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

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Presentation on theme: "Mariana Bridi Costa, Brazilian model Pope John-Paul II Etta James, singer All of them died secondary to sepsis."— Presentation transcript:

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

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

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

5  Primary Care Providers  Hospitalists  Medical Students  Residents  Hospital Administrators  Specialists

6  No pertinent financial disclosures

7  A brief review of the last 12 years…

8  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

9  12 years ago Dr. Emanuel Rivers published in the NEJM an article that would change our approach to sepsis

10  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

11 1. We have to be willing to evolve with the evidence based medicine and be able to look at it critically 2. We have to be open to the idea of aggressive management 3. We have to put away our old notions of the “look” of sepsis

12 1. We have to be willing to evolve with the evidence based medicine and be able to look at it critically 2. We have to be open to the idea of aggressive management 3. We have to put away our old notions of the “look” of sepsis

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14  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

15  To understand the definition we have to understand the process

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

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

18 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

19 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?

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21 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…

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25  Used to visualize sublingual microcirculation

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

27 Rev. bras. ter. intensiva vol.23 no.3 São Paulo July/Sept. 2011 Septic Shock

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

29 This is why peripheral hypoxia (i.e. SvO2) can continue despite normal vitals, CVP etc.

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31  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

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33 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

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

35 2 SIRS CRITERIA An infection or suspected infection +

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

37 Sepsis Syndrome Hypotension (Systolic BP <90) Lactate >4 End Organ Damage +

38 Sepsis Syndrome Hypotension (Systolic BP <90) Lactate >4 End Organ Damage +

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

40 Persistent Hypotension (Systolic BP <90) Lactate >4 End Organ Damage Refractory to IVF Challenge +

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

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43 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

44 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

45 He is evaluated by a moonlighting resident Vital Signs BP: 109/89 HR: 101 Temp: 102.1 RR: 16 SpO2 98%

46 Physical exam of the right lung base reveals rhonchi but is otherwise unremarkable Chest X-ray demonstrates:

47 His lab work at the urgent care is: Na140 (135-148 mEq/L) K4.0(3.5-5.3 mEq/L) Cl107(95-108 mEq/L) CO211(25-35 mEq/L) BUN27(6-19 mEq/L) Cr2.1(0.7-1.5 mg/dL) Glucose152(70-105 mg/dL)

48 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

49 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

50 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

51 Within 2 hours: 3 liters of normal saline 1 liter in the ambulance 2 liters (500 cc every 30 mins) Vital Signs BP: 105/72 HR: 101 Temp: 99.9 RR: 16 (on vent) SpO2 97% FIO2 of 80%

52 He is stabilized in the ED and transferred to the ICU for further care Throughout his 6 day stay in the hospital, Jimmy suffers from acute renal failure, persistent hypoxemia, and an NSTEMI He is discharged home with home health services and eventually makes a full recovery

53 Question: When was Jimmy Septic?

54  Remembering our steps…

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

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60 Question: When was Jimmy septic? Answer: At urgent care.

61 Barcelona, Spain

62 6 Hour Bundle Measure serum lactate Blood Cultures prior to antibiotics Broad spectrum antibiotics within 3 hours of presentation, 1 hour in hospital Initial fluid resuscitation with 20-40 mL/kg crystalloid (or equivalent colloid) if hypotensive (SBP 4 mmol/L Vasopressors If septic shock or lactate > 4 mmol/L: CVP and ScvO 2 or SvO 2 measured CVP maintained 8-12 mm Hg Inotropes (and/or PRBCs if Hct 8 mmHg 24 Hour Bundle Glucose control maintained < 150 mg/dL Steroids given for septic shock requiring continued use of vasopressors for > 6 hours Lung protective strategy with plateau pressures < 30 cm H 2 O for mechanically ventilated patients http://www.ihi.org

63  But what does that mean for us practically when we see a patient presumed to be sick from an infection?

64 VITAL SIGNS THROUGH THE LENS OF SIRS CRITERIA

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66  Sepsis with end organ damage, hypotension or lactate > 4  Central Line  Arterial Line  Early Intubation  Labs (ACC CLUE)  ABG  CMP/CBC/Coags  CXR/Cardiac Enzymes  Cultures (B/U/S)  Lactate  UA  EKG

67  Remembering that… Are all physical exam signs of end organ damage

68 6 Hour Bundle Measure serum lactate Blood Cultures prior to antibiotics Broad spectrum antibiotics within 3 hours of presentation, 1 hour in hospital Initial fluid resuscitation with 20-40 mL/kg crystalloid (or equivalent colloid) if hypotensive (SBP 4 mmol/L Vasopressors If septic shock or lactate > 4 mmol/L: CVP and ScvO 2 or SvO 2 measured CVP maintained 8-12 mm Hg Inotropes (and/or PRBCs if Hct 8 mmHg 24 Hour Bundle Glucose control maintained < 150 mg/dL Steroids given for septic shock requiring continued use of vasopressors for > 6 hours Lung protective strategy with plateau pressures < 30 cm H 2 O for mechanically ventilated patients http://www.ihi.org

69  Broad spectrum antibiotics covering the organisms that affect the infected area

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71  But how much do you give?

72  Here is where the central venous catheter comes into play

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75 Recommendation is 500 cc bolus of normal saline every 30 mins until you reach a CVP of 8-12

76 Vasopressors

77 Norepinephrine vs Dopamine Neither has shown replicable superiority Either may be first line agent of choice

78 When to use?

79 Then check SVO2 And if < 70% transfuse to a HCT 30% And if still <70% add dobutamine to increase cardiac output

80  Steroids intially showed a 10% decrease in mortality

81 CORTICUS had patients whose mortality was 30-40% vs the JAMA article which had mortality 56% In addition, a subset analysis showed that patient with a similar severity level to the original trial in JAMA had a similar 10% outcome benefit.

82 Conclusion: If a patient is adequately volume resuscitated and isn’t on pressors, they don’t need steroids Steroids should be withheld for 6-8 hours until you can gauge adequately whether the patient is volume replete or not

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84 What do these all have in common?

85 CHEST September 2010 vol. 138 no. 3 476-480

86  In a recent multicenter preimplementation (n = 1,554) and postimplementation (n = 4,801) study, hospital length of stay was reduced by 5.02 days, and hospital charges were $47,923 less between groups ( P <.0001).  A hospital seeing 250 patients per year can realize a cost savings of > $11.98 million per year and an average decrease in hospital length of stay of 5 days or 1,250 bed days saved per year by implementing EGDT. CHEST September 2010 vol. 138 no. 3 476-480

87  Should we adhere to EGDT, and does it matter? Yes. The real question is why we are continuing to accept the old paradigm because by doing so, we not only are depriving our patients of the best and most cost-efficient care but also are accepting death as an alternative. CHEST September 2010 vol. 138 no. 3 476-480

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