Infectious Diseases: Sepsis & Shock Flashcards

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1
Q

Systemic inflammatory response syndrome (SIRS)

A
  • Dysregulated host inflammatory response.
  • Presence of two or more of the following:
    • Temperature >38oC (100.4oF) or <36oC (96.8oF)
    • Heart rate >90 beats/min
    • Respiratory rate >20 breaths/min
    • WBC >12,000 cells/mm3, <4000 cells/mm3, or >10 percent immature (band) forms
  • Can be result of noninfectious processes
  • Sepsis = SIRS + Infection
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2
Q

Severe sepsis

A
  • Hypotension
    • Systolic blood pressure <90 mmHg
    • drop of >40 mm Hg from baseline
    • Reversible with intravenous fluid resuscitation
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3
Q

Septic shock

A
  • Sepsis not responding to IVF resuscitation
  • Requires vasopressors
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4
Q

Some causes of sepsis

A
  • Meningitis: N. meningitides, S. pneumoniae, L. monocytogenes
  • Pneumonia:
    • Community-acquired (top 3): S. pneumoniae, M. pneumoniae, H. influenzae
    • Nosocomial pneumonia (top 3): MRSA, Pseudomonas, E. coli
  • Pyelonephritis: E. coli, Proteus, Klebsiella
  • Peritonitis: aerobic and anaerobic gram -ve
  • Cholangitis: E. coli, Klebsiella, Enterobacter
  • Cellulitis: S. aureus (MSSA, MRSA), beta-hemolytic strep
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5
Q

Sepsis & Shock Pathogenesis

A
  • “Malignant intravascular inflammation”
  • Balance of pro- and anti- inflammatory processes
  • Small amounts lead to
    • Fever
    • Leukocytosis
    • Activation of complement
  • Excessive production/release lead to
    • Dysregulated
    • Capillary leakage, hypovolemia → hypotension and poor tissue perfusion
    • DIC
    • Shock
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6
Q

Effect of shock & sepsis on pulmonary

A
  • Vascular permeability due to heart failure
  • Noncardiogenic pulmonary edema
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7
Q

Effect of shock & sepsis on renal

A

Decrease effective intravascular volume due to systemic hypotension -> Acute tubular necrosis

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8
Q

Effect of shock & sepsis on CNS

A
  • Hypotension can lead to brain hypoperfusion.
  • Result of hepatic or renal dysfunction, metabolic encephalopathy
  • Delirium? vs. CNS infection?
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9
Q

Endocarditis Etiopath

A

Risk factors:

  • Stenosis, sclerosis, prolapse
  • Prosthetic valve
  • Rheumatic
  • IVDU
  • Congenital: Tetraology
  • VSD, bicuspid AV

Etiology

Secondary to primary focus of infection

  • Usually transient
  • Skin- Abscess
  • GU- Pyelonephritis
  • Pulmonary- Pneumonia
  1. Endovascular source
  • Usually sustained
  • Infected intravascular device- (Catheter)

Pathogenesis

  • Trauma to endothelium as result of turbulent flow
  • Stimulates fibrin, platelet deposition
  • Episode of transient bacteremia
  • Likely suspects – staph, strep viridans (alpha hemolytic), enterococcus, coagulase -ve staph, HACEK (liver around mouth and cause subacute)
  • Beta hemolytic organisms are uncommon causes of endocarditis: S.pyogenes Group A, S.agalactiae, GBS
  • However, IV drug users, any microbe can cause endocarditis (bacteria & fungi)
  • Virulence factors: biofilm

Sx: fever, new murmur, vascular embolic event, splenomegaly, splinter hemorrhages, Osler’s nodes (immune complex deposition) , Janeway’s lesions (septic emboli, microabscesses), Roth spots, hypopion, mitral valve vegatation,

  • pulm: septic pulmonary emboli
  • Spleen & liver: infarcts & abscesses
  • MSK: septic arthritis, vertebral osteomyelitis
  • CNS: Embolic stroke, infarct, hemorrhage
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