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Sepsis & Shock

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on 26 November 2014

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Transcript of Sepsis & Shock

Stats Continued
After cardiac disease, sepsis is the second leading cause of death among ICU patients

Patients hospitalized for sepsis had an average length of stay 75% longer than for other conditions

Patients hospitalized for sepsis were more than eight times as likely to die during hospitalization

In 2008, an estimated 14.6 billion was spent on hospitalizations for sepsis
(Hall, Williams, DeFrances, & Golosinskiy, 2011)
(Colon-Franco, 2012)
Why the Rise in Sepsis Rates?
Growing elderly population

Increased use of invasive surgery

Increased incidence of bacterial resistance (widespread use of antibiotics creating “superbugs”)

Increased number of immuno-compromised patients

(Nimmo, 2006)
Diagnostics and labs
Conclusion
“Individual registered nurses bear primary responsibility for the nursing care that their patients receive and are individually accountable for their own practice”
(ANA Code of Ethics for Nurses)


Carefully observe for subtle changes in the patient status

Trust your intuition

Act quickly!

Don't rely on machines

Educate yourself and others
Sepsis & Shock
Sepsis and septic shock is a complex systemic response that is initiated when a microorganism enters the body and stimulates the inflammatory/immune system


Sepsis can arise from various infections, including the skin, lungs, abdomen, and urinary tract
What is Sepsis and Septic Shock?
(Urden, Stacy, & Lough, 2013, p. 902)
Sepsis Statistics
The number and rate per 10,000 population of hospitalizations for sepsis more than doubled from 2000-2008


(Hall, Williams, DeFrances, & Golosinskiy, 2011)
Pathophysiology
Shock
Imbalance between oxygen supply and demand
4 types:
Hypovolemic
Cardiogenic
Neurogenic
Distributive/Vasodilatory (Anaphylactic & Septic Shock)
Sepsis: Infectious process that facilitated SIRS
Severe Sepsis: Sepsis + 1 or more organ dysfunction
Septic Shock: Severe sepsis + cardiovascular dysfunction NOT responsive to fluids
(Baird & Bethel, 2011 P. 294-926)
Four Main Factors
Hyperinflammation
Hypercoagulation
Microvascular obstruction
Increased endothelial permeability
Management of Sepsis
HAND WASHING, ASEPTIC TECHNIQUE

Identification of patients at risk and reduction of their exposure to invading microorganisms.

Early identification = early treatment and decreases mortality.

Monitor and treat complications.

Our Role as Nurses
Finding and eradicating the cause of infection
Pan culture
Antibiotic therapy should be started within 1 hour of recognition
Each hour of delay is associated with a substantial drop in the survival rate.

A key measure in treatment:

TO BE COMPLETED WITHIN 6 HOURS:

5) Apply vasopressors (for hypotension that does not respond to initial fluid resuscitation) to maintain a mean arterial pressure (MAP) ≥65 mm Hg

6) In the event of persistent arterial hypotension despite volume resuscitation (septic shock) or initial lactate ≥4 mmol/L (36 mg/dL):      
1.Measure central venous pressure (CVP)* 2.Measure central venous oxygen saturation(ScvO2)*

7) Remeasure lactate if initial lactate was elevated*
***CVP of ≥8 mm Hg; ScvO2 of ≥70%, and normalization of lactate.

Continued...
TO BE COMPLETED WITHIN 3 HOURS:

1) Measure lactate level
2) Pan cultures prior to administration of antibiotics
3) Administer broad spectrum antibiotics
4) Administer 30 ml/kg crystalloid for hypotension or lactate ≥4mmol/L

Surviving Sepsis Campaign Bundle

It is a medical emergency

Early treatment reduces mortality.

Goal: reverse pathophysiologic responses, control the source of infection, maintain circulatory stability.

Management & Treatment of Sepsis/Septic Shock
http://www.survivingsepsis.org/Bundles/Pages/default.aspx
*Hallmark of severe sepsis:
Endothelial damage
Coagulation Dysfunction
Refactory Stage
Progressive Stage
Compensatory Stage
Stages of Shock
1. Initial
2. Compensatory
3. Progressive
4. Refactory
1. Initial Stage:
- Decreased cardiac output (CO)
- Threatened tissue perfusion
Body attempts to maintain CO, BP, and tissue perfusion through the SNS.

Neural
Increased HR & contractility
Arterial and venous vasoconstriction
Shunting of blood to the vital organs.

Hormonal
Renin response
Anterior pituitary & adrenal medulla.

Chemical: Inflammatory response
Unmet metabolic needs

Ineffective tissue perfusion

Aerobic --> anaerobic metabolism

Endo- & epithelial hypoxia --> vasodilation & increased permeability
Invasion of microorganism causes tissue injury & release of intracellular proteins
Tissue factor (TF) & monocytes
Nitric oxide

Result:
Intravascular hypovolemia
Tissue edema
Tissue hypoxia
Systemic Inflammatory Response (SIRS)
Irreversible damage
Uncontrolled inflammation
Inflammatory response:
Protection
Vasodilation
Hypovolemia
Maldistriubtion
Microvascular shunting
Signs of SIRS
Temp: > 38 degrees or < 36 degrees
HR: > 90
Resp > 20 or PaCO2 < 32 mmHg
WBC > 12,000 or < 4,000
> 10 % bands (immature form)

Patient with sepsis presents with 2 or more SIRS criteria
Myocardial Depression
Adequate fluid resuscitation -->
Hyperdynamic state: increased CO & decreased SVR

Decreased EF
Ventricular dilation
Failing compensation after fluid resuscitation

Caused by microorganisms
Cerebral hypoperfusion
Cardiac depression, resp depression, thermoregulatory failure
Pulmonary dysfunction:
- increased permeability
- micro-emboli
- vasoconstricion
Acute respiratory distress syndrome (ARDS)
Renal dsyfunction

GI dysfunction
Severe Sepsis
Sepsis associated with:
1. organ dysfunction
2. hypoperfusuion
or 3. hypotension

A/M/B: Lactic acidosis, oliguria, acute altered mental status
Disseminated Intravascular Coagulation (DIC)
Diffused damage impairing anticlotting mechnisms
Consumes coagulation factors
Bleeding
Hemorrhage
Septic shock:
Hypotension - despite adequate fluid resuscitation
Perfusion abnormalities - lactic acidosis, oliguria, ALOC
Unresponsive to therapy = Irreversible
MODS = failure of 2 or more organs
Death
R/T ineffective tissue perfusion
(Baird & Bethel, 2011; Bridges & Dukes, 2005; Urden et al, 2014)
(Baird & Bethel, 2011)
(Urden et al, 2014, p. 903-905; Bridges & Dukes, 2005)
(Baird & Bethel, 2011 P. 294-926)
Imbalance of O2 supply & demand =
Cell hypoxia, damage, hibernation, & death

Epinephrine & norepinephrine
Hypermetabolic state
Vasoconstriction

Metabolic derangement = inability of cells to use O2 even if blood flow is adequate

Apoptosis & suicide
Etiology & Statistics
(Urden et al, 2014)
Education
Life after sepsis:
- Exhaustion and pain
- Post-sepsis syndome

http://www.sepsisalliance.org/

Listen!
Don’t ignore the patient or family

Protocols and education materials
http://www.survivingsepsis.org/Resources/Pages/Media.aspx


Beware:
Pulse ox:
NOT
a good indicator - measures ARTERIAL hemoglobin saturation
The septic patient has
VENOUS hypoxia

Hypotension =
LATE SIGN


Other signs:
Slurred speech
Extreme muscle pain
Inability to pass urine
Severe breathlessness
Mottled or discolored skin
Feeling of impending doom



Infection control:
Hand washing
Cover cough & sneeze
Take antibiotics as prescribed
Life sustaining measures
End-of-life care
Patient & Family Education
Sepsis six mnemonic:

Give 3, take 2, monitor 1
Give 3: Oxygen, IV fluids, antibiotics
Take 2: blood cultures & hemoglobin/lactate
Monitor 1: urine output

Infection control – hand washing
Assess and monitor
Documentation – time
Communication with patient and family
Explain procedures and interventions
End-of-life care
Life sustaining measures
Care for Septic Patient
Early detection!
Temperature: > 38 C (100.4) or < 36 C (98.6)
Heart rate: >90
Respirations: tachypnea (>20) within 12-24 hours
PaCO2 < 32

Initial stage: may have early signs & symptoms or asymptomatic from compensation




Education for Nurses
Goal:
Infection prevention

Early detection

Astute Assessments.
Educational Needs
(Urden et al, 2014; McCormick, 2009)
(Ernst, 2012; Emergency Nursing, 2013).
(McCormic, 2009)
(McCormick, 2009)
References
American Nurses Association. (2001). Code of ethics for nurses with interpretive statements. Silver Springs, MD: Nursesbooks.org.

Balentine, J.R. (2013). Sepsis (blood infection). eMedicneHealth. Retrieved November 29, 2013, from
http://www.emedicinehealth.com/sepsis_blood_infection/article_em.htm#sepsis_overview

Colón-Franco, J.M. (2012). Identification of models to predict early sepsis in medical ICU (MICU) patients. Vanderbilt University
Medical Center. Retrieved from http://www.aacc.org/members/loc_sections/southeast/LSSEMtgAnnouncements/Documents/ColonFranco_SE%20conference.pdf

The Commercial Appeal (2012). Healthy memphis: Sepsis is on the rise as a life-threatening condition. The Commercial Appeal.
Retrieved from http://www.commercialappeal.com/news/2012/jan/09/sepsis-is-on-the-rise-as-a-life-threatening/?print=1


Deaths from severe sepsis due to care failures, report claims. (2013). Emergency Nurse, 21(6),
8-9. doi:10.7748/en2013.10.21.6.8.s9

Ernst, Y. (2012). “Sepsis – an often missed diagnosis.” The Bolus. Retrieved from
http://thebolus.org/sepsis-an-often-missed-diagnosis/


Hall, M.J., Williams, S.N., DeFrances, C.J., Golosinskiy, A. (2011). Inpatient care for septicemia or sepsis: A challenge for patients and
hospitals. Center for Disease Control and Prevention NCHS Data Brief No. 62, 1-8.

Kalil, A., & Bailey, K.L. (2013). Septic Shock. Medscape. Retrieved November 26, 2013
from http://emedicine.medscape.com/article/168402-overview

McCormic, M. (2009). Recognizing the signposts for sepsis. Nursing made incredibly easy, 40-53.
References


Odell, M. (2002). Sepsis: Early detection and care. Nursing Times.net. Retrieved fromhttp://www.nursingtimes.net/sepsis-early-detection-and-care/199645.article

Nimmo, G.R. (2006). Identifying sepsis early. Identifying Sepsis Early Group 1-18. Retrieved fromhttp://www.scottishintensivecare.org.uk/education/ise.pdf


Society of Critical Care Medicine. (2013). Bundles. Surviving Sepsis Campaign. Retrieved November 28,
2013, from http://www.survivingsepsis.org/Bundles/Pages/default.aspx

Urden, L.D., Stacy, K.M., & Lough, M.E. (2010). Critical care nursing: diagnosis and management (6th ed). St. Louis, Mo.: Mosby/Elsevier.

PAN CULTURE
White blood cell count: Leukocytosis or leukopenia (Endotoxemia may cause early leukopenia)

Platelet count: Thrombocytosis or thrombocytopenia (High value early may be seen as acute-phase response; low platelet counts seen in overt DIC)

Coagulation cascade Protein C deficiency; antithrombin deficiency; elevated D-dimer level; prolonged PT and PTT Abnormalities can be observed before onset of organ failure and without frank bleeding.

Creatinine level: Elevated from baseline Doubling-indicates acute renal injury

Lactic acid level: Lactic acid > 4 mmol/L (36 mg/dL) Indicates tissue hypoxia

Liver enzyme levels: Elevated alkaline phosphatase, AST, ALT, bilirubin levels Indicates acute hepatocellular injury caused by hypoperfusion

Serum phosphate level: Hypophosphatemia Inversely correlated with proinflammatory cytokine levels

C-reactive protein (CRP) level: Elevated Acute-phase response

Procalcitonin level: Elevated Differentiates infectious SIRS from noninfectious SIRS
FLUID RESUSCITATION/VASOPRESSORS/CORTICOSTEROIDS
Antibiotics
Surgical Management
Administer 1st dose of broad spectrum antibiotic within one hour
Community acquired infection: Ceftriaxone, Gentamycin, moxifloxacin
Hospital acquired organism or pseudomonas or MRSA: Cefepime, Piperacillin, Ciprofloxacin,ADD Vancomycin if MRSA is likely , if exposed to prior antibiotics use Meropenem
Initiate .9% NS or RL 500ml bolus q 15 min to increase MAP >65mmhg within the first hour
Norepinephrine and Dopamine are the first line of vasopressors to administer
Epinephine and Vasopressors are the second line of vasopressors to administer
Also fluid expanders are sometimes given, such as Albumin for plasma volume expansion and maintence of cardiac output.
Corticosteroids (anti-immflamatory agents) are given to maintain vascular tone in severe septic shock. Ex: Hydrocortisone,Dexamethasone
Certain conditions will not respond to standard treatment for septic shock until the source of infection is surgically removed. Some of these common foci of infection include intra-abdominal sepsis (perforation or abscess), empyema, mediastinitis, cholangitis, pancreatic abscess, pyelonephritis or renal abscess from ureteric obstruction, infective endocarditis, septic arthritis, infected prosthetic devices, and necrotizing fasciitis.
Whenever possible, percutaneous drainage of abscesses and other well-localized fluid collections is preferred to surgical drainage
MECHANICAL VENTILATION/ARDS

The goals of mechanical ventilation include the following:
Improving gas exchange
Reducing work of breathing
Avoiding oxygen toxicity
Minimizing high airway pressures
Avoiding further lung damage
Allowing the injured lung to heal
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