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A review of the latest guidelines
By Julie Miller, BSN, RN, CCRN


AFFECTING MILLIONS OF people worldwide, sepsis is a systemic response to an overwhelming inflammatory process caused by an infection. Approximately one in four people who develop sepsis will die.1 In January 2013, the international Surviving Sepsis Campaign Guidelines
Committee published its 2012 surviving sepsis guidelines
(SSG), an update to the 2008 guidelines for early identification and management of sepsis in adults.1 The guidelines highlight the importance of screening every potentially infected patient for sepsis and providing best-practice interventions for managing sepsis, severe sepsis, and septic shock. This article provides an overview of care for the adult patient with sepsis, focusing on sepsis identification and the first 6 hours of goal-directed treatment according to current guidelines.
Defining sepsis
Sepsis is the presence of infection along with systemic manifestations of infection. If sepsis isn’t recognized and treated early, it progresses rapidly to severe sepsis, defined as sepsis plus sepsis-induced organ dysfunction or tissue hypoperfusion. Sepsis-induced tissue hypoperfusion is defined as infection-induced hypotension, elevated lactate level, or oliguria.1 24 l Nursing2014 l April

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Patients with severe sepsis may have low systolic or mean arterial pressure (MAP), a lactate level above
2 mmol/L, or a urine output of less than 0.5 mL/kg/hr for at least 2 hours despite adequate fluid resuscitation.1 Recognizing that a patient has sepsis before it progresses to severe sepsis is essential for early intervention to prevent further progression to septic shock.

Septic shock is sepsis-induced hypotension that persists despite adequate fluid resuscitation. Sepsisinduced hypotension is defined as systolic BP (SBP) less than 90 mm
Hg, MAP less than 70 mm Hg, or a decrease in SBP greater than 40 mm
Hg or less than two standard deviations below normal for age in the absence of other causes of hypotension.1 Screening patients for sepsis includes monitoring for signs and symptoms of infection and identifying subtle changes in vital signs, mental status, urine output, lab values, and/or markers of tissue perfusion. (See Screening patients for sepsis, severe sepsis, or septic shock.)
Identifying sepsis quickly allows for early goal-directed therapy, potentially reducing the patient’s mortality

Screening patients for sepsis, severe sepsis, or septic shock1

Severe sepsis

Septic shock

Suspected or documented infection plus some of the following:

Criteria from previous column plus any of the following thought to be due to the infection:

All of the criteria from previous columns plus: • sepsis-induced hypotension

• SBP 140 mg/dL in the absence of diabetes)
Inflammatory variables
• white blood cell (WBC) count >12,000/mm3 or 10% immature forms (bands)

• acute lung injury with PaO2/FiO2
2.0 mg/dL
• bilirubin >2 mg/dL
• platelet count 40 mm Hg or less than two standard deviations below normal for age in the absence of other causes of hypotension • plasma C-reactive protein more than two standard deviations above the normal value
• plasma procalcitonin more than two standard deviations above the normal value
Hemodynamic variables
• SBP 60 seconds)
• ileus (absent bowel sounds)
• thrombocytopenia (platelet count 4 mg/dL)
Tissue perfusion variables
• serum lactate >1 mmol/L
• decreased capillary refill or mottling

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Targeted time frames and goals of initial therapy1
Within 1 hour of recognition of severe sepsis or septic shock initiate the following and complete within 3 hours:

Within 6 hours of recognition of severe sepsis or septic shock:

• Obtain blood culture specimens before antibiotic administration.

• Infuse vasopressors (for hypotension that doesn’t respond to initial fluid resuscitation or for abnormally low diastolic
BP) to maintain MAP of 65 mm Hg or greater; I.V. norepinephrine is first choice.

• Obtain serum lactate level.
• Administer broad-spectrum antibiotic (don’t delay more than
45 min for blood cultures).
• Initiate 30 mL/kg isotonic crystalloid fluids for hypotension or lactate level of 4 mmol/L or greater (may use albumin as part of initial fluid resuscitation in patients requiring substantial amounts of crystalloids; avoid hydroxyethyl starches).
• Goals are to achieve MAP of 65 mm Hg and urine output
>0.5 mL/kg/hr.

risk. To illustrate, let’s look at a case study. Recognizing sepsis
Ms. C, 45, embedded a fishhook in her right foot 3 days ago on a fishing excursion with friends. She removed it and didn’t seek emergency care for the injury.
Because she’s been feeling “off” for the last 2 days and her right foot is tender and swollen, a friend brought her to the
ED. The friend reports that Ms. C’s been acting odd and saying “crazy things.”
Assessment reveals a cool, edematous right foot with patches of erythema on the foot and ankle; oral temperature
101° F (38.3° C); heart rate 102; respirations 24; and BP 88/42 (MAP 57).
She’s alert and oriented to person, time, and place but can’t describe her current situation of needing to seek medical attention for her infected foot. She doesn’t remember when she last urinated. Her friend reports she had a tetanus shot last year. An infection in her right foot is suspected and she has signs and symptoms of systemic inflammation (tachycardia, fever, tachypnea, mottling, altered mental status, hypotension, and probable oliguria). Ms. C is identified as having sepsis.
She may have severe sepsis, so the healthcare provider initiates early goaldirected therapy. It’s been 10 minutes since
Ms. C was first suspected of having sepsis.
Initiating goal-directed therapy The SSG recommend early goaldirected therapy for patients suspected • In the event of persistent arterial hypotension despite volume resuscitation (septic shock) or initial lactate of
4 mmol/L or more, measure CVP with a target of 8-12 mm
Hg; measure ScvO2 and target ScvO2 or SvO2 >70% or 65%, respectively. • Remeasure lactate if initial level was elevated.

of having severe sepsis or septic shock and provide targeted time frames and goals for these interventions. Early sepsis management is considered to be similar to management of polytrauma, acute myocardial infarction, or stroke, where the speed and appropriateness of therapy administered in the initial hours are likely to influence the patient’s outcome.1 (See Targeted time frames and goals of initial therapy.)
Upon recognizing severe sepsis or septic shock:
• obtain at least two sets of blood cultures using aerobic and anaerobic bottles before starting I.V. antibiotics.
• determine the serum lactate level.
• administer broad-spectrum antibiotics within 1 hour of recognition of severe sepsis or septic shock; antibiotic administration shouldn’t be delayed more than 45 minutes to obtain the blood cultures.
• initiate isotonic crystalloid fluid resuscitation at 30 mL/kg to treat hypotension or a lactate level of 4 mmol/L or greater.1
Initiating therapy for Ms. C
Within 1 hour after clinicians recognize severe sepsis in Ms. C, peripheral venous access is obtained and specimens are drawn for blood cultures, serum lactate level, basic metabolic panel, complete blood cell count and differential, prothrombin time/international normalized ratio (PT/INR), and an activated partial thromboplastin time (aPTT). An I.V.

broad-spectrum antibiotic is administered for the suspected foot infection. An infusion of 0.9% sodium chloride solution is initiated at a rate of 1,000 mL every 30 to 60 minutes to a total of 3 L (3,000 mL) in 3 hours (Ms. C weighs 220 lb
[100 kg] so she receives 30 mL/kg). Her
BP is assessed frequently, focusing on achieving a MAP of 65 mm Hg or greater. Because Ms. C couldn’t recall her last void and she’s hemodynamically unstable, an indwelling urinary catheter is inserted to closely monitor her urine output. Initial resuscitation goals for Ms. C include a urine output of 0.5 mL/kg/hr or more and a MAP of 65 mm Hg or greater.
At the 2-hour mark after severe sepsis was recognized, Ms. C’s BP is 92/36 (MAP
55), she’s receiving the third liter of 0.9% sodium chloride solution, her urine output is 0.3 mL/kg/hr, and her initial lactate level is 4.5 mmol/L (normal, 0.5 to
1.5 mmol/L). Lactic acidosis is generally defined as a plasma lactate concentration greater than 4 mmol/L, even without overt acidemia.2 Because she isn’t responding to fluid resuscitation and her MAP and urine output remain low, the healthcare provider prescribes I.V. vasopressor therapy using a norepinephrine infusion to achieve a MAP of 65 mm Hg. Meanwhile, the initial fluid resuscitation continues at 30 mL/kg. Once this is complete, the healthcare provider prescribes another infusion of 0.9% sodium chloride solution at 100 mL/hr. Because
Ms. C’s been started on vasopressors, the
ICU is notified of a probable admission and possible central venous catheter
(CVC) placement.
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Ms. C’s vital signs are reviewed, particularly her BP of 92/36 (MAP 55).
The abnormally low diastolic pressure creates a wide pulse pressure (the difference between the systolic and diastolic
BP normally one-third the systolic). Ms.
C’s pulse pressure is 56 mm Hg (92-36).
Her pulse pressure should normally be one-third the systolic BP or 30 (92 ÷ 3).3
In sepsis as well as other systemic inflammatory syndromes, the arterioles and capillary beds vasodilate, resulting in a widened pulse pressure and at times a low diastolic pressure.
As the capillary beds dilate, fluid leaks into the interstitial spaces, resulting in an intravascular volume deficit. The dilated capillary beds and resulting dehydration impair oxygen delivery to the tissues and promote intravascular thrombosis.3 Early goaldirected therapy focusing on fluid resuscitation at 30 mL/kg restores circulating blood volume, increases tissue perfusion, and lessens the chance of thrombus formation. If fluid fails to restore an adequate BP
(MAP of 65 mm Hg or more), I.V. vasopressors such as norepinephrine are added to constrict the arteriole beds and restore homeostasis.
Ms. C is transferred to the ICU, a triple-lumen CVC is placed in her right subclavian vein, and a central venous pressure (CVP) reading of 6 mm Hg is

amounts of crystalloids to restore circulating volume, a colloid such as albumin may be added. Hydroxyethyl starches should be avoided.

Norepinephrine is recommended as the first-line vasopressor if fluid fails to restore an adequate BP. obtained. The SSG recommend a target
CVP reading of 8-12 mm Hg to indicate adequate circulating volume.1
Fluid continues to leak into the interstitial spaces, requiring Ms. C to continue receiving fluid replacement and I.V. norepinephrine to restore hemodynamic stability. As Ms. C is receiving substantial

Sorting out causes of altered ScvO2 or SvO25,8
Low ScvO2 or SvO2

High ScvO2 or SvO2

Low delivery

High delivery

• low hemoglobin

• excessive oxygen

• low cardiac output
• low FiO2

• increases in cardiac output, hemoglobin, SaO2, PaO2

High consumption

Low consumption

• positive inotropic drugs (norepinephrine, epinephrine, dobutamine, dopamine)

• tissue extraction failure– cell death

• agitation, shivering

• hypothermia

• pain

• anesthesia or sedation

• increased work of breathing
• nursing interventions (such as bathing and turning)
• seizures
• infection and sepsis
• noisy environment

When fluids fail
Norepinephrine is recommended as the first-line vasopressor if fluid fails to restore an adequate BP1 Norepi. nephrine is a strong alpha-adrenergic receptor agonist that causes peripheral arteriolar vasoconstriction.4 This action slows the leakage of fluid into the interstitial spaces and helps maintain circulating blood volume. Norepinephrine also acts on the beta1 receptors in the heart, increasing myocardial contractility and heart rate.4 This may increase oxygen consumption by the tissues, so the patient’s oxygen saturation and response to therapy must be closely monitored.
To gauge the patient’s oxygen consumption, the healthcare provider may want to measure central venous oxygen saturation (ScvO2) using blood obtained from the CVC distal port. ScvO2 is an indicator of tissue perfusion and reflects the percentage of oxygen being returned to the right side of the heart after tissue consumption.5 The target ScvO2 for Ms. C is
70%. An abnormally low or high
ScvO2 or mixed venous oxygen saturation (SvO2) should be evaluated for cause. (See Sorting out causes of altered
ScvO2 or SvO2.)
One hour after starting the norepinephrine infusion (4 hours since severe sepsis was identified), a venous blood gas sample and a lactate level are obtained from the distal port of Ms. C’s CVC. Her
ScvO2 is 68% and her lactate level has dropped to 2.8 mmol/L; both values indicate improving tissue perfusion. Her skin is warm and moist, her urine output is
0.8 mL/kg/hr, and she’s asking the staff why she’s in the hospital, indicating improving mental status. Over the next few days, Ms. C is continually monitored for signs and symptoms of improvement in clinical status and deterioration into septic shock.
Early identification and rapid goal-directed therapy to treat severe

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sepsis in the first 6 hours from identification are essential to reducing mortality. Ms. C’s severe sepsis was identified early, her altered tissue perfusion corrected with rapid administration of I.V. antibiotics, I.V. fluids, and the addition of an I.V. vasopressor when fluid failed to maintain the targeted MAP of 65 mm Hg and CVP of 8-12 mm Hg.
The healthcare provider may discontinue antibiotic therapy using procalcitonin levels or similar biomarkers. Procalcitonin levels that drop to 0.5 mcg/L or by more than
80% to 90% from baseline have been used as a marker for timing antibiotic discontinuation.6 The SSG offer supportive therapy recommendations for patients who continue to deteriorate or who don’t respond to early goal-directed measures. Other hemodynamic therapies that may be added include additional vasopressors and inotropic agents
(see Vasopressors and inotropic choices for managing sepsis).
In the 2008 SSG, dopamine was recommended as a substitute for norepinephrine.7 Dopamine is now recommended only as an alternative to norepinephrine in cases where the risk of tachydysrhythmias is low or the patient is experiencing bradycardia.1 Additional hemodynamic support includes adding I.V. hydrocortisone daily if the patient fails to achieve hemodynamic stability with
I.V. fluids and vasopressors.1 Because
Ms. C achieved hemodynamic stability with fluids and vasopressors, she didn’t need a course of hydrocortisone. Other recommendations to support the care of the patient with severe sepsis after the first 6 hours are outlined in the guidelines. Recommendations for transfusing packed red blood cells after tissue hypoperfusion has resolved and in the absence of extenuating circumstances (myocardial ischemia, acute hemorrhage, severe hypoxemia, or myocardial infarction) include a hemoglobin level less than
7 g/dL. For patients with severe sepsis, Vasopressors and inotropic choices for managing sepsis1,4
I.V. vasopressors in order of initiation

Add I.V. inotropic therapy

• norepinephrine

Dobutamine is suggested to be administered or added to vasopressor support when patient shows signs of myocardial dysfunction as suggested by elevated cardiac filling pressures and low cardiac output, or ongoing signs of hypoperfusion, despite achieving adequate intravascular volume and adequate MAP.

• epinephrine added to or substituted for norepinephrine • vasopressin added to norepinephrine to increase
MAP or decrease norepinephrine dose
• dopamine substituted for norepinephrine only in patients with low risk for tachydysrhythmias or experiencing bradycardia
• don’t use low-dose dopamine to increase renal perfusion • use phenylephrine only if patient is experiencing serious dysrhythmias known to have been caused by norepinephrine, cardiac output is known to be high and BP persistently low, or as salvage therapy when combined inotrope/vasopressor drugs and low-dose vasopressin have failed to achieve MAP target

prophylactic platelet transfusions are recommended only if the platelet count is 10,000/mm3 or less in the absence of severe bleeding, or 20,000/ mm3 or less for a high risk of bleeding. For patients who are actively bleeding, going to surgery, or having another invasive procedure, the guidelines suggest platelet transfusion for counts of 50,000/mm3 or less.1
In the past, immune-modulating nutritional supplements such as I.V. selenium and the administration of
I.V. immunoglobulins have been tried to improve sepsis outcomes.
Neither of these interventions is recommended in the 2012 SSG.
The administration of recombinantactivated protein C is discussed in the guidelines but isn’t available for administration since its withdrawal from the market.1
Supportive recommendations
For severely ill patients with sepsis who may need mechanical ventilator support, the guidelines provide ventilator strategies for reducing mortality from sepsis-induced acute respiratory distress syndrome. The guidelines recommend using the least amount of sedation and avoiding administration of neuromuscular blocker agents

to patients with sepsis who are receiving mechanical ventilation.1
For ICU patients with severe sepsis, the guidelines provide recommendations for glucose control. The
SSG recommend not treating with insulin infusions until two consecutive glucose readings are above 180 mg/dL. Glucose control is targeted at maintaining the blood glucose level at less than 180 mg/dL and monitoring blood glucose every 1 to 2 hours until glucose values and insulin infusion rates are stable, and then every
4 hours thereafter.1
Other recommendations address managing patients who may need dialysis, bicarbonate administration, stress ulcer prophylaxis, prevention of deep vein thrombosis (DVT), and nutrition. • In patients who require renal replacement therapy for acute renal failure, continuous renal replacement therapies and intermittent hemodialysis are seen as equivalent.
• The guidelines recommend against treating sepsis-induced lactic acidemia with bicarbonate therapy for pH levels greater than or equal to 7.15.
• The guidelines support preventing
DVT by administering prophylactic anticoagulation with subcutaneous
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low-molecular-weight heparin or unfractionated heparin.
• The guidelines also support the use of intermittent pneumatic compression devices, both for patients receiving prophylactic anticoagulation and for those with contraindications to anticoagulant therapy.
• The guidelines support administration of proton pump inhibitors or
H2 blockers to prevent stress ulcers in patients with severe sepsis/septic shock who have risk factors for bleeding. • Nutritional support (oral or enteral nutrition) should be started within
48 hours of recognizing severe sepsis in combination with low-dose I.V. glucose (up to 500 kcal/day) for the first week. If the patient requires parenteral nutrition, the guidelines recommend combining it with enteral feedings.1 The final supportive recommendation involves guidelines for setting goals of care. As sepsis is associated with high mortality, the guidelines recommend discussing and setting


goals of care (including end-of-life care) with the family and patient as soon as possible but no longer than
72 hours after admission.1
Ms. C’s tissue perfusion continued to improve and she was weaned off her vasopressor support on day 3 in the
ICU. On day 4 she was transferred to the medical-surgical unit and her antibiotic therapy was transitioned to oral preparations. Her central line was discontinued and her urinary catheter was removed. She was discharged home on oral antibiotics on day 6 following admission. Timing is key
Early identification and initiation of goal-directed therapies for sepsis are essential for reducing mortality. By learning how to identify and screen every potentially infected patient for sepsis, nurses can save lives. ■

2. Emmett M. Causes of lactic acidosis. UpToDate.
3. Carlson B. Fitzsimmons L. Shock, sepsis, and multiple organ dysfunction syndrome. In: Urden
LD, Stacy KM, Lough ME. Critical Care Nursing:
Diagnosis and Management. 7th ed. St. Louis, MO:
Mosby; 2014.
4. Micromedex.
5. Headley JM, Giuliano KK. Continuous venous oxygen saturation monitoring. In: Lynn-McHale
Weigand D, ed. AACN Procedure Manual for
Critical Care. 6th ed. St. Louis, MO: Saunders;
6. Schuetz P, Chiappa V, Briel M, Greenwald JL.
Procalcitonin algorithms for antibiotic therapy decisions: a systematic review of randomized controlled trials and recommendations for clinical algorithms. Arch Intern Med. 2011;171(15):13221331.
7. Dellinger RP, Levy MM, Carlet JM, et al. Surviving sepsis campaign: international guidelines for management of severe sepsis and septic shock:
2008. Intensive Care Med. 2008;34(1):17-60.
8. Preuss T, Lynn-McHale Weigand D. Blood sampling from a central venous catheter In:
Lynn-McHale Weigand D, ed. AACN Procedure
Manual for Critical Care. 6th ed. St. Louis, MO:
Saunders; 2011.
Julie Miller is staff development educator in critical care at Trinity Mother Frances Hospitals and Clinics in
Tyler, Tex.

1. Dellinger RP, Levy MM, Rhodes A, et al. Surviving sepsis campaign: international guidelines for management of severe sepsis and septic shock:
2012. Crit Care Med. 2013;41(2):580-637.

The author and planners have disclosed no potential conflicts of interest, financial or otherwise.

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