Beruflich Dokumente
Kultur Dokumente
Akmal Syaroni
Div. Of Tropical and Infectious Disease Dept. Of Internal Medicine Faculty of Medicine Sriwijaya University/ Moh Hoesin Hospital Palembang Indonesia
DEFINITIONS of SEPSIS: The hosts reaction to invading microbes or the systemic response to microbial invasion.
infections
Bacteremia Fungemia Viremia Parasitemia
SIRS
Burns Panreatitis Trauma Surgery
sepsis
Sepsis
Definition: Bacteremia:microorganisms in bloodstream Fungemia Viremia # Clinical S/S may be or not. # Almost half septic Pt had Neg culture.
Sepsis
Sepsis or septicemia Clinical syndrome ( SIRS ) + microorganisms or their toxic product in bloodstream or infection. # Clinical manifectations: chills, fever, tachycardia ,tachypnea, altered metation.
Sepsis
Septic syndrome ( severe sepsis ): Sepsis + MODS Multiple organ dysfunction syndrome: # metabolic acidosis, oliguria,consciousness disturbanced,coagulation abnormality, acute respiratory failure,abnormal liver
Sepsis
Septic shock: Sepsis + hypotension and inadequate organ perfusion. # systolic blood pressure(SBP)< 90 mmHg or reduction of > 40 mmHg from base-line. Refractory septic shock: shock >1 hr, and does not repond to fluid or pressor administration.
Etiology
Fungus : 2-3 % ( Candida spp ) Others: Virus (Dengue fever,Hanta virus, Ebola virus,Herpes virus. Mycobacteria, protozoa.
Predisposing Factors
Malignancy:leukemia,lymphoma,dis semi-nated carcinoma. Immunosupressed : chemotherapy, steroid ,organ transplantation Indwelling cath: E-T tube,CVP line, Foleys tube,drain tube(PTCD, PCN ) Liver cirrhosis,Uremia,DM,Alcoholism.
Sepsis
Poor
prognosis: Microbial factor: P.aeruginosa Host factor: immunocompromised host, leukemia, SLE, AIDS, neutropenia. Septic syndrome: DIC, ARDS, latic acidosis, shock.
Pathogenesis
Gram negative sepsis: most from G-I tract, G-U tract, biliary tract, Resp tract, less: skin ,bone, joint. Gram positive sepsis: cath-related infection, IV drug abuser, Resp tract, skin & soft tissue infection
Pathology
Involvement of target organ: Lung: pul edema, hemorrhage, hyaline menbrane change, & ARDS. Kidney: tubular or cortical necrosis. Heart: patchy necrosis in myocardium. GI tract: superficial ulcer or hemorrhage. Vascular: WBC-PLT or fibrin thrombi in the capillaries, DIC.
Pathophysiology
Microbial factors: G(-) : Endotoxin : lipopolysaccharides (lipid A) G(+): Exotoxin, streptokinase. Host mediators:TNF-, Interleukin1,6, cytokine,complement,Kinin.
Complication
Cardio-vascular system: Hypotension Decreased myocardial contractility Pooling of blood in the microcirculation Two phases: early: hyperdynamic phase later : hypodynamic phase
Complication
Lung: ventilation- perfusion mismatching decreased PaO2. increased capillary permeability increased lung water and infiltrate @ Sepsis is the leading cause of ARDS #DDx: pul edema (PCWP>18 mm Hg ) & pneumocystis carinii infection are similar to ARDS in CXR findings.
Complication
Kidney :acute renal failure most due to acute tubular necrosis(ATN) induced by hypotension or capillary injury. Oliguria,azotemia,proteinuria. Liver : increased ALT,AST,bilirubin, Alk.P, LDH,CRP. G-I tract: ileus,ulcers, ischemic bowel.
Complication
Coagulation system: Thrombocytopenia, DIC (disseminated intra-vascular coagulation ) Metabolic: latic acidosis impaired of gluconeogenesis and insulin resistant, poor control of blood sugar in diabetic patients.
Treatment
Removal of infection source: indwelling catheter,prosthetic device. Drainage of abscess: Relief of obstruction:hydronephrosis, CBD obstruction,urine retention.
Treatment
DC or hold immunosupressed drug G-CSF for leukopenia (WBC< 1000) Respiratory support: O2 therapy, ventilator, PEEP for ARDS. Hemodynamic support:PCWP:12-15 CVP:10-12 cm H2O, correct anemia. Urine output:30mL/h, furosemide if need
Treatment
Dopamine: keep SBP> 90 mmHg. Low dose: 5-10 ug/Kg/min, dopaminergic effect -1 adrenergic effect. High dose: adrenergic effect. Adrenal insufficiency:prior steroid use, meningococemia,TB,AIDS. hydrocortisone 50 mg iv q6h.
Treatment
Metabolic acidosis: NaHCO3 administered if pH< 7.2 DIC: FFP and platelet transfusion. successful Tx of underlying disease is essential to reverse both acidosis & DIC
Antibiotics
Urosepsis:GNB most common, B-lactam + aminoglycoside Meningitis: 3rd generation cephalosporin + crystal penicillin. Endocarditis:PCN or oxacillin + GM. Liver abscess & BTI :cefazolin + GM Intra-abd infection: polymicrobial.
GNB: Gram negative bacili, BTI : Biliary Tract infections,GM : Gentamicin, PCN: Penicilin
Antibiotics
Community acquired pneumonia: pneumococci: PCN, cefotaxime,Rocephin vancomycin. H.influenzae or M.catalarris:2nd cephem Atypical pneumonia: erythromycin or new macrolide Hospital acquired pneumonia:GNFGNB MRSA,ESBL-E.coli, K.P,P aeruginosa.
Antibiotics
Cellulitis: Face & mandible:oral cavity bacteria Deep neck infection: K.P in diabetic Extremities:Gr A streptococcus L.cirrhosis:eat raw oester: V.vulnificus Fournieres gangrene Toxic shock syndrome:staph or strepto..
Antibiotics
Asplenic patients: S.pneumoniae, H.influenzae, N.meningitidis PCN or vancomycin + 3rd cephem. Catheter-associated infection: MRSA,coag-negstaph,GNB,enterococci Neutropenic patients: P.aeruginosa.
Antibiotics
NO obvious infectious source: Broad spectrum antibiotics cover, B-lactam + aminoglycoside NEW MEASURES: Anti-endotoxin agents:neutralize effect. Anti-mediator agents: antagonist of TNF and interleukin receptor.
Thank You