Sepsis dan syok sepsis
description
Transcript of Sepsis dan syok sepsis
-
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.