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Mariana Bridi Costa, Brazilian model

All of them died secondary to sepsis. Pope John-Paul II. Mariana Bridi Costa, Brazilian model. Etta James, singer. Practical Sepsis. Curtis J. Merritt D.O. Chief Internal Medicine Resident Danville Regional Medical Center Danville Virginia. “.

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Mariana Bridi Costa, Brazilian model

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  1. All of them died secondary to sepsis Pope John-Paul II Mariana Bridi Costa, Brazilian model Etta James, singer

  2. Practical Sepsis Curtis J. Merritt D.O. Chief Internal Medicine Resident Danville Regional Medical Center Danville Virginia

  3. With that in mind the single goal of this presentation is to demonstrate a stepwise approach to make sepsis practical

  4. Target Audience • Primary Care Providers • Hospitalists • Medical Students • Residents • Hospital Administrators • Specialists

  5. Disclosures • No pertinent financial disclosures

  6. SEPSIS • A brief review of the last 12 years…

  7. By The Numbers • Annual cost = $16.7 billion in the US in 2000 • 1,400 people die each day from sepsis • Roughly 2 million cases per year • 30% dying within one month of diagnosis • 80% of patients who die from major injuries are actually killed by sepsis Survivingsepsis.org

  8. 12 years ago Dr. Emanuel Rivers published in the NEJM an article that would change our approach to sepsis

  9. In that study, Dr. Rivers and colleagues proved that early recognition and aggressive treatment of severe sepsis and septic shock resulted in a 16% reduction in absolute mortality. • That translates to NNT = 6 - 8 N Engl J Med 2001; 345:1368-1377: November 8, 2001

  10. If you fancy a journey… • We have to be willing to evolve with the evidence based medicine and be able to look at it critically • We have to be open to the idea of aggressive management • We have to put away our old notions of the “look” of sepsis

  11. If you fancy a journey… • We have to be willing to evolve with the evidence based medicine and be able to look at it critically • We have to be open to the idea of aggressive management • We have to put away our old notions of the “look” of sepsis

  12. There’s the rub…

  13. The Rub • Many physicians do not use the current definition of sepsis despite attempts to standardize terminology and diagnostic criteria. Indeed, only 17% of clinicians agree on a definition of sepsis (12), and this disparity results in missed diagnosis and delayed treatment. The challenges include: • Lack of awareness of frequency and mortality rate of sepsis • No universally accepted definition of sepsis • No single or combination of tests or markers for a reliable diagnosis of sepsis • Need for earlier diagnosis and treatment of septic patients • Lack of adequate healthcare professional training in the diagnosis and treatment of sepsis *http://www.survivingsepsis.org/Background/Pages/barcelona_declaration.aspx

  14. Sepsis model • To understand the definition we have to understand the process

  15. The River… What do you notice about the river? -fast -churning -high rate of aeration -large volume in a confined space -faces of horror

  16. This river is very similar to normal physiology -fast turn over -adequate O2 -adequate volume

  17. Now picture that same volume in that river after the rock walls have been removed and the width of the channel is much larger Much like a stagnant swamp

  18. Now that same volume is moving through a much larger area So… What happens to flow? What happens to O2 content? What happens to the fish?

  19. In sepsis, toxins and cytokines produce a profound vasodialation and the venous side of the circulator system experiences a low-flow, low O2 state But that’s not the whole story…

  20. Orthogonal polarization spectral imaging • Used to visualize sublingual microcirculation

  21. Orthogonal polarization spectral imaging Normal No embolisms Flow speed is adequate that individual RBCs can’t be seen Normal vessel caliber Rev. bras. ter. intensiva vol.23 no.3 São Paulo July/Sept. 2011

  22. Orthogonal polarization spectral imaging Septic Shock Rev. bras. ter. intensiva vol.23 no.3 São Paulo July/Sept. 2011

  23. Microthrombi • Stagnant flow • Small caliber Rev. bras. ter. intensiva vol.23 no.3 São Paulo July/Sept. 2011

  24. This is why peripheral hypoxia (i.e. SvO2) can continue despite normal vitals, CVP etc. Rev. bras. ter. intensiva vol.23 no.3 São Paulo July/Sept. 2011

  25. How to define something seemingly amorphous

  26. First things first • We have to put our old definitions of sepsis away • We have to realize that sepsis is often difficult to diagnose without a stepwise approach

  27. SEPSIS STEPS

  28. SIRS Systemic Inflammatory Response Syndrome (SIRS) with 2 of the following: • Temp: >38 C (100.4 F) <36 C (96.8 F) • Heart Rate: >90 beats/min • Resp Rate: >20 breaths/min • PCO2: <32 mmHg • WBC: >12,000 <4,000 >10% Bands N Engl J Med 2001; 345:1368-1377 November 8, 2001

  29. SEPSIS STEPS SIRS T: >100.4 F < 96.8 F RR: >20 HR: >90 WBC: >12,000 <4,000 >10% bands PCO2 < 32 mmHg

  30. Sepsis Syndrome An infection or suspected infection + 2 SIRS CRITERIA

  31. SEPSIS STEPS SEPSIS SIRS 2 SIRS + Confirmed or suspected infection T: >100.4 F < 96.8 F RR: >20 HR: >90 WBC: >12,000 <4,000 >10% bands PCO2 < 32 mmHg

  32. SEVERE SEPSIS Hypotension (Systolic BP <90) Lactate >4 End Organ Damage Sepsis Syndrome +

  33. SEVERE SEPSIS Hypotension (Systolic BP <90) Lactate >4 End Organ Damage Sepsis Syndrome +

  34. SEPSIS STEPS SEVERESEPSIS SEPSIS Sepsis + Signs of End Organ Damage Hypotension (SBP <90) Lactate >4 mmol SIRS 2 SIRS + Confirmed or suspected infection T: >100.4 F < 96.8 F RR: >20 HR: >90 WBC: >12,000 <4,000 >10% bands PCO2 < 32 mmHg

  35. Septic Shock Persistent Hypotension (Systolic BP <90) Lactate >4 End Organ Damage Refractory to IVF Challenge Severe Sepsis +

  36. SEPSIS STEPS SEPTICSHOCK SEVERESEPSIS Severe Sepsis with persistent: Hypotension Signs of End Organ Damage Lactate >4 mmol SEPSIS Sepsis + Signs of End Organ Damage Hypotension (SBP <90) Lactate >4 mmol SIRS 2 SIRS + Confirmed or suspected infection T: >100.4 F < 96.8 F RR: >20 HR: >90 WBC: >12,000 <4,000 >10% bands PCO2 < 32 mmHg

  37. Case 1: Jimmy

  38. Case 1: “Jimmy” Jimmy is a 45 year old gentleman who presents to the local urgent care with a complaint of cough It began 4 days ago, steadily has worsened, producing thick green/yellow sputum He complains of subjective fevers and chills and a general feeling of un-wellness

  39. Case 1: “Jimmy” PMHx Jimmy is a smoker of 10 years ½ ppd Denies alcohol or drug use No past medical history No surgeries He takes no medications

  40. Case 1: “Jimmy” He is evaluated by a moonlighting resident Vital Signs BP: 109/89 HR: 101 Temp: 102.1 RR: 16 SpO2 98%

  41. Case 1: “Jimmy” Physical exam of the right lung base reveals rhonchi but is otherwise unremarkable Chest X-ray demonstrates:

  42. Case 1: “Jimmy” His lab work at the urgent care is: Na 140 (135-148 mEq/L) K 4.0 (3.5-5.3 mEq/L) Cl 107 (95-108 mEq/L) CO2 11 (25-35 mEq/L) BUN 27 (6-19 mEq/L) Cr 2.1 (0.7-1.5 mg/dL) Glucose 152 (70-105 mg/dL)

  43. Case 1: “Jimmy” He is sent home with a diagnosis of: Right Lower Lobe Pneumonia Dehydration Cough He is prescribed moxifloxacin 400 mg daily x 7 days and told to drink plenty of fluids

  44. Case 1: “Jimmy” He arrives at the hospital 8 hours later unresponsive Vital Signs BP: 80/61 HR: 115 Temp: 102.0 RR: 30 SpO2 81% on 15L NRB

  45. Case 1: “Jimmy” Within 30 mins of arriving: He has been intubated He has a central line He has an arterial line He has been cultured (U/B/S) and labs drawn He has started to receive: 3.375 gm of pipercillian/tazobactam 1.25 gm of vancomycin

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