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Shock and Systemic Inflammatory Shock and Systemic Inflammatory Response Syndrome Response Syndrome By: Bryan Mae H. Degorio, RN By: Bryan Mae H. Degorio, RN

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Page 1: Shock and SIRS

Shock and Systemic Inflammatory Shock and Systemic Inflammatory Response SyndromeResponse Syndrome

By: Bryan Mae H. Degorio, RN By: Bryan Mae H. Degorio, RN

Page 2: Shock and SIRS

ShockShock- - is a is a life threateninglife threatening condition with a condition with a

variety of underlying causes.variety of underlying causes.

- Characterized by - Characterized by inadequate tissue inadequate tissue perfusion that ,if untreated , perfusion that ,if untreated ,

results in cell death.results in cell death.

- - Systematic blood pressure is Systematic blood pressure is inadequate to deliver oxygeninadequate to deliver oxygen and and nutrients to support vital organs nutrients to support vital organs and cellular functions.and cellular functions.

Page 3: Shock and SIRS

- Blalock in 1934, categorized shock - Blalock in 1934, categorized shock into 4 etiology or causes:into 4 etiology or causes:

a. Hematogenica. Hematogenic

b. Neurogenicb. Neurogenic

c. Vasogenicc. Vasogenic

d. Cardiogenicd. Cardiogenic

- 3 Major Factors that Regulate the - 3 Major Factors that Regulate the Circulatory Mechanism:Circulatory Mechanism:

a. Preloada. Preload

b. Ventricular contractionb. Ventricular contraction

c. Afterloadc. Afterload

Page 4: Shock and SIRS

--typestypes::1. Hypovolemic Shock1. Hypovolemic Shock2. Cardiogenic Shock2. Cardiogenic Shock3. Circulatory Shock (Distributive Shock)3. Circulatory Shock (Distributive Shock)

> Septic Shock> Septic Shock> Neurogenic Shock> Neurogenic Shock> Anaphylactic Shock> Anaphylactic Shock

*Obstructive Shock*Obstructive Shock-Vascular Responses-Vascular Responses

1. Central Regulatory Mechanisms1. Central Regulatory Mechanisms2. Local Regulatory Mechanisms2. Local Regulatory Mechanisms

Page 5: Shock and SIRS

--Blood Pressure RegulationBlood Pressure RegulationBP= CO x TPRBP= CO x TPR CO= SV x HRCO= SV x HR

>Maintained by:>Maintained by:a. nervous systema. nervous systemb. endocrine systemb. endocrine systemc. chemicalsc. chemicals

>Maintain tissue/organ perfusion:>Maintain tissue/organ perfusion:a. MAP= a. MAP= systolic BP + 2 (diastolic BP)systolic BP + 2 (diastolic BP)

33*should exceed 70-80 mmHg*should exceed 70-80 mmHg

--Stages of ShockStages of Shock1. Compensatory Stage1. Compensatory Stage

>BP is maintained within normal limits >BP is maintained within normal limits due to the due to the effect of normally effect of normally

functioning functioning regulatory mechanismsregulatory mechanisms

Page 6: Shock and SIRS

>s/sx:>s/sx:

- - cold clammy skincold clammy skin

- oliguria- oliguria

- hypoactive bowel sounds can be - hypoactive bowel sounds can be assessed. assessed.

>medical management:>medical management:a. identify the cause of shocka. identify the cause of shock

b. correction of shockb. correction of shock

c. support of the regulatory c. support of the regulatory mechanismsmechanisms

>nursing management:>nursing management:

a. monitoring tissue perfusiona. monitoring tissue perfusion

*LOC*LOC*urine output*urine output *V/S*V/S*skin*skin*laboratory values*laboratory values

Page 7: Shock and SIRS

b. reducing anxietyb. reducing anxietyc. promoting safetyc. promoting safety

2. Progressive Stage2. Progressive Stage-exhaustion of the compensatory -exhaustion of the compensatory

mechanismsmechanisms- - In this stage, the mechanisms that In this stage, the mechanisms that

regulate blood pressure can no regulate blood pressure can no longer longer compensate and the compensate and the mean mean arterial arterial pressure falls.pressure falls.

Page 8: Shock and SIRS

-assessment and dxtic findings:-assessment and dxtic findings:a. respiratory effectsa. respiratory effects

hypoxemia and hypercarbiahypoxemia and hypercarbia

intense inflammatory responseintense inflammatory response

decreased surfactant productiondecreased surfactant production

acute respiratory distress syndromeacute respiratory distress syndrome

(acute lung injury, shock lung, non (acute lung injury, shock lung, non cardiogenic pulmonary edema)cardiogenic pulmonary edema)

Page 9: Shock and SIRS

b. cardiovascular effectsb. cardiovascular effects

dysrhythmiasdysrhythmias

myocardial infarctionmyocardial infarction

cardiac depressioncardiac depression

c. neurologic effectsc. neurologic effects

decreased cerebral perfusiondecreased cerebral perfusion

*mental status change*mental status change

*behavioral change*behavioral change

*pupillary dilation*pupillary dilation

d. renal effectsd. renal effects

MAP<80mmHgMAP<80mmHg

acute renal failureacute renal failure

Page 10: Shock and SIRS

e. hepatic effectse. hepatic effectsdecreased blood flowdecreased blood flow

less ability to perform hepatic functionsless ability to perform hepatic functions

f. gastrointestinal effectsf. gastrointestinal effectsdecreased blood flowdecreased blood flow

*PUD*PUD *bloody diarrhea*bloody diarrhea *sepsis*sepsis

g. hematologicg. hematologic

DIC DIC

shockshock

Page 11: Shock and SIRS

-medical management:-medical management:a. depends on the type of shocka. depends on the type of shock

b. depends on the decompensation of the b. depends on the decompensation of the organ systemsorgan systems

Management Common To All Types Of ShockManagement Common To All Types Of Shocka. optimize intravascular volumea. optimize intravascular volume

b. supporting the pumping action of the heartb. supporting the pumping action of the heart

c. improving the competence of the vascular c. improving the competence of the vascular systemsystem

Nursing ManagementNursing Management::a. preventing complicationsa. preventing complications

b. promoting rest and comfortb. promoting rest and comfort

c. supporting family membersc. supporting family members

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3. 3. Irreversible StageIrreversible Stage

-severe organ damage-severe organ damage

-can no longer respond to treatment-can no longer respond to treatment

-survival is less likely-survival is less likely

-medical management:-medical management:a. same with the progressive stagea. same with the progressive stage

b. b. the use of life supporting drugs the use of life supporting drugs like epinephrine and investigational like epinephrine and investigational medicationsmedications. .

-nursing management:-nursing management:a. same with progressive shocka. same with progressive shock

b. moral support to the familyb. moral support to the family

c. ethical issues (living will) c. ethical issues (living will)

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Clinical Findings in the Stages of ShockClinical Findings in the Stages of Shock

FindingFinding CompensatoryCompensatory ProgressiveProgressive IrreversibleIrreversible

BPBP normalnormal Systolic <80 -Systolic <80 -90mmHg90mmHg

Mechanical or Mechanical or pharma supportpharma support

HRHR >100bpm>100bpm >150bpm>150bpm erratic, asystoleerratic, asystole

RespirationRespiration >20 breaths/ >20 breaths/ minmin

Rapid, shallow Rapid, shallow cracklescrackles

IntubationIntubation

SkinSkin cold, clammycold, clammy Mottled, Mottled, petechiaepetechiae

JaundiceJaundice

Urine Urine OutputOutput

decreaseddecreased 0.5ml/kg/hr0.5ml/kg/hr anuria, needs anuria, needs dialysisdialysis

MentationMentation confusionconfusion LethargyLethargy ComaComa

Page 14: Shock and SIRS

FindingFinding CompensatoryCompensatory ProgressiveProgressive IrreversibleIrreversible

A/B BalanceA/B Balance Resp AlkalosisResp Alkalosis Met AcidosisMet Acidosis Profound Profound AcidosisAcidosis

Page 15: Shock and SIRS

General Management for ShockGeneral Management for Shock

• fluid replacement to restore fluid replacement to restore intravascular volumeintravascular volume

• vasoactive medications to restore vasoactive medications to restore vasomotor tone and improve cardiac vasomotor tone and improve cardiac functionfunction

• nutritional support to address the nutritional support to address the metabolic requirements that are metabolic requirements that are dramatically increased in shockdramatically increased in shock

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A.A. Fluid Replacement:Fluid Replacement:

- - Is administered in all types of Is administered in all types of shocks. The type of fluids administered shocks. The type of fluids administered and the speed of delivery vary, but fluids and the speed of delivery vary, but fluids are given to improve cardiac and tissue are given to improve cardiac and tissue oxygenation.oxygenation.

- may include - may include CRYSTALLOIDSCRYSTALLOIDS (electrolyte solutions that move freely (electrolyte solutions that move freely between intravascular and interstitial between intravascular and interstitial space), space), COLLOIDSCOLLOIDS (large-molecule (large-molecule intravenous solutions) or blood intravenous solutions) or blood components.components.

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COMLICATIONS OF FLUID ADMINISTRATIONCOMLICATIONS OF FLUID ADMINISTRATION

- The most common and serious - The most common and serious side effect of fluid replacement are side effect of fluid replacement are

cardiovascular overload and pulmonary cardiovascular overload and pulmonary edema.edema.

B.  B.  VASOACTIVE MEDICATION THERAPYVASOACTIVE MEDICATION THERAPY

- - Administered in all forms of Administered in all forms of shocks to improve the patients shocks to improve the patients hemodynamic stability when fluid hemodynamic stability when fluid therapy alone cannot maintain therapy alone cannot maintain adequate MAP. adequate MAP.

Page 18: Shock and SIRS

-Vasoactive medications are -Vasoactive medications are selected for their action on receptors of selected for their action on receptors of the sympathetic nervous system.the sympathetic nervous system.

- when vasoactive medications - when vasoactive medications are administered, vital sign must be are administered, vital sign must be monitored frequently(at least every monitored frequently(at least every 15min until stable or more often if 15min until stable or more often if

indicated)indicated)

Page 19: Shock and SIRS

C. C. NUTRITIONAL SUPPORT NUTRITIONAL SUPPORT --Nutritional support is an Nutritional support is an

important aspect of care for the patient important aspect of care for the patient with shocks. with shocks.

-Increased metabolic rates during -Increased metabolic rates during shock increase energy requirements. shock increase energy requirements. The patients in shocks requires more The patients in shocks requires more than 3000 calories daily. than 3000 calories daily.

- The release of catecholamines - The release of catecholamines early in the shocks continuum causes early in the shocks continuum causes glycogen stores to the depleted in glycogen stores to the depleted in

about 8 to 10 hours.about 8 to 10 hours.

  

Page 20: Shock and SIRS

TYPES OF SCHOCKTYPES OF SCHOCK

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HYPOVOLEMIC SHOCKHYPOVOLEMIC SHOCK

-most common type of shock-most common type of shock

-characterized by decreased intravascular -characterized by decreased intravascular volume of 15-25%volume of 15-25%

-predisposing factors:-predisposing factors:

External: External: Fluid LossesFluid Losses Internal: Internal: Fluid Fluid ShiftsShifts

a. traumaa. trauma a. hemorrhagea. hemorrhage

b. surgeryb. surgery b. burnsb. burns

c. vomitingc. vomiting c. ascitesc. ascites

d. diarrhead. diarrhea d. peritonitisd. peritonitis

e. diuresise. diuresis e. dehydratione. dehydration

f. diabetes insipidusf. diabetes insipidus

Page 22: Shock and SIRS

Manifestations:Manifestations:

1. Decreased Level of Consciousness1. Decreased Level of Consciousness

2. Tachycardia (pulse: weak and 2. Tachycardia (pulse: weak and thready)thready)

3. Decreased B/P3. Decreased B/P

4. Decreased Cardiac Output (CO= 4. Decreased Cardiac Output (CO= SV x HR)SV x HR)

5. Decreased Urinary Output5. Decreased Urinary Output

6. Cool, Clammy Skin6. Cool, Clammy Skin

Page 23: Shock and SIRS

DECREASED IN BLOOD VOLUME

DECREASE IN VENOUS RETURN

DECREASE IN STROKE VOLUME

DECREASE IN TISSUE PERFURION

DECREASED IN CARDIAC OUTPUT

PATHOPHYSIOLOGY

Page 24: Shock and SIRS

-medical management:-medical management:

>goals:>goals:

a. restore intravascular volumea. restore intravascular volume

b. redistribute fluid volumeb. redistribute fluid volume

c. correct the underlying causec. correct the underlying cause

*pharmacologic therapy*pharmacologic therapy

desmopressindesmopressin anti-emeticanti-emetic

insulininsulin anti-diarrheaanti-diarrhea

-nursing management:-nursing management:

a. administer O2 as ordereda. administer O2 as ordered

b. administering blood and fluids safelyb. administering blood and fluids safely

c. assess type client hydration statusc. assess type client hydration status

Page 25: Shock and SIRS

d. monitor hemoglobin and hematocrit d. monitor hemoglobin and hematocrit levellevel

e. Monitor the circulatory status (HR, e. Monitor the circulatory status (HR, arterial pressure, peripheral arterial pressure, peripheral perfusion, and UO.)perfusion, and UO.)

f. Monitor Vs and for hypotensionf. Monitor Vs and for hypotension

g. Monitor I and O, urine output, and g. Monitor I and O, urine output, and insert FBC as orderedinsert FBC as ordered

h. Monitor LOCh. Monitor LOC

e. Administer small doses of narcotic e. Administer small doses of narcotic analgesic as orderedanalgesic as ordered

f. Antibiotic for severely injuredf. Antibiotic for severely injured

g. Pressure on site- severe traumag. Pressure on site- severe trauma

Page 26: Shock and SIRS

CARDIOGENIC SHOCKCARDIOGENIC SHOCK

-failure of the heart to pump blood adequately to -failure of the heart to pump blood adequately to the circulation causing reduction in COthe circulation causing reduction in CO

-due to cardiac failure-due to cardiac failure

-either coronary and non coronary-either coronary and non coronary

Coronary FactorsCoronary Factors Non Coronary FactorsNon Coronary Factors

a. myocardial a. myocardial a. cardiomyopathiesa. cardiomyopathies infarction infarction b. valvular damageb. valvular damage

c. cardiac tamponadec. cardiac tamponade

d. dysrhythmiasd. dysrhythmias

-signs and symptoms:-signs and symptoms:

a. anginal paina. anginal pain

b. hemodynamic instabilityb. hemodynamic instability

c. dysrhythmiasc. dysrhythmias

Page 27: Shock and SIRS

Decreased cardiac contractility

Decreased stroke volume and Cardiac output

Pulmonary congestion

Decreased systemic tissue perfusion Decreased coronary

artery perfusion

Pathophysiology

Ineffective ventricular emptying

Page 28: Shock and SIRS

--medical managementmedical management::

a. correction of underlying causea. correction of underlying cause

b. initiation of first line b. initiation of first line treatmenttreatment

*supplemental oxygen*supplemental oxygen*vasoactive medications*vasoactive medications

*controlling chest pain*controlling chest pain*controlling HR*controlling HR

*selected fluid support*selected fluid support*mechanical cardiac support*mechanical cardiac support

Page 29: Shock and SIRS

c. pharmacologic therapyc. pharmacologic therapy

*dobutamine*dobutamine*nitroglycerine*nitroglycerine

*dopamine*dopamine*vasoactive meds*vasoactive meds

*anti-arrhythmic meds*anti-arrhythmic meds

d. fluid therapyd. fluid therapy

--nursing managementnursing management::

a. administer IV morphine sulfatea. administer IV morphine sulfate

b. administer O2b. administer O2

c. Prepare client for mechanical ventilationc. Prepare client for mechanical ventilation

d. administer diuretics and nitrates while d. administer diuretics and nitrates while constantly monitoring the BPconstantly monitoring the BP

Page 30: Shock and SIRS

e. Administer vasopressin, and postive e. Administer vasopressin, and postive inotropicinotropic

f. Prepare the client for the insertion of f. Prepare the client for the insertion of intraaortic balloon pump.intraaortic balloon pump.

g. Prepare for emergency reperfusion such g. Prepare for emergency reperfusion such as transluminal coronary angioplastyas transluminal coronary angioplasty

h. Monitor blood gash. Monitor blood gas

i. UO monitori. UO monitor

Page 31: Shock and SIRS

CIRCULATORY SHOCKCIRCULATORY SHOCK

- is also called distributive shock- is also called distributive shock

- occurs when the blood is - occurs when the blood is abnormally abnormally distributed in the vasculaturedistributed in the vasculature

maldistribution of blood volume

vasodilation

decreased tissue perfusion

decreased stroke volume

decreased cardiac output

decreased venous return

Pathophysiology:

Page 32: Shock and SIRS

Types of Circulatory shock:Types of Circulatory shock: Septic shockSeptic shock Anaphylactic shockAnaphylactic shock Neurogenic shockNeurogenic shock

Risk Factors for Circulatory Shock

Septic shock

ImunnosuppresionExtreme ages (<1 and >65)MalnourishmentChronic illnessInvasive procedure

Anaphylactic shock

Penicillin sensitivityTransfusionBee sting allergyLatex sensitivity

Neurogenic shock

Spinal cord injurySpinal anesthesiaDepressant actionGlucose deficiency

Page 33: Shock and SIRS

A.A. SeSeptic Shockptic Shock

- circulatory collapse due to infection- circulatory collapse due to infection

- due to invasive infection such as - due to invasive infection such as viruses, parasites and bacteriaviruses, parasites and bacteria

- - Gram (-) bacteriaGram (-) bacteria is the most is the most common common causecause

- - genito-urinary systemgenito-urinary system- the most - the most common source of causative common source of causative organism usually after organism usually after instrumentation in the tractinstrumentation in the tract

Page 34: Shock and SIRS

- caused by the released of bacteria - caused by the released of bacteria toxin that directly act on the on toxin that directly act on the on the blood vessel causing the blood vessel causing vasodilation and pooling of vasodilation and pooling of

blood , blood , resulting mostly from gram resulting mostly from gram negative septicemianegative septicemia

- the goal of treatment is controlling - the goal of treatment is controlling the cause of sepsisthe cause of sepsis

Page 35: Shock and SIRS

Manifestations:Manifestations:a. The a. The HYPERDYNAMIC PHASEHYPERDYNAMIC PHASE

High cardiac output with systemic High cardiac output with systemic vasodilatation. vasodilatation.

The BP remains within normal limits. The BP remains within normal limits. TachycardiaTachycardia Hyperthermic and febrile with warm, Hyperthermic and febrile with warm,

flushed skin and bounding pulsesflushed skin and bounding pulsesb. The b. The HYPODYNAMIC or irreversible phase HYPODYNAMIC or irreversible phase

LOW cardiac output with LOW cardiac output with VASOCONSTRICTIONVASOCONSTRICTION

The blood pressure drops, the skin is cool The blood pressure drops, the skin is cool and pale, with temperature below normal. and pale, with temperature below normal.

Heart rate and respiratory rate remain Heart rate and respiratory rate remain RAPID! RAPID!

The patient no longer produces urine.The patient no longer produces urine.

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MEDICAL MANAGEMENT:MEDICAL MANAGEMENT:• Current treatment involves identifying Current treatment involves identifying

and eliminating the cause of infection.and eliminating the cause of infection.• Fluid replacement must be instituted to Fluid replacement must be instituted to

correct Hypovolemiacorrect Hypovolemia• Intravenous antibiotics are prescribed Intravenous antibiotics are prescribed

based on culture and sensitivity.based on culture and sensitivity. Nursing management:Nursing management:

a.a.Control of infectionControl of infection

b.b.Administer IV antibioticsAdminister IV antibiotics

c.c.Administer O2, IV, vasoactive durgsAdminister O2, IV, vasoactive durgs

d.d.Monitor for CVP or pulmonary wedge pressureMonitor for CVP or pulmonary wedge pressure

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e. Obtain specimen for C and Se. Obtain specimen for C and S

f. Assess hydration and electrolyte f. Assess hydration and electrolyte imbalanceimbalance

B. Anaphylactic ShockB. Anaphylactic Shock

- - circulatory collapse due to massive circulatory collapse due to massive vasodilation from an allergic vasodilation from an allergic reactionreaction

- - massive vasodilation massive vasodilation resulting resulting from from serious dramatic allergic serious dramatic allergic reaction reaction causing release of causing release of histamine and histamine and related substances for related substances for damaged damaged cellcell

Page 38: Shock and SIRS

- can be due to venom, medication, - can be due to venom, medication, and dyes use in radiologic study and dyes use in radiologic study

MEDICAL MANAGEMENTMEDICAL MANAGEMENT: : Treatment of anaphylactic shock Treatment of anaphylactic shock

requires removing the causative requires removing the causative antigen, administering medications antigen, administering medications that restore vascular tone, and that restore vascular tone, and providing emergency support of basic providing emergency support of basic life functions.life functions.

EPINEPHRINE is the drug of choice EPINEPHRINE is the drug of choice given to reverse the vasodilatationgiven to reverse the vasodilatation

Page 39: Shock and SIRS

• Nursing management:Nursing management:

a. Establish a patent airwaya. Establish a patent airway

b. Prepare for the administration of b. Prepare for the administration of epinephrene, benadyril, epinephrene, benadyril,

corticosteroidcorticosteroid

c. administer o2 and IV fluidsc. administer o2 and IV fluids

d. administer vasoactive drugsd. administer vasoactive drugs

Page 40: Shock and SIRS

C. Neurogenic ShockC. Neurogenic Shock

-occurs due to the loss of sympathetic -occurs due to the loss of sympathetic tonetone

- an interference in the balance of the - an interference in the balance of the vasoregulation influences vessels vasoregulation influences vessels resulting in massive vasodilation resulting in massive vasodilation

and and pooling of bloodpooling of blood

- Aka- - Aka- Primary shockPrimary shock

- vasodilation of both arterioles and - vasodilation of both arterioles and venules increases the reservoir venules increases the reservoir capacity thereby decreasing the capacity thereby decreasing the venous returnvenous return

Page 41: Shock and SIRS

Manifestations:Manifestations:

a. The patient who suffers a. The patient who suffers from neurogenic shock may from neurogenic shock may

have have warm, dry skin and warm, dry skin and BRADYCARDIA!, BRADYCARDIA!,

poiklothermic poiklothermic temp.temp.

Management:Management:

- This involves restoring - This involves restoring sympathetic sympathetic tone, either through the tone, either through the stabilization of stabilization of a spinal cord a spinal cord injury or in anesthesia, proper injury or in anesthesia, proper

positioning. positioning.

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-nursing management:-nursing management:

a. elevate the head of the bed 30 a. elevate the head of the bed 30 degreesdegrees

( in spinal/epidural anesthesia)( in spinal/epidural anesthesia)

b. immobilize the patientb. immobilize the patient

(in spinal cord injury)(in spinal cord injury)

c. elastic compression stockingsc. elastic compression stockings

d. feet elevationd. feet elevation

e. heparin/low molecular weight heparine. heparin/low molecular weight heparin

f. pneumatic compression of the legsf. pneumatic compression of the legs

g. passive ROMg. passive ROM

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Systemic Inflammatory Systemic Inflammatory Response SyndromeResponse Syndrome

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SIRSSIRS

- clinical response to a nonspecific - clinical response to a nonspecific insult of either infectious or insult of either infectious or noninfectious origin.noninfectious origin.

- is nonspecific and can be caused by - is nonspecific and can be caused by ischemia, inflammation, trauma, ischemia, inflammation, trauma, infection, or a combination of infection, or a combination of several insults.several insults.

SEPSISSEPSIS- is the systemic response to infection - is the systemic response to infection and is defined as the presence of and is defined as the presence of

SIRS SIRS in addition to a documented or in addition to a documented or presumed infectionpresumed infection

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Epidemiology:Epidemiology: 500,000 – 750,000 cases annually in the United 500,000 – 750,000 cases annually in the United

States and risingStates and rising Most common cause of death in non-coronary ICU Most common cause of death in non-coronary ICU

and two-thirds of cases occur in hospitalized and two-thirds of cases occur in hospitalized patientspatients

Increasing incidence of severe sepsis is Increasing incidence of severe sepsis is attributable to the aging population with chronic attributable to the aging population with chronic diseasesdiseases

Widespread use of antimicrobial agents, Widespread use of antimicrobial agents, indwelling catheters, mechanical devices and indwelling catheters, mechanical devices and ventilatorsventilators

increase incidenceincrease incidence

·30% mortality when shock is present·30% mortality when shock is present

· Severe sepsis $22K/pt, $16 billion/year· Severe sepsis $22K/pt, $16 billion/year

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Criteria for Diagnosing:Criteria for Diagnosing: Systemic Inflammatory Response Systemic Inflammatory Response

System(SIRS)System(SIRS)

o Widespread inflammatory responseo Widespread inflammatory response

o Two or more of the followingo Two or more of the following

Temp > 38°C or ˂ 36°CTemp > 38°C or ˂ 36°C

Heart Rate > 90 bpmHeart Rate > 90 bpm

Tachypnea (RR > 20) or Tachypnea (RR > 20) or hyperventilation (PaCoz ˂ 32 hyperventilation (PaCoz ˂ 32 mmHg)mmHg)

WBC > 12,000 cells/mm3, < 4000 WBC > 12,000 cells/mm3, < 4000 cells/mm3 or presence of >10% cells/mm3 or presence of >10% immature neutrophilsimmature neutrophils

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SepsisSepsis

-SIRS + definitive source of infection-SIRS + definitive source of infection Severe SepsisSevere Sepsis

-Sepsis + organ dysfunction, -Sepsis + organ dysfunction, hypoperfusion, or hypotensionhypoperfusion, or hypotension

-Hypoperfusion and perfusion -Hypoperfusion and perfusion abnormalities may include but abnormalities may include but

not not limited to lactic acidosis, oliguria limited to lactic acidosis, oliguria or an acute mental state.or an acute mental state.

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Septic ShockSeptic Shock

- Sepsis + hypotension despite fluids- Sepsis + hypotension despite fluids

-Perfusion abnormalities-Perfusion abnormalities

a. Lactic acidosisa. Lactic acidosis

b. Oliguriab. Oliguria

c. Acute AMSc. Acute AMS Multiple Organ System FailureMultiple Organ System Failure

-Abnormal function of two or more -Abnormal function of two or more organs such that homeostasis cannot organs such that homeostasis cannot be achieved without interventionbe achieved without intervention

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Pathophysiology:Pathophysiology:

Local Injury (trauma, infection, ischemia)

Bacteria enters the damage tissue

Release of bacterial toxin

Toxin enters the blood and is circulated in the body

Release of systemic chemical mediators: a. Bradykinin b. Histamine c. interleukin-1 d. TNF e. complement

Damage the endothelial cells

Massive vasodilation

Multiple organ damage

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Pathophysiology of SIRSPathophysiology of SIRS

The antigen-antibody reaction The antigen-antibody reaction stimulates multiple interacting stimulates multiple interacting systems such as:systems such as:• Complement CascadeComplement Cascade• Cytokine cascadesCytokine cascades• Arachidonic Acid MetabolitesArachidonic Acid Metabolites• Cell Mediated ImmunityCell Mediated Immunity• Humoral Immune MechanismsHumoral Immune Mechanisms• Clotting CascadeClotting Cascade

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Cytokines Cytokines

Are Intercellular signaling proteins or Are Intercellular signaling proteins or messengersmessengers

More than 30 recognizedMore than 30 recognized Act through binding to specific Act through binding to specific

receptors on the target cells receptors on the target cells triggering other cascades or its own triggering other cascades or its own cascadecascade

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Pathophysiology of SIRS

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TNF-TNF-αα

The earliest and most potent mediator in The earliest and most potent mediator in SIRSSIRS

It activates neutrophils, causing the It activates neutrophils, causing the production of Interleukin-1(IL-1), production of Interleukin-1(IL-1), Interleukin-6 (INL-6), and Interleukin -8 Interleukin-6 (INL-6), and Interleukin -8 (INL-8).(INL-8).

It stimulates platelet activating factors It stimulates platelet activating factors and prostaglandin, and prostaglandin,

and promotes leukocyteand promotes leukocyte

or vessel cell wall adhesion.or vessel cell wall adhesion.

Pathophysiology of SIRS

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Pathophysiology of SIRS

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IL-1IL-1 During an inflammatory response, it facilitates the During an inflammatory response, it facilitates the

movement of WBCs toward the injury, ischemia, or movement of WBCs toward the injury, ischemia, or infected areainfected area

It stimulates the release of arachidonic acid from It stimulates the release of arachidonic acid from phospholipids in the plasma membranes, leading phospholipids in the plasma membranes, leading to fever, hypotension, and decrease systemic to fever, hypotension, and decrease systemic vascular resistance.vascular resistance.

IL-1 also leads to muscle protein breakdownIL-1 also leads to muscle protein breakdown IL-1 works with other cellular immunity IL-1 works with other cellular immunity

components to produce IL-2, which decreases components to produce IL-2, which decreases blood pressure, systemic vascular resistance, and blood pressure, systemic vascular resistance, and left ventricular ejection fraction.left ventricular ejection fraction.

IL-2 may also increase left ventricular end diastolic IL-2 may also increase left ventricular end diastolic volume, cardiac output, and heart rate volume, cardiac output, and heart rate

Pathophysiology of SIRS

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IL-6IL-6

Is a key messenger that can either Is a key messenger that can either trigger the rest of the cascade or its trigger the rest of the cascade or its arrestarrest

Stimulates the release of acute Stimulates the release of acute phase reactorsphase reactors

Its serum levels are consistent with Its serum levels are consistent with the gravity of the immune reaction the gravity of the immune reaction

Pathophysiology of SIRS

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Nitric OxideNitric Oxide

Nitric oxide is synthesised by inducible Nitric oxide is synthesised by inducible nitric oxide synthase (iNOS) in the nitric oxide synthase (iNOS) in the vascular endothelium and smooth muscle vascular endothelium and smooth muscle in response to pro-inflammatory cytokines in response to pro-inflammatory cytokines

NO is the vasoactive mediator responsible NO is the vasoactive mediator responsible for the fall in systemic vascular resistance for the fall in systemic vascular resistance underlying the hypotension in the late underlying the hypotension in the late stages of SIRS and septic shock stages of SIRS and septic shock

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Arachidonic Acid CascadeArachidonic Acid Cascade

Thromboxane AThromboxane A22

• Is a potent vasoconstrictor and platelet Is a potent vasoconstrictor and platelet aggregatoraggregator

• Leads to tissue ischemia from Leads to tissue ischemia from hypoperfusion.hypoperfusion.

Leukotrienes Leukotrienes leads toleads to• ↑↑Capillary endothelial permeabilityCapillary endothelial permeability• BronchoconstrictionBronchoconstriction• Activation of neutrophilsActivation of neutrophils

Pathophysiology of SIRS

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The Complement CascadeThe Complement Cascade

Controls the inflammatory processControls the inflammatory process• Chemotaxis Chemotaxis • Opsonization Opsonization • Promotion of phagocytosis Promotion of phagocytosis

Pathophysiology of SIRS

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Clotting CascadeClotting Cascade

Fibrin is formed due to the injury of the Fibrin is formed due to the injury of the vascular endotheliumvascular endothelium

Chemical mediators stimulate the release Chemical mediators stimulate the release of Hageman Factor and Thromboplastinof Hageman Factor and Thromboplastin

These form clots at the site of the injury, These form clots at the site of the injury, attempting to stabilize the siteattempting to stabilize the site

Fibrinolysis is activated by the coagulation Fibrinolysis is activated by the coagulation cascade, leading to mediator induced cascade, leading to mediator induced (DIC).(DIC).

Pathophysiology of SIRS

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BradykininBradykinin

The activation of the Hageman The activation of the Hageman Factor stimulates the release of Factor stimulates the release of bradykininbradykinin

Bradykinin creates vasodilatation Bradykinin creates vasodilatation and capillary leakage, therefore and capillary leakage, therefore volume depletion.volume depletion.

Pathophysiology of SIRS

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Myocardial Depressant FactorMyocardial Depressant Factor

Myocardial depressant factor is a Myocardial depressant factor is a serum protein released by the serum protein released by the hypoperfused and ischemic cells of hypoperfused and ischemic cells of the pancreasthe pancreas

It decreases the velocity of It decreases the velocity of contractions of myocardial cells, contractions of myocardial cells, leading to decreased right and left leading to decreased right and left ventricular ejection fractionsventricular ejection fractions

Pathophysiology of SIRS

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Beta EndorphinsBeta Endorphins

Beta endorphins are released, by the Beta endorphins are released, by the pituitary and hypothalamus, in pituitary and hypothalamus, in response to hypoperfusionresponse to hypoperfusion

They cause peripheral vasodilatation, They cause peripheral vasodilatation, and decrease cardiac contractilityand decrease cardiac contractility

Pathophysiology of SIRS

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Stages of SIRSStages of SIRS

4 stages according to the gravity of the 4 stages according to the gravity of the situation situation

Pathophysiology of SIRS

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SIRS 1SIRS 1

Release of proinflammatory Release of proinflammatory mediatorsmediators• These mediators create a web of These mediators create a web of

reactions designed to limit new reactions designed to limit new damage and ameliorate whatever damage and ameliorate whatever damage has already occurreddamage has already occurred

Pathophysiology of SIRS

Stages

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SIRS 2SIRS 2

Pro-inflammatory and anti-Pro-inflammatory and anti-inflammatory mediators appear inflammatory mediators appear in the systemic circulationin the systemic circulation• Pro-inflammatory mediators recruit Pro-inflammatory mediators recruit

neutrophils, lymphocytes, platelets, neutrophils, lymphocytes, platelets, and coagulation factorsand coagulation factors

Stages

Pathophysiology of SIRS

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SIRS 3SIRS 3

Massive Systemic InflammationMassive Systemic Inflammation• Progressive endothelial dysfunction Progressive endothelial dysfunction

occurs increasing microvascular occurs increasing microvascular permeabilitypermeability

• Vessels lose tone and profound Vessels lose tone and profound vasodilatation occurs resulting in vasodilatation occurs resulting in severe shocksevere shock

Pathophysiology of SIRS

Stages

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SIRS 4SIRS 4

Most patients do not make it this Most patients do not make it this far --but if they do--far --but if they do--• A compensatory anti-inflammatory A compensatory anti-inflammatory

response occurs trying to suppress response occurs trying to suppress inflammationinflammation

Stages

Pathophysiology of SIRS

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Clinical PictureClinical Picture

The typical 2 or more of:The typical 2 or more of:• Temp. >38°C or <36°CTemp. >38°C or <36°C• HR >90 bpmHR >90 bpm• RR > 20 cpm or PaCO2 < 4.3 kPaRR > 20 cpm or PaCO2 < 4.3 kPa• WBCs WBCs

>12 x 109/lit>12 x 109/lit < 4 x 109/lit< 4 x 109/lit > 10% immature forms> 10% immature forms

Symptoms & Signs of each organ sequels Symptoms & Signs of each organ sequels

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Organ ManifestationsOrgan Manifestations

CardiovascularCardiovascular• Skin warm and flushedSkin warm and flushed• Widened pulse pressureWidened pulse pressure• Cardiac output is Cardiac output is ⇑⇑ but SVR is but SVR is ⇓⇓• Eventually C.O. declines Eventually C.O. declines

exacerbating hypoperfusionexacerbating hypoperfusion

Clinical Picture

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Organ ManifestationsOrgan Manifestations

PulmonaryPulmonary• Hypoxemia may be masked by Hypoxemia may be masked by

hyperventilationhyperventilation• Respiratory alkalosisRespiratory alkalosis• Pulmonary edemaPulmonary edema• Respiratory failureRespiratory failure• BronchoconstrictionBronchoconstriction• ARDSARDS

Clinical Picture

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Organ ManifestationsOrgan Manifestations

CNSCNS• Altered mental Altered mental

statusstatus• ConfusionConfusion• IrritabilityIrritability• AgitationAgitation• DisorientationDisorientation• LethargyLethargy• SeizuresSeizures• ComaComa

RenalRenal• Oliguria:    < 500 Oliguria:    < 500

ml/dayml/day• Metabolic Metabolic

AcidosisAcidosis

Clinical Picture

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Organ ManifestationsOrgan Manifestations

GITGIT• Impaired motilityImpaired motility• ⇑ ⇑ SGPT & SGOTSGPT & SGOT• HyperbilirubinemiHyperbilirubinemi

a a • Hepatic necrosisHepatic necrosis• HypoprothrombinHypoprothrombin

emiaemia• HypoglycemiaHypoglycemia

BloodBlood• ⇑ ⇑ or ⇓ or ⇓ WBCsWBCs• ⇑ ⇑ PT and PTTPT and PTT• ⇑ ⇑ or ⇓ Plateletsor ⇓ Platelets• AnemiaAnemia

Clinical Picture

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Investigations Investigations

Cytokines assay (IL-6, IL-8 & TNF)Cytokines assay (IL-6, IL-8 & TNF) Blood CultureBlood Culture Burn eschar biopsy with culture & Burn eschar biopsy with culture &

sensitivitysensitivity Serum ProcalcitoninSerum Procalcitonin

• The only lab test that differentiates The only lab test that differentiates SIRS (0.5 -2 ng/dl) from SIRS (0.5 -2 ng/dl) from Sepsis (>2 & <10 ng/dl) fromSepsis (>2 & <10 ng/dl) from MOD (>10 and often >100ng/dl)MOD (>10 and often >100ng/dl)

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TreatmentTreatment

= Elimination of triggering factor (LPC = Elimination of triggering factor (LPC & LPS)& LPS)

LPSLPS• Antibiotics according to C&SAntibiotics according to C&S• Gut decontaminationGut decontamination

LPC throughLPC through Prompt early surgical eschar excisionPrompt early surgical eschar excision Chemical elimination eg. Cerium NitrateChemical elimination eg. Cerium Nitrate

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TreatmentTreatment

SupportiveSupportive MedicalMedical Surgical Surgical

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Supportive TherapySupportive Therapy

Volume replacementVolume replacement +ve inotropes & vasopressors+ve inotropes & vasopressors Ventilation (Pressure support or PEEP)Ventilation (Pressure support or PEEP) Nutritional Support Nutritional Support

• Iso-Osmotic Feedings Iso-Osmotic Feedings • TPNTPN• PPNPPN• Immune Modulatory Foods such as Arginine, Immune Modulatory Foods such as Arginine,

Glutamine & fish oilsGlutamine & fish oils

Treatment

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Medical Medical

Potent anti-oxidants Potent anti-oxidants • Methylene Blue given IVMethylene Blue given IV• Acetyl CysteineAcetyl Cysteine• Vitamin CVitamin C

Immune ModulatorsImmune Modulators• Ibuprofen (proved of limited value)Ibuprofen (proved of limited value)• Centoxin: an Ab to endotoxinsCentoxin: an Ab to endotoxins• NOSI (nitric oxide synthetase inhibtor) very NOSI (nitric oxide synthetase inhibtor) very

much acceptedmuch accepted• IL-6 blockers ExperimentalIL-6 blockers Experimental

Treatment

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Surgical ExcisionSurgical Excision

Best option = Early excision + Best option = Early excision + coveragecoverage

Best performed within the 1Best performed within the 1stst 72 72 hours and after resuscitationhours and after resuscitation

Is the only way to break the circleIs the only way to break the circle

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Surgical Excision Surgical Excision

⇓⇓ ⇓⇓ incidence of burn wound colonizationincidence of burn wound colonization

Barret et al, 2003

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Prognosis Prognosis

Death in 60% of cases of late stages Death in 60% of cases of late stages & shock in patients with no previous & shock in patients with no previous history of medical conditionshistory of medical conditions

Death rate is higher if MOD develops Death rate is higher if MOD develops & is dependant on no. of organs & is dependant on no. of organs affectedaffected• 3 organs 85%3 organs 85%• 4 organs 95%4 organs 95%• 5 organs 99%5 organs 99%

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Thank YouThank You