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SHOCK SHOCK “A rude unhinging of the machinery of life” - Gross -: RAJAN KUMAR

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Page 1: Shock n Sepsis

SHOCKSHOCK“A rude unhinging of the machinery of

life”

- Gross -: RAJAN

KUMAR

Page 2: Shock n Sepsis

DefinitionDefinition Shock is a systemic state of low Shock is a systemic state of low

tissue perfusion, which is tissue perfusion, which is inadequate for normal cellular inadequate for normal cellular respiration. With insufficient respiration. With insufficient delivery of oxygen and glucose, cells delivery of oxygen and glucose, cells switch from aerobic to anaerobic switch from aerobic to anaerobic metabolism. If perfusion is not metabolism. If perfusion is not restored in a timely fashion, cell restored in a timely fashion, cell death ensues.death ensues.

Page 3: Shock n Sepsis

PathophysiologyPathophysiology Physiologic response to hypovolemia Physiologic response to hypovolemia

directed at preservation of perfusion to directed at preservation of perfusion to vital organsvital organs

-Increase cardiac contractility & -Increase cardiac contractility & peripheral peripheral vascular tone via ANSvascular tone via ANS

-Hormonal response to preserve salt & -Hormonal response to preserve salt & waterwater

-Change in local micro circulation to -Change in local micro circulation to regulate regulate

regional blood flow regional blood flow

Page 4: Shock n Sepsis

Cellular responseCellular response Inadequate delivery of oxygen Inadequate delivery of oxygen

& substrates leads to in & substrates leads to in oxidative phosphorylation & ATP oxidative phosphorylation & ATP generation.generation.

Anaerobic respiration leads to Anaerobic respiration leads to lactic acidosis.lactic acidosis.

Page 5: Shock n Sepsis

Na+,K+ ATP ase activity Na+,K+ ATP ase activity decrease leading to decrease leading to accumulation of Na+ & leak of accumulation of Na+ & leak of K+K+

Intracellular lysosomes release Intracellular lysosomes release autodigestive enzymes & cell autodigestive enzymes & cell lysis ensues leading to release of lysis ensues leading to release of K+ into bloodstream.K+ into bloodstream.

Cellular responseCellular response

Page 6: Shock n Sepsis
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MicrovascularMicrovascularProgressive tissue ischemiaProgressive tissue ischemia

Change in local milieuChange in local milieu

(hypoxia & acidosis)(hypoxia & acidosis)

Activation of immune & coagulation Activation of immune & coagulation systemsystem

(compliment & prime neutrophils)(compliment & prime neutrophils)

Page 8: Shock n Sepsis

O2 free radical & cytokineO2 free radical & cytokine

Injury of capillary endothelial cellsInjury of capillary endothelial cells

(becomes ‘leaky’)(becomes ‘leaky’)

Tissue oedemaTissue oedema

Cellular hypoxiaCellular hypoxia

Contd.

Page 9: Shock n Sepsis

SystemicSystemic CardiovascularCardiovascular

in preload & afterloadin preload & afterload

Compensatory baroreceptor activationCompensatory baroreceptor activation

Sympathetic activitySympathetic activity

Tachycardia & systemic Tachycardia & systemic vasoconstrictionvasoconstriction

Page 10: Shock n Sepsis

Arterial Baroreceptors

Page 11: Shock n Sepsis

Autonomic Responses toBaroreceptor Activity

Arterial baroreceptor firing inhibits sympathetic outflow and stimulates parasympathetic outflow

Therefore, reduced firing, which occurs during hemorrhage, leads to sympathetic activation and parasympathetic inhibition

Page 12: Shock n Sepsis

Cardiopulmonary Baroreceptors

• Location: Venoatrial Junction – Tonically active • Receptor firing decreases ADH

(vasopressin) release leading to diuresis and vasodilation

• Hemorrhage → increase ADH (reduced urine formation and increased vasoconstriction)

• Location: Atria and Ventricles – Tonically active • affect vagal and sympathetic outflow

similar to arterial baroreceptors • reinforce arterial baroreceptor responses

during hypovolemia

Page 13: Shock n Sepsis

Baroreceptor Reflexes

Page 14: Shock n Sepsis

Chemoreceptor Reflexes

Peripheral chemoreceptors – Carotid bodies – Aortic bodies

Central chemoreceptors – Medulla (associated with

cardiovascular control “centers”)

Page 15: Shock n Sepsis

Increasingly important when mean arterial pressure falls below 60 mmHg (i.e., when arterial baroreceptor firing rate is at minimum)

Acidosis resulting from decreased organ perfusion stimulates central and peripheral chemoreceptors → sympathetic activation

Stagnant hypoxia in carotid bodies enhances peripheral vasoconstriction

Respiratory stimulation may enhance venous return (abdominothoracic pump)

Contd.

Page 16: Shock n Sepsis

RespiratoryRespiratoryMetabolic acidosis & sympathetic Metabolic acidosis & sympathetic

responseresponse

R.Rate & MVR.Rate & MV

(excretion of Co2)(excretion of Co2)

Compensatory respiratory Compensatory respiratory alkalosisalkalosis

Page 17: Shock n Sepsis

RenalRenal

Page 18: Shock n Sepsis

EndocrineEndocrine Vasopressin (ADH) released from Vasopressin (ADH) released from

hypothalamus in response to preload hypothalamus in response to preload vasoconstriction & reabsorption vasoconstriction & reabsorption of water in collecting system.of water in collecting system.

Cortisol released from adrenal cortex Cortisol released from adrenal cortex Na+ & H2O reabsorption and Na+ & H2O reabsorption and sensitising the cells to sensitising the cells to catecholamines.catecholamines.

Page 19: Shock n Sepsis

HypothalamusHypothalamus

HyperglycemiaLypolysisGluconeogenesisGlycogenolysis

Cortisol

ACTH

CRH

Hormonal responseHormonal response

Page 20: Shock n Sepsis

Ischaemia-reperfusion Ischaemia-reperfusion syndromesyndrome

During the period of systemic During the period of systemic hypoperfusion, cellular and organ hypoperfusion, cellular and organ damage progresses because of direct damage progresses because of direct effects of hypoxia & local activation of effects of hypoxia & local activation of inflammation.inflammation.

Further injury occurs once normal Further injury occurs once normal circulation is restored to these tissues.circulation is restored to these tissues.

The acid & K+ load can lead toThe acid & K+ load can lead to

-direct myocardial depression-direct myocardial depression

-vascular dilatation & further -vascular dilatation & further hypotension.hypotension.

Page 21: Shock n Sepsis

HypoxiaHypoxia

Cellular & humoral componentsCellular & humoral components

Flushed back into circulationFlushed back into circulation

Endothelial injury(lungs,kidney)Endothelial injury(lungs,kidney)

Ischaemia-reperfusion Ischaemia-reperfusion syndromesyndrome

Page 22: Shock n Sepsis

Acute lung,kidney injury,Acute lung,kidney injury,

multi organ failure & deathmulti organ failure & death

This injury can be attenuated by This injury can be attenuated by reducing the extent and duration of reducing the extent and duration of tissue hypoperfusiontissue hypoperfusion

Ischaemia-reperfusion Ischaemia-reperfusion syndromesyndrome

Page 23: Shock n Sepsis

ClassificationClassification HypovolaemicHypovolaemic CardiogenicCardiogenic ObstructiveObstructive DistributiveDistributive EndocrineEndocrine

Page 24: Shock n Sepsis

TypesTypes

Hypovolaemic shockHypovolaemic shock -Due to reduced circulating volume.-Due to reduced circulating volume.

1.1. HaemorrhagicHaemorrhagic

2.2. Non-HaemorrhagicNon-Haemorrhagic Causes of non-haemorrhagic shockCauses of non-haemorrhagic shock

--Dehydration,diarrhoea,vomiting,evaDehydration,diarrhoea,vomiting,evaporation,3poration,3rdrd space loss, bowel space loss, bowel obstruction or pancreatitis.obstruction or pancreatitis.

Page 25: Shock n Sepsis
Page 26: Shock n Sepsis

Cardiogenic shockCardiogenic shock Primary failure of the heart to pump.Primary failure of the heart to pump.

CausesCauses

-MI, cardiac dysrhytmias, valvular -MI, cardiac dysrhytmias, valvular heart disease,blunt myocardial heart disease,blunt myocardial injury,cardiomyopathy.injury,cardiomyopathy.

-d/t endogenous factors (in sepsis)-d/t endogenous factors (in sepsis)

-d/t exogenous factors (drugs)-d/t exogenous factors (drugs)

TypesTypes

Page 27: Shock n Sepsis
Page 28: Shock n Sepsis

Obstructive shockObstructive shock Reduction in preload due to Reduction in preload due to

mechanical obstruction of cardiac mechanical obstruction of cardiac filling.filling.

CausesCauses

- cardiac tamponade, tension - cardiac tamponade, tension pneumothorax, massive pulmonary pneumothorax, massive pulmonary embolus, air embolus.embolus, air embolus.

TypesTypes

Page 29: Shock n Sepsis

Distributive shockDistributive shock Inadequate organ perfusion Inadequate organ perfusion

accompanied byaccompanied by

1.1. Vascular dilatation with Vascular dilatation with hypotensionhypotension

2.2. Low SVRLow SVR

3.3. Inadequate afterloadInadequate afterload

4.4. Abnormally high cardiac outputAbnormally high cardiac output

TypesTypes

Page 30: Shock n Sepsis

CausesCauses

--Septic shockSeptic shock -Anaphylaxis-Anaphylaxis

-Spinal cord injury-Spinal cord injury

TypesTypes

Page 31: Shock n Sepsis

Endocrine shockEndocrine shock Combination of hypovolaemic, Combination of hypovolaemic,

cardiogenic & distributive cardiogenic & distributive shock.shock.

CausesCauses

-Hypo- & hyperthyroidism-Hypo- & hyperthyroidism

-Adrenal insufficiency-Adrenal insufficiency

TypesTypes

Page 32: Shock n Sepsis

Cardiovascular & metabolic Cardiovascular & metabolic characteristicscharacteristics

hypovolaehypovolaemiamia

cardiogecardiogenicnic

obstructobstructiveive

distributdistributiveive

Cardiac Cardiac outputoutput

lowlow lowlow lowlow HighHigh

VasculaVascular r resistanresistancece

highhigh highhigh highhigh lowlow

Venous Venous pressurpressuree

LowLow HighHigh highhigh LowLow

Base Base deficitdeficit

highhigh highhigh highhigh highhigh

Page 33: Shock n Sepsis

Severity of shockSeverity of shock Compensated shockCompensated shock DecompensationDecompensation Mild shockMild shock Moderate shockModerate shock Severe shockSevere shock

Page 34: Shock n Sepsis

Clinical featuresClinical featurescompensacompensa

tedtedmildmild moderatmoderat

eeseveresevere

Lactic Lactic acidosisacidosis

++ ++++ ++++ ++++++

UOPUOP normalnormal normalnormal oliguricoliguric AnuricAnuric

Level of Level of consciouconsciou

snesssness

NormalNormal Mild Mild anxietyanxiety

drowsydrowsy ComatComatoseose

R.RateR.Rate NormalNormal IncreasedIncreased IncreaseIncreasedd

LabourLaboureded

PulsePulse Mild Mild increaseincrease

increasedincreased increaseincreasedd

increasincreaseded

B.P.B.P. normalnormal normalnormal Mild lowMild low Severe Severe lowlow

Page 35: Shock n Sepsis

Clinical MarkersClinical Markers Brachial systolic blood pressure:

<110mmHg Sinus tachycardia: >90 beats/min Respiratory rate: <7 or >29

breaths/min Urine Output: <0.5cc/kg/hr Metabolic acidemia:

[HCO3]<31mEq/L or base deficit>3mEq/L

Page 36: Shock n Sepsis

Hypoxemia: 0-50yr: <90mmHg; 51-70yr: <80mmHg; >71yo; <70mmHg;

Cutaneous vasoconstriction vs. vasodilation.

Mental Changes: anxiousness, agitation, indifference, lethargy, obtundation

Prolonged capillary refill timeProlonged capillary refill time

Contd.

Page 37: Shock n Sepsis

PitfallsPitfalls Capillary refillCapillary refill -prolonged-prolonged

-not a specific marker. (varies in -not a specific marker. (varies in adults)adults)

-if short then may be early stage of -if short then may be early stage of shockshock

-in -in septic shockseptic shock:- BRISK despite :- BRISK despite of profound shockof profound shock

Page 38: Shock n Sepsis

TachycardiaTachycardia- Not always accompany shockNot always accompany shock- Who on Who on ββ-blocker or have implanted -blocker or have implanted

pacemakers unable to mount pacemakers unable to mount tachycardiatachycardia

- A pulse rate of 80 in a fit young adult A pulse rate of 80 in a fit young adult who normally has a pulse of 50 is who normally has a pulse of 50 is abnormalabnormal

Contd.

Page 39: Shock n Sepsis

Blood pressureBlood pressure- Hypotension is one of the last signHypotension is one of the last sign- Children & fit young adults are able to Children & fit young adults are able to

maintain B.P. until the final stages maintain B.P. until the final stages (compensatory mechanism lead to in SV (compensatory mechanism lead to in SV & peripheral vasoconstriction)& peripheral vasoconstriction)

- Elderly hypertensive pts may present Elderly hypertensive pts may present with ‘normal’ BP but be hypovolemic & with ‘normal’ BP but be hypovolemic & hypotensivehypotensive

- ββ-blocker may prevent tachycardic -blocker may prevent tachycardic responseresponse

Contd.

Page 40: Shock n Sepsis

Consequences Consequences Unresuscitable shockUnresuscitable shock- Profound shock for a prolonged period of Profound shock for a prolonged period of

timetime- Cell death follows from cellular ischemiaCell death follows from cellular ischemia- Ability to compensate lostAbility to compensate lost- Myocardial depressionMyocardial depression- Non responsive to fluid or ionotropesNon responsive to fluid or ionotropes- Peripherally loss of ability to maintain Peripherally loss of ability to maintain

SVRSVR- Further hypotension ensuesFurther hypotension ensues- Death is inevitableDeath is inevitable

Page 41: Shock n Sepsis

Multiple organ failureMultiple organ failure- Defined as 2 or more failed organ Defined as 2 or more failed organ

systemssystems- No specific treatmentNo specific treatment- Supporting organ systems with Supporting organ systems with

ventilation, cardiovascular support & ventilation, cardiovascular support & dialysis until there is recovery of dialysis until there is recovery of functionfunction

- Mortality rate 60%Mortality rate 60%- Prevention by early aggressive Prevention by early aggressive

identification & reversal of shockidentification & reversal of shock

Contd.

Page 42: Shock n Sepsis

Effects of organ failureEffects of organ failure

Lung Lung ARDSARDS

Kidney Kidney Acute renal Acute renal insufficiencyinsufficiency

Liver Liver Acute liver Acute liver insufficiencyinsufficiency

Clotting Clotting CoagulopathyCoagulopathy

Cardiac Cardiac Cardiovascular Cardiovascular failure failure

Page 43: Shock n Sepsis

ResuscitationResuscitationA – airwayA – airwayB – breathing i.e. B – breathing i.e.

oxygenation & ventilationoxygenation & ventilationC – circulation C – circulation

(cardiovascular (cardiovascular resuscitation) resuscitation)

Page 44: Shock n Sepsis

Conduct of resuscitationConduct of resuscitation- Should not be delayedShould not be delayed- Timing & nature of resuscitation Timing & nature of resuscitation

depend on type of shock and timing & depend on type of shock and timing & severity of insultseverity of insult

- Rapid examination to make a diagnosis Rapid examination to make a diagnosis & detect the source& detect the source

- If there is doubt about cause it is safer If there is doubt about cause it is safer to assume the cause is hypovolemia. to assume the cause is hypovolemia. Begin with fluid resuscitationBegin with fluid resuscitation

Contd.

Page 45: Shock n Sepsis

The pts who are actively bleeding it is The pts who are actively bleeding it is counterproductive to institute high counterproductive to institute high volume fluid therapyvolume fluid therapy

Operative hemorrhage control should Operative hemorrhage control should not be delayed & resuscitation should not be delayed & resuscitation should proceed in parallel with surgeryproceed in parallel with surgery

A pt with bowel obstruction & A pt with bowel obstruction & hypovolemic shock must be hypovolemic shock must be adequately resuscitated before adequately resuscitated before undergoing surgeryundergoing surgery

Contd.

Page 46: Shock n Sepsis

Fluid therapyFluid therapy- Hypovolemia & inadequate preload Hypovolemia & inadequate preload

must be addressed 1must be addressed 1stst

- First-line therapy is IV access and First-line therapy is IV access and administration of IV fluidsadministration of IV fluids

- Short wide bore catheters preferredShort wide bore catheters preferred- Central venous catheters are more Central venous catheters are more

appropriate for monitoringappropriate for monitoring

Contd.

Page 47: Shock n Sepsis

Type of fluidType of fluid- There is no ideal resuscitation fluidThere is no ideal resuscitation fluid- It is more important to understand It is more important to understand

how & when to administer themhow & when to administer them- Crystalloid vs ColloidCrystalloid vs Colloid- Their O2 carrying capacity zeroTheir O2 carrying capacity zero- Blood should be replaced with bloodBlood should be replaced with blood- Hypotonic solution like dextrose Hypotonic solution like dextrose

should not be used unless the deficit should not be used unless the deficit is free water loss(DI) or Na+ is free water loss(DI) or Na+ overload (cirrhosis)overload (cirrhosis)

Contd.

Page 48: Shock n Sepsis

Dynamic fluid responseDynamic fluid response- Shock status can be determined by Shock status can be determined by

the cardiovascular response to the the cardiovascular response to the rapid administration of a fluid bolusrapid administration of a fluid bolus

- InterpretationInterpretation

1.1. RespondersResponders

2.2. Transient respondersTransient responders

3.3. Non-respondersNon-responders

Contd.

Page 49: Shock n Sepsis

Vasopressor and inotropic supportVasopressor and inotropic support- Not indicated as 1Not indicated as 1stst line therapy in line therapy in

hypovolemiahypovolemia- Vasopressor agents (phenylepherine, nor-Vasopressor agents (phenylepherine, nor-

adrenaline) used in distributive shock stateadrenaline) used in distributive shock state- If vasodilation is resistant to If vasodilation is resistant to

catecholamines, vasopressin may be usedcatecholamines, vasopressin may be used- Inotropic therapy required for cardiogenic Inotropic therapy required for cardiogenic

shockshock- Inodilator dobutamine is agent of choiceInodilator dobutamine is agent of choice

Contd.

Page 50: Shock n Sepsis

MonitoringMonitoring MinimumMinimum- ECGECG- Pulse oximetryPulse oximetry- Blood pressureBlood pressure- Urine outputUrine output

Additional Additional modalitiesmodalities

- Central venous Central venous pressurepressure

- Invasive Blood Invasive Blood pressurepressure

- Cardiac outputCardiac output- Base deficit and Base deficit and

serum lactateserum lactate

Page 51: Shock n Sepsis

Cardiovascular Cardiovascular monitoringmonitoring Central venous pressureCentral venous pressure- There is no ‘normal’ CVP for a shocked pt.There is no ‘normal’ CVP for a shocked pt.- It varies patient to patientIt varies patient to patient- Ventricular compliance can change Ventricular compliance can change

rapidlyrapidly- It is a poor reflection of preloadIt is a poor reflection of preload- Measurement during fluid challenge testMeasurement during fluid challenge test- Normal response is a rise of 2-5 cmH2ONormal response is a rise of 2-5 cmH2O- Pt with no change,require more fluidPt with no change,require more fluid- With large CVP have high preloadWith large CVP have high preload

Page 52: Shock n Sepsis

Cardiac outputCardiac output- AssesesAsseses

1.1. Cardiac functionCardiac function

2.2. Systemic vascular resistanceSystemic vascular resistance

3.3. Preload (end-diastolic volume)Preload (end-diastolic volume)

4.4. Blood volumeBlood volume

Contd.

Page 53: Shock n Sepsis

Systemic & organ Systemic & organ perfusionperfusion

Goal of t/t is to restore cellular & Goal of t/t is to restore cellular & organ perfusionorgan perfusion

UOP is the best monitorUOP is the best monitor Level of consciousness – marker of Level of consciousness – marker of

cerebral perfusioncerebral perfusion Clinical indicators of perfusion of GIT Clinical indicators of perfusion of GIT

& muscular beds are lactate & base & muscular beds are lactate & base deficit and the mixed venous oxygen deficit and the mixed venous oxygen saturationsaturation

Page 54: Shock n Sepsis

ClinicalClinical InvestigationaInvestigationall

SystemSystemic ic perfusiperfusionon

Base deficit; lactate; Base deficit; lactate; mixed venous O2 sat.mixed venous O2 sat.

Organ Organ perfusiperfusionon

Muscle Muscle -- Near infrared Near infrared spectroscopyspectroscopy

Gut Gut -- Sublingual Sublingual capnometry;pcapnometry;pH;flowmetryH;flowmetry

Kidney Kidney UOPUOP --

Brain Brain Level of consciousnessLevel of consciousness Near infrared Near infrared spectroscopyspectroscopy

Page 55: Shock n Sepsis

Base deficit and lactateBase deficit and lactate

Sensitive tool for both diagnosis and Sensitive tool for both diagnosis and monitoringmonitoring

>6mmol/l have higher morbidity & >6mmol/l have higher morbidity & mortalitymortality

Occult hypoperfusion- state of normal Occult hypoperfusion- state of normal vital signs and continued vital signs and continued underperfusion manifested by ed underperfusion manifested by ed base deficitbase deficit

ABG measurementABG measurement

Page 56: Shock n Sepsis

Mixed venous oxygen Mixed venous oxygen saturationsaturation % saturation of oxygen returning to % saturation of oxygen returning to

heart from bodyheart from body Measure of O2 delivery & extraction Measure of O2 delivery & extraction

by tissuesby tissues measurement ;- sample from rt atriummeasurement ;- sample from rt atrium 50-70% normal50-70% normal <50% indicate inadequate O2 <50% indicate inadequate O2

delivery & ed O2 extraction by cellsdelivery & ed O2 extraction by cells In hypovolemic or cardiogenic shockIn hypovolemic or cardiogenic shock

Page 57: Shock n Sepsis

>70% in sepsis>70% in sepsis Disordered utilisation of O2 at Disordered utilisation of O2 at

cellular levelcellular level Arteriovenous shunting of bloodArteriovenous shunting of blood Rapid correction required withRapid correction required with- Fluid therapyFluid therapy- InotropesInotropes

Contd.

Page 58: Shock n Sepsis

Endpoints of Endpoints of resuscitationresuscitation

Resuscitation complete when oxygen Resuscitation complete when oxygen debt repaid,tissue acidosis corrected debt repaid,tissue acidosis corrected & aerobic metabolism restored & aerobic metabolism restored

Systemic ParametersSystemic Parameters LactateLactate Base deficitBase deficit Tissue ParametersTissue Parameters Gastric tonometeryGastric tonometery Near infrared spectroscopy Near infrared spectroscopy

Page 59: Shock n Sepsis

Sepsis in a Sepsis in a surgical patientsurgical patient

Page 60: Shock n Sepsis

Shock associated with sepsis is Shock associated with sepsis is found to be major cause of death found to be major cause of death in surgical intensive carein surgical intensive care

Incidence of sepsis has increased Incidence of sepsis has increased steadily over timesteadily over time

Cause of this is Cause of this is - widespread use of - widespread use of

antimicrobials, steroids, antimicrobials, steroids, indwelling catheters & ventilatorsindwelling catheters & ventilators

Page 61: Shock n Sepsis

What is sepsis?What is sepsis? Sepsis can be response to any class of Sepsis can be response to any class of

micro organism that may spread micro organism that may spread beyond invaded tissuebeyond invaded tissue

Microbial bloodstream invasion not Microbial bloodstream invasion not essentialessential

Fever or hypothermia, tachypnea, Fever or hypothermia, tachypnea, tachycardia herald onsettachycardia herald onset

When counter regulatory mechanisms When counter regulatory mechanisms overwhelmed, homeostasis fails causing overwhelmed, homeostasis fails causing organ dysfunction and further organ dysfunction and further imbalance leads to hypotensionimbalance leads to hypotension

Page 62: Shock n Sepsis
Page 63: Shock n Sepsis

Definitions in sepsisDefinitions in sepsis Bacteremia Bacteremia – presence of bacteria in blood – presence of bacteria in blood

with +ve blood cultureswith +ve blood cultures

SepticemiaSepticemia – presence of bacteria + toxins in – presence of bacteria + toxins in bloodblood

Systemic inflammatory response Systemic inflammatory response syndromesyndrome (SIRS) – may have infectious or (SIRS) – may have infectious or noninfectious aetiologynoninfectious aetiology

2 or more of following conditions2 or more of following conditions - fever or hypothermia- fever or hypothermia - tachycardia- tachycardia - tachypnea- tachypnea - leukocytosis or leukopenia or > 10% bands- leukocytosis or leukopenia or > 10% bands

Page 64: Shock n Sepsis

SepsisSepsis – SIRS with a documented – SIRS with a documented INFECTIONINFECTION

Severe SepsisSevere Sepsis or or Sepsis SyndromeSepsis Syndrome – Sepsis with evidence of one or – Sepsis with evidence of one or more organ failures [respiratory more organ failures [respiratory (ARDS), cardiovascular (compromise (ARDS), cardiovascular (compromise of cardiac function & in PVR ), renal of cardiac function & in PVR ), renal (ATN), hepatic, blood coagulation (ATN), hepatic, blood coagulation system or CNS]system or CNS]

Contd.

Page 65: Shock n Sepsis

SUSPECT SEVERE SUSPECT SEVERE SEPSIS IFSEPSIS IF

systolic BP <90 mm Hg or > 40 mm systolic BP <90 mm Hg or > 40 mm Hg fall from pts normal BPHg fall from pts normal BP

hypoxemiahypoxemia lactic acidemialactic acidemia oliguriaoliguria acute encephalopathyacute encephalopathy Hypotension unresponsive to fluid Hypotension unresponsive to fluid

resuscitation denotes septic shockresuscitation denotes septic shock

Page 66: Shock n Sepsis

OMINOUS SIGNSOMINOUS SIGNS

Septic shock lasts for > 1 hr and Septic shock lasts for > 1 hr and does not respond to fluid or pressor does not respond to fluid or pressor administration : Refractory septic administration : Refractory septic shockshock

Dysfunction of > 1 organ requiring Dysfunction of > 1 organ requiring intervention to maintain intervention to maintain homeostasis: Multiple organ homeostasis: Multiple organ dysfunction syndrome –dysfunction syndrome –

Page 67: Shock n Sepsis

Organisms causing Organisms causing sepsissepsis

Gram +ve Gram +ve - staph. Aureusstaph. Aureus- enterococcus,enterococcus,- coagulase –ve staphcoagulase –ve staph Gram –ve Gram –ve - E. coliE. coli- KlebsiellaKlebsiella- Pseudomonas Pseudomonas

Page 68: Shock n Sepsis

PathophysiologyPathophysiology

Septic insult

Complement activation Macrophage activation

TNF, IL – 1,6

Neutrophil activation

Endothelial cellUp regulation

bradykinin coagulationArachidonic metabolites N2O Oxygen radicals

Capillary leak microthrombosis vasodilation vasodilationTissue

destruction

Organ injury

Page 69: Shock n Sepsis

Complications of sepsisComplications of sepsis

Cardiopulmonary – ARDS, arteriolar Cardiopulmonary – ARDS, arteriolar vasodilatation, myocardial dysfunctionvasodilatation, myocardial dysfunction

Renal – acute tubular necrosisRenal – acute tubular necrosis

Coagulation – thrombocytopenia, Coagulation – thrombocytopenia, disseminated intravascular coagulationdisseminated intravascular coagulation

Neurological - polyneuropathyNeurological - polyneuropathy

Page 70: Shock n Sepsis

Initial ResuscitationInitial Resuscitation

Should begin as soon as severe sepsis or sepsis induced tissue hypoperfusion recognized

Elevated Serum lactate identifies tissue hypoperfusion in patients not hypotensive

Page 71: Shock n Sepsis

Initial ResuscitationInitial Resuscitation

Goals of therapy within first 6 hours

- - Central Venous Pressure 8-12 mm Central Venous Pressure 8-12 mm Hg (12-15 in ventilator pts)Hg (12-15 in ventilator pts)

- Mean arterial pressure > 65 mm HgMean arterial pressure > 65 mm Hg- Urine output > 0.5 mL/kg/hrUrine output > 0.5 mL/kg/hr- ScvO2 or SvO2 ≥ 70%; ScvO2 or SvO2 ≥ 70%;

Page 72: Shock n Sepsis

Initial ResuscitationInitial Resuscitation

- if not achieved with fluid if not achieved with fluid resuscitation during first 6 hours:resuscitation during first 6 hours:

- Transfuse RCC to hematocrit > Transfuse RCC to hematocrit > 30%30%

- Administer dobutamine (max 20 Administer dobutamine (max 20 mcg/kg/min) to goalmcg/kg/min) to goal

Page 73: Shock n Sepsis

DiagnosisDiagnosis

Before the initiation of Before the initiation of antimicrobial, at least antimicrobial, at least two blood two blood culturescultures should be obtained should be obtained

- At least one drawn At least one drawn percutaneouslypercutaneously

- At least one drawn through At least one drawn through each vascular access device if each vascular access device if inserted longer than 48 hoursinserted longer than 48 hours

Page 74: Shock n Sepsis

DiagnosisDiagnosis

Cultures such as urine, Cultures such as urine, cerebrospinal fluid, wounds, cerebrospinal fluid, wounds, respiratory secretions obtained as respiratory secretions obtained as clinical situation dictatesclinical situation dictates

Imaging and sampling performed Imaging and sampling performed promptly to determine source promptly to determine source and causative organism and causative organism

may be limited by patient stabilitymay be limited by patient stability

Page 75: Shock n Sepsis

Source ControlSource Control

Evaluate patients for focus of infection Evaluate patients for focus of infection amenable to source control measuresamenable to source control measures

Drainage of an abscess or local focus of Drainage of an abscess or local focus of infectioninfection

Debridement of infected necrotic tissueDebridement of infected necrotic tissue Removal of a potentially infected deviceRemoval of a potentially infected device Definitive control of a source of ongoing Definitive control of a source of ongoing

microbial contaminationmicrobial contamination

Source control methods must weigh Source control methods must weigh benefits and risks of specific benefits and risks of specific interventionintervention

Page 76: Shock n Sepsis

Antibiotic TherapyAntibiotic Therapy

Start i.v. antibiotics within 1st Start i.v. antibiotics within 1st hr of recognition of severe hr of recognition of severe sepsis after obtaining cultures sepsis after obtaining cultures

Page 77: Shock n Sepsis

Antibiotic TherapyAntibiotic Therapy Empirical choice of antimicrobials Empirical choice of antimicrobials

should include 1 or more drugs with should include 1 or more drugs with activity against likely pathogens, activity against likely pathogens, bacterial & fungalbacterial & fungal1.1. Penetrate presumed source of infectionPenetrate presumed source of infection

2.2. Guided by susceptibility patterns in Guided by susceptibility patterns in hospitalhospital

3.3. Continue broad spectrum therapy until Continue broad spectrum therapy until causative organism and causative organism and susceptibilities definedsusceptibilities defined

Page 78: Shock n Sepsis

Reassess after 48-72 hours to Reassess after 48-72 hours to narrow spectrum of therapynarrow spectrum of therapy

Duration of therapy should be 7-Duration of therapy should be 7-

10 days and guided by clinical 10 days and guided by clinical responseresponse

Antibiotic TherapyAntibiotic Therapy

Page 79: Shock n Sepsis

Some experts prefer combination Some experts prefer combination therapy for therapy for Pseudomonas Pseudomonas infections or neutropenic patientsinfections or neutropenic patients

Stop antimicrobials promptly if Stop antimicrobials promptly if clinical syndrome is determined clinical syndrome is determined to be noninfectiousto be noninfectious

Antibiotic TherapyAntibiotic Therapy

Page 80: Shock n Sepsis

Fluid Therapy: Choice of Fluid Therapy: Choice of FluidFluid

Fluid resuscitation consists of natural Fluid resuscitation consists of natural or artificial colloids or crystalloidsor artificial colloids or crystalloids

No evidenced-based support for one No evidenced-based support for one type of fluid over anothertype of fluid over another

- Crystalloids have much larger volume Crystalloids have much larger volume of distribution compared to colloidsof distribution compared to colloids

- Crystalloid resuscitation requires more Crystalloid resuscitation requires more fluid to achieve same endpoints as fluid to achieve same endpoints as colloidcolloid

- Crystalloids result in more edemaCrystalloids result in more edema

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Fluid Therapy: Fluid Fluid Therapy: Fluid ChallengeChallenge

Fluid challenge in patients with Fluid challenge in patients with suspected hypovolemia may be givensuspected hypovolemia may be given

500 - 1000 mL of crystalloids over 30 mins500 - 1000 mL of crystalloids over 30 mins 300 - 500 mL of colloids over 30 mins300 - 500 mL of colloids over 30 mins Repeat based on response and toleranceRepeat based on response and tolerance Input is greater than output due to Input is greater than output due to

venodilation and capillary leakvenodilation and capillary leak Most patients require continuing Most patients require continuing

aggressive fluid resuscitation during the aggressive fluid resuscitation during the first 24 hours of managementfirst 24 hours of management

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VasopressorVasopressor

Initiate vasopressor therapy if fluid Initiate vasopressor therapy if fluid challenge fails to restore adequate challenge fails to restore adequate blood pressure and organ perfusionblood pressure and organ perfusion

Vasopressor therapy used Vasopressor therapy used transiently in face of life-transiently in face of life-threatening hypotension, even when threatening hypotension, even when fluid challenge is in progressfluid challenge is in progress

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Vasopressor Vasopressor Norepinephrine or dopamine Norepinephrine or dopamine

first line agents to correct first line agents to correct hypotension in septic shockhypotension in septic shock

Norepinephrine more potent than Norepinephrine more potent than dopamine and more effective at dopamine and more effective at reversing hypotensionreversing hypotension

Dopamine particularly useful in Dopamine particularly useful in patients with compromised patients with compromised systolic function but causes more systolic function but causes more tachycardia and more tachycardia and more arrhythmogenicarrhythmogenic

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VasopressorVasopressor Low dose dopamine should Low dose dopamine should not be used not be used

for renal protection in severe sepsisfor renal protection in severe sepsis An arterial catheter placed as soon as An arterial catheter placed as soon as

practical in all patients requiring practical in all patients requiring vasopressorsvasopressors

Arterial catheters provide more accurate Arterial catheters provide more accurate and reproducible measurement of and reproducible measurement of arterial pressure in shock states arterial pressure in shock states compared to a cuffcompared to a cuff

Vasopressin considered in refractory Vasopressin considered in refractory shock patients refractory to fluid shock patients refractory to fluid resuscitation and high dose vasopressorsresuscitation and high dose vasopressors

Infusion rate of 0.01-0.04 units/min in adultsInfusion rate of 0.01-0.04 units/min in adults May decrease stroke volumeMay decrease stroke volume

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Inotropic TherapyInotropic Therapy

In patients with low cardiac output In patients with low cardiac output despite adequate fluid resuscitation, despite adequate fluid resuscitation,

dobutaminedobutamine may be used to may be used to increase cardiac outputincrease cardiac output

Combined with vasopressor therapy Combined with vasopressor therapy in hypotensionin hypotension

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Steroids I.V corticosteroids recommended in I.V corticosteroids recommended in

patients with septic shock requiring patients with septic shock requiring vasopressors to maintain blood vasopressors to maintain blood pressurepressure

Administer i.v. hydrocortisone 200-300 Administer i.v. hydrocortisone 200-300 mg/day for 7 days in 3 or 4 divided mg/day for 7 days in 3 or 4 divided doses or by continuous infusiondoses or by continuous infusion

Reduces mortality rate in patients with Reduces mortality rate in patients with relative adrenal insufficiencyrelative adrenal insufficiency

In absence of shock, corticosteroids not In absence of shock, corticosteroids not be used for treatment of sepsisbe used for treatment of sepsis

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Blood Product Blood Product AdministrationAdministration

Blood transfusion when Blood transfusion when hemoglobin decreases to < 7 g/dLhemoglobin decreases to < 7 g/dL

- Once tissue hypo-perfusion has Once tissue hypo-perfusion has resolved and in the absence of resolved and in the absence of significant coronary artery significant coronary artery disease, acute hemorrhage or disease, acute hemorrhage or lactic acidosislactic acidosis

- Target hemoglobin of 7 – 9 g/dLTarget hemoglobin of 7 – 9 g/dL

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Blood Product Blood Product AdministrationAdministration

Erythropoietin not Erythropoietin not recommended for treatment of recommended for treatment of anemia associated with severe anemia associated with severe sepsissepsis

- Unless septic patients have - Unless septic patients have other accepted reasons for other accepted reasons for administration of erythropoietin administration of erythropoietin

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Blood Product Blood Product AdministrationAdministration

Routine use of Routine use of fresh frozen fresh frozen plasmaplasma to correct laboratory to correct laboratory clotting abnormalities in absence of clotting abnormalities in absence of bleedingbleeding

Platelets administered when platelet Platelets administered when platelet counts are <5000/mmcounts are <5000/mm33 regardless of regardless of apparent bleedingapparent bleeding

Platelet transfusion when counts are Platelet transfusion when counts are 5000 - 30,000/mm5000 - 30,000/mm3 3 and significant and significant risk of bleedingrisk of bleeding

Platelet counts Platelet counts 50,000/ mm 50,000/ mm33 for for surgery or invasive proceduressurgery or invasive procedures

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Glucose ControlGlucose Control

Following initial stabilization of Following initial stabilization of patients, maintain blood glucose patients, maintain blood glucose to < 150 mg/dLto < 150 mg/dL

Best results when blood glucose Best results when blood glucose maintained between 80 and 110 maintained between 80 and 110 mg/dlmg/dl

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Glucose ControlGlucose Control Glycemic control strategy includes a Glycemic control strategy includes a

nutrition protocol with preferential nutrition protocol with preferential use of the enteral routeuse of the enteral route

Risk of hypoglycemia minimized Risk of hypoglycemia minimized by providing a continuous supply by providing a continuous supply of glucose substrate of glucose substrate

Accomplished by 5% or 10% Accomplished by 5% or 10% dextrose IV infusion ,followed by dextrose IV infusion ,followed by initiation of feeding preferably initiation of feeding preferably by enteral routeby enteral route

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Renal ReplacementRenal Replacement

Continuous venovenous hemofiltration and intermittent hemodialysis considered equivalent in acute renal failure (in absence of hemodynamic instability)

Continuous hemofiltration offers Continuous hemofiltration offers easier management of fluid balance easier management of fluid balance in hemodynamically unstable in hemodynamically unstable patients patients

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Bicarbonate TherapyBicarbonate Therapy Bicarbonate not recommended for

improving hemodynamics or reducing vasopressor requirements for hypoperfusion induced lactic acidemia with pH 7.15

No difference in vasopressor No difference in vasopressor requirements or hemodynamic requirements or hemodynamic variables between bicarbonate and variables between bicarbonate and normal saline for treating normal saline for treating hypoperfusion-induced acidemiahypoperfusion-induced acidemia

Effects of bicarbonate therapy at pH Effects of bicarbonate therapy at pH levels < 7.15 not studiedlevels < 7.15 not studied

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DVT prophylaxisDVT prophylaxis DVT prophylaxis with low-dose

unfractionated heparin or low molecular weight heparin

Use mechanical prophylactic device Use mechanical prophylactic device or intermittent compression in or intermittent compression in patients with contraindications to patients with contraindications to heparinheparin

Use a combination of Use a combination of pharmacological and mechanical pharmacological and mechanical therapy in very high risk patients therapy in very high risk patients (eg, severe sepsis and history of (eg, severe sepsis and history of DVT)DVT)

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Stress ulcer prophylaxisStress ulcer prophylaxis

Stress ulcer prophylaxis given to all patients with severe sepsis

H2 receptor blockers more H2 receptor blockers more efficacious than sucralfate efficacious than sucralfate and are preferred agents and are preferred agents

Proton pump inhibitorsProton pump inhibitors

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Basics of managementBasics of management

Suspect sepsis if clinical signs presentSuspect sepsis if clinical signs present Resuscitation should be started Resuscitation should be started

immediately (fluids/pressors/steroid as immediately (fluids/pressors/steroid as indicated)indicated)

Identify source if possibleIdentify source if possible Baseline investigations and blood Baseline investigations and blood

cultureculture Start empirical antibiotics according to Start empirical antibiotics according to

center policycenter policy Close monitoring and periodic review Close monitoring and periodic review

are vital for successful outcome are vital for successful outcome

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ConclusionConclusion Sepsis is a widespread problem in a Sepsis is a widespread problem in a

surgical set upsurgical set up Sepsis is reversible in early stagesSepsis is reversible in early stages Hence early detection and prompt Hence early detection and prompt

treatment necessarytreatment necessary High index of suspicion, active High index of suspicion, active

resuscitation and judicious use of resuscitation and judicious use of antibiotics, pressors etc are antibiotics, pressors etc are cornerstones of therapycornerstones of therapy

Antibiotic choice dictated by culture Antibiotic choice dictated by culture results. Empirical therapy is institution results. Empirical therapy is institution dependentdependent

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