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Sepsis Guidelines 2015Sepsis Guidelines 2015
Dr. T.R.ChandrashekarDr. T.R.Chandrashekar IntensivistIntensivist, Liver transplantation. , Liver transplantation. BMC & RI super-specialty Hospital. BMC & RI super-specialty Hospital. Bangalore. Bangalore.
Case ScenarioCase Scenario 35 year old male patient brought to ICU with 3 35 year old male patient brought to ICU with 3
day old perforation, day old perforation, Posted for emergency Posted for emergency LapratomyLapratomy
Has chills with feverHas chills with fever Tachypneic- RR 40/mt, has respiratory distress, Tachypneic- RR 40/mt, has respiratory distress, Tense abdomen, bilateral crepts, Tense abdomen, bilateral crepts, Spo2 on 4l/O2 on RBM 95%,Spo2 on 4l/O2 on RBM 95%, Pulse 130/mt well felt, BP 80/60 mm Hg, Pulse 130/mt well felt, BP 80/60 mm Hg,
Restless,Restless, InvestigationsInvestigations WBC – 19,000 T.B 3.5, Enzymes NormalWBC – 19,000 T.B 3.5, Enzymes Normal SC-2.0 INR 2.0, Platelets 1.2 lac SC-2.0 INR 2.0, Platelets 1.2 lac Lactate 5.0Lactate 5.0
Is he in septic shock ?
Terminology and Terminology and DefinitionsDefinitions
Shock definition Shock definition Shock Shock is defined as a life-threatening, is defined as a life-threatening,
generalized generalized maldistributionmaldistribution of blood flow of blood flow resulting in failure to deliver and/or utilize resulting in failure to deliver and/or utilize adequate amounts of oxygen, leading to tissue adequate amounts of oxygen, leading to tissue dysoxia.dysoxia.
Hypotension [SBP Hypotension [SBP < < 90 mmHg, SBP decrease of 90 mmHg, SBP decrease of 40 mmHg from baseline, or mean arterial 40 mmHg from baseline, or mean arterial pressure (MAP) pressure (MAP) < < 65 mmHg], while commonly 65 mmHg], while commonly present, should present, should not be required to define shocknot be required to define shock. . Shock requires evidence of inadequate tissue Shock requires evidence of inadequate tissue perfusion on physical examinationperfusion on physical examination..
Relationship Of Infection, SIRS, Relationship Of Infection, SIRS, Sepsis Severe Sepsis and Septic Sepsis Severe Sepsis and Septic
ShockShock
SIRSINFECTION
PANCREATITIS
BURNS
TRAUMA
OTHER
SEPSIS
SEVERESEPSIS
SEPTICSHOCKBacteria
Fungus ParasitesVirus
Sepsis: Defining a Disease Continuum
A clinical response arising from a nonspecific insult, including 2 of the following:
•Temperature 38oC or 36oC •HR 90 beats/min•Respirations 20/min / PCo2 30 cms H2O•WBC count 12,000/mm3 or 4,000/mm3 or >10% immature neutrophils
SIRSSystemic Inflammatory Response Syndrome
SIRS with a presumed or confirmed infectious process
SepsisSepsisSIRSSIRSInfectionInfection Severe Severe SepsisSepsis
SEPTIC SHOCK
Inflammatory response to microorganisms or invasion of normally sterile tissues
SepsisSepsisSIRSSIRSInfection/Infection/TraumaTrauma
Severe Severe SepsisSepsis
Sepsis with 1 sign of organ failureCardiovascular ( hypotension)Lungs: early fall in arterial
PO2, (ARDS):Kidneys -oliguria, anuria,
azotemia, proteinuria SC more than 2
Liver TB more than 2Digestive tract- vomiting,
diarrhea and ileus Brain - confusion
SEPTICSEPTICShockShock
Hypotension despite adequate fluid resuscitation/Requiring vasopressors/Inotropes
Disease continuum
Arterial hypotensionTachycardia
Increased cardiac output/low SVR/high SvO2
Altered skin perfusionDecreased urine output
Hyperlactatemia – increased base deficit
Altered WBC countIncreased CRP,
IL-6, PCT concentrations
Rigor– fever(sometimes hypothermia)
Tachypnea/respiratory alkalosis
Positive fluid balance – edema
General signs & symptomsGeneral inflammatory reaction
Hemodynamic alterations
Signs of organ dysfunction
HypoxemiaCoagulation abnormalities
Altered mental status
Expanded signs of SIRS
Acute Organ DysfunctionAcute Organ DysfunctionTachycardiaHypotension
CVP PAOP
Jaundice Enzymes Albumin
PT
Altered Consciousness
ConfusionPsychosis
TachypneaPaO2 <70 mm Hg
SaO2 <90%PaO2/FiO2 300
OliguriaAnuria
Creatinine
Platelets PT/APTT Protein C D-dimer
Balk. Crit Care Clin 2000;16:337-52
Pathophysiology Pathophysiology
Pathogenesis of shockPathogenesis of shock
Microcirculatory Mitochondrial dysfunction
Cardiac dysfuction, microemboli, microvasular injury, increasaed Nitric oxide- vasoplegia
Cytokines & inflammatory mediator cascade
Interaction with human cells- macrophages Monocytes, Neutrophils, Endothelial cells
Infectious trigger
Sepsis is a disease of the microcirculation
Pathogenisis of Pathogenisis of SepsisSepsis
TRIGGER INTERACTION WITH HUMAN CELLS
Coagu
lation
abno
rmalit
iesPro-inflammatory
Anti inflammatory
Endothelial injuryNitric oxide
over productionCardiac dysfunction
HypotensionMicro-emboli
Hypoperfusion Mitochondrial
dysfunction Organ injury MODS
Death
Primary mediators
Secondary mediators
Monocytes Macrophages
NeutophilsPlasma
Endothelial cells
Immune Response to Injury/ Immune Response to Injury/ InfectionInfectionInfection/injuryInfection/injury
Prompt coordinatedPrompt coordinatedprotectsprotects
Excessive, poor regulationExcessive, poor regulationharmsharms
Deficient, weakDeficient, weakInf establishedInf established
Immunologic Cascade1.1. Cytokine releaseCytokine release2.2. Activation of macrophage/ neutrophilsActivation of macrophage/ neutrophils3.3. Activation of neuro endocrine reflexActivation of neuro endocrine reflex4.4. Activation of plasma protein cascades Activation of plasma protein cascades
(Complement,Coagulation, fibrinolysis)(Complement,Coagulation, fibrinolysis)
Toll receptors (TLR)Toll receptors (TLR) Key mediators of the innate immune
system Expressed on macrophage, dendritic cells,
neutrophils, endothelial cells and mucosal epithelial cells
TLR are transmembrane proteins with the ability to promote signaling pathways downstream, triggering cytokine release and neutrophil activation and stimulating endothelial cells
Why different bacteria Why different bacteria stimulate different Effects ?stimulate different Effects ?
Most microorganisms present more than one TLR ligand, therefore, it is likely that microbes with differing patterns of molecular motifs can cause differential activation of a number of TLRs, allowing differential responses to various classes of pathogen.
ImmunosuppressedExtremes of age
Malnutrition Alcohol, Drug Abuse
MalignancyHIV/AIDS
Chronic Health Issues – Diabetes, Liver Failure, Heart
Disease, Corticosteroids, ChemotherapyMultiple invasive procedures
or invasive lines
Microcirculation Microcirculation
Key steps in oxygen Key steps in oxygen cascadecascade
Macrocirculation
Microcirculation
Why the microcirculation is important in Why the microcirculation is important in shockshock..
1. It is where oxygen exchange takes place.
2. It plays a central role in the immune system.
3. During sepsis and shock it the first to go and last to recover.
4. Rescue of the microcirculation = resuscitation end-point.
Local
ShuntPrecapillary sphincter= vasodilatation/vasoconstriction
cell
= cellular utilization O2 in sepsis
Interstitial matrix= edema causes barrier to O2
delivery to the cell
Postcapillary venule
Microcirculatory defects
Spronk P, Zandstra D, Ince C (2004) Critical Care 8:462-468
Sepsis is a disease of the microcirculation
Microcirculation Microcirculation Microvascular abnormalities appear
early in septic shock, and their persistence is closely associated with organ failure and prognosis.
Septic shock perfusion is characterized by heterogeneity of organ perfusion and the discrepancy between the overall hemodynamics and local blood flow
Microcirculation Microcirculation Global parameters such as heart
rate and mean arterial pressure (MAP) cannot identify or quantify microcirculatory abnormalities.
Impaired microcirculatory perfusion may persist despite correction of systemic oxygen delivery variables like MAP or cardiac output.
Markers of Macro-Markers of Macro-circulation and Micro circulation and Micro
circulationcirculation
Resuscitation end Resuscitation end pointspoints
Orthogonal polarizationspectral (OPS) imaging
Gastric Tonometry
Microdialysis
Sublingual capnometry
ScVO2Base deficitMediators
Microcirculation Microcirculation assessmentassessment
Tissue perfusionTissue perfusion Gastric tonometryGastric tonometry
Orthogonal polarizationOrthogonal polarizationspectral (OPS) imagingspectral (OPS) imaging
Capillary flow in sepsisCapillary flow in sepsis
Understanding oxygen Understanding oxygen delivery to cellular leveldelivery to cellular level
Matching delivery Matching delivery
== Requirement
Assessment of OxygenationO2 delivery is a Cardio-Respiratory function
DODO22/VO/VO2 2 Oxygen delivery vs Oxygen delivery vs RequirementRequirement
Patients have to be kept well above the Critical Point so that
Does not plateau- Consumption remains supply dependent even with supraphysiological levels
VO2 is supply dependent
VO2 is supply independent
Oxygenation to the tissue is not compromised
MMDS and O2 extraction failureShunting due to micro-emboli
OO22
COCO22
AlveoliPAO2
Atmospheric air /FIO2
Water vapour is added- Nose/ upper airway
Alveolar Oxygen
PaO2 (2% dissolved O2)
Measured in ABG
P(A-a)O2
SaO2
O.
D.
C.Temp H+2,3-DPG
98% of O2 is Hb bound-
1.34 x Hb% x Sao2CaO2-oxygen content +PaO2 x 0.003ml
Oxygen Delivery=CaO2 x Cardiac output
Cardiac output - SV x HR Preload / Afterload/ Contractility
Oxygen delivery DO2 is a Cardio- Respiratory Function
=
Volume Vesseltone
Heart function
If shock is prolonged, mechanisms of shock are combined
Physiologic Classification of Physiologic Classification of Acute Circulatory InsufficiencyAcute Circulatory Insufficiency
Fluids / blood Vasopressors Inotropes
TIME TIME isis
TISSUETISSUE
Oxygen DonOxygen Don’’t Go t Go Where the Blood WonWhere the Blood Won’’t t FlowFlow!!
From these two statements three things are obviousEarly therapy before mitochondria gets damaged.
Macro circulation should be optimised first.Micro circulation optimisation to prevent
Mitochondrial injury is the target
Sepsis Management Sepsis Management BundleBundle
Macrocirculation Macrocirculation optimization to correct optimization to correct
MicrocirculationMicrocirculation
Sepsis Management Sepsis Management BundleBundle
First 3 hours bundleFirst 3 hours bundle Measure lactate level Obtain blood cultures prior to
administration of antibiotics Administer broad spectrum
antibiotics Administer 30ml/kg crystalloid for
hypotension or lactate ≥4mmol/L
Time of presentation “Time of presentation” is defined as
the time of triage in the emergency department or, if presenting from another care venue, from the earliest chart annotation consistent with all elements of severe sepsis or septic shock ascertained through chart review.
TO BE COMPLETED WITHIN 6 HOURS
( Bundle) OF TIME OF PRESENTATION Apply vasopressors (for hypotension that
does not respond to initial fluid resuscitation) to maintain a mean arterial pressure (MAP) ≥65mmHg
In the event of persistent hypotension after initial fluid administration (MAP < 65 mm Hg) or if initial lactate was ≥4 mmol/L, re-assess volume status and tissue perfusion and document findings according to Table 1.
Re-measure lactate if initial lactate elevated.
DOCUMENT REASSESSMENT OF DOCUMENT REASSESSMENT OF VOLUME STATUS AND TISSUE VOLUME STATUS AND TISSUE
PERFUSION WITHPERFUSION WITHEITHEREITHERRepeat focused exam (after initial fluid Repeat focused exam (after initial fluid resuscitation) by licensed independent practitioner resuscitation) by licensed independent practitioner including vital signs, cardiopulmonary, capillary including vital signs, cardiopulmonary, capillary refill, pulse, and skin findings.refill, pulse, and skin findings.OR TWO OF THE FOLLOWINGOR TWO OF THE FOLLOWING::Measure CVP / Measure ScvOMeasure CVP / Measure ScvO22 / Bedside / Bedside cardiovascular ultrasoundcardiovascular ultrasoundDynamic assessment of fluid responsiveness with Dynamic assessment of fluid responsiveness with passive leg raise or fluid challengepassive leg raise or fluid challenge
Of note, the 6-hour bundle has been updated; The 3-hour SSC bundle is not affected.
DiagnosisDiagnosis For patients suspected to be in severe sepsis or septic shock, For patients suspected to be in severe sepsis or septic shock,
body fluid culturesbody fluid cultures should be obtained as quickly as is feasible. should be obtained as quickly as is feasible. Collect at least Collect at least 2 sets of aerobic and anaerobic blood 2 sets of aerobic and anaerobic blood culturescultures; these should be drawn ; these should be drawn before giving antibioticsbefore giving antibiotics -- -- as long as cultures can be collected without delaying as long as cultures can be collected without delaying antimicrobial therapy by antimicrobial therapy by >45 minutes>45 minutes..
At least one blood culture bottle set should be collected At least one blood culture bottle set should be collected percutaneouslypercutaneously (through a needle stick), and one drawn (through a needle stick), and one drawn from from each venous or arterial cathetereach venous or arterial catheter (IVs, dialysis access, central (IVs, dialysis access, central line, surgical port, arterial line, etc). line, surgical port, arterial line, etc).
If a line or device has been placed in the last 48 hours, it can be If a line or device has been placed in the last 48 hours, it can be considered non-infected and no culture drawn.considered non-infected and no culture drawn.
Other culturesOther cultures (e.g., urine) should be collected, if clinically (e.g., urine) should be collected, if clinically indicated, with the same imperative to avoid undue delay of indicated, with the same imperative to avoid undue delay of antibiotics.antibiotics.
DiagnosisDiagnosis In the uncommon situation in which invasive In the uncommon situation in which invasive
candidiasis is being considered as a cause of candidiasis is being considered as a cause of sepsis, collect blood for the sepsis, collect blood for the 1,3 beta-D-1,3 beta-D-glucan assayglucan assay, and/or the , and/or the mannan and mannan and anti-mannan antibody assaysanti-mannan antibody assays, which can , which can help diagnose invasive candida infections.help diagnose invasive candida infections.
Appropriate Appropriate imaging studiesimaging studies be be performed quickly, to help confirm potential performed quickly, to help confirm potential sources of infection. sources of infection.
Source ControlSource Control Evaluate patient for a focused Evaluate patient for a focused
infection amendable to source infection amendable to source control measures including control measures including abscess drainage or tissue abscess drainage or tissue debridement.debridement.• Move rapidlyMove rapidly• Consider physiologic upset of Consider physiologic upset of
measuremeasure• Intravascular access devicesIntravascular access devices
Antibiotic TherapyAntibiotic Therapy Begin intravenous antibiotics Begin intravenous antibiotics
within first hour of recognition within first hour of recognition of severe sepsis.of severe sepsis.
Antibiotic TherapyAntibiotic Therapy “Hit hard’ with a high dose of broad-
spectrum antibiotic “Get to the point’: take
pharmacodynamics into account “Focus, focus, focus’: tailor or stop
therapy according to microbiological results
“Listen to your hospital’: tailor antibiotic policy regularly
“Look at your patient’: administer antibiotics according to comorbidities, intubation period and previous antibiotic exposure
Antibiotics
Always look at you
local organisms and resistance patterns
Antibiotic TherapyAntibiotic TherapyReassess antimicrobial Reassess antimicrobial regimen at 48-72 hrsregimen at 48-72 hrs• Microbiologic and clinical Microbiologic and clinical
datadata• Narrow-spectrum antibioticsNarrow-spectrum antibiotics• Non-infectious cause Non-infectious cause
identifiedidentified• Prevent resistance, reduce Prevent resistance, reduce
toxicity, reduce coststoxicity, reduce costs
Fluid therapyFluid therapyInitial fluid challenge in sepsis-Initial fluid challenge in sepsis-
induced tissueinduced tissuehypoperfusion (hypotension or hypoperfusion (hypotension or
elevated lactate)elevated lactate)
A minimum of 30ml/kg of crystalloids A minimum of 30ml/kg of crystalloids (a portion of this may be albumin (a portion of this may be albumin
equivalent)equivalent)
Three different scenariosThree different scenarios
2- Patients in the ER for high suspicion of septic shock2- Patients in the ER for high suspicion of septic shock
3- Patients in the ICU, already resuscitated for several 3- Patients in the ICU, already resuscitated for several hours or dayshours or days
1- Patients in the ER for acute blood losses or body fluid losses1- Patients in the ER for acute blood losses or body fluid losses
3- 3- Patients in the ICU, already resuscitated for sePatients in the ICU, already resuscitated for several hours or daysveral hours or days
How to deal with this therapeutic dilemma?
Prediction Prediction of volume responsiveness ?of volume responsiveness ?
Fluid challenge ?Fluid challenge ?
- with hemodynamic instability requiring therapy- with hemodynamic instability requiring therapy
- without certainty of volume responsiveness- without certainty of volume responsiveness
- with potential risks of pulmonary edema with potential risks of pulmonary edema and/or excessive cumulative fluid balanceand/or excessive cumulative fluid balance
A fluid challenge A fluid challenge is a method of
identifying those patients likely to benefit from an increase in intravenous volume in order to guide further volume resuscitation. It is a dynamic test of the circulation. The use of a ‘test’ that uses a small amount of fluid to assess the volume respon- siveness may reduce the risk of a too liberal fluid strategy and the possible consequences of fluid overload
Fluid challengeFluid challenge 250ml or 3ml/kg over 5 to 10 250ml or 3ml/kg over 5 to 10
minutesminutes 500ml in 30 min500ml in 30 min CVP increase by 2 cms of h2oCVP increase by 2 cms of h2o ScVO2 increase by 4%ScVO2 increase by 4% SV by 10 to 15 %SV by 10 to 15 % Increase in MAP UOIncrease in MAP UO
Passive Leg RaisingPassive Leg Raising
45 °45 °
Venous blood shiftVenous blood shift(Rutlen et al. (Rutlen et al. 19811981, , Reich et al. 1989)Reich et al. 1989)
Increase in right ventricular preload Increase in right ventricular preload (Thomas et al 1965)
Increase in left ventricular preload Increase in left ventricular preload (Rocha 1987, Takagi 1989, De Hert 1999, Kyriades 1994 )
Transient effect Transient effect (Gaffney 1982)(Gaffney 1982)
PLR could be used as a test to detect volume responsiveness PLR could be used as a test to detect volume responsiveness rather than as a therapyrather than as a therapy
Parameters to guide fluid Parameters to guide fluid administrationadministration
Vasopressors / InotropesVasopressors / Inotropes
. .
Vasopressors Vasopressors VasopressorsVasopressors should be begun initially to target a mean should be begun initially to target a mean
arterial pressure of 65 mm Hg (arterial pressure of 65 mm Hg (Grade 1CGrade 1C).). An An arterial catheterarterial catheter for hemodynamic monitoring should for hemodynamic monitoring should
be placed as soon as practical, if resources are available, for be placed as soon as practical, if resources are available, for all patients requiring vasopressors (ungraded all patients requiring vasopressors (ungraded recommendation).recommendation).
NorepinephrineNorepinephrine (Levophed) should be provided as the first- (Levophed) should be provided as the first-line vasopressor (line vasopressor (Grade 1BGrade 1B).).
EpinephrineEpinephrine is considered the next-line agent for septic is considered the next-line agent for septic shock after norepinephrine in the Surviving Sepsis shock after norepinephrine in the Surviving Sepsis Guidelines. When norepinephrine is insufficient to maintain Guidelines. When norepinephrine is insufficient to maintain MAP 65 mm Hg, epinephrine should be added to or MAP 65 mm Hg, epinephrine should be added to or substituted for norepinephrine (substituted for norepinephrine (Grade 2BGrade 2B))..
VasopressinVasopressin VasopressinVasopressin at 0.03 units/minute is appropriate to at 0.03 units/minute is appropriate to
use with norephinephrine, either to improve use with norephinephrine, either to improve perfusion (increase MAP) or to reduce the required perfusion (increase MAP) or to reduce the required dose of norepinephrine (ungraded recommendation).dose of norepinephrine (ungraded recommendation).
Vasopressin is not recommended for use as a single Vasopressin is not recommended for use as a single vasopressor for septic shock (ungraded vasopressor for septic shock (ungraded recommendation).recommendation).
Vasopressin doses higher than 0.03 - 0.04 units/min Vasopressin doses higher than 0.03 - 0.04 units/min are recommended to be reserved only for dire are recommended to be reserved only for dire situations of septic shock refractory to standard situations of septic shock refractory to standard doses of multiple vasopressors (ungraded doses of multiple vasopressors (ungraded recommendation).recommendation).
Dobutamine Dobutamine DobutamineDobutamine should be tried for patients in septic shock should be tried for patients in septic shock
who have low cardiac output with high filling pressures who have low cardiac output with high filling pressures while on vasopressors, or who have persistent evidence of while on vasopressors, or who have persistent evidence of hypoperfusion after attaining an adequate mean arterial hypoperfusion after attaining an adequate mean arterial pressure and intravascular volume (with or without pressure and intravascular volume (with or without vasopressors).vasopressors).
A dobutamine infusion up to 20 mcg/kg/min can be added A dobutamine infusion up to 20 mcg/kg/min can be added to any vasopressor(s) in use. Dobutamine is also an to any vasopressor(s) in use. Dobutamine is also an appropriate first-line agent in patients with severe sepsis appropriate first-line agent in patients with severe sepsis and low cardiac output, with a preserved mean arterial and low cardiac output, with a preserved mean arterial pressure (i.e., who are not in septic shock).pressure (i.e., who are not in septic shock).
Dobutamine is recommended Dobutamine is recommended notnot to be used to deliberately to be used to deliberately raise cardiac output to higher than normal levels in an raise cardiac output to higher than normal levels in an attempt to improve perfusion.attempt to improve perfusion.
DopamineDopamine DopamineDopamine is suggested to is suggested to not not be used as an alternative to be used as an alternative to
norepinephrine in septic shock, except in highly selected norepinephrine in septic shock, except in highly selected patients such as those with inappropriately low heart rates patients such as those with inappropriately low heart rates (absolute or relative bradycardia) who are at low risk for (absolute or relative bradycardia) who are at low risk for tachyarrhythmias. Dopamine is recommended to not be used tachyarrhythmias. Dopamine is recommended to not be used in low doses in a so-called renal-protective strategy.in low doses in a so-called renal-protective strategy.
PhenylephrinePhenylephrine is recommended to not be used for septic is recommended to not be used for septic shock, except when 1) septic shock persists despite the use shock, except when 1) septic shock persists despite the use of 2 or more inotrope/vasopressor agents along with low-of 2 or more inotrope/vasopressor agents along with low-dose vasopressin; 2) cardiac output is known to be high, or dose vasopressin; 2) cardiac output is known to be high, or 3) norepinephrine is considered to have already caused 3) norepinephrine is considered to have already caused serious arrhythmias.serious arrhythmias.
SteroidsSteroids Treat patients who still require
vasopressors despite fluid replacement with hydrocortisone 200-300 mg/day, for 7 days in three or four divided doses or by continuous infusion.
ACTH stimulation test is ACTH stimulation test is notnot recommended.recommended.
Steroid therapy may be weaned once Steroid therapy may be weaned once vasopressors are no longer required.vasopressors are no longer required.
Glucose ControlGlucose Control After initial stabilizationAfter initial stabilization
Glucose < 180 mg/dLGlucose < 180 mg/dL Continuous infusion insulin and Continuous infusion insulin and
glucose or feeding (enteral glucose or feeding (enteral preferred)preferred)
MonitoringMonitoring Initially q30–60 minsInitially q30–60 mins After stabilization q4hAfter stabilization q4h
Blood Product Blood Product AdministrationAdministrationRed Blood CellsRed Blood Cells
Tissue hypoperfusion resolvedTissue hypoperfusion resolvedNo extenuating circumstancesNo extenuating circumstances
Coronary artery diseaseCoronary artery disease Acute hemorrhageAcute hemorrhage Lactic acidosisLactic acidosis
Transfuse < 7.0 g/dl to maintain 7.0-Transfuse < 7.0 g/dl to maintain 7.0-9.0 g/dL9.0 g/dL
Supportive careSupportive care Deep vein thrombosis prophylaxis.Deep vein thrombosis prophylaxis. Stress ulcer prophylaxis.Stress ulcer prophylaxis. Glucose control.Glucose control. Maintain a Plateau pressure of Maintain a Plateau pressure of
less than equal to 30 cmH2O and less than equal to 30 cmH2O and low tidal volume 4-6 ml/kg of low tidal volume 4-6 ml/kg of Predicted body weight for Predicted body weight for mechanically ventilated patientsmechanically ventilated patients . .
Consideration for limitation Consideration for limitation of supportof support
Discuss advance care planning with Discuss advance care planning with patients and families. Describe likely patients and families. Describe likely outcomes and set realistic outcomes and set realistic expectations.expectations.
Focus on early diagnosis, targeted Focus on early diagnosis, targeted management, and standardization of management, and standardization of the care process use SSGthe care process use SSG
•Even with the ‘best’ parameters it is not always easy to make the right decision.………
Conclusions Conclusions Sepsis is a disease of Sepsis is a disease of
microcirculation. microcirculation. Oxygen DonOxygen Don’’t Go t Go
Where the Blood WonWhere the Blood Won’’t Flow- t Flow- Optimise the Macrocirculation Optimise the Macrocirculation first.first.
Monitoring microcirculation at Monitoring microcirculation at bedside is difficult- Lactate/ SCVO2 bedside is difficult- Lactate/ SCVO2
Treatment –SS guidelinesTreatment –SS guidelines
Thank you
Suspected infectionBlood cultures
SBP< 90 even after20-30ml/kg fluid or Lactate > 4mmol/l
Appropriate Empirical Antibiotics with in 1 hr/
source control
CVP
MAP
Goal achieved
SCVO2
< 8 Fluids NS, RL/ Colloid
8-12
>60-90mmHg
< 60-90Vasopressors
Noradrenaline/dopamine
<70%
< 30 HCt-Packed cellsSCVO2< 70%
InotropeDobutamine
SCVO2 >70%
DecreaseOxygen
consumption
Michard F et al, Am J Respir Crit Care Med 1999; 159:935-Michard F et al, Am J Respir Crit Care Med 1999; 159:935-99
Michard F et al, Am J Respir Crit Care Med 2000; 162:134-Michard F et al, Am J Respir Crit Care Med 2000; 162:134-88
Pulse Pressure Variation Pulse Pressure Variation (PPV)(PPV)
• The arterial PP is The arterial PP is directly proportional to directly proportional to the SVthe SV• The systolic BP may be The systolic BP may be influenced by changes in influenced by changes in the pleural pressure the pleural pressure 120 120
mmHgmmHg
4040
PPPPmaxmax
PPPPminmin
PPPPmaxmax - PP - PPminmin
(PP(PPmax max + PP+ PPminmin)/2)/2∆∆PP =PP =
Arterial Arterial Pressure Pressure
Stroke Volume Variation (SVV)Stroke Volume Variation (SVV)(pulse-contour analysis by the PiCCO monitor)(pulse-contour analysis by the PiCCO monitor)
SV maxSV max
SV minSV min
SV meanSV mean
SV max + SV minSV max + SV min
SVmeanSVmeanSVV =SVV =
The difference between the maximal and minimal SV values over a floating period of 7.5 seconds
Cellular Oxygen Delivery
(1) central
Cardiacoutput
PaO2
O2 contentPaO2
HbSaO2
Cardiac outputPreloadAfterloadcontractility
= Oxygendelivery
The questionThe question ““Will my patient respond Will my patient respond to fluids?to fluids?”” cannot be accurately cannot be accurately
answered by any answered by any ‘‘preloadpreload’’ parameter parameterPrinciples of Volume challenge
To test Starling’s law the fluid needs to be given quickly – the faster it is given the less that is needed
It makes no sense to test “preload” responses over long periods of time (eg Kumar et al 2004)
The type of fluid is not critical if given quickly enough
There needs to be a change in CVP to know that Starling’s Law has been tested
ICU Treatment ICU Treatment During the first 6 hrs of resuscitation, During the first 6 hrs of resuscitation, Central venous pressure 8–12 mm HgCentral venous pressure 8–12 mm Hg Mean arterial pressure (MAP) more than Mean arterial pressure (MAP) more than
equal to 65 mm Hgequal to 65 mm Hg Urine output more than equal to 0.5 Urine output more than equal to 0.5
mL/kg/hrmL/kg/hr Central venous (superior vena cava) or Central venous (superior vena cava) or
mixed venous oxygen saturation more than mixed venous oxygen saturation more than equal to 70% or more than equal to 65%, equal to 70% or more than equal to 65%, respectively respectively
PRELOAD assessment-PRELOAD assessment-Volume Volume To look at CVP/ PAOPTo look at CVP/ PAOP
Always CVP is in relation to COAlways CVP is in relation to CO
Volume responsive
Volume unresponsive
Add dopamine or dobutamine
Volume
SV
Decreased contractility
Right atrial volume
–The actual value of the CVP is determined by the interaction of Cardiac function and return function
return function
cardiac function
EGDTEGDTSuspected infection
Blood cultures
Obtain two or more BCsOne or more BCs should be percutaneous
One BC from each vascular access device in place more than equal to 48 hrsCulture other sites as clinically indicated.
Other diagnostic/imaging as indicated
Appropriate Empirical Antibiotics with in 1 hr/
source controlHost factors/ local antibiogram/ suspected site
Combination antibiotics/ right dose
SBP< 90 even after20-30ml/kg fluid or Lactate > 4mmol/l