2. Erin's Story
It is the clinical syndrome that results from a
dysregulated inflammatory response to an
infection (UpToDate, 2012).
Sepsis is not a specific event in time, but rather
a syndrome that occurs on a continuum.
3. ~750,00 cases annually (trend has been on a
steady increase since the 70’s)
Thought to be influenced by:
aging population
increase in immune suppressed population
increased drug resistant diseases
~200,000 deaths/year
Patients >65 account for nearly 60% of all cases
(Angus, et all, 2001).
4. Increased incidence during winter
months
30-50% mortality, severity
dependent
Septic patients have 2x as long
hospital stay as patients without
Costs the health care system over
$16 billion dollars annually
7. Clinical syndrome that results from a
dysregulated inflammatory response, but is due
to a non-infectious source.
Examples:
Acute pancreatitis
Trauma
Burns
Surgery
8. SIRS requires 2 or more of the following
derangements:
Temp >38.3: (100.4:F) or <36:C (96.8:F)
HR >90
RR >20 or PaCO2 >32 (normal 35-45)
WBC >12,000 or <4,000 or >10% immature
cells (bands)
9. A systemic inflammatory response to infection,
triggers cascade of inflammation, coagulation
and impaired fibrolysis.
This out of control inflammatory process results
in vasodilitation, increased capillary
permeability and clotting.
Same criteria as SIRS, however, occurs within a
context of known infection.
10. Sepsis plus at least one of the following signs of
hypoperfusion or end organ damage
Areas of mottled skin
Delayed capillary refill
Urine output of <0.5 mL/kg for at least one hour or
renal replacement therapy
Lactate >2 mmol/L
AMS
Abnormal EEG findings
Platelet count <100,000
DIC
Acute lung injury or ARDS
Cardiac dysfunction
11. Exists if there is severe sepsis & one or both of
the following:
Systemic mean blood pressure <60 mmHg despite
adequate fluid resuscitation
Maintaining systemic mean blood pressure >60
mmHg requires vasopressors despite adequate
fluid resuscitation
Vassopressor use is a significant predictor of
mortality
12.
13. Altered function of one or more organs
Primary and secondary MODS
Primary: direct injury/insult to organs that results
from a specific event (i.e. pulmonary
contusion, liver laceration)
Secondary: indirect injury/insult to organs as a
result of systemic event (i.e. SIRS, sepsis)
Mortality with MODS is very high; proportionate
to the number of organs involved
2 organ failure mortality 45-55%
3 organ failure mortality >80%
16. Localized site of infection, initiates a localized
inflammatory response
White blood cells converge to the site of infection
Neutrophils, macrophages
Localized infection can lead to bloodstream
infection (bactermia), this is sepsis
Bacteria release endotoxins
Immune system releases proinflammatory
mediators (prostaglandins, cytokines)
Endotoxins
17. Cytokines are immunomodulators (interleukons
& interferons) released by WBCs and cause:
Vasodilitation
Increased capillary permeability
Increased coagulation
Prostaglandins in the inflammatory process
cause vasodilitation, inhibit platelet aggregation
and effect the hypothalamus with regards to
thermoregulation (fever)
18. Vasodilitation is mechanism used to increase
blood flow to affected areas allowing for better
transport of WBCs
Without corresponding increase in blood volume,
hypotension follows
Increased capillary permeability leads to fluid
leak third spacing & further volume loss
Impaired fibrinolysis causes decreased clot
breakdown microthrombi, then tissue
hypoperfusion, necrosis & organ failure
20. In septic shock, the body’s compensatory
mechanisms are overwhelmed by malignant
inflammatory response.
Leading to:
Reduced coronary blood flow with decreased CO, BP &
tissue perfusion
Pro-inflammatory cytokines cause imbalances between
clotting & lysis, impairing circulation to
tissues/organs, third spacing & worsening hypotension
Brain fails to respond with vasomotor responses to
hypotension
Peripheral ischemia occurs due to prolonged shunting &
microemboli
Survival at this stage in the cascade is <10%
23. WBCs elevated or suppressed (>12,000<4,000)
or normal with >10% bands
Documented infection
Increased lactate >4 mmol/L
Coagulation disturbances
Low fibrinogen, increased fibrin split products
Thrombocytopenia
Elevated INR or PTT
Elevated CRP (C Reactive Protein)
Hyperglycemia
24. The key to sepsis treatment is: PREVENTION
HAND WASHING
Proper line management
VAP protocols
Hand washing
Catheter removal
Early mobility
Did I mention hand washing already?
25.
26. Broad spectrum antibiotics within first 1-3 hours
Corticosteroids, if persistent hypotension
despite adequate fluid resuscitation; may
indicate adrenal insufficiency
no longer requires cortisol stim test to start therapy
Vasopressors, for hemodynamic support after
adequate fluid resuscitation
Xigris (drotrecogin alfa) voluntarily pulled from
the market in 10/2011 as studies showed no
benefit
27. Stroke: Time is brain
MI: Time is muscle
Sepsis: Time is tissue
With every hour that intervention is delayed,
survival drops by 10%
Early recognition and intervention are key to
successful outcomes
Prevention is the key to sepsis
29. HighImpactGraphics. (2011, August 14). Sepsis {Video file}. Retrieved from
http://www.youtube.com/watch?v=xm437bHXsrY
LoyolaHealth. (2012, September 24). Code sepsis {Video file}. Retrieved from
https://www.youtube.com/watch?v=t3qWMcDK-ME
Angus, B., Linde-Zwinde, W., Lidicker, J., Clemont, G., Carcillo, J., & Pinsky, M. (2001).
Epidemiology of severe sepsis in the United States: Analysis of incidence, outcome
and associated costs of care. Critical Care Medicine, 29(7), 1303-1310.
Bone, R., Balk, R., Cerra, F., Dellinger, R., Fein, A., Knaus, W., . . . Sibbald, W. (1992).
Definitions for sepsis and organ failure and guidelines for the use of innovative
therapies in sepsis. The ACCP/SCCM Consensus Conference Committee, (pp. 1644-55).
30. Angus, B., Linde-Zwinde, W., Lidicker, J., Clemont, G., Carcillo, J., & Pinsky, M. (2001).
Epidemiology of severe sepsis in the United States: Analysis of incidence, outcome
and associated costs of care. Critical Care Medicine, 29(7), 1303-1310.
Bone, R., Balk, R., Cerra, F., Dellinger, R., Fein, A., Knaus, W., . . . Sibbald, W. (1992).
Definitions for sepsis and organ failure and guidelines for the use of innovative
therapies in sepsis. The ACCP/SCCM Consensus Conference Committee, (pp. 1644-55).
Dellacroce, H. (2009). Surviving sepsis: The role of the nurse. RN, July, 16-21.
Dellinger, R.P.; Levy, M.M.; Rhodes, A.; Annane, D.; Gerlach, H.; opal, S.M.;
Sevrasky, J.E.; Sprung, C.L.; Douglas, I.S.; Jaeschke, R.; Osborn, T.M.; Nunnally, M.E.;
Townsend, S.R.; Reinhart, K.; Kleinpell, R.M.; Angus, D.; Deutschman, C.S.;
Machado, F.R.; Rubenfeld, G.D.; Webb, S.A.; Beale, R.J.; Vincent, JL; Moreno, R.;
Surviving Sepsis Campaign Guidelines Committee including the Pediatric Subgroup.
(2012, January 20). Surviving sepsis campaign: International guidelines for
management of severe sepsis and septic shock: 2012. Society of Critical Care
Medicine's 42nd Congress, (41)2, 580-637. DOI: 10.1097/CCM.0b013e31827e83af
31. McCormick, M.J. Recognizing the signposts for sepsis. Nursing Made Incredibly
Easy!, (7)3, 40-51. doi: 10.1097/01.NME.0000350939.27283.30
Woodruff, D.W. Why you need to know about sepsis syndrome {Webinar notes}.
(2011, July 22). Retrieved from
http://www.ed4nurses.com/resources/1/pdf/Sepsis.pdf
Wood, S.; Lavieri, M.C.; Durkin, T. (2007). What you need to know about sepsis.
Nursing2007, 37(3), 46-51
Editor's Notes
Average cost of each case of sepsis approx. $22,000
Cytokine: TNF…..central mediator in the inflammatory response. Effects fever, increases insulin resistance, stimulates phagocytosis. Locally, TNF causes traditional signs of inflammation: heat, redness, swelling, pain. High concentrations produce shock-like symptoms. IL6….part of the acute response phase crosses blood/brain barrier and effects fever, as well. Also triggers marrow production of neutrophils.
Shunting occurs to preserve perfusion to vital organs-periphery feels cold to touch. Also shunts from the bowel, as digestion is considered a nonvital function. Blood is diverted to heart, lungs & brain. Activated Protein C suppresses inflammatory response-reduces clotting, improves fibrinolysis.
