Infectious Diseases: Sepsis & Shock Flashcards
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
2
Q
Severe sepsis
A
- Hypotension
- Systolic blood pressure <90 mmHg
- drop of >40 mm Hg from baseline
- Reversible with intravenous fluid resuscitation
3
Q
Septic shock
A
- Sepsis not responding to IVF resuscitation
- Requires vasopressors
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
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
6
Q
Effect of shock & sepsis on pulmonary
A
- Vascular permeability due to heart failure
- Noncardiogenic pulmonary edema
7
Q
Effect of shock & sepsis on renal
A
Decrease effective intravascular volume due to systemic hypotension -> Acute tubular necrosis
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?
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
- 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