Case 3 SLOs

List the signs and symptoms of septicemia, and identify the most likely etiological agents.
Signs and Symptoms-Two or more of the following conditions: Fever, oral temp>38 degrees Celsius, hypothermia,
tachypnea, tachycardia, leukocytosis (high WBC) or leukopenia.
Most likely etiological agents
Site of Infection

Microorganisms

Therapeutic Choices

Community-

Streptococcus pneumoniae, Haemophilus

Third-generation cephalosporin with macrolide or

acquired

influenzae, Legionella pneumophila, Mycoplasma

respiratory quinolone

pneumonia

pneumoniae

Early hospital-

S. pneumoniae, H. influenzae, L. pneumophila,

Ceftriaxone, respiratory quinolone or ampicillin-

acquired

M. pneumonia; nonresistant gram-negative rods

sulbactam, or ertapenem

Late hospital-

Pseudomonas aeruginosa,

Antipseudomonal cephalosporin or carbapenem, or

acquired

Klebsiellaspp., Acinetobacter spp., methicillin-

antipseudomonal beta-lactam or beta-lactamase

pneumonia

resistant Staphylococcus aureus

inhibitor, plus linezolid or vancomycin

Intra-abdominal

Enteric gram-negative rods and anaerobes

Third-generation cephalosporin with metronidazole,

pneumonia (<5
days)

infections

or beta-lactam or beta-lactamase inhibitor, or

carbapenem or moxifloxacin

Urinary tract
infections

Gram-negative rods; Enterococcus spp.

Extended-spectrum beta-lactam or aztreonam, with

or without an aminoglycoside; ampicillin or
vancomycin ifEnterococcus is present

Describe the mechanisms of antibiotics given as empirical antibiotic therapy during suspected urosepsis.
Antibiotic therapy: Extended-spectrum beta-lactam (inhibits cell wall synthesis) or aztreonam (used for gram rods and
prevents peptidoglycan cross-linking), with or without an aminoglycoside (inhibits translocation traditionally for gram
negative bacteria), ampicillin or vancomycin (if enterococcus is present)both cell wall synthesis inhibition and broad
spectrum.
*Important to know that treat broad spectrum first before specifying treatment. No Bactrim because sulfonimides can
cause kidney issues, so stick to penicillin or cephlasporins.
Describe the different types of trauma that can lead to the introduction of bacteria into the blood.
Open wounds, surgical procedures, surgical device placements.
Restate the rationale of giving different antibiotics before and after specific identification of a bacterial pathogen.
First line: Broad spectrum
Once you find out about specific bacteria, modify treatment based on gram + or gram -.

Illustrate the pathway of molecules involved in the progression of septic shock and propose novel therapeutic interventions
based on this pathway.

P
Platelets and Heparin for DIC.
Review the four stages of shock.
1. Initial: Hypoperfusion causes hypoxia. This leads to mitochondrial dysfunction. The cells become leaky and switch to anaerobic
metabolism. This switch produces lactic acid and a resultant metabolic acidosis.
2. Compensatory: During this phase the body employs several mechanisms in an attempt to correct the metabolic upset of shock:
a. Hyperventilation: This will create a respiratory alkalosis in an attempt to neutralize the metabolic acidosis of shock
returning the body to a normal pH or hydrogen ion concentration. Clearly if lung function or respiratory drive mechanisms
are impaired this compensation will be less effective.
b. Catecholamine response: In response to hypotension, noradrenaline and adrenaline will be released in an attempt to
maintain both SVR and CO
c. Renin-angiotensin response: Vasopressin excretion is increased leading to fluid retention (to maintain circulating volume)
and vasoconstriction.
3. Progressive: The mechanisms listed above can only compensate for worsening shock for so long. Eventually they will begin to fail.
At this point cellular dysfunction begins to spiral out of control, metabolic acidosis worsens and the arteriolar and precapillary
sphincters constrict such that blood remains in the capillaries. The pressure within the capillaries will increase. This, combined with
membrane dysfunction, will lead to fluid loss into the extravascular interstitial spaces. This will further worsen the intravascular
volume status.
4. Refractory: At this stage organs fail and the shock can no longer be reversed. Death normally occurs rapidly.