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SEPTIC SHOCKSEPTIC SHOCKBy
Marian D. Williams RN BN CEN CFRN CCRN
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SEPTIC SHOCK
Most common cause of death in non-cardiac ICU’s in the US
Most cases are nosocomial Increased incidence due to advanced
invasive technology Elderly are at greatest risk Mortality:40%-85%
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SEPTIC SHOCK
10th leading cause of death in the United States
139% increase from 1979 - 1987
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SEPTIC SHOCK
DEFINITIONS– Bacteremia
Presence of BACTERIA in the blood Body’s defense systems effectively destroy
bacteria
– Septicemia Presence of MICROBES in the blood
associated with systemic infection
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SEPTIC SHOCK
Sepsis– Systemic inflammatory response to
infection.
Severe Sepsis/SIRS– Sepsis associated with evidence of one or
more acute organ dysfunctions
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SEPTIC SHOCK RISK FACTORS
Patient related– < 1 year of age– > 65 years of age– Debilitated– Malnourished– Chronic health problems
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SEPTIC SHOCK RISK FACTORS
Treatment Related– Invasive lines and
procedures– Surgical procedures– Treatment for burns
or traumatic wounds– Immuno-suppression
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SEPTIC SHOCK CAUSATIVE MICROORGANISMS
Gram Negative– Most cases– E. COLI
– Most likely
– Klebsiella pneumoniae
– Enterobacter aerogenes
– Serratia marcescens
Gram Positive– Less common– Staphylococcus
aureus
Viruses Fungi Rickettsiae Protozoans
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SEPTIC SHOCK CAUSATIVE MICROORGANISMS
Gram Negative– Responsible for the
majority of the cases
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ENTRY SITES FOR SEPTIC SHOCK
Most common - GU Tract
GI Tract
Respiratory Tract
Skin
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SEPTIC SHOCK PATHOGENESIS
Proinflammatory and procoagulation responses dominate and lead to uncontrolled inflammation and advanced coagulopathy
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SEPTIC SHOCK PATHOGENESIS
Three known problems1. Excess Coagulation
2. Exaggerated or malignant inflammation
3. Impaired fibrinolysis
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SEPTIC SHOCK PATHOGENESIS
Balance of coagulation and fibrinolysis shifts toward increased coagulation via the extrinsic pathway
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SEPTIC SHOCK PATHOGENESIS
In mice, microthrombi developed in the hepatic circulation within 5 minutes of injection of endotoxin
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SEPTIC SHOCK PATHOGENESIS
Endotoxin is within the Gram Negative bacteria wall
Released into the blood during bacterial cell lysis
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PATHOGENESIS OF SEPTIC SHOCK
Macrophages– Phagocytic cells
found in the lung interstitium and alveoli, liver, sinuses etc.
– Activated by endotoxin to release cytokines
Cytokines– Tumor necrosis
factor Major endogenous
toxin *
– Interleukin-1– Interleukin-2
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PATHOGENESIS OF SEPTIC SHOCK
Endotoxins activatesEndotoxins activates GRANULOCYTES– Releases toxic
mediators e.g. platelet activating factor, Oxygen derived free radicals
– Proteolytic enzymes
Endotoxins activate Endotoxins activate arachidonic acid arachidonic acid cascadecascade– Results in
prostaglandin, leukotrienes, thromboxane A etc effecting smooth muscle
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PATHOGENESIS OF SEPTIC SHOCK
Thromboxane A2 and B2– Pulmonary
vasoconstriction– Mediate broncho-
onstriction– Potent platelet
aggregator
Prostaglandin E and Prostacyclin– Potent vasodilator– May be responsible
for hypotension
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PATHOGENESIS OF SEPTIC SHOCK
Complement System Activated– Produce microemboli– Endothelial cell
destruction
Histamine– Potent Vasodilator– Released by mast
cells– Increases Capillary
permeability (Fluid moves from vascular bed)
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PATHOGENESIS OF SEPTIC SHOCK
Myocardial Depressant factor (MDF)– Released from
pancreas– Decreases
contractility of the heart
– Coagulation system is activated
Kinin System activated– Bradykinin is
released– Vasodilation– Increased capillary
permeability
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PATHOGENESIS OF SEPTIC SHOCK
MYOCARDIAL DEPRESSANT FACTOR– MAY ENHANCE
DEVELOPMENT OF MICRO EMBOLI
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HEMODYNAMIC ALTERATIONS OF SEPTIC
SHOCK Profound Vasodilation
– Systemic vascular resistance is decreased– Blood Pressure falls– Veins dilate– Intravascular pooling in the venous
capacitance system
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HEMODYNAMIC ALTERATIONS OF SEPTIC
SHOCK Mal-distribution of blood flow
– Some tissues under-perfused and some tissues are over-perfused
– Excessive flow rates to areas of low metabolic demand limits O2 extraction
– Therefore, difference in arterial and venous O2 content
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HEMODYNAMIC ALTERATIONS IN SEPTIC
SHOCK Decreased ejection
fraction– Definition:
Percent of diastolic volume that is ejected during systole
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HEMODYNAMIC ALTERATIONS IN SEPTIC
SHOCK Decreased Ejection Fraction
– Depressed myocardial contractility despite increased cardiac output
– Right ventricular dysfunction is common – usually as a result of pulmonary hypertension and myocardial depression
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HEMODYNAMIC ALTERATIONS IN SEPTIC SHOCK
Increased capillary permeability– Fluid movement out of the vascular beds
and into the interstitial space– Generalized soft tissue edema results– Edema can interfere with tissue
oxygenation and organ function
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HEMODYNAMIC ALTERATIONS IN SEPTIC
SHOCK Microembolization
– Results in sluggish blood flow– Decreased oxygen utilization therefore
increased risk of
D. I. C.D. I. C.
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HYPERDYNAMIC PHASECLINICAL MANIFESTATIONS
BP Falls– Decreased SVR– Decreased venous
return
Decreased sympathetic tone– Diastolic pressure
falls
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HYPERDYNAMIC PHASE -CLINICAL MANIFESTATIONS
Increased sympathetic tone– Widened pulse pressure– Heart rate increases in attempt to increase
CO to compensate for decreased blood pressure
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HYPERDYNAMIC PHASE -CLINICAL MANIFESTATIONS
Impaired gas exchange– Pulmonary blood
congestion– Pulmonary blood
flow decreases
Respiratory rate and depth increase– Early respiratory
alkalosis
Crackles may be audible– Interstitial pulmonary
edema
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HYPERDYNAMIC PHASE - CLINICAL MANIFESTATIONS
Impaired Gas Exchange
Pulmonary vascular resistance increases
Pulmonary congestion results
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HYPERDYNAMIC PHASE-CLINICAL MANIFESTATIONS
Febrile Possible associated
chills Skin pink and warm
– Peripheral vasodilation
LOC may be altered– Cerebral ischemia
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HEMODYNAMIC MANIFESTATIONS-
HYPERDYNAMIC PHASE Decreased SVR
– Cardiac output high– Cardiac Index high
Decreased venous return– Pulmonary artery
pressures below normal
– PCWP below normal
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HEMODYNAMIC MANIFESTATIONS-
HYPERDYNAMIC PHASE Maldistribution of blood flow
Oxygen consumption is decreased
SVO2 levels are above normal
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HYPODYNAMIC PHASE-CLINICAL MANIFESTATIONS
Decreased cardiac output– Rapid, shallow respirations– Crackles and wheezes
Pulmonary congestion
– Decreased Urinary output Renal hypoperfusion
– Lethargic
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HYPODYNAMIC PHASE- CLINICAL MANIFESTATIONS
SNS Stimulation– Peripheral vasoconstriction
Narrowing pulse pressure Cool, clammy skin Increased afterload Decreased contractility PROFOUND HYPOTENSION
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HEMODYNAMIC MANIFESTATIONS-
HYPODYNAMIC PHASE SVR increased CO decreased CI decreased
SEVERE MYOCARDIAL DEPRESSION
PA and PAWP pressures increased
Metabolic and respiratory acidosis with hypoxemia
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CLINICAL MANAGEMENT
1. Fluid Administration– To restore adequate ventricular preload
Maintain PAWP: 12 MM HG Colloids vs. crystalloids
– Colloids my cause movement of fluid into interstitial space because of the capillary permeability
2. If ineffective, may need Dopamine and Dobutamine
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CLINICAL MANAGEMENT
3. Mechanical Ventilation– Greater risk for acute lung injury and ARDS– Low tidal volume of 6 ml/kg
– Maintain plateau pressures at 30 cm H2O or less
• Reduction of mortality of 9%
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CLINICAL MANAGEMENT
4. Glycemic Control Blood sugar 80-100 mg/dl
Mortality reduced by 3.4%
Blood glucose levels of 110-150 mg/dl were associated with a worse outcome
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CLINICAL MANAGEMENT
5. Prevention of Infection– Prevent ventilator associated pneumonia
(VAP) Maintain head of bed elevated at 30 degrees
– Increase 23% infection in supine position
– Oral Care – mouth is colonized within 24 hours
– Deep oral suctioning above the ET cuff
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CLINICAL MANAGEMENT
6. Xigris (Drotrecognifa-activated) aka Drotrecogin alfa (activated)– Approved by US Food and Drug in 2001– Recombinant form of human activated
protein C PROWESS Trial
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CLINICAL MANAGEMENT
Xigris Guidelines– Known or suspected
infection– 2 or more signs of
SIRS– At least 1 failing
organ– High risk for death
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CLINICAL MANAGEMENT
Xigris Contraindications– Active internal
bleeding– Recent hemorrhagic
stroke (3 mos)– Head traum (recent)– Epidural catheter– Intracranial mass
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CLINICAL MANAGEMENT
XigrisCost - $6800/96 hour infusion
Dosage:
24 mcg/kg/hour
Dedicated IV line
80% of the drug’s effects cleared within 30 minutes
Activity is reduced substantially in 15 minutes
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CLINICAL MANAGEMENT
7.Antibiotic therapy – Instituted after the cultures are obtained
– Third generation cephalosporins plus an aminoglycoside
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CLINICAL MANAGEMENT
Possible anti-endotoxin drugs– In research phase– Have been shown to decrease mortality
significantly in patients with septic shock and gram negative bacteremia
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COMPLICATIONSCOMPLICATIONS OF OF SHOCKSHOCK
ARDS
ACUTE RENAL FAILURE
DIC
ACUTE RENAL FAILURE
MULTIPLE ORGAN DYSFUNCTION SYNDROME
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SEVERE SEPSIS/SIRS
Sepsis with acute organ dysfunction
750,000 cases /year 28%-50% mortality
– Definition:
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SIRS
Systemic Inflammatory Response Syndrome– 2 or more of:
Body Temperature > 38 degrees C or < 36 degrees F
Heart Rate >90/min RR - >20/min; or PaCO2
<32 mm Hg WBC - > 12,000 or >
10% bands
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SEVERE SEPSIS/SIRS
Associated with organ dysfunction, hypoperfusion or hypotension– May include but are
not limited to: Lactic acidosis Oliguria Acute alteration in
mental status
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SEPSIS (SIRS)-INDUCED HYPOTENSION
Systolic BP of < 90 mm Hg or a reduction of > 40 mm Hg from baseline in the absence of other causes for hypotension
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SEPTIC SHOCK / SIRS SHOCK
Subset of severe sepsis and defined as sepsis (SIRS)-induced hypotension despite adequate fluid resuscitation along with the presence of perfusion abnormalities that may include but not limited to:
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SEPTIC SHOCK / SIRS SHOCK
– Lactic acidosis– Oliguria– Acute alteration in
mental status
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MODS
Multiple Organ Dysfunction Syndrome– Presence of altered
organ dysfunction in an acutely ill patient such that homeostasis cannot be maintained without intervention
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MODS
Factors in the development– Result of
Bacterial factors Inflammatory
mediators Endothelial injury Disturbed hemostasis Microcirculatory
failure
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MODS
Factors– Patients
Advancing age Pre-existing illness
– Primary Cellular Injury
Underlying disease processes
Toxic effects of certain mediators
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MODS
Factors– Microaggregates
Platelets, neutrophils, RBC’s and fibrin impair microcirculatory blood flow and produce tissue ischemia
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MODS
Factors– Endothelial Cell
Injury Proinflammatory
cytokines Alters vasomotor tone Capillary leakage-
pulmonary edema
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MODS
Factors– Metabolic
Derangement Mitochondrial
dysfunction– Oxidants are
produced during endotoxin induced shock
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MODS
Factors– Humoral Mediators
TNF- and IL-1– Attract leukocytes
to site of infection
– Excess levels cause general response
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MODS
Factors– Therapy –induced
dysfunction Mechanical ventilation at
higher volumes Blood transfusions Hyperglycemia
– Activates tissue factor pathway for coagulation
• Enhanced thrombin formation
• Acute thrombosis
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MODS
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MODS
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MODS
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MODS
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MODS
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SIRS
Systemic Inflammatory Response Syndrome
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SIRS
Systemic Inflammatory Response Syndrome
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SIRS
Systemic Inflammatory Response Syndrome
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SIRS
Systemic Inflammatory Response Syndrome
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SIRS
Systemic Inflammatory Response Syndrome
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SEVERE SEPSIS
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SEVERE SEPSIS
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SEVERE SEPSIS
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SEVERE SEPSIS
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SEVERE SEPSIS
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SEVERE SEPSIS
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IN SUMMARY......
SEPTIC SHOCK IS A MASSIVE INFECTION CAUSING VASODILATION AND INADEQUATE TISSUE PERFUSION
THERAPY IS AIMED AT IMPROVING DISTRIBUTION OF BLOOD FLOW AND TREATING INFECTION
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THANK YOU