1. Faheem Guirgis MD, FACEP
Assistant Professor of Emergency Medicine
Division of Research
Department of Emergency Medicine
UF Health Jacksonville
8 Tips for Treating Sepsis
3. Objectives
Learn rapid stepwise assessment of possible
sepsis patients
Learn how to evaluate patients for organ
dysfunction
Review evidence-based early sepsis management
Discuss common pitfalls and how to avoid them
Review and discuss recent literature and
implications for sepsis management
5. Stepwise Assessment for sepsis
in patients with infection
Assess and Address:
1. Critical instability
2. Clinical signs of organ dysfunction (qSOFA)
3. Subtle signs of organ dysfunction
12. Case 1
A 60-year-old man w/ PMH prostate CA (in remission)
presents with burning with urination and fever for the 3
days.
HR 110, BP 130/90, RR 20, SpO2 98%,Temp 102 F.
Exam – Mild suprapubic tenderness, B CVA tenderness
WBC 18k with 5% bands, Cr 1.5, Platelets 130k, UA 80
WBCs, + Nit/LE; Lactate 1.2
AfterTylenol and Fluids, the patient wants to leave…
13. Case 2
A 70 yof with PMH DM, HTN, CVA arrives via EMS from a local
NH for fever and right leg pain.
NH Staff say she’s “not acting right”
EMSVitals: BP 85/50, HR 105, RR 20, 99.5 F, O2 96%, glucose
270 mg/dL.
Exam – AOx1; tender, warm and erythematous right leg;
Crepitus to foot
What next?
17. Empiric Fluids
Currently CMS requires 30 ml/kg fluids to be
given to patients with septic shock in the first
3 hours
CMS definition of shock =
Lactate > 4
Hypotension not responsive to fluids
18. 11k patients, multi-center study
Improved outcomes for early fluids
compared to delayed fluids (> 120
min)
Mortality OR increased 1.09 per hr
19. 49k patients, multicenter study
Higher risk-adjusted mortality
> 3 hr to bundle completion (1.04 per
hour)
longer time to antibiotics (1.04 per hour)
Longer time to fluids was not associated
with increased risk of mortality (1.01)
28. Use a full loading dose of
early, broad-spectrum
antibiotics
29. Antibiotics
Antibiotics in the 1st hour (all sepsis)
Studies
49k - 1.04 per hour mortality (Seymour, et al)
35k - increased odds of death (1.09) (Liu et al)
Kumar study – 8% mortality increase/hr
Post-shock = OR 2.4 mortality (Puskarich et al)
31. “Sepsis is a compulsive search
for a source of infection”
1. Treat the patient like a trauma – fully expose
2. The less the patient can tell you the more
compulsive the search
32. Source Severity should be
proportional to severity of
illness
Don’t blame the UA!
Source control ASAP
Remove infected lines
IR/Surgery
33. 5. Know your vasoactive meds
2016 Guidelines
Norepinephrine 1st agent
Vaso or Epi as 2nd agent
Dopamine – increased risk of
mortality in septic shock and
cardiogenic shock
34. Adult patients on norepinephrine of 0.2
mcg/kg/min
Improved MAP ≥ 75 mm Hg (p< 0.001)
Improved CV SOFA at 48 hours (p = 0.01)
No difference in mortality
FDA warning – increased thrombosis?
35.
36. Shock, mechanical ventilation, + pressors ≥ 4 hrs
3800 patients (HC 200 mg/day vs placebo)
No 90 day mortality difference (27.9% HC,
28.8%P)
HC patients, shorter time to:
Shock resolution (3 vs. 4 days, p < 0.001)
ICU discharge (10 vs. 12 days, p < 0.001)
Cessation of initial mechanical ventilation (6 vs. 7 days)
40. Failure to normalize lactate
Repeat Lactate ≥ 5 has 90% specificity for early death
41. Lactate Limitations
Lactate can come from many different sources
Anaerobic metabolism
Reduced clearance (liver/kidney)
B1 adrenergic stimulation (Na+/K+ ATPase)
Altered mitochondrial function or “cytopathic
hypoxia”
Lactate can be normal in septic shock
42. 26% of High shock index patients became
hypotensive post induction
Low shock index patients became
hypertensive
8. Optimize Hemodynamics prior
to Intubation
43. Fluid load
Push-dose vasopressors or norepinephrine drip
initiated prior to intubation
Half dose induction meds for RSI, Max dose
paralytics
Intubation for Shock
45. Case 1 - Stepwise Assessment
60 yom with Fever, Back pain, + UA
1. Critical Instability? No
2. Bedside assessment?
qSOFA negative
3. Subtle organ dysfunction?
Yes
Cr of 1.5 mg/dL
Platelet count of 130 x 103/mm3
46. Case 1 – 60 yom w/ UTI
SOFA of 2
Treated with sepsis bundle
After his vital signs remained stable, the
patient was admitted to a monitored hospital
bed and was discharged to continue oral
antibiotics 2 days later.
47. Case 2 – Stepwise Assessment
70 yof with AMS and leg pain
1. Critical Instability?
Yes - Address hypotension with Fluid bolus
2. Bedside assessment?
qSOFA positive (hypotension + AMS)
48. Management
Resus bay – Sepsis bundle, large bore IVs, 30
ml/kg fluid bolus
Required norepinephrine (initiated at 10
mcg/min) to maintain a MAP > 65 mm Hg
XRAY?
49. OR then SICU – discharged back to NH after 10
day hospital admission
50. The End!
Thank you!
Email with questions:
Faheem.Guirgis@jax.ufl.edu
Editor's Notes
Discuss this idea?
Sick/Not sick
What makes sepsis so difficult to diagnose?
lack of a gold standard diagnostic test
Progression of symptoms and change in clinical condition (slow vs rapid)
Indolent organ dysfunction difficult to recognize
This will work in every possible case if you adhere to it.
Clinical signs = bedside
Immediately observable signs of organ dysfunction
Are there signs that this patient is having an abnormal, systemic response to infection, ie organ dysfunction.
Dangerous as a screening tool - Rule in for high risk sepsis
38% sensitive, 85% specific for death
Use it – but understand the limitations
Positive = move to resus bay, jump on this patient
Neg = further evaluate organ dysfunction
This patient is QSOFA negative – what does that mean?
Jama EVEN RECENTLY published a paper by Raith et all that showed an AUROC Of 0.60 for qSOFA, 0.589 for SIRS, and 0.75 for SOFA – they are essentially admitting that qSOFA is insensitive
Dangerous as a screening tool - Rule in for high risk sepsis
Use it – but understand the limitations
Positive = move to resus bay, jump on this patient
Neg = keep looking
Robust scoring system – very well –studied
Look for new changes in SOFA components
Accurate prognosis for death
associated with need for intensive care
Associated with long-term organ dysfunction and poor outcomes as well as sepsis recidivism
NOT USER FRIENDLY – EPIC AUTO CALCULATOR?
Patient is alert but not oriented. During transfer from the EMS stretcher to her bed, the patient screams in pain as her right leg bumps the bed rail.
a. Figure it out early qSOFA - rule in for high risk sepsis Simple SOFA - components, Platelets, Cr, GCS, MAP pressor use, O2 requirement (indicator of increased disease severity) Biomarkers - Lactate, procalcitonin, cholesterolb. Fill tank - fluid tolerance, fluids till IVC full then look for B-lines US-based decision making - 2 H's and 2T's in trauma - hypoxia, hemorrhage, tension pneumo, tamponade Similar in a non-trauma shock patient - differential not quite as narrow but
Not enough fluids, or too much?
US guided - Heart, IVC, lung
Why do we give fluids? To improve cardiac output; bicycle analogy reference article by JL Vincent
Reference this article http://journal.publications.chestnet.org/article.aspx?articleid=2589098&utm_source=newsletter_340&utm_medium=email&utm_campaign=critical-care-reviews-newsletter-274
c. Fight bugsd. Fix perfusion
Lower hospital mortality, mechanical ventilation, ICU admission, length of stay, ICU days
Mean fluid volumes in the < 30 minute and 31 – 120 minute groups were 29 ml/kg and 27 ml/kg, respectively
Obese patients - A study of 4157 patients, of whom 31.3% (1293) were obese (body mass index > 30)
Fluid dosing based on adjusted BW (ideal BW + 40% of actual - ideal BW) vs. actual body weight in obese patients was associated with improved mortality. (Taylor SP et al. J Crit Care. 2018;43:7-12)
CHF/ESRD – In the Leisman et al study, these pts were treated with lower fluid volumes (15 ml/kg) and experienced delays to fluid administration
This was not associated with an increased mortality
In general, rec. for an initial dose of 30 ml/kg intravenous fluids for CMS septic shock patients
What does Anne Landers say?
“SEEK PROFESSIONAL HELP”
The effect of intubation on pulmonary pressures negatively affects hemodynamics; you essentially reverse what the patient was doing prior to intubation
On MV, PPV causes an increase in intrathoracic pressure during inspiration which causes IVC diameter to increase relative to expiration where the IVC collapses
High TV (8-10 mL/kg), Rate 12, I:E 1:2, PEEP 0
(Dmax - Dmin)/Dmin
Size variation 15-18% = fluid responsive
PPV 93%, NPV 92%
Changed from 3 hrs for sepsis, 1 hr for shock in 2012 guidelines
Liu VX et al. Am J Respir Crit Care Med. 2017;196(7):856-863.)
Recount the Nec Fasc case I had in room 28 when I was a Pre-attending
Case I had where patient had perf’d viscus and I thought it was UTI
Dobutamine is not a pressor! It’s an inotrope! But Epi is prob a better choice
Arterial line as soon as possible
Remember –
Epi can be bad for splanchnic circulation and increases lactate and may preclude lactate normalization as a resuscitation endpoint (stimulates skeletal muscle B2 receptors)
Vaso at higher doses cardiac, digital, and splanchnic ischemia
What about steroids for septic shock?
Nec Fasc patient I had at Jacobi
Asplenic pneumonia patient went into DIC and died later that night in < 12 hours
Patient with sepsis from ischemic bowel died within 6 hours
Warning Signs:
WBC >= 30k
High lactate
Hyponatremia
AKI
Strength - lactate is probably the most reliable, clinically useful biomarker we have for sepsis
High lactate is associated with poor outcomes
Failure to normalize lactate (when elevated) is a stronger predictor of poor outcome than lactate clearance (Adnan's study)
Failure to clear lactate -
Mostly trauma patients
Mean Ketamine dose in HSI group was 1.2 mg/kg (median 1.7) vs 1.4 mg/kg in the LSI group
Talk about what happens to hemodynamics s/p intubation
Piperacillin/tazobactam 4.5 g IV was given in the first hour of arrival to the ED (Plus Clindamycin and Vancomycin)