pathophysiology of septic & septic shock, dr christian a johannes span
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Dr. Christian A Johannes, SpAn, KIC
Tempat/ Tanggal Lahir : Jakarta, 27 November
Pendidikan : Dokter umum FK UNSRAT 1979
Anastesi logist FK UNDIP 1990Konsultan ICU IDSAI 1996
Pekerjaan : Kepala ICU RSPAD GS Jakarta
Team Dokter Kepresidenan RI
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Pathophysiology of Septic
and Septic Shock
Chris JohannesHead of Intensive Care Unit Centralrmy Hospital Gatot Subroto
JAKARTA
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ACCP/SCCM ConsensusDefinitions
Infection Inflammatory response to
microorganisms, or Invasion of normally sterile
tissues
Systemic InflammatoryResponse Syndrome(SIRS)
Systemic response to a variety
of processes
Sepsis Infection plus 2 SIRS criteria
Severe Sepsis Sepsis Organ dysfunction
Septic shock
Sepsis Hypotension despite fluidresuscitation
Multiple OrganDysfunction Syndrome
(MODS) Altered organ function in anacutely ill patient
Homeostasis cannot bemaintained withoutintervention
Bone RC et al. Chest. 1992;101:1644-55.
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Mortality of severe sepsis in most centers
remainsunacceptable highThe speed and appropriateness of therapy
administered in the initial hours after the
syndrome develops likely influenceoutcome
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Mortality
SepticShock
53-63%
20-53%Severe Sepsis300,000
7-17%Sepsis
400,000
Incidence
Balk, R.A. Crit Care Clin 2000;337:52
Mortality Increases in Septic Shock Patients
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INCIDENCE ANDMORTALITY
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0
50,000
100,000
150,000
200,000
250,000
D e a
t h s
/ Y e a r
Severe Sepsis:Comparison With Other Major Diseases
National Center for Health Statistics, 2001.American Cancer Society, 2001.
0
50
100
150
200
250
300
AIDS* Colon BreastCancer
CHF SevereSepsis
C a s e s
/ 1 0 0
, 0 0 0
Incidence of Severe Sepsis
AIDS* SevereSepsis
AMI BreastCancer
*American Heart Association. 2000.Angus DC et al. Crit Care Med 2001 In Press).
Mortality of Severe Sepsis
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Mortality Severe Sepsis:
Angus DC et al. Cr i t Ca re Med . 2001 (In Press). Sands KE et al. J A M A . 1997;278:234-40. Zeni F et al. Cri t Care Med . 1997;1095-100.
28% 34%
50%
0
20
40
60
M o r t a
l i t y
( % )
2001
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Brazilian Sepsis
Epidemiological Study
Mortalitas
Sepsis 33.9%
Severe sepsis 46.9%
Septic shock 52.2%
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Hospital mortality (%)
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The interrelationship between SIRS, sepsis, and infection
Chest 1992;101:1645
INFECTION SIRSSEPSIS
PANCREATITIS
BURNS
TRAUMA
OTHER
OTHER
VIREMIA
PARASITEMIA
FUNGEMIA
BACTERIEMIA
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Sepsis: A Complex DiseaseThis Venn diagram
provides a conceptualframework to viewthe relationships
between variouscomponentsof sepsis.
The inflammatory
changes of sepsis aretightly linked todisturbed hemostasis.
Adapted from: Bone RC et al. Chest. 1992;101:1644-55.
Opal SM et al. Crit Care Med . 2000;28:S81-2.
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SIRS: More Than Just a Systemic
Inflammatory ResponseSIRS: A clinical responsearising from a nonspecificinsult manifested by
2 of the following: Temperature
38C or 36C HR 90 beats/min Respirations 20/min WBC count 12,000/ mL or
4,000/ mL or >10% immatureneutrophils
Recent evidence indicatesthat hemostatic changes arealso involved
Adapted from: Bone RC et al. Chest. 1992;101:1644-55.Opal SM et al. Crit Care Med . 2000;28:S81-2.
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Sepsis: More Than JustInflammation
Sepsis : Known or suspected
infection Two or more
SIRS criteria
A significant linkto disorderedhemostasis
Adapted from: Bone RC et al. Chest. 1992;101:1644- 55.
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Severe Sepsis: Acute OrganDysfunction and DisorderedHemostasisSevere Sepsis:
Sepsis with signs oforgan dysfunction in 1of the followingsystems:
Cardiovascular Renal Respiratory Hepatic Hemostasis CNS Unexplained metabolic
acidosis Adapted from: Bone RC et al. Chest. 1992;101:1644- 55.
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Identifying Acute OrganDysfunction as a Marker ofSevere Sepsis
TachycardiaHypotension
CVPPAOP
JaundiceEnzymes Albumin
PT
AlteredConsciousness
ConfusionPsychosis
TachypneaPaO 2
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Angus DC et al. Crit Care Med . 2001; (In Press).
Zeni F et al. Crit Care Med . 1997;25:1095-100.Wheeler AP et al. N Engl J Med . 1999;340:207-14.
Severe Sepsis: A Complex and
Unpredictable Clinical SyndromeHigh mortality rate(28%-50%)
Heterogeneous patient population
Unpredictabledisease progression
Unclear etiologyand pathogenesis
SystemicInflammation
ImpairedFibrinolysis
Coagulation
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Sepsis: Defining a Disease Continuum
Bone et al. Chest. 1992;101:1644; Wheeler and Bernard. N Engl J M ed . 1999;340:207.
Sepsis SIRS Insult Severe Sepsis
Sepsis with 1 sign of organfailure
Cardiovascular (refractoryhypotension)
Renal
RespiratoryHepaticHematologicCNSMetabolic acidosis
Shock
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Initial Resuscitation Diagnosis Antibiotic therapy Source Control Fluid therapy Vasopressors Inotropic Therapy Steroids Recombinant Human
Activated Protein C(rhAPC) [drotrecoginalfa (activated)]
Blood Product Administration Mechanical Ventilation
Sedation, Analgesia, and NeuromuscularBlockade in Sepsis
Glucose Control
Renal Replacement
Bicarbonate Therapy
Deep Vein Thrombosis Prophylaxis
Stress Ulcer Prophylaxis
Limitation of Support
Index
Dellinger, et. al. Crit Care Med 2004, 32: 858-873.
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SEPSIS
Systemic Inflammatory Response (SIRS) toINFECTION manifested by two or > of following:
Temp > 38 or < 36 centigrade HR > 90 RR > 20 or PaCO2 < 32
WBC > 12,000/cu mm or > 10% Bands (immature wbc)
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Risk Factors Associated with Septic
Shock Age
Malnutrition
General debilitation
Use of invasive
catheters
Traumatic wounds
Drug Therapy
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Pathophysiology of Septic shock
Initiated by gram-negative (most common) orgram positive bacteria, fungi, or virusesCell walls of organisms contain Endotoxins
Endotoxins release inflammatory mediators(systemic inflammatory response) causes... Vasodilation & increase capillary permeability leadstoShock due to alteration in peripheral circulation &massive dilation
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Pathophysiology of Septic Shock
IMMUNE / INFLAMMATORY RESPONSE
Microorganisms enter body
Mediator Release
Activation of Complement, kallikrein / kinin/ coagulation
& fibrinolytic factors platelets, neutrophils ¯ophages>>damage to endothelial cells.
ORGAN DYSFUNCTION
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Sequelae of Septic Shock
The effects of the bacterias endotoxins cancontinue even after the bacteria is dead!!!
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ISF DEBATES:CONTROVERSIES IN SEPSIS
Vasopressor Therapyof Septic Shock:
Norepinephrine vs. DopamineSummary
Phillip Dellinger, MDJean-Louis Vincent, MD
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No high level evidence exists to
support better clinical outcomewith either dopamine ornorepinephrine when compared tothe other drug.
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Either dopamine or norepinephrine, as acombined inotrope/vasopressor, ispreferred over alternative drugs as firstline agents to treat hypotension in septicshock.
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Non-clinical outcome physiological
studies may be used to offer potentialadvantages of norepinephrine ordopamine, one over the other.
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In patients with poor contractility as a
major component of the hypotension,dopamine may be a better initialchoice.
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Some patients who do not achieveacceptable blood pressure with dopaminewill achieve that goal withnorepinephrine.
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Surviving Sepsis Campaign (SSC)Guidelines- Vasopressors
Either norepinephrine or dopamine(through a central line as soon as
available) is the first-choicevasopressor agent to correcthypotension in septic shock.
Grade D
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Low dose dopamine should not be used forrenal protection in severe sepsis
An arterial catheter should be placed as soonas practical in all patients requiringvasopressors Arterial catheters provide more accurate
and reproducible measurement of arterial pressure in shock states when compared tousing a cuff
Vasopressin may be cons idered in refractoryshock patients that are ref ractory to fluidresuscitation and high dose vasopressors
Vasopressors (cont)
Grade B
Grade E
Grade E
Dellinger, et. al. Crit Care Med 2004, 32: 858-873.
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.
http://www.sccm.org/professional_resources/guidelines/table_of_contents/index.asphttp://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=11505120&itool=iconabstrhttp://www.sccm.org/professional_resources/guidelines/table_of_contents/index.asphttp://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=11191541&itool=iconabstrhttp://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=11505120&itool=iconabstrhttp://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=11505120&itool=iconabstrhttp://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=11505120&itool=iconabstrhttp://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=11505120&itool=iconabstrhttp://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=11191541&itool=iconabstrhttp://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=11191541&itool=iconabstrhttp://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=11191541&itool=iconabstrhttp://www.sccm.org/professional_resources/guidelines/table_of_contents/index.asphttp://www.sccm.org/professional_resources/guidelines/table_of_contents/index.asphttp://www.sccm.org/professional_resources/guidelines/table_of_contents/index.asp -
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In patients with low cardiac output despiteadequate 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 cardiacindex to target an arbitrarily predefinedelevated level Patients with severe sepsis failed to benefit from
increasing oxygen delivery t o supranormal levels by use of dobutamine
Inotropic TherapyGrade E
Grade A
Gattinoni L. N Eng J Med 1995;333:1025-1032.
Hayes MA. N Eng J Med 1994;330:1717-172 2.
Dellinger, et. al. Crit Care Med 2004, 32: 858-873.
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=7675044http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=7675044http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=7993413http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=7993413http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=7993413http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=7993413http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=7993413http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=7993413http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=7993413http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=7675044http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=7675044http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=7675044 -
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Location of gun shoot N---------------------------------------------------------------
1. Abdomen 6
2. Thorax 23. Thoraco Abdominal 14. Head 25. Musculosceletal 1
--------------------------------------------------------------Total 12
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Clasification of Sepsis N---------------------------------------------------------------
1. Sepsis 3
2. Severe Sepsis 43. Septic Shock 5
--------------------------------------------------------------
Total 12
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Isolated micro organism from blood1. Klebsiella sp ( 4 pts )2. Enterobacter sp ( 2 pts )
3. Pseudomonas aerogenosa ( 2 pts )4, Escheria coli ( 1 pts )
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On Ventilator : 8 pts. ( e.c. ARDS ) All pts we give Fluid. ( Crystalloid an Colloid)Antibiotic : Meropenem
CefipimeSource ControlVasopressors ( Noerepinephrine, Dopamine,Dobutamine ) Glucocorticoid if there any indication.Glucose ControlNutrition Therapy
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Polyclonal IVIGTight Monitoring.
- Hemodynamic monitoring.
- SaO2- BGA
- Blood Glucose.
- Urine Output
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RESULT8 pts ( 66,6 % ) survived
4 pts ( 33,3 % ) died.
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CONCLUSION
IF WE USE THE GUIDELINES FROMSURVIVING SEPSIS CAMPAIGN, THEMORTALITY IN SEPSIS COULD BEDECREASED.
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