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S IRS
SYSTEMIC INFLAMMATORY RESPONSE SYNDROM
Manifested by two or more of the following:
• Temperature > 38C or < 36C
• Heart rate > 90 beats/min
• Respiratory rate > 20 /min or PaCO2 < 32 mm Hg
• WBC > 12,000, < 4000, or > 10% immature (band)
forms

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 SIRS- LACK SPECIFICITY
SIRS criteria c a n b e p r es en t in many hospitalised pt
who d onot develop infection.
NON INFECTIOUS CONDITIONS WITH SIRS
PANCREATITIS
VASCULITIS
AUTO IMMUNE DISORDERS
BURNS
SURGERY
THROMBOEMBOLISM
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 S EP S IS
INFECTION
Inflammatory response to microorganisms or invasion of normally
sterile tissues

SEPSIS
The systemic response to infection – i.e., confirmed or suspected
infection plus ≥ 2 SIRS criteria

ACCP/SCCM Consensus Statement. Chest. 1992;

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 Why new definitions
Definitions of sepsis and septic shock were last
revised in 2001.
Considerable advances have since been made into the
pathobiology (changes in organ function, morphology,
cell biology, biochemistry, immunology, and circulation),
management, and epidemiology of sepsis,
ECONOMIC BURDEN,, MORTALITY
suggesting the need for reexamination
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 SEPSIS 3

Sepsis is life-threatening organ dysfunction

caused
by a dys-regulated host response to infection

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SEPSIS is life-threatening o rg an dysfunction caused
by a dys-regulated h o s t r e s p o n s e to infection

• So … “sepsis” now = the old “severe sepsis

• As opposed to the “regulated host response”
that characterizes the non-septic response to infection

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 NEW DEFINATION
ADVANTAGES
• Incorporates most up-to-date thinking on sepsis pathobiology
• Provides closest approximation possible to describing
“what sepsis is”

CONCERNS
• Of limited practical utility a s they contain elements that cannot
be clinically identified
• “organ dysfunction”
• “dysregulated host response
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 RISK FACTORS SEPSIS
• ICU Admissions ( nosocomial infections)
• Bacteremia
• Advanced age ≥65 yrs
• Immunosuppresion ( comorbidies, drugs)
• DM, CANCER
• CAP ( approx 50% sepsis)
• Previous hospitalisation
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 The Validity of SIRS challenged
• SIRS criteria have been used to diagnose
sepsis for more than 20 years.
• “SIRS no longer has any legs ….. Itsounded
like a good idea in 1990 , but it has lost
steam…..”
• Poor concurrent Validity

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SOFA SCORE
 Limitations of SOFA
• The SOFA score identifies Pt septic both in &out of
ICU. But it involves the use of many lab tests and is a
bit complex.
• Cumbersome due to multiple variables
• Not well known outside ICU setting
• Variables &cutoff values developed by consensus
• For patients not in the ICU, the performance of Quick
SOFA score was similar to that of the SOFAscore .
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SOFA &LODS Superior in ICU

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qSOFA similar to complex scores outside the ICU

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 Q SOFA
• Poor man’s SOFA
• Quick and repeat bedside test
• No laboratory test required
• Outside ICU settings
• Emergency, WARDS.

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To Summarize….

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SEPTIC SHOCK

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 1991 &2001 Septic Shock definitions
1991
Sepsis-induced hypotension, persisting despite adequate
fluid resuscitation, along with the presence of hypoperfusion
abnormalities or organ dysfunction
2001
State of acute circulatory failure characterized by persistent
arterial hypotension unexplained by other causes
Neither definition p r o p o s e d explicit criteria
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Shankar-Hari M, Phillips GS, Levy ML et al.

Developing a New Definition a n d A s s e s s i n g New Clinical Criteria for Septic

Shoc k For the Third International C o n s e n s u s Definitions for S e p s i s a n d
Septic Shoc k (Sepsis-3)

JAMA 2016; 315: 775-787

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 SEPTIC SHOCK 2016
SEPTIC SHOCK is a subset of sepsis
in which profound
circulatory, cellular and metabolic abnormalities
are associated with a
greater risk of mortality than with sepsis alone
(40% vs 10%)

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 Clinical criteria for Septic shock

Meta-analysis a n d sy stemic reviews from Ja nua ry 1, 1992- December 25,2015

44 septic s h o c k st udi e s
166,479 patients
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 Three variables identified
• Hypotension
• Elevated serum lactate level
• Sustained need for vasopressor therapy

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Lactate > 2 mmol/L for predicting mortality in Septic Shock
• Sensitivity = 82.5 %
• Specificity = 22.4 %
• Mortality significantly higher in patients with fluid resistant
hypotension requiring vasopressors &hyperlactatemia (42.3 %)
vs
Hyperlactatemia alone “or”
Fluid resistant hypotension requiring vasopressors
but Lactate level ≤ 2 mmol/L (30.1%)
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WHY HYPOTENSION &
HYPERLACTATEMIA
 How it differs from old defination
• Both serum lactate level and vasopressor-
dependent hypotension instead of either alone
• Lower serum lactate level cutoff of 2 mmol/L vs 4
mmol/L a s currently used in the SSC definitions

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 Conclusions
DEFINITION
Septic shock is defined a s a subset of sepsis in which
underlying circulatory, cellular and metabolic abnormalities are
associated with a greater risk of mortality than sepsis alone
CLINICAL CRITERIA
• Hypotension requiring use of vasopressors to maintain MAP
≥65 mmHg
• having a serum lactate >2 mmol/l
• Persisting despite adequate fluid resuscitation
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FLOWCHART

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2002 2016
X

X
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 Controversies and limitations
• Most data extracted from US database
• q SOFA and SOFA can miss occult organ dysfunction
• Specific infections can cause local organ dysfunction
without dysregulated systemic host response
• Non- availability of lactate measurements in resource
poor settings
• Task force focused on adult patients

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 Some of the concerns raised …
• ‘SOFA won’t be measured daily on every patient’
• ‘do I need to measure SOFA twice to measure change’
• ‘lactate should be in the sepsis criteria’
• ‘lactate should go from the septic shock criteria’
• ’80% of the world cannot measure lactate’
• ‘why not shock = hyperlactatemia OR hypotension?’
• ‘patients will die if we wait until qSOFA hits ≥2 before treating’
• ‘why don’t we just use qSOFA to diagnose sepsis?’
• ‘the coders won’t like it’
• ‘what about children?’ …
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 Treat the patient in front of you
• NOT suggesting that infected patients shouldn’t be
actively managed until qSOFA≥2 or SOFA ≥2
• so treat infection, oliguria, hypoxaemia etc a s
indicated
• .. do not wait until criteria met

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