Drnitinpresentation Surgery

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Department of Surgery

G.R. MEDICAL COLLEGE, GWALIOR SEMINAR PRESENTATIONSEMINAR PRESENTATION

Septic Shock and Its ManagementSeptic Shock and Its Management

Chairperson

Prof. Dr. L.P. VermaM.S., F.A.I.S.

Prof. & Head

Department of Surgery

G.R. Medical College Gwalior

Presented byDr. Nitin Aggarwal

R.S.O. Surgery

Guide

Prof. Dr. B.R. ShrivastavaM.S.,M.Ch.Phd

ProfessorDepartment of Surgery

G.R. Medical College Gwalior



Definition

Shock is the clinical syndrome that resultsfrom inadequate tissue perfusion.

Classification of shock Hypovolumic

Cardiogenic

Septic

Hyperdynamic Hypodynamic

Neurogenic



Physiology characteristics of

the various forms of shock

Type of shock CVP &

PCWP

CO SVR Venous O2

saturation

Hypovolumic q q o q

Cardiogenic o q o q

Septic

- Hyperdynamic- Hypodynamic qoqo oq qo ooq

Neurogenic q q q q



Bacteremia

Infection SIRS

Pancreatitis

Fungemia

Other

Trauma

Burns

Parasite

Virus

other

Sepsis



DefinitionsDefinitions

Infection=Infection= microbial phenomenonmicrobial phenomenon

characterized by an inflammatory responsecharacterized by an inflammatory response

to the presence of microorganisms or theto the presence of microorganisms or the

invasion of normally sterile host tissue byinvasion of normally sterile host tissue bythose organisms.those organisms.

Bacteremia =Bacteremia = the presence of viablethe presence of viable

bacteria in the blood.bacteria in the blood. SepticemiaSepticemia == the presence of microbes or the presence of microbes or

their toxins in blood.their toxins in blood.



Systemic inflammatory responseSystemic inflammatory response

syndrome (SIRS)syndrome (SIRS)

The systemic inflammatory response to aThe systemic inflammatory response to avariety of severe clinical insults. Thevariety of severe clinical insults. Theresponse is manifested byresponse is manifested by two or more of two or more of

the followingsthe followings:: Temperature >38Temperature >38°°C or <36C or <36°°CC

Heart rate >90 beats/minHeart rate >90 beats/min

Respiratory rate >20 breaths/minRespiratory rate >20 breaths/min

WBC >12,000 cells/mmWBC >12,000 cells/mm33,,<4000cells/mm<4000cells/mm33, or >10 % immature, or >10 % immature(band) forms(band) forms



SepsisSepsis vsvs Severe SepsisSevere Sepsis

Sepsis = the systemic response toSepsis = the systemic response to

infection. That is, SIRS with definitiveinfection. That is, SIRS with definitive

evidence of infection.evidence of infection.Severe sepsis = Sepsis associated withSevere sepsis = Sepsis associated with

organ dysfunction, hypoperfusion, or organ dysfunction, hypoperfusion, or

hypotension.hypotension.

The manifestations of hypoperfusion include,The manifestations of hypoperfusion include,systolic B P < 90 mm Hg, lactic acidosis,systolic B P < 90 mm Hg, lactic acidosis,

oliguriaoliguria, or an acute alteration in mental status., or an acute alteration in mental status.



Septic ShockSeptic Shock

Patient with severe sepsis who :Patient with severe sepsis who :

Are not responsive to intravenous fluid infusionAre not responsive to intravenous fluid infusionfor resuscitationfor resuscitation

RequireRequire inotropicinotropic or or vasopressor vasopressor agents toagents tomaintain systolic blood pressuremaintain systolic blood pressure



Multiple Organ DysfunctionMultiple Organ Dysfunction

Syndrome (M

ODS /M

OF)Syndrome (M

ODS /M

OF)

MODS /MOF = the presence of altered organMODS /MOF = the presence of altered organ

function in an acutely ill patient such thatfunction in an acutely ill patient such thathomeostasis cannot be maintained withouthomeostasis cannot be maintained withoutintervention.intervention.



Homeostasis Is Unbalanced inHomeostasis Is Unbalanced in

Severe SepsisSevere Sepsis



Etiology

Sepsis can be a response to any class of

microorganism

Blood culture

(+) 20-40% in severe sepsis.

(+) 40-70% in septic shock



Main Pathogens in Septic Shock

Gram-positive bacteria- 30-50%

coagulase-negative staphylococci,Staphylococcus aureus, Streptococcus

pneumoniae, Enterococcus, other

Gram-negative bacteria- 25-30%

E. coli, Ps. aeruginosa, K. pneumoniae, other

Fungi- 1-3%

Candida albicans, other

Parasites (1-3%) and Viruses (

2-4%)



CONDITION THAT MAY PREDISPOSE TO CONDITION THAT MAY PREDISPOSE TO

INFECTION IN +VE BLOOD CULTUREINFECTION IN +VE BLOOD CULTURE

GramGram veve bacteriabacteria D M , cirrhosis , burns , invasive procedureD M , cirrhosis , burns , invasive procedure

foleysfoleys catheter , perforatedcatheter , perforated viscuscocciviscuscocci

GramGram ++veve bacteriabacteria II V V cathetercatheter ,indwelling,indwelling mechanicalmechanical devicesdevices

burnsburns ,, II V V drugdrug abuseabuse

FungiFungi NeutropeniaNeutropenia,, immunocompromisedimmunocompromised



Pathogenesis of Septic Shock

Infectious Triggers

Cytokine and inflammatory mediator cascade

Cardiac dysfunction and microvascular

injury

Hypotension and shock



Primary Cytokine Mediators of

Septic ShockSystemic Macrophage activation by microbes

Systemic Interleukin-1, Tumor Necrosis Factor-

Endothelial/Leukocyte molecular activation

Secondary mediators (NO,PAF, PG, LT, IL)

Vasodilation, capillary leak, endothelial damage

Shock MODS Death



Severe Sepsis: The Final CommonSevere Sepsis: The Final Common

PathwayPathway

Endothelial Dy sfu nction and

Microv asc u lar Thrombosi s

H ypoper fusion/I schemia

Ac u te Organ Dy sfu nction

(Sev ere Sepsi s)

Death

Cytokine storm



Microbial Triggers = Pathogen

Associated Molecular Patterns Gram-negative bacteria:

lipopolysaccharide, lipoproteins

Gram-positive bacteria:

Lipoteichoic acid, peptidoglycan

acterial flagellin

Viral and bacterial nucleic acid



Identifying Acute Organ DysfunctionIdentifying Acute Organ Dysfunction

as a Marker of Severe Sepsisas a Marker of Severe Sepsis

Tachycardia

Hypotension

o CVP

o PAOP

Jaundice

o Enzymes

q Albumin

o PT

Altered

Consciousn

ess

Confusion

Psychosis

Tachypnea

PaO2 <70 mm

Hg

SaO2 <90%

PaO2 /FiO2 e300

Oliguria

Anuria

o Creatinine

q Platelets

o PT /APTT

q Protein C

o D-dimer



DiagnosisDiagnosis

Obtain appropriate cultures before starting antibioticsprovided this does not significantly delay antimicrobialadministration (1C) obtain two or more BCs

One or more BCs should be percutaneous

One BC from each vascular access device in place 48 hrs

Culture other sites as clinically indicated

Perform imaging studies promptly to confirm and sample

any source of infection, if safe to do so (ex. Sonographysuitable, transport outside unit may be dangerous)



Guidelines for Management of Severe Sepsis andGuidelines for Management of Severe Sepsis andSeptic ShockSeptic Shock

I. MANAGEMENT OFSE VERE SEPSIS Initial Resuscitation

Diagnosis Antibiotics Therapy Source Control Fluid therapy Vasopressors Inotropic Therapy Corticosteroid Recombinant Human

Activated Protein C (rhAPC) Blood Product

Administration

II. SUPPORTI VE THER APYOF SE VERE SEPSIS Mechanical Ventilation ofSepsis-induced ALI/ ARDS

Sedation, Analgesia, and N-M Blockade in Sepsis

Glucose Control Renal Replacement Bicarbonate Therapy DVT Prophylaxis Stress Ulcer Prophylaxis Selective Digestive TractDecontamination (SDD)

Consideration forLimitation of Support

III. Pediatric Consideration



Early GoalEarly Goal--Directed TherapyDirected Therapy

1000 ml of crystalloid or 3001000 ml of crystalloid or 300--500 ml bolus500 ml bolusof colloid q 30 min to keep C VP 8of colloid q 30 min to keep C VP 8--12 cm H12 cm H22OO

Vasoactive agents (M AP: Vasoactive agents (M AP: 65 mmHg)65 mmHg)

Vasopressors if M AP < 65 mmHg Vasopressors if M AP < 65 mmHg

Vasodilator if M AP > 90 mmHg Vasodilator if M AP > 90 mmHg

Transfusion (Transfusion ( Hct > 30%) and Dopamine/Hct > 30%) and Dopamine/

Dobutamine if ScvODobutamine if ScvO22 < 70% or mixed venous << 70% or mixed venous <65%65%

Keep urine output : Keep urine output : 0.5 ml.kg0.5 ml.kg--11.hr.hr



Antibiotic Therapy Antibiotic Therapy

Begin intravenous antibiotics as early as possibleand always within the first hour of recognizingsevere sepsis and septic shock

In the presence of septic shock, each hour delay inachieving administration of effective antibiotics isassociated with a measurable increase in mortality

Broad-spectrum: one or more agents activeagainst likely bacterial/fungal pathogens and

with good penetration into presumed source




Reassess antimicrobial regimen dailyto optimize efficacy, prevent

resistance, avoid toxicity, andminimize costs consider combinationtherapy in Pseudomonas infections

Consider combination empiric therapyin neutropenic patients




Combination therapy 35 days and de-escalation following susceptibilities (Tosingle therapy)

Duration of therapy typically limited to 710 days; longer if response is slow orthere are undrainable foci of infection or

immunologic deficiencies

Stop antimicrobial therapy if cause isfound to be noninfectious









InotropicInotropic TherapyTherapy

Use dobutamine in patients withmyocardial dysfunction as supported byelevated cardiac filling pressures and lowcardiac output (check cardiac output)

Do not increase cardiac index topredetermined supranormal levels



Corticosteroid in Septic ShockCorticosteroid in Septic Shock

High doses of corticosteroids do not improve survivalHigh doses of corticosteroids do not improve survivaland may worsen outcomes by increasing the frequencyand may worsen outcomes by increasing the frequencyof secondary infectionsof secondary infections

LowLow--dose (?physiologic?) steroids may be beneficialdose (?physiologic?) steroids may be beneficial

because of relative adrenal insufficiencybecause of relative adrenal insufficiency Treat patients who still require vasopressors despite fluidTreat patients who still require vasopressors despite fluid

replacement with hydrocortisone 200replacement with hydrocortisone 200--300 mg/day, for 7 days in300 mg/day, for 7 days inthree or four divided doses or by continuous infusionthree or four divided doses or by continuous infusion



Human Activated Protein C inHuman Activated Protein C in

Septic ShockSeptic Shock

Activated protein C had anti Activated protein C had anti--thrombotic, thrombotic, antianti--inflammatory and proinflammatory and pro--fibrinolyticfibrinolyticpropertiesproperties

DrotrecoginDrotrecogin Alfa is the first anti Alfa is the first anti--inflammatoryinflammatoryagent that proved effective in the treatment agent that proved effective in the treatment of sepsisof sepsis

Dose : 24 microgram / kg /min in infusionDose : 24 microgram / kg /min in infusion



FD A labelingFD A labelingRecombinant human activated protein C (rh APC)Recombinant human activated protein C (rh APC)

Patients who have severe sepsis and with a highPatients who have severe sepsis and with a highrisk of deathrisk of death

Such as with an APACHE II score of at least 25Such as with an APACHE II score of at least 25

Evidence of endEvidence of end--organ dysfunctionorgan dysfunction Shock, acidosis, oliguria, or hypoxemiaShock, acidosis, oliguria, or hypoxemia

Be given within 24 hours of the first organBe given within 24 hours of the first organfailurefailure

Not be given to mildNot be given to mild--toto--moderate sepsis who domoderate sepsis who donot have evidence of endnot have evidence of end--organ injuryorgan injury



Contraindications to Use of Recombinant

Human Activated Protein C (rhAPC)

Active internal bleeding Recent (within 3 months) hemorrhagic stroke Recent (within 2 months) intracranial or

intraspinal surgery,or severe head trauma

Trauma with an increased risk of life threateningbleeding

Presence of an epidural catheter Intracranial neoplasm or mass lesion or evidence

of cerebral herniation Known hypersensitivity to rh APC or any

component of the product



Blood Product AdministrationBlood Product Administration

Administer platelets when

Counts are 5000/mm3 (5x 109 /L) regardless of bleeding

Counts are 5000 ±30,000/mm3 (5 ±30x109 /L) andthere is significant bleeding risk

Higher platelet counts (50,000/mm3 [50x 109 /L])are required for surgery or invasive procedures

Blood transfudion : Hb <7 gm



Glucose ControlGlucose Control

After initial stabilization After initial stabilization

Glucose be maintained <150 mg/dlGlucose be maintained <150 mg/dl

Continuous infusion insulin and glucose orContinuous infusion insulin and glucose orfeeding (feeding (enteralenteral preferred)preferred)

MonitoringMonitoring

Initially: q30Initially: q30--6060 minsmins

After After stabilizaitonstabilizaiton: q4h: q4h



Renal ReplacementRenal Replacement

Absence of hemodynamic instability Absence of hemodynamic instability Intermittent hemodialysis and continuousIntermittent hemodialysis and continuous

venovenous filtration equal (C VVH)venovenous filtration equal (C VVH)

Hemodynamic instabilityHemodynamic instability C VVH preferred C VVH preferred ------ to facilitate managementto facilitate management

of fluid balance in septic patients, noof fluid balance in septic patients, noimproved in regional perfusion and survivalimproved in regional perfusion and survivalbenefitbenefit



Bicarbonate therapy not recommended toimprove hemodynamics in patients with

hypoperfusion-induced lactic acidemiapH >7.15

Will increase Na, fluid overload,increase lactate and PCO2

Bicarbonate Therapy



Prognosis

Approximately 20 to 35% of patients

with severe sepsis and 40 to 60% of

patients with septic shock die within 30 days.

Late death often result from poorly

controlled infection, complications of

intensive care, failure of multiple organ .



Prevention

Reducing the number of invasive procedureundertaken by limiting the use of indwellingvascular and bladder catheters.

Incidence and duration of profoundnutropenia <500 neutrophils/QL

Aggressively treating localize nosocomial

infection. Indiscriminate use of antimicrobial agents

and glucocorticoids should be avoided.



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