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Septic Shock
Maternal MortalityMaternal Mortality-- Safe Motherhood Initiative Safe Motherhood Initiative --
In 2002 the “Safe Motherhood Initiative” was
launched as a joint venture between NYS Dept
of Health and ACOG District II. of Health and ACOG District II.
The goals of the program :
1. - Overall decrease in maternal mortality:
2. - Eliminates the disparity between white and black women
Maternal MortalityMaternal Mortality-- Safe Motherhood Initiative Safe Motherhood Initiative --
Reporting Maternal Deaths through the S.M.I.
was on a voluntary basis � from 8/03 through
6/05 there were 37 Maternal Deaths reported6/05 there were 37 Maternal Deaths reported
to ACOG District II through the S.M.I.
Maternal MortalityMaternal Mortality-- Safe Motherhood Initiative Safe Motherhood Initiative --
Embolism 24%
Most common causes of M.M.
PIH 24%
Hemorrhage 15%
Infectious 15%
Cardiac 6%
Maternal MortalityMaternal Mortality-- Safe Motherhood Initiative Safe Motherhood Initiative --
1.- Hemorrhage Protocol
2.- Preconceptional counselling2.- Preconceptional counselling
3.- Management of Sepsis and septic shock
4.- Obesity
5.- Critical Care in Obstetrics
Septic Shock- Case presentation -
C/O - Fever, nausea, vomiting 2-3d
- Other fam members � same symptoms
Mrs X , 36y old P2 at 34wks
V.S. -Temp 104, BP 97/57, Pulse 150, R.R. 22
P.E. - Non-focal: Lungs clear, Abd non-tender
Labs - WBC 8,000 Hct 33%, Hb 11g
Fever etiology ?? - Hydration, �Temp, EFM
- Sepsis workup
Septic Shock- Case presentation -
Initial FHR:
- Bseline 200bpm, �variability, no decels
Hospital Course
- Bseline 200bpm, �variability, no decels
2hrs after Adm:
- Temp 102, BP 94/45, Pulse 150, R.R. 18, O Sat 95%
4 hrs after Adm:
- FHR Decelerations
430 hrs after Adm:
- Decision for C/S
Adhesion molecules
Septic Shock- Case presentation -
Septic Shock-Case presentation –
Septic Shock- Case presentation -
Delivery 401 A.M. (EBL=800cc)
To R.R. 430 A.M.
4:45A.M. Temp 98.9o F
5:00A.M. BP 80/40 Ephedrine BP 100/55
6:45A.M. O2 Sat 85%, -75% � O2 � Rpt Sat 95%
7:00A.M. pH=7.27 pO2=47 pCO2=41 HCO3=18
7:30A.M. Temp 99.5o F, CxR Bil pleural effusion
Septic Shock- Case presentation -
Delivery 401 A.M. (EBL=800cc)
To R.R. 430 A.M. Urinary Output
5A.M. 50cc5 50cc6A.M. 50cc7A.M. 45cc8A.M. 25cc9A.M. 25cc10A.M. 20cc11A.M. 10cc 12P.M. 30cc1P.M. 60cc
� Fluids
Septic Shock- Case presentation -
PregnancyPost surgery Ac resp distress
R/O Pulmonary Embolus
- 8A.M. Heparin theray started
- 2P.M. CT - No evidence of Emboli- Infiltrates sugg of pulm. edema
- 8A.M. Heparin theray started- CT of chest requested
Temp 99-101o F, O2 Sat 95-97%, UO > 30cc/h
Septic Shock- Case presentation -
CT � Bil Infiltrates
Rpt WBC � 15,000
Fever 1010 F
O2 desaturation
Pneumonia – Sepsis -ARDS
O2 desaturation
Low BP’s- 5P.M. Antibiotic Rx � ICU
-10P.M. Respiratory DistressIntubated � Vent (PEEP=15cm H2 O)Rpt CxR � ARDS
Septic Shock- Case presentation -
No improvement Pulmonary StatusLevophed Maintain BP’sBlood Culture Strep PneumoniaRx Imipenem, Gentamycin
Day 1-7
Rx Imipenem, GentamycinXigris (APC) started
WBC’s 18-33,000Temp 102-103 F
Day 8-9
2nd Septic Source ?
Septic Shock- Case presentation -
CxR No empyemaNo other studies done (Pat unstable)
#9 Explor laparotomy � TAH* in ICU
2nd Septic Source
#9 Explor laparotomy � TAH* in ICU
Temp’s � 98-100 FWBC’s � 17,000
Pulmonary – No ChangePressor agents – No Change
#14 Cardiac Arrest � Death
* Endomyometritis with abcess formation
Septic Shock- Case presentation -
-Delay in Dg
-Delay in initiation of antibiotic therapy
Mrs X , 36y old P2 at 34wks ���� 2A.M.
-Delay in initiation of antibiotic therapy
-Delay in initiation of hemodynamic monitoring
- Delay in initiation of aggressive fluid management
ICU Admission in Septic Shock � 5 P.M.
Maternal Mortality 2wks later
Septic Shock
Consensus conference of American College of Chest Physicians and Society of Critical Care Medicine on Sepsis and related disorders – 1992
- Systemic inflamatory response syndrome- Systemic inflamatory response syndrome
- Sepsis
- Severe Sepsis
- Septic Shock
- Multiple Organ Dysfunction Syndrome
Systemic Inflamatory Response Syndrome
Septic Shock
The organisms response to any insult
SIRS*
- Infectious, Trauma, Toxic
>2 of the following :
Definition
Diagnosis
*Systemic Inflamatory Response Syndrome
>2 of the following :-Temperature >380C or <360C- Heart Rate > 90 bpm- Respiratory Rate >20/min-WBC >12,000 or <4,000- Organ dysfunction
(Neuro, Renal, Clotting, Acidosis, etc)
Diagnosis
Septic Shock
BacteremiaPresence of bacteria in the blood
SIRSSystemic Inflamatory Response Syndrome
Sepsis
Severe sepsis
Septic Shock
Documented infection + Evidence of SIRS
SIRS
Sepsis associated with organ dysfunction (MODS)
Sepsis induced hypotension despite adequate hydration
Response Syndrome
Septic Shock
1.- Individual entities ?Increasingly severe responses to same insult
2.- Do they develop sequentially ?
Progression after 2.- Do they develop sequentially ?
3.- Risk of specific end-organ failure ?
4.- Mortality Rates ?
Progression after hospitalization ?
ARDS, DIC, ARF
Septic Shock
A large study of 2,527 patients that met at least 2 criteria for SIRS and were followed for 28d in the hospital or until discharge/death.28d in the hospital or until discharge/death.
Rangel-Fausto et al JAMA-1995
Septic Shock
SIRS 1301 (52%)
Sepsis 649 (26%)
Final Diagnosis
Rangel-Fausto et al JAMA-1995
Sepsis 649 (26%)
Severe Sepsis 467 (18%)
Septic Shock 110 (4%)
Septic Shock
Final Dg Present on Admission
Progressed in Hospital
Sepsis 56% 44%
Rangel-Fausto et al JAMA-1995
Sepsis 56% 44%
Severe Sepsis 42% 58%
Septic Shock 29% 71%
Septic Shock
SIRS Advance to higher level
Advance to Septic Shock
Rangel-Fausto et al JAMA-1995
2 criteria 32% 11%
3 criteria 36% 21%
4 criteria 45% 27%
Septic Shock
Sepsis 16%
⊕⊕⊕⊕ Blood Cultures
Rangel-Fausto et al JAMA-1995
Sepsis 16%
Severe Sepsis 25%
Septic Shock 69%
Septic Shock
Dg ARDS DIC ARF
SIRS-2 2% 8% 9%
SIRS-3 3% 15% 13%
Rangel-Fausto et al JAMA-1995
SIRS-3 3% 15% 13%
SIRS-4 6% 19% 19%
Sepsis 6% 16% 19%
Severe Sepsis 8% 18% 23%
Septic Shock 18% 38% 31%
Septic Shock
Septic Shock
SIRS and related conditions represent a hierarchical continuum of increased inflammatory response to infection
Conclusions
Rangel-Fausto et al JAMA-1995
response to infection
End organ failure rates blood culture rates and mortality rates are all increased with each subsequent stage of systemic inflamatory response.
Septic Shock
Diagnosis- Clinical presentation
- Lab workupPathophysiology
- Lab workup
Treatment
Septic Shock- Pathophysiology -
Infection
Bacteremia Release of toxins
Complex Complex inflammatory response
Multiple Organ Dysfunction
Death
Septic Shock- Pathophysiology -
Coagulation system
Endothelium
Cell metabolismBacterial toxins
Bacteremia
Cell metabolism
Lungs
Kidney
Cardio-vascular
Bacterial toxins
Inflamatory Response
Septic Shock-Coagulation –
Procoagulants Anticoagulants
- Coagulation cascade
- Platelet Activation Factor
- Vasoconstriction
- TF Inhibitor
- AT Complex
- Prot C Complex
- Fibrinolysis
Septic Shock- Coagulation -
Activated Protein C
- Inhibits Factor VIII-a, V-a
- � TF expression
- Inhibits PAI – 1
Anticoagulant
Fibrinolysis- Inhibits PAI – 1
- � Leukocytes adhesion
- � TNF levels
Fibrinolysis
Anti-Inflamatory
Low Prot C and APC Mortality Rates
Septic Shock
Septic Shock- Coagulation -
���� Procoagulants
� AnticoagulantsBacterial Toxins
Bacterial Toxins
-� Expression of TF- Edothelial damage-� Platelet agregation
-� levelTF Inhibitor
- � level ofAT
- � level of Prot C
- � Prot C to APC
- � Fibrinolysis
Microvascular thrombosis
Septic Shock- Cellular metabolism -
Sepsis
-Hypoxemia
- Hypotension
-Microvascular abn Microvascular thrombosis
Tissue hypoxia
-Microvascular abn Microvascular thrombosis
Shunting
Mitochondrial dysfunction
Anaerobic metabolism� ATP � Lactic ac
Septic Shock- Cellular metabolism -
Acidosis ( pH < 7.35 )
Respiratory� pCO2 > 45mmHg
Metabolic � HCO3 < 22mEq/L� pCO2 > 45mmHg
� HCO3 22-26 mEq/L� HCO3 < 22mEq/L
⊕Anion Gap-Lactic ac-Ketoacidosis-Intoxication
∅ Anion Gap-Renal ac
Anion Gap = (Na + K ) – (Cl + HCO3 ) ⊕ Anion Gap >14mEq/L
Septic Shock- Endothelial Cell -
Endothelial cell
- Prevent coagulation
- Prevent migration of cells
TM,, APC receptors �TF
� Adhesion molecules- Prevent migration of cells
- Regulate vasopermeability
- Regulate microcirculation
� Adhesion molecules
� Leukocyte activation
Vasoactive substances
Septic Shock- Endothelial Cell -
�Adhesion molecules
Complement activation� Permeability
Sepsis Endothelial cells
Complement activation
� TF, � PAF
� Permeability
� Coagulation
Leakage � Edema
Microvascular thrombosis
Cell death
Septic Shock
Endothelial cell injury
Alveolar flooding
� Lung compliance
� Capillary permeability
- ARDS -
� Lung compliance
Shunting
Hypoxemia
Recovery DeathPulmonary fibrosis
Pulmonary HTN
Septic Shock- ARDS -
Onset Acute
PaO / FiO < 200mmHgHypoxemia PaO2 / FiO2 < 200mmHg
Chest X-ray Bilateral alveolar or interstitial infiltrates
PCWP < 18mmHg
Septic Shock- Cardio-vascular -
Myocardial Depression
Refractory Vasodilation
Sepsis
Hypotension
Tissue perfusion
Capillary permeability
Loss of intravascular volume
Cell Death
Septic Shock- Diagnosis -
Coagulation - Hypoxemia- CxR changes
- Metabolic ac. Renal
Pulmonary
Tissue -Ac renal failure
-D.I.C.- Thrombosis
-Decreased E.F.-Hypotension
- Metabolic ac.(Anion gap)
- � Lactic acid
RenalTissue metabolism
Cardio vascular
-Ac renal failure
-Hepatic failureLiver
-Alteration of mental status
C.N.S.
Septic Shock- Diagnosis -
Fever - Common symptom- Viral syndrome- Non infectious
-Regional anesthesia
- Anxiety- Pain
Pulse
BP
- Pregnancy- Steroids (FLM)- Labor
-Regional anesthesia-Supine hypotension
- NPO- Nausea/Vomiting
WBC’s
BP
Output
Septic Shock- Diagnosis -
Coagulation
-Low BP (Refractory), PCWP, EF
- pH, HCO3 BD, Anion gap, LactateTissue metabolism
Cardio-vascular
-Fibrinogen, FSP, PT, PTT, INR, Plts
-Low BP (Refractory), PCWP, EF
- O2 Sat, CxR
Renal
Pulmonary
Cardio-vascular
- Urinary Output, BUN, CR, Lytes
- Liver function tests
C.N.S.
Liver
- Physical exam
Septic Shock- Diagnosis -
Acidosis
Oliguria
Hypotension
Hypoxemia
FeverAbn WBC’s�BP, �Pulse Hypoxemia
Coagulopathy
Abn mental status
�Pulse� R.R.
Prompt Dg andManagement
Septic Shock- Management -
Patients seen in the E.R. with the Dg of septic shock were randomly allocated to
Rivers et al NEJM 2001
1.- Standard therapy (n=133)
2.- Early goal-directed therapy (n=130)
Septic Shock- Management -
“Early goal directed therapy” is a complex approach to septic shock involving manipulation of cardiac preload afterload and contractility to achieve a balance between O2delivery and O2 demand.delivery and O2 demand.
End points used to confirm that balance
- Mixed venous O2 Sat- Lactate level- Base Deficit- pH
Rivers et al NEJM 2001
Septic Shock- Management -
Controls A-lines, CVP placed
Management of fluids, drugs up to MD’s
Study A-line, CVP placed
Rivers et al NEJM 2001
StudyFluids 500cc q 30min � CVP = 8-12mmHg
If MAP < 65mmHg � Vasopressors
If CV O2 Sat < 70% � Blood Hct > 30%
If CV O2 Sat still < 70% � Dobutamine
During the 1st 6hrs
Septic Shock- Management -
Therapy 0-6hrs 0-72hrs
Fluids-Control 3,499ml 13,300ml
Fluids-Study 4,981ml* 13,400mlns
Rivers et al NEJM 2001
Fluids-Study 4,981ml* 13,400ml
Blood-Control 18% 44%
Blood-Study 64%* 68%*
Dobutamine-Control 1% 9%
Dobutamine-Study 14%* 15%ns
*p< 0.01
Septic Shock- Management -
End-Point Baseline 0-6hrs 7-72hrs
CVP-C 6.1 11.8 11.6
CVP-S 5.3ns 13.8* 11.9ns
MAP-C 76 81 80
Rivers et al NEJM 2001
MAP-C 76 81 80
MAP-S 74ns 95* 87*
Lactate-C 6.9 4.9 3.9
Lactate-S 7.7ns 4.3* 3.0*
Base Deficit-C 8.9 8.0 5.1
Base deficit-S 8.9ns 4.7* 2.0*
C � Control, S � Study *p< 0.01
Septic Shock- Management -
End-Point Baseline 0-6hrs 7-72hrs
PT-C 16.5 17.5 17.3
PT-S 15.8ns 16.0* 15.4ns
PTT-C 32.9 37.6 37.0
Rivers et al NEJM 2001
PTT-C 32.9 37.6 37.0
PTT-S 33.3ns 32.6* 34.6*
FSP-C 39 54.9 62.0
FSP-S 44ns 45.8ns 39.2*
MODS-C 7.3 6.8 6.4
MODS-S 7.6ns 5.9* 5.1*
C � Control, S � Study *p< 0.01
Septic Shock- Management -
Mortality Controls(n=133)
Study(n=130)
All inpatients 59(46%) 38(30%)*
Rivers et al NEJM 2001
All inpatients 59(46%) 38(30%)*
28 day 61(49%) 40(33%)*
60 Day 70(57%) 50(44%)*
*p< 0.01
Septic Shock- Management -
To determine the impact of delays in initiating
Objective
Kumar et al Crit Care Med, 2006
To determine the impact of delays in initiating adequate antibiotic therapy on mortality rates of patients in septic shock
Septic Shock- Management -
A retrospective cohort study including 14 ICU’s
Methods
Kumar et al Crit Care Med, 2006
A retrospective cohort study including 14 ICU’s in the USA and Canada. A total of 2,731 adult patients with documented septic shock were included.
Septic Shock- Management -
A. The primary outcome variable was survival to hospital discharge.
Methods
Kumar et al Crit Care Med, 2006
hospital discharge.
B. The primary independent variable was the time to initiation of effective antimicrobial therapy relative to the first occurrence of shock (persistent hypotension)
Septic Shock- Management -
A. Mortality for the entire population � 56%
B. Survival was similar:
Outcome
Kumar et al Crit Care Med, 2006
B. Survival was similar:
- Infection documented or suspecetd
- A plausible pathogen identified or not
- Bacteremia present or absent
Septic Shock- Management -
Antibiotics Rx(from onset of shock)
Mortality Rates
< 1hr 82%
Kumar et al Crit Care Med, 2006
At 6hrs 42%
< 1hr 82%
Septic Shock- Management -
Antibiotics Rx(from onset of shock)
Mortality Rates
< 1hr 82%
Kumar et al Crit Care Med, 2006
At 6hrs 42%
Each hour of delay was associated with a � in survival of 7.6%
Septic Shock- Management -
Antibiotic Rx and Intensive therapy (goal directed therapy ) started at the earliest stages of severe sepsis/septic shockstages of severe sepsis/septic shock
Lower mortality rates