Gracias - Shock and Euvolemic Resuscitation

Shock and Euvolemic
Resuscitation
Vicente H. Gracias MD, FACS, FCCP
Associate Professor of Surgery
Chief Surgical Critical Care
Medical Director Critical Care
University of Pennsylvania School of Medicine
Hemodynamic Monitoring
Multimodality Therapy
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Agreement of terms
Shock
• An abnormality of the circulatory system
that results in inadequate organ
perfusion and tissue oxygenation
– International Consensus Conference-Hemodynamic monitoring in shock
and implications for management. Intensive Care Medicine (2007) 33:575590
“A momentary pause in the act of death.”
-John Collins Warren, 1800s
Agreement of Terms
Sepsis
• Source of infection (positive blood cultures)
• Plus two or more (SIRS)
– Temperature <36 (0C) or >38 (0C)
– Leukocytes <4,000(nL) or > 12,000 or 10%
immature cell
– Heart rate > 90 beats/minute
– Respiratory rate >20 breaths/min or
PCO2<32mmHg
ACCP/SECM Consensus Conference 1991,
published 1992
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Agreement of Terms
Host response
Improved specificity for defining SIRS
• Sepsis
– Clinical syndrome characterized by the presence of
both infection and a systemic inflammatory response
• Severe sepsis- organ dysfunction, hypoperfusion
responsive to volume loading
• Septic shock – arterial hypotension, vasopressors
• Multiple Organ Dysfunction Syndrome
SCCM/ ACCP/ ESICM/ ATS/ SIS
Consensus Conference Revised 2001
The Obvious
Hemorrhage
↓
Massive transfusion &
Shock
↓
Hypothermia
Acidosis ∆ Coagulopathy
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Importance
Sepsis incidence
•
•
•
•
750,000 new cases/year in US
Surviving sepsis campaign- SCCM
More than a third trauma related
> 50% of surgical patients present with
possible infective insult
• 20% SIRS/sepsis rate of severely injured
patients (ISS >15)
• 19%- 43% Mortality
Importance
Etiology Major Sources
•
•
•
•
Thoracic/ Pulmonary
Intra-abdominal / abscess
Extremity wounds/ injured tissue
Catheter related complication
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Importance
Abdominal Sepsis
• Re-exploration- 3-6% misdiagnosis
• CT scan – 10% misdiagnosis
• Autopsy results- 3% trauma patients
– 1970s to the 2000s 3-5% rate for missed
diagnosis of intra-abdominal sepsis among
patients who died from MODS
CCM 1988, Chest 2001, JACS 2002,
SCCM/ESICM Proceedings 2002
Importance
ICU Sources- miscellaneous
•
•
•
•
•
•
•
Wound infection
Acalculous cholecystitis
Antibiotic-associated colitis
Sinusitis and otitis media
Meningitis
Endocarditis
Septic thrombophlebitis
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Mechanism: Acute phase response
One hit Vs Two hit Model
One Hit
• Single insult initiates
SIRS response
• Ongoing underresuscitation
•
•
•
•
•
•
Two hit
Shock- induces PMN
priming and activation
Blood transfusion
Bacterial translocation
Second insult
Infection- Pneumonia
Surgery
ACS
ACUTE INFLAMMATORY RESPONSE
Other:
Interferons
MIPs
Complement
CSFs
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End Results
Pulmonary
• Blunt Trauma ISS> 15
• Most common organ to fail following
severe sepsis
• 17% to 40% incidence of pneumonia
• H. influenza and Staph. aureus - early
• Gram negative – late, VAP
Nast-Kolb JOT 2001
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End results
ARDS
•
•
•
•
•
Female sex
ISS>20
Multiple Transfusions
Pulmonary contusion
Multiple fractures (long bones, pelvis)
– 25% will develop ARDS
End result
Intra-abdominal Complications
Parameters
ATI
Crystalloid (L)
Fascia closed (%)
IAC (n=5)
44.6 +/- 11.7
15.8 +/- 7.4
0/5 (0)
No IAC (n=21)
33.1 +/- 11.7
8.2 +/- 6.0
12/16 (75)
p value
<0.05
<0.05
<0.01
ACS
Gracias et.al. 2002 (unpublished )
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End result
Nutrition & Post-injury Hypercatabolism
“Nitrogen death”
Muscle Mass
Visceral protein
Organ Function
Immune response
“INFECTIONS”
Multiple Organ failure
Mattox, Moore, Feliciano Fourth edition
Multisystem Organ dysfunction
• Clinical disorder characterized by the acute but
potentially reversible physiologic dysfunction
involving at least two organ systems
• Infectious Vs inflammatory
• Causative
– Epi-phenomenon
• Changing etiologies
– Pulmonary and Abdominal
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SIRS/Sepsis
Multiple Organ Dysfunction Syndrome
Number of Organs
Mortality (%)
0
1
2
0.8
6.8
26.2
3
48.5
4
5
68.8
83.3
*Adapted from Irwin and Rippe’s Critical Care Medicine 5th Edition, pg 1837
Unfortunately…
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Shock
The Spiral
Balanced Physiologic Response
Shock
• SIRS
• CARS- compensatory anti-inflammatory
response syndrome
• DIC
• Apoptosis
• MODS/MOF
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Balanced Resuscitation
Shock
Imbalance in host immune defense
Therapy
First Steps
• Infection surveillance
• Blood cultures/ Physical exam if possible (ileus)
• DPL- high negative predictive value
• Broad spectrum antibiotics
• Mono-therapy as good as classic (Amp/Gent/Flagyl)
• Quick D/C if no source identified
• Antifungal therapy
• Early intervention for non-responders
• Within 24-48 hours of suspician
• CT scan Vs OR
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Therapy
When to get aggressive?
• Aggressive monitoring with early end point
resuscitation- ongoing acidosis
• Cardiac efficiency
• SVO2, Lactate, CVP Oxymetry
• Early inotropic support with failed preload
• Norepinephrine
• Vasopressin
• Protective ventilator management
• Low tidal volume, best PEEP, low inflation pressures
The Problem
• Inadequate resuscitation of the patient
in shock leads to MODS and/or death
• Patients may appear to be adequately
resuscitated based on traditional
parameters (vital signs, urine output),
but have occult hypoperfusion and
ongoing tissue acidosis
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The Problem
No agreement
• Compensated shock may lead to organ
dysfunction and death
• What measures can we use to guide
our resuscitation?
• Do these measures predict survival?
• Do these measures improve survival?
Hemodynamics
Cardiac efficiency
• No preload marker is infallible, “ the
trend is your friend”
• Stoke volume may have better functional
correlation with target value 0.75cc to 1cc/kg
than CVP or PCWP
» Lacking validation
• PAC lacks validating outcomes studies.
• Some data in severely injured patients
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Hemodynamics
Cardiac efficiency
EDEMA ZONE
Cardiac
Index
CVP/Stroke volume/ EDVI
PAC Utility
• No study has ever proven benefit of
PAC on critical care patients
• Several studies have pointed toward
adverse outcomes
• Meta analysis show use of PAC neither
increased nor decreased overall
mortality or days in hospital nor
conferred benefit.
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PAC Utility
• Why doesn’t it work?
– Data incorrect
– Interpretation incorrect
– Management schemes incorrect
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PAC Utility
• Why doesn’t it work?
– Data incorrect
– Interpretation incorrect
– Management schemes incorrect
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PAC Utility
• Why doesn’t it work?
– Data incorrect
– Interpretation incorrect
– Management schemes incorrect
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PAC Utility
• Why doesn’t it work?
– Data incorrect
– Interpretation incorrect
– Management schemes incorrect
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Does RVEDVI indicate preload?
• The RVEDVI predicts a CI response to preload better
than the PCWP
– Diebel 1992, 1994
– Durham 1995
– Chang 1996
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Hemodynamics in sepsis
Determinants of oxygen delivery (DO2)
Heart rate
Cardiac
output
DO2
Stroke volume
O2 Sat %
Oxygen
content
PaO2
Hct
Hemodynamics in sepsis
Endpoints of resuscitation
C
O
N
S
U
O
M
2
P
T
I
O
N
Flow Independent
Flow Dependent
OXYGEN DELIVERY
Bishop,Shoemaker :CCM 1993
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Hemodynamics in sepsis
Lactate
• Marker of anaerobic metabolism
• Classically increased organic acidosis
• Metabolized by liver
– increased with hepatic dysfunction
– Increased with shunting due to sepsis
Hemodynamics in sepsis
Lactate
Weil & Afifi, Circulation 1970.
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Euvolemic Resuscitation
Too
MUCH
E
n
d
p
o
i
n
t
Too
LITTLE
1/SVO2
Lactate
Flow sufficiency
Cardiac inefficiency
Hemodynamic sufficiency
Just RIGHT
Flow inefficiency
Cardiac efficiency
OXYGEN DELIVERY
Adapted from: Gracias, McGonigal:SCNA 2000
Sepsis
Prophylaxis
• Antibiotics- early cessation without
source
• Enteral nutrition
• Sucralfate Vs H2 Blockade
• Selective Gut Decontamination
• I/S, CPT
• Operative Timing
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Hemodynamics in sepsis
Priorities
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•
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Early identification
Early initiation of antibiotics
Control of septic source
Understand hemodynamics
Rapid resuscitation and hemodynamic
management
• Early mechanical ventilation?
International Sepsis Forum (ISF) 2001
Rivers NEJM 2001
Discussion
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