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Bakteriemia, sepsis dan

syok septik
dr Putra Hendra SpPD
UNIBA

Current Management of Severe Sepsis and Septic Shock l February 27, 2020 l 1
Current Management of Severe Sepsis and Septic Shock l February 27, 2020 l 2
Source
(usually an endogenous source of
• intestinal tract infection)
• oropharynx
• instrumentation sites
• contaminated inhalation therapy equipment
• IV fluids.
• Most frequent sites of infection: Lungs, abdomen,
and urinary tract.
• Other sources include the skin/soft tissue and the
CNS.

Angus DC, et al. Crit Care Med 2001, 29:1303-


1310.
Patients at increased risks of
developing sepsis

• Underlying diseases: neutropenia, solid tumors, leukemia,


dysproteinemias, cirrhosis of the liver, diabetes, AIDS,
serious chronic conditions.
• Surgery or instrumentation: catheters.
• Prior drug therapy: Immuno-suppressive drugs, especially
with broad-spectrum antibiotics.
• Age: males, above 40 y; females, 20-45 y.
• Miscellaneous conditions: childbirth, septic abortion,
trauma and widespread burns, intestinal ulceration.
Normal Systemic Response
to Infection and Injury (1)
• Leukocytosis Mobilizes neutrophils into the
circulation
• Tachycardia Increases cardiac output, blood flow
to injuried tissue
• Fever temperature central ↑ peripheral
vasoconstriction shunts blood flow to
injuried tissue

Mandell et al. Principals and Practice of Infectious Diseases6th


ed;906:906-926.
Normal Systemic Response
to Infection and Injury (2)
• Acute-Phase Responses
– Anti-infective
• Increases synthesis of complement factors,
microbe pattern-recognition molecules(mannose-
binding lectin, LBP, CRP, CD14, Others)

Mandell et al. Principals and Practice of Infectious Diseases6th


ed;906:906-926.
Normal Systemic Response
to Infection and Injury (3)
• Anti-inflammatory
– anti-inflammatory neuroendocrine hormones ↑
(cortisol, ACTH, epinephrine, α-MSH)
• Increases synthesis of proteins that help
prevent inflammation within the systemic
compartment
• Cytokine antagonists (IL-1Ra, sTNF-Rs)
• Anti-inflammatory mediators (e.g.,IL-4, IL-6, IL-
6R, IL-10, IL-13, TGF-β)
• Protease inhibitors (e.g.,α1-antiprotease)
• Antioxidants (haptoglobin)
Normal Systemic Response
to Infection and Injury (4)
• Procoagulant
– Walls off infection, prevents systemic spread
• Increases synthesis or release of fibrinogen,
PAI-1, C4b
• Decreases synthesis of protein C, anti-thrombin
III
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Current Management of Severe Sepsis and Septic Shock l February 27, 2020 l 12
Patogenesis
Current Management of Severe Sepsis and Septic Shock l February 27, 2020 l 14
Pathogenesis of Severe
Sepsis
Infection

Microbial Products
(exotoxin/endotoxin)

Cellular Responses
Platelet Coagulation Kinins Cytokines
Activation Activation Oxidases Complement TNF, IL-1, IL-6

Coagulopathy/DIC
Vascular/Organ System Injury

Multi-Organ Failure

Death
Current Management of Severe Sepsis and Septic Shock l February 27, 2020 l 16
The Sepsis Continuum
Severe Septic
SIRS Sepsis Sepsis Shock

• A clinical response
arising from a SIRS with a Sepsis with Refractory
nonspecific insult, presumed organ failure hypotension
with 2 of the or confirmed
following: infectious
• T >38oC or <36oC process
• HR >90 beats/min
• RR >20/min SIRS = systemic inflammatory
• WBC >12,000/mm3 or response syndrome
<4,000/mm3 or >10%
bands Chest 1992;101:1644.
Severe Sepsis

• Sepsis with organ hypoperfusion


one of the followings :
– SBP < 90 mmHg
– Acute mental status change
– PaO2 < 60 mmHg
– Increased lactic acid/acidosis
– Oliguria
– DIC or Platelet < 80,000 /mm3
– Liver enzymes > 2 x normal
MODS
(Multiple Organ Dysfunction Syndrome)

• Sepsis with multiorgan hypoperfusion


Two or more of the followings:
– SBP < 90 mmHg
– Acute mental status change
– PaO2 < 60 mmHg
– Increased lactic acid/acidosis
– Oliguria
– DIC or Platelet < 80,000 /mm3
– Liver enzymes > 2 x normal
Corticosteroid
CNS disease, CS use
Insufficiency in Acute
Cytokine
Illness
+- • Adrenal insufficiency
(low basal serum
cortisol level or poor
response to
Pituitary apoplexy, CS use
cirticotropin) is
common in
Cytokine,
anesthetic,
– critically ill patients
antiinfective ( 30%),
- –
agents,
hemorrhage, septic shock (50-
infection 60%)

 CS-binding
globulin
 Glucocorticoid
The Cardiovascular
System
Septic Shock

Decreased Decreased Abnormal


Volume Pump Vessel
Function Tone
Definition of Shock

• Inadequate tissue perfusion


• Decreased oxygen supply
• Anaerobic metabolism
• Accumulation metabolic waste
Complications
• Adult respiratory distress syndrome (ARDS)
• Disseminated Intravascular Coagulation (DIC)
• Acute Renal failure (ARF)
• Intestinal bleeding
• Liver failure
• Central Nervous System dysfunction
• Heart failure
• Death

Angus DC, et al. Crit Care Med 2001, 29:1303-


1310.
Sepsis management bundle
• Fluid resuscitation

• Appropriate cultures prior to antibiotic


administration, anti fungal

• Removal of source : kateter

• Use of vasopressors/inotropes when fluid

resuscitation optimized

Surviving Sepsis Campaign Management Guidelines Committee. Crit Care Med 2004;
32:858-873.
Sepsis management bundle
• Evaluation for adrenal insufficiency :
dopamin
• Stress dose corticosteroid administration
• Recombinant human activated protein C
(xigris) for severe sepsis
• Low tidal volume mechanical ventilation for
ARDS
• Tight glucose control
Surviving Sepsis Campaign Management Guidelines Committee. Crit Care Med 2004; 32:858-
873.
Early Goal-
Directed Therapy

CVP : central
venous
pressure

MAP : mean
arterial
pressure

ScvO2: central
venous
oxygen
saturation

NEJM 2001;345:1368-
77.
Current Management of Severe Sepsis and Septic Shock l February 27, 2020 l 33
SEPTIC SHOCK
MINIMIZING INFLAMMATION
Recombinant human activated protein C
(Xigris)
– Inhibits thrombin
– Inhibits apoptosis
– Improves survival in patients with multi-organ
dysfunction
– suppression of inflammation
– prevention of microvascular coagulation (DIC)
– reversal of impaired fibrinolysis
Current Management of Severe Sepsis and Septic Shock l February 27, 2020 l 35
Conclusion

Current Management of Severe Sepsis and Septic Shock l February 27, 2020 l 36

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