Sepsis
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SEPSIS
DR UNNIKRISHNAN P / CCU
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.• “SEPSIS AT ITS INCEPTION IS DIFFICULT
TO RECOGNIZE BUT EASY TO TREAT;
LEFT UNATTENDED IT BECOMES EASY
TO RECOGNIZE BUT DIFFICULT TO
TREAT”
Machiavelli
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INFECTION
• .
microbial phenomenon characterised by an inflammatory response to the presence of micro organisms or the invasion of normally sterile host tissue by these organisms
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BACTEREMIA
Presence of viable bacteria in blood
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SYSTEMIC INFLAMMATORY RESPONSE SYNDROME
• Generalized inflammatory response of the body to a variety of clinical conditions including infection, but not limited to infection
• 2 or more of the following
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SIRS•Systemic response to infection manifested by ≥ 2 of:
–Temp > 38oC or < 36oC–HR > 90 bpm–RR > 20 bpm or PaCO2 < 32 mmHg–WBC > 12 x 109/L, < 4 x 109/L or >10% band
form
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SEPSIS• SIRS due to infection
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SEVERE SEPSIS• Sepsis associated with organ dysfunction,
hypoperfusion or hypotension• May include lactic acidosis,oliguria,altered
mentation
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ORGAN DYSFUNCTION
• Arterial hypotension
SBP<90 MAP<70 x 1hour
despite fluid resuscitation
perfusion abnormalities
(that could include,lactic acidosis, oliguria, and/or acute change in mental status).
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ORGAN DYSFUNCTION• Thrombocytopenia
drop by >30% within 24 hrs OR count <100G/L
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ORGAN DYSFUNCTION• Arterial hypoxaemia
PaO2 < 75 mm of Hg (room air) OR
PaO2 /FiO2 < 250 (oxygen supplimentation)
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ORGAN DYSFUNCTION• Renal dysfunction
Urine output < 0.5 ml/ kg x 2 hrs despite fluid loading OR S. creatinine > 2x reference range
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ORGAN DYSFUNCTION• Metabolic acidosis
BE < 5 mmol/L OR S.lactate > 1.5 x upper value
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MODS• Presence of altered organ function lasting for
> 24 hrs in an acutely ill patient, such that homeostasis cant be maintained without intervention.
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Organ wise…
0
10
20
30
40
50
60
70
80
Per
cen
t o
f P
atie
nts
Shock
Respiratory
Renal
Metabolic
Coag
DIC
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HOW?OR
GANISM
HOST
SEPSIS
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True or false…..?
• The immune response by the host is minimal in sepsis..
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Bacterial infection
Sepsis and septic shock
Excessive host response
Host factors lead to cellular damage
Organ damage
Death
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PATHOGENESIS
INFLAMMATION
COAGULATION
CYTOKINE
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The events…..
Proinflammatory cytokines
Antiinflammatorycytokines
CARSSevere sepsis ,
shock vs infections
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Coagulation and sepsis
Less anticoagulant activity
Less profibrinolytic activity
PROCOAGULANT STATE
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.INFLAMM
ATION VASODIL
ATION
SHOCK
COAGULATION DISTURBANCE
MULTIPLE ORGAN FAILURE
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MANAGEMENT
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Be on the lookout for disaster
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INITIAL RESUSCITATION [1st 6 hrs]• Central venous pressure (CVP): 8–12 mm
Hg / 12-15 if mechanical ventilation• Mean arterial pressure (MAP) >65 mm Hg• Urine output >0.5 mL/kg/hour• Central venous (superior vena cava) or
mixed venous oxygen saturation >70% or >65%, respectively
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if central venous oxygen saturation not achieved
• FLUID• PRBC ( Hct >30)• DOBUTAMINE : max 20µ/kg/min
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DIAGNOSIS
BLOOD CULTURE
OTHER CULTURES
IMAGING STUDIES
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BLOOD CULTURE.2 .O
NE P/C
.ONE FROM EACH IV device
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ANTIBIOTICS
1 HOUR BROAD SPECTRUM
REASSESS
COMBINATION 3-5 days
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SOURCE IDENTIFICATION/CONTROL
SITE -WITHIN6 HRS
?DRAINABLE FOCUS
IMPLEMENT SOON
MAX EFFICACY MIN UPSET
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HEMODYNAMIC SUPPORT
Challenge:1000 ml crystalloid/300-500 ml colloid over 30 mins
CVP >8 / >12Reduce if no improvement
and filling pressures increase
More..Increase if improves
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VASOPRESSORS
NOREPINEPHRINE / DOPAMINE
EPINEPHRINE ADDED IF POOR RESPONSE
VASOPRESSIN0.03 UNITS/MIN
No low dose Dopamine!
MAP >65
Arterial catheter
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INOTROPES
LOW CO
DOBUTA
MINE
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STEROIDS• Poorly responsive hypotension• Hydrocortisone > dexamethasone• Hydrocortisone <300 mg / day• Fludrocortisone 50 µg OD optional• Weaned when no vasopressors• No steroid if no shock
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Recombinant Activated Protein C
• APACHE II >25
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BLOOD PRODUCTS
Hb: 7-9gSepsis related
anemia- no erythropoetin
FFP: only if bleeding / invasive
procedures
FFP not a nutrient!
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PLATELETS
•Give it….•,< 5000•SIGNIFICANT BLEEDING RISK•.
5000-30000
•SURGERY•INVASIVE PROCEDURES> 50000
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MECHANICAL VENTILATION-ARDS
TIDAL VOLUME: 6 ML/KG
PLATEAU PRESSURE MAX 30 CM H2O
PERMISSIVE HYPERCAPNEA
PEEP
PRONE POSITION VENTILATION
SEMIRECUMBENT : 30-45º
STABLE/AROUSABLE/REFLEXES/FAST RECOVERY NIV
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MECHANICAL VENTILATION-ARDSWEANING PROTOCOL
SBT: LOW LEVEL PS † PEEP-5 CM H2O OR T-PIECE
AROUSABLE
STABLE HEMODYNAMICS
NO NEW SERIOUS CONDITIONS
LOW PEEP REQUIREMENT
LOW FiO2 REQUIREMENT
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SEDATION- ANALGESIA- NMB
Sedation
• Protocol-based with interruption
NMB
• Only when necessary
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GLUCOSE CONTROLIV INSULIN
RBS < 150 mg%
Calorie source provided
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GLUCOSE CONTROLQ 1-2 h,
Q 4 h if stable
Interpret with caution
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RENAL REPLACEMENT
• Intermittent HD = CVVH• CVVH if hypotension
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Bicarbonate therapy• Not for hypoperfusion induced lactic
acidemia with pH >7.15
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DVT PROPHYLAXIS
PHARMACOLOGIC
UFH
LMWH
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STRESS ULCER PROPHYLAXIS
GI BLEED
VAP
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SEPSIS RESUSCITATION BUNDLE- 6 h
LACTATECULTUR
E
ANTIBIOTICS
BP LESS-FLUID 20 ml/kg Pressors
MAP >65
CVP>8ScvO2 > 70%
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SEPSIS MANAGEMENT BUNDLE – 24HR
STEROIDDROTECOG
EN α
GLUCOSE <150
PIP<30 CM
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OUTCOME IMPROVED BY• Early goal directed therapy
• Lung protective ventilation
• Appropriate antibiotic coverage
• Activated protein C
• Tight control of sugars 80-100mg/dl
• Steroids
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A clinician, armed with the sepsis bundles, attacks the three heads of severe sepsis: hypotension, hypoperfusion and organ dysfunction
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T H A N K Y O U
.
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