Department of Surgery

G.R. MEDICAL COLLEGE, GWALIOR

SEMINAR PRESENTATION

Septic Shock and Its Management

Chairperson Guide
Prof. Dr. L.P. Verma Prof. Dr. B.R. Shrivastava
M.S., F.A.I.S.
M.S.,M.Ch.Phd
Prof. & Head
Professor
Department of Surgery
Department of Surgery
G.R. Medical College Gwalior
G.R. Medical College Gwalior
Presented by
Dr. Nitin Aggarwal
R.S.O. Surgery
 Definition
 Shock is the clinical syndrome that results
from inadequate tissue perfusion.
 Classification of shock
 Hypovolumic
 Cardiogenic
 Septic
 Hyperdynamic
 Hypodynamic

 Neurogenic
 Physiology characteristics of
the various forms of shock
Type of shock CVP & CO SVR Venous O2
PCWP saturation

Hypovolumic    
Cardiogenic    
Septic
- Hyperdynamic    
- Hypodynamic    

Neurogenic    
 Bacteremia
Other
Infection SIRS
Fungemia Sepsis Trauma
Parasite

Virus Burns
other
Pancreatitis
 Definitions

 Infection= microbial phenomenon

characterized by an inflammatory response
to the presence of microorganisms or the
invasion of normally sterile host tissue by
those organisms.
 Bacteremia = the presence of viable
bacteria in the blood.
 Septicemia = the presence of microbes or
their toxins in blood.
 Systemic inflammatory response
syndrome (SIRS)
 The systemic inflammatory response to a
variety of severe clinical insults. The
response is manifested by two or more of
the followings:
 Temperature >38°C or <36°C
 Heart rate >90 beats/min
 Respiratory rate >20 breaths/min
 WBC >12,000 cells/mm3,
<4000cells/mm3, or >10 % immature
(band) forms
 Sepsis vs Severe Sepsis

Sepsis = the systemic response to

infection. That is, SIRS with definitive
evidence of infection.
Severe sepsis = Sepsis associated with
organ dysfunction, hypoperfusion, or
hypotension.
 The manifestations of hypoperfusion include,
systolic B P < 90 mm Hg, lactic acidosis,
oliguria, or an acute alteration in mental status.
 Septic Shock
Patient with severe sepsis who :

Are not responsive to intravenous fluid infusion

for resuscitation

Require inotropic or vasopressor agents to

maintain systolic blood pressure
 Multiple Organ Dysfunction
Syndrome (MODS/MOF)

MODS/MOF = the presence of altered organ

function in an acutely ill patient such that
homeostasis cannot be maintained without
intervention.
 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
INFECTION IN +VE BLOOD CULTURE
Gram –ve bacteria D M , cirrhosis , burns , invasive procedure
foleys catheter , perforated viscuscocci

Gram +ve bacteria I V catheter ,indwelling mechanical devices

burns , I V drug abuse

Fungi Neutropenia, immunocompromised

Pathogenesis of Septic Shock
Infectious Triggers

Cytokine and inflammatory mediator cascade

Cardiac dysfunction and microvascular

injury

Hypotension and shock

Primary Cytokine Mediators of
Septic Shock
Systemic Macrophage activation by microbes

Systemic Interleukin-1, Tumor Necrosis Factor-α

Endothelial/Leukocyte molecular activation

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

Vasodilation, capillary leak, endothelial damage

Shock MODS Death

Severe Sepsis: The Final Common
Pathway
Cytokine storm
Endothelial Dysfunction and
Microvascular Thrombosis

Hypoperfusion/Ischemia

Acute Organ Dysfunction

(Severe Sepsis)

Death
 Microbial Triggers = Pathogen
Associated Molecular Patterns
 Gram-negative bacteria:

lipopolysaccharide, lipoproteins
 Gram-positive bacteria:

– Lipoteichoic acid, peptidoglycan

 Bacterial flagellin
 Viral and bacterial nucleic acid
Identifying Acute Organ Dysfunction
as a Marker of Severe Sepsis
Altered
Consciousn
Tachycardia
ess
Hypotension
Confusion
 CVP
Psychosis
 PAOP

Tachypnea
PaO2 <70 mm Oliguria
Hg Anuria
SaO2 <90%  Creatinine
PaO2/FiO2 300

 Platelets
Jaundice  PT/APTT
 Enzymes  Protein C
 Albumin  D-dimer
 PT
 Diagnosis
 Obtain appropriate cultures before starting antibiotics
provided this does not significantly delay antimicrobial
administration (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. Sonography
suitable, transport outside unit may be dangerous)
Guidelines for Management of Severe Sepsis and
Septic Shock
 I. MANAGEMENT OF  II. SUPPORTIVE THERAPY
SEVERE SEPSIS OF SEVERE SEPSIS
 Initial Resuscitation  Mechanical Ventilation of
 Diagnosis Sepsis-induced ALI/ARDS
 Antibiotics Therapy  Sedation, Analgesia, and
N-M Blockade in Sepsis
 Source Control
 Fluid therapy
 Glucose Control
 Vasopressors
 Renal Replacement
 Inotropic Therapy
 Bicarbonate Therapy
 DVT Prophylaxis
 Corticosteroid
 Recombinant Human
 Stress Ulcer Prophylaxis
Activated Protein C  Selective Digestive Tract
(rhAPC) Decontamination (SDD)
 Blood Product  Consideration for
Administration Limitation of Support
 III. Pediatric Consideration
 Antibiotic Therapy
 Begin intravenous antibiotics as early as possible
and always within the first hour of recognizing
severe sepsis and septic shock
 In the presence of septic shock, each hour delay in
achieving administration of effective antibiotics is
associated with a measurable increase in mortality
 Broad-spectrum: one or more agents active
against likely bacterial/fungal pathogens and
with good penetration into presumed source
 Antibiotic Therapy
 Reassess antimicrobial regimen daily
to optimize efficacy, prevent
resistance, avoid toxicity, and
minimize costs consider combination
therapy in Pseudomonas infections
 Consider combination empiric therapy

in neutropenic patients
 Antibiotic Therapy
 Combination therapy 3–5 days and de-
escalation following susceptibilities (To
single therapy)
 Duration of therapy typically limited to 7–10
days; longer if response is slow or there are
undrainable foci of infection or immunologic
deficiencies
 Stop antimicrobial therapy if cause is found
to be noninfectious
 Vasopressors
Dopamine 2-5 µg/kg/min Pharmacologic effects
(dopaminergic range) are dose dependent:
5-10 µg/kg/min renal and mesentric
(dopaminergic &  vasodilation
range) predominate at lower
10-20 µg/kg/min dose; cardiac
( range) stimulation and
20-50 µg/kg/min vasoconstriction
( range) develop as the dose is
increased
Dobutamine 2.5-25 µg/kg/min Selective 1 agonist

Noreepinephrin 0.02-0.25 µg/kg/min  and 1 agonist

Vasopressin 0.4-1.0 unit/min V1 receptor agonist

 Inotropic Therapy
 Use dobutamine in patients with
myocardial dysfunction as supported by
elevated cardiac filling pressures and low
cardiac output (check cardiac output)
 Do not increase cardiac index to
predetermined supranormal levels
 Human Activated Protein C in
Septic Shock
 Activated protein C had anti-thrombotic,
anti-inflammatory and pro-fibrinolytic
properties
 Drotrecogin Alfa is the first anti-inflammatory
agent that proved effective in the treatment
of sepsis
 Dose : 24 microgram / kg /min in infusion
 Blood Product Administration

 Administer platelets when

 Counts are 5000/mm3 (5x 109/L) regardless of
bleeding
 Counts are 5000–30,000/mm3 (5–30x109/L) and
there 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
 Renal Replacement
 Absence of hemodynamic instability
 Intermittent hemodialysis and continuous
venovenous filtration equal (CVVH)

 Hemodynamic instability
 CVVH preferred --- to facilitate management
of fluid balance in septic patients,
no improved in regional perfusion and survival
benefit
 Bicarbonate Therapy

 Bicarbonate therapy not recommended to

improve hemodynamics in patients with
hypoperfusion-induced lactic acidemia pH
>7.15
• Will increase Na, fluid overload,
increase lactate and PCO2
 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 procedure
undertaken by limiting the use of indwelling
vascular and bladder catheters.
• Incidence and duration of profound
nutropenia <500 neutrophils/L
• Aggressively treating localize nosocomial
infection.
• Indiscriminate use of antimicrobial agents
and glucocorticoids should be avoided.