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

http://images.google.com/imgres?imgurl=www.tomklare.com/glitch/glitchgifs/e-coli.gif&imgrefurl=http://www.tomklare.com/glitch/ecoli.html&h=360&w=455&prev=/images%3Fq%3De.%2Bcoli%26svnum%3D10%26hl%3Den%26lr%3D%26ie%3DUTF-8%26oe%3DUTF-8%26sa%3DN

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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

http://www.cat.cc.md.us/courses/bio141/lecguide/unit1/bacpath/images/lps.gif

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)

http://images.medscape.com/pi/editorial/cmecircle/2002/1817/peden/slide40.jpg

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

http://www.meddean.luc.edu/lumen/MedEd/medicine/pulmonar/images/leischne/Scan51.jpg

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

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http://www.rchc.rush.edu/rmawebfiles/chd/vsd/normal_pulse_pressure.jpg

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

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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

http://www.liu.edu/cwis/bklyn/acadres/facdev/FacultyProjects/WebClass/micro-web/images/antibiotics.gif

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