NEW SEPSIS GUIDELINES

1. PRESENTED BY
MAJ SANKAR J

2. DEFINITION
2012 2016
Sepsis: Presence of infection together
with systemic manifestation of
infection.
Sepsis : life threatening organ
dysfunction caused by dysregulated
host response to infection.
Severe sepsis : sepsis-induced organ
dysfunction or tissue hypo perfusion.
Septic shock : sepsis-induced
hypotension persisting despite fluid
resuscitation.
Septic shock: is a subset of sepsis with
underlying circulatory and
cellular/metabolic abnormalities.

3. INITIAL RESUSCITATION
2012 2016
1.Goals during first 06 hours of
resuscitation.
2.Normalisation of lactate levels.
1.Immediate resuscitation.
2.Atleast 30 ml/kg crystalloid with in 3 hrs.
3.Additional fluids be guide by frequent
assessment of hemodynamic status.
5.Dynamic over static variables.
6.MAP 65 mm Hg .
7.Normalize lactate.

4. SCREENING FOR SEPSIS AND
PERFORMANCE IMPROVEMENT
2012 2016
1.Routine screening of potentially
infected seriously ill patients.
2.Hospital based performance
improvement efforts.
1.Hospitals and hospital systems have a
performance improvement program for
sepsis.

5. DIAGNOSIS
2012 2016
1.Cultures as clinically appropriate.
2.Use of 1-3 b –D –glucan assays and
anti mannan antibody assays.
3. Prompt imaging studies
1.Routine microbiological cultures to
be obtained before antimicrobials.

6. ANTIMICROBIAL THERAPY2012 2016
1.Effective antimicrobials with in first
hour.
2.Emperical anti infective therapy.
3.Re assessment for de-escalation.
4. Procalcitonin levels.
5.Combination therapy for neutropenic
patient with severe sepsis and MDR
pathogens.
6. Duration of empirical antibiotics.
7.Duration of therapy.
1.Early IV antimicrobials .
2.Emperical broad spectrum therapy.
3.Descalation.
4. Procalcitonin levels .
5.Dosing strategies based on accepted
pharmacodynamic/pharmacokinetic
and specific properties of the drug.

7. ANTIMCROBIAL THERAPY
2012 2016
8.Antiviral therapy .
9.Antimicrobial agents should not be used
in severe inflammatory states of non
infectious cause.
6.Combination therapy not to be used in
sepsis with out shock.
7.No antibiotic prophylaxis in inflammatory
states of non infectious origin.
8.De-escalation .
9.Antimicrobial duration .
10.Short courses of antimicrobials where
rapid clinical resolution.

8. SOURCE CONTROL
2012 2016
1.Specific anatomic diagnosis of
infection, source control and
intervention.
2.Effective intervention associated with
least physiologic insult.
3. Removal of intravascular access.
1.Specific anatomic diagnosis of
infection source control, intervention.
2.Prompt removal of intravascular
access and devices.

9. FLUID THERAPY
2012 2016
1.Crystalloids .
2.Use of hydroxy ethyl starches .
3.Albumin in fluid resuscitation.
4.Initial fluid challenge of 30 ml/kg.
5. Improvement based on dynamic or
static variables.
1.Fluid challenge technique.
2.Crystalloids .
3.Either balanced crystalloids or saline .
4.Hydroxy ethyl starch .

10. VASO ACTIVE MEDICATION2012 2016
1. Target MAP of 65 mm Hg.
2.Norepinephrine is the first choice.
3.Epinephrine as an additional agent is
required.
4.Vasopressin.03 units/min can be
added to nor epinephine.
5.Low dose vasopressin is not
recommended as the initial choice.
1. Nor epinephrine as the first choice
vasopressor.
2. Adding vasopressin to nor
epinephine.
3. Dopamine in selected patients.
4. Low dose dopamine for renal
protection is not recommended.

11. VASO ACTIVE MEDICATION
2012 2016
6.Dopamine in highly selected
patients.
7.Low dose dopamine should not be
used for renal protection.
8. Arterial catheter.
9.Dobutamine infusion.
5.Dobutamine in patients with
persistent hypo perfusion .
6. Arterial catheter.

12. CORTICOSTEROIDS
2012 2016
1.IV hydrocortisone at dose of 200
mg/day .
2.Not using ACTH stimulation test.
3.Tapering of steroids.
4. No corticosteroid in the absence of
shock.
1. IV hydrocortisone at dose of 200
mg/day .

13. BLOOD PRODUCTS
2012 2016
1.Blood transfusion when Hb less
than 7g/dl t, target Hb 7-9 g/dl.
2.No erythropoietin.
3. No FFP in absence of bleeding or
planned invasive procedures.
4.No anti thrombin.
5.Administation of platelets.
1.Blood transfusion occur only when
Hb <7.0g/dl .
2.No erythropoietin.
3.Use of FFP to correct clotting
abnormalities in absence of bleeding
not recommended.
5.Administation of platelets.

14. IMMUNOGLOBULINS
2012 2016
1.Not using IV immunoglobulin in adult
patients with severe sepsis or septic
shock.
1.Not using IV immunoglobulin in adult
patients with severe sepsis or septic
shock.

15. BLOOD PURIFICATION
2012 2016
Not applicable No recommendations

16. ANTI COAGULANTS
2012 2016
Not applicable 1.Use of antithrombin for the
treatment of sepsis and septic shock
not recommended.
2.No recommendation regarding the
use of thrombomodulin or heparin

17. MECHANICAL VENTILATION2012 2016
1.Tidal volume 6ml/kg.
2.Plateau pressure<30 cm H2O.
3.Positive and high PEEP.
4.Recruitment manners .
6.Prone position
.
7.Head end elevation 30-45 degrees.
8.NIV .
9.Weaning protocol.
10. pulmonary artery catheter.
1. Tidal volume 6 ml/kg.
2. Plateau pressure 30 cm H2O.
3.Higher PEEP.
4.Recruitment manouevers.
5.Prone ventilation.
6.Recommend against using HFV.
7.No recommendation for NIV.
8.Neuro muscular blocking agents.

18. MECHANICAL VENTILATION
2012 2016
11.Conservative fluid strategy.
12.In the absence of specific
indications such as
brochospasm,not using beta 2
agonists for the sepsis induced
ARDS.
9.Conservative fluid strategy .
12.In the absence of specific indications
such as brochospasm,not using beta 2
agonists for the sepsis induced ARDS.
13. pulmonary artery catheter.
14.Low tidal volume in adults with
adults with sepsis induced
respiratory failure with out ARDS.
15.Spontaneous breathing trials .
16.Head end elevation.

19. SEDATION AND ANALGESIA
2012 2016
1.Continous intermittent sedation
should be minimized.
2.NMBA to be avoided.
3.Short course of NMBA in early sepsis
induced ARDS.
1.Continous and intermittent sedation
be minimized.

20. GLUCOSE CONTROL
2012 2016
1.Upper target glucose level <180 mg/dl.
2.Blood glucose monitoring.
3.Capillary blood glucose should be
interpreted with caution.
1.Upper target glucose level <180 mg/dl.
2.Blood glucose monitoring.
3.Capillary blood glucose should be
interpreted with caution.
4.Arterial blood rather than
capillary blood for glucose
monitoring .

21. RENAL REPLACEMENT THERAPY
2012 2016
1.Continous RRT and intermittent
haemodialysis are equivalent in patients
with severe sepsis and renal failure.
2.Use continuous therapies to facilitate
management of fluid balance in
haemodynamically unstable patients.
1.Continous RRT and intermittent
haemodialysis are equvalent .
2.Use continous therapies to facilitate
management of fluid balance.
3.Against the use of RRT in patients
with sepsis and acute kidney injury
for increase in creatinine or oliguria
with out other definitive indications
for dialysis.

22. BICARBONATE THERPY
2012 2016
1.Not using sodium bicarbonate therapy
for the purpose of improving
haemodynamics or reducing
vasopressor requirements in patients
hypoperfusion-induced lactic acidemia
with Ph>7.15.
1.Not using sodium bicarbonate therapy
for the purpose of improving
haemodynamics or reducing
vasopressor requirements in patients
hypoperfusion-induced lactic acidemia
with Ph>7.15.

23. VTE PROPHYLAXIS
2012 2016
1.Daily prophylaxis against VTE with
LMWH or UFH.
2.Combination of pharmacological and
intermittent pneumatic compression.
3.In case of contraindication to heparin
mechanical prophylactic treatment.
1.Pharcacological prophylaxis against
UFH or LMWH against VTE .
2.We recommend LMWH rather
than UFH for VTE prophylaxis.
3.Combination of pharmacological and
intermittent pneumatic compression.
4.Mechahnical VTE prophylaxis where
pharmacologic VTE is contraindicated.

24. STRESS ULCER PROPHYLAXIS
2012 2016
1.Stress ulcer prophylaxis using H2
blockers or PPI in patients with
bleeding risk factors.
2.PPI is preferred to H2 blockers.
3.No prophylaxis in patients with out
risk factors.
1.Stress ulcer prophylaxis using H2
blockers or PPI in patients with
bleeding risk factors.
2.Either PPI or H2 blockers is
indicated.
3.No prophylaxis in patients with out
risk factors.

25. NUTRITION
2012 2016
1.Either oral or enteral feeding as
tolerated with in the first 48 hrs.
2.Avoid mandatoy full calorie feeding.
3.Use IV glucose and enteral nutrition
rather than TPN alone in the first 7
days.
4.Use nutrition with no
immunomodulating supplementation.
5.No using IV selenium .
1.Early parentral nutrition alone or
parentral nutrition in combination with
enterall feedings in critical patients who
can fed enterally is not recommended.
2.Initiate IV glucose and advance enteral
feeds as tolerated in the first 7 days
where enteric feeding not possible.
3.Early initiation of enteral feeding.
4.Trophic/hypocaloric feed is the initial
startegy.

26. NUTRITION
2012 2016
5.Omega 3 fatty acids not
recommended.
6.Routine monitoring of gastric
residual volume not recommended.
7. Prokinetic agents.
8. Post pyloric feeding tubes .
9.Use of IV selenium not
recommended.
10 Arginine,glutamine and carnitine not
recommended.

27. SETTING GOALS OF CARE
2012 2016
1.Discuss the goals of care and prognosis
with patients and families.
2.Incorporate goals of care into
treatment and end of life care planning
,utilizing palliative care principles .
3.Address goals of care as early as
possible.
1.Discuss the goals of care and prognosis
with patients and families.
2.Incorporate goals of care into
treatment and end of life care planning
,utilizing palliative care principles.
3.Address goals of care as early as
possible.

28. INVESTIGATIONAL THERAPIES
1.Inhibition of innate immunity.
2.Cytokine and endotoxin inactivation or removal.
3.Interferon gamma.
4.GM-CSF.
5.Augmentation of immunomodulation.
6.Inhibition of pro inflammatory gene expression.
7.Haemofiltration.
8.Naloxone.
9.Pentoxiphyline.
10.Statins.
11.Beta blockade

29. INHIBITION OF INNATE IMMUNITY
 TLR-4 antagonist-Eritoran.
 Resatorvid.

30. CYTOKINE AND ENDOTOXIN
INACTIVATION.
 Haemoperfusion through a membranous polymixin B
fibre coloumn.
 Haemoperfusion through sorbent containing
catridges(haemeadsorption)
 Cytosorb appears to be more promising.
 Does not remove potentially inflammatory
molecules,endotoxin and interleukin-10.
 Plasma or whole blood exchange.
 Coupled plasma filtration adsorption(CPFA).

31. INTERFERON -GAMMA
 May restore monocytic cell function.

32. GM-CSF
 Increased peripheral cell count.
 May reduce the length of hospital stay and infectious
complicatons and duration of antimicrobial therapy.
 Large trials are necessary.

33. AUGMENTATION OF
IMMUNOMODULATION
 Antibodies against macrophage inhibition factor.
 Might restore or augment the immunomodulatory
action of endogenous glucocorticoids.
 Not yet studied in humans.

34. ANTI PRO INFLAMMATORY GENE
EXPRESSION
 Inhibits super antigen induced expression of certain
pro inflammatory genes by limiting T-cell activation.

35. HEMOFILTRATION
 Initial studies suggested benefit.
 Recent meta analysis and multicentre prospective
study (IVORE )suggested no benefit.

36. NALOXONE
 Led to haemodynamic improvement.
 Did not improve case fatality rate.

37. PENTOXYPHYLINE
 Decreased red cell deformity and platelet aggregation
are migitated by pentoxyphyline.
 Inhibits neutrophil adhesion and activation and
modulates endotoxin-induced expression of pro
inflammatory cytokines.

38. STATINS
 Supression of endotoxin induced up regulation of
TLR-4 and TLR-2.

39. BETA BLOCKADE
 Greater decline from the base line heart rate.
 Reduced need for vasopressors.
 Reduced need for fluid replacement therapy.

40. THANK YOU