1. The document outlines new definitions and guidelines for diagnosing and managing sepsis and septic shock according to the Surviving Sepsis Campaign: International Guidelines for Management of Sepsis and Septic Shock: 2016. 2. Key changes include removing SIRS criteria and defining sepsis as a life-threatening organ dysfunction caused by a dysregulated host response to infection. Septic shock requires vasopressors to maintain blood pressure and elevated lactate levels. 3. Management guidelines cover initial patient assessment, diagnostic testing, antimicrobial therapy, fluid resuscitation, vasopressors, corticosteroids, mechanical ventilation, glucose control, nutrition, and thromboembolism prophylaxis

1. Sepsis andSepticShock
(SEPSIS–3)
Surviving Sepsis Campaign: International Guidelines
for Management of Sepsis and Septic Shock: 2016
Amiteshwar Singh
SETH G.S. MEDICAL COLLEGE AND KEM HOSPITAL, MUMBAI

2. New
Definitions  The SIRS criteria have been removed.
 It may present in simple, non-complicated
infection, or in response to non infectious-
triggers (i.e. polytrauma, pancreatitis, post-
cardiac arrest syndrome),
 Or may even be absent in critically ill patients
with obvious evidence of a life-threatening
infection.
Sepsis is defined as
LIFE-THREATENING
ORGAN DYSFUNCTION
CAUSED BY A DYSREGULATED HOST
RESPONSE
TO INFECTION.

3. New
Definitions
 Septic shock is defined by persisting
hypotension requiring vasopressors to
maintain a mean arterial pressure of 65
mm Hg or higher and a serum lactate
level greater than 2 mmol/L (18 mg/dL)
despite adequate volume resuscitation.
 Septic shock is a subset of sepsis with
circulatory and cellular/metabolic
dysfunction associated with a higher
risk of mortality.
Terms like Severe Sepsis/Septicemia
has been removed

5. Clinical
Presentation
Signs and symptoms of sepsis
are often nonspecific and
include the following:
Fever, chills or rigors
Confusion
Anxiety
Difficulty breathing
Fatigue, malaise
Nausea and vomiting

6.  Physical examination should first involve
assessment of patients general
condition including the ABCs.
 Followed by identification of localizing
signs to a particular organ system.
 Shock can be identified with presence of
signs of poor perfusion such as cool skin,
cold extremities and delayed capillary
refill.
Clinical
Presentation

7. MANAGEMENT

8. Diagnosis
 CBC
 Coagulation studies
 Blood chemistry (eg, sodium, chloride,
magnesium, calcium, phosphate, glucose,
lactate)
 Arterial blood gas analysis
 RFT and LFT (eg, creatinine, blood urea
nitrogen, bilirubin, alkaline phosphatase, alanine
aminotransferase, aspartate aminotransferase,
albumin, lipase)
 Blood cultures
 Urinalysis and urine cultures
 Gram stain and culture of secretions and tissue

9. Imaging  Chest, abdominal, or extremity
radiography
 Abdominal ultrasonography
 Computed tomography of the body
part suspected to be origin of sepsis.

10. DIAGNOSIS
 Two or more sets (aerobic and
anaerobic) of blood cultures are
recommended before initiation of any
new antimicrobial in all patients with
suspected sepsis
 Other sites and bodily fluids may be
Cultured as clinically appropriate.
 Within 45 minutes

11. Initial
Resuscitation
 In the resuscitation from sepsis induced
hypoperfusion, at least 30 mL/kg of IV
crystalloid fluid be given within the first 3 hours
 Additional fluids should be guided by frequent
reassessment of hemodynamic status
 Reassessment should include evaluation of
available physiologic variables
 heart rate
 blood pressure
 arterial oxygen saturation
 respiratory rate
 urine output ≥ 0.5 mL/kg/hr
 CVP of 8–12 mm Hg
 Target mean arterial pressure of 65 mm Hg in
patients with septic shock requiring
vasopressors.
 Decrease in lactate levels may be used to guide
resuscitation.

12.  IV antimicrobials be initiated as soon as
possible after recognition and within
one hour for both sepsis and septic
shock.
 Empiric broad-spectrum therapy with
one or more antimicrobials is
recommended.
 Antimicrobial therapy should be
narrowed once pathogen identification
and sensitivities are established and/or
adequate clinical improvement is noted.
 7 to 10 days is adequate for most serious
infections associated with sepsis and
septic shock.
ANTIMICROBIAL
THERAPY

13.  Decision for empiric antimicrobial is driven by
factors such as
 Anatomic site of infection
 Prevalent pathogens within the community,
hospital, and even hospital ward
 The resistance patterns of those prevalent
pathogens
 The presence of specific immune defects
such as neutropenia, splenectomy, poorly
controlled HIV infection,
 Age and patient comorbidities including
chronic illness (e.g., diabetes) and chronic
organ dysfunction (e.g., liver or renal
failure) that compromise the defense to
infection.
ANTIMICROBIAL
THERAPY

14. SOURCE
CONTROL
 The principle of source control in the
management of sepsis and septic shock
includes removal of the potential source
of ongoing microbial contamination.
 For example
 The drainage of an abscess,
 Debridement of infected necrotic
tissue
 Peritoneal wash and closing
gastrointestinal perforation
 A time lag of no more than 6 to 12 hours
after diagnosis should be targeted for
source control after initial resuscitation.

15. FLUID
THERAPY
 Crystalloids are the fluid of choice for
initial resuscitation and subsequent
intravascular volume replacement
 Albumin should be used in addition to
crystalloids for initial resuscitation and
subsequent intravascular volume
replacement when substantial amounts
of crystalloids are required
 Crystalloids to be preferred over
Gelatins
 Use of hydroxyethyl starches is not
recommended

16. VASOACTIVE
MEDICATIONS
 InitiateVasopressor therapy if MAP is
persistently below 65 mm Hg despite adequate
fluid resuscitation.
 Noradrenaline as the first-choice vasopressor
 2nd line vasopressors include adrenaline or
vasopressin
 Dopamine as an alternative vasopressor agent to
norepinephrine may be used only in highly
selected patients (e.g., patients with low risk of
tachyarrhythmias or with low heart rate)
 Low-dose dopamine for renal protection is no
longer recommended.
 Dobutamine may be administered or added to
vasopressor (if in use) in the presence of (a)
myocardial dysfunction or (b) persistent
hypoperfusion, despite achieving adequate
intravascular volume and adequate MAP

17. CORTICO-
STEROIDS
 IV hydrocortisone at a dose of 200 mg
per day is recommended if adequate
fluid resuscitation and vasopressor
therapy are unable to restore
hemodynamic stability.
 Taper steroids once vasopressors are not
required.

18. BLOOD
PRODUCTS
 Transfuse packed RBC only when hemoglobin
concentration decreases to < 7.0 g/dL in adults in
the absence of extenuating circumstances, such as
myocardial ischemia, severe hypoxemia, or acute
haemorrhage.
 Fresh frozen plasma (FFP) may be transfused only
when there is a documented deranged coagulation
profile (increased PT/INR) and the presence of
active bleeding or before surgical or invasive
procedures.
 Prophylactic platelet transfusion is recommended
when counts are < 10,000/mm3 in the absence of
apparent bleeding and when counts are <
20,000/mm3 if the patient has a significant risk of
bleeding. Higher platelet counts (≥ 50,000/mm3)
are advised for active bleeding, surgery, or
invasive procedures

19. MECHANICAL
VENTILATION
 The goals of mechanical ventilation
include the following:
 Improving gas exchange
 Reducing work of breathing
 Avoiding oxygen toxicity
 Minimizing high airway pressures
 Avoiding further lung damage
 Allowing the injured lung to heal
 Management of ARDS using lung
protective proctocols.

20. GLUCOSE
CONTROL
 Target an upper blood glucose level ≤
180 mg/dL
 Monitor Blood Glucose Q2H till glucose
and insulin infusion rates are stable,
then every 4 hours thereafter.

21. BICARBONATE
THERAPY
 No to use of sodium bicarbonate
therapy to improve
hemodynamics or to reduce
vasopressor requirements in
patients with hypoperfusion-
induced lactic acidemia with pH ≥
7.15

22. VENOUS
THROMBO-
EMBOLISM
PROPHYLAXIS
 Combination pharmacologicVTE
prophylaxis and mechanical
prophylaxis is recommended,
whenever possible.
 LMWH rather than UFH for
PharmocologicalVTE prophylaxis
in the absence of contraindications
to the use of LMWH

23. STRESS
ULCER
PROPHYLAXIS
 Use of either proton pump
inhibitors or histamine-2 receptor
antagonists is recommended for
stress ulcer prophylaxis

24. NUTRITION
 Early initiation of enteral feeding rather
than a complete fast or only IV glucose is
recommended in critically ill patients with
sepsis or septic shock who can be fed
enterally.
 Use of parenteral nutrition alone or in
combination with enteral feeding is not
recommended in the first 7 days
 Use of arginine, glutamine, omega-3 fatty
acids as an immune supplement is not
recommended.
 Consider placement of post-pyloric feeding
tubes in critically ill patients with feeding
intolerance or who are considered to be at
high risk of aspiration

25. TAKE HOME
MESSAGE
 Start adequate antibiotic therapy (proper
dosage and spectrum) as early as possible.
 Resuscitate the patient, using supportive
measures to correct hypoxia, hypotension,
and impaired tissue oxygenation
(hypoperfusion)
 Identify the source of infection, and treat
with antimicrobial therapy, surgery, or both
(source control)
 Earlier inotropes, use noradrenaline
 Maintain adequate organ system function,
guided by cardiovascular monitoring, and
interrupt the progression to multiple organ
dysfunction syndrome (MODS)