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Adult Sepsis Nursing Competency

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Presentation on theme: "Adult Sepsis Nursing Competency"— Presentation transcript:

1 Adult Sepsis Nursing Competency
Jonna Bobeck BSN, RN, CEN

2 Competency Instructions
Listen to Competency Read linked policies/guideline Read article Print test and complete. Return test to Clinical Education

3 What is Sepsis? Systemic Inflammatory Response Syndrome (SIRS) Sepsis
Severe Sepsis Septic Shock Systemic inflammatory response syndrome criteria includes: temperature >100.4F or <98.6F, heart rate >90bpm, respiratory rate >20 breaths per minute, and WBC count > 12,000 or <4000 or >10% immature forms. Sepsis is defined as two or more SIRS criteria plus suspected or proven infection. Severe Sepsis is sepsis plus sepsis induced organ dysfunction or tissue hypoperfusion : hypotension, hypoxemia, oliguria, thrombocytopenia, hyperbilirubinemia, elevated lactate, altered mental status, and acidosis. Septic shock is defined as severe sepsis plus persistent arterial hypotension despite adequate volume resuscitation: Systolic blood pressure ,90mm hg Mean arterial pressure < 70mm hg >40% decrease in systolic blood pressure from patient’s baseline

4 The Sepsis Continuum Sepsis SIRS Severe Septic Shock SIRS with a
A clinical response arising from a nonspecific insult, with 2 of the following: T >38oC or <36oC HR >90 beats/min RR >20/min WBC >12,000/mm3 or <4,000/mm3 or >10% bands SIRS with a presumed or confirmed infectious process Sepsis with organ failure Refractory hypotension

5 Epidemiology of Sepsis
Sepsis in the United States Major cause of Morbidity and Mortality Leading cause of death in non-cardiac ICU in US 10th leading cause of death overall Annually in >200,000 sepsis deaths Average cost per patient is $60,000 Average annual cost to health care system = 16.7 billion Average hospital length of stay is 19.6 days Severe sepsis, the leading cause of death in America's non-coronary intensive care units, is a rapidly growing problem in the United States in terms of the number of patients afflicted by the condition and the complexity of their cases There are approximately 750,000 new sepsis in the US cases each year, with at least 210,000 fatalities. More than 500 patients die of sepsis on a daily basis. The average cost per patient is approximately $60,000 with the annual cost to the US healthcare system being 16.7 billion. As medicine becomes more aggressive, with invasive procedures and immunosuppression, the incidence of sepsis is likely to increase even more.

6 Surviving Sepsis Campaign (SSC)
A collaboration of three leading professional organizations Efforts to improve treatment and decrease mortality Click below to visit SSC website: The Surviving Sepsis Campaign (SSC) is the first initiative of its kind to bring together three leading professional organizations in the field of sepsis: the European Society of Intensive Care Medicine, the Society of Critical Care Medicine, and the International Sepsis Forum. The purpose of the SSC is to create an international collaborative effort to improve the treatment of sepsis and reduce the high mortality rate associated with the condition.

7 Early Goal Directed Therapy
Early initiation of supportive care to correct physiologic abnormalities, such as hypoxemia and hypotension [6-9]. Distinguishing sepsis from systemic inflammatory response syndrome (SIRS) (table 1 and table 2) because, if an infection exists, it must be identified and treated as soon as possible (table 3). This may require a surgical procedure (eg, drainage), as well as appropriate antibiotics. EARLY MANAGEMENT — The first priority in any patient with severe sepsis or septic shock is stabilization of their airway and breathing. Next, perfusion to the peripheral tissues should be restored [7,10].

8 Therapy Across the Sepsis Continuum
SIRS Severe Septic Shock Insulin and tight glucose control across the continuum, antibiotics and source control with suspected infection. Early goal directed therapy for sepsis, severe sepsis, and septic shock and xigris when indicated. Early Goal Directed Therapy Antibiotics and Source Control Insulin and tight glucose control

9 Sepsis Management Guidelines
Initial resuscitation (first 6 hours) Begin immediately for elevated lactate or hypotension Resuscitation goals: CVP 8-12 mmhg MAP > 65mmhg Urine output > 0.5 ml/kg/hr Central venous oxygenation > 70%, mixed venous > 65% Initial resuscitation begins in the emergency department. Once sepsis is recognized early goal directed therapy should begin within 6 hours. Rationale. Early goal-directed resuscitation has been shown to improve survival for emergency department patients presenting with septic shock in a randomized, controlled, single-center study. If the patient presents with hypotension or elevated lactate is resulted begin sepsis resuscitation efforts immediately. The goals of resuscitation are a central venous pressure of 8 – 12 mmhg, mean arterial pressure of greater than or equal to 65mm hg, urine output greater than or equal to 0.5 ml/kg/hr, and central venous in the superior vena cava oxygen saturation greater than or equal to 70% or mixed venous greater than or equal to 65%. If venous oxygen saturation target is not achieved consider further fluid, transfusing PRBC’s, and/or dopamine infusion with a max of 20 mcg/kg/min,

10 Diagnosis Careful history and physical Obtain appropriate cultures
Do not delay antibiotics Obtain blood cultures before starting antibiotic therapy provided this does not significantly delay administration of antibiotics. Obtain two or more blood cultures, one or more should be percutaneous. One or more blood culture should be from each vascular device in place. Additionally, culture other sites as indicated.

11 Antibiotic Therapy Begin as soon as possible Broad-spectrum Reassess
Duration Begin intravenous antibiotics as early as possible, always within the first hour of recognizing sepsis. Broad-spectrum antibiotics are used, one or more agents active against likely bacteria and/or fungal pathogens. Antibiotic therapy should be reassessed daily to optimize efficacy, prevent resistance, avoid toxicity, and minimize costs. Duration of therapy is usually 7 – 10 days, longer if the patients response is slow, undrainable foci of infection, or immunological deficiencies. Therapy should be stopped if the cause is found to be non-infectious.

12 Source Identification and Control
Site of infection Evaluate for focus of infection Source control measures Remove infected devices It is recommended that a specific anatomical diagnosis of infection requiring consideration for emergent source control (e.g., necrotizing fasciitis, diffuse peritonitis, cholangitis, intestinal infarction) be sought and diagnosed or excluded as rapidly as possible and within the first 6 hrs following presentation. All patients presenting with severe sepsis be evaluated for the presence of a focus on infection amenable to source control measures, specifically the drainage of an abscess or local focus on infection, the debridement of infected necrotic tissue, the removal of a potentially infected device, or the definitive control of a source of ongoing microbial contamination. 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. when source control is required, the effective intervention associated with the least physiologic insult be employed (e.g., percutaneous rather than surgical drainage of an abscess. Lastly, when intravascular access devices are a possible source of severe sepsis or septic shock, they be promptly removed after other vascular access has been established.

13 Safe Study and Fluid Therapy
Resuscitate using crystalloids or colloids CVP > 8mmhg Use fluid challenge technique Monitor for overload 1. It is recommended fluid resuscitation with either natural/artificial colloids or crystalloids. There is no evidence based support for one type of fluid over another. the Rationale being The SAFE study indicated that albumin administration was safe and equally as effective as crystalloid. There was an insignificant decrease in mortality rates with the use of colloid in a subset analysis of septic patients. Previous meta-analyses of small studies of ICU patients had demonstrated no difference between crystalloid and colloid fluid resuscitation. Although, the volume of distribution is much larger for crystalloids than for colloids, resuscitation with crystalloids requires more fluid to achieve the same end points and results in more edema. Crystalloids are less expensive. fluid resuscitation should initially target a central venous pressure of 8 mm Hg (12 mm Hg in mechanically ventilated patients). Further fluid therapy is often required. A fluid challenge technique should be applied wherein fluid administration is continued as long as the hemodynamic improvement (e.g., arterial pressure, heart rate, urine output) continues (grade 1D). fluid challenges in patients with suspected hypovolemia should be started with 1000 mL of crystalloids or 300–500 mL of colloids over 30 mins. More rapid administration and greater amounts of fluid may be needed in patients with sepsis-induced tissue hypoperfusion. The rate of fluid administration be reduced substantially when cardiac filling pressures (central venous pressure or pulmonary artery balloon-occluded pressure) increase without concurrent hemodynamic improvement because Fluid challenge must be clearly separated from simple fluid administration; it is a technique in which large amounts of fluids are administered over a limited period of time under close monitoring to evaluate the patient’s response and avoid the development of pulmonary edema. The degree of intravascular volume deficit in patients with severe sepsis varies. With venodilation and ongoing capillary leak, most patients require continuing aggressive fluid resuscitation during the first 24 hrs of management. Input is typically much greater than output, and input/output ratio is of no utility to judge fluid resuscitation needs during this time period.

14 PRH Fluid Therapy Instructions
SIRS/Early Sepsis Bolus 0.9 NS 20ml/kg Sepsis If MAP less than 65 mmHg give 0.9 NS at 20ml/kg as a bolus; repeat x 1 if MAP continues less than 65 mmHg

15 PRH Fluid Therapy Instructions
Severe Sepsis/Septic Shock If MAP less than 65 mmHg give 0.9 NS at 20ml/kg as a bolus; repeat x 1 if MAP continues less than 65 mmHg. If MAP les than 65 mmHg following 40ml/kg then begin: Norepinephrine up to 20mcg/min to maintain MAP >65 Vasopressin 0.04 units/minute to maintain MAP >65

16 Vasopressors Maintain MAP > 65 mm Hg Norepinephrine or dopamine
1. The Surviving Sepsis Campaign recommends that mean arterial pressure (MAP) be maintained 65 mm Hg. Rationale being Vasopressor therapy is required to sustain life and maintain perfusion in the face of life-threatening hypotension, even when hypovolemia has not yet been resolved. Below a certain mean arterial pressure, autoregulation in various vascular beds can be lost, and perfusion can become linearly dependent on pressure. Thus, some patients may require vasopressor therapy to achieve a minimal perfusion pressure and maintain adequate flow. The titration of norepinephrine to as low as MAP 65 mm Hg has been shown to preserve tissue perfusion. In addition, preexisting comorbidities should be considered as to most appropriate MAP target. For example, a MAP of 65 mm Hg might be too low in a patient with severe uncontrolled hypertension, and in a young previously normotensive, a lower MAP might be adequate. Supplementing end points,such as blood pressure, with assessment of regional and global perfusion, such as blood lactate concentrations and urine output, is important. Adequate fluid resuscitation is a fundamental aspect of the hemodynamic management of patients with septic shock and should ideally be achieved before vasopressors and inotropes are used, but using vasopressors early as an emergency measure in patients with severe shock is frequently necessary. When that occurs, great effort should be directed to weaning vasopressors with continuing fluid resuscitation. We recommend either norepinephrine or dopamine as the first choice vasopressor agent to correct hypotension in septic shock (administered through a central catheter as soon as one is available. We suggest that epinephrine, phenylephrine, or vasopressin should not be administered as the initial vasopressor in septic shock. We suggest that epinephrine be the first chosen alternative agent in septic shock that is poorly responsive to norepinephrine or dopamine (grade 2B). Rationale. There is no high-quality primary evidence to recommend one catecholamine over another. Much literature exists that contrasts the physiologic effects of choice of vasopressor and combined inotrope/vasopressors in septic shock (73– 85). Human and animal studies suggest some advantages of norepinephrine and dopamine over epinephrine (the latter with the potential for tachycardia as well as disadvantageous effects on splanchnic circulation and hyperlactemia) and phenylephrine (decrease in stroke volume). There is, however, no clinical evidence that epinephrine results in worse outcomes, and it should be the first chosen alternative to dopamine or norepinephrine. Phenylephrine is the adrenergic agent least likely to produce tachycardia but as a pure vasopressor would be expected to decrease stroke volume. Dopamine increases mean arterial pressure and cardiac output, primarily due to an increase in stroke volume and heart rate. Norepinephrine increases mean arterial pressure due to its vasoconstrictive effects, with little change in heart rate and less increase in stroke volume compared with dopamine. Either may be used as a first-line agent to correct hypotension in sepsis. Norepinephrine is more potent than dopamine and may be more effective at reversing hypotension inpatients with septic shock. Dopamine may be particularly useful in patients with compromised systolic function but causes more tachycardia. 5. We recommend that low-dose dopamine not be used for renal protection Rationale being A large randomized trial and meta-analysis comparing low-dose dopamine to placebo found no difference in either primary outcomes 6. We recommend that all patients requiring vasopressors have an arterial catheter placed as soon as practical ifresources are available. Rationale. In shock states, estimation of blood pressure using a cuff is commonly inaccurate; use of an arterial cannula provides a more appropriate and reproducible measurement of arterial pressure. These catheters also allow continuous analysis so that decisions regarding therapy can be based on immediateand reproducible blood pressure information

17 Inotropic Therapy Dobutamine in patients with myocardial dysfunction
Combined inotrope/vasopressor It is recommended that a dobutamine infusion be administered in the presence of myocardial dysfunction as suggested by elevated cardiac filling pressures and low cardiac output. Rationale being Dobutamine is the firstchoice inotrope for patients with measured or suspected low cardiac output in the presence of adequate left ventricular filling pressure (or clinical assessment of adequate fluid resuscitation) and adequate mean arterial pressure. Septic patients who remain hypotensive after fluid resuscitation may have low, normal, or increased cardiac outputs. Therefore, treatment with a combined inotrope/ vasopressor, such as norepinephrine or dopamine, is recommended if cardiac output is not measured. When the capability exists for monitoring cardiac output in addition to blood pressure, a vasopressor, such as norepinephrine, may be used separately to target specific levels of mean arterial pressure and cardiac output. Two large prospective clinical trials that included critically ill ICU patients who had severe sepsis failed to demonstrate benefit from increasing oxygen delivery to supranormal targets by use of dobutamine (99, 100). These studies did not specifically target patients with severe sepsis and did not target the first 6 hrs of resuscitation. The first 6 hrs of resuscitation of sepsis-induced hypoperfusion need to be treated separately from the later stages of severe sepsis (see Initial Resuscitation recommendations)

18 Glucocorticoids Low-dose glucocorticoids Choice of steroid
Adrenal insuffieiency Prolonged survival For patients with severe septic shock (which we define as a systolic blood pressure <90 mmHg for more than one hour despite both adequate fluid resuscitation and vasopressor administration), we suggest initiation of intravenous corticosteroid therapy within eight hours after the onset of shock (Grade 2B). Response to ACTH testing should not be used to select patients for corticosteroid therapy. (See 'Clinical evidence' above.) We suggest that corticosteroids be administered for five to seven days (Grade 2C). A tapering course is optional; however, close observation of those patients whose steroid therapy is stopped without being tapered is warranted. (See 'Administration' above.) We suggest that fludrocortisone NOT be added to the corticosteroid regimen (Grade 2C). (See 'Administration' above.)

19 Blood Transfusion PRBC’s Oxygen delivery impairment
Target hemoglobin of 7.0 – 9.0 g/dL Red blood cell transfusions — Early goal-directed therapy aggressively utilizes red blood cell transfusions to raise the ScvO2. In the trial discussed above, nearly 70 percent of patients in the early goal-directed therapy group received transfusions, compared to 45 percent in the conventional therapy group [13]. However, other data support a more cautious approach to transfusion in critically ill patients [32]. (See "Use of blood products in the critically ill", section on 'Red blood cells'.) There are several possible explanations for the conflicting data. - Outcome may be related to when a red blood cell transfusion is given. Transfusions administered as part of early goal-directed therapy were given early in the course of illness, whereas studies that support a more cautious approach typically gave transfusions later in the course of illness. - The apparent benefit of red blood cell transfusions may be due to other interventions. In other words, red blood cell transfusion was just one of several interventions during early goal-directed therapy and it is possible that the benefit was due to one or more of the other interventions, not the red blood cell transfusion per se.

20 Scv02 Measure the mixed central venous 02 saturation (Scv02) by obtaining ABG from distal port of CVC line. If Scv02 >70% - therapy achieved If Scv02 is <70% check hematocrit and follow protocol

21 Mechanical Ventilation
Mechanical ventilation of sepsis-induced acute lung injury (ALI)/ARDS Targets Peep Conservative fluid strategies

22 Glucose Control Hyperglycemia associated with poor outcomes
Target glucose 140 – 180mg/dL NICE-SUGAR trial PRH Insulin Order Guideline Hyperglycemia is associated with poor clinical outcomes in critically ill patients. (See 'Effects of hyperglycemia' above.) While most clinicians agree that such glycemic control is a desirable intervention, the optimal blood glucose range is controversial. (See 'Glycemic control' above.) For hyperglycemic critically ill patients: We recommend a blood glucose target of 140 to 180 mg/dL (7.7 to 10 mmol/L), rather than a more stringent target (eg, 80 to 110 mg/dL [4.4 to 6.1 mmol/L]) (Grade 1A). (See 'General approach' above.) We also suggest a blood glucose target of 140 to 180 mg/dL (7.7 to 10 mmol/L), rather than a more liberal target (eg, 180 to 200 mg/dL [10 to 11.1 mmol/L]) (Grade 2C). (See 'General approach' above.) To achieve our target blood glucose, we minimize our use of intravenous fluids that contain glucose and administer insulin only when necessary. A widely accepted insulin regimen has not been established. (See 'General approach' above.) Use of UpToDate is subject to the Subscription and License Agreement. There is insufficient information from randomized controlled trials to determine the optimal target range of blood glucose in the severely septic patient. (1) The NICE-SUGAR trial is the largest most compelling study to date on glucose control in ICU patients given its inclusion of multiple ICUs and hospitals, and a more general patient population. (2) Based on the results of this trial, we recommend against intravenous insulin therapy titrated to keep blood glucose in the normal range ( mg/dl) in patients with severe sepsis. It is clear that attempts to normalize blood glucose with IV insulin during critical illness results in higher rates of hypoglycemia. (1,3) Until additional information is available, teams seeking to implement glucose control should consider initiating insulin therapy when blood glucose levels exceed 180 mg/dL with a goal blood glucose approximating 150 mg/dl as was observed in the beneficial arm of the NICE-SUGAR trial. 1)

23 DVT Prophylaxsis Low molecular weight heparin Mechanical prophylaxis
For patients who are at high risk for DVT use either low dose unfractionated heparin or low molecular weight heparin unless contrindicated. Use mechanical prophylactic devices such anti-embolism stockings or intermittent compression devices.

24 Evaluation for Sepsis Screening Tool
Press Ctrl and click link to view tool: - Surviving Sepsis Campaign There are specific criteria for severe sepsis as distinct from non-severe sepsis. Patients ought to be evaluated for severe sepsis based on these formal criteria when making clinical decisions. This tool provides a simple method to rapidly screen patients in any clinical setting (e.g., in the emergency department, the clinical wards, or the intensive care unit) for appropriateness of enrollment in a severe sepsis treatment protocol.

25 Severe Sepsis Bundles Sepsis Resuscitation Bundle
Sepsis Management Bundle

26 Sepsis Resuscitation Bundle: (To be accomplished ASAP and scored over 6 hours)
Serum lactate measured Blood cultures obtained prior to antibiotic administration From the time of presentation, broad-spectrum antibiotics administered within 3 hours for ED admissions and 1 hour for non-ED ICU admissions In the event of hypotension and/or lactate > 4 mmol/L (36 mg/dl): Deliver an initial minimum of 20 ml/kg of crystalloid (or colloid equivalent) Apply vasopressors for hypotension not responding to initial fluid resuscitation to maintain mean arterial pressure (MAP) > 65 mm Hg In the event of persistent hypotension despite fluid resuscitation (septic shock) and/or lactate > 4 mmol/L (36 mg/dl): Achieve central venous pressure (CVP) of > 8 mm Hg Achieve central venous oxygen saturation (SvO2) of > 70% The Severe Sepsis Bundles are a distillation of the concepts and recommendations found in the practice guidelines published by the Surviving Sepsis Campaign in 2004. The Severe Sepsis Bundles are designed to allow teams to follow the timing, sequence, and goals of the individual elements of care, in order to achieve the goal of a 25 percent reduction in mortality from severe sepsis. Individual hospitals should use the bundles to create customized protocols and pathways specific to their institutions.  However, all of the elements in the bundles must be incorporated in those protocols. The addition of other strategies not found in the bundles is not recommended.  The bundle will form the basis for the measurements that improvement teams will conduct to follow their progress as they make changes. Hospitals should implement two different Severe Sepsis Bundles.  Each bundle articulates requirements for specific timeframes. Sepsis Resuscitation Bundle: Tasks that should begin immediately, but must be done within 6 hours for patients with severe sepsis or septic shock. Sepsis Management Bundle: Tasks that should begin immediately, but must be done within 24 hours for patients with severe sepsis or septic shock. 

27 Sepsis Management Bundle: (To be accomplished ASAP and scored over 24 hours)
Low-dose steroids Activated Protien C - administered in accordance with a standardized ICU policy Glucose control maintained > lower limit of normal, but < 180 mg/dl Inspiratory plateau pressures maintained < 30 cm H2O for mechanically ventilated patients

28 Read Article and Take Test

29 References Surviving Sepsis Campaign, Initials. (2009). Surviving sepsis campaign. Retrieved from Angus, DC, Linde-Zwirble, WT, Lidicker, J, et al. Epidemiology of severe sepsis in the United States: analysis of incidence, outcome, and associated costs of care. Crit Care Med 2001; 29:1303. Bernard, GR, Wheeler, AP, Russell, JA, et al. The effects of ibuprofen on the physiology and survival of patients with sepsis. The Ibuprofen in Sepsis Study Group. N Engl J Med 1997; 336:912. McCloskey, RV, Straube, RC, Sanders, C, et al. Treatment of septic shock with human monoclonal antibody HA-1A. A randomized double-blind, placebo-controlled trial. Ann Intern Med 1994; 121:1. Zeni, F, Freeman, B, Natanson, C, et al. Anti-inflammatory therapies to treat sepsis and septic shock: a reassessment. Crit Care Med 1997; 25:1095. Sasse, KC, Nauenberg, E, Long, A, et al. Long-term survival after intensive care unit admission with sepsis. Crit Care Med 1995; 23:1040. Annane, D, Bellissant, E, Cavaillon, JM. Septic shock. Lancet 2005; 365:63. Dellinger, RP, Levy, MM, Carlet, JM, et al. Surviving Sepsis Campaign: international guidelines for management of severe sepsis and septic shock: Crit Care Med 2008; 36:296. Hollenberg, SM, Ahrens, TS, Annane, D, et al. Practice parameters for hemodynamic support of sepsis in adult patients: 2004 update. Crit Care Med 2004; 32:1928. Practice parameters for hemodynamic support of sepsis in adult patients in sepsis. Task Force of the American College of Critical Care Medicine, Society of Critical Care Medicine. Crit Care Med 1999; 27:639. Sessler, CN, Perry, JC, Varney, KL. Management of severe sepsis and septic shock. Curr Opin Crit Care 2004; 10:354. Luce, JM. Pathogenesis and management of septic shock. Chest 1987; 91:883. Ghosh, S, Latimer, RD, Gray, BM, et al. Endotoxin-induced organ injury. Crit Care Med 1993; 21:S19. Rivers, E, Nguyen, B, Havstad, S, et al. Early goal-directed therapy in the treatment of severe sepsis and septic shock. N Engl J Med 2001; 345:1368.


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