Sepsis dan syok sepsis

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sepsis dan tatalaksana syok septik

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  • sepsisDr.AbdulWAHID M SalihPh.D. Surgery

  • How to manage ?54yr male24 hr Fever and deliriumInitial ObsHR 162, RR 30,O2 sats 95% , BP 116/82, GCS 13/15HistoryMigratory abdominal pain and fever 1/7Past HistoryLeft ureteric stone, 6mm

  • Differential DiagnosisPancreatitisIscheamic GutHypovolaemic shockGI bleed / AAA rupture / ectopic / dehydrationCardiogenic shockAMI / Myocarditis / TamponadePEToxic ShockAddisonian crisis (note relative adrenocorticoid insufficiency in many septic patients)Thyroid Storm

  • Consensus Definitions

  • eitherBacteraemia (or viraemia/fungaemia/protozoan)is the presence of bacteria within the bloodstream

    Septic focus (abscess / cavity / tissue mass)

    Infection

  • 2/4 of;Temp >38 or 90Respiratory Rate >20 or PaCO2 12 or 10% bands (immature forms)

    SIRS

  • Is the systemic response to infection

    Sepsis

  • Sepsis - SIRS + Infection

    Severe Sepsis- Sepsis+ Organ dysfunction

    Septic shockSepsis+ Hypotension despite fluid resuscitation

  • Complications

  • Organ System InvolvementCirculationHypotension, increases in microvascular permeabilityShock

    LungPulmonary Edema, hypoxemia, ARDS

    HematologicDIC, coagulopathy(DVT)

  • Organ System Involvement

    GI tractstress ulcer Translocation of bacteria, Liver Failure, Gastroparesis and ileus, Cholestasis

    Kidney Acute tubular necrosis, Renal Failure

  • Organ System Involvement

    Nervous SystemEncephalopathy

    Skeletal Muscle Rhabdomyolysis

    EndocrineAdrenal insufficiency

  • Sources of SepsisThe International Cohort StudySevere SepsisSeptic Shock35% mortality

    Respiratory6653Abdomen920Bacteremia1416Urinary1111Multiple--

  • PathophysiologyExcessive anti-inflammatory responseSepsis: auto-destructive process allowing normal responses to infection/injury to involve normal tissues

  • Severe Sepsis: The Final Common PathwayEndothelial Dysfunction and Microvascular ThrombosisHypoperfusion/IschemiaAcute Organ Dysfunction (Severe Sepsis)Death

  • High Risk PatientsFor Sepsis and DyingMiddle-aged, elderlyPost op / post traumaPost splenectomy Transplant immune supressedAlcoholic / MalnourishedGenetic predispositionDelayed appropriate antibioticsComorbidities : AIDS, renal or liver failure, neoplasms

  • Identification of septic focushistory physical examination imaging cultures Blood cultures, urine culture, sputum culture, abscess culture.

  • InvestigationsBasicWBCPlateletsCoagsRenal functionGlucoseAlbuminLFTABGSpecific ?Source

    UrineCxRBlood Cultures Biopsy

    May all be normal early on!

  • Differentiate sepsis from noninfectious SIRS

    ProcalcitoninC-reactive protein (CRP) IL-6protein complement C3aLeptin

    test is not yet readily available for clinical practice

  • Treatment of SepsisAntibiotics

    Early aggressive fluid resuscitation

    Inotropes for BP support (Dopamine, vasopressin, norepinephrine)

    Source control

    Steroid therapy (adrenal insufficiency)

    Activated protein C

    Ventilatory Strategies

    Glycemic control

    Newer therapies.

  • I.V. antibiotics Initiated as soon as cultures are drawn.

    Severe sepsis should receive broadspectrum antibiotic.

    Empiric antifungal drug; Neutropenic patients, DM, chronic steroids.

  • AntibioticsAbx within 1 hr hypotension: 79.9% survivalSurvival decreased 7.6% with each hour of delayMortality increased by 2nd hour post hypotension Time to initiation of Antibiotics was the single strongest predictor of outcome

  • Antibiotics dosing Dosage for intravenous administration (normal renal function).Imipenem-cilastin 0.5g q 6hMeropenem 1.0g q 8hPiperacillin-tazobactam 3.375gq 4h or 4.5 g q 6hCefepime1-2 q 8hrGatifloxacin 400mg iv q dCeftriaxone 2.0g q 24hrLevofloxacin500mg q d

  • Source controlEarly recognition of the Sepsis syndrome.Surgical intervention when indicated.Aggressive supportive care in intensive care units.

  • Surgery

    Get the pus outabscesses or foci of infection should be drained

    Early definitive care ;e,.g; ruptured appendix, cholecystitis

  • SupportiveOxygenate / Ventilate

    Volume

    Electrolyte homeostasis

    Inotropes

    (DVT) and stress ulcer prophylaxis

  • ARDS causes respiratory failurein patients with severe Sepsis

    Assess the airway, respiration, and perfusion

    Supplemental oxygenation,

    Ventilator for respiratory failure

  • Sepsis-induced hypotensionsystolic less than 90 mm Hg or a reduction of more than 40 mm Hg from baseline in the absence of other causes of hypotension."

    A loss of plasma volume into the interstitial space, Decreases in vascular tone, Myocardial depression.

  • Treatment of HypotensionIntravenous fluids : Crystalloids vs. Colloids.need more than maintenance + replace losses

  • Fluid TherapyNo mortality difference between; colloid vs. crystalloid

  • Goals for initial resuscitation

    Central venous pressure 8 to 12 mmHg.

    Mean arterial pressure 65 mmHg.

    Urine output 0.5 mL per kg per hr.

    Pulmonary capillary wedge pressure exceeds 18 mmHg

  • Steroids For Non-responders;

    Improved refractory hypotension Reduced mortality 10%

    50mg of hydrocortisone iv q 6hrs With fludrocortisone 50mcg ngtfor 7 days

  • Stress hyperglycemiain critically ill patients Due to;

    A decreased release of insulin

    increased release of hormoneswith effects countering insulin

    increased insulin resistance

    Hyperglycemia diminishes the ability of neutrophils and macrophages to combat infections.

  • Tight Glycemic control

    Continuous insulin infusion

    Maintaining serum glucose levels between 80 and 110 mg/dl

    Decreased mortality development of renal failure

  • Failed therapiesCorticosteroidshigh dose methylprednisolone

    Anti-endotoxin antibodies

    TNF antagonistssoluble TNF receptor

    Ibuprofen

  • MortalitySepsis: 30% - 50%

    Septic Shock: 50% - 60%

    ****This chart shows the site of infection for cases within the categories of severe sepsis or septic shock. This information is useful for guiding investigations and initial empiric treatment.*The endothelial cell is the focal point of interactions between the inflammatory events and disordered hemostasis of patients with severe sepsis. Although vascular bed-specific factors are operative, endothelial cell injury or death can shift the cells phenotype from antithrombotic to prothrombotic and induce sequestration of inflammatory cells and platelets in the damaged vessel(s). The resultant hypoperfusion/ischemia produces acute organ dysfunction. Uninterrupted, a viscous cycle ensues that can end in death.