Transcript septic shock - donaldhudson.org

SEPTIC SHOCK
By
Marian D. Williams RN BN CEN CFRN CCRN
SEPTIC SHOCK
Most common cause of death in noncardiac 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
problems
1. Excess Coagulation
2. 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 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
PATHOGENESIS OF
SEPTIC SHOCK

Thromboxane A2
and B2
– Pulmonary
vasoconstriction
– Mediate bronchoonstriction
– 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.
HYPERDYNAMIC PHASE
CLINICAL 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 PHASECLINICAL MANIFESTATIONS



Febrile
Possible associated
chills
Skin pink and warm
– Peripheral
vasodilation

LOC may be altered
– Cerebral ischemia
HEMODYNAMIC MANIFESTATIONSHYPERDYNAMIC PHASE

Decreased SVR
–
–
Cardiac output high
Cardiac Index high

Decreased venous
return
– Pulmonary artery
pressures below
normal
– PCWP below normal
HEMODYNAMIC MANIFESTATIONSHYPERDYNAMIC PHASE

Maldistribution of blood flow

Oxygen consumption is decreased

SVO2 levels are above normal
HYPODYNAMIC PHASECLINICAL 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 MANIFESTATIONSHYPODYNAMIC PHASE



SVR increased
CO decreased
CI decreased
SEVERE
MYOCARDIAL
DEPRESSION


PA and PAWP
pressures increased
Metabolic and
respiratory acidosis
with hypoxemia
CLINICAL MANAGEMENT
Fluid Administration
1.
–
To restore adequate ventricular preload


Maintain PAWP: 12 MM HG
Colloids vs. crystalloids
–
2.
Colloids my cause movement of fluid into interstitial
space because of the capillary permeability
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
associated with a worse outcome
were
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

Xigris
Cost - $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
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
COMPLICATIONS OF
SHOCK

ARDS

ACUTE RENAL
FAILURE

ACUTE RENAL
FAILURE

MULTIPLE ORGAN
DYSFUNCTION
SYNDROME

DIC
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 leakagepulmonary 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

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