulmonary edema
 This is characterized by rapid onset of respiratory failure in the setting of raised intracranial pressure. It is
thought to be due to pulmonary capillary endothelial damage.
 Most of these patients are comatose.
 Treatment includes reduction of intracranial pressure, mechanical ventilation with positive-end expiratory
pressure and attaining the lowest central venous or pulmonary wedge pressure that maintains an effective
cardiac output by cautious diuresis.
 Look for ECG changes.
 Prognostication Unfavorable outcome was associated with increasing age, worsening
neurological grade, ruptured posterior circulation aneurysm, larger aneurysm size,
intracerebral hematoma or intraventricular hemorrhage, elevated systolic blood pressure
on admission, fever 8 days after SAH, use of anticonvulsants, symptomatic vasospasm
and cerebral infarction.