Neurocritical Care
for Stroke
WENDY L. WRIGHT, MD, FCCM, FNCS
CHIEF OF NEUROLOGY AND DIRECTOR OF THE
NEUROSCIENCE CRITICAL CARE UNIT
EMORY UNIVERSITY HOSPITAL MIDTOWN
ASSOCIATE PROFESSOR OF NEUROLOGY
AND NEUROSURGERY
EMORY UNIVERSITY SCHOOL OF MEDICINE
ATLANTA, GA
Greetings from the Stroke Belt
Mohr
Stroke Belt & Buckle
Stroke Belt & Buckle
Nahab
Objectives
 Determine the role of the NeuroICU in the stroke “chain of survival”
Systems of delivery
 Identify unique opportunities for the multidisciplinary,
multiprofessional neurocritical care team to impact stroke care
 SAH, ICH, CVST
 Early detection of neuro changes
 Monitoring and managing increased intracranial pressure
 Examine the basic treatment principles that guide neurointensive
stroke care
 Interventions
 Medical management

No financial disclosures
Stroke
remains a
leading cause
of death and
disability in
the U.S., with
more than
750,000
cases per
year.
Strokes
cause
200,000
deaths and
cost more
than $57
billion per
year in the
U.S. alone.
Gonzales
Meyers
Stroke Care
Prevention
Reperfusion
Neuroprotection
Penumbral
perfusion
Supportive
care
Rehabilitation
Gonzales
Jovin
Systems of Care: Chain of Survival
 Prehospital management
 Rapid transport to designated stroke center
 Emergency evaluation
 Early diagnosis
 Rapid implementation of treatment
 General “supportive” care
 Management of complications
 Rehabilitation
 Secondary prevention
Systems of Care: Chain of Survival
 Prehospital management
 Rapid transport to designated stroke center
 Emergency evaluation
 Early diagnosis
 Rapid implementation of treatment
 General “supportive” care
 Management of complications
 Rehabilitation
 Secondary prevention
Expanding role of
neurocritical care
Indications for Intensive Care
 Patients with stroke who meet medical criteria for intensive care
Respiratory, cardiac, etc.
 Patients who need for intensive neurologic
monitoring/management
 All subarachnoid hemorrhage



Acute intracerebral hemorrhage


Risk of cerebral edema
Stroke or hemorrhage in the posterior fossa


Risk of rebleed and cerebral edema
Large hemispheric ischemic stroke


Risk of re-rupture, high-risk treatment modalities, risk of hydrocephalus,
risk of vasospasm
Imminent risk of neurologic deterioration due to hydrocephalus and
cerebral edema
Intracranial pressure monitoring
Traditional Role of NeuroICU in Stroke Care
 Diagnosis
 Acute reperfusion strategies
 “Supportive” measures
 Penumbral perfusion
 Prevent secondary brain injury
 Including
neuroprotection
 Prevent/treat stroke complications
Diagnosis: Stroke Mimics
 Metabolic disturbance
 Hypo- or hyperglycemia, drug toxicity, hypo- or
hypernatremia, renal or hepatic failure, post-anoxic
encephalopathy
 Meningitis/encephalitis
 Hypertensive encephalopathy
 Hypotension
 Seizures with persistent neurologic deficit
 Migraine with persistent neurologic deficit
 Intracranial mass
 Tumor, hematoma, abscess
 Craniocerebral/cervical trauma
Acute Reperfusion Strategies
 Measures to restore or improve perfusion
 IV thrombolytics
 Endovascular therapies
 Anticoagulants or antiplatelets


Volume expansion, vasodilators and induced hypertension


Role is secondary prevention, not reperfusion
Not recommended outside a of research setting
Surgical interventions

Not recommended as a reperfusion strategy outside of a research
setting
Adams
“Brain-Oriented” Intensive Care
 Balance cerebral metabolic (oxygen and glucose)
supply


Cerebral perfusion pressure, cerebral oxygenation
Controlling intracranial pressure
 With cerebral metabolic demand

Fever, seizures, agitation, pain, shivering
 And minimize compounds that will worsen
neurologic damage

Excess cerebral glucose, lactic acid, excitotoxic neurotransmitters,
inflammatory mediators, etc.
DeGeorgia 2005
Loss of autoregulation
Reperfusion injury
Free radicals
Cerebral
ischemia
Mitochondrial
dysfunction
Loss of ion
homeostasis,
including
prolonged Ca++
influx
Loss of membrane integrity
Release of excitotoxins
Inflammatory reactions,
proinflammatory cytokines
Tisdall, Polderman,
Mulvey, DeGeorgia
Loss of autoregulation
Reperfusion injury
Free radicals
Cerebral
ischemia
Loss of ion
homeostasis,
including
prolonged Ca++
influx
Mitochondrial
dysfunction
Loss of membrane integrity
Release of excitotoxins
Inflammatory reactions,
proinflammatory cytokines
Apoptosis
Cellular swelling=>↑ICP
Tisdall, Polderman,
Mulvey, DeGeorgia
Continuous
EEG
Cerebral
Blood
Flow
Monitor
Cerebral
Microdialysis
Membrane
degradation
products,
excitotoxic
neurotransmiters,
inflammatory
markers, etc.
Brain Tissue
Oxygenation
Monitor
DeGeorgia 2005
Wright 2007
Stroke Critical Care
 Emergency measures

Airway/breathing/circulation
 Penumbral perfusion

BP delivery
 Secondary injury/neuroprotection





Seizures
Glucose
Infection
Temperature management
ICP management
 Complications





DVT/PE
Infection
Alimentation
Hemorrhagic transformation
Recurrent stroke
 Rehab initiation

Early mobilization
Supportive Measures After Stroke
 Airway

Intubate if compromised
 Breathing

Maintain sats >94% (avoid hypoxia)

Supplemental O2 not recommended
 Circulation



Cardiac monitoring
Cardiac rhythm
Treat/avoid hypovolemia



With fluids that do not contain glucose and are not hypotonic
Treat high or low BP
Improve blood flow to penumbra?

Volume expanders, vasodilators, induced hypertension and
hemodilution
Jaunch
BP treatment after stroke
 If patient received tPA
 Treat to keep SBP > 180, DBP> 105 for the first 24 hrs
 Nicardipine, labetolol are the first line recommendations
 If patient did not receive tPA
 Treat if SBP>220, DBP>120
 Target 15% reduction on the first day
 Oral antihypertensives can probably be added (or
restarted) slowly following 24-48 hours of symptoms
onset

Some use 24-48 hours after symptom stabilization
Wartenberg 2007
Blood Pressure after Acute Ischemic Stroke
*BP Goal:
Allow for
enough
cerebral
perfusion
pressure and
penumbral
perfusion, but
not so much to
cause
hemorrhagic
transformation
*One goal
unlikely to fit all
patients
Gonzales
Meyers
Enhancing Perfusion of the Ischemic Penumbra
 Hemodilution
 Intentional hemodilution does not reduce mortality or
improve outcome in survivors and is therefore not
recommended (Class III, Level A)
 Only possible exception is in patients with severe polycythemia
vera
 Volume expansion
 Trials ongoing with albumin (ALIAS), but not currently
recommended
 Vasodilators
 Not recommended based on current data (Class III, Level A)
 Induced hypertension
Induced Hypertension- AHA Guidelines
 Optimal management of blood pressure remains
controversial
 Inducing hypertension is attractive in experimental
studies Wityk, Hillis, Koenig
 Guidelines Adams


In exceptional cases, may prescribe vasopressors to improve
cerebral blood flow; if used, close neurologic and cardiac
monitoring is recommended (Class I, Level C)
Drug-induced hypertension, outside of the setting clinical
trials, is not recommended for most patients with acute
ischemic stroke (Class III, Level B)
Induced Hypertension in Clinical Practice
 In general, if neurologic symptoms are fluctuating
over the first 48-72 hours, there are many
neurocritical care units that will try a modest
increase in blood pressure

Starting with bolus fluid administration to increase MAP by
10-20%, then using vasopressors if needed to see if neurologic
deficits stabilize or improve
If so, MAP goals are then reset to this level until symptoms
stabilize, then slowly weaned over ensuing days
 Similar steps are taken if symptoms fluctuate or worsen to sudden
changes in BP with change in body position, medication
administration, etc.

General Supportive Measures After Stroke
 Admit to stroke unit, standard stroke orders
 Alimentation
 Early dysphagia screen
 NG/PEG if needed for feeding and meds
 Infection
 Avoid foley
 Glucose
 Avoid/treat hypoglycemia and hyperglycemia
 Venous thromboembolism prophylaxis
 Anticoagulation for DVT prophylaxis
 SCDs if they cannot tolerate anticoagulation
 Early mobilization
 Early meds to prevent stroke recurrent stroke
 ASA is appropriate in most patients
 Statin as indicated (do not discontinue if already taking)
Jaunch
Supportive Measures After Stroke
 Hyperthermia

Evaluate and treat causes of fever
 Neuroprotective strategies



No medications to date have been efficacious in clinical trial
 Calcium channel blockers
 NMDA-receptor antagonists
 Early administration of magnesium in the field (FAST-MAG)
 Nitric oxide synthetase inhibitors
 Interferon-В
 Erythropoietin
 And many more…
Hyperbaric O2 data inconclusive
Hypothermia
Jaunch
Hypothermia
 Has been shown to be neuroprotective in experimental
and focal brain injury models
 Rational is strong, especially since it is multifactorial





May delay depletion of energy reserves
Lessen intracellular acidosis
Slow influx of calcium into ischemic cells
Suppress production of oxygen free radicals
Lessen impact of excitatory amino acids
 Studies are on going to look at factors such as optimal
temperature, and timing of rewarming, etc.
 Hypothermia is commonly used in neurocritical care
units to treat refractory cerebral edema
Treating Complications After Stroke
 Infection
 Avoid foley catheter placement
 Treat pneumonia, urinary tract infections per usual
 Prophylactic antibiotics not recommended
 Recurrent seizures should be treated
 Prophylactic AEDs not recommended
 Hemorrhagic transformation
 Avoid/stop high dose anticoagulants, antiplatelets
 Ventricular drain for hydrocephalus
 Brain edema
 Do not give corticosteriods
 Suboccipital craniotomy for cerebellar strokes
 Decompressive hemicraniectomy is lifesaving in the setting of malignant
cerebral edema from large artery strokes
Jaunch
Don’t Underestimate These Strokes!
 Posterior circulation strokes


Can look like intoxication or infection (CNS or inner ear)
Image vessels with CT-angiography or MR-angiography
 Cerebellar strokes


Swelling can cause hydrocephalus and herniation, and can be rapidly fatal
Neurosurgical consult is required for ventriculostomy drain or suboccipital
craniotomy
 Large ischemic strokes



“Large” is >1/3 the MCA territory, or with mass effect on the ventricle or
midline shift
At risk for life-threatening cerebral edema which could lead to herniation
and death
Early decompressive hemicraniectomy can be life saving
 Cerebral venous sinus thrombosis


Often misdiagnosed
Reluctance to anticoagulate persists
Brain Edema
 Tends to occur with infarction of major intracranial
arteries and leads to multilobar infarctions
 Usually peaks 3-5 days after stroke
 Can be a problem in the first 24 hours after large
cerebellar infarction
Adams
Increased Intracranial Pressure
The Ultimate Compartment Syndrome!
Intracranial Pressure & Cerebral Perfusion Pressure
 Normal ICP varies with age, but in adults it is usually
5-15 mm Hg
 Cerebral perfusion pressure (CPP) is the mean
arterial pressure (MAP) minus the ICP

If the ICP is high, blood can not reach cerebral tissues
 ICP of 20-30 mm Hg is generally considered
elevated, but cerebral herniation can occur at lower
values, especially with pressure gradients across
cerebral compartments
Signs and Symptoms of Increased ICP
 Declining mental status
 Headache
 Nausea, vomiting
 Papilledema
 Reliable, but uncommon
 Pupillary dilation
 Decerebrate posturing
 Apnea
 “Cushing's Triad” of HTN, bradycardia, change in
respiratory pattern
Rangel-Castillo
ICP Treatment Based on MKD
 Plan to quickly assess for and treat any underlying
causes such as a subdural hematoma or cerebral
abscess

This will usually require neurosurgical intervention
 Mass-targeted
 CSF-targeted
 Brain-targeted
 Blood-targeted
ICP Management
 General (targets blood compartment)
Avoid shivering, agitation, fever; head midline and elevated to
30º; maintain euvolemia or slightly hypervolemic
Hyperventilation (targets blood compartment)
 Lower PaCO2 30-35 in emergent situations
Osmotherapy (targets brain compartment)
 Hypertonic saline (Na 145-155), mannitol (osm 300-320),
furosemide (less desirable but still used)
Metabolic suppression (targets blood compartment)
 Narcotics, benzodiazepines, barbiturate coma, propofol
CSF drainage (targets CSF compartment)
 Especially in pts with hydrocephalus or IVH
Neurosurgical (targets brain or “mass” compartment)
 Hematoma/infarcted tissue removal, hemicraniectomy
Hypothermia (targets brain compartment)







Bhardwaj
Bedside Interventions for ICP Crisis
 Immediate steps
 HOB up, head midline (blood targeted)
 Hyperventilate with ambu bag (blood targeted)
 Osmotherapy (brain targeted)
30-60cc of 23.4% saline through central line
 250-500cc of 3% saline is an alternative
 or 1 gm/kg of mannitol through a peripheral line
 This must go through a filter

 Try to reverse the herniation (i.e., return pupil to normal)
or ICP spike and get patient to CT scanner to look for
reversible and/or neurosurgical causes
Bedside Interventions for ICP Crisis
 ADVANCED management options
 Cool the patient
 Can pack in ice if a cooling blanket is not available
 Watch for shivering!
 Propofol 0.05-0.1mg/kg bolus
or 125-250 mg of thiopental IV
 Will drop the MAP/CPP, and may make it difficult to
examine the patient
 If an ICP monitor is in, consider vasopressors to support
cerebral perfusion pressure
Don’t Underestimate These Strokes!
 Posterior circulation strokes


Can look like intoxication or infection (CNS or inner ear)
Image vessels with CT-angiography or MR-angiography
 Cerebellar strokes


Swelling can cause hydrocephalus and herniation, and can be rapidly fatal
Neurosurgical consult is required for ventriculostomy drain or suboccipital
craniotomy
 Large ischemic strokes



“Large” is >1/3 the MCA territory, or with mass effect on the ventricle or
midline shift
At risk for life-threatening cerebral edema which could lead to herniation
and death
Early decompressive hemicraniectomy can be life saving
 Cerebral venous sinus thrombosis


Often misdiagnosed
Reluctance to anticoagulate persists
Cerebral Venous Thrombosis
 CVT accounts for 0.5% to 1% of all strokes
 Mostly affects young people, especially women of
childbearing age
 Commonly presents with headache

Though some present with a focal neurological deficit,
decreased level of consciousness, seizures or intracranial
hypertension without focal signs
 Insidious onset can create a diagnostic challenge
 2011 guideline
Cerebral Venous Thrombosis
 A prothrombotic factor or direct cause is identified in
about 2/3 of patients
 Diagnosis is usually made by venographic studies
with CT (CTV) or MRI (MRV) to demonstrate
obstruction of the venous sinuses
Risk Factors
 Acquired

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




Surgery
Trauma
Pregnancy
Puerperium
Antiphospholipid syndrome
Cancer
Exogenous hormones


Infections



Oral contraceptives
Mainly in parameningeal locations
CVT caused by infection is more
common in children
Mechanical precipitants



Epidural blood patch
Spontaneous intracranial
hypotension
Lumbar puncture
 Genetic risks

Inherited thrombophilia/
hypercoaguability






Antithrombin III deficiency
Protein C deficiency
Protein S deficiency
Factor V Leiden positivity
Hyperhomocysteinemia
Mutation G2020A of factor II
 Hematologic disorders


Paroxysmal nocturnal
hemoglobinuria
Polycythemia, thrombocythemia
 Systemic diseases


Systemic lupus erythematosus
Inflammatory bowel disease
Pregnancy and the Puerperium
 Common causes of prothrombotic states
 Most pregnancy related CVTs occur in the third
trimester or 6-8 weeks after birth
 During the puerperium, additional risk factors
include infection; increasing maternal age;
hypertension; vomiting; and instrumental delivery or
Cesarean section
Treatment
 Initiate anticoagulation, unless there is a
contraindication

In the presence of CVT, intracranial hemorrhage is NOT an
contraindication to anticoagulation
 Treat any underlying cause, if able
 Including antibiotics for infection, or surgical drainage of
purulent collections of infectious sources associated with CVT
when appropriate
 Treat a seizure if one occurs, but routine use of
prophylatic antibiotics is not recommended
 Put the treatment algo.
Increased Intracranial Pressure
 Monitor for visual field loss
 May require cerebrospinal fluid diversion
 Guidelines say that acetazolamide is reasonable to
decrease CSF production
 Patients with neurologic deterioration due to severe
mass effect or intracranial hemorrhage causing
intractable intracranial hypertension may be eligible
for hemicraniectomy
 Steroids are not indicated to treat cerebral edema

Unless needed for another underlying disease
Systems of Care
 Primary stroke center certification
 Preferential routing of stroke patients whose symptoms started
within time windows amenable to intervention
 Comprehensive stroke centers
 Act as a regional resource for stroke care and will be pivotal for
further advancement in acute stroke care, stroke prevention
and rehabilitation Dion, Rymer, Silverman
 Designed to care for patients with
Complicated types of stroke, intracerebral hemorrhage or
subarachnoid hemorrhage
 And those requiring specific interventions (surgery or
endovascular procedures) or an intensive care setting


Currently about 75 in the US, estimated need is 300
Mobile Stroke Units
Studies showed a reduction in EMS
activation-to-treatment time from
104 minutes to 64 minutes
Future Directions
 Continued move toward regionalization of stroke
care
 Focus on candidate selection for acute stroke therapy


For recanalization, hemicraniectomy, hypothermia and other
advanced therapies
Advanced radiology techniques to assess core vs. penumbra
 The quest for neuroprotection continues
 Fine tune care delivery systems
Conclusions
 Stroke remains an actively advancing field of
medicine
 We are all a link in the chain of survival
 Due to multidisciplinary, multiprofessional
collaboration, neurocritical care unit teams have a
specialized ability to detect and manage



Patients in need of acute stroke interventions
Secondary brain injury after stroke
Complications after stroke
References
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