1. Sepsis is a major cause of morbidity and mortality worldwide, with mortality rates ranging from 15-60% depending on the severity. The guidelines provide recommendations for the management of sepsis, severe sepsis, and septic shock. 2. The initial focus is on early recognition and treatment within the first hour including antibiotics, fluid resuscitation, lactate monitoring, and source control. Vasopressors, inotropes, steroids and other supportive care measures are also addressed. 3. Goals are to diagnose and treat the infection while restoring tissue perfusion and organ function through a coordinated response and supportive therapies.

1. International Guidelines for
Management of Severe
Sepsis and Septic Shock
2012

2. Presented by
Dr.Nabina Lala
IMO(Medicine)
CMCH

4. INTRODUCTION
•Major cause of morbidity and mortality
worldwide.
•Mortality
Sepsis: 15% - 30%
Severe sepsis & Septic Shock :40%-60%
Mortality is highest among the elderly

5. Risk factors
•Extemesof age(<10yrs and > 70 yrs)
•DM,CLD,alcoholism,malignancy
•Immunosupression(immunosupressive
therapy,corticosteroid,IV drug abusers,organ
and bone marrow transplant
recipients,complement deficiencies)
•Major surgery ,trauma ,burns

6. •Invasive procedures
(catheters,intravascular device,prosthetic
device,hemodialysis and peritoneal dialysis
catheters,or endotracheal tubes)
•Previous antibiotic treatment
•Prolonged hospitalization
•Malnutrition,child birth,abortion.

7. Definitions

8. Widespread inflammatory response to a
variety of severe clinical insults is known to as
SIRS.
Clinically recognized by the presence of 2 or
more of the following:
-Temperature >38C or < 36C
-Heart Rate >90
-Respiratory Rate > 20 or PaCO2 <32
-WBC > 12,000, < 4000 or > 10% immature forms

9. Sepsis is defined as the presence of infection
together with systemic manifestations of
infection.
Severe sepsis is defined as sepsis plus
sepsis-induced organ dysfunction or tissue
hypo perfusion.

10. Sepsis-induced hypotension is defined as
a systolic blood pressure(SBP) < 90 mm
Hg or mean arterial pressure (MAP) < 70
mmHg or a absence of other causes of
hypotension.
Septic shock is defined as sepsis-induced
hypotension persisting despite adequate
fluid resuscitation

14. MANAGEMENT
• Initial Resuscitation and Infection Issues
• Hemodynamic Support &
AdjunctiveTherapy
• Supportive Therapy of Severe Sepsis

15. Initial Resuscitation and Infection Issues

16. A. Initial Resuscitation
1.During the first 6 hrs of resuscitation, the goals of
initial resuscitation of sepsis-induced hypoperfusion
should include all of the following as a part of a
treatment protocol:
a) CVP 8–12 mm Hg
b) MAP ≥ 65 mm Hg
c) Urine output ≥ 0.5 mL ・ kg ・ hr
d) Superior vena cava oxygenation saturation (Scvo2)
or mixed venous oxygen saturation (Svo2) 70% or
65%,respectively.
2. We suggest targeting resuscitation to normalize
lactate in patients with elevated lactate levels as a
marker of tissue hypoperfusion

17. B. Screening for Sepsis and
Performance Improvement
•Routine screening of seriously ill patients
for severe sepsis to increase the early
identification of sepsis allow implementation
of early sepsis therapy.
•Performance improvement efforts to
improve patient outcomes and decrease
sepsis-related mortality.

18. The SSC guidelines and bundles can be
used as the basis of a sepsis performance
improvement program.
Application of the SSC sepsis bundles led
to sustained, continuous quality
improvement in sepsis care and was
associated with reduced mortality.

20. C. Diagnosis
• Cultures before antibiotic therapy
-Without causing significant delay
• At least 2 blood cultures (both aerobic and
anaerobic)
-percutaneous
-drawn through each lumen of each vascular
access device(if >48 hrs)
• Imaging studies in attempts to confirm a
potential source of infection

21. Other Cultures if indicated- Urine, CSF,
sputum etc.
Vol of blood sample > 10ml
1,3 β-d-glucan assay , mannan and anti-
mannan antibody assays
-If invasive candidiasis suspected

22. D. Antimicrobial Therapy
1.The administration of effective intravenous
antimicrobials within the first hour of
recognition of septic shock and severe
sepsis without septic shock should be the
goal of therapy.

23. 2a. Initial empiric anti-infective therapy of one
or more drugs that have activity against all
likely pathogens and that penetrate in
adequate concentrations into tissues
presumed to be the source of sepsis .
2b. Antimicrobial regimen should be
reassessed daily for potential de escalation .

24. 4a.Combination empiric therapy (>=2 )
-Neutropenic patients with severe sepsis
-Difficult-to-treat,multidrug-resistant bacterial
pathogens such as Acinetobacter and
Pseudomonas.
-For patients with severe infections
associated with respiratory failure and septic
shock.

25. Extended spectrum beta-lactam + AGS/FQs
for P. aeruginosa bacteremia
Beta-lactam and macrolide for bacteremic
Streptococcus pneumoniae infections
Not for more than 3–5 days
-

26. De-escalation to the most appropriate
single therapy as per susceptibility.
Duration of therapy 7–10 days.
Longer courses if
-slow clinical response
-undrainable foci of infection
-bacteremia with S. aureus
some fungal and viral infections
-immunologic deficiencies

27. E. Source Control
•Specific anatomical diagnosis of infection
•Intervention for source control within the
first 12 hr of diagnosis.
•Source control with least physiological
insult in severe sepsis.

28. Intravascular access suspected to be
source of severe sepsis or septic shock –
remove promptly after other vascular
access has been established.
Surgical intervention done when minimally
invasive approaches are inadequate / when
diagnostic uncertainty persists despite
imaging.

29. F. Infection Prevention
•Selective oral decontamination with Oral
chlorhexidine gluconate has been shown
to reduce VAP
•Selective digestive decontamination

30. HAEMODYNAMIC SUPPORT &
ADJUNCTIVE THERAPY

31. •FLUID THERAPY
•VASOPRESSORS
•INOTROPIC SUPPORT
•CORTICOSTEROIDS

32. FLUID THERAPY

33. •Crystalloids
•Against the use of hydroxyethyl starches.
Albumin for fluid resuscitation when patients
require substantial amounts of crystalloids
•Initial fluid challenge in patients with sepsis-
induced tissue hypoperfusion & suspected of
hypovoluemia @ 30 mL/kg of crystalloids.`

34. VASOPRESSORS

35. •Target a mean arterial pressure (MAP) of 65 mm
Hg
•Norepinephrine as the first choice
Epinephrine added when an additional agent is
needed to maintain adequate B.P.
•Vasopressin 0.03 U/min added to NE for raising
MAP or decreasing NE dosage .

36. •Low dose vasopressin not recommended
as the single initial vasopressor for sepsis-
induced hypotension
•Vasopressin doses > 0.03-0.04 U/min
reserved for salvage therapy
•Dopamine as an alternative vasopressor
agent to NE only in highly selected patients
with low risk of tachyarrhythmias
absolute or relative bradycardia

37. •Phenylephrine not recommended
except when
–NE associated with serious arrhythmias
–cardiac output high and BP persistently
low
–as salvage therapy when combined
inotrope/vasopressor drugs and low dose
vasopressin have failed to achieve MAP
–Low dose dopamine should not be used
for renal protection

38. INOTROPIC THERAPY

39. •Trial of dobutamine infusion up to 20
mcg/kg/min be administered or added to
vasopressor if
–myocardial dysfunction suggested by elevated
cardiac filling pressures and low cardiac output
–ongoing signs of hypoperfusion, despite
achieving adequate intravascular volume and
adequate MAP.

40. CORTICOSTEROID

41. Not indicated if adequate fluid resuscitation
and vasopressor therapy able to restore
hemodynamic stability.
In case not achievable, iv hydrocortisone at
a dose of 200 mg per day.
Corticosteroids not be administered for
treatment of sepsis in the absence of shock

42. OTHER SUPPORTIVE THERAPY

43. OTHER SUPPORTIVE THERAPY
•Blood products administration
•Immunoglobulins*
•Selenium*
•Mechanical ventilation of sepsis induced
ARDS
•Sedation, anaelgesia & neuromuscular
blockade
•Glucose control

44. •Renal replacement therapy
•Bicarbonate therapy
•DVT prophylaxis
•Stress ulcer prophylaxis
•Nutrition*
•Setting goals of care

45. BLOOD PRODUCT ADMINISTRATION

46. •RBC transfusion only when Hb <7.0 g/dl
•EPO not be used as specific treatment of
anemia associated with severe sepsis.
FFP not be used to correct laboratory clotting
abnormalities in the absence of bleeding or
planned invasive procedures.
•Not using antithrombin for the treatment of
severe sepsis and septic shock.

47. Platelet transfusion
<10,000/mm3 in the absence of apparent
bleeding.
< 20,000/mm3 if the patient has a
significant risk of bleeding.
Higher platelet counts (≥50,000/mm3)
advised for active bleeding, surgery, or
invasive procedures.

48. GLUCOSE CONTROL

49. •A protocolised approach to blood glucose
management in ICU patients with severe
sepsis commencing insulin dosing when
-2 consecutive blood glucose levels are >180
mg/dL.
•Blood glucose values be monitored every
1 to 2 hrs until glucose values and insulin
infusion rates are stable and then every 4 hrs
thereafter.

50. RENAL REPLACEMENT
THERAPY

51. •Continuous renal replacement therapies and
intermittent hemodialysis are equivalent in
patients with severe sepsis and acute renal
failure.
•Use continuous therapies to facilitate
management of fluid balance in
hemodynamically unstable septic patients.

52. DVT PROPHYLAXIS

53. •VTE prophylaxis required using daily
subcutaneous LMWH.
•If creatinine clearance <30 mL/min, use
dalteparin.
•Patients with severe sepsis should be
treated with a combination of pharmacologic
therapy and intermittent pneumatic
compression devices whenever possible.

54. •Septic patients who have a contraindication
for heparin use (eg, thrombocytopenia,
severe coagulopathy, active bleeding, recent
intracerebral hemorrhage) not to receive
pharmacoprophylaxis but receive
mechanical prophylactic treatment, such
as graduated compression stockings or
intermittent compression devices , unless
contraindicated.

55. STRESS ULCER PROPHYLAXIS

56. •Stress ulcer prophylaxis using H2 blocker or
proton pump inhibitor be given to patients
with severe sepsis/septic shock who
have bleeding risk factors .
•When stress ulcer prophylaxis is used,
proton pump inhibitors rather than H2RA.
•Patients without risk factors do not receive
prophylaxis

57. NUTRITION

58. •Administer oral or enteral (if necessary)
feedings, as tolerated, rather than either
complete fasting or provision of only
intravenous glucose within the first 48 hours
after a diagnosis of severe sepsis/septic
shock.
• Avoid mandatory full caloric feeding in the
first week but rather suggest low dose feeding
(eg, up to 500 calories per day),advancing
only as tolerated.

59. Use i/v glucose + enteral nutrition rather than
TPN alone or parenteral nutrition in the first 7
days after a diagnosis of severe sepsis/septic
shock.
Nutrition without specific immunomodulating
supplementation.

60. SETTING GOALS OF CARE

61. •Discuss goals of care and prognosis with
patients and families.
•Incorporate goals of care into treatment and
end-of-life care planning, utilizing palliative
care principles where appropriate .
•Address goals of care as early as feasible,
but no later than within 72 hours of ICU
admission.

62. The Third International Consensus
Definitions for Sepsis and Septic Shock
(Sepsis-3)