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SEPTIC SHOCK

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By 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 ... – PowerPoint PPT presentation

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Title: SEPTIC SHOCK


1
SEPTIC SHOCK
  • By
  • Marian D. Williams RN BN CEN CFRN CCRN

2
SEPTIC SHOCK
  • Most common cause of death in non-cardiac ICUs
    in the US
  • Most cases are nosocomial
  • Increased incidence due to advanced invasive
    technology
  • Elderly are at greatest risk
  • Mortality40-85

3
SEPTIC SHOCK
  • 10th leading cause of death in the United States
  • 139 increase from 1979 - 1987

4
SEPTIC SHOCK
  • DEFINITIONS
  • Bacteremia
  • Presence of BACTERIA in the blood
  • Bodys defense systems effectively destroy
    bacteria
  • Septicemia
  • Presence of MICROBES in the blood associated with
    systemic infection

5
SEPTIC SHOCK
  • Sepsis
  • Systemic inflammatory response to infection.
  • Severe Sepsis/SIRS
  • Sepsis associated with evidence of one or more
    acute organ dysfunctions

6
SEPTIC SHOCK RISK FACTORS
  • Patient related
  • lt 1 year of age
  • gt 65 years of age
  • Debilitated
  • Malnourished
  • Chronic health problems

7
SEPTIC SHOCK RISK FACTORS
  • Treatment Related
  • Invasive lines and procedures
  • Surgical procedures
  • Treatment for burns or traumatic wounds
  • Immuno-suppression

8
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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11
SEPTIC SHOCK CAUSATIVE MICROORGANISMS
  • Gram Negative
  • Responsible for the majority of the cases

12
ENTRY SITES FOR SEPTIC SHOCK
  • Most common - GU Tract
  • GI Tract
  • Respiratory Tract
  • Skin

13
SEPTIC SHOCK PATHOGENESIS
  • Proinflammatory and procoagulation responses
    dominate and lead to uncontrolled inflammation
    and advanced coagulopathy

14
SEPTIC SHOCK PATHOGENESIS
  • Three known problems
  • Excess Coagulation
  • Exaggerated or malignant inflammation
  • Impaired fibrinolysis

15

16
SEPTIC SHOCK PATHOGENESIS
  • Balance of coagulation and fibrinolysis shifts
    toward increased coagulation via the extrinsic
    pathway

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18
SEPTIC SHOCK PATHOGENESIS
  • In mice, microthrombi developed in the hepatic
    circulation within 5 minutes of injection of
    endotoxin

19
SEPTIC SHOCK PATHOGENESIS
  • Endotoxin is within the Gram Negative bacteria
    wall
  • Released into the blood during bacterial cell
    lysis

20
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

21
PATHOGENESIS OF SEPTIC SHOCK
  • Endotoxins activates GRANULOCYTES
  • Releases toxic mediators e.g. platelet activating
    factor, Oxygen derived free radicals
  • Proteolytic enzymes
  • Endotoxins activate arachidonic acid cascade
  • Results in prostaglandin, leukotrienes,
    thromboxane A etc effecting smooth muscle

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23
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

24
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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26
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

27
PATHOGENESIS OF SEPTIC SHOCK
  • MYOCARDIAL DEPRESSANT FACTOR
  • MAY ENHANCE DEVELOPMENT OF MICRO EMBOLI

28
HEMODYNAMIC ALTERATIONS OF SEPTIC SHOCK
  • Profound Vasodilation
  • Systemic vascular resistance is decreased
  • Blood Pressure falls
  • Veins dilate
  • Intravascular pooling in the venous capacitance
    system

29
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

30
HEMODYNAMIC ALTERATIONS IN SEPTIC SHOCK
  • Decreased ejection fraction
  • Definition
  • Percent of diastolic volume that is ejected
    during systole

31
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

32
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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35
HEMODYNAMIC ALTERATIONS IN SEPTIC SHOCK
  • Microembolization
  • Results in sluggish blood flow
  • Decreased oxygen utilization therefore increased
    risk of
  • D. I. C.

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37
HYPERDYNAMIC PHASE CLINICAL 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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42
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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44
HYPERDYNAMIC PHASE - CLINICAL MANIFESTATIONS
  • Impaired Gas Exchange
  • Pulmonary vascular resistance increases
  • Pulmonary congestion results

45
HYPERDYNAMIC PHASE- CLINICAL MANIFESTATIONS
  • Febrile
  • Possible associated chills
  • Skin pink and warm
  • Peripheral vasodilation
  • LOC may be altered
  • Cerebral ischemia

46
HEMODYNAMIC MANIFESTATIONS- HYPERDYNAMIC PHASE
  • Decreased SVR
  • Cardiac output high
  • Cardiac Index high
  • Decreased venous return
  • Pulmonary artery pressures below normal
  • PCWP below normal

47
HEMODYNAMIC MANIFESTATIONS- HYPERDYNAMIC PHASE
  • Maldistribution of blood flow
  • Oxygen consumption is decreased
  • SVO2 levels are above normal

48
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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50
HYPODYNAMIC PHASE- CLINICAL MANIFESTATIONS
  • SNS Stimulation
  • Peripheral vasoconstriction
  • Narrowing pulse pressure
  • Cool, clammy skin
  • Increased afterload
  • Decreased contractility
  • PROFOUND HYPOTENSION

51
HEMODYNAMIC MANIFESTATIONS- HYPODYNAMIC PHASE
  • SVR increased
  • CO decreased
  • CI decreased
  • SEVERE MYOCARDIAL DEPRESSION
  • PA and PAWP pressures increased
  • Metabolic and respiratory acidosis with hypoxemia

52
CLINICAL MANAGEMENT
  • 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
  • If ineffective, may need Dopamine and Dobutamine

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54
CLINICAL MANAGEMENT
  • 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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56
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

57
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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59
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

60
CLINICAL MANAGEMENT
  • Xigris Guidelines
  • Known or suspected infection
  • 2 or more signs of SIRS
  • At least 1 failing organ
  • High risk for death

61
CLINICAL MANAGEMENT
  • Xigris Contraindications
  • Active internal bleeding
  • Recent hemorrhagic stroke (3 mos)
  • Head traum (recent)
  • Epidural catheter
  • Intracranial mass

62
CLINICAL MANAGEMENT
  • Xigris
  • Cost - 6800/96 hour infusion
  • Dosage
  • 24 mcg/kg/hour
  • Dedicated IV line
  • 80 of the drugs effects cleared within 30
    minutes
  • Activity is reduced substantially in 15 minutes

63
CLINICAL MANAGEMENT
  • 7. Antibiotic therapy
  • Instituted after the cultures are obtained
  • Third generation cephalosporins plus an
    aminoglycoside

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65
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

66
COMPLICATIONS OF SHOCK
  • ARDS
  • ACUTE RENAL FAILURE
  • DIC
  • ACUTE RENAL FAILURE
  • MULTIPLE ORGAN DYSFUNCTION SYNDROME

67
SEVERE SEPSIS/SIRS
  • Sepsis with acute organ dysfunction
  • 750,000 cases /year
  • 28-50 mortality
  • Definition

68
SIRS
  • Systemic Inflammatory Response Syndrome
  • 2 or more of
  • Body Temperature gt 38 degrees C or lt 36 degrees F
  • Heart Rate gt90/min
  • RR - gt20/min or PaCO2 lt32 mm Hg
  • WBC - gt 12,000 or gt 10 bands

69
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

70
SEPSIS (SIRS)-INDUCED HYPOTENSION
  • Systolic BP of lt 90 mm Hg or a reduction of gt 40
    mm Hg from baseline in the absence of other
    causes for hypotension

71
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

72
SEPTIC SHOCK / SIRS SHOCK
  • Lactic acidosis
  • Oliguria
  • Acute alteration in mental status

73
MODS
  • Multiple Organ Dysfunction Syndrome
  • Presence of altered organ dysfunction in an
    acutely ill patient such that homeostasis cannot
    be maintained without intervention

74
MODS
  • Factors in the development
  • Result of
  • Bacterial factors
  • Inflammatory mediators
  • Endothelial injury
  • Disturbed hemostasis
  • Microcirculatory failure

75
MODS
  • Factors
  • Patients
  • Advancing age
  • Pre-existing illness
  • Primary Cellular Injury
  • Underlying disease processes
  • Toxic effects of certain mediators

76
MODS
  • Factors
  • Microaggregates
  • Platelets, neutrophils, RBCs and fibrin impair
    microcirculatory blood flow and produce tissue
    ischemia

77
MODS
  • Factors
  • Endothelial Cell Injury
  • Proinflammatory cytokines
  • Alters vasomotor tone
  • Capillary leakage-pulmonary edema

78
MODS
  • Factors
  • Metabolic Derangement
  • Mitochondrial dysfunction
  • Oxidants are produced during endotoxin induced
    shock

79
MODS
  • Factors
  • Humoral Mediators
  • TNF-? and IL-1
  • Attract leukocytes to site of infection
  • Excess levels cause general response

80
MODS
  • Factors
  • Therapy induced dysfunction
  • Mechanical ventilation at higher volumes
  • Blood transfusions
  • Hyperglycemia
  • Activates tissue factor pathway for coagulation
  • Enhanced thrombin formation
  • Acute thrombosis

81
MODS
82
MODS
83
MODS
84
MODS
85
MODS
86
SIRS
  • Systemic Inflammatory Response Syndrome

87
SIRS
  • Systemic Inflammatory Response Syndrome

88
SIRS
  • Systemic Inflammatory Response Syndrome

89
SIRS
  • Systemic Inflammatory Response Syndrome

90
SIRS
  • Systemic Inflammatory Response Syndrome

91
SEVERE SEPSIS
92
SEVERE SEPSIS
93
SEVERE SEPSIS
94
SEVERE SEPSIS
95
SEVERE SEPSIS
96
SEVERE SEPSIS
97
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

98
THANK YOU
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