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SEPSIS
Stephanie Tang
Page #1:
 10:40pm:
“Patient Chen spiked fever to 38.7oC.
Other vitals are BP 100/60, HR 110, RR
20, SaO2 95% on RA”
Fever
 work up should include (at least) the following:
 blood cultures
 at least two with one being peripheral
 if pt has central access, must culture each port
 UA and urine culture
 CXR
 a careful exam
Page #2
 12:15am:
“Patient Peterson spiked fever to 38.7oC.
Other vitals are BP 92/55, HR 120, RR
24, SaO2 95% on RA”
SIRS sepsis
severe
sepsis
septic
shock
multiple
organ
dysfunction
syndrome
(MODS)
Systemic Inflammatory Response
Syndrome (SIRS)
 T >38.3oC OR T <36oC
 HR >90/min
 RR >20/min OR PaCO2 <32mmHg
 WBC >12,000 OR <4,000
OR >10% immature forms
American College of Chest Physicians & Society of Critical Care Medicine 1991
Systemic Inflammatory Response
Syndrome (SIRS)
 dysregulated inflammatory response to
an insult
 autoimmune disorder
 pancreatitis
 vasculitis
 thromboembolism
 burns
 surgery
Sepsis
 SIRS + source of infection
(probable or documented source)
Severe Sepsis
 sepsis + evidence of hypoperfusion
 oliguria or acute renal failure
 encephalopathy
 coagulopathy
 acute respiratory failure
 ischemic hepatopathy
 skin mottling
 elevated lactate
 low central venous saturation
Septic Shock
 severe sepsis refractory to fluid resuscitation
of 30mL/kg
- ex. 70 kg  2.1 L of IVF
 distributive shock
Why Do We Care about Sepsis?
 1,665,000 cases in the United States each year
Chest. 2011;140(5):1223-1231
In-hospital mortality
N Engl J Med. 2003;348(16):1546
Long term Mortality
Crit Care Med. 1995 Jun;23(6):1040-7.
Long term Mortality
Crit Care Med. 1995 Jun;23(6):1040-7.
WHAT HAPPENS?
Normally…
proinflammatory
mediators
TNFα, IL-1
anti-inflammatory
mediators
IL-10, transforming growth factor
β, IL-1 receptor antagonist
Sepsis
 occurs these responses to an infection
exceeds the boundaries of the local
environment, leading to a more
generalized response
Mitochondrial Dysfunction
 Peripheral blood
monocytes in
sepsis
 Assay membrane
potential at
admission, 3 days
and at hospital
discharge
Christophe et al. Am. J. Respir. Crit. Care Med 2001 164: 389-395
Circulatory Failure
↑ nitric oxide
↑ prostacyclin
(improve metabolic
autoregulation)
hypotension
(high CO, low SVR state)
Endothelial Damage
Mutunga et al. Am. J. Respir. Crit. Care Med., Volume 163, 2001, 195-200
Myocardial Dysfunction
 circulating depressant factors
Parrillo. J Clin Invest. 1985;76:1539–1553
Myocardial Dysfunction
 reduced
ventricular
function
 even in setting of
elevated CO
 reversible (usually
7-10 days)
Kumar et al J Exp Med 1996;183:949-953
TNF
IL-1
Coagulopathy
 Endothelial
expression of
Tissue Factor
 Decreased
endothelial
expression of
thrombomodulin
Marshall Nature Rev Drug Disc 2003;2-391-405.
Coagulopathy of Sepsis
 In-situ thrombosis
 Skin biopsy in meningococcal sepsis
Faust et al.N Engl J Med 345 (6): 408, August 9, 2001
In Summary…
Riedemann et al, Novel strategies for the treatment of sepsis, Nat Med, 9(5):517-524
TREATMENT OF SEVERE
SEPSIS
Monitoring
 close monitoring of heart rate and blood pressure
 foley (to monitor urine output)
 frequent clinical reassessments
Goals
fluid
resuscitation
stabilize
breathing
source
control
SEPSIS
Resuscitation
 Fluids should be bolused
 Large bore IVs are best
 22g IV = max 35 ml/minute
 20g IV = max 60 ml/min
 18g IV = max 105 ml/min
 16g IV = max 205 ml/min
 14g IV = max 333 ml/min
rate ∞
length
radius4
Resuscitation
 crystalloid
 lactated ringers
 normal saline
 nongap (hyperchloremic) acidosis
 hypokalemia
 colloid
 blood
 albumin
130 109
154 154
4
+ lactate 28
HCO3
(by liver)
Respiratory Status
oxygenation ventilation airway
Respiratory Status
oxygenation
pulmonary edema
ARDS
ventilation airway
Respiratory Status
oxygenation ventilation
primary respiratory alkalosis
↑ work of breathing ↔ ↑ O2 consumption
airway
Respiratory Status
oxygenation ventilation airway
altered mental status
Source Control
 appropriate antibiotic coverage
 abscesses or closed space infections
 ascending cholangitis
 obstructive pyelonephropathy
Early Goal-Directed Therapy in the Treatment of
Severe Sepsis and Septic Shock
Emanuel Rivers, M.D., M.P.H., Bryant Nguyen, M.D., Suzanne Havstad, M.A., Julie Ressler, B.S.,
Alexandria Muzzin, B.S., Bernhard Knoblich, M.D., Edward Peterson, Ph.D., Michael Tomlanovich,
M.D., for the Early Goal-Directed Therapy Collaborative Group
N Engl J Med 2001;345: 1368-1377
Early Goal-Directed Therapy
 Rationale: early hemodynamic assessment
(physical findings, vital signs, CVP, UOP) fail to
detect persistent global tissue hypoxia
 Goal: resuscitation strategy targeted to
optimize cardiac preload, afterload, and
contractility to achieve balance between
systemic oxygen delivery and oxygen demand
 Endpoints: mixed venous O2 sat, arterial
lactate, base deficit, pH
Early Goal-Directed Therapy
 n = 263
 In ED:
SIRS +
sBP< 90 or lactate >4
 after 30cc/kg fluid bolus
 Randomized to:
usual care
vs.
early goal-directed
therapy protocol
In-hospital mortality
 Mortality: 30.5% vs. 46.5% (p=0.009)
 ARR 16%, NNT 6.3
 Larger initial fluid resuscitation in EGDT arm
 4.9L vs. 3.5L (p<0.001)
Lessons from EGDT
 up front aggressive monitoring for
hypoperfusion is critical
 early aggressive IVF is beneficial
 clinical markers are important but we need to
also track markers for occult hypoperfusion
(mixed venous sat, lactate)
Sepsis for TYs

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Sepsis for TYs

Notas del editor

  1. Hypovolemic, cardiogenic, distributive
  2. Risk Factors: bacteremia age >=65 immunosuppression DM and cancer CAP genetic factors
  3. N Engl J Med. 2003 Apr 17;348(16):1546-54. The epidemiology of sepsis in the United States from 1979 through 2000. Martin GS, Mannino DM, Eaton S, Moss M. We analyzed the occurrence of sepsis from 1979 through 2000 using a nationally representative sample of all nonfederal acute care hospitals in the United States. Data on new cases were obtained from hospital discharge records coded according to the International Classification of Diseases, Ninth Revision, Clinical Modification.
  4. Long-term survival after intensive care unit admission with sepsis. Sasse KC, Nauenberg E, Long A, Anton B, Tucker HJ, Hu TW Crit Care Med. 1995;23(6):1040. All patients admitted to the ICU from January 1, 1987 to March 31, 1991 who both demonstrated clinical evidence of the systemic inflammatory response syndrome and yielded blood cultures positive for a bacterium or fungus (n = 153). Follow-up evaluation utilizing the National Death Index provided survival outcome for all patients 1 yr after hospital discharge. The mortality rate at hospital discharge was 51.0%, and mortality rates at 1 month, 6 months, and 1 yr after admission date were 40.5%, 64.7%, and 71.9%, 
  5. Long-term survival after intensive care unit admission with sepsis. Sasse KC, Nauenberg E, Long A, Anton B, Tucker HJ, Hu TW Crit Care Med. 1995;23(6):1040. All patients admitted to the ICU from January 1, 1987 to March 31, 1991 who both demonstrated clinical evidence of the systemic inflammatory response syndrome and yielded blood cultures positive for a bacterium or fungus (n = 153). Follow-up evaluation utilizing the National Death Index provided survival outcome for all patients 1 yr after hospital discharge. The mortality rate at hospital discharge was 51.0%, and mortality rates at 1 month, 6 months, and 1 yr after admission date were 40.5%, 64.7%, and 71.9%, 
  6. PRO: stimulate PMNs, macrophages and endothelial cells to release a number of downstream inflammatory mediators, including platelet activating factor and nitric oxide (NO), further amplifying the inflammatory response ANTI:
  7. Hypotension due to diffuse vasodilation unintended consequence of the release of vasoactive mediators, whose purpose is to improve metabolic autoregulation (the process that matches oxygen availability to changing tissue oxygen needs) by inducing appropriate vasodilation. Mediators include the vasodilators prostacyclin and nitric oxide (NO), which are produced by endothelial cells.
  8. Blood samples were taken from 11 healthy volunteers, nine ventilated intensive care unit (ICU) control patients without sepsis, eight patients with sepsis but without shock, and 15 patients with septic shock. Circulating endothelial cells were identified by indirect immunofluorescence, using antibodies to von Willebrand factor (vWf).  Distributive shock, capillary leak
  9. NOT myocardial hypoperfusion/hypoxia
  10. Also feedsback to microcirculatory hypoperfusion
  11. n=263 with severe sepsis or septic shock urban ED randomized to early goal-directed therapy v. standard therapy x 6 hrs --> then to ICU ICU team blinded in-hospital morality 30.5% v. 46.5% (p=0.009) central venous sat 70.4% v. 65.3% (p<0.02) lactate 3.0 v. 4.4 (p<0.02) APACHE II score 13.0 v. 15.9 (p<0.001)
  12. Usual care group = target CVP 8-12, MAP>65, UOP>0.5mL/kg/hr  ICU ASAP Early goal-directed = protocol x 6 hours All rec’d: a-line, central line Early goal-directed group: constant central venous sat monitoring CVP 500cc PRN until 8-12 arterial sBP if<65 start pressors arterial MAP  if>95 start vasodilators central venous sat  if <70% transufse to Hct>30% if still <70% start dobutamine @ 2.5ug/kg/min and uptitrate until 20 if HD optimization could not achieved, mechanical ventilation + sedatives to decr O2 demand
  13. During initial 6 hours: no difference in HR, CVP MAP lower in standard therapy group, although everyone MAP>65 Central venous sat met by 60% in standard therapy v. 95% in early-goal directed group & lower avg value similar lactate and pH values Hours 7-72: HR higher and MAP lower in standard therapy group similar CVPs Lower central venous sat, higher lactate, greater base deficit, lower pH in standard group