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					Sepsis
• DEFINITIONS of SEPSIS:
  The host’s reaction to invading microbes or
  the systemic response to microbial invasion.
    Systemic inflammatory
   response syndrome(SIRS)
• Two or more following conditions:
1. Fever(> 38c ) or hypothermia (<36c)
2. Tachypnea (> 24/min) or PaCO 2<32.
3. Tachycardia( > 90/min ).
4. Leukocytosis( WBC>12000, )or leukopenia
   (WBC<4000,) or >10% bands form.
     infections            SIRS

Bacteremia
                                    Burns
Fungemia          sepsis       Panreatitis
Viremia
Parasitemia                    Trauma
                              Surgery
                 Sepsis
• Definition:
• Bacteremia:microorganisms in
  bloodstream
• Fungemia
• Viremia
# Clinical S/S may be or not.
# Almost half septic P’t 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
  and heart function.
                 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
  dose not repond to fluid or pressor
  administration.
               Etiology
• Gram negative bacteria: 60-70 %
• Gram positive bacteria: 20-30 %
  (Staphylococcus,Streptococcus,Pneumo..)
• Fungus : 2-3 % ( Candida spp )
• Others: Virus (Dengue fever,Hanta virus,
  Ebola virus,Herpes virus.
  Mycobacteria, protozoa.
      Predisposing Factors
• Malignancy:leukemia,lymphoma,dissemi-
  nated carcinoma.
• Immunosupressed : chemotherapy,
  steroid ,organ transplantation
• Indwelling cath: E-T tube,CVP line,
  Foley’s 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) α
  G(+): Exotoxin, streptokinase.
• Host mediators:TNF-α,Interleukin-1,6,
         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
             β-1 adrenergic effect.
  High dose:α 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.
               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
   Fourniere’s 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-neg- staph,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.

				
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