The Critically Ill Neurological
Patient:
Why Neuro ICU Matters
Julia Durrant, MD
Division of Neurosciences Critical Care
Department of Neurology
Oregon Health and Science University
Disclosures
 No external sources of financial support to
disclose
Outline
• The Dedicated Neuro ICU
• The Art of the Neuro ICU
– Cerebral edema/ICP management
– Fever control
– Seizure control
• Does it work?
Neuro ICU at OHSU
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Founded in 2005
17 bed unit
24 hour CT/MRI access
24 Hour access to EEG techs, Epilepsy faculty
Proximity to OR and Angio suites
24-7 Neuro-Intensivist coverage with 8 faculty
Patient Population
• Severe ischemic stroke:
at risk for cytotoxic
edema
• Ischemic stroke
following thrombolysis
with tPA or
thrombectomy
• Cerebral venous
thrombosis
Who should be admitted?
• ICU admission:
– Stroke complicated by respiratory failure,
myocardial decompensation or uncontrollable
hypertension.
– Large mismatch between core infarction and
territory
• complex hemodynamic management.
Patient Population
• Intracerebral and
intraventricular
hemorrhage
• Subdural and
epidural hematoma
Patient Population
• Subarachnoid
hemorrhage
• Cerebral aneurysms
• Cerebral and spinal
vascular
malformations
• Brain tumors
Patient Population
• Status epilepticus
• Meningitis and
encephalitis
• Neuromuscular
disorders in crisis
(myasthenia gravis,
Guillain-Barre
syndrome) and acute
myelopathies
Neuroprotection: the goal of
neurocritical care
• Assessment of end organ perfusion
– No direct laboratory measurements
– Physical exam
– MRI/CT imaging
• Interval to end-organ failure under adverse
conditions can be rapid.
• Further injury to even small regions of brain
can have devastating consequences.
What Can We Offer?
• Cerebral resuscitation
– “The Brain Code”
• Disease-specific
management
• Full complement of
subspecialists
• Cutting-edge
technology
Cerebral Resuscitation: acute
catastrophic neurologic injury
• Catastrophic neurologic injury: ICP
herniation
Cranial Vault Mechanics
csf
blood
brain
normal
• Monroe and Kellie
– Skull is a rigid container
– Cranial contents (brain,
blood, CSF) are viscous gel
and incompressible
– Additional volume
(pathologic or expansion of
the 3 normal contents) will
lead to the displacement of
another content
9%
4%
150mL 75mL
87%
1400 mL
abnormal
4% 4%
mass
1%
20%
92%
abnormal
79%
Saunders NR, Habgood MD, Dziegielewska KM (1999). "Barrier mechanisms in the brain, I. Adult brain". Clin.
Exp. Pharmacol. Physiol. 26 (1): 11–9
Cranial vault mechanics
CPP = MAP - ICP
CBF = CPP/CVR
CD02 = CBF x Ca02
ICP<20, CPP>60 = mortality reduction by> 50% in TBI
Bratton SL et al. J Neurotrauma 24 (S1): S59-S64, 2007
Narotam P, Morrison J et al. Brain tissue oxygen monitoring in traumatic brain injury and major
trauma: outcome analysis of a brain tissue oxygen-directed therapy. JNS (2009) 111 (4): 672-682
Rosner M J, Rosner S D & Johnson A H. "Cerebral perfusion: management protocol and
clinical results." J.Neurosurgery 1985; 83: 949-962.
Cerebral Resuscitation: herniation
syndromes
Subfalcine Herniation
Cerebral cortex under falx
•Ipsi/contra leg weakness
• mental status
Upward Herniation
Brainstem up through
tentorium
•  mental status
•Dilated pupil (CNIII),
ophthalmoplegia
•Ipsi paresis/posturing
(contra cerebral crus)
Tonsillar Herniation
Cerebellar tonsils in foramen magnum
•Awake, quadriparesis
•Arrhythmia/cardiac arrest
•Respiratory arrest
Central Herniation
Brainstem down through
tentorium
• mental status
•Dilated pupil (CNIII),
ophthalmoplegia
•Ipsi paresis/posturing
(contra cerebral crus)
•Basilar stroke
Uncal Herniation
 mental status
Uncus over tentorial notch
•Dilated pupil (CNIII),
ophthalmoplegia
•Ipsi paresis/posturing
(contra cerebral crus)
• PCA stroke
Medical Interventions
Reduce Cranial Contents:
Blood – vasodilation to constriction
Venous Return
Hyperventilation
Reduction of CMR02
Brain water
Osmolar therapy for edema
Surgical Interventions
Drain CSF
Surgical removal of mass
Break the rigid skull - craniectomy
Brain Code
Airway: O2 sat>90%
Breathing: normal CO2
Circulation CPP> 60mmHg
Head of Bed:
•30 degree, midline
Hyperventilation:
•pCO2 30 +/- 2 mmHg
Hyperosmolar therapy
•Mannitol IV 1 gm/kg IV
•Hypertonic saline (CVL)
o3% NaCl or 23.4% NaCl
Normothermia/?Hypothermia
Pharmacologic Coma
Cerebral Resuscitation: compartment
approach to ICP management
Venous blood
-HOB up
-Neck straight
-No IJ lines, do not lay flat
for lines
-Do no use venodilating BP
agents
Arterial blood
-Hyperventilate
-Avoid hyperemia: MAP
target 60, Pa02>50
-Decrease metabolism:
sedation, cooling
CSF
-Place IVC
-Change popoff
Brain parenchyma
-Osmotherapy (mannitol,
hypertonic saline)
-Steroids only if appropriate
(Vasogenic edema)
Lesion
-Blood, tumor, pus -> surgery
-Air-> 100% NRB, surgery
Cerebral Resuscitation: arterial
compartment
Arterial blood
-Hypervent
-Avoid
hyperemia:
MAP target
60, Pa02>50
-Decrease
metabolism:
sedation,
cooling
Kramer A, Zygun D. Anemia and red cell transfusion in neurocritical care. Critical Care 2009 13:R89
Cerebral Resuscitation: compartment
approach to ICP management
Venous blood
-HOB up
-Neck straight
-No IJ lines, do not lay flat
for lines
-Do no use venodilating BP
agents
Arterial blood
-Hyperventilate
-Avoid hyperemia: MAP
target 60, Pa02>50
-Decrease metabolism:
sedation, cooling
CSF
-Place IVC
-Change popoff
Brain parenchyma
-Osmotherapy (mannitol,
hypertonic saline)
-Steroids only if appropriate
(Vasogenic edema)
Lesion
-Blood, tumor, pus -> surgery
-Air-> 100% NRB, surgery
Cerebral Resuscitation: venous
compartment
Venous blood
-HOB up
-Neck straight
-No IJ lines, do not lay flat
for lines
-Do no use venodilating BP
agents
If CVP exceeds ICP,
CPP = MAP - CVP
Ropper: n=19. 52% had ICP when HOB increased from 0->60°. 2% had ICP.
Davenport: n=8. Median ICP from 18->15 with 20° elevation, no in CPP until > 60°.
Lee: n=30. Trendelenburg positioning ICP from 20->24, but ICP in 20% of pts. (!)
Davenport A, Will EJ, Davison AM. Effect of posture on intracranial pressure and cerebral perfusion
pressure. Crit Care Med 1990; 18(3):286-289.
Lee ST. Intracranial pressure changes during positioning of patients with severe head injury. Heart Lung
1989; 18(4):411-414.
Ropper AH, O'Rourke D, Kennedy SK. Head position, intracranial pressure, and compliance. Neurology
1982; 32(11):1288-1291.
Cerebral Resuscitation: compartment
approach to ICP management
Venous blood
-HOB up
-Neck straight
-No IJ lines, do not lay flat
for lines
-Do no use venodilating BP
agents
Arterial blood
-Hyperventilate
-Avoid hyperemia: MAP
target 60, Pa02>50
-Decrease metabolism:
sedation, cooling
CSF
-Place IVC
-Change popoff
Brain parenchyma
-Osmotherapy (mannitol,
hypertonic saline)
-Steroids only if appropriate
(Vasogenic edema)
Lesion
-Blood, tumor, pus -> surgery
-Air-> 100% NRB, surgery
Cerebral Resuscitation: CSF
compartment
CSF
-Place IVC
-Change
popoff
Cerebral Resuscitation: compartment
approach to ICP management
Venous blood
-HOB up
-Neck straight
-No IJ lines, do not lay flat
for lines
-Do no use venodilating BP
agents
Arterial blood
-Hyperventilate
-Avoid hyperemia: MAP
target 60, Pa02>50
-Decrease metabolism:
sedation, cooling
CSF
-Place IVC
-Change popoff
Brain parenchyma
-Osmotherapy (mannitol,
hypertonic saline)
-Steroids only if appropriate
(Vasogenic edema)
Lesion
-Blood, tumor, pus -> surgery
-Air-> 100% NRB, surgery
Cerebral Resuscitation: Brain
parenchyma
Brain parenchyma
-Osmotherapy
(mannitol,
hypertonic saline)
-Steroids only if
vasogenic edema
- Surgery (hemicrani,
SOC)
Cytotoxic
Vasogenic
Hydrostatic
Cerebral Resuscitation: Brain
parenchyma
Reflection Coefficient
Osmotic Load
Solution Concentration
Sodium Concentration
(mEq/L)
Ringer's lactate
Osmolarity (mOsm/L)
130
275
0.90%
154
308
2.00%
242
684
3.00%
513
1062
Mannitol 20%
n/a
1098
Mannitol 25%
n/a
1375
7.50%
1283
2566
23.40%
4004
8008
P.S. 1L of NS is 3.5g of Na+ in 1 liter of free water
Hinson et al, J Intensive Care Med (2011)
Cerebral Resuscitation: Brain
parenchyma
• Both improve rheology of erythrocytes  increases
deformability through small capillaries
•Mannitol easier to give: no central line
•HS increases vascular volume  improves CBF up to
23%
 HS reduces inflammatory response by reducing PMN
adhesion to microvasculature
Pascual J et al. Hypertonic saline resuscitation of hemorrhagic shock diminishes neutrophil rolling and
adherence to endothelium and reduces in vivo vascular leakage. Ann Surg. 2000 Nov; 236 (5): 634-642
Tseng M, Pippa G et al. Effect of hypertonic saline on cerebral blood flow in poor grade patients with
subarachnoid hemorrhage. Stroke 2003;34:1389-1396
Recent Trials
Author/Year
Type of
Prospective Trial
Agent
3% sodium
lactate v. 20%
mannitol
Ichai/2009
Randomized
Controlled
Francony/2008
Randomized
Controlled
Battison/2005
Randomized
Controlled
Harutjunyan/2005
Randomized
Controlled
7.5% HS v. 20%
mannitol
20mL 20%
mannitol v.
100mL 7.5% HS
dextran
7.2% HS + 6%
HES v. 15%
mannitol
Vialet/2003
Randomized
Controlled
7.5% HS v. 20%
mannitol
Condition(s) Number of
Treated
Patients?
TBI
TBI +
Stroke
TBI + SAH
34
HS>Mannitol
for ICP,
GOS
20
Both ICP
similarly
9
Neurosurg
patients
40
TBI
20
Hinson et al, J Intensive Care Med (2011)
Outcome
HS>mannitol
for ICP
HS>mannitol
for ICP
HS>Mannitol
for reducing
elevated ICP
episodes
Adverse Effects
Complication
Mannitol
Hypertonic Saline
Renal Failure
Avoid prolonged
Avoid continuous infusion, hypernatremia
repeat high dosing
>160mEq/L
Rebound
Allow clearance prior to
repeat dosing
Allow clearance prior to
repeat dosing
Metabolic Acidosis
n/a
Reduce chloride in
admixture
Hypokalemia
n/a
Add potassium to fluids
Hypovolemia
Concurrent volume
resuscitation
n/a
Hinson et al, J Intensive Care Med (2011)
Cerebral Resuscitation: compartment
approach to ICP management
Venous blood
-HOB up
-Neck straight
-No IJ lines, do not lay flat
for lines
-Do no use venodilating BP
agents
Arterial blood
-Hyperventilate
-Avoid hyperemia: MAP
target 60, Pa02>50
-Decrease metabolism:
sedation, cooling
CSF
-Place IVC
-Change popoff
Brain parenchyma
-Osmotherapy (mannitol,
hypertonic saline)
-Steroids only if appropriate
(Vasogenic edema)
Lesion
-Blood, tumor, pus -> surgery
-Air-> 100% NRB, surgery
Cerebral Resuscitation: Lesion
• Surgical evacuation: STICH
– Subjects with ICH (≥2cm) randomized to early (<24
hours) surgical evacuation v. medical management
– No benefit to early surgery in general
– Superficial lesions, large cerebellar lesions (≥3cm) may
benefit
– Summary: “Except for possibly those with superficial
ICHs, craniotomy at 1 day or longer after onset is not
better than initial conservative medical treatment
with or without later craniotomy for patients who
have deterioration.”
Mendelow AD, et. al. STICH investigators. Lancet. 2005; 365 (9457): 387–97.
Malignant Middle Cerebral Artery
Stroke
• 1-10% of patients with
supratentorial infarcts
– life-threatening edema with
peak edema on day 2-5
• Mortality of entire MCA
territory is 78%, thus
“malignant MCA infarction”
– Including maximal medical
intervention
• Midline shift peaked after
2-4 days for those who
died,
– 3-7 days for survivors.
Cerebral Resuscitation: Lesion
• Hemicraniectomy in stroke: DECIMAL,
DESTINY, HAMLET
– All small trials showed non-significant trend
toward benefit of hemicraniectomy
– Meta-analysis suggests an absolute risk reduction
of 13%
– Patient selection?
• Non dominant hemisphere
• Age of patient
Jüttler E. Stroke. 2007 Sep;38(9):2518-25.
Disease Specific Management:
Ischemic Stroke
• Hemorrhagic Transformation
• CT study shows ~1-5% hemorrhagic
transformation
– ranges from minor petechial bleeding to major
mass-producing hemorrhage
• Use of antithrombotics, anticoagulants,
thrombolytics increase risk
– NINDS ICH: 6.4% of tPA treated patients versus
0.6% in the placebo group, and mortality was 47%
Disease Specific Management:
Subarachnoid Hemorrhage
• Feared Complications:
– Hydrocephalus
– Aneurysm re-rupture
– Seizures
– Vasospasm
– Stressed myocardium
– Neurogenic pulmonary edema
Disease Specific Management:
Subarachnoid Hemorrhage
 Blood pressure management
 Use of intermittent labetalol boluses or continuous infusion of
nicardipine to maintain SBP less than 140 mmHg (unsecured)
 Vasospasm prophylaxis
 Nimodipine 60 mg every 4 hours for 21 days
 Vasospasm monitoring
 Daily transcranial doppler sonography for 14 days
 Hydrocephalus treatment
 Extraventricular Drain (EVD) placement
Cardiac Support after SAH
• Reduced Ejection Fraction or Symptomatic
Vasospasm
– Fluids, vasopressors
– Hemodynamic monitoring
Fever
• ~50% of stroke patients develop fever1
• Body temp > 37.5°C significantly correlates
with poor outcomes2
• Fever in first 24 hours linked to infarct
volume3
• Induced normothermia may reduce metabolic
stress4
1. Stroke 1998;29: 2455–60. 2. Stroke 1995;26:2040–3. 3. Acta Neuropathol 1991;81:615–25. 4. Stroke 2009;40:1913–16
Fever and Hypothermia
• Fever treatment
– Acetaminophen
– Cooling blankets
– Intravascular cooling devices
• Hypothermia
– Not Standard of Care
– No clinical evidence yet to support its use
– National Acute Brain Injury Study: Hypothermia II
terminated early for futility1
1. GL Clifton, A Valadka, D Zygun et al. Lancet Neurol, 10 (2011), pp. 131–139
Glucose
• Elevated serum glucose increases tissue necrosis and
edema.
• Hyperglycemia >200mg/dl is a predictor of poor
outcome in ICU patients.
• Hypoglycemia (<60mg/dl) can result in focal
neurological deficits.
• The goal of care is to achieve normoglycemia (80-140
mg/dl) with insulin infusion.
Seizures after Stroke
• Seizures occur in ~ 9% of patients1
– Greater risk after hemorrhagic stroke
– ~2.5% have recurrent seizures
– Stroke location modifies risk
• Routine prophylaxis not recommended2
• Seizure always on differential in depressed
mental status
– Continuous EEG helpful in making diagnosis
1. Arch Neurol. 2000 Nov;57(11):1617-22. 2. Stroke. 2010; 41: 2108-2129
Cardiac management
• ST-T changes can be seen in large ischemic
strokes
• Diffuse or confined to a cardiovascular territory
• Myocardial ischemia should always be excluded
• “Brain T-wave changes” do not predict cardiac
morbidity
• Autonomic reciprocal innervation to the temporal
lobes may produce arrhythmias in patients
without pre-existing coronary disease
Does Neurocritical Care matter?
• Improved Mortality
for ICH patients
Critical Care Medicine. 29(3):635-640, March 2001.
Does Neurocritical Care matter?
• Reduced
Mortality
• Shorter LOS
• More
discharges
to
home/rehab
Journal of Neurosurgical Anesthesiology. 13(2):83-92, April 2001.
Does Neurocritical Care matter?
• Reduction in
mortality after
Neurointensivist
appointed
Critical Care Medicine. 32(11):2191-2198, November 2004.
Cerebral Resuscitation: outcomes
Long-term outcome after medical reversal of transtentorial herniation in
patients with supratentorial mass lesions
Qureshi,,Geocadin,Suarez, Ulatowski, CRITICAL CARE MEDICINE 2000;28:1556-1564


11/28 (40%) survived to discharge
7/11 (59%) survivors functionally independent
Does Neurocritical Care matter?
YES!
Thank you!
• Questions?