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Surviving Sepsis Campaign 2012 Guideline Algorithm

Overview for Initial Resuscitation for Surviving Sepsis. Geared at the medical student / general medical resident level.
by

Clinton Pong

on 6 February 2013

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Transcript of Surviving Sepsis Campaign 2012 Guideline Algorithm

Surviving Sepsis Campaign:
2012 Guidelines SIRS Other Trauma Burns Pancreatitis Other Viremia Parasitemia Fungemia Bacteremia Sepsis Infection 2+ of the following:
THReW 1. T > 38°C or < 36°C
2. HR > 90
3. RR > 20 or PaCO2 < 32 mm Hg
4. WBC >12K, <4K, or >10% immature (band) forms Infection, documented or suspected, and "some" of the following: Fever (> 38.3°C)
Hypothermia (core temperature < 36°C)
Heart rate > 90/min–1 or more than two
sd above the normal value for age
Tachypnea
Altered mental status
Significant edema or positive fluid
balance (> 20 mL/kg over 24 hr)
Hyperglycemia (plasma glucose > 140
mg/dL or 7.7 mmol/L) in the
absence of diabetes Leukocytosis (WBC count > 12,000 μL–1)
Leukopenia (WBC count < 4000 μL–1)
Normal WBC count with greater than
10% immature forms
Plasma C-reactive protein more than two
sd above the normal value
Plasma procalcitonin more than two sd
above the normal value Arterial hypotension
SBP < 90 mm Hg
MAP < 70 mm Hg
or an SBP decrease > 40 mm Hg in
adults or less than two sd below
normal for age) Arterial hypoxemia (Pao2/Fio2 < 300)
Acute oliguria (urine output < 0.5 mL/kg/hr
for at least 2 hrs despite adequate fluid resuscitation)
Creatinine increase > 0.5 mg/dL or 44.2 μmol/L
Coagulation abnormalities (INR > 1.5 or aPTT > 60 s)
Ileus (absent bowel sounds)
Thrombocytopenia (platelet count < 100,000 μL–1)
Hyperbilirubinemia (plasma total bilirubin > 4 mg/dL
or 70 μmol/L)
Tissue perfusion variables
Hyperlactatemia (> 1 mmol/L)
Decreased capillary refill or mottling General Variables Inflammatory Variables Hemodynamic Variables Organ dysfunction variables Severe Sepsis = sepsis-induced tissue hypoperfusion or organ dysfunction
(any of the following thought to be due to the infection) Sepsis-induced hypotension
Lactate above upper limits laboratory normal
Urine output < 0.5 mL/kg/hr for more than 2 hrs despite adequate fluid resuscitation
Acute lung injury with Pao2/Fio2 < 250 in the absence of pneumonia as infection source
Acute lung injury with Pao2/Fio2 < 200 in the presence of pneumonia as infection source
Creatinine > 2.0 mg/dL (176.8 μmol/L)
Bilirubin > 2 mg/dL (34.2 μmol/L)
Platelet count < 100,000 μL
Coagulopathy (international normalized ratio > 1.5) a) CVP 8–12 mm Hg
b) MAP ≥ 65 mm Hg
c) Urine output ≥ 0.5 mL·kg·hr
d) Superior vena cava oxygenation saturation (Scvo2 % >70%) or mixed venous oxygen saturation (Svo2>65%) Initial Resuscitation Goals DO NOT use IV hydrocortisone to treat adult septic shock patients if adequate fluid resuscitation and vasopressor therapy are able to restore hemodynamic stability.

In case this is not achievable:
USE IV hydrocortisone: 200 mg/day continuous infusion (grade 2C)
Taper hydrocortisone when vasopressors have been discontinued (2D) ACTH test NOT recommended (Grade 2B) Vasopressors (targeting MAP of at least 65 mmHg)
* Norepinephrine (NE) is the vasopressor of choice (1B)
* Epinephrine (EPI) if an additional agent is required; can be added to or substituted for NE (2B)
* Vasopressin (0.03 units/minute) can be added to NE; it should not be titrated or used as a single agent (ungraded).
* In selected patients (e.g., bradycardia or low-risk of tachyarrhythmia), dopamine may be considered (2C). Low-dose dopamine (for renal protection) should not be used (1A).
* Phenylephrine (PE) is not recommended, except if (1C):
** Serious NE associated arrhythmias
** Cardiac output can be measured and is increased with low MAP (PE can reduce cardiac output)
** Other therapies cannot achieve the target MAP Fluid therapy
* An initial fluid bolus of at least 30 mL/kg is recommended; crystalloids should be the initial fluid (1B)
* Consider albumin when “substantial” amounts of crystalloid have been given (2C).
* Use of hydroxyethyl starch is not recommended (1B) Diagnosis 1. Cultures before antimicrobial therapy if no significant delay (> 45 mins) in the start of antimicrobial(s) (1C).
-- BCx x2 (both aerobic & anaerobic) before antibiotics
-- Extra draws through each vascular access device, unless the device was recently (<48 hrs) inserted (1C).

2. Use of the 1,3 beta-D-glucan assay (2B), mannan and anti-mannan antibody assays (2C), if invasive candidiasis is in the differential dx

3. Imaging studies performed promptly to confirm a potential source of infection (UG). Antibiotics 1. Give effective IV antibiotics/antivirals/antifungals w/in the FIRST HOUR of recognition of septic shock (1B) and severe sepsis w/o septic shock (1C)

2 a. Initial empiric treatment: 1+ drugs against all likely pathogens (bacterial/fungal/viral) that penetrate into tissue source of sepsis (1B).
b. Regimen should be reassessed daily for potential deescalation (1B).

3. In cases initially appearing septic, but have no subsequent evidence of infection, use low procalcitonin to D/C of empiric abx (2C).

4 a. Combo empiric tx for neutropenic pt w/ severe sepsis (2B) and for pt with difficult-to-treat, MDR bacterial pathogens like Acinetobacter and Pseudomonas spp. (2B). For pt w/ severe infxn assoc w/ respiratory failure & septic shock, combine tx w/ an extended spectrum beta-lactam + either a) aminoglycoside or b) a fluoroquinolone for P. aeruginosa bacteremia (2B). Combine of beta-lactam and macrolide for patients with septic shock from bacteremic S. pneumoniae infections (2B). 4b. Empiric combo tx should NOT be administered for more than 3–5 days. De-escalate to the most appropriate single therapy when the susceptibility profile is known (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 (2C).

6. Antiviral therapy initiated as early as possible in patients with severe sepsis or septic shock of viral origin (2C).

7. Antimicrobial agents should NOT be used in patients with severe inflammatory states determined to be of noninfectious cause (UG). Source Control 1. Seek out a specific anatomic dx of infection source, diagnose and/or excluded ASAP and control w/in the FIRST TWELVE HOURS after diagnosis(1C).

2. When infected peripancreatic necrosis is identified as a potential source of infection, delay intervention until demarcation of viable and nonviable tissues is adequate(2B).

3. Use the least invasive and least harmful methods for source control if possible. (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 after
other vascular access has been established (UG). 1a. Oral and digestive decontamination should be introduced and investigated as a method to reduce the incidence of VAP (2B)

1b. 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). Infection Prevention <21-27% >21-27% Although less applicable to septic patients, results of a randomized trial in patients undergoing cardiac surgery with cardiopulmonary bypass support a restrictive transfusion strategy using a threshold hematocrit of < 24% (hemoglobin 8 g/dL) as equivalent to a transfusion threshold of hematocrit of < 30% (hemoglobin 10 g/dL)
1. Once tissue hypoperfusion has resolved and in the absence of extenuating circumstances
(i.e. MI, hypoxemia, acute hemorrhage, or IHD, transfuse RBCs only when Hgb <7.0 g/dL with a target Hgb of 7.0 –9.0 g/dL (1B).

Avoid using:
-- EPO for anemia associated with severe sepsis (1B).
-- FFP to correct lab abnormalities in the absence of bleeding or planned invasive procedures (2D).
-- antithrombin for the treatment of severe sepsis and septic shock (1B).

5. In patients with severe sepsis, administer Platelets when <10,000/mm^3 (<10 x 10^9/L) in the absence of apparent bleeding.
transfuse at < 20K if the patient has a significant risk of bleeding
transfuse at ≥50K for active bleeding, surgery, or invasive procedures (2D). Blood Product Administration Mechanical Ventilation of Sepsis-Induced Acute Respiratory Distress Syndrome (ARDS) 1. TV of 6 mL/kg predicted BW (vs. 12 mL/kg) (1A).
2. Plateau pressure initial upper limit ≤30 cm H2O (1B).
3. PEEP to avoid alveolar collapse at end expiration (atelectotrauma) (1B).
4. Use higher rather than lower PEEP for sepsis-induced moderate or severe ARDS (2C).
5. Recruitment maneuvers be used in sepsis patients with severe refractory hypoxemia (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 (2B).
7. HOB elevated to 30-45 degrees to limit aspiration risk and to prevent the development of VAP (1B).
8. NIV used in a minority of patients in whom the benefits outweigh the risks (2B).






9. Weaning protocol in place and mechanically ventilated patients with severe sepsis undergo SBT 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;
e) low Fio2 requirements which can be met safely delivered with a face mask or NC.
If successful, consider extubation (1A).
10. Against the routine use of the pulmonary artery catheter for patients with sepsis-induced ARDS (1A).
11. A conservative rather than liberal fluid strategy for patients with established sepsis-induced ARDS who do not have evidence of
tissue hypoperfusion (1C).
12. In the absence of specific indications such as bronchospasm, not using beta 2-agonists for treatment of sepsis-induced ARDS (grade 1B). insulin dosing when 2 consecutive blood glucose levels are >180 mg/dL. . POC glucose levels should be interpreted with caution, as such measurements may not accurately estimate arterial blood or plasma glucose values (UG).
1. Target: upper blood glucose </=180 mg/dL rather than an upper target blood glucose ≤ 110 mg/dL (1A).

2. Monitor BG Q1–2 hr until glucose and insulin infusion are stable; then Monitor Q4 hrs thereafter (1C). Sepsis Adapted from Levy MM, Fink MP, Marshall JC, et al: 2001 SCCM/ESICM/ NICE-SUGAR Leuven Protocol demonstrated a reduction in ICU mortality with intensive intravenous insulin target of 80-110 mg/dL (in a predominantly cardiac SICU).

In 3 MICUs for pt with LOS >3 days, overall mortality was not reduced.

RCTs studied mixed populations of surgical and medical ICU patients and found that intensive insulin therapy did not significantly decrease mortality, whereas the NICE-SUGAR trial demonstrated an increased mortality.

All studies reported a higher incidence of severe hypoglycemia (≤ 40 mg/dL) (6%−29%) with intensive insulin therapy.
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