Principals of Neurocritical Care
in the Acute Stroke Patient
Alexander Y. Zubkov, MD, PhD, FAHA
Clinical Associate Professor of Neurology
Director of Stroke Center
Fairview Southdale Hospital
Minneapolis Clinic of Neurology
Kari Olson, RN, BSN, CNRN
Neuroscience Nurse Clinician
DISCLOSURE
Relevant Financial Relationship(s)
• None
Off Label Usage
• None
Objectives
Learning Objectives: Upon completion of this
call, participants will be able to:
– Describe Neuro Critical Care management of acute
stroke patients.
– Explain advances in neurosurgery for the stroke patient
including decompressive hemicraniectomy for malignant
cerebral edema
– Describe nursing care guidelines for the pre and post
neurosurgical stroke patient
Pressing Issues in Acute Ischemic
Stroke
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Restoring blood flow
Monitoring for edema and swelling
Managing risk of bleeding with tPA
Preventing and minimizing secondary injury
General Care Principles
• Maximize standard medical management
– B/P, fever, hyperglycemia, seizure activity
• Neuroprotection
• Improve cerebral blood flow
– Induce HTN
– Recanilization with thrombolysis
– Large vessel intra-arterial thombolectomy/lysis
• Prevention of complications
Airway and Mechanical Ventilation
• Management of the airway and mechanical ventilator is
different in neurologic critically ill patients.
• Many patients admitted to NICU have normal baseline
pulmonary function
• Mode of mechanical ventilation in acutely ill neurologic
patient is often limited to intermittent mandatory or assist
control modes
• Ventilator dependency is much less common
Airway and Mechanical Ventilation
• Any amount of hypoxia of the injured brain will add
a significant damage to the brain.
• Thus, intubation should be preferably performed in
the controlled settings, and sometimes it is safest
to perform in the anticipation of the respiratory
problems rather than when the respiratory failure
will occur.
Volume Status and Blood Pressure
• Very few patients admitted to NICU are euvolemic
and correction of volume status is one the first steps
in the management of critically ill neurological or
neurosurgical patient
• Initial correction of hypovolemia should be done
with crystalloids (normal saline). Glucose containing
solutions may precipitate increased lactate
production and secondary brain injury
Volume Status
• 200 mL/hr
• .9% sodium cloride
• Correct insensible loss
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GI 250 mL
Skin 750 mL
Fever 500 mL/degree C
Sweating
• Fluid balance 750-1,000
mL/ day excess
• Maintain body weight
• Hematocrit < 55%
• Osmolality <350
mosm/L
• Serum sodium < 150
meq/L
The Importance of Blood Pressure
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Hypertension is a physiological response in stroke
BP reduction is associated with worse outcome
BP fluctuations are associated with worse outcome
BP augmentation may be safe and effective at least
in selected cases
Management of Blood pressure
• Current recommendations include cutoff point in
treatment of hypertension if systolic pressure is
above 230 mm Hg, or diastolic pressure is above
125 mm Hg, or mean pressure above 130 mm Hg.
• It is reasonable to gradually decrease blood pressure
with rapid-acting antihypertensive medications if
mean pressure is getting above 130 mm Hg.
Detrimental effect of BP reduction in first
24 hours after stroke onset:
• Prospective assessment of 115 pts evaluated within
24 hr of stroke onset
• Mean NIHSS 4.5
• Most common mechanism: cardioembolism (30%)
• Predictors of poor outcome at 3 mo on multivariable
analysis:
- Higher NIHSS
(OR 1.55 per 1 point increase in score)
- Degree of SBP reduction in first 24 hr
(OR 1.89 per 10% SBP decrease)
Oliveira-Filho et al. Neurology 2003;61:1047-51
The Importance of Blood
Glucose
• Hyperglycemia in acute stroke is associated
with:
- Worse functional outcome
- Lower rates of recanalization
- Higher rates of hemorrhagic complications
• Trials of acute intensive glycemic control
ongoing
Infections / Fever
• Fever develops in 25-50% of NICU patients.
• 52% percent of fevers were explained by infectious
etiology with most predominant pulmonary
pathology.
• Non-infectious etiologies of fever may occur and
include reaction to blood products, deep vein
thrombosis, drug fever, postsurgical local tissue
injury, pulmonary embolism and central fever with
its extreme autonomic storms (episodes of profuse
sweating, tachycardia, tachypnea, bronchial
hypersecretion).
The Importance of Body
Temperature
• Fever after acute stroke is associated with
worse functional outcome
• Preliminary evidence suggests that aggressive
control of hyperthermia (and perhaps
induced hypothermia in cases of massive
brain infarction) may be beneficial
• Rigorous, larger interventional trials needed
Nutrition
• The main goal of nutrition should be to
preserve muscle mass, and to provide
adequate fluids, minerals and fats
• It is prudent to consider postpyloric feeding
in patient with neurological catastrophies,
because gastric atony increases the risk of
aspiration.
• Enteral feeding should be preferably done by
continuous infusion with a volumetric pump.
Seizures
• Acute injury to the cortical structures can
elicit seizures.
• Seizures may be focal or generalized, single
or continuous
• Tonic–clonic status epilepticus is commonly
defined as repetitive seizures without full
recovery between the episodes, usually with
seizure intervals of 5 to 10 minutes
Seizures
• Nonconvulsive status epilepticus is much
difficult to diagnose and likely is less
common.
• Clinical hallmarks are decrease in the level of
consciousness or fluctuation in
responsiveness.
• Patient may have fluttering of the eyelids or
eye deviation as only signs of nonconvulsive
status epilepticus.
Seizure Assessment
• Continuous clinical assessment
• Continuous vEEG monitorin
– 20 minute EEG will demonstrate 15% of
seizures
– 60 minute EEG – 50%
– 24 hours monitoring – close to 90%
Seizure Management
• Benzodiazepins
– Ativan 4 mg IV push
• Antiepileptic medications
– Dilantin may be toxic for the acutely injured
brain
– Depakote may cause severe platelet dysfunction
and bleeding
– Keppra seems to avoid significant side effects
and used widely in NICU
Seizure Management
• Failure of lorazepam and fosphenytoin in adequate
doses to control seizures indicates transition to
refractory status epilepticus.
• At this point either increasing doses of barbiturates
or midazolam should be used for treatment.
• Propofol is another alternative but high dosis are
needed. Propofol infusion syndrome – sudden
cardiovascular collapse with metabolic acidosis-is a
serious complication that limits the routine use of
this otherwise very effective medication.
Anticoagulation
• Neurological patients has a higher incidence of DVT due to
lack of mobility in the affected limbs, associated with
neurological injury.
• Clinically apparent DVT was reported in 1.7% to 5% of
patients with ischemic stroke
• Subclinical DVT occurred in 28 to 73%, mostly in the
paralyzed extremity
• 5% of the patient with ICH died of pulmonary embolism
(PE) within the first 30 days.
Anticoagulation
• Only mechanical methods (intermittent pneumatic
compression with or without elastic stockings)
should the standard of care.
• The use of unfractionated heparin was left on the
discretion of the practitioner
• One study in TBI patients demonstrated no increase
risk of hemorrhage in patients treated with
unfractionated heparin within 72 hours
Large Hemispheric Stroke Issues
• High risk for deterioration in first 24-72
hours
– Neurologic causes: edema, hemorrhagic
transformation, restroke
– Systemic causes: fever, infection, hypotension,
hypoxia, hypercarbia
Malignant MCA Syndrome
• Malignant brain edema
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Mortality up to 80%
Starts days 1-3
Peaks days 3-5
Subsides by 2 weeks
Who is at Risk for Developing
Malignant MCA Syndrome?
Clinical Picture:
• hemispheric syndrome with
hemiparesis,
hemianesthesia
• eye deviation
• those requiring early
intubation for airway
protection
• global asphasia
• somnolence
Radiographic Picture
• CT findings in 1st 6 hours
• Large early hypodensity
• Loss of gray/white matter
distinction
• Hyperdense MCA sign
• CT findings at 24 hours
• Mass effect
Intracranial pressure
Monro-Kelly doctrine
ICP depends on the
volumes of blood,
cerebrospinal fluid and
brain to be in the balance.
Intracranial pressure
• CSF shift from ventricular or subarachnoid
space into spinal compartment.
• Reduction of intracranial blood volume
achieved by collapsing of veins and dural
sinuses and by changes in the diameter of
cerebral vessels.
• If the limits of compensatory mechanisms
are exceeded, minimal increase in the
intracranial volume will lead to precipitous
rise of ICP.
Intracranial Pressure
• Intracranial pressure monitoring is an integral
part of NICU.
• The indications for placement of ICP
monitors include GCS < 8, severe traumatic
brain injury, massive cerebral edema from
infarction
Intracranial Pressure Management
• Head position should be neutral to reduce
any possible compression of jugular veins.
• Head elevation of 30º is considered standard
• Patients should be made comfortable, avoid
pain, bladder distention, and agitation,
because all of them might increase ICP.
Intracranial Pressure Management
• Hyperventilation
– Aggressive hyperventilation might decrease
cerebral blood flow to the levels approaching
ischemia.
– Hyperventilation should only be used as a bridge
measure while other means of ICP control are
instituted
Intracranial Pressure Management
• Osmotic diuresis – mainstay of the therapy
– Mannitol is not only facilitates movement of extracellular
water, but also might be increasing CSF absorption
• The effect is apparent within 15 minutes and failure to respond
to mannitol is usually a bad prognostic sign
• 100 grams IV over 30 minutes
• 50 grams IV q6h with osmolality monitoring.
– Hypertonic Saline
• 3% NaCl - continuous infusion
• 7.5% NaCl - mostly used in trauma centers
• 23.4% saline
• Sixty-eight patients met criteria for TTH and received 23.4%
saline, and there were a total of 76 TTH events in these
patients.
• The 23.4% saline was administered as a bolus of 30 mL in 65
events (85.5%) and 60 mL in 11 events (14.5%).
Neurology, Mar 2008; 70: 1023 - 1029
Hypertonic Saline Effect
• Clinical reversal of TTH occurred in 57/76 events (75.0%).
• Median (IQR) GCS increased from 4(3-5) at the time of
herniation to 6(4-7) (p<0.01) 1 hour and 7(5-9) 24 hours
following TTH (p<0.001).
Neurology, Mar 2008; 70: 1023 - 1029
Intracranial Pressure Management
• Hypothermia
– Need to continue the study of safety and
effectiveness in the Neuro ICU.
– Guidelines needed for best practice temperature
thresholds and rates of rewarming.
Decompressive Hemicraniectomy
• Allows for the expansion of edematous tissue
outside the cranial vault
• Decreases mortality and disability
• Issues:
– Patient Selection
– Timing of surgery
– Dominant vs. non-dominant hemisphere strokes
Outcome at 1 year by treatment group
for all three studies combined
Lancet Neurology, 8( 7); 603-604, 2009
Subarachnoid hemorrhage
• Hydration with normal saline should be
started immediately and patient should
receive at least 2-3L of fluids in the first 24
hours.
• Attention should be paid to possible
neurogenic pulmonary edema and fluid
management should be adjusted accordingly.
• Cardiac stunning might occur in the poor
grade SAH and might contribute to
pulmonary edema
Subarachnoid hemorrhage
• Management of hypertension depends on the
stage of the treatment.
• In the patients with unsecured aneurysm we
tend to keep mean arterial pressure below 100
mm Hg.
• In patients who underwent aneurysmal repair,
mean blood pressure should be liberalized up
to 130 mm Hg.
Subarachnoid hemorrhage
• Nutrition usually delays to the second day.
Nausea and vomiting are common on the
first day, in addition to gastroparesis in more
severely impaired patients
• Deep vein thrombosis prophylaxis should
utilize mechanical means only.
• Gastric ulcer prophylaxis is important in all
patients due to high incidence of stress ulcers.
Subarachnoid hemorrhage
• Stool softeners should be used in all patients to
prevent straining, which may lead to rerupture of
the aneurysm.
• Indwelling catheters should be used to close
monitoring in outputs due to potential of the
development of SIADH.
• Headache may be relieved by acetaminophen with
codeine or tramadol.
• Vomiting should be aggressively treated.
Subarachnoid hemorrhage
• Deterioration in patients with SAH can be
delayed and related to rebleeding,
hydrocephalus, vasospasm, or enlargement of
frontal or temporal intraparenchymal
hematoma.
Intracerebral hemorrhage
• Hemorrhages have a potential of enlargement in about a
third of the patients and management should be directed
towards supportive measures.
• Very aggressive decrease of blood pressure may precipitate
ischemia
• Comatose patients could benefit from the monitoring in
intracranial pressure.
• Intracranial pressure should remain below 20 mm Hg and
cerebral perfusion pressure must remain in the range of 60
to 80 mm Hg to provide adequate cerebral blood flow
AAICH
• Anticoagulation-associated intracerebral
hemorrhages should be immediately reversed
with fresh frozen plasma and vitamin K.
• Factor VIIa - works within 10 minutes
– It is short lived factor.
– Treatment should be followed by administration
of FFP and Vitamin K
– INR should be monitored for at least 72 hours
Time is Brain
• For every minute’s delay, the brain loses:
– 1.9 million neurons;
– 14 billion synapses;
– 7.5 miles of myelinated fibers.
• If a stroke runs its full course – an estimated 10
hours on average – the brain loses:
– 1.2 billion neurons;
– 8.3 trillion synapses;
– 4,470 miles of myelinated fibers.
Stroke 2006;37:263-266
Nursing management of Acute Stroke
• Airway management/ventilator management
• Assessment and evaluation of neurologic status to detect
patient deterioration
• Blood pressure management
• General supportive care and prevention of complications
associated with:
– Dysphagia, HTN, hyperglycemia, dehydration, malnourishment,
fever, cerebral edema, infection, and DVT, immobility, falls, skin
care, bowel and bladder dysfunction.
Nursing Management of Acute Stroke
• Coordination of interdisciplinary team and
plan of care
• Support and counsel for patient & family
Intensive Nursing Management
• Monitor for bleeding complications after tPA
– ICH-Hemorrhagic transformation
– retroperitoneal bleed, genitourinary and
gastrointestinal hemorrhages
– Patients over age of 80 with higher NIHSS score
at greater risk of ICH
Intensive Nursing Management
• Management of suspected ICH after tPA
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Notify physician, possible neurosurgery consult
Stop tPA infusion
Prepare for stat brain imaging, lab, type and cross
Prepare to administer platelets, cryoprecipitate,
FFP
– Increase frequency of nursing assessment
Intensive Nursing Management
Cerebral Edema after stroke
Usually peaks 3-5 days after stroke
Can be an issue in first 24 hours in cerebellar
infarct and younger stroke patients
If not detected and treated can lead to increased
intracranial pressure, brain herniation and
death
Recognizing Increased ICP
• Early signs:
– Decreased LOC
– Deterioration in motor
function
– Headache
– Changes in vital signs
• Late signs
– Pupillary abnormalities
– Changes in respiratory
pattern
– Changes in ABG’s
Nursing Care of the Decompressive
Hemicraniectomy Patient
• Airway management adequate O2 saturation
• Preventing increased ICP and providing supportive
care.
• Hourly vitals/neuros including ICP, CPP, CVP.
• Maintaining BP to ensure adequate CPP
• Seizure precautions
• Antibiotic prophylaxis
Nursing Care of the Decompressive
Hemicraniectomy Patient
• Place a sign on bed to alerting care providers which
side of the skull is missing the bone flap
• Do not turn patients onto side of missing flap
• Monitor hemicraniectomy site for changes in
appearance- bulging, inflammation, CSF leakage
• Fit with head gear to protect surgical site when up
Decompressive Hemicraniectomy
• Bone flap stored in a Bone Bank or sewn into
a pouch in patient’s abdomen.
• Bone replaced at around 3 months from the
time of the infarction.
Team Work
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Key to the care of the NICU patient
Stabilization
Prevention of complications
Monitoring neuro status
Family support and education
Resources
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Adams, H. et al (2007). Guidelines for the Early Management of Adults with
Acute Ischemic Stroke. Stroke 38, 1655-1711.
Ropper, A.H., Gress, D.R., Diringer, M.N., Green, D.M. , Mayer, S.A. , Bleck,
T.P. Neurological and Neurosurgical Intensive Care. Fourth edition. Lippincott
Williams & Wilkins.2004. Philadelphia, PA
Summers, et al. (2009) Comprehensive Overview of Nursing and Interdisciplinary
Care of the Acute Ischemic Stroke Patient. Stroke 40, 2911-2944.
Tazbir, J., Marthaler, M.T., Moredich, C., Keresztes, P. Decompressive
Hemicraniectomy with Duraplasty: A treatment for Large-Volume Ischemic
Stroke. Journal of Neuroscience Nursing. August 2005. 37(4).
Wojner Alexandrof, A. W., Hyperacute Ischemic Stroke
Management:Reperfusion and Evolving Therapies. Critical Care Nurse Clinician
North America. 21(2009) 451-470.