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    Sepsis: Pathophysiology and Management in The ICU

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    prashsubbu
    1. Sepsis is defined as a systemic inflammatory response due to infection along with signs of organ dysfunction. It is a complex syndrome caused by an imbalance between pro-inflammatory and anti-inflammatory responses. 2. The Surviving Sepsis Campaign guidelines provide evidence-based recommendations for management of sepsis and septic shock focusing on early goal-directed resuscitation and treatment of organ dysfunctions. 3. Initial management involves fluid resuscitation, vasopressors, steroids, mechanical ventilation, glucose control, renal replacement therapy, DVT prophylaxis and stress ulcer prophylaxis aimed at reversing hypoperfusion and preventing further organ injury.

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    Sepsis: Pathophysiology and Management in The ICU

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    1. Sepsis is defined as a systemic inflammatory response due to infection along with signs of organ dysfunction. It is a complex syndrome caused by an imbalance between pro-inflammatory and anti-inflammatory responses. 2. The Surviving Sepsis Campaign guidelines provide evidence-based recommendations for management of sepsis and septic shock focusing on early goal-directed resuscitation and treatment of organ dysfunctions. 3. Initial management involves fluid resuscitation, vasopressors, steroids, mechanical ventilation, glucose control, renal replacement therapy, DVT prophylaxis and stress ulcer prophylaxis aimed at reversing hypoperfusion and preventing further organ injury.

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    1. Sepsis is defined as a systemic inflammatory response due to infection along with signs of organ dysfunction. It is a complex syndrome caused by an imbalance between pro-inflammatory and anti-inflammatory responses. 2. The Surviving Sepsis Campaign guidelines provide evidence-based recommendations for management of sepsis and septic shock focusing on early goal-directed resuscitation and treatment of organ dysfunctions. 3. Initial management involves fluid resuscitation, vasopressors, steroids, mechanical ventilation, glucose control, renal replacement therapy, DVT prophylaxis and stress ulcer prophylaxis aimed at reversing hypoperfusion and preventing further organ injury.

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    645 views38 pages

    Sepsis: Pathophysiology and Management in The ICU

    Uploaded by

    prashsubbu
    1. Sepsis is defined as a systemic inflammatory response due to infection along with signs of organ dysfunction. It is a complex syndrome caused by an imbalance between pro-inflammatory and anti-inflammatory responses. 2. The Surviving Sepsis Campaign guidelines provide evidence-based recommendations for management of sepsis and septic shock focusing on early goal-directed resuscitation and treatment of organ dysfunctions. 3. Initial management involves fluid resuscitation, vasopressors, steroids, mechanical ventilation, glucose control, renal replacement therapy, DVT prophylaxis and stress ulcer prophylaxis aimed at reversing hypoperfusion and preventing further organ injury.

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    Sepsis: Pathophysiology and

    Management in the ICU


    Systemic inflammatory response syndrome
    Diagnostic criteria:

    (at least 2 of the following)


    1.Temperature >38º C or <36ºC
    2.Heart rate >90/min
    3.Respiratory rate > 20 breaths/min or arterial PCO2 <32 mm Hg
    4.WBC count > 12,000/cmm or <4000/cmm or > 10 % immature
    (band) forms
    Definitions
    Sepsis : SIRS as a result of infection
    Severe Sepsis : Sepsis + dysfunction of 1 or more vital organs
    Sepsis Induced Hypotension : SBP <90 mm Hg or MAP< 70 mm Hg or a
    decrease in SBP by 40 mm Hg or 2 SD below normal
    Septic Shock : Severe sepsis with hypotension refractory to volume
    infusion
    MODS : Abnormal function in more than 1 vital organ
    MOF : Failure of more than one organ system
    Determinants of the Sepsis Syndrome

    Virulence of the organism


    • Inoculum of the organism
    • Site of Infection
    • Host response
    – Inflammatory
    – Anti-inflammatory
    – “Balance”
    • Genetic factors
    – Susceptibility
    – Regulation
    Common Etiology

    1)Bacteria-
    Aerobes –
    gram negative rods- klebsiella,serratie
    - pseudomonas
    gram posive cocci - strepto,staph
    gram negatiev cocci - meningococci
    Mycobacteria
    2)Viruses -flavivirus,coronaviridae
    3)Rickettsia
    4) Fungi- candida,histoplasma,aspergillus
    Pathophysiology
    -Loss of hemostatic balance + endothelial dysfunction
    - Compromising the circulatory system, intracellular homeostasis.
    - Cellular hypoxia and apoptosis .
    Systemic involvement
    1.Vascular System
    Micocirculatory shunting due
    to:
    1)Microthrombi
    2)Endothelial cell swelling
    narrowing the capillary lumen
    3)Activated leukocytes
    adhering to endothelial cells
    4)Dysfunctional RBC
    (decreased deformability)
    2.Cardiac dysfunction
    Myocardial contractility compromised
    Diastolic dilatation of the left ventricle increasing left ventricular end
    diastolic volume to maintain sufficient stroke volume
    Rightward shift of frank starling law
    3.Endocrine dysfunction
    •Corticosteroids-
    •Vasopressin-
    •Insulin-
    Diagnostic criteria for sepsis
    SSC guidelines 2008

    A) Infection, documented or suspected, and some of the following:


    1)General variables :
    Fever (38.3°C), Hypothermia (core temperature 36°C), Heart rate >90 /min
    or > 2 SD , Tachypnea, Altered mental status, Significant edema or positive
    fluid balance (20 mL/kg over 24 hrs), hyperglycemia (plasma glucose 140
    mg/dL or 7.7 mmol/L) in the absence of diabetes

    2) Inflammatory variables:
    Leukocytosis (WBC > 12,000 /L), Leukopenia(WBC < 4000 /L)
    Normal WBC count with 10% immature forms, Plasma C-reactive protein
    >2 SD, Plasma procalcitonin >2 SD

    3) Hemodynamic variables
    Arterial hypotension (SBP 90 mm Hg; MAP 70 mm Hg; or an SBP decrease 40
    mm Hg in adults or 2 SD below normal for age)
    B)Organ dysfunction variables
    • Arterial hypoxemia (PaO2/FIO2 300)
    • Acute oliguria (urine output 0.5 mL/Kg hr or 45 mmol/L for at least 2 hrs,
    despite adequate fluid resuscitation)
    • Creatinine increase by 0.5 mg/dL or 44.2 mol/L
    • Coagulation abnormalities (INR 1.5 or a PTT 60 secs)
    • Ileus (absent bowel sounds)
    • Thrombocytopenia (platelet count, 100,000 L1)
    • Hyperbilirubinemia (plasma total bilirubin 4 mg/dL or 70 mol/L)
    • Tissue perfusion variables
    Hyperlactatemia ( upper limit of lab normal)
    Decreased capillary refill or mottling
    Surviving Sepsis Campaign: International guidelines
    for management of severe sepsis and septic shock:
    2008

    Grading Quality of Evidence Grading Strength of Recommendation


    1- strong recommendation – Do it we
    A- high quality Randomized recommend
    controlled trial (RCT) 2- weak recommendation – Probably
    B- intermediate Downgraded do it. We suggest
    RCT or upgraded Determinants of strength
    observational
    Quality of evidence
    C- low Observational or
    cohort Relative importance of outcomes
    D- very low Case series or Risks and costs
    expert opinion Absolute magnitude and precision
    Upgrade capability of effect
    I. MANAGEMENT OF SEVERE
    SEPSIS
    A)Initial resuscitation (first 6 hrs)
    ● Begin resuscitation immediately in patients with hypotension or elevated serum
    lactate 4 mmol/L; do not delay pending ICU admission (1C)
    ● Resuscitation goals (1C)
    CVP 8–12 mm Hga
    Mean arterial pressure 65 mm Hg
    Urine output 0.5 mLkg1hr1
    Central venous (superior vena cava) oxygen saturation 70% or mixed venous 65%
    If venous oxygen saturation target is not achieved (2C)
    • Consider further fluid
    • Transfuse packed red blood cells if required to hematocrit of 30% and/or
    • Start dobutamine infusion, maximum 20 gkg1min1
    • higher target CVP of 12–15 mm Hg is recommended in the presence of
    mechanical ventilation or preexisting decreased ventricular compliance.
    Hemodynamic support and adjunctive therapy

    1)Fluid therapy
    ● Crystalloids or Colloids (1B)
    ● Target a CVP of 8 mm Hg (12 mm Hg if mechanically ventilated) (1C)
    ● fluid challenge technique (1D)
    ● Rate of fluid administration should be reduced if cardiac filling pressures
    increase without concurrent hemodynamic improvement (1D)
    2)Vasopressors
    ● Maintain MAP 65 mm Hg (1C)
    ● Norepinephrine and dopamine centrally administered are the initial
    vasopressors of choice (1C)
    Epinephrine, phenylephrine, or vasopressin?
    ● Do not use low-dose dopamine for renal protection (1A)
    ● In patients requiring vasopressors, insert an arterial catheter as soon as
    practical (1D)
    ● use of dobutamine (1C)
    Role of CVP:
    currently the most readily obtainable target for fluid resuscitation.

    Transfusion of packed red blood cells,Dobutamine infusion:


    When ScvO2 or SV¯O2 of 70% or 65%,respectively, not achieved with
    fluid resuscitation
    3)Steroids
    -Hypotension responding poorly to adequate fluid resuscitation and vasopressors
    - ACTH stimulation test is not recommended
    - Hydrocortisone (300 mg/day) is preferred to dexamethasone
    - Fludrocortisone (50 g OD) may be included if an alternative to hydrocortisone
    - Steroid therapy may be weaned once vasopressors are no longer required (2D)

    Do not use corticosteroids to treat sepsis in the absence of shock unless the patient’s
    endocrine or corticosteroid history warrants it (1D)
    4)Recombinant human activated protein C

    - in adult patients with sepsis-induced organ dysfunction with clinical


    assessment of high risk of death (typically APACHE II 25 or multiple
    organ failure) if there are no contraindications

    - Adult patients with severe sepsis and low risk of death (typically,
    APACHE II 20 or one organ failure) should not receive rhAPC (1A)
    5)Blood product administration

    a) PRBC: when Hb < 7.0 g/dL to target a Hb of 7.0–9.0 g/dL in adults (1B).
    A higher hemoglobin level - myocardial ischaemia, severe hypoxemia, acute hemorrhage,
    cyanotic heart disease, or lactic acidosis)
    b) erythropoietin : not to be used to treat sepsis-related anemia.
    c) fresh frozen plasma : not to correct laboratory clotting abnormalities unless there is
    bleeding or planned invasive procedures (2D)
    d) Do not use antithrombin therapy (1B)
    e) Platelets when (2D)
    Counts are 5000/mm3 (5 109/L) regardless of bleeding
    Counts are 5000–30,000/mm3 (5–30 109/L) and there is significant bleeding risk
    Higher platelet counts (50,000/mm3 [50 109/L]) for surgery or invasive procedures
    Mechanical ventilation of sepsis-induced ALI/ARDS

     Tidal volume of 6 mL/kg (predicted) body weight in patients with ALI/ARDS (1B)
     Initial upper limit plateau pressure 30 cm H2O. (1C)
     Allow PaCO2 to increase above normal, if needed (1C)
     use of PEEP , prone position, semirecumbent position
     Noninvasive ventilation
     Use a weaning protocol and SBT
    Before the SBT

    patients should be arousable,


    hemodynamically stable without vasopressors
    have no new potentially serious conditions ,
    have low ventilatory and end-expiratory pressure requirement,
    require FIO2 levels that can be safely delivered with a face mask or nasal
    cannula
    Sedation, analgesia, and neuromuscular blockade in sepsis

     sedation protocols with a sedation goal(1B)


     Use either intermittent bolus sedation or continuous infusion sedation
     daily interruption/lightening to produce awakening.
     Avoid neuromuscular blockers where possible.
     Monitor depth of block with train-of-four when using continuous infusions (1B)
    Glucose control
    IV insulin to control hyperglycemia
    Aim to keep blood glucose 150 mg/dL (8.3 mmol/L) using a validated protocol for insulin dose
    adjustment (2C)
    glucose calorie source and monitor blood glucose values every 1–2 hrs (4 hrs when stable)
    Interpret with caution low glucose levels

    Renal replacement
    Intermittent hemodialysis and CVVH are considered equivalent (2B)
    CVVH offers easier management in hemodynamically unstable patients (2D)

    Bicarbonate therapy
    Do not use bicarbonate therapy for the purpose of improving hemodynamics or reducing
    vasopressor requirements when treating hypoperfusioninduced
    lactic acidemia with pH 7.15 (1B)
    Deep vein thrombosis prophylaxis
    ● low-dose UFH or LMWH
    ● Mechanical prophylactic device when heparin is contraindicated (1A)
    Use a combination of pharmacologic and mechanical therapy for patients at very high risk for
    deep vein thrombosis (2C)
    In patients at very high risk, LMWH should be used rather than UFH (2C)

    Stress ulcer prophylaxis


    Provide stress ulcer prophylaxis using H2 blocker (1A) or proton pump inhibitor (1B).
    Benefits of prevention of upper gastrointestinal bleed must be weighed against the potential
    for
    development of ventilator-acquired pneumonia

    Consideration for limitation of support


    ● Discuss advance care planning with patients and families. Describe likely outcomes and set
    realistic expectations (1D)
    B) Diagnosis

    Obtain appropriate cultures before starting antibiotics (1C)


    Obtain two or more BCs
    One or more BCs should be percutaneous
    One BC from each vascular access device in place for 48 hrs or more
    Culture other sites as clinically indicated

    ● Perform imaging studies promptly to confirm and sample any source of


    infection, if safe to do so (1C)
    C) Antibiotic therapy

    ● IV antibiotics as early as possible and always within the 1st hour of recognizing severe sepsis
    (1D) and septic shock (1B)
    ● Broad-spectrum: one or more agents active against likely bacterial/fungal pathogens and with
    good penetration into presumed source (1B)
    ● Reassess antimicrobial regimen daily (1C)
    Combination therapy in Pseudomonas infections (2D)
    Empiric therapy in neutropenic patients (2D)
    Combination therapy 3–5 days and de-escalation following susceptibilities (2D)
    ● Duration of therapy typically limited to 7–10 days; longer if response is slow or there are
    undrainable foci of infection or immunologic deficiencies (1D)
    ● Stop antimicrobial therapy if cause is found to be noninfectious (1D)
    D) Source identification and control

    ● Specific anatomic site of infection


    ● Formally evaluate for a focus of infection (e.g.abscess drainage, tissue debridement)
    ● Implement source control measures as soon as possible
    ● Choose source control measure with maximum efficacy and minimal physiologic upset
    ● Remove intravascular access devices if potentially infected (1C)
    Sepsis in the Paediatric population

    Diagnostic criteria :

    Signs and Symptoms of inflammation plus


    Infection with hyper- or hypothermia (rectal temperature 38.5°C or 35°C),
    Tachycardia (may be absent in hypothermic patients),
    and at least one of the following indications of altered organ function:
    altered mental status,
    hypoxemia,
    increased serum lactate level
    bounding pulses.
    Specific to the paediatric age group:
    1) Hydrocortisone therapy to be reserved for use in children with
    catecholamine resistance and suspected or proven adrenal insufficiency .
    2) rhAPC not to be used in children.
    3) use of ECMO be limited to refractory pediatric septic shock and/or
    respiratory failure not supported by conventional therapies .
    4) DVT prophylaxis can be given in postpubertal children with severe
    sepsis.
    5)Immunoglobulin be considered in children with severe sepsis.
    6)Sedation protocols can be used. Propofol to be avoided.
    7) optimal hemoglobin for a critically ill child with severe sepsis is not
    known.
    8) no graded recommendations for stress ulcer prophylaxis, renal
    replacement therapy and glycemic control.

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