Kuliah Sepsis Septik Syok

November 2014
Dr.Budi Riyanto,MSc,SpPD,KPTI
INFECTION AND SEPSIS
Surrounded by pathogens
Infection is the exception
Protective from infection
Physical barriers
Chemical barriers
Immunological function
Physical and Chemical
Barriers to Infection
Skin
stronger in hands and feet
sebaceous secretions lower pH
Mucous membranes
ciliary function
mucous barrier
acid mileu in stomach
 Immune Defense
Humoral defense
antibodies
complement

Cellular defense
Cytokines
potential for deleterious effects
Interaction of mechanisms
 Breakdown of Host Defense
Physical, chemical and immunological
breakdown -act synergistically
e.g. patient with
diabetes
immunosuppresion
surgery
Potential for deleterious effects
 Infection Manifestation
Local signs
pain,redness,swelling, warmth loss
of function
Systemic signs
Fever, somnolence, confusion, ileus,
hypotension
Lab tests
TW,polymorphs, Cultures
Non infective- causes may manifest
as infection
Sepsis and Septic Shock
 Sepsis and Septic Shock

Definitions

Epidemiology

Pathogenesis

Principles of management

Budi Riyanto workshop PIT PAPDI 2009

 Definitions

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
Bacteraemia: the presence of bacteria in the
bloodstream
Septicaemia: no longer used
ACCP/SCCM Consensus Conference: Bone et al, Chest 1992 101:1644
 Definitions
Sepsis: 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
Septic shock: sepsis with hypotension despite
adequate fluid resuscitation, with perfusion
abnormalities that could include, but are not limited
to, lactic acidosis, oliguria, and/or acute mental
status.

ACCP/SCCM Consensus Conference: Bone et al, Chest 1992 101:1644

Budi Riyanto workshop PIT PAPDI 2009
 SIRS and Sepsis

SIRS: Systemic Inflammatory

Response Syndrome
Fever, leucocytosis, organ failure
Recognises difficulty of always
identifying infection, but
As a result, high sensitivity but low
specificity

Budi Riyanto workshop PIT PAPDI 2009

 Parasite

Virus
Severe
Infection Sepsis SIRS
Sepsis
Fungus
shock Severe
SIRS Trauma

Bacteria
BSI
Burns
Adapted from SCCM ACCP Consensus Guidelines Budi Riyanto workshop PIT PAPDI
2009
Budi Riyanto workshop PIT PAPDI 2009
 Sepsis and septic shock

Bacterial infection

Excessive host response

Host factors lead to cellular damage

Organ damage

Death

Budi Riyanto workshop PIT PAPDI 2009

Cohen, Nature: 2002 420:885
 Management of Sepsis
Recognition
Supportive care
Source control
Antibiotics
Specific (adjunctive)
therapy

Budi Riyanto workshop PIT PAPDI 2009

 Surviving Sepsis Campaign

Guidelines for Management of Severe

Sepsis and Septic Shock

Dellinger RP, Carlet JM, Masur H, et al. for the Surviving Sepsis Campaign
Management Guidelines Committee. Crit Care Med 2004; 32:858-873.
Initial Resuscitation
Resuscitation should begin as soon as severe sepsis or sepsis
induced tissue hypoperfusion is recognized
Elevated Serum lactate identifies tissue hypoperfusion in
patients at risk who are not hypotensive
Goals of therapy within first 6 hours are Grade B
- Central Venous Pressure 8-12 mm Hg (12-15 in ventilator pts)
- Mean arterial pressure > 65 mm Hg
- Urine output > 0.5 mL/kg/hr
-
- ScvO2 or SvO2 70%;
if not achieved with fluid resuscitation during first 6 hours:
- Transfuse PRBC to hematocrit > 30% and/or
- Administer dobutamine (max 20 mcg/kg/min) to goal

Rivers E. N Engl J Med 2001;345:1368-77.

Dellinger, et. al. Crit Care Med 2004, 32: 858-873.
 Surviving Sepsis Campaign Guidelines

Early Goal-Directed Therapy Results

28-day Mortality
60
49.2%
50 P = 0.01*

40
33.3%
30

20

10

0
Standard Therapy EGDT
n=133 n=130
*Key difference was in sudden CV collapse, not MODS
Rivers E. N Engl J Med 2001;345:1368-77.
Diagnosis
Before the initiation of antimicrobial therapy, at least two
blood cultures should be obtained Grade D
At least one drawn percutaneously
At least one drawn through each vascular access device
if inserted longer than 48 hours
Other cultures such as urine, cerebrospinal fluid, wounds,
respiratory secretions or other body fluids should be Grade D
obtained as the clinical situation dictates
Other diagnostic studies such as imaging and sampling
should be performed promptly to determine the source and
causative organism of the infection Grade E
may be limited by patient stability

Weinstein MP. Rev Infect Dis 1983;5:35-53

Blot F. J Clin Microbiol 1999; 36: 105-109.

Dellinger, et. al. Crit Care Med 2004, 32: 858-873.

Antibiotic Therapy
Start intravenous antibiotic therapy within the first Grade E
hour of recognition of severe sepsis after obtaining
appropriate cultures

Empirical choice of antimicrobials should include one

or more drugs with activity against likely pathogens, Grade D
both bacterial or fungal
Penetrate presumed source of infection
Guided by susceptibility patterns in the
community and hospital
Continue broad spectrum therapy until
the causative organism and its
susceptibilities are defined

Kreger BE. Am J Med 1980;68:344-355.

Ibrahim EH. Chest 2000;118:146-155.
Hatala R. Ann Intern Med 1996;124-717-725.

Dellinger, et. al. Crit Care Med 2004, 32: 858-873.

Antibiotic Therapy
Grade E
Reassess after 48-72 hours to narrow
the spectrum of antibiotic therapy
Grade E
Duration of therapy should typically be
7-10 days and guided by clinical
response
Some experts prefer combination Grade E
therapy for Pseudomonas infections or
neutropenic patients
Stop antimicrobials promptly if clinical
syndrome is determined to be Grade E
noninfectious
Ali MZ. Clin Infect Dis 1997;24:796-809

Dellinger, et. al. Crit Care Med 2004, 32: 858-873.

Source Control
Grade E
Evaluate patients for focus of infection amenable to
source control measures
Drainage of an abscess or local focus of infection
Debridement of infected necrotic tissue
Removal of a potentially infected device
Definitive control of a source of ongoing microbial
contamination
Source control methods must weigh benefits and Grade E
risks of the specific intervention

Jimenez MF. Intensive Care Med 2001;27:S49-S62.

Bufalari A. Acta Chir Belg 1996;96:197-200.

Dellinger, et. al. Crit Care Med 2004, 32: 858-873.

Source Control (cont)
Once a focus of infection has been identified, source Grade E
control should be implemented as soon as possible
following initial resuscitation
Especially important for patients with necrotizing soft
tissue infection or intestinal ischemia
If intravascular access devices are suspected to be Grade E
the source of infection, remove them promptly after
establishing other vascular access
It may be reasonable to leave access devices in place
when patients develop sepsis of unknown source, until
the source of infection is determined

Moss RL. J Pediatr Surg 1996;31:1142-1146.

CDC. MMWR 2002;51:1-29.

Dellinger, et. al. Crit Care Med 2004, 32: 858-873.

Fluid Therapy: Fluid Challenge
Grade E
Fluid challenge in patients with
suspected hypovolemia may be given

500 - 1000 mL of crystalloids over 30 mins

300 - 500 mL of colloids over 30 mins
Repeat based on response and tolerance
Input is typically greater than output due to venodilation
and capillary leak
Most patients require continuing aggressive fluid
resuscitation during the first 24 hours of management

Dellinger, et. al. Crit Care Med 2004, 32: 858-873.

 Vasopressors
Grade E
Initiate vasopressor therapy if appropriate fluid challenge fails
to restore adequate blood pressure and organ perfusion
Vasopressor therapy should also be used transiently in the face of life-
threatening hypotension, even when fluid challenge is in progress

Either norepinephrine or dopamine are first line agents to

correct hypotension in septic shock Grade D
Norepinephrine is more potent than dopamine and may be more
effective at reversing hypotension in septic shock patients
Dopamine may be particularly useful in patients with compromised
systolic function but causes more tachycardia and may be more
arrhythmogenic

LeDoux D. Crit Care Med 2000;28:2729-2732. Regnier B. Intensive Care Med 1977;3:47-53.
Martin C. Chest 1993;103:1826-1831. Martin C. Crit Care Med 2000;28:2758-2765.
DeBacker D. Crit Care Med 2003;31:1659-1667. Hollenberg SM. Crit Care Med 1999; 27: 639-660.

Dellinger, et. al. Crit Care Med 2004, 32: 858-873.

Vasopressors (cont)
Low dose dopamine should not be used for renal Grade B
protection in severe sepsis
An arterial catheter should be placed as soon as
practical in all patients requiring vasopressors Grade E
Arterial catheters provide more accurate and
reproducible measurement of arterial pressure in
shock states when compared to using a cuff
Vasopressin may be considered in refractory shock
patients that are refractory to fluid resuscitation and
high dose vasopressors Grade E
Infusion rate of 0.01-0.04 units/min in adults
May decrease stroke volume

Hollenberg SM. Crit Care Med 1999; 27:639-660.

Bellomo R. Lancet 2000; 356: 2139-2143.
Kellum J. Crti Care Med 2001; 29: 1526-1531.

Dellinger, et. al. Crit Care Med 2004, 32: 858-873.

Inotropic Therapy
Grade E
In patients with low cardiac output despite adequate
fluid resuscitation, dobutamine may be used to
increase cardiac output
Should be combined with vasopressor therapy in the presence
of hypotension
It is not recommended to increase cardiac index to Grade A
target an arbitrarily predefined elevated level
Patients with severe sepsis failed to benefit from increasing
oxygen delivery to supranormal levels by use of dobutamine

Gattinoni L. N Eng J Med 1995;333:1025-1032.

Hayes MA. N Eng J Med 1994;330:1717-1722.

Dellinger, et. al. Crit Care Med 2004, 32: 858-873.

Steroids
Grade C
Intravenous corticosteroids are
recommended in patients with septic
shock who require vasopressor
therapy to maintain blood pressure
Administer intravenous hydrocortisone 200-300 mg/day
for 7 days in three or four divided doses or by continuous
infusion
Shown to reduce mortality rate in patients with relative
adrenal insufficiency

Annane, D. JAMA, 2002; 288 (7): 868

Dellinger, et. al. Crit Care Med 2004, 32: 858-873.

THANK YOU