BP management in TBI Mustapha Ezzeddine, MD - Neurocritical Care University of Minnesota Medical Center
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BP management in TBI Mustapha Ezzeddine, MD Neurocritical Care University of Minnesota Medical Center
Hypertension is common in acute TBI • Patients presenting with isolated TBI often present acutely hypertensive. • A catecholamine surge occurs as stress response to the brain trauma, similarly to other types of acute brain injury • to a massive release of epinephrine and norepinephrine in the systemic circulation can occur without increased ICp
Hypotension is also common in early TBI • About a third of all TBI patients are hypotensive • Often related to systemic trauma, hypoxia and blood loss • Can be present in isolated brain injury in about a third of the cases • Isolated TBI/hypotension more common in pediatrics.? Related to neurogenic cardiac injury
Early Hypotension is linked to worse
outcomes
• Hypotension on presentation linked to
150% increase in mortality in one study
• BP lower than 75% percentile linked to
worse outcome even with SBP>90
• Patients with early hypotension did worse
than patients with delayed hypotension.Secondary Injury
Hypotension = Devastation
• Chesnut RM, Marshall SB, Piek J, Blunt BA,
Klauber MR, Marshall LF.
Early and late systemic hypotension as a
frequent and fundamental source of cerebral
ischemia following severe brain injury in the
Traumatic Coma Data Bank.
Acta Neurochir Suppl (Wien) 1993;59:121-5Secondary Injury
Hypotension
• Severe head injury in the Traumatic Coma Data Bank
– GCS score < or = 8
– Hypotension = SBP < 90 mm Hg
• Early Hypotension: (248 of 717 patients)
– Mortality: 55% vs 27%
– If shock present, mortality was 65%
• Late Hypotension: In ICU (156 of 493 patients)
– Mortality or vegetative state: 66% vs 17%
• Logistic Regression Modeling
– Early and late shock were the most powerful independent
predictors of mortalitySecondary Injury
Hypotension & Hypoxia
• Chesnut RM, Marshall LF, Klauber MR, Blunt
BA, Baldwin N, Eisenberg HM,Jane JA,
Marmarou A, Foulkes MA.
The role of secondary brain injury in determining
outcome from severe head injury.
J Trauma 1993 Feb;34(2):216-22.Secondary Injury
Hypotension & Hypoxia
• Severe head injury (GCS score < or = 8) in 717
cases in the Traumatic Coma Data Bank
• Impact on outcome of hypotension and hypoxia
– Hypotension = SBP < 90 mm Hg
– Hypoxia = Pao2 < 60 mm Hg, apnea or cyanosis
• Hypoxia and hypotension were independently
associated with significant increases in morbidity
and mortality from severe head injurySecondary Injury Cascade
AnemiaIschemia and TBI
• Early ischemia (first 12 hrs post-injury)
– Global ischemia
• severe intracranial hypertension (mass lesion, diffuse
swelling)
• hypotension
• severe diffuse injury
– Regional ischemia
• contusions
• vascular injuries/compression
• Early CBF reflects severity of injury
• Early ischemia is strongly predictive of early
mortalityIschemia and TBI
• Late Ischemia (>12 hr after trauma)
– Global - secondary ischemic insults
• Intracranial hypertension
• Hypotension
• Hypoxia
• Hypocarbia
• Anemia
• Fever
– Regional - evolving contusions, vasospasm
• Late ischemia often can be prevented, or treated if
detected early
• Late ischemia worsens outcomePHYSIOLOGY
High energy requirements of the
brain
• Brain 2% body mass
• 20% of cardiac output
• 60% of body’s glucose
• 20% of consumed oxygen
• Low oxygen extraction reserve ( high
extraction under normal conditions)CBF=CPP/CVR CPP=MAP-ICP (CVP) CPP: Cerebral Perfusion Pressure MAP: Mean Arterial Pressure ICP: Intracranial Pressure CBF: Cerebral Blood Flow CVR: Cerebrovascular resistance
CBF
Impaired
autoregulation
Vasogenic
edema Chronic
Hypertension
Ischemia
l l
50 150
MAPCoupling of CMRO2 and CBF mediated by
local signals, ATP, nitric oxide NO,
adenosine, phospholipid metabolites
Very minimal neurogenic influence
(sympathetic or parasympathetic)
Hydrogen
ion mediatedFalling cerebral perfusion
Cerebral perfusion pressure
Autoregulation, no symptoms
Ischaemic symptoms
Cerebral blood volume
Exhausted reserve
O2 extraction fraction
Cerebral blood flow
Cerebral metabolic rate of O2Current Opinion in Neurology 2004, 17:705–709
Cerebral ischemia - duration
Normal flow, normal function
50
Low flow, raised O2 extraction, normal function
CBF (ml/100g brain)
20
Reversible
reduced
Irreversible
function
reduced
function
0
TimeCompartmentalization of ICP
Brain Tissue
Oxygenation Bpt02
Cerebral
Multimodal Microdyalisis
Neuro-
Focal CBF
monitoring monitors
Continuous EEG
monitoringBrain Tissue Oxygenation
• Intraprenchymal catheter with sensor tip
• Measures local Po2, PCO2, and pH
• Placed similarly to an ICP monitor
• Ideally need to target placement in tissue
at risk/ischemic penumbraCerebral Microdialysis • Intraparenchymal microdialysis catheter inserted in a similar fashion to ICP bolt • Typically measure glucose, lactate, pyruvate to detect ischemia • Excitatory amino-acids • Can measure other molecules (drugs, inflammatory markers
Jugular Bulb Oximetry • Central venous oximetry catheter placed retrograde in IJ, to jugular bulb • Continuous venous saturation Sjo2 • Can detect brain increased oxygen extraction • 55-85% nl values,
Transcranial Doppler • cerebral blood flow velocities • Asses cerebrovascular reserve • Detect cessation of circulation-Brain Death • Pulsatility index for monitoring of edema
Why Regional CBF After TBI?
Heterogeneity of CBF after TBI
Histogram of Average rCBF in Cortical ROIs
Patients with < 5mm shift Patients with shift and/or mass lesion
40 60
Number of ROI's
30 Diffuse I 50
Number of ROI's
20 40
Diffuse IV
10
30
40
20
Number of ROI's
30
10
Diffuse II
20
40
Number of ROI's
10
30
40
20
Number of ROI's
Mass Lesion
30
10
Diffuse III
20
0
100
10 rCBF in ROI
0
100
rCBF in ROIGlobal Continuous Monitors –
SjvO2 Catheter Indirect Measures of CBF
Local
PbtO2 CatheterCPP
Cerebral perfusion pressure
• CPP=MAP-ICP
– original recommendations for CPP were extrapolated from
effects of changing CPP in normals, who have intact
autoregulation
• ‘CPP management’ stresses primacy of CPP over
the actual ICP value
– the ‘Lund protocol’ is diametrically opposed, lowering
MAP to decrease edema production
– both claim improved outcome compared to historical
controls
• current AANS guidelines specify CPP of 60 mmHg
– lower: poorer outcome
– higher: more ARDSCPP: What Target
• Reduction in CPP < 60-70 leads to secondary
injury from release of glutamate (Vespa et al J
Neurosurg 1998)
• One CPP does not fit all
– Heterogeneous cerebral blood flow
– At any given CPP, there are regions of the brain
that are oligemic
– Different CPP thresholds for different regions of the
brainThe Lund Protocol
Brain Volume Regulation With Preserved Microcirculation
• Based on Physiological Principles
• Aim to decrease cranial fluid volume
• Maintain cerebral flow
• Protect brain from sympathetic mediated
fluctuation of CBFThe Lund Protocol
• Increase interstitial fluid resorbtion
– Maintain COP with normovolemia, normal serum
albumin & haemoglobin
• Veno-constriction to decrease CBV
– Dihydroergotamine
• Vasoconstriction of pre-capillary sphincter
– Low dose thiopentone & dihydroergotamine
• Lower BP : CPP > 50
– Beta 1 (metoprolol) & alfa 2 (clonidine) blockers
• Drain CSF via EVD for acute rise of ICPThe Lund Protocol
• CCM 1998;26:1881-6
– 5 year study
– 53 head injured patients (ICP> 25 & GCS < 8)
– Study group
• Mortality 8% & Severe brain damage 13%
– Historical controls
• Mortality 47% & Severe brain damage 11%
• CCM 1998;26:1787-8 Comment on above studyThe Lund Protocol
• 3 independent non randomized trials, using main
principles of Lund protocol with good outcome
– Naredi S et al. ICM 1998;24:446-51
– Eker et al. CCM 1998;26:1881-6
– Naredi S et al. Acta Anaest. Scand. 2001;45:402-6
• Elf et al CCM 2002;30:129-134
– Good outcome: Principles based ? More on Lund
protocol than US guidelines
• Naredi S et al. Treatment of traumatic head injury-
US/European Guidelines of the Lund Concept. Crit Care
Med 2003;31:2713-4Maximize CPP vs Hyperventilate & Decrease ICP • Staged problems and management in traumatic acute brain injury • Phase of Hypoperfusion – Correct BP & CPP with conventional means • Phase of Hyperemia – Decrease cerebral blood flow with hyperventilation • Phase of Vasospasm – Volume expansion with induced hypertension
Fluid thresholds and outcome from
severe brain injury
• Retrospective study (from the NIH
multicenter hypothermia trial data) of the
effect on GOS of ICP, MAP, CPP, and fluid
balance at 6 mo after injury
• Univariate predictors of poor outcome:
– ICP >25 mm Hg
– MAPFluid thresholds and outcome from
severe brain injury
• Significant variables in a stepwise
logistic regression:
– GCS score at admission
– Age
– MAP 25 mm HgFluid thresholds and outcome from
severe brain injury
• Conclusions: Exceeding thresholds of ICP,
MAP, CPP, and fluid volume may be detrimental
to severe brain injury outcome.
• Fluid balance lower than -594 mL was
associated with an adverse effect on outcome,
independent of its relationship to intracranial
pressure, mean arterial pressure, or cerebral
perfusion pressure.Maximize CPP vs Hyperventilate & Decrease ICP
• Claudia S. Robertson et al Critical Care
Medicine 1999;27:2086-2095
– RCT 189 adults
– CPP group: CPP>70 & CO2 ~35 mmHg
– ICP group:CPP>50 & CO2 25-30
– CPP group had less frequency of jugular
desaturation: 50.6% to 30% (p = .006)
• Risk of cerebral ischemia 2.5 time greater in ICP group
– No difference in neurological outcome
– CPP group had 5 fold increase in ARDS (15 vs 3%)
• TCDB data: ARDS associated with X 3 mortality in TBIEffect of various medications on:
ICP/CBF
Decreases No Change Increases
INDUCTION AGENTS
Barbiturates Midazolam Ketamine
Etomidate Propofol Droperidol
MUSCLE RELAXANTS Vecuronium Succinylcholine
Atracurium
Pancuronium
IV AGENTS Lidocaine Narcotics (rare paradox: fentanyl)
Benzodiazepines
ANTI-HYPERTENSIVES Labetolol Nitroglycerine
Beta blockers Nitroprusside
ACE inhibitors Hydralazine
CA CHANNEL BLOCKERS Nicardipine Nifedipine
Verapamil
INHALATION AGENTS N2O Isoflurane
Enflurane Halothane
Adapted from: Manual of Neuroanesthesia, Sperry,1989 Figure 2-3BP IN OTHER BRAIN INJURIES
Stroke
Blood pressure Management
BP reduction in acute ischemic
stroke might worsen ischemia
BP reduction in acute
intracerebral hemorrhage might
limit hematoma growthDetrimental effect of blood pressure reduction in the
first 24 hours of acute stroke onset
NEUROLOGY 2003;61:1047-1051
115 acute stroke patients within 24 hrs
OR 95% CI p
Age 1.51 per 10-year increase 0.87 –2.64 0.15
NIHSS score 1.55 per 1-point increase 1.28 –1.87INTERACT • 404 patients with ICH < 6hours • Randomized to SBP
HYPOTENSION
Hypotension after TBI
• A common phenomena after brain injury,
occuring in one in five cases.
• Numerous observational studies have
confirmed the association between systemic
hypotension occurring at any point after injury
and poor outcome.
• A single episode of hypotension is associated
with approx doubling of mortality and a
parallel increase in morbidity.
– Persists when age and the presence of hypoxia and extracranial
injuries are taken into account
• Most commonly due to inadequate volume
resuscitationFluid Resuscitation:
Hypertonic Saline
Mechanism of Action Osmotic effect
Osmotic effect Via properties of sodium chloride
1. Low permeability across BBB
Anti-inflammatory effects 2. Hi reflection coefficient (1.0)
Modulation of neuroendocrine Hyperosmolar concentrations
system (ANP, VSP) Create a gradient to pull water
from interstitial and intracellular
spaces into the intravascular
Maintain BBB integrity via compartment
membrane stabilization
Improve regional cerebral blood
flow (rCBF)Hypertonic Saline –
Clinical Evidence
Cooper et al (JAMA 2004; 291: 1350)
Design
Prospective RCT of 229 severe TBI and
hypotension in the field
Bolus with 250 cc 7.5% LR or LR
Results
No baseline differences between groups
Median GCS = 4, ISS 38, fluid = 1250
No difference in Bp on arrival to ED
No difference in morbidity or mortalityHypertonic saline out of hospital TBI • blunt trauma and a prehospital GCSof 8 or less not in hypovolemic shock. • 250 cc bolus 7.5% saline vs NS • Survival at 28 days was 74.3% with hypertonic saline/dextran, 75.7% with hypertonic saline, and 75.1% with normal saline • No difference in functional outcomes JAMA. 2010 Oct 6;304(13):1455-64.
2007 BTF Guidelines A. Hypotensive patients should be treated with isotonic fluids. B. Hypertonic resuscitation is a treatment option for TBI GCS < 8.
2007 BTF Guidelines • B. Level II Blood pressure should be monitored and hypotension (systolic blood pressure < 90 mm H B. Level II Aggressive attempts to maintain CPP above 70 mm Hg with fluids and pressors should be avoided because of the risk of ARDS. C. Level III CPP of < 50 mm Hg should be avoided.
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