Review of Sepsis Pre-Reading for Sepsis Pilot Project

1. Review of SepsisPre-Reading for Sepsis Pilot Project

2. You probably have SIRS… or Sepsis….

3. Systemic Inflammatory Response Syndrome • a.k.a. SIRS • Refers to an initial systemic response believed to precede the development of Sepsis and Septic Shock • Defined as the presence of 2 or moreof the following objective signs of systemic inflammation: • 1. Temperature (T) >38 C or <36 C • 2. Heart Rate (HR) >90/ min • 3. Respiratory Rate (RR) >20 breaths/ min • 4. White Blood Cells (WBC) >12,000 or <4,000 • 5. Change in LOC

4. SIRS Cont’d • Can arise from a variety of non-specific sources including but not limited to infection • Other potential sources of SIRS include burns, trauma and pancreatitis • Very important to identify the syndrome early, monitor patients closely for hypotension and evidence of hypoperfusion which can indicate progression from SIRS to Sepsis to Severe Sepsis and Septic Shock

5. Sepsis • Defined as SIRS in the presence of a presumed or confirmed infection thus treated with antibiotic therapy • More than 90% of sepsis is bacterial in origin • Frequent causes of sepsis are Pneumonias and UTI’s • Sites of infection include: 1. Respiratory 4. Lines 2. Genito-urinary 5. Wounds/ Surgical Wound 3. Gastro-intestinal 6. Vascular

6. Bacteremia • Presence of bacteria in the blood • Bacteria can enter the bloodstream through a primary site of infection such as from infected wounds, infected indwelling lines or catheters, pneumonias, during surgeries, etc. • Bacteria can also use the blood to spread to other parts of the body causing infections away from the original site of infection and examples include endocarditis, osteomyelitis, etc.

7. Severe Sepsis • Defined as the systemic inflammatory response (SIRS), plus infection (SEPSIS), plus the presence 1 or more organ dysfunctions. • Organ dysfunction can include acute lung injury, coagulation abnormalities, thrombocytopenia, altered mental status, renal, liver, or cardiac failure, • Hypoperfusion with lactic acidosis • Lactate level of greater than or equal to 4.0 mmol/L is commonly used to define severe sepsis

8. What does hypoperfusion look like?

9. Lactic Acidosis Lactic acid is the normal endpoint of the anaerobic breakdown of glucose in the tissues. The lactate exits the cells and is transported to the liver, where it is oxidized back to glucose. In the setting of decreased tissue oxygenation, lactic acid is produced as the anaerobic cycle is utilized for energy production. Lactic acidosis is a physiological condition characterized by low pH in body tissues and blood (acidosis) accompanied by the build up of lactate, and is considered a distinct form of metabolic acidosis. Lactic acidosis reflectsincreased anaerobic metabolism in the bodies of the cells due to poor circulatory perfusion and reduced oxygen delivery to tissues.

10. Hyperlactatemia is defined as a persistent, mild to moderate (2-4 mmol/L) increase in blood lactate concentration without metabolic acidosis, whereas lactic acidosisis characterized by persistently increased blood lactate levels (> 4 mmol/L) in association with metabolic acidosis. Normal lactate level: 0.5-2.2 mmol/L

11. Septic Shock • Patients in septic shock have marked hypotension (SBP<90mmHg), insufficient blood flow (hypoperfusion) or critical reduction in perfusion to one or more organs despite aggressive fluid resuscitation • May respond to fluids initially but subsequently develops refractory hypotension • Is present when cardiovascular dysfunction requires the support of inotropic agents or vasopressors (given during Code Blue or admission to a critical care areas)

12. SIRSSEPSISSEVERE SEPSISSEPTIC SHOCKSepsis can lead to multiple organ dysfunction syndrome (MODS) (formerly known as multiple organ failure), and death

13. Stages of Sepsis to Septic Shock: Body’s Responses • Initial: During this stage, the hyperinflammatory/ hypoperfused state may cause: • Decreased LOC/ Restlessness/ Agitation/ Anxiety/ Confusion or Delirium • Slight increase in Temperature/ Pyrexia • Elevated WBCs • Flushed skin • Rigors/ chills

14. 2. Compensatory: This stage is characterised by the body employing physiological mechanisms, including neural, hormonal and bio-chemical mechanisms in an attempt to reverse the condition and may cause: • Tachycardia • Sustained or slight increase in BP • Hyperventilation due to sympathetic nervous system stimulation • Prolonged cap refill, cool, clammy, and mottled skin • Electrolyte abnormalities • Oliguria, concentrated urine and rise in creatinine

15. 3. Progressive: Should the cause of the crisis not be successfully treated, this will proceed to the progressive stage and the compensatory mechanisms begin to fail due to the decreased perfusion to vital organs and may cause: • Fatigue and lethargy • Profound hypotension • Rapid, weak, thready pulse • Hypothermia • Coagulopathies • Ischemic bowel • Anuria

16. 4. Refractory: At this stage, the vital organs have failed and the shock can no longer be reversed • Brain damage and cell death occur • Death

17. What can we do?

18. Vision Reduce Sepsis morbidity and mortality rates by: • Identifying sepsis patients early • Applying the BC In patient Sepsis Guidelines • Achieving seamless transitions of care

19. Assessments • Assess Vital Signs including trends in blood pressure to monitor for hypotension and determine ongoing changes. • Assess neurological vital signs using Glasgow coma scale (GCS) to assess LOC changes • Do a thorough head-to-toe assessment as sepsis involves and affects all organs of the body. • Monitor respiratory status and apply oxygen therapy tosupport and optimize oxygenation. Page and notify RT if oxygen needs are increasing and patient is decompensating.

20. Screening • Utilize the Adult In-patient Sepsis Screening Toolso that you can identify the condition early and act quickly.

21. Identification of Sepsis

22. If the patient has SEPSIS: • CALL THE PHYSICIAN • Report Assessment Findings and • Discuss initiating the In-patient Ward Early Sepsis Investigation and Treatment

23. Taking Action

24. In-patient Ward Early Sepsis Investigation and Treatment DIET:□ NPO LABORATORY: All investigations are STAT Lactate (Venous Plasma). Notify physician immediately if lactate greater than 2 mmol/L □ Repeat lactate 2 hours after the first lactate is drawn. Notify physician of results CBC and differential, INR, PTT, electrolytes, BUN, creatinine, glucose, liver function tests, lipase, troponin Blood cultures X 2 sets BEFORE antibiotics (include culture from central line, if present) □ Urinalysis and urine C&S (as per VCH guidelines) □ Sputum for C&S Other ____________________

25. DIAGNOSTIC: All investigations are STAT □ 12 lead ECG □ Chest X-ray Other_____________________ INTRAVENOUS: Initial intravenous infusion and hydration orders: Ensure at least #20 gauge IV access is in place. May insert a second IV access as necessary. □ Start IV bolus: □ Sodium chloride 0.9% (NS) _______________ mL (max 2 L) □ Ringer’s Lactate at _______________ mL (max 2 L) □Plasmalyte _______________mL (max 2 L) Give IV fluid over __________ minutes (physician to assess post-bolus)

26. MEDICATIONS: □ Physician to initiate appropriate antibiotic therapy ________________________________________________________________________________ ________________________________________________________________________________ MONITORING: • Vital Signs and oxygen saturation Q1H X 6H • Glasgow Coma Score (GCS) Q1H X 6 H • Monitor urine output if able– May insert a foley catheter as necessary. TREATMENTS: ________________________________________________________________________________

27. ** Confirm Early Sepsis Investigation and Treatment is congruent with patient’s goals of care ** URGENT CONSIDERATIONS • If patient develops hypotension (SBP less than 90 mmHg) despite initial fluid bolus, or lactate greater than 4 mmol/L, notify physician that SEVERE SEPSIS/SEPTIC SHOCK is present and call Critical Care Outreach Team (CCOT). Physician to consider ICU consultation • If drainable focus of infection identified, organize early source control/drainage • Physician to determine further management and disposition

28. NURSING GUIDELINES: • Ensure IV fluid start and stop times and IV fluid bolus amounts are documented in the 24 Hour Fluid Flowsheet. • Monitor vital signs with oxygen saturation and perform respiratory assessment and documentation prior to and after completion of each fluid bolus to determine ongoing changes. • Contact MD for deterioration in vital signs or clinical status using SBAR. • Ensure thorough documentation and accurate nursing handover with shift changes.

29. THANK YOU!