principles of surgery - pgy 1 and pgy 2 shock – evidence based sandro rizoli, md, frcsc, phd, facs...

Principles of Surgery - PGY 1 and PGY 2Principles of Surgery - PGY 1 and PGY 2

SHOCK – EVIDENCE BASEDSHOCK – EVIDENCE BASED

Sandro RizoliSandro Rizoli, MD, FRCSC, PhD, FACS, MD, FRCSC, PhD, FACSAssociate Professor Surgery and Critical Care MedicineAssociate Professor Surgery and Critical Care Medicine

De Souza Trauma Research ChairDe Souza Trauma Research ChairCIHR New InvestigatorCIHR New Investigator

GOALGOAL

1. Preparation for the exams1. Preparation for the exams

2. Theoretical basis for practice2. Theoretical basis for practice

MASTER PLANMASTER PLAN

1.1. DefinitionDefinition2.2. ClassificationClassification3.3. HistoryHistory4.4. PathophysiologyPathophysiology5.5. Hypovolemic ShockHypovolemic Shock

• TherapyTherapy• Novel ideasNovel ideas

6.6. Septic shockSeptic shock• DefinitionDefinition• Current guidelinesCurrent guidelines

QUESTION #1QUESTION #1

With regards to the distribution and composition of the bodyfluid compartments, which of the following statements is/are correct?

a) Most intracellular water is in skeletal muscle.b) The major intracellular cation is sodium.c) The major intracellular anions are proteins and phosphates.d) The major extracellular cation is sodium.

DEFINITIONDEFINITION

• Inadequate tissue perfusionInadequate tissue perfusion

• Imbalance between substrate supply (DOImbalance between substrate supply (DO22))

and demand (VOand demand (VO22) at a cellular level) at a cellular level

• Dysfunction of cellular biochemistryDysfunction of cellular biochemistrycell membrane pump dysfunctioncell membrane pump dysfunctionintracellular edemaintracellular edemaleak intracellular contentsleak intracellular contentsinadequate regulation intracellular pHinadequate regulation intracellular pH

DEFINITIONDEFINITION

• Initially reversibleInitially reversible

• Cell death – organ damage – failure MO – deathCell death – organ damage – failure MO – death

• Mortality:Mortality:septic shock = 35-40% mortalityseptic shock = 35-40% mortalitycardiogenic shock = 60-90% mortalitycardiogenic shock = 60-90% mortalityhemorrhagic = variable mortalityhemorrhagic = variable mortality

DETERMINANTS TISSUE PERFUSIONDETERMINANTS TISSUE PERFUSION

CO = HR x stroke volumeCO = HR x stroke volume (preload+contractility+afterload) (preload+contractility+afterload)

DODO2 2 = CaO= CaO22 x cardiac output x cardiac output

VOVO22 = (CaO = (CaO22 - CvO - CvO22) x cardiac output) x cardiac output

OO22 content = (1.38 x Hg) x O content = (1.38 x Hg) x O22 sat + (0.03 X PaO sat + (0.03 X PaO2 2 ))

SVR = vessel length, blood viscosity, vessel diameterSVR = vessel length, blood viscosity, vessel diameter

CLASSIFICATIONCLASSIFICATION

1.1. Hypovolemic – Hypovolemic – decreased pre-loaddecreased pre-load hemorrhage/fluid losshemorrhage/fluid loss

2. Distributive –2. Distributive – sepsis, vasodilatory, pancreatitis, sepsis, vasodilatory, pancreatitis, anaphylaxis, Addison, SIRSanaphylaxis, Addison, SIRS

3. Cardiogenic –3. Cardiogenic – pump failure pump failure heart, arrhythmias, obstructive heart, arrhythmias, obstructive (PE, pneumotx, tamponade, pulm. hypert.) (PE, pneumotx, tamponade, pulm. hypert.)

4. Neurogenic –4. Neurogenic – hypotension NOT tachyc, vasoconstriction hypotension NOT tachyc, vasoconstriction

CLASSIFICATIONCLASSIFICATION

PCWP CO SVR SPCWP CO SVR SVO2VO2

HypovolemicHypovolemic

DistributiveDistributive

CardiogenicCardiogenic

History Shock ResuscitationHistory Shock Resuscitation

TimeTime Focus Focus Resusc Resusc Outcome Outcome

WW IWW I wound toxins wound toxins none none early death early death

WW IIWW II IV repletion IV repletion blood blood ARF ARF

colloidcolloid

VietnamVietnam IV + EC repletion blood IV + EC repletion blood ARDS ARDS

crystalloidcrystalloid

70-80’s70-80’s organ support organ support ICU ICU ARDS, MOF ARDS, MOF

Trauma Trauma

QUESTION #2QUESTION #2

Metabolic effects of the neuroendocrine response to injuryinclude which of the following events?

a) Gluconeogenesis.b) Glycogen synthesis.c) Lipolysis.d) Proteolysis.e) Hypoglycemia.

PATHOPHYSIOLOGY IPATHOPHYSIOLOGY I

HypovolemiaHypovolemia(decresase C.O.)(decresase C.O.)

VasoconstrictionVasoconstrictionTachycardiaTachycardia

Decrease blood flowDecrease blood flow• SplanchnicSplanchnic• Loss gut barrierLoss gut barrier• Renal redistributionRenal redistribution• Renin-angiotensin-aldostRenin-angiotensin-aldost

Cellular dysfunctionCellular dysfunctionFall transmemb potentialFall transmemb potential

Na-K pumpNa-K pump

PATHOPHYSIOLOGY IPATHOPHYSIOLOGY I

Na=9.9Na=9.9K=173K=173Cl=3.9Cl=3.9

Na=18.4Na=18.4K=162K=162Cl=11.1Cl=11.1

Extracellular water 49%Extracellular water 49%

Intracellular water 6%Intracellular water 6%

QUESTION #3QUESTION #3

Which of the following is/are elevated during acute responseto injury?

a) Glucagon.b) Glucocorticoids.c) Cathecolamines.d) Insulin.e) Thyroid stimulating hormone (TSH).

PATHOPHYSIOLOGY IIPATHOPHYSIOLOGY II

hypovolemiahypovolemiatissue injurytissue injury

painpainfearfear

sympatho-sympatho-adrenaladrenal

responseresponse

hypothalamic-hypothalamic-hypophyseal-hypophyseal-

adrenaladrenalresponseresponse

hypermetabolichypermetabolicstatestate

catecholcatecholBP, HRBP, HR

contractilitycontractilityvasoconstrictionvasoconstriction

hypoxiahypoxiaendoth – macrophages cytokines, PAF, eicosanoid,endoth – macrophages cytokines, PAF, eicosanoid, neutrophils ROS, coagulationneutrophils ROS, coagulation

reperfusion injuryreperfusion injurySIRS/MODSSIRS/MODStranslocationtranslocation

cortisol, glucagoncortisol, glucagon

1.1. AcidemiaAcidemia – low pH, lactate, BE – low pH, lactate, BE

2.2. Ischemic organsIschemic organs

3.3. SIRSSIRS

4.4. MODSMODS

CONSEQUENCESCONSEQUENCES

QUESTION #4QUESTION #4

Which of the following statements accurately characterizesfluid shifts in hemorrhagic shock?

a) Loss of IV volume is fully compensated by interstitial fluid movinginto the vascular space.

b) Intracellular fluid volume decreases as fluid shifts from the ICto the EC compartment to compensate for the IV loss.

c) There is movement of interstitial fluid into the IC space even thoughfull compensation of IV losses has not yet occurred.

d) Transmembrane potential falls resulting in increased Na permeabilityand influx of Na into the cell.

ClassificationClassification

• Up to 15%Up to 15% (compensated) (compensated)HR<100, RR 14-20, N urine/BP, anxiousHR<100, RR 14-20, N urine/BP, anxious

• 30%30% (up to 1500ml)(up to 1500ml)

• 40%40%

• >40%>40%

HYPOVOLEMIC SHOCKHYPOVOLEMIC SHOCK

ManagementManagement

1.1. ABCDE – oxygen + 2L NS or RLABCDE – oxygen + 2L NS or RL2.2. Identify source bleedingIdentify source bleeding3.3. Control bleedingControl bleeding4.4. Resuscitate until perfusion correctedResuscitate until perfusion corrected

Massively transfused patientsMassively transfused patients

HYPOVOLEMIC SHOCKHYPOVOLEMIC SHOCK

Direct control of bleedingDirect control of bleeding

- surgery- surgery

- cauterization- cauterization

- topical agents- topical agents

- angio-embolization- angio-embolization

Control Bleeding - SurgeryControl Bleeding - Surgery

Restore circulating volumeRestore circulating volume

crystalloids vs. colloidscrystalloids vs. colloids

SAFE trialSAFE trial::

NEJM 2004; 350:2247NEJM 2004; 350:2247

NEJM 2007; 357:874NEJM 2007; 357:874 - TBI severe 42% vs 22% - TBI severe 42% vs 22%

FluidsFluids

Replace blood lossesReplace blood losses

- RBC- RBC

- other blood products- other blood products

TRICC trialTRICC trial::

NEJM 1999; 340:409NEJM 1999; 340:409

J Trauma 2004; 57:563 J Trauma 2004; 57:563

BloodBlood

Crystalloid Side EffectsCrystalloid Side Effects

• Abdominal compartment syndromeAbdominal compartment syndrome• Extremity compartment syndromeExtremity compartment syndrome

• Pro inflammatory Pro inflammatory • Increased organ dysfunction (ARDS)Increased organ dysfunction (ARDS)• Increased hospital stayIncreased hospital stay• Longer ventilation daysLonger ventilation days

• dilutiondilution• consumptionconsumption• hypothermiahypothermia• platelet dysfunctionplatelet dysfunction• excessive fibrinolysisexcessive fibrinolysis• DIC (????)DIC (????)

Diffuse CoagulopathyDiffuse Coagulopathy

hypothermiahypothermia

acidosisacidosis coagulopathycoagulopathy

deathdeath

massivemassivetransfusedtransfused(10-20U RBC)(10-20U RBC)

Triangle of DeathTriangle of Death

Damage control resuscitation:

• 5% massively bleeding

• Restrict crystalloids

• Reconstituted whole blood RBC 1:1 FFP (:1 platelet)

Evidence 1FFP:1RBCEvidence 1FFP:1RBC

Borgman Borgman (J.Trauma 2007;63:805)(J.Trauma 2007;63:805)

• Retrospective chart reviewRetrospective chart review• 246 at US Combat Army Hospital246 at US Combat Army Hospital• ≥≥10U RBC/24h (including whole blood)10U RBC/24h (including whole blood)

mortalitymortality death by exsanguinationdeath by exsanguination

1:81:8 65% 65% 92%92%

1:21:2 34% 34% 78%78%

1:11:1 19% 19% 37%37%

Evidence 1FFP:1RBC

Borgman (J.Trauma 2007;63:805)

• Survivorship bias• Crystalloids

mortality crystalloids

1:8 65% 1.8L/h

1:1 19% 0.5L/h

Kashuk (J. Trauma 2008, 65:261)

• Retrospective (Civilian - Denver)• 133 patients; >10 RBC in 6h

• 1:1 NO survival benefit• Crystalloids NOT risk factor coagulopathy• Temperature risk factor (ISS ??)

Evidence 1FFP:1RBC

Guidelines – ATLSGuidelines – ATLS (95% patients) (95% patients)

Endpoints Trauma RoomEndpoints Trauma Room

Fluid resuscitationFluid resuscitation EndpointsEndpoints

2L crystalloids 2L crystalloids blood pressureblood pressure

search bleedingsearch bleeding heart rateheart rate

repeat bolusrepeat bolus urine outputurine output

start RPBCstart RPBC85% inadequate tissue O85% inadequate tissue O22

Endpoints – ICUEndpoints – ICU

GlobalGlobal RegionalRegionalsupranormal DOsupranormal DO22 gastric tonometrygastric tonometry

mixed venous Omixed venous O22 sat sat skin/brain blood flowskin/brain blood flow

RVEDV - LVPRVEDV - LVP

base deficitbase deficit

lactatelactate

Current ResuscitationCurrent Resuscitation

GOAL-DIRECTED SUPRANORMAL VALUESGOAL-DIRECTED SUPRANORMAL VALUES

ShoemakerShoemaker (late 80’s) (late 80’s)post op, trauma pre-op patientspost op, trauma pre-op patients

Boyd & HayesBoyd & Hayes (1999) (1999)no improvement overallno improvement overallreduced mortality if 8-12h (8RCT)reduced mortality if 8-12h (8RCT)92% survival if achieved 24h92% survival if achieved 24h93% mortality if not and lactate high >24h93% mortality if not and lactate high >24h

THERAPYTHERAPY

598 patients598 patients• penetratingpenetrating• BP BP 90 mmHg 90 mmHg

STANDARDSTANDARDn = 309n = 309• 870 cc p.h.870 cc p.h.• 1608 cc ER1608 cc ER

NO FLUIDNO FLUIDn = 289n = 289• 90 cc p.h.90 cc p.h.• 280 cc ER280 cc ER

62%62% survived survived 70%70% survived survived

TIMINGTIMING for fluids for fluids

1.1. Bleeding – surgical hemostasisBleeding – surgical hemostasis2.2. NO TBI – allow hypotensionNO TBI – allow hypotension

ManagementManagement1.1. ABCDE – oxygen + 2L NSABCDE – oxygen + 2L NS2.2. Identify & control bleedingIdentify & control bleeding3.3. Resuscitate until perfusion correctedResuscitate until perfusion corrected

Massively transfused patientsMassively transfused patients1.1. Blood-based resuscitationBlood-based resuscitation2.2. Reconstituted whole blood Reconstituted whole blood (1:1 RBC:FFP)(1:1 RBC:FFP)

3.3. Restrict crystalloidRestrict crystalloid

HYPOVOLEMIC SHOCKHYPOVOLEMIC SHOCK

QUESTION #5QUESTION #5

Which one or more of factors determines cardiac output?

a) End-diastolic volume.b) Afterload.c) Contractility.d) Heart rate.e) Ventricular interaction.

QUESTION #6QUESTION #6

Which factors directly affect oxygen delivery?

a) Blood transfusions.b) Oxygen consumption (VO2).c) Cardiac output (CO).d) Fraction of inspired oxygen (FiO2). e) Metabolic alkalosis.

SIRSSIRS

SepsisSepsisdocumented infectiondocumented infection

Severe sepsisSevere sepsislactic acidosis, oliguria (<0.5ml/h), mental, lactic acidosis, oliguria (<0.5ml/h), mental, platelet <100,000, cap refill platelet <100,000, cap refill ≥ 3sec, mottled≥ 3sec, mottled

Septic shockSeptic shockhypotension despite fluids (40-60 ml/Kg)hypotension despite fluids (40-60 ml/Kg)

SEPTIC SHOCKSEPTIC SHOCK

At least two of:At least two of:

• RR>20 or PaCORR>20 or PaCO22<32mmHg<32mmHg

• HR>90HR>90

• Temperature >38Temperature >3800C or <35C or <3500CC

• WBC>12,000 or <4,000WBC>12,000 or <4,000

DEFINITION SIRSDEFINITION SIRS

1.1. FLUIDS **FLUIDS **

2.2. DIAGNOSISDIAGNOSIS

3.3. SOURCE CONTROLSOURCE CONTROL

4.4. ANTIBIOTICSANTIBIOTICS

THERAPY THERAPY

1.1. FLUIDS **FLUIDS **

CVP 8-12CVP 8-12MAP MAP 65 65U.O. U.O. 0.5cc/h 0.5cc/hSvOSvO22 70% (or S 70% (or SVCVCOO22))

THERAPY THERAPY

Rivers Rivers NEJM 2001NEJM 2001

controlcontrol

CVP, MAP, U.O.CVP, MAP, U.O.

interventionintervention

CVP, MAP, U.O., CVP, MAP, U.O., SvOSvO22

more fluidmore fluidmore bloodmore bloodmore inotropesmore inotropes

0 to 6h0 to 6h

7 to 72h7 to 72h more fluidmore fluidmore bloodmore bloodmore inotropesmore inotropesMORE DEATHSMORE DEATHS

5. PRESSOR 5. PRESSOR (2(2ndnd line, nor, epi or dopamine) line, nor, epi or dopamine)

6. INOTROPES 6. INOTROPES (dobutamine)(dobutamine)

THERAPY THERAPY

Heart Rate ContractilityHeart Rate Contractility Constriction Constriction

DopamineDopamine ++++ ++ ++ ++ ++EpiEpi ++++++ +++ +++ ++ ++NorepiNorepi ++++ ++ ++ +++ +++PhenylephrinePhenylephrine 00 0 0 +++ +++

7. STEROIDS 7. STEROIDS (ACTH, low raise <9mcg/dl + hemod effect)(ACTH, low raise <9mcg/dl + hemod effect)

8.8. rhAPC rhAPC (PROWESS = APACHE>25, MOD x2(PROWESS = APACHE>25, MOD x2 ADDRESS = not for low risk death)ADDRESS = not for low risk death)

THERAPY THERAPY

9. TRANSFUSION TRIGGER9. TRANSFUSION TRIGGER

10.10. PROTECTIVE VENTILATIONPROTECTIVE VENTILATIONTV 6ml/k; PP<30, PEEPTV 6ml/k; PP<30, PEEP

11. SEDATION, PARALYSIS11. SEDATION, PARALYSIS

12. NUTRITION, GLUCOSE CONTROL12. NUTRITION, GLUCOSE CONTROL

THERAPY THERAPY

1.1. ShockShock• Definition, classificationDefinition, classification• Overview physiopathologyOverview physiopathology

2.2. Hypovolemic shockHypovolemic shock• Stop bleeding then volumeStop bleeding then volume• Damage control resuscitationDamage control resuscitation

3.3. Septic shockSeptic shock• DefinitionDefinition• Current guidelinesCurrent guidelines

CONCLUSIONSCONCLUSIONS