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Infectious Disease [SEPSIS]

Introduction SIRS Criteria


An infection usually causes a local inflammatory response with Temperature > 38 or < 36
symptoms. Lung infections cause a cough, while UTIs cause Tachycardia > 90
dysuria. But when an infection jumps the shark and goes systemic Respiratory RR > 20 or PCO2 < 32
WBC > 12 or < 4
- effects are felt systemically - start thinking of sepsis. Sepsis
itself doesn’t require septicemia (bacteria in the blood) and
therefore may be culture negative, but the systemic effects of SIRS “Types”
inflammatory mediators can wreak havoc on the body. SIRS 2 or more criteria met, Ø source
Sepsis SIRS source
SIRS Criteria Severe Sepsis Sepsis with low blood pressure or elevated
The Systemic Inflammatory Response Syndrome (SIRS) must lactic that is responsive to fluids
meet 2 of 4 criteria that signal physiologic responses to Septic Shock Sepsis with low blood pressure or elevated
inflammation. Inflammatory mediators will cause ↑ CO (↑ HR) lactate that is non-responsive to fluid.
MODS Multiple Organ Dysfunction Syndrome, the
either directly on the heart or reflexively from vasodilation.
patient is circling the drain with septic
Tachypnea follows. Fever is a product of IL-6 + TNF-α. Finally, shock and multiple organs failing
the response to infection is ↑ WBC (leukocytosis). But, because
some infections may ↓ WBC or a person can have sepsis in the
presence of HIV, both count. Evaluation beyond sepsis involves Organs in Dysfunction
looking for end organ damage: 1) Renal Failure (↑ Cr and Hypotension
BUN), 2) liver failure with coags and an LFT 3) Blood Vessels
with a blood pressure, 4) Brain with mental status checks, and 5)
Heart with an ECG or Troponins. Still further, one needs to
AMS
evaluate for tissue hypoxemia with a lactic acid level. Depending
on the number and severity of organ dysfunction, the patient is
stratified into a sepsis “type.” (SIRS, Sepsis, Severe Sepsis,
Septic Shock, MODS). Creatinine

Therapy
Regardless of “type,” the treatment is the same: Early Goal
Directed Therapy. This takes place in the first six hours of LFTs, Coags
hospitalization (early) and is designed to ↑ Tissue Perfusion, ↓
Tissue Hypoxia, and control the source. Controlling the source
begins by eliminating sources of infection (IV sites, Abscess Other Lactate
Drainage, and Wound Debridement) and starting empiric
antibiotics for the suspected agent. Blood Cultures should be
drawn prior to antibiotics, but do NOT delay the treatment with
broad-spectrum antibiotics. In order to meet tissue perfusion
demands certain criteria should be monitored. To maintain Early Goal Directed Therapy
perfusion (MAP > 65, CVP 8-16) a 30cc/kg bolus is the first CVP 10-12mmHg
MAP >65mmHg
step. If responsive, nothing more needs be done. Failure of the
Uoutput >0.5cc/kg/hr
fluid challenge will require the need for pressors. To maintain SvcO2 >70%
oxygenation (oxygen deliver > oxygen consumption, or SvO2 > 1) Give 30cc/kg IV Bolus
70%) both oxygen and blood (if Hgb < 7) should be given. 2) Remove all source of infection
3) O2 as needed
4) Pressors if fluid bolus fails
5) Empiric abx while waiting for cultures


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