wendy l. wright, md, fccm, fncs chief of neurology and director of the neuroscience critical care...
TRANSCRIPT
WENDY L. WRIGHT, MD, FCCM, FNCSCHIEF OF NEUROLOGY AND DIRECTOR OF THE
NEUROSCIENCE CRITICAL CARE UNITEMORY UNIVERSITY HOSPITAL MIDTOWNASSOCIATE PROFESSOR OF NEUROLOGY
AND NEUROSURGERYEMORY UNIVERSITY SCHOOL OF MEDICINE
ATLANTA, GA
Neurocritical Care for Stroke
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.
MeyersGonzales
Gonzales
Stroke Care
Prevention Reperfusion Neuroprotection
Penumbral perfusionSupportive care
Rehabilitation
Jovin
Systems of Care: Chain of Survival
Prehospital managementRapid transport to designated stroke centerEmergency evaluationEarly diagnosisRapid implementation of treatmentGeneral “supportive” careManagement of complicationsRehabilitationSecondary prevention
Systems of Care: Chain of Survival
Prehospital managementRapid transport to designated stroke centerEmergency evaluationEarly diagnosisRapid implementation of treatmentGeneral “supportive” careManagement of complicationsRehabilitationSecondary 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
Risk of re-rupture, high-risk treatment modalities, risk of hydrocephalus, risk of vasospasm
Acute intracerebral hemorrhage Risk of rebleed and cerebral edema
Large hemispheric ischemic stroke Risk of cerebral edema
Stroke or hemorrhage in the posterior fossa Imminent risk of neurologic deterioration due to hydrocephalus
and cerebral edema Intracranial pressure monitoring
Traditional Role of NeuroICU in Stroke Care
DiagnosisAcute reperfusion strategies“Supportive” measures
Penumbral perfusionPrevent secondary brain injuryIncluding neuroprotectionPrevent/treat stroke complications
Diagnosis: Stroke Mimics
Metabolic disturbance Hypo- or hyperglycemia, drug toxicity, hypo- or
hypernatremia, renal or hepatic failure, post-anoxic encephalopathy
Meningitis/encephalitisHypertensive encephalopathyHypotensionSeizures with persistent neurologic deficitMigraine with persistent neurologic deficitIntracranial mass
Tumor, hematoma, abscessCraniocerebral/cervical trauma
Acute Reperfusion Strategies
Measures to restore or improve perfusion IV thrombolytics Endovascular therapies Anticoagulants or antiplatelets
Role is secondary prevention, not reperfusion Volume expansion, vasodilators and induced
hypertension 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
Cerebral ischemia
Free radicals
Reperfusion injury
Loss of membrane integrity
Release of excitotoxins
Mitochondrial dysfunction
Loss of ion homeostasis, including prolonged Ca++
influx
Tisdall, Polderman, Mulvey, DeGeorgia
Inflammatory reactions, proinflammatory cytokines
Loss of autoregulation
Cerebral ischemia
Free radicals
Reperfusion injury
Loss of membrane integrity
Release of excitotoxins
Mitochondrial dysfunction
Apoptosis
Cellular swelling=>↑ICP
Loss of ion homeostasis, including prolonged Ca++
influx
Tisdall, Polderman, Mulvey, DeGeorgia
Inflammatory reactions, proinflammatory cytokines
DeGeorgia 2005
Cerebral Blood Flow Monitor
Brain Tissue Oxygenation Monitor
Cerebral Microdialysis
Continuous EEG
Membrane degradation products, excitotoxic neurotransmiters, inflammatory markers, etc.
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
Airway Intubate if compromised
Breathing Maintain sats >94% (avoid hypoxia)
Supplemental O2 not recommendedCirculation
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
Supportive Measures After Stroke
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
*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
MeyersGonzales
Blood Pressure after Acute Ischemic Stroke
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
recommendedVasodilators
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.
Admit to stroke unit, standard stroke ordersAlimentation
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 mobilizationEarly meds to prevent stroke recurrent stroke
ASA is appropriate in most patients Statin as indicated (do not discontinue if already taking)
General Supportive Measures After Stroke
Jaunch
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
Supportive Measures After Stroke
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 hydrocephalusBrain 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 craniotomyLarge 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 savingCerebral 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 strokeCan 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 statusHeadacheNausea, vomitingPapilledema
Reliable, but uncommonPupillary dilationDecerebrate posturingApnea“Cushing's Triad” of HTN, bradycardia,
change in respiratory patternRangel-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-targetedCSF-targetedBrain-targetedBlood-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 craniotomyLarge 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 savingCerebral venous sinus thrombosis
Often misdiagnosed Reluctance to anticoagulate persists
Cerebral Venous Thrombosis
CVT accounts for 0.5% to 1% of all strokesMostly affects young people, especially
women of childbearing ageCommonly 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 Surgery Trauma Pregnancy Puerperium Antiphospholipid syndrome Cancer Exogenous hormones
Oral contraceptives Infections
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 statesMost pregnancy related CVTs occur in the
third trimester or 6-8 weeks after birthDuring 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 anticoagulationTreat 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 lossMay require cerebrospinal fluid diversionGuidelines say that acetazolamide is reasonable
to decrease CSF productionPatients 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 interventionComprehensive 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.
penumbraThe quest for neuroprotection continuesFine tune care delivery systems
Conclusions
Stroke remains an actively advancing field of medicine
We are all a link in the chain of survivalDue 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
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