SEPSIS

DR UNNIKRISHNAN P / CCU

.• “SEPSIS AT ITS INCEPTION IS DIFFICULT

TO RECOGNIZE BUT EASY TO TREAT;

LEFT UNATTENDED IT BECOMES EASY

TO RECOGNIZE BUT DIFFICULT TO

TREAT”

Machiavelli

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

BACTEREMIA

Presence of viable bacteria in blood

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

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

SEPSIS• SIRS due to infection

SEVERE SEPSIS• Sepsis associated with organ dysfunction,

hypoperfusion or hypotension• May include lactic acidosis,oliguria,altered

mentation

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).

ORGAN DYSFUNCTION• Thrombocytopenia

drop by >30% within 24 hrs OR count <100G/L

ORGAN DYSFUNCTION• Arterial hypoxaemia

PaO2 < 75 mm of Hg (room air) OR

PaO2 /FiO2 < 250 (oxygen supplimentation)

ORGAN DYSFUNCTION• Renal dysfunction

Urine output < 0.5 ml/ kg x 2 hrs despite fluid loading OR S. creatinine > 2x reference range

ORGAN DYSFUNCTION• Metabolic acidosis

BE < 5 mmol/L OR S.lactate > 1.5 x upper value

MODS• Presence of altered organ function lasting for

> 24 hrs in an acutely ill patient, such that homeostasis cant be maintained without intervention.

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

HOW?OR

GANISM

HOST

SEPSIS

True or false…..?

• The immune response by the host is minimal in sepsis..

Bacterial infection

Sepsis and septic shock

Excessive host response

Host factors lead to cellular damage

Organ damage

Death

PATHOGENESIS

INFLAMMATION

COAGULATION

CYTOKINE

The events…..

Proinflammatory cytokines

Antiinflammatorycytokines

CARSSevere sepsis ,

shock vs infections

Coagulation and sepsis

Less anticoagulant activity

Less profibrinolytic activity

PROCOAGULANT STATE

.INFLAMM

ATION VASODIL

ATION

SHOCK

COAGULATION DISTURBANCE

MULTIPLE ORGAN FAILURE

MANAGEMENT

Be on the lookout for disaster

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

if central venous oxygen saturation not achieved

• FLUID• PRBC ( Hct >30)• DOBUTAMINE : max 20µ/kg/min

DIAGNOSIS

BLOOD CULTURE

OTHER CULTURES

IMAGING STUDIES

BLOOD CULTURE.2 .O

NE P/C

.ONE FROM EACH IV device

ANTIBIOTICS

1 HOUR BROAD SPECTRUM

REASSESS

COMBINATION 3-5 days

SOURCE IDENTIFICATION/CONTROL

SITE -WITHIN6 HRS

?DRAINABLE FOCUS

IMPLEMENT SOON

MAX EFFICACY MIN UPSET

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

VASOPRESSORS

NOREPINEPHRINE / DOPAMINE

EPINEPHRINE ADDED IF POOR RESPONSE

VASOPRESSIN0.03 UNITS/MIN

No low dose Dopamine!

MAP >65

Arterial catheter

INOTROPES

LOW CO

DOBUTA

MINE

STEROIDS• Poorly responsive hypotension• Hydrocortisone > dexamethasone• Hydrocortisone <300 mg / day• Fludrocortisone 50 µg OD optional• Weaned when no vasopressors• No steroid if no shock

Recombinant Activated Protein C

• APACHE II >25

BLOOD PRODUCTS

Hb: 7-9gSepsis related

anemia- no erythropoetin

FFP: only if bleeding / invasive

procedures

FFP not a nutrient!

PLATELETS

•Give it….•,< 5000•SIGNIFICANT BLEEDING RISK•.

5000-30000

•SURGERY•INVASIVE PROCEDURES> 50000

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

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

SEDATION- ANALGESIA- NMB

Sedation

• Protocol-based with interruption

NMB

• Only when necessary

GLUCOSE CONTROLIV INSULIN

RBS < 150 mg%

Calorie source provided

GLUCOSE CONTROLQ 1-2 h,

Q 4 h if stable

Interpret with caution

RENAL REPLACEMENT

• Intermittent HD = CVVH• CVVH if hypotension

Bicarbonate therapy• Not for hypoperfusion induced lactic

acidemia with pH >7.15

DVT PROPHYLAXIS

PHARMACOLOGIC

UFH

LMWH

STRESS ULCER PROPHYLAXIS

GI BLEED

VAP

SEPSIS RESUSCITATION BUNDLE- 6 h

LACTATECULTUR

E

ANTIBIOTICS

BP LESS-FLUID 20 ml/kg Pressors

MAP >65

CVP>8ScvO2 > 70%

SEPSIS MANAGEMENT BUNDLE – 24HR

STEROIDDROTECOG

EN α

GLUCOSE <150

PIP<30 CM

OUTCOME IMPROVED BY• Early goal directed therapy

• Lung protective ventilation

• Appropriate antibiotic coverage

• Activated protein C

• Tight control of sugars 80-100mg/dl

• Steroids

A clinician, armed with the sepsis bundles, attacks the three heads of severe sepsis: hypotension, hypoperfusion and organ dysfunction

T H A N K Y O U

.

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