TUESDAY - California Society of Anesthesiologists

2014 Fall Anesthesia Seminar
Preeclampsia Update:
2014-15
Mark Zakowski, M.D.
Chief Obstetrical Anesthesiology
Cedars-Sinai Medical Center
Los Angeles CA 90048
Associate Prof, Adjunct
Drew University, Los Angeles
Disclosures
• No relevant financial relationship with any
commercial interest.
• Member, CMQCC Task Force Preeclampsia
• Passionate about Maternal and Baby well
being
• Quantum Birthing, LLC
Learning Objectives
• Recognize preeclampsia in the peripartum period.
• Understand assessments of patients for
preeclampsia and preeclampsia related
complications.
• Implement current guidelines and practices for
preeclampsia therapies.
• Understand the role of communication in
prevention, recognition and treatment of
preeclampsia related maternal and neonatal
complications.
OUTLINE
•
•
•
•
•
Preeclampsia
Recognition
Current treatment protocols 2014-15
Communication – keys to success
Bonus
Hypertensive Disorders of Pregnancy
•
•
•
•
•
•
•
6-10% of pregnancies worldwide
Preeclampsia increased 25%/20yr USA
50,000+ maternal deaths/yr worldwide
50-100x more ‘near miss’
Major cause of prematurity, infant mortality
Long term sequelae Maternal and Offspring
Less than optimal care contributes
– Communication large part of that
-ACOG Task Force HTN Preg rev 5-2014
Age-adjusted incidence per 1,000 deliveries for women with gestational hypertension (b
0.0024; P < 0.0001) or preeclampsia (b = 0.0009; P = 0.009) for 2-year periods, 1987–2004
Wallis A B et al. Am J Hypertens 2008;21:521-526
© 2008 by the American Journal of Hypertension, Ltd.
CA-PAMR: Chance to Alter Outcome
Grouped Cause of Death; 2002-2004 (N=145)
Grouped Cause of Death
Chance to Alter Outcome
Strong / Some
Good (%) (%)
None
(%)
Total
N (%)
Obstetric hemorrhage
69
25
6
16 (11)
Deep vein thrombosis/
pulmonary embolism
53
40
7
15 (10)
Sepsis/infection
50
40
10
10 (7)
Preeclampsia/eclampsia
50
50
0
25 (17)
Cardiomyopathy and other
cardiovascular causes
25
61
14
28 (19)
Cerebral vascular accident
22
0
78
9 (6)
Amniotic fluid embolism
0
87
13
15 (10)
All other causes of death
46
46
8
26 (18)
Total (%)
40
48
12
145
Preventability Maternal Death
Cause
% of deaths
Preventable %
Cardiomyopathy
21
22
Hemorrhage
14
93
Preeclampsia spectrum
10
60
CVA
9
0
Chronic Medical problem
9
89
AFE
7
0
Infection
7
43
Pulm Embolism
6
17
CV condition
5
40
North Carolina maternal deaths, n=108, 1995-1999
-Berg Obstet Gynecol 2005:106:1228-34
Preeclampsia: an Evolving Disease
• Starts 1st trimester
– abnormal placental implantation
– Altered remodeling spiral arteries
• 2nd trimester
– Angiogenic imbalance
• 3rd trimester
– Endothelial dysfunction
– Maternal effects widespread
– Clinical symptoms
Preeclampsia: an Evolving Disease
• Early onset (<34 weeks GA)
– Placental origin
• Late Onset (>34 weeks GA)
– Maternal Origin
• Increased Maternal CV risk later
– Unmasking disease vs. altering the course
– Offspring have altered health.
Risk Factors Preeclampsia
•
•
•
•
•
•
•
•
•
Prior preeclampsia (OR 7) or family Hx (OR 2-4)
Primiparity
IVF
Diabetes – type I OR type II
Maternal age >40
Obesity
Chronic HTN or renal disease
Multiple Gestation
Lupus
-ACOG 2013 Task Force HTN Pregnancy
Placental Implantation Normal
• Anaerobic
• Placenta releases PlGF, VEGF – grows
into endometrium
• Invades and dilates spiral arteries to
increase blood flow
• Low resistance – high flow
• Increases oxygen delivery for
development
Placenta Preeclampsia
• Incorrect growth placenta/invasion
endometrium
• Spiral arteries maintain smooth muscle and
thickness
• Smaller diameter => higher blood flow
velocity
• Relatively under-perfused = less oxygen
delivery
• Higher oxidative stress
• Antiangiogenic sFlt-1 binds to VEGF, PlGF
Genetic Causes Preeclampsia
• STOX1 overexpression
– Modulates trophoblast proliferation and
migration
– Placental preeclampsia
• ACVR2A
– Maternal preeclampsia
-Biochimica et Biophysica Acta 2012:1960-9
Hum Genet 2007:120:607-12
Early Onset Preeclampsia (<34
weeks)
• Higher maternal mortality
• Higher recurrence rate
• More placental pathology
Higher rate remote postpartum medical
problems
• Higher remote risk maternal CV disease
• Higher remote risk maternal Diabetes
-Hypertension 2013:61:932-42
ONE SUGGESTED PATHOPHYSIOLOGIC MODEL
-Hypertension 2013:61:932-42
ONE SUGGESTED PATHOPHYSIOLOGIC MODEL
-Biochimica et Biophysica Acta 2012:1960-9
Late Onset Preeclampsia
•
•
•
•
Maternal (late onset) preeclampsia
IUGR absent
Less severe generally
Fewer long term consequences
Late Onset Preeclampsia
• >34 weeks gestation, 80% of all
preeclampsia
• Maternal causes
• Maternal Risk factors
Maternal Risk Factor
OR Increased Preeclampsia
Diabetes – Type I or II
3.5
Multiple Gestation
3
BMI increased
2.5
Maternal Age >40
2
Cardiovascular disease
3.8
-Hum Genet 2007:120:607-612
OUTLINE
•
•
•
•
Preeclampsia
Recognition
Current treatment protocols 2014-15
Communication – keys to success
Preeclampsia Definitions - OLD
Preeclampsia (mild)
• HTN >140/90 mmHg
• Proteinuria >0.3 g/24hr
Severe Preeclampsia
• BP >160/110 mmHg
• Proteinuria >5 g/24hr
• HELLP syndrome
• CNS symptoms
-ACOG Practice Bulletin 33, 2002
Preeclampsia Definitions - NEW
Preeclampsia without severe features (new term)
• BP >140/90
• Proteinuria >300 mg/24hr OR dipstick 1+ OR
protein/creatinine ratio >0.3
Absence of proteinuria with any:
• Platelets <100k
• Creatinine >1.1
• LFT elevation
• CNS symptoms
-ACOG Task Force HTN Pregnancy Nov 2013
Preeclampsia Definitions NEW
Severe Preeclampsia = ANY ONE of:
• BP >160/110 – must TREAT within 1hr
• Platelets <100k
• LFT elevation
• Creatinine >1.1
• Pulmonary edema
• CNS symptoms
-ACOG Task Force HTN Pregnancy Nov 2013
Post-Partum Preeclampsia
• Occurs up to 6 weeks postpartum
– De novo increase of BP
– First diagnosis post-partum
Physiology:
• BP rises again 3-6 days postpartum
– BP usually decreases 1-2 days postpartum
-CMQCC Preeclampsia Toolkit 5-2014
Preeclampsia Foundation
Preeclampsia Overview
• Classification
– Preeclampsia
– Chronic Hypertension
– Chronic Hypertension with Superimposed
Preeclampsia
– Gestational HTN
-Druzin, CMQCC/ACOG/Stanford
Classification HTN Pregnancy
• Pre-Pregnancy
– Chronic hypertension
• After 20 weeks
– Preeclampsia/eclampsia
• Chronic hypertension with superimposed
preeclampsia
– 50% chronic HTN develop superimposed Preecl.
• After 20 weeks
– Gestational hypertension HTN and no other sx.
Often evolve into something more
-Druzin, CMQCC/ACOG/Stanford
Forecast: Preeclampsia
HTN alone
OR
Proteinuria alone
• 40% develop classic preeclampsia
-. Obstet Gynecol. 2008;112(2 PART 1): 359-372.
Preeclampsia Update 2014-15
• Why the big secret? People are smart, they can
handle it. -Agent J(Will Smith)
• A person is smart. People are dumb, panicky,
dangerous animals and you know it. Fifteen
hundred years ago everybody knew the Earth was
the center of the universe. Five hundred years
ago, everybody knew the Earth was flat, and
fifteen minutes ago, you knew that humans were
alone on this planet...
• Imagine what you'll know tomorrow
Agent K(Tommy Lee Jones)
-Men in Black 1997
-
Preeclampsia Blood Tests
Angiogenic:
• Placental Growth Factor (PlGF)
• Vascular Endothelial Growth Factor (VEGF)
Anti-angiogenic factors:
• Soluble fms-like tyrosine kinase-1 (sFLT-1)
• Soluble Endoglin (sENG)
Endothelial dysfunction:
• Endocan
Placenta
• Placental protein 13
Predicting Preeclampsia
• Uterine artery Dopper velocimetry
– Early onset Preeclampsia, OR 5-20
• Angiogenesis
• sFlt-1 rises 4-5 weeks prior to clinical sx
– Early onset preeclampsia
• PlGF starts to decreases 9-11weeks,
accelerates 5 weeks prior to clinical sx
• Placental protein-13 low 1st trimester
– Early onset preeclampsia
-ACOG 2013 Task Force HTN Pregnancy
Predicting Preeclampsia
• PlGF/Endoglin ratio mid-trimester
– Sensitivity 100% specificity 98% early onset PE
• Multivariable algorithm
– Uterine pulsatility, MAP, pregnancy-associated
plasma protein A, PlGF, BMI, nulliparity, prior PE
– 93% predictive, OR 16 early onset PE
-ACOG 2013 Task Force HTN Pregnancy
NEJM 2004:350:672-83
Hypertension 2009:53:812-8
OUTLINE
• Preeclampsia
• Recognition
• Current treatment protocols 2014-15
• Communication – keys to success
Pitfalls and Protocols:
Preventing Maternal Death
• Delayed response to triggers
• Maternal mortality Preeclampsia
– 92% delayed recognition and treatment
– Calif Pregnancy Assoc Mortality Review 2002-5
• Written criteria to observe change or
deterioration
– Joint Commission Sentinel Event Alert #44:
Preventing Maternal Death 2010
-Calif Pregnancy Assoc Mortality Review 2002-5
Maternal Early Obstetric Warning
System (MEOWS)
1 point/Yellow Trigger
2 Points/Red Trigger
SBP
150-160 or 90-100
>160 or <90
DBP
90-100
>100
HR
100-120 or 40-50
>120 or <40
Oxygen Saturation%
<95%
Temp oC
35-36
<35 or >38
Neurologic
response to voice
(motor block >2 hrs PACU)
unresponsive
(motor block >3 PACU)
Call physician to evaluate patient for 2 points or more
-NHS U.K., CMQCC, et al.
The Joint Commission
• 2010 Sentinel Alert #44, Preventing
Maternal Death
• All centers have process for
RECOGNITION and RESPONSE to
patient’s deteriorating condition with
WRITTEN CRITERIA describing EARLY
WARNING SIGNS for when to seek
assistance
-CMQCC Preeclampsia Toolkit revised 5-2014
-CMQCC Preeclampsia Toolkit revised 5-2014
Fluid Restriction Guideline
• Generally fluid restricted
• Oliguria <30 ml/hr x2 hr
– Fluid bolus 250-500 ml crystalloid NS/LR
– After 1 L and considered hypovolemic:
• Albumin
• Must use pulse oximetry
• Furosemide if suspect pulmonary edema
• Consider cardiac dysfunction
– ECHO, BNP
-CMQCC Preeclampsia Toolkit revised 5-2014
-ACOG Task Force HTN Pregnancy 2013
Post-Partum Preeclampsia
• Occurs up to 6 weeks postpartum
• BP rises again 3-6 days postpartum
• Only 1/3 women who had Sx postpartum
sought care
• Follow-up BP within 7 days - NEW
• Patient education - NEW
• Preeclampsia Foundation
– www.preeclampsia.org
-CMQCC Preeclampsia Toolkit 5-2014
Preeclampsia Foundation
Timing of Delivery Preeclampsia
• <37 weeks GA - 1.5% Preeclampsia
• <34 weeks GA – 0.3% Preeclampsia
• Deliver by Vaginal or Cesarean:
– >37 weeks preeclampsia
– >34 weeks Severe Preeclampsia
• <34 weeks GA – wait unless unstable [NEW]
• Deliver for Eclampsia, HELLP, Pulm Edema,
Coagulopathy, BP not controlled, Clinical Sx
persist (HA, Vision, RUQ pain)
-CMQCC Preeclampsia Toolkit revised 5-2014
-ACOG Task Force HTN Pregnancy 2013
Preeclampsia
• Treat BP >160/105-110 within 1 hr
• Seizure – first line Rx Magnesium
• Cocaine/Amphetamine + BP Rx –>
resistant hypotension
• 40% new onset HTN or proteinuria ->
Preeclampsia
• Early onset preeclampsia often more
severe
Cause of U.S. Maternal Mortality
• CDC Review of 14 years of coded data: 1979-1992
• 4024 maternal deaths
• 790 (19.6%) from preeclampsia
90%
of CVA were
from
hemorrhage
MacKay AP, Berg CJ, Atrash HK. Obstetrics and Gynecology 2001;97:533-538
Preeclampsia Mortality Rates
in California and UK
Cause of Death among
Preeclampsia Cases
CA-PAMR (2002-04)
Rate/100,000
Live Births
UK CMACE (2003-05)
Rate/100,000
Live Births
Stroke
1.0
.47
Pulmonary/Respiratory
.06
.00
Hepatic
.25
.19
OVERALL
1.6
.66
The overall mortality rate for
preeclampsia in California
is greater than 2 times that of the UK,
largely due to differences in deaths
caused by stroke.
Acute HTN Rx 2014
• Timely – Rx <1 hr of BP>160/105-110 - NEW
– preferably <30 min of confirm 2nd BP by 15 min
– Systolic important
• First Line Rx one of:
– Labetalol 20 mg IV
– Hydralazine 5-10 mg IV
– PO Nifedipine 10 mg
• NO to SL Nifedipine 10 mg
-CMQCC Preeclampsia Toolkit revised 5-2014
-ACOG Task Force HTN Pregnancy 2013
Acute HTN Rx 2014
• Timely – RX <1 h of BP>160/105-110 - NEW
– preferably <30 min of confirm 2nd BP by 15 min
• Second Line RX one of:
– Labetalol 40 mg IV, 80 mv IV in ten min
• Max dose 300 mg
– Hydralazine 5-10 mg IV, repeated every 15-20
min
– Nifedipine 10 mg oral
– Nitropusside must have A-line
– Consult anesthesiologist
-CMQCC Preeclampsia Toolkit revised 5-2014
-ACOG Task Force HTN Pregnancy 2013
Magnesium
• Prevention or TREATMENT of seizures in Severe
preeclampsia
• 4-6 g load/20 min
• Recurrent seizure - 2 g/5min additional
• Infused at 1-2 g/h
– NEW: Continue Intra-op cesarean!
• Preeclampsia without severe features (formerly
mild)
– SOGC (Canada), WHO yes to magnesium,
– ACOG – not needed, OB may choose to use
-CMQCC Preeclampsia Toolkit revised 5-2014
-ACOG Task Force HTN Pregnancy 2013
Eclampsia
• Maternal mortality 0.3-1%
• Morbidity serious – pulmonary edema,
renal failure, stroke, arrest
Long term effects
• White matter brain lesions – 36%
• Cognitive failures – 50%+
• Depression and Anxiety
-AJOG 2014:211:37:e1-9
• Visual changes
ACOG Task Force HTN Preg 2013
Obstet Gynecol 2012:119:959-66
Eclampsia
-AJOG 2014:211:37:e1-9
Another NEW rule?
• NSAIDs – OLD – the best!
• New- may be bad!
NSAIDs – may increase BP
• Suggest using other analgesics if patient
has HTN beyond day 1 postpartum
Politics: Narcotic Rx overdoses – pressure
to use less Oxycodone, hydrocodone
-ACOG Task Force HTN Preg rev 5-2014
OUTLINE
•
•
•
•
Preeclampsia
Recognition
Current treatment protocols 2014-15
Communication – keys to success
Preeclampsia Overview
• Obstetric Management
– BP control (acute for >160/105-110)
– Seizure prophylaxis
– Delivery NSVD or Cesarean
• 34 weeks if Severe Preeclampsia
• 37 weeks if not Severe Preeclampsia
– Post Partum follow-up BPs
-Druzin, CMQCC, ACOG, Stanford
Communication
•
•
•
•
•
Triggers
Maternal agitation, confusion
Severe headache
Shortness of breath
Prolonged motor block after regional
anesthesia
• Oliguria <0.5 ml/kg/hr for 2 hours
-NY Times 2006
Teamwork
• Escalation – people, equipment, place
• Alert physician or qualified clinician
• BEDSIDE evaluation (phone misses key
clues)
• Local protocols
• Multi-disciplinary team work
• Proper communication (e.g. SBAR)
• Team trainings/simulations
Communications
• Communication failure - top 3 leading causes
of maternal and newborn sentinel events TJC
• Communication, teamwork, shared decision
making – fundamental
• Preeclampsia #2 maternal death CA-PAMR 2002-3
• Clinician factors 78%
• Facility/system issues 57%
• Preeclampsia deaths – 48% good chance to
change outcome
– Delays Diagnosis, Treatment, Denial severity
-CA-PAMR 2011, 2002-3 Maternal Death Review
Communication Skills
• Briefings
• Debriefings
• Language- Concerned, Uncomfortable,
Safety issue
• SBARRR– situation, background,
assessment, recommendation, reasoning,
ratification
• Closed Loop communication – read back
• Call outs – confirm phase of process
-CMQCC Preeclampsia Toolkit revised 5-2014
-ACOG Task Force HTN Pregnancy 2013
Communication
• Signs and Symptoms of Preeclampsia
– Antepartum
• Office – consult?
• Upon L&D admission
– Postpartum
– Up to 6 weeks post delivery – Emergency Dept.
• Severe BP >160/105-110 mmHg
– Repeat 5 min, but must treat within 1 hr first BP
• Reduce risk stroke, ICH
Communication
• Preeclampsia – lifetime disease
– CV risk equal to smoking, hyperlipidemia
– Death
– Diabetes
• Preop History
• Children of Preeclamptic mothers
– Higher BP
– Fetal programming
OUTLINE
•
•
•
•
•
Preeclampsia
Recognition
Current treatment protocols 2014-15
Communication – keys to success
Bonus
0
20
years from birth
40
-Skjaerven BMJ 2012;345:bmj.e7677
Preeclampsia: Maternal Health
Long-Term Effects
Disease in future
OR
HTN
Dose effect – severity, #
Early onset > Late onset PreE
3-4
CV Disease
2
dose effect, risks
7
End Stage Renal Disease
3-5
Hypothyroidism
1.8
Diabetes
3
-Chen Cardiovasc Res 2014:101:579-86
Preeclampsia: Children’s Health
Long-Term Effects
Children 9-12 years old
Control
Gestational
HTN
Preeclampsia
P
BMI
17.6
18.1
17.9
.001
SBP
104
106
107
.001
DBP
60
61
62
.001
Also effects biomarkers HDL relative IL-6, CRP – small but statistically significant
-Eur Heart J 2012:33:335-45
Risk Factors CV Disease
Risk Factor
OR Coronary Artery Dis
95% Confidence Interval
Smoking
2.1
1.5-2.9
HTN
2.1
1.4-3
LDL >4.1 mmol/L
1.7
1.2-2.4
Preeclampsia
2.2
1.9-2.5
Preeclampsia as bad as smoking and chronic HTN !!!
PMH – h/o Preeclampsia = pertinent information
-Heart Lung Circ 2014:23:203-12
Posterior Reversible Encephalopathy
Syndrome (PRES)
• MRI diagnosis – bilateral vasogenic edema
posterior cerebral circulation white matter
Occipital and posterior parietal lobes
• Sx: HTN, seizure, altered mental status, HA,
vision
• Pathophysiology: endothelial dysfunction,
cerebral autoregulation dysfunction, leaky
• Up to 6 weeks postpartum
MRI – Posterior Reversible Encephalopathy Syndrome (PRES)
-CMQCC Preeclampsia Toolkit revised 5-2014
Posterior Reversible Encephalopathy
Syndrome (PRES)
• Treatment same as preeclampsia/eclampsia
• Antihypertensive medication
– ED also likes IV Nicardipine
• Anti-seizure medication
– Magnesium
-CMQCC Preeclampsia Toolkit revised 5-2014
Patient Education Materials
This and many other
patient education
materials can be
ordered from
www.preeclampsia.org/
market-place
Upcoming Events
CSA Winter Anesthesia Seminar
January 12-16, 2015 | Wailea Maui, Hawaii
Fairmont Kea Lani
CSA Spring Anesthesia Seminar
April 16-19, 2015| San Francisco, California
Hyatt Regency San Francisco, 5 Embarcadero Center
CSA Fall Anesthesia Seminar
November 2-6, 2015| Kauai, Hawaii
Grand Hyatt Resort and Spa
Visit www.csahq.org/CMEevents for more information.
2014 Fall Anesthesia Seminar
New Modes of Mechanical
Ventilatory Support:
What every Anesthesia Provider
Should Know
Michael A. Gropper, MD, PhD
Professor and Interim Chair
Department of Anesthesia and
Perioperative Care
UCSF
Disclosures
I have received research support
from:
• NIH
• The Gordon and Betty Moore
Foundation
Learning Objectives
• At the conclusion of the activity participants
should be able to:
• Define barotrauma, volutrauma,
atelectrauma, biotrauma and their relevance
to mechanical ventilation.
• Discuss the relationship between tidal volume
and acute lung injury.
• Describe factors associated with tidal volume
reduction and improved patient outcomes.
1st Published Scientific Paper on
Positive Pressure Ventilation
"But that life may ... be restored to the
animal, an opening must be attempted
in the trunk of the trachea, in which a
tube of reed or cane should be put; you
will then blow into this, so that the lung
may rise again and the animal take in
air. ... And as I do this, and take care
that the lung is inflated in intervals, the
motion of the heart and arteries does
not stop..."
Andreas Wesele Vesalius, 1543
Early Mechanical Ventilation
6
New Modes of Mechanical
Ventilatory Support
•
•
•
•
•
Ventilator Associated Lung Injury
Protective Mechanical Ventilation
Prone Mechanical Ventilation
High Frequency Ventilation
Post-extubation CPAP
Ventilator Associated Lung Injury
• Barotrauma
• Volutrauma
• Atelectrauma
• Biotrauma
7
Barotrauma
• Parenchymal injury resulting from
high intrapulmonary air pressures
• Most studies estimate that
barotrauma occurs when plateau
pressures exceed 35 cmH2O
Barotrauma in ALI/ARDS
High Airway Pressure Increases Pulmonary
Vascular Permeability
.6
Permeability
Kf,c
(ml/min/cmH20/10
0g)
.4
.2
0
0
20
40
Peak Airway Pressure (cmH2O)
70
Parker et al, JAP, 1984
Volutrauma
• Direct injury to the lung parenchyma
from overdistention
• Results from regional variability in lung
compliance
• Significant overdistention may occur in
normal areas of lung
Peri-Vascular Hemorrhage
Is it the Pressure or the Volume?
Dreyfuss et al, Am Rev. Respir. Dis. 137:1159–1164.
Lung Water
HiP-HiV LoP-HiV HiP-LoV
Protein Permeability
HiP-HiV LoP-HiV HiP-LoV
Atelectrauma
• Injury to alveoli resulting from the cyclic
collapse and opening of atelectatic
alveoli.
• Very high shear forces can be created
at the air-liquid interface with alveolar
collapse
• Exacerbated by surfactant depletion
Collapsed
alveolus
Atelectrauma
Inflated alveolus
Cytokine release
Cytokine release
Biotrauma
• Lung and distant organ injury
resulting from the release of
inflammatory mediators into the
airspaces and into the systemic
circulation.
• Mediators may originate from the
lung, or from other organs
• Is perpetuated by mechanical
ventilation
Physiologic Changes with VILI
NEJM 369;22, 2013
Ventilator Induced Lung Injury
Lung injury
Mechanical ventilation
Alveolar collapse
Regional
overdistention
Neutrophil activation
inflammation
Edema formation
Surfactant inactivation
Worsening lung injury
Are you using protective
mechanical ventilation in
patients with acute lung
injury?
Sepsis-induced ARDS
23
CT in Early ARDS
Normal
Lung
Pleural
effusion
Consolidation in dependent lung
zones
Pressure-volume relationship
appropriate
Vt
V
excessive
Vt
protective
Vt
Pflex
Paw
Respiratory failure and mechanical
ventilation
• Respiratory failure is the leading cause
for admission to the ICU.
• Approximately 45% of our patients are
mechanically ventilated.
• Strong evidence suggests that patients
with acute lung injury and acute
respiratory distress syndrome should be
managed with a protective ventilation
strategy.
Respiratory failure and mechanical
ventilation
Definitions:
ALI:
ARDS:
Acute onset
bilateral infiltrates on CXR
PaO2/FiO2<300 mmHg
No evidence of LA hypertension
Same as above, except
PaO2/FiO2<200 mmHg
Berlin Definition of ARDS
JAMA, June 20, 2012—Vol 307, No. 23
ARDSnet Trial: Ventilator
Procedures
All Patients
• Mode: Volume-Assist Control
• Rate: Set rate < 35; adjust for pH goal
= 7.30-7.45 (if possible)
• I:E:
1:1 - 1:3
• Weaning by Pressure Support when
PEEP/FiO2 < 8/.40
PaO2 / FiO2
*
*
Ventilator-Free Days
Mortality Prior to Hospital
Discharge
P=0.0054
6 ml/kg
12 ml/kg
ARDS Protocol @ UCSF
• Multicenter, double-blind, parallel-group trial of 400 pts with major abd
surgery
• Control group had 10-12 ml/kg tidal volume, no PEEP or recruitment
maneuvers
• Intervention was 6-8 ml/kg tidal volume, PEEP 6-8 cnH2O, recruitment
maneuver of 30 cmH2O for 30 seconds every 30 minutes
• Primary outcome was a composite of major pulmonary and extrapulmonary
complications within 7 days after surgery: (atelectasis, pneumonia,
ALI/ARDS, need for ventilation, sepsis, death)
Futier et al, NEJM 2013
Intraoperative Procedures
Futier et al, NEJM 2013
Variable
Control
(N = 200)
Lung Protection
(N = 200)
P Value
Tidal volume (ml)
719 + 128
406 + 76
<0.001
Tidal volume (ml/kg)
11.1 + 1
6.4 + 1
<0.001
PEEP (cmH2O)
0
6
<0.001
# Recruitments
0
9
<0.001
Peak Pressure (cmH2O)
20.1 + 4.9
18.9 + 3.6
0.04
Plateau Pressure
(cmH2O)
16.1 + 4.3
15.2 + 3.0
0.02
Compliance ml/cmH2O
45.1 + 12.9
55.2 + 26.7
<0.001
FiO2
0.47 + 7.6
0.46 + 7.3
0.27
Fluids (liters)
2.0 crystalloid
0.5 colloid
1.5 crystalloid
0.5 colloid
0.47
0.97
(at end of surgery)
Futier et al, NEJM 2013
Variable
Control
(N=200)
Lung
protection
(N=200)
Primary
composite
outcome (30d)
58(29.0)
25(12.5)
0.45(0.28-0.73)
<0.001
Pulmonary
complication
42(21.0)
10(5.0)
0.23(0.11-0.49)
<0.001
Atelectasis
34(17.0)
13(*6.5)
0.37(0.19-0.73)
0.004
Pneumonia
16(8.0)
3(1.5)
0.19(0.05-0.66)
0.009
Need for
ventilation
7(3.5) IV
29(14.5)NIV
2(1.0) IV
9(4.5) NIV
0.40(0.08-1.97)
0.29(0.13-0.65
0.26
0.002
29(14.5)
13(6.5)
0.48(0.25-0.93)
0.03
30d mortality
7(3.5)
6(3.0)
1.13(0.36-3.61)
0.83
Hospital LOS
13
11
-2.45(-4.17 to -0.72)
0.006
ICU LOS
7
6
-1.21(-4.98 to 7.40)
0.69
Sepsis
Adjusted relative risk
P Value
Probability of Composite Event
(pneumonia, ventilation, sepsis, death)
Futier et al, NEJM 2013
Managing Severe Hypoxemia
Recruitment Maneuvers
Hypothesis:
• Sustained lung inflation to recruit
atelectatic alveoli
• Usually done with CPAP at 15-20
cmH2O
• May be accompanied by hypotension,
especially in volume depleted patients
Canine Oleic Acid Injury
Maximum Inspiratory Capacity [%]
100
80
IC = 100%
60
IC = 93%
IC = 81%
40
IC = 59%
20
IC = 22%
0
IC = 0%
Best PEEP ?
0
10
20
30
40
After Gattinoni L, Pelosi
P, Marini JJ et al, with
permission: Ref
AJRCCM, 2001:164.
50
60
Recruitment Maneuver
Before recruitment
After recruitment
Recruitment
• Prospective trial of 68 pts with ALI/ARDS
• Whole body CT at different lung volumes
• Measured percentage of potentially
recruitable lung.
CT Measurement of Recruitable Lung
Gattinoni et al, NEJM 2006
Mortality as Function of Recruitable Volume
Gattinoni et al, NEJM 2006
What about PEEP?
• Pro: Anesthesia and surgery cause
atelectasis, leading to hypoxemia. May
contribute to overdistention and lung
injury
• Con: PEEP increases intrathoracic
pressure, which decreases venous
return, and may contribute to
hypotension
• Randomized, controlled trial at 30 centers in
Europe, Americas
• 900 Patients at risk for postoperative pulmonary
complications
• Tidal volume set at 8 ml/kg
• Randomized to either high PEEP (12 cmH2O) with
recruitment maneuvers or to low PEEP (< 2 cmH2O)
without recruitment maneuvers
• Measure composite pulmonary outcomes
High PEEP plus RM’s vs Low PEEP and no RM
Lancet, 2014
High PEEP plus RM’s vs Low PEEP and no RM
Lancet, 2014
Probability of Postoperative Pulmonary
Complications by Day 5
Lancet, 2014
• Multicenter, double-blind trial of 340 patients with early-onset,
severe ARDS
• Randomized to cisatracurium or placebo
• All other management identical
• Primary outcome was 90-day mortality
N Engl J Med 2010;363:1107-16.
N Engl J Med 2010;363:1107-16.
Cisatracurium
(N=177)
Placebo
(N=162)
RR with
Cisatracurium
(95% CI)
P Value
42%
52%
57%
54%
63%
67%
0.71(0.51-1.00)
0.76(0.56-1.02)
0.78(0.59-1.03)
0.05
0.06
0.08
Vent Free Days
(D1-D90)
53.1+35.8
44.6+37.5
0.03
Days without any
organ failure
15.8 + 9.9
12.2 + 11.1
0.01
9 (5.1 [2.7-9.4])
19 (11.7 [7.6-17.6])
0.43 (0.20-0.93)
0.03
7 (4.0 [2.0-8.0])
19 (11.7 [7.6-17.6])
0.34 (0.15-0.78)
0.01
72/112
(64.3 [55.1-72.6])
61/89
(68.5 [58.3-77.3])
Outcome
Mortality
28D
ICU
Hospital
Barotrauma
N(%[RR})
Pneumothorax
N(%[RR})
Days without ICUacquired paresis
N(%[RR})
0.51
N Engl J Med 2010;363:1107-16.
Prone Positioning
Prone Positioning
Hypothesis:
• Dependent atelectasis causes V/Q
mismatching and shunt
• Improves weight distribution of
edematous lung and heart, allowing
improved lung expansion
• Last year I recommended against using
it
Prone Positioning
Supine
Prone
Prone Positioning: Meta-analysis
Abroug et al, Crit Care. 2011
PROSEVA Trial
PROSEVA: Protocol
• 474 pts randomized
• Dose of proning:
– Within 55 minutes of
randomization
– PP daily duration of
17 + 3 hours
• All patients
ventilated with lung
protective strategy
• Criteria for cessation
of PP:
–
–
–
–
P/F > 150
PEEP < 10
FiO2 < 0.6
All criteria persist at
least 4 hours in
supine position
Guerin et al, NEJM 2013
Survival
Guerin
et al,
NEJM
2013
Prone Positioning: Recommendation
• PROSEVA more effective than previous
studies
• More complications than expected in
supine group (13% incidence cardiac
arrest)
• Highly experienced centers: no adverse
events with proning
– Watch video at NEJM.org
• Most patients received NMB’s
Guerin et al, NEJM 2013
High Frequency Ventilation
High Frequency Ventilation
Rationale:
• Low tidal volumes protect the lung from
ventilator associated lung injury
• Maximize mean airway pressure,
prevent atelectasis
• Limit peak pressures
High Frequency Ventilation
• Refers to rates > 100 breaths/min in adult and >
300 breaths/min in neonates
• Jet ventilation
– exhalation is passive
– set frequency, jet volume, entrainment volume
inspiratory time, and baseline pressure
• Oscillatory ventilation
– piston or microprocessor gas controllers
– bias flow through circuit determines Paw
– set oscillator frequency, displacement, I:E times,
bias flow
High Frequency Ventilation
Ventilator Type
Frequency
Breaths/min
Inspiration
Expiration
CV
2 - 40
Active
Passive
HFPPV
60 - 100
Active
Passive
HFJV
100 - 200
Active
Passive
HFO
200 - 2400
Active
Active
Gas Transport During HFV
1.
2.
3.
4.
Bulk flow
Taylor dispersion
Pendeluft
Assymetric velocity
profiles
5. Cardiogenic mixing
6. Molecular Diffusion
High Frequency Jet Ventilation
High Frequency Oscillation
• Original design was
a home stereo
speaker
• Oscillator creates
inspiratory and
expiratory flow
• Changing inspiratory
bias flow adjusts
mean airway
pressure
• Multicenter, randomized, controlled trial
• 548 patients 39 ICU’s in 5 countries
Ferguson et al, NEJM. 2013
OSCILLATE Trial
Ferguson et al, NEJM. 2013
HFOV
(N=275)
Control
N=273
Relative Risk
(95%CI)
P Value
Death in
hospital
129 (47%)
96 (35%)
1.33 (1.091.64)
0.005
Death in ICU
123 (45%)
84 (31%)
1.45 (1.171.81)
0.001
Barotrauma
46/256 (18%)
34/259 (13%)
1.37 (0.912.06)
0.13
Refractory
hypoxemia
19 (7%)
38 (14%)
0.50 (0.290.84)
0.007
9 (3%)
8 (3%)
1.12 (0.442.85)
0.82
ICU LOS (D)
15
14
0.93
0.93
Hosp LOS (D)
30
25
0.74
0.74
Outcome
Refractory
acidosis
Ferguson et al, NEJM. 2013
• Multicenter, randomized, controlled trial comparing
HFOV to usual ventilator care
• 800 Patients randomized in 29 hospitals
Young et al, NEJM. 2013
OSCAR Trial
OSCAR vs OSCILLATE
• Different oscillators
• Different algorithms for adjustment:
– Mean airway pressure in oscillator arm:
• OSCILLATE: 31 + 2.6 cmH2O
• OSCAR: : 27 + 6.2 cmH2O
• Different ventilation in control groups
– Control mortality:
• 35% in OSCILLATE
• 41% in OSCAR
Wavering on Oscillation?
• Taken together, no benefit, potential
harm with HFOV in ARDS
• Negative effects may be due to:
– Ventilator-associated lung injury
– ? Higher vasopressor, fluid, sedatives
• Control arm not ARDSnet protocol
Other strategies for severe
hypoxemia
Airway pressure release ventilation
(APRV)
• Time-triggered, pressure-limited, and
time-cycled mode
• high continuous positive airway
pressure (P high) is delivered for a long
duration (T high) and then falls to a
lower pressure (P low) for a shorter
duration (T low)
• allows spontaneous breathing (with or
without PS) during both the inflation and
deflation phases
Gonza ĺ ez et al. Intensive Care Med (2010) 36:817–827
Airway Pressure Release Ventilation
Airway pressure release ventilation
(APRV)
• Potential benefits:
– improved alveolar recruitment and oxygenation
– Some observational studies show decreased
peak airway pressure, improved alveolar
recruitment, increased ventilation of the
dependent lung zones and improved
oxygenation
– No mortality benefit
• Potential risks: In severe obstructive
disease, could lead to hyperinflation and
barotrauma
Biphasic Ventilation
• Similar to APRV, except that T low
is longer during biphasic ventilation,
allowing more spontaneous breaths
to occur at P low
• AKA Bi-Vent, BiLevel, BiPhasic,
and DuoPAP ventilation.
Biphasic Ventilation
Post-Extubation CPAP
• Randomized, unblinded
study of postop laparotomy
patinents with hypoxemia
• 209 patients in 15 hospitals
• Randomized to oxygen vs
CPAP
• Primary outcome was
reintubation
Post-extubation CPAP
1322 Patients enrolled
230 met postop criteria
209 randomized
104 assigned to oxygen by
facemask
105 assigned to oxygen + CPAP
2 unable to tolerate
4 unable to tolerate
104 included in analysis
105 included in analysis
Squadrone et al, JAMA 2004.
Reintubation Rate
10
8
Intubation
%
6
4
2
0
0
20
60
100
140
Time (hours)
Squadrone et al, JAMA 2004.
Postextubation CPAP: Secondary Outcomes
Outcome
Control
(104)
CPAP
(105)
Relative
Risk
P Value
ICU LOS
(d)
2.6
1.4
.09
Hosp LOS
(d)
17
15
.10
Pneumoni
a #(%)
10(10)
2(2)
0.19
0.02
Infection
#(%)
11(10)
3(3)
0.27
.03
Sepsis
#(%)
9(9)
2(2)
0.22
.03
Deaths
#(%)
3(3)
0(0)
.12
Squadrone et al, JAMA 2004.
Meta analysis of 9 clinical trials.
Annals Surgery, 2008.
CPAP and Postop Complications
Conclusions
• Ventilator associated lung injury is
multifactorial
• 6 ml/kg IBW tidal volume should be
used in the ICU and OR for all high-risk
patients, even those without lung injury
• Consider early use of NMB’s in patients
with ARDS
• In a recent trial, prone positioning has
been shown to reduce mortality
Conclusions (cont)
• HFOV may improve oxygenation, but
has not shown mortality benefit
• APRV and Bilevel ventilation may
improve oxygenation, but have no other
proven benefit.
• Post-extubation CPAP in the PACU can
prevent reintubation in high risk patients
Upcoming Events
CSA Winter Anesthesia Seminar
January 12-16, 2015 | Wailea Maui, Hawaii
Fairmont Kea Lani
CSA Spring Anesthesia Seminar
April 16-19, 2015| San Francisco, California
Hyatt Regency San Francisco, 5 Embarcadero Center
CSA Fall Anesthesia Seminar
November 2-6, 2015| Kauai, Hawaii
Grand Hyatt Resort and Spa
Visit www.csahq.org/CMEevents for more information.
2014 Fall Anesthesia Seminar
Perioperative Management of
Neurovascular Procedures
Keith J Ruskin, MD
Professor of Anesthesiology and
Neurosurgery
Yale University School of Medicine
Disclosures
• Consultant: Masimo Corporation
Learning Objectives
• Explain the pathophysiology of intracranial
aneurysms and arteriovenous
malformations.
• Discuss the unique challenges of working
in the interventional radiology suite.
• Manage critical events that occur during
neurointerventional procedures, including
hemorrhage and vascular occlusion.
Neurovascular Surgery






Intracranial aneurysms
Arteriovenous malformations
Stroke
Endovascular vs open management
Intraoperative management
Vasospasm, cerebral protection
Intracranial Aneurysm



3% US population: Unruptured aneurysm
Case control study
Reasons for imaging (unruptured)
Atherosclerotic disease (23%)
 Positive family history (18%)
 Headache (8%)
 Preventive screening (3%)
 “Other” (46%)

Aneurysm Risk Factors




Current smoking
Hypertension
Family history of stroke other than
subarachnoid hemorrhage
Reduced risk:
Regular physical exercise
 Hypercholesterolemia

Vlak MH et al. Stroke. 2013 Apr;44(4):984-7.
Risk Factors (Rupture)



Smoking
History of migraine
Decreased risk factors:
Hypertension
 Hypercholesterolemia
 Heart disease


Why?
Vlak MH et al. Stroke. 2013 May;44(5):1256-9.
Subarachnoid Hemorrhage




Incidence: 8-10 per 100,000 people
Most common at 55-60 years
75% of SAH: Ruptured cerebral aneurysm
20% idiopathic origin
Subarachnoid Hemorrhage



Risk of rupture: 1 - 2% annually
16,000 patients per year in US
30-day mortality: 45%
Priebe HJ. Br J Anaesth 2007 Jul; 99(1):102-18.
Cardiac Involvement

ECG changes in 50 - 100%


ST depressions, T wave inversions
Dysrhythmias
Ventricular ectopy
 Sinus bradycardia, tachycardia
 Atrial fibrillation


? Hypothalamic injury
Jain: AJNR Am J Neuroradiol. 2004 Jan;25(1):126-9.
Fluid, Electrolyte Balance

30% SAH patients hypovolemic
Increases risk of vasospasm
 Impairs perfusion


Electrolyte disturbances
Hyponatremia (30%)
 Hypokalemia
 Hypocalcemia


Salt wasting, SIADH
Autoregulation



Impairment correlates with clinical grade
Decreased CBF, CMRO2
PaCO2 response preserved post-bleed
Endovascular or Craniotomy




Randomized controlled trial
2143 patients with ruptured aneurysm
42 institutions (UK and Europe)
Primary outcomes:


Death, dependence at 1 year
Secondary outcomes:

Rebleeding, seizures
ISAT Trial: Results

Death: 7.4% Absolute risk reduction



Early survival advantage maintained 7 years
Rebleed rate: 0.2%
Fewer seizures (relative risk 0.52)
Molyneux AJ. Lancet. 2005 Sep 3-9;366(9488):809-17.
Arteriovenous Malformations

Incidence 0.05% in autopsy series


Occur predominantly in males
Congenital abnormality
20%- 60% Seizures
 25% Headache, bruit



Peak diagnosis: 10 - 30 years
Yearly mortality: 1.5%

Mortality from hemorrhage: 10 – 15%
AVMs: Physiology


Mass of thin-walled vessels, no capillaries
Low pressure, high flow A-V shunt


60 mmHg proximal to AVM
Distal autoregulation impaired
Resistance arterioles maximally dilated
 Normal pressure breakthrough bleeding

Dural A-V fistulas

Outside pia, involve dura
Direct: Well-defined AV shunt, few feeders
 Indirect (sinus): Small arterial feeders drain
into dural sinus


Can cause a “steal” phenomenon
AVMs: Management

Endovascular procedure


Stereotactic radiotherapy



Vascular occlusion with glue
“Gamma knife”
Surgical excision
Combined procedure
Acute Ischemic Stroke

Intravenous rtPA:
Persistent neurologic deficits, < 3 hours
 Not suggestive of subarachnoid hemorrhage


Intra-Arterial rtPA:
Major stroke, < 6 hour duration
 MCA occlusion
 IV thrombolysis contraindicated

Meyers PM. Circulation 2009;119(16):2235–49.
Preop Evaluation

History, physical examination
Hemorrhage severity
 Neurologic examination


Laboratory values


Electrolytes, coagulation studies
Radiologic examination

CT, angiography
Hunt and Hess Grading
Grade 0
Unruptured aneurysm
Grade 1
Asymptomatic, minimal
headache
Moderate to severe
headache, rigidity
Drowsiness, confusion,
mild focal deficit
Stupor, hemiparesis
Grade 2
Grade 3
Grade 4
Grade 5
Coma, decerebrate
rigidity
Anesthetic Management




Hemodynamic stability
Brain relaxation (if open procedure)
Cerebral protection?
Rapid emergence
Premedication



Continue Ca++ antagonists (nimodipine),
anticonvulsants
H2 antagonists (e.g., ranitidine)
Sedatives?
Decrease anxiety, catecholamines
 May mask changes in mental status

Monitoring



Routine monitors
Intra-arterial catheter
Anticoagulation (ACT or aPTT)


If endovascular treatment planned
Consider EP monitoring if temporary
occlusion planned
Anesthetic Management

Induction
Hemodynamic stability
 Patient may be hypovolemic


Maintenance
Volatile anesthetics increase ICP
 N2O increases ICP, CMRO2
 Narcotic, low-dose potent volatile agents


Emergence
Endovascular Anesthesia

Remote location


Limited equipment, supplies, assistance
Patient access
Intravenous, intra-arterial catheters
 Secure airway, extension tubes on circuit



Radiation safety
Catastrophic events…
Blood Pressure (Aneurysm)


Establish normal range
Fighting with medication
Ca++ antagonists
 Nitroglycerine to prevent vasospasm


Autoregulation:
Describes a population, not an individual
 Consider MAP lower limit 70 mmHg

Patel PM. In: Miller RD, et al, eds. Miller’s anesthesia. New York: Churchill Livingstone;
2010. pp. 305–39.
Transmural Pressure
Gradient

TMPG = MAP – ICP
Same formula for CPP: TMPG = CPP!
 Maintain adequate CPP, avoid “spikes”


Antihypertensives: Labetalol, nicardipine
Blood Pressure (AVM)



Impaired distal autoregulation
Hypotension may cause ischemia
During resection:

Increased PO2, pH; decreased PCO2
Charbel FT. Neurol Med Chir (Tokyo) 1998; 38(Suppl):171–6.

After resection:
Resistance arterioles: Impaired
vasoconstriction
 Normal perfusion pressure breakthrough

Spetzler RF: Clin Neurosurg. 1978;25:651-72.
Management Strategy
(Stroke)

General anesthesia or MAC?

No clear data; depends upon patient status
SNACC. J Neurosurg Anesthesiol. 2014 Apr;26(2):95-108.

Maintain cerebral perfusion pressure:
Within 10-20% of admission BP
 Less than 185/105 mmHg


Avoid hyperglycemia
Tarlov N. Neurology. 2012 Sep 25;79(13 Suppl 1):S182-91.
Intracranial Catastrophe
Intracranial Catastrophe



Communicate with team, call for help
Secure the airway
Hemorrhage:
Reverse anticoagulation
 Low normal MAP


Occlusion

Hypertension guided by exam, imaging
Catastrophe (Cont’d)



Head up 15º if possible
Adjust PaCO2 as appropriate
Consider…
Mannitol 0.5 g/kg
 EEG burst suppression
 Passive cooling to 33° to 34°
 Ventriculostomy
 Anticonvulsants

Intraoperative Rupture






High morbidity and mortality
Prevention: Manage transmural pressure
Incidence: 11% if previously ruptured
Maintain normovolemia
Temporary occlusion of blood supply
Consider transient hypotension
Cerebral Relaxation

Timing important




Prevent abrupt transmural pressure changes
Moderate hypocapnia (25 - 30 mmHg)?
Mannitol (0.25 - 1.0 g / kg)
CSF drainage

Lumbar drain, ventricular catheter
Hypocapnia


102 mechanically ventilated SAH patients
92%: ETCO2 below 35 mmHg
Mean duration: 4 days
 68% while breathing spontaneously


Hypocapnia correlated with poor outcome,
symptomatic vasospasm
Solaiman O. J Neurosurg Anesthesiol. 2013 Jul;25(3):25461.
Hypothermia

No benefit from mild hypothermia
Todd et al: N Engl J Med. 2005 Jan 13;352(2):135-45.

Fever worsens neurologic outcome
Todd et al: Neurosurgery. 2009 May;64(5):897-908

For giant aneurysms, consider:
Profound hypothermia
 Circulatory arrest

Brain Protection


Ischemia during temporary occlusion
“Classical” brain protection:
Hypothermia
 Barbiturates


IHAST temporary occlusion subgroup
Hypothermia, protective drugs
 Thiopental, etomidate
 No effect on outcome

Hindman BJ et al. Anesthesiology. 2010 Jan;112(1):86-101.
Cerebral Vasospasm



30%-70% incidence after SAH
3-12 days post-bleed
Diagnosis:
Clinical symptoms
 Angiography


Etiology unclear
Prevention and Treatment

Nimodipine
Class 1, level A
 Prevents 1 poor outcome / 13 patients





Prevent hypotension, maintain euvolemia
Positive fluid balance?
Triple-H therapy?
Cerebral angioplasty
Lazaridis C. Neurosurg Clin N Am. 2010 Apr;21(2):353-64.
Triple-H Therapy





Hypertension, hypervolemia, hemodilution
Increase in pressure, decrease in viscosity
improves CBF in spastic vessels
SBP 160-200 mmHg after clipping
CVP 8-12 mmHg, PCWP 15-18 mmHg
Hematocrit 30%-35%
Triple-H Therapy

No current standard approach


Consensus for symptomatic vasospasm


Indications, contraindications, methods
Hypertension, hypervolemia
No endpoints to guide therapy
Meyer R. Neurocrit Care. 2011 Feb;14(1):24-36.
Conclusions

Skilled anesthesiologist


Pathophysiology of neurovascular disease
Skilled surgeon / proceduralist
Rapid, atraumatic procedure
 Rapid control of intraoperative bleeding



Attention to details (BP control)
Postoperative management
Upcoming Events
CSA Winter Anesthesia Seminar
January 12-16, 2015 | Wailea Maui, Hawaii
Fairmont Kea Lani
CSA Spring Anesthesia Seminar
April 16-19, 2015| San Francisco, California
Hyatt Regency San Francisco, 5 Embarcadero Center
CSA Fall Anesthesia Seminar
November 2-6, 2015| Kauai, Hawaii
Grand Hyatt Resort and Spa
Visit www.csahq.org/CMEevents for more information.
2014 Fall Anesthesia Seminar
Management of Traumatic
Brain Injury
Keith J Ruskin, MD
Professor of Anesthesiology and
Neurosurgery
Yale University School of Medicine
Disclosures
• Consultant, Masimo Corporation
Learning Objectives
• Discuss the pathophysiology of TBI.
• Explain how to manage the airway and
ventilate patients who have a TBI.
• Discuss fluid management in the braininjured patient.
Common: 1.7 million / year (US)
Poor outcome when severe
Leading cause of death < 45 years old
50% of survivors: moderate or severe disability
Thornhill S: BMJ. 2000 Jun 17;320(7250):1631-5.
Early cognitive deficits common
Complete recovery: 6 months – 1 year
Possible association: psychiatric illness, suicide
Carroll LJ. Arch Phys Med Rehabil. 2014 Mar;95(3 Suppl):S152-73.
Death rate increased for 7 years after event
McMillan TM Brain. 2007 Oct;130(Pt 10):2520-7.
Axonal injury
Shearing, compressive forces
Physical destruction, loss of homeostasis
Swelling, hypoperfusion, neurotoxic events
Ischemic injury
Decreased glucose use, lactate accumulation
Ca2+ influx causes depolarization
Excitotoxicity
Algattas H. Int J Mol Sci. 2013 Dec 30;15(1):309-41.
Messengers, immune cells enter brain
Neutrophilic infiltration
Astrocytosis
Cytokines
Edema
Proposed therapy:
Hyperosmolar agents
Decompressive craniectomy
Hormones (progesterone)
Algattas H. Int J Mol Sci. 2013 Dec 30;15(1):309-41.
Small proportion of TBI patients
Two broad groups:
Early deaths: Severe extracranial injuries, traumatic
shock
Late deaths: Older patients with less severe
extracranial injuries, lower incidence of
hypotension on arrival
Anticoagulation therapy in both groups
Davis DP. J Trauma. 2007 Feb;62(2):277-81.
Maintain cerebral perfusion, oxygenation
Avoid iatrogenic injury
Avoid hypo- and hypercapnia
Avoid hyperglycemia
No clear evidence, practice based on guidelines
Usually responds to medical therapy
Medically untreatable in 10-15% of patients
Sustained ICP > 20 mmHg: 100% mortality
Reduces cerebral perfusion pressure
May cause herniation
Early intubation may improve outcome in some
patients, but may harm others
Time from injury to intubation does not affect
mortality
Indications for endotracheal intubation:
Glasgow Coma Score < 8
Inability to maintain airway
Impending respiratory failure
No clear evidence for prehospital intubation
187,709 adults; 16,078 cervical spine injury
Risk factors:
Older age
Skull, facial fractures
Spine fracture, dislocation
Upper limb injury
Thoracic injury
Hypotension
Axial CT required (plain films unreliable)
Fuji T. J Emerg Trauma Shock. 2013 Oct;6(4):252-8.
Hypercapnia increases brain volume
Hypocapnia may worsen injury:
Causes cerebral ischemia
Increases “zero-flow” pressure
Maintain normocapnia
Maintain SpO2 > 90% - 95%
Hypotension associated with poor outcome
Avoid hypotension
Systolic pressure > 120 mmHg
MAP > 90 mmHg
Theoretical concern about cerebral edema after
massive resuscitation
No evidence of exacerbation in clinical practice
BTF: Treat increased ICP with mannitol
May decrease mortality
Guide treatment with intracranial pressure
Hypertonic saline may be more effective
Wakil A. Cochrane Database Syst Rev. 2013 Aug 5;8:CD001049.
Prospective cohort study
Adult TBI patients, sustained ICP > 30 mmHg
14.6% hypertonic saline, 40 ml bolus dose
11 patients, 56 doses of HS, 3 survivors
Mean ICP decreased: 40 mmHg to 33 mmHg
Eskandari R. J Neurosurg. 2013 Aug;119(2):338-46.
Improves cerebral venous outflow
Decreases CBV, capillary leak
CSF moves to spinal subarachnoid space
May decrease CPP in hypotensive patients
Reduces intracranial volume
Enhanced clearance of edema
Role unclear in severe head injury
Propensity score: decompressive craniectomy
2602 patients matched criteria
450 patients received DC
No difference in mortality
No difference in neurologic outcome
Nirula R. J Trauma Acute Care Surg. 2014 Apr;76(4):944-55.
Retrospective review
Patients with GCS < 8, no evidence of shock
Normalized for age, sex, injury severity, GCS,
hemodynamics
28 day mortality increased if Hgb > 10 g/dL
Each unit increased multiorgan dysfunction
score by 0.45
Elterman J et al. J Trauma Acute Care Surg. 2013 Jul;75(1):8-14.
Anemia is a risk factor for secondary brain injury
Increased risk when combined with hypoxia
Treating anemia improves oxygenation
No level I evidence for RBC transfusion trigger
Large trials needed
LeRoux P. Curr Opin Crit Care. 2013 Apr;19(2):83-91.
Hyperglycemia worsens outcome
Hyperglycemia, glucose variability increases
mortality, prolongs length of stay
Jacka MJ: Can J Neurol Sci. 2009 Jul;36(4):436-42.
Perioperative hyperglycemia
200 nondiabetic patients with TBI
20%: intraoperative glucose > 180 mg/dL
Routine glucose monitoring
Bhattacharjee S. J Neurosurg Anesthesiol. 2014 Mar 13.
Titrate to burst suppression, isoelectricity
Reduce CMRO2
Extensive support
Hypotension in 25% of patients
Continuous hemodynamic monitoring
Intubation, mechanical ventilation
Hypotension offsets decreased ICP
No evidence for improved outcome
Roberts I. Cochrane Database Syst Rev. 2012 Dec 12;12:CD000033.
Seizures common after traumatic brain injury
4-25% within one week
Negative effects:
Increased cerebral metabolic rate, ICP
Enhanced neurotransmitter release
Multiple risk factors:
GCS < 10
Cortical contusions, depressed skull fracture
Hematoma, penetrating head wound
Temkin NR. N Engl J Med. 1990 Aug 23;323(8):497-502.
Phenytoin, carbamazepine reduce early seizures
No effect on mortality, long-term seizure risk
US guidelines recommend seizure prophylaxis
European guidelines do not discuss seizures
Levetiracetam: Binds synaptic vesicle
glycoprotein 2A; probably inhibits Ca2+
May improve neurobehavioral outcome
Benge JF. Front Neurol. 2013 Dec 2;4:195.
Improves outcome in animal models of TBI
Systematic review: 20 trials, 1885 patients
Significant reduction in mortality, poor outcome
No evidence for association with pneumonia
Conclusions:
Majority of studies poor quality
Need high-quality randomized controlled trials
Crossley S. Crit Care. 2014 Apr 17;18(2):R75.
Nimodipine (Ca2+ channel antagonist)
Demonstrated benefit after aneurysmal
subarachnoid hemorrhage
No significant effect after TBI
Magnesium
Ca2+ antagonist, NMDA antagonist
No demonstrated benefit
Trial stopped: increased mortality
Affects multiple parts of injury cascade
Limits vasogenic, cytotoxic edema
May reduce free radical formation
Upregulates antioxidant enzymes
Decreases inflammation
Modulates cytokine release
Limits neuronal apoptosis
May promote central, peripheral remyelination
100 adults, TBI, GCS 4-12
Intravenous progesterone vs placebo
Blinded observers
Neurologic events, 30-day outcome
Progesterone group:
Lower 30-day mortality
More likely to have “moderate to good” outcome
Wright DW. Ann Emerg Med. 2007 Apr:49(4):391-402.
Rat model of permanent MCA occlusion
Intraperitoneal progesterone
Brains examined 22 days after stroke
8, 16 mg/kg attenuated infarct volume
Functional outcomes improved
Movement
Grip
Spatial navigation
Improves outcome
Wali B. Brain. 2014 Feb;137(Pt 2):486-502
Maintain cerebral perfusion, oxygenation
Avoid iatrogenic injury
Avoid hypo- and hypercapnia
Avoid hyperglycemia
No clear evidence, practice based on guidelines
Progesterone: Promising “new” agent
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