2012 Surviving Sepsis Campaign Guidelines

This podcast was originally posted on the Practical Evidence Podcast

The 2012 SSC Guidelines were just published and I saw the preview in Puerto Rico

2012 Surviving Sepsis Campaign Guidelines

See the Guidelines at (CCM 2013;41(2):580)

Diagnosis of Sepsis

sepsis-diag-criteria

Diagnosis of Severe Sepsis

severe-sepsis

The New Bundles

bundles

A. Initial Resuscitation

  1. Protocolized, quantitative resuscitation of patients with sepsis- induced tissue hypoperfusion (defined in this document as hypotension persisting after initial fluid challenge or blood lactate concentration ? 4 mmol/L). Goals during the first 6 hrs of resuscitation:
    • Central venous pressure 8–12 mm Hg
    • Mean arterial pressure (MAP) ? 65 mm Hg
    • Urine output ? 0.5 mL/kg/hr
    • Central venous (superior vena cava) or mixed venous oxygen saturation 70% or 65%, respectively (grade 1C).
  2. In patients with elevated lactate levels targeting resuscitation to normalize lactate (grade 2C).

B. Screening for Sepsis and Performance Improvement

  1. Routine screening of potentially infected seriously ill patients for severe sepsis to allow earlier implementation of therapy (grade 1C).
  2. Hospital–based performance improvement efforts in severe sepsis (UG).

C. Diagnosis

  1. Cultures as clinically appropriate before antimicrobial therapy if no significant delay (> 45 mins) in the start of antimicrobial(s) (grade 1C). At least 2 sets of blood cultures (both aerobic and anaerobic bottles) be obtained before antimicrobial therapy with at least 1 drawn percutaneously and 1 drawn through each vascular access device, unless the device was recently (<48 hrs) inserted (grade 1C).
  2. Use of the 1,3 beta-D-glucan assay (grade 2B), mannan and anti-mannan antibody assays (2C), if available and invasive candidiasis is in differential diagnosis of cause of infection.
  3. Imaging studies performed promptly to confirm a potential source of infection (UG).

D. Antimicrobial Therapy

  1. Administration of effective intravenous antimicrobials within the first hour of recognition of septic shock (grade 1B) and severe sepsis without septic shock (grade 1C) as the goal of therapy.
  2. Initial empiric anti-infective therapy of one or more drugs that have activity against all likely pathogens (bacterial and/or fungal or viral) and that penetrate in adequate concentrations into tissues presumed to be the source of sepsis (grade 1B). Antimicrobial regimen should be reassessed daily for potential deescalation (grade 1B).
  3. Use of low procalcitonin levels or similar biomarkers to assist the clinician in the discontinuation of empiric antibiotics in patients who initially appeared septic, but have no subsequent evidence of infection (grade 2C).
  4. Combination empirical therapy for neutropenic patients with severe sepsis (grade 2B) and for patients with difficult-to-treat, multidrugresistant bacterial pathogens such as Acinetobacter and Pseudomonas spp. (grade 2B). For patients with severe infections associated with respiratory failure and septic shock, combination therapy with an extended spectrum beta-lactam and either an aminoglycoside or a fluoroquinolone is for P. aeruginosa bacteremia (grade 2B). A combination of beta-lactam and macrolide for patients with septic shock from bacteremic Streptococcus pneumoniae infections (grade 2B). Empiric combination therapy should not be administered for more than 3–5 days. De-escalation to the most appropriate single therapy should be performed as soon as the susceptibility profile is known (grade 2B).
  5. Duration of therapy typically 7–10 days; longer courses may be appropriate in patients who have a slow clinical response, undrainable foci of infection, bacteremia with S. aureus; some fungal and viral infections or immunologic deficiencies, including neutropenia (grade 2C).
  6. Antiviral therapy initiated as early as possible in patients with severe sepsis or septic shock of viral origin (grade 2C).
  7. Antimicrobial agents should not be used in patients with severe inflammatory states determined to be of noninfectious cause (UG).

E. Source Control

  1. A specific anatomical diagnosis of infection requiring consideration for emergent source control be sought and diagnosed or excluded as rapidly as possible, and intervention be undertaken for source control within the first 12 hr after the diagnosis is made, if feasible (grade 1C).
  2. When infected peripancreatic necrosis is identified as a potential source of infection, definitive intervention is best delayed until adequate demarcation of viable and nonviable tissues has occurred (grade 2B).
  3. When source control in a severely septic patient is required, the effective intervention associated with the least physiologic insult should be used (eg, percutaneous rather than surgical drainage of an abscess) (UG).
  4. If intravascular access devices are a possible source of severe sepsis or septic shock, they should be removed promptly after other vascular access has been established (UG).

F. Infection Prevention

  1. Selective oral decontamination and selective digestive decontamination should be introduced and investigated as a method to reduce the incidence of ventilator-associated pneumonia; This infection control measure can then be instituted in health care settings and regions where this methodology is found to be effective (grade 2B).
  2. Oral chlorhexidine gluconate be used as a form of oropharyngeal decontamination to reduce the risk of ventilator-associated pneumonia in ICU patients with severe sepsis (grade 2B).

G. Fluid Therapy of Severe Sepsis

  1. Crystalloids as the initial fluid of choice in the resuscitation of severe sepsis and septic shock (grade 1B).
  2. Against the use of hydroxyethyl starches for fluid resuscitation of severe sepsis and septic shock (grade 1B).
  3. Albumin in the fluid resuscitation of severe sepsis and septic shock when patients require substantial amounts of crystalloids (grade 2C).
  4. Initial fluid challenge in patients with sepsis-induced tissue hypoperfusion with suspicion of hypovolemia to achieve a minimum of 30 mL/kg of crystalloids (a portion of this may be albumin equivalent). More rapid administration and greater amounts of fluid may be needed in some patients (grade 1C).
  5. Fluid challenge technique be applied wherein fluid administration is continued as long as there is hemodynamic improvement either based on dynamic (eg, change in pulse pressure, stroke volume variation) or static (eg, arterial pressure, heart rate) variables (UG).

H. Vasopressors

  1. Vasopressor therapy initially to target a mean arterial pressure (MAP) of 65 mm Hg (grade 1C).
  2. Norepinephrine as the first choice vasopressor (grade 1B).
  3. Epinephrine (added to and potentially substituted for norepinephrine) when an additional agent is needed to maintain adequate blood pressure (grade 2B).
  4. Vasopressin 0.03 units/minute can be added to norepinephrine (NE) with intent of either raising MAP or decreasing NE dosage (UG).
  5. Low dose vasopressin is not recommended as the single initial vasopressor for treatment of sepsis-induced hypotension and vasopressin doses higher than 0.03–0.04 units/minute should be reserved for salvage therapy (failure to achieve adequate MAP with other vasopressor agents) (UG).
  6. Dopamine as an alternative vasopressor agent to norepinephrine only in highly selected patients (eg, patients with low risk of tachyarrhythmias and absolute or relative bradycardia) (grade 2C).
  7. Phenylephrine is not recommended in the treatment of septic shock except in circumstances where (a) norepinephrine is associated with serious arrhythmias, (b) cardiac output is known to be high and blood pressure persistently low or (c) as salvage therapy when combined inotrope/vasopressor drugs and low dose vasopressin have failed to achieve MAP target (grade 1C).
  8. Low-dose dopamine should not be used for renal protection (grade 1A).
  9. All patients requiring vasopressors have an arterial catheter placed as soon as practical if resources are available (UG).

I. Inotropic Therapy

  1. A trial of dobutamine infusion up to 20 micrograms/kg/min be administered or added to vasopressor (if in use) in the presence of (a) myocardial dysfunction as suggested by elevated cardiac filling pressures and low cardiac output, or (b) ongoing signs of hypoperfusion, despite achieving adequate intravascular volume and adequate MAP (grade 1C).
  2. Not using a strategy to increase cardiac index to predetermined supranormal levels (grade 1B).

J. Corticosteroids

  1. Not using intravenous hydrocortisone to treat adult septic shock patients if adequate fluid resuscitation and vasopressor therapy are able to restore hemodynamic stability (see goals for Initial Resuscitation). In case this is not achievable, we suggest intravenous hydrocortisone alone at a dose of 200 mg per day (grade 2C).
  2. Not using the ACTH stimulation test to identify adults with septic shock who should receive hydrocortisone (grade 2B).
  3. In treated patients hydrocortisone tapered when vasopressors are no longer required (grade 2D).
  4. Corticosteroids not be administered for the treatment of sepsis in the absence of shock (grade 1D).
  5. When hydrocortisone is given, use continuous flow (grade 2D).

K. Blood Product Administration

  1. Once tissue hypoperfusion has resolved and in the absence of extenuating circumstances, such as myocardial ischemia, severe hypoxemia, acute hemorrhage, or ischemic heart disease, we recommend that red blood cell transfusion occur only when hemoglobin concentration decreases to <7.0 g/dL to target a hemoglobin concentration of 7.0 –9.0 g/dL in adults (grade 1B).
  2. Not using erythropoietin as a specific treatment of anemia associated with severe sepsis (grade 1B).
  3. Fresh frozen plasma not be used to correct laboratory clotting abnormalities in the absence of bleeding or planned invasive procedures (grade 2D).
  4. Not using antithrombin for the treatment of severe sepsis and septic shock (grade 1B).
  5. In patients with severe sepsis, administer platelets prophylactically when counts are <10,000/mm3 (10 x 109/L) in the absence of apparent bleeding. We suggest prophylactic platelet transfusion when counts are < 20,000/mm3 (20 x 109/L) if the patient has a significant risk of bleeding. Higher platelet counts (?50,000/mm3 [50 x 109/L]) are advised for active bleeding, surgery, or invasive procedures (grade 2D).

L. Immunoglobulins

  1. Not using intravenous immunoglobulins in adult patients with severe sepsis or septic shock (grade 2B).

M. Selenium

  1. Not using intravenous selenium for the treatment of severe sepsis (grade 2C).

N. History of Recommendations Regarding Use of Recombinant Activated Protein C (rhAPC)

A history of the evolution of SSC recommendations as to rhAPC (no longer available) is provided.

O. Mechanical Ventilation of Sepsis-Induced Acute Respiratory Distress Syndrome (ARDS)

  1. Target a tidal volume of 6 mL/kg predicted body weight in patients with sepsis-induced ARDS (grade 1A vs. 12 mL/kg).
  2. Plateau pressures be measured in patients with ARDS and initial upper limit goal for plateau pressures in a passively inflated lung be ?30 cm H2O (grade 1B).
  3. Positive end-expiratory pressure (PEEP) be applied to avoid alveolar collapse at end expiration (atelectotrauma) (grade 1B).
  4. Strategies based on higher rather than lower levels of PEEP be used for patients with sepsis- induced moderate or severe ARDS (grade 2C).
  5. Recruitment maneuvers be used in sepsis patients with severe refractory hypoxemia (grade 2C).
  6. Prone positioning be used in sepsis-induced ARDS patients with a Pao2/Fio2 ratio ? 100 mm Hg in facilities that have experience with such practices (grade 2B).
  7. That mechanically ventilated sepsis patients be maintained with the head of the bed elevated to 30–45 degrees to limit aspiration risk and to prevent the development of ventilator-associated pneumonia (grade 1B).
  8. That noninvasive mask ventilation (NIV) be used in that minority of sepsis-induced ARDS patients in whom the benefits of NIV have been carefully considered and are thought to outweigh the risks (grade 2B).
  9. That a weaning protocol be in place and that mechanically ventilated patients with severe sepsis undergo spontaneous breathing trials regularly to evaluate the ability to discontinue mechanical ventilation when they satisfy the following criteria: a) arousable; b) hemodynamically stable (without vasopressor agents); c) no new potentially serious conditions; d) low ventilatory and end-expiratory pressure requirements; and e) low Fio2 requirements which can be met safely delivered with a face mask or nasal cannula. If the spontaneous breathing trial is successful, consideration should be given for extubation (grade 1A).
  10. Against the routine use of the pulmonary artery catheter for patients with sepsis-induced ARDS (grade 1A).
  11. A conservative rather than liberal fluid strategy for patients with established sepsis-induced ARDS who do not have evidence of tissue hypoperfusion (grade 1C).
  12. In the absence of specific indications such as bronchospasm, not using beta 2-agonists for treatment of sepsis-induced ARDS (grade 1B).

P. Sedation, Analgesia, and Neuromuscular Blockade in Sepsis

  1. Continuous or intermittent sedation be minimized in mechanically ventilated sepsis patients, targeting specific titration endpoints (grade 1B).
  2. Neuromuscular blocking agents (NMBAs) be avoided if possible in the septic patient without ARDS due to the risk of prolonged neuromuscular blockade following discontinuation. If NMBAs must be maintained, either intermittent bolus as required or continuous infusion with train-of-four monitoring of the depth of blockade should be used (grade 1C).
  3. A short course of NMBA of not greater than 48 hours for patients with early sepsis-induced ARDS and a Pao2/Fio2 < 150 mm Hg (grade 2C).

Q. Glucose Control

  1. A protocolized approach to blood glucose management in ICU patients with severe sepsis commencing insulin dosing when 2 consecutive blood glucose levels are >180 mg/dL. This protocolized approach should target an upper blood glucose ?180 mg/dL rather than an upper target blood glucose ? 110 mg/dL (grade 1A).
  2. Blood glucose values be monitored every 1–2 hrs until glucose values and insulin infusion rates are stable and then every 4 hrs thereafter (grade 1C).
  3. Glucose levels obtained with point-of-care testing of capillary blood be interpreted with caution, as such measurements may not accurately estimate arterial blood or plasma glucose values (UG).

R. Renal Replacement Therapy

  1. Continuous renal replacement therapies and intermittent hemodialysis are equivalent in patients with severe sepsis and acute renal failure (grade 2B).
  2. Use continuous therapies to facilitate management of fluid balance in hemodynamically unstable septic patients (grade 2D).

S. Bicarbonate Therapy

  1. Not using sodium bicarbonate therapy for the purpose of improving hemodynamics or reducing vasopressor requirements in patients with hypoperfusion-induced lactic acidemia with pH ?7.15 (grade 2B).

T. Deep Vein Thrombosis Prophylaxis

  1. Patients with severe sepsis receive daily pharmacoprophylaxis against venous thromboembolism (VTE) (grade 1B). This should be accomplished with daily subcutaneous low-molecular weight heparin (LMWH) (grade 1B versus twice daily UFH, grade 2C versus three times daily UFH). If creatinine clearance is <30 mL/min, use dalteparin (grade 1A) or another form of LMWH that has a low degree of renal metabolism (grade 2C) or UFH (grade 1A).
  2. Patients with severe sepsis be treated with a combination of pharmacologic therapy and intermittent pneumatic compression devices whenever possible (grade 2C).
  3. Septic patients who have a contraindication for heparin use (eg, thrombocytopenia, severe coagulopathy, active bleeding, recent intracerebral hemorrhage) not receive pharmacoprophylaxis (grade 1B), but receive mechanical prophylactic treatment, such as graduated compression stockings or intermittent compression devices (grade 2C), unless contraindicated. When the risk decreases start pharmacoprophylaxis (grade 2C).

U. Stress Ulcer Prophylaxis

  1. Stress ulcer prophylaxis using H2 blocker or proton pump inhibitor be given to patients with severe sepsis/septic shock who have bleeding risk factors (grade 1B).
  2. When stress ulcer prophylaxis is used, proton pump inhibitors rather than H2RA (grade 2D)
  3. Patients without risk factors do not receive prophylaxis (grade 2B).

V. Nutrition

  1. Administer oral or enteral (if necessary) feedings, as tolerated, rather than either complete fasting or provision of only intravenous glucose within the first 48 hours after a diagnosis of severe sepsis/septic shock (grade 2C).
  2. Avoid mandatory full caloric feeding in the first week but rather suggest low dose feeding (eg, up to 500 calories per day), advancing only as tolerated (grade 2B).
  3. Use intravenous glucose and enteral nutrition rather than total parenteral nutrition (TPN) alone or parenteral nutrition in conjunction with enteral feeding in the first 7 days after a diagnosis of severe sepsis/septic shock (grade 2B).
  4. Use nutrition with no specific immunomodulating supplementation rather than nutrition providing specific immunomodulating supplementation in patients with severe sepsis (grade 2C).

W. Setting Goals of Care

  1. Discuss goals of care and prognosis with patients and families (grade 1B).
  2. Incorporate goals of care into treatment and end-of-life care planning, utilizing palliative care principles where appropriate (grade 1B).
  3. Address goals of care as early as feasible, but no later than within 72 hours of ICU admission (grade 2C).
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Comments

  1. Leong Ka Weng says:

    How to use albumin as part of fluid therapy in septic shock ?
    What concentration (4-5% or 20% albumin) to be used ?
    What is the “dosage” ?
    – how much ?
    – how fast (the rate) ?

    • BIJU JOHN says:

      Ever since we started talking about the glycocalyx and modified Starling’s equation concerning fluid transport across the capillary membrane, we have known that hyperoncotic solutions are BAD for the endothelial surface layer. So 20 %albumin is kinda out!!. Also, there is no evidence of any survival benefit with its use from the literature. 4-5% Albumin is safe, and the dose equivalence to crystalloids is 1:1.4ml.
      ( SAFE and VISEP studies…) Also, there is some evidence that albumin infact protects the glycocalyx a bit.

      Hope this helps.

  2. I was hoping for the guidelines to include something about “prehospital recognition and initial treatment”. Currently unappreciated in the prehospital realm and a push from the “guidelines” side could help move this along (e.g. wider adoption of something like the Denver Sepsis Alert program).

  3. At our shop, patients usually get up to the ICU within 1-2 hours.
    I love starting central lines. However, the culture at my facility is to not start them in the ED in most cases, as frustrating as that sounds.
    Given that reality, has anyone looked at the safety and efficacy of giving norepinephrine peripherally in a concentration that is more dilute than standard? Instead of 8mg/250ml of D5W, why not 1 or 2mg/250ml and increase the flow rate?
    To provide 16mcg/min, instead of 30ml/hr the rate would be 120ml/hr for a 2mg/250ml preparation.
    I don’t see that this has ever been studied. Do you know if it’s been looked at?
    If this were adopted, phentolamine could be kept on standby. However, I’d imagine that extravasation occurring at a flow rate of 120ml would quickly become obvious due to IV pump alarms.

    • That is exactly what Paul Mayo (of the RSI debate) has been doing in the MICU at Long Island Jewish. I assume he will publish his results. I think the ideal for this is to place a longer cath in the AC (peds central line or a femoral a-line kit). I will shoot him an email and see if he responds.

      • That is the issue we face, in a generally very busy community department. Our times to ICU are not bad, but having the time to place central lines in a truly optimal fashion is rare, and giving peripheral pressors creates a workflow benefit. The discussion previously had included using phenylephrine as a safer peripheral agent, but the skylines pretty much shoot that down.
        Love to hear what Paul has to say, Scott!

  4. Minh Le Cong says:

    thanks Scott. great way to review the new guidelines!

    Over the last few years, I have stopped recommending CVC line placement in prehospital and retrieval medicine. cause more trouble than they are worth usually in the retrieval setting. I advocate use of norepinephrine or preferably epinephrine infusions via secure PIV for the few hours or less a retrieval mission will take. Norepi drips I recommend as Joe says in a dilute preparation. One time during the H1N1 epidemic I had a flu patient in septic shock, SBP 60, turn up at a remote clinic I was working. For initial resus, we had to make up a epinephrine drip via 18G PIV by putting 1 mg epi into a 1 L saline bag. Gravity dripped it in and titrated to BP and HR. Vasopressor and fluids at same time. Anyway it worked well enough to stabilise his BP prior to RSI. ..and in fact BP did not falter during RSI and post RSI period.

    • Mattia Quarta says:

      This might be tedious but it’s something that had me thinking recently.
      There is no recommended dosage infusions for norepinephrine despite being the first choice pressor.
      I had been searching the literature on sepsis and found ranges that varies from 0.02 mcg/kg/min to 5 mcg/kg/min.
      I generally prefer weight based dosages but at my institution norepinephrine scheme has always been unrelated to patients’ weight. If I got it right you are not following a weight based scheme either.
      Do you have any suggestion on starting dose and maximum dose? Is there any particular advantage in your opinion in using a weight based protocol?

      Thanks!

      • No I see no advantage and a number of disadvantages. Norepi is a titratable drug, so it really doesn’t matter if you dose by weight except for the starting dose; after that you are just moving up and down by MAP. The disadvantage to weight base dosing is you may start too high. Often, 1-2 mcg/min of norepi does the job. I will start at these low doses if the patient is not crashing and move up from there.

  5. Let’s say it’s found that pressors, when appropriately diluted, are safe given peripherally. If this were found to be the case, do you think there could be a subset of patients manageable in the ICU without the need for a central line? It sounds like that is what Dr. Mayo is doing. There may be other advantages to having the central line in place that we in the ED aren’t aware of.

    If there are any research directors reading this-how about a randomized trial? Could study outcomes of ICU patients managed without a central line and administration of pressors by PIV vs current standard of care.

  6. Panos Zotos says:

    Dr Weingart I would really like to thank you for your very precise remarks about the new SSC guidelines! I am a greek intensivist doctor and a new member of your blog.
    I learned about your blog recently while I was in New York for an ED training program. Since then I am a real fan of you and your interesting
    notes! Thank you!

  7. Mathias Tschopp says:

    Always a good read on why CVP must be put to rest:
    http://socmob.blogspot.ch/2012_10_01_archive.html

  8. Dave Barounis says:

    Scott,

    Love the podcast as always, couple questions/comments

    1. Why is there so much stress on the need for blood cultures? I mean every time I am about to give abx, I get a call from pharmacy or nursing to ask if they need blood cultures first. In the guidelines it seems as though they recommend blood cultures for all septic patients, is this including patients without shock? It seems that the diagnostic utility of blood cultures in your run of the mill septic patient is low, and between 1-5% of patients will have a false positive, and rarely the choice of antibiotics are changed. I think using a prediction rule or common sense is more appropriate (indwelling catheter, suspected endocarditis, post-surgical, evidence of shock, neutropenia etc.) for deciding who needs cultures.

    2. What do you do about fever control? It seems as though the evidence for patients with severe infections do worse with fever control, especially when looking at using NSAID’s. Rectal Tylenol, cooling blanket, nothing? The evidence is merky, but it makes physiologic sense.

    3. Also you didn’t mention when you start mechanical ventilation in patients who have a continued elevated lactate despite initial resus, but their work of breathing is increased. This increased work of breathing seems to contribute significantly to metabolic demand and the persistent hyperlactatemia. Taking control of the patient’s respiratory drive may reduce metabolic requirements by up to 30%. This is obviously somewhat of a judgment call, but any general opinions?

    4. What fluids are you using (chloride liberal like NS, or chloride restrictive like LR or PL) for resuscitation. I think at my shop NS is 13cents LR 17cents and PL $1.13. With the recent JAMA article covering this topic (sort of) is emcrit using chloride restrictive fluid for the initial resuscitation?

    5. Lastly you have mentioned using US guided IVC collapse for fluid responsiveness. I guess if you use it as a guide to force you to use more fluid it seems reasonable, but in a spontaneously breathing individual the negative intrathoracic pressure generated on a breath-to-breath basis is constantly varying. Shallow breaths may only cause minimal negative intrathoracic pressure changes, which therefore cause smaller increases in venous return, which might be missed when evaluating the IVC. If there is marked collapse then patients are likely fluid responsive, but usually this is clinically evident, as you mentioned in your podcasts like patients with CVP’s of 0 on initial resus. Also the type of breathing will vary the IVC collapse chest wall breathing (pulling abdomen in) or abdominal breathing (pushing your abdomen out) so it makes me question the utility of IVC collapse

    Anyways, I think identifying fluid responsiveness in a patient not on mechanical ventilation continues to prove to be a bit of a quagmire in terms of when to stop fluid resuscitation.

    Thanks

    Dave

    • Blood cultures matter a ton for hospital/health care assoc. infections; not as much for community. But when we are dealing with severe infection, it is nice to know the bug and especially the sensitivities. Often the yield is higher in the patients as well. If the pt has CA-MRSA as the cause of their severe sepsis pneumonia, I’d like to know. I would not wait one second to start abx though. If you can’t get cx with first draw, start abx and keep working to get cx while the abx is infusing.

      Have no idea on fever control.

      I have other podcasts about the need for intubation for severe acidosis, poor tissue ox. This is just a review of guidelines.

      I use alternating NS and plasmalyte liter for liter.

      IVC collapse should be an indication to give more fluid, non-collapsing is not an indication to not for all the reasons you mention.

  9. Sean sue md says:

    Septic dialysis pt with map 64 , lactate 7. Alert but confused. Airway patent. Med. effusions on ct long windows. None on cxr. What do you do with fluid resuscitation in the Ed over 1st 3 hrs

  10. Hi. I’m very interested in changes you have made to comply with the new recommendations for Sepsis Campaign, as well as what barriers you anticipate. Does your facility use a sepsis database?

  11. Seth Trueger says:

    Are art lines always necessary for patients on pressors? http://resus.me/non-invasive-bp-in-shock/

  12. Scott,

    Great review thanks. A few quick questions:

    – In Marik’s study a significant number of his patients were post-CABG: how does this effect the extension of this study’s findings to septic MICU patients?

    – Marik’s “responders” and “non-responders” had CVPs of 8.7 and 9.7 respectively: what’s the likelihood these guys are already on the flat part of the startling curve?

    – Lactate vs. Scv02: what about the significant number of initially lactate negative patients that go on to vasopressor dependent shock? Might seeing a (pre-dysoxic state) falling Scv02 have promoted more aggressive, potentially life-saving, resuscitation?

    Thanks!

    • Insightful points. We all believe that when the cvp is very low<5 they pt likely will be fluid responsive. Most of the CABG pts were fluid replete in the OR, so the cohort cuts out the easy patients, but this is a better test of a test. THis si the opposite of a case-control conundrum, If CVP works great for profoundly dehydrated patients and pts in cardiogenic pulm edema but no well for the middle ground, then it is a failure as a test. Sort of like BNP.

      What the literature is showing in 3 separate trials now is that vasopressor dependent shock with no lactate elevation is a relatively benign situation. The initial fluids, abx, and vasopressor is all they need. Acutally the Jones trial consisted almost entirely of these patients. The better question is what about the lactate of 8 patient who clears to 6.5; have we really done enough for this patient. The Jones trial did not have many of these.

  13. mike mathieson says:

    Scott, We are working on an institution wide sepsis protocol in anticipation that CMS will soon require it.(most of our ed folks have been following the EGDT guidlines already) I agree that the non invasive strategy is a great option for many patients and would love to avoid central lines if possible. The question came up about using PICC lines for cvp monitoring. I have found conflicting information about this. Just wondering what you thought about it? Thanks for the great material. Mike

  14. Tony Ashton says:

    I find the diagnosis section confusing.
    “Sepsis is defined as the presence (probable or documented) of infection together with systemic manifestations of infection.” Okay got it. SIRS now includes a plethora of new variables and the statement in Table 1 “Infection, documented or suspected, and some of the following:” is wooly but presumably increases sensitivity.
    “Severe sepsis is defined as sepsis plus sepsis-induced organ dysfunction or tissue hypoperfusion”. Table 2 has organ dysfunction variables that are different from the organ dysfunction variables in table 1 (Bilirubin, Creatinine, acute lung injury). The threshold for bilirubin is higher for use as a Sepsis diagnostic criteria than for Severe sepsis and the Creatinine criteria is an increment of 0.5 mg/dL for Sepsis but a rise above an absolute value of 2.0mg/dL in Severe sepsis.

  15. Thanks for a great review. You mentioned you wouldn’t wait for blood cultures to start antibiotics. Do you know of data on how long after starting antibiotics valid blood cultures can be obtained ? I would be very curious to see data on that…

    However, the literature finds that most blood cultures obtained in the ED are not helpful. They are almost as likely to be false positive (contaminants) as true positive, true positives may not be noted by the inpatient team, and even if they are, culture results are less likely to influence management than the patient’s “clinical picture.” There is slightly more support for obtaining cultures in healthcare-acquired infections and ICU patients. The literature does NOT support obtaining blood cultures in a septic patient with CAP unless going to the ICU (and ACEP clinical policy on pna reflects this as well). Your thoughts?

  16. Andrew DeWolf says:

    Scott: Surviving Sepsis Campaign is dear to my heart, and as an advanced practitioner Paramedic we are looking to implement as much of the reccomended bundles as appropriate and practical for EMS. The problem on our end is cost and reimbursements…. trying to sell administration on training/screening/Finger stick lactate levels/ Sepsis Alert –> Any literature you are aware of that may help with this? Thanks!

  17. Øyvind S Holen says:

    Scott: I know that you advocate the use of lactate clearance as a resuscitation goal. I was wondering if you have had the chance to take a look at this article by PE Marik? It is suggesting that lactate clearance is a flawed concept and that lactic acidosis in fact is no associated with anaerobic metabolism. Pretty controversial stuff I would say! Must I unlearn all that I have learned??? Do you have any thoughts or comments?

    http://www.oapublishinglondon.com/article/431

    • Nothing controversial about this at all. Most of lactate in severe sepsis is not from anaerobic metabolism, it is from the cytokine-storm induced changes in metabolism. Paul’s facts are all true, the conclusion doesn’t follow. When Jones performed the LACTATE study it was with full knowledge that what we are seeing is not anaerobic metabolism. This was discussed way back in the all about lactate podcast.

  18. Aleksandar says:

    Dear Sir,
    I’m a medical doctor, and I desperately need your help about one question. The question is:
    Solutions of choice in the treatment of sepsis and septic shock are (one answer is correct):
    a. crystalloid solutions;
    b. colloidal solutions;
    c. there is no evidence that one type of solution has the advantage over the other, and can both can be aplied

    My dilemma is: are the crystalloids recommended as initial fluid due to hard clinical evidence, or just because of their lower cost? What would you answer on this question? Thanks in advance

    • The only colloid that may have a role in sepsis is albumin. The data is not clear how advantageous it is over crystalloid if at all, and it is radically more expensive. Based on that you make your choices.

  19. We can draw a continuum in sepsis: infection -> sepsis -> severe sepsis -> septic shock. Where does “Sepsis Induced Tissue Hypoperfusion” fit? By other words, what´s the difference between “Sepsis Induced Tissue Hypoperfusion” and “Septic Shock”?

    • shock is being used to refer to hypotension as opposed to the better definition of tissue hypoperfusion. So severe sepsis is the better term.

      • Thanks for your reply!
        As a far as I know that was a term introduced in the new SSC Guidelines 2012 and I was having trouble understanding it. To my opinion, I patient with hyperlactatemia > 4mmol/L after fluid-challenge is also in shock – cryptic shock, to be more precisely.

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