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Systemic Inflammatory Response Syndrome SIRS

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Title: Systemic Inflammatory Response Syndrome SIRS


1
Systemic Inflammatory
Response Syndrome (SIRS)
  • PRANEE
    SITAPOSA, MD.

2
SEPSIS and Its Disease spectrum
  • Various stages of disease
  • Bacteremia
  • SIRS
  • Sepsis syndrome
  • Sepsis shock early and refractory

3
Definition
  • Infection
  • Presence of microorganisms in a normally sterile
    site.
  • Bacteremia
  • Cultivatable bacteria in the blood stream.
  • Sepsis
  • The systemic response to infection.
    If associated with proven or clinically
    suspected infection, SIRS is called sepsis.

American College of Chest Physicians/Society of
Critical Care Medicine Consensus Conference
Committee. Crit Care Med. 199220864-874.
4
SIRS
(Systemic Inflammatory Response Syndrome)
  • The systemic response to a wide range of
    stresses.
  • Temperature gt38C (100.4) or lt36C (96.8F).
  • Heart rate gt90 beats/min.
  • Respiratory rate gt20 breaths/min or
    PaCO2 lt32 mmHg.
  • White blood cells gt 12,000 cells/ml or lt 4,000
    cells/ml or gt10 immature (band) forms.
  • Note
  • Two or more of the following must be present.
  • These changes should be represent acute
    alterations from baseline in the absence of other
    known cause for the abnormalities.

American College of Chest Physicians/Society of
Critical Care Medicine Consensus Conference
Committee. Crit Care Med. 199220864-874.
5
Severe Sepsis
  • Sepsis with organ hypoperfusion
    one of the followings
  • SBP lt 90 mmHg
  • Acute mental status change
  • PaO2 lt 60 mmHg on RA (PaO2 /FiO2 lt 250)
  • Increased lactic acid/acidosis
  • Oliguria
  • DIC or Platelet lt 80,000 /mm3
  • Liver enzymes gt 2 x normal

American College of Chest Physicians/Society of
Critical Care Medicine Consensus Conference
Committee. Crit Care Med. 199220864-874.
6
MODS(Multiple Organ Dysfunction Syndrome)
  • Sepsis with multiorgan hypoperfusion
  • Two or more of the followings
  • SBP lt 90 mmHg
  • Acute mental status change
  • PaO2 lt 60 mmHg on RA (PaO2 /FiO2 lt 250)
  • Increased lactic acid/acidosis
  • Oliguria
  • DIC or Platelet lt 80,000 /mm3
  • Liver enzymes gt 2 x normal










American College of Chest Physicians/Society of
Critical Care Medicine Consensus Conference
Committee. Crit Care Med. 199220864-874.
7
Relationship between SIRS and Sepsis
Bone RC et al, Chest1992101164-55.
8
The Sepsis Continuum
  • A clinical response arising from a nonspecific
    insult, with ?2 of the following
  • T gt38oC or lt36oC
  • HR gt90 beats/min
  • RR gt20/min
  • WBC gt12,000/mm3 or lt4,000/mm3 or gt10 bands
  • SIRS with a
  • presumed
  • or confirmed
  • infectious
  • process

Sepsis with organ failure
Refractory hypotension
SIRS systemic inflammatory response
syndrome
Chest 19921011644.
9
Mortality rate in SIRS
Rangel-Frausto, et al. JAMA 273117-123, 1995.
10
The Response to Pathogens Cross-Talk
NEJM 2003348138-150.
11
Inflammatory Response to Sepsis
NEJM 20063551699-1713.
12
Procoagulant Response in Sepsis
NEJM 20063551699-1713.
13
Pathogenesis of sepsis and septic shock
Angus DC, et al. Crit Care Med 2001,
291303-1310.
14
Pathogenesis of Severe Sepsis
Infection
Microbial Products (exotoxin/endotoxin)
Cellular Responses
Platelet Activation
Cytokines TNF, IL-1, IL-6
CoagulationActivation
Kinins Complement
Oxidases
Coagulopathy/DIC Vascular/Organ System Injury
Endothelial damage
Endothelial damage
Multi-Organ Failure
Death
15
Normal Systemic Response to Infection and Injury
(1)
  • Leukocytosis Mobilizes neutrophils into the
    circulation
  • Tachycardia Increases cardiac output, blood
    flow to injuried tissue
  • Fever Raises core temperature peripheral
    vasoconstriction shunts blood flow to
    injuried tissue. Occurs much more often
    when infection is the trigger for systemic
    responses

Mandell et al. Principals and Practice of
Infectious Diseases6th ed906906-926.
16
Normal Systemic Response to Infection and Injury
(2)
  • Acute-Phase Responses
  • Anti-infective
  • Increases synthesis of complement factors,
    microbe pattern-recognition molecules(mannose-bind
    ing lectin, LBP, CRP, CD14, Others)
  • Sequesters iron (lactoferrin) and zinc
    (metallothionein)

Mandell et al. Principals and Practice of
Infectious Diseases6th ed906906-926.
17
Normal Systemic Response to Infection and Injury
(3)
  • Anti-inflammatory
  • Releases anti-inflammatory neuroendocrine
    hormones (cortisol, ACTH, epinephrine, a-MSH)
  • Increases synthesis of proteins that help prevent
    inflammation within the systemic compartment
  • Cytokine antagonists (IL-1Ra, sTNF-Rs)
  • Anti-inflammatory mediators (e.g.,IL-4, IL-6,
    IL-6R, IL-10, IL-13, TGF-ß)
  • Protease inhibitors (e.g.,a1-antiprotease)
  • Antioxidants (haptoglobin)
  • Reprograms circulating leukocytes (epinephrine,
    cortisol, PGE2, ?other)

Mandell et al. Principals and Practice of
Infectious Diseases6th ed906906-926.
18
Normal Systemic Response to Infection and Injury
(4)
  • Procoagulant
  • Walls off infection, prevents systemic spread
  • Increases synthesis or release of fibrinogen,
    PAI-1, C4b
  • Decreases synthesis of protein C, anti-thrombin
    III
  • Metabolic
  • Preserves euglycemia, mobilizes fatty acids,
    amino acids
  • Epinephrine, cortisol, glucagon, cytokines
  • Thermoregulatory
  • Inhibits microbial growth
  • Fever

Mandell et al. Principals and Practice of
Infectious Diseases6th ed906906-926.
19
Risk factors of sepsis
  • aggressive oncological chemotherapy and radiation
    therapy
  • use of corticosteroid and immunosuppressive
    therapies for organ transplants and inflammatory
    diseases
  • longer lives of patients predisposed to sepsis,
    the elderly, diabetics, cancer patients, patients
    with major organ failure, and with
    granulocyopenia.
  • Neonates are more likely to develop sepsis (ex.
    group B Streptococcal infections).
  • increased use of invasive devices such as
    surgical protheses, inhalation equipment, and
    intravenous and urinary catheters.
  • indiscriminate use of antimicrobial drugs that
    create conditions of overgrowth, colonization,
    and subsequent infection by aggressive,
    antimicrobial-resistant organisms.

Angus DC, et al. Crit Care Med 2001,
291303-1310.
20
Patients at increased risks of developing sepsis
  • Underlying diseases neutropenia, solid tumors,
    leukemia, dysproteinemias, cirrhosis of the
    liver, diabetes, AIDS, serious chronic
    conditions.
  • Surgery or instrumentation catheters.
  • Prior drug therapy Immuno-suppressive drugs,
    especially with broad-spectrum antibiotics.
  • Age males, above 40 y females, 20-45 y.
  • Miscellaneous conditions childbirth, septic
    abortion, trauma and widespread burns, intestinal
    ulceration.

Angus DC, et al. Crit Care Med 2001,
291303-1310.
21
Source
(usually an endogenous source of infection)
  • intestinal tract
  • oropharynx
  • instrumentation sites
  • contaminated inhalation therapy equipment
  • IV fluids.
  • Most frequent sites of infection Lungs, abdomen,
    and urinary tract.
  • Other sources include the skin/soft tissue and
    the CNS.

Angus DC, et al. Crit Care Med 2001,
291303-1310.
22
Diagnosis
  • History
  • community or nosocomially acquired infection
  • immunocompromised patient
  • exposure to animals, travel, tick bites,
    occupational hazards, alcohol use, seizures, loss
    of consciousness, medications
  • underlying diseases specific infectious agents
  • Some clues to a septic event include
  • Fever or unexplained signs with malignancy or
    instrumentation
  • Hypotension
  • Oliguria or anuria
  • Tachypnea or hyperpnea
  • Hypothermia without obvious cause
  • Bleeding

Angus DC, et al. Crit Care Med 2001, 291303-1310.
23
Specific Infectious agents
  • Splenectomy (traumatic or functional)
  • S pneumoniae, H influenzae, N meningitidis
  • Neutropenia (lt500 neutrophil/ml)
  • Gram-negative, including P aeruginosa,
    gram-positives, including S aureus
  • Fungi, especially Candida species
  • Hypogammaglobulinemia (e.g.,CLL)
  • S pneumoniae, E coli
  • Burns
  • MRSA, P aeruginosa, resistant gram-negatives

MacArthur RD, et al.
Mosby, 20013-10. Wheeler AP, et
al. NEJM 1999340207-214. Chaowagul W, et
al. J Infect Dis 1989159890-899.
24
Specific Infectious agents
  • Aids
  • P aeuginosa (if neutropenic), S aureus, PCP
    pneumonia
  • Intravascular devices
  • S aureus, S epidermidis
  • Nosocomial infections
  • MRSA, Enterococcus species, resistant
    gram-negative, Candida species
  • Septic patients in NE of Thailand
  • Burkholderia pseudomallei


MacArthur RD, et al.
Mosby, 20013-10.
Wheeler AP, et
al. NEJM 1999340207-214.
Chaowagul W, et
al. J Infect Dis 1989159890-899.
25
Diagnosis
  • Physical Examination
  • essential
  • In all neutropenic patients and in patients with
    as suspected pelvic infection the physical exam
    should include rectal, pelvic, and genital
    examinations
  • perirectal, and/or perineal abscesses
  • pelvic inflammatory disease and/or abscesses, or
    prostatitis

Angus DC, et al. Crit Care Med 2001,
291303-1310.
26
Signs and Symptoms
  • Nonspecific symptoms of sepsis not
    pathognomonic
  • fever
  • chills
  • constitutional symptoms of fatigue, malaise
  • anxiety or confusion
  • absent symptoms in serious infections, especially
    in elderly individuals

Angus DC, et al. Crit Care Med 2001, 291303-1310.
27
Complications
  • Adult respiratory distress syndrome (ARDS)
  • Disseminated Intravascular Coagulation (DIC)
  • Acute Renal failure (ARF)
  • Intestinal bleeding
  • Liver failure
  • Central Nervous System dysfunction
  • Heart failure
  • Death

Angus DC, et al. Crit Care Med 2001, 291303-1310.
28
Surviving Sepsis Campaign
Guidelines for Management of Severe Sepsis and
Septic Shock
Dellinger RP, et al. Crit Care Med 2004
32858-873.
29
Diagnosis
  • Before the initiation of antimicrobial therapy,
    at least two blood cultures should be obtained
  • At least one drawn percutaneously
  • At least one drawn through each vascular access
    device if inserted longer than 48 hours
  • Other cultures such as urine, cerebrospinal
    fluid, wounds, respiratory secretions or other
    body fluids should be obtained as the clinical
    situation dictates
  • Other diagnostic studies such as imaging and
    sampling should be performed promptly to
    determine the source and causative organism of
    the infection
  • may be limited by patient stability

Weinstein MP. Rev Infect Dis 1983535-53Blot F.
J Clin Microbiol 1999 36 105-109.
Dellinger, et. al. Crit Care
Med 2004, 32 858-873.
30
Sepsis resuscitation bundle
  • Serum lactate measured
  • Blood cultures obtained before antibiotics
    administered
  • Improve time to broad-spectrum antibiotics
  • In the event of hypotension or lactate gt 4 mmol/L
    (36 mg/dL)
  • a. Deliver an initial minimum of 20 mL/kg of
    crystaloid (or colloid
    equivalent)
  • b. apply vasopressors for ongoing hypotension
  • In the event of persistent hypotension despite
    fluid resuscitation or lactate gt 4 mmol/L (36
    mg/dL)
  • a. achieve central venous pressure of gt 8 mmHg
  • b. achieve central venous oxygen saturation of gt
    70

Hurtado FJ. et al. Crit Care Clin2006
22521-9.
31
Sepsis management bundle
  • Fluid resuscitation
  • Appropriate cultures prior to antibiotic
    administration
  • Early targeted antibiotics and source control
  • Use of vasopressors/inotropes when fluid
  • resuscitation optimized

Surviving Sepsis Campaign Management Guidelines
Committee. Crit Care Med 2004 32858-873.
32
Sepsis management bundle
  • Evaluation for adrenal insufficiency
  • Stress dose corticosteroid administration
  • Recombinant human activated protein C (xigris)
    for severe sepsis
  • Low tidal volume mechanical ventilation for ARDS
  • Tight glucose control

Surviving Sepsis Campaign Management Guidelines
Committee. Crit Care Med 2004 32858-873.
33
Infection Control
  • Appropriate cultures prior to antibiotic
  • administration
  • Early targeted antibiotics and source control

Surviving Sepsis Campaign Management Guidelines
Committee. Crit Care Med 2004 32858-873.
34
Early Goal-Directed Therapy
CVP central venous
pressure MAP mean arterial
pressure ScvO2 central
venous oxygen
saturation
NEJM 20013451368-77.
35
Early Goal-Directed Therapy Results
28-day Mortality
60
49.2
P 0.01
50
40
33.3
30
20
10
0
Standard Therapy n133
EGDT n130
Key difference was in sudden CV collapse, not
MODS



NEJM 20013451368-77.
36
Antibiotic use in Sepsis (1)
  • The drugs used depends on the source of the
    sepsis
  • Community acquired pneumonia
  • third (ceftriaxone) or fourth (cefepime)
    generation cephalosporin is given with an
    aminoglycoside (usually gentamicin)
  • Nosocomial pneumonia
  • Cefipime or Imipenem-cilastatin and an
    aminoglycoside
  • Abdominal infection
  • Imipenem-cilastatin or Pipercillin-tazobactam and
    aminoglycoside

Angus DC, et al. Crit Care Med 2001,
291303-1310.
37
Antibiotic use in Sepsis (2)
  • Nosocomial abdominal infection
  • Imipenem-cilastatin and aminoglycoside or
    Pipercillin-tazobactam and Amphotericin B
  • Skin/soft tissue
  • Vancomycin and Imipenem-cilastatin or
    Piperacillin-tazobactam
  • Nosocomial skin/soft tissue
  • Vancomycin and Cefipime
  • Urinary tract infection
  • Ciprofloxacin and aminoglycoside

Angus DC, et al. Crit Care Med 2001,
291303-1310.
38
Antibiotic use in Sepsis (3)
  • Nosocomial urinary tract infection
  • Vancomycin and Cefipime
  • CNS infection
  • Vancomycin and third generation cephalosporin or
    Meropenem
  • Nosocomial CNS infection
  • Meropenem and Vancomycin
  • Drugs will change depending on the most likely
    cause of the patient's sepsis
  • Single drug regimens are usually only indicated
    when the organism causing sepsis has been
    identified and antibiotic sensitivity testing

Angus DC, et al. Crit Care Med 2001, 291303-1310.
39
New Drug in Treating Severe Sepsis
  • It is the first agent approved by the FDA
    effective in the treatment of severe sepsis
    proven to reduce mortality. Activated Protein C
    (Xigris) mediates many actions of body
    homeostasis. It is a potent agent for the
  • suppression of inflammation
  • prevention of microvascular coagulation
  • reversal of impaired fibrinolysis

Angus DC, et al. Crit Care Med 2001, 291303-1310.
40
NEJM3551699-1723.
41
Sepsis Cascade
42
Activated Protein C (Xigris)
NEJM3551640,
October 19, 2006.
43
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