Post on 25-Feb-2016
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SEPTIC SHOCKSEPTIC SHOCKBy
Marian D. Williams RN BN CEN CFRN CCRN
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%
SEPTIC SHOCK 10th leading cause of death in the United
States 139% increase from 1979 - 1987
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
SEPTIC SHOCK Sepsis
– Systemic inflammatory response to infection.
Severe Sepsis/SIRS– Sepsis associated with evidence of one or
more acute organ dysfunctions
SEPTIC SHOCK RISK FACTORS
Patient related– < 1 year of age– > 65 years of age– Debilitated– Malnourished– Chronic health problems
SEPTIC SHOCK RISK FACTORS
Treatment Related– Invasive lines and
procedures– Surgical procedures– Treatment for burns
or traumatic wounds– Immuno-suppression
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
SEPTIC SHOCK CAUSATIVE MICROORGANISMS
Gram Negative– Responsible for the
majority of the cases
ENTRY SITES FOR SEPTIC SHOCK
Most common - GU Tract
GI Tract
Respiratory Tract
Skin
SEPTIC SHOCK PATHOGENESIS
Proinflammatory and procoagulation responses dominate and lead to uncontrolled inflammation and advanced coagulopathy
SEPTIC SHOCK PATHOGENESIS
Three known problems1. Excess Coagulation2. Exaggerated or
malignant inflammation
3. Impaired fibrinolysis
SEPTIC SHOCK PATHOGENESIS
Balance of coagulation and fibrinolysis shifts toward increased coagulation via the extrinsic pathway
SEPTIC SHOCK PATHOGENESIS
In mice, microthrombi developed in the hepatic circulation within 5 minutes of injection of endotoxin
SEPTIC SHOCK PATHOGENESIS
Endotoxin is within the Gram Negative bacteria wall
Released into the blood during bacterial cell lysis
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
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
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
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)
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
PATHOGENESIS OF SEPTIC SHOCK
MYOCARDIAL DEPRESSANT FACTOR– MAY ENHANCE
DEVELOPMENT OF MICRO EMBOLI
HEMODYNAMIC ALTERATIONS OF SEPTIC
SHOCK Profound Vasodilation
– Systemic vascular resistance is decreased– Blood Pressure falls– Veins dilate– Intravascular pooling in the venous
capacitance system
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
HEMODYNAMIC ALTERATIONS IN SEPTIC
SHOCK Decreased ejection
fraction– Definition:
Percent of diastolic volume that is ejected during systole
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
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
HEMODYNAMIC ALTERATIONS IN SEPTIC
SHOCK Microembolization
– Results in sluggish blood flow– Decreased oxygen utilization therefore
increased risk of
D. I. C.D. I. C.
HYPERDYNAMIC PHASECLINICAL MANIFESTATIONS
BP Falls– Decreased SVR– Decreased venous
return Decreased
sympathetic tone– Diastolic pressure
falls
HYPERDYNAMIC PHASE -CLINICAL MANIFESTATIONS
Increased sympathetic tone– Widened pulse pressure– Heart rate increases in attempt to increase
CO to compensate for decreased blood pressure
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
HYPERDYNAMIC PHASE - CLINICAL MANIFESTATIONS
Impaired Gas Exchange
Pulmonary vascular resistance increases
Pulmonary congestion results
HYPERDYNAMIC PHASE-CLINICAL MANIFESTATIONS
Febrile Possible associated
chills Skin pink and warm
– Peripheral vasodilation
LOC may be altered– Cerebral ischemia
HEMODYNAMIC MANIFESTATIONS-
HYPERDYNAMIC PHASE Decreased SVR
– Cardiac output high– Cardiac Index high
Decreased venous return– Pulmonary artery
pressures below normal
– PCWP below normal
HEMODYNAMIC MANIFESTATIONS-
HYPERDYNAMIC PHASE Maldistribution of blood flow
Oxygen consumption is decreased
SVO2 levels are above normal
HYPODYNAMIC PHASE-CLINICAL MANIFESTATIONS
Decreased cardiac output– Rapid, shallow respirations– Crackles and wheezes
Pulmonary congestion– Decreased Urinary output
Renal hypoperfusion– Lethargic
HYPODYNAMIC PHASE- CLINICAL MANIFESTATIONS
SNS Stimulation– Peripheral vasoconstriction
Narrowing pulse pressure Cool, clammy skin Increased afterload Decreased contractility PROFOUND HYPOTENSION
HEMODYNAMIC MANIFESTATIONS-
HYPODYNAMIC PHASE SVR increased CO decreased CI decreased
SEVERE MYOCARDIAL DEPRESSION
PA and PAWP pressures increased
Metabolic and respiratory acidosis with hypoxemia
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
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%
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
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
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
CLINICAL MANAGEMENT Xigris Guidelines
– Known or suspected infection
– 2 or more signs of SIRS
– At least 1 failing organ
– High risk for death
CLINICAL MANAGEMENT Xigris
Contraindications– Active internal
bleeding– Recent hemorrhagic
stroke (3 mos)– Head traum (recent)– Epidural catheter– Intracranial mass
CLINICAL MANAGEMENT
XigrisCost - $6800/96 hour infusionDosage:
24 mcg/kg/hourDedicated IV line80% of the drug’s effects cleared within 30 minutesActivity is reduced substantially in 15 minutes
CLINICAL MANAGEMENT
7.Antibiotic therapy – Instituted after the cultures are obtained
– Third generation cephalosporins plus an aminoglycoside
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
COMPLICATIONSCOMPLICATIONS OF OF SHOCKSHOCK
ARDS
ACUTE RENAL FAILURE
DIC
ACUTE RENAL FAILURE
MULTIPLE ORGAN DYSFUNCTION SYNDROME
SEVERE SEPSIS/SIRS Sepsis with acute
organ dysfunction 750,000 cases /year 28%-50% mortality
– Definition:
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
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
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
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:
SEPTIC SHOCK / SIRS SHOCK
– Lactic acidosis– Oliguria– Acute alteration in
mental status
MODS Multiple Organ
Dysfunction Syndrome– Presence of altered
organ dysfunction in an acutely ill patient such that homeostasis cannot be maintained without intervention
MODS Factors in the
development– Result of
Bacterial factors Inflammatory
mediators Endothelial injury Disturbed hemostasis Microcirculatory
failure
MODS Factors
– Patients Advancing age Pre-existing illness
– Primary Cellular Injury
Underlying disease processes
Toxic effects of certain mediators
MODS Factors
– Microaggregates Platelets, neutrophils,
RBC’s and fibrin impair microcirculatory blood flow and produce tissue ischemia
MODS Factors
– Endothelial Cell Injury
Proinflammatory cytokines
Alters vasomotor tone Capillary leakage-
pulmonary edema
MODS Factors
– Metabolic Derangement
Mitochondrial dysfunction
– Oxidants are produced during endotoxin induced shock
MODS Factors
– Humoral Mediators TNF- and IL-1
– Attract leukocytes to site of infection
– Excess levels cause general response
MODS Factors
– Therapy –induced dysfunction
Mechanical ventilation at higher volumes
Blood transfusions Hyperglycemia
– Activates tissue factor pathway for coagulation
• Enhanced thrombin formation
• Acute thrombosis
MODS
MODS
MODS
MODS
MODS
SIRS Systemic
Inflammatory Response Syndrome
SIRS Systemic
Inflammatory Response Syndrome
SIRS Systemic
Inflammatory Response Syndrome
SIRS Systemic
Inflammatory Response Syndrome
SIRS Systemic
Inflammatory Response Syndrome
SEVERE SEPSIS
SEVERE SEPSIS
SEVERE SEPSIS
SEVERE SEPSIS
SEVERE SEPSIS
SEVERE SEPSIS
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
THANK YOU