Sepsis chapter - Philadelphia University



Care of the Patient with Sepsis

Learning Outcome 1

1. Sepsis is a potentially life-threatening complication of an infection. Sepsis occurs when chemicals released into the bloodstream to fight the infection trigger inflammatory responses throughout the body. This inflammation can trigger a cascade of changes that can damage multiple organ systems, causing them to fail.

2. Recognition of the patient with sepsis.

This first phase of sepsis process has been described as the presence of two or more of the following indicators:

• Temperature greater than 38◦C (100◦F) or less than 36◦C (96.8◦F)

• Pulse greater than 90 beats per minute

• Respiratory rate greater than 20 breaths/minute or PaCO2 less than 32

• White blood cells (WBCs) greater than 12,000/mm3 or less than 4,000/mm3

Figure 18-4 Possible sources of infection in the hospitalized patient with sepsis.

[pic]

3. Recognition of the patient with septic shock

Septic shock is defined as the presence of sepsis and refractory hypotension. Refractory hypotension is:

• systolic BP of less than 90 mm Hg,

• MAP of less than 65 mm Hg (MAP= systolic pressure + 2×diastolic/3) normally 70-105 mm Hg, or

• Decrease of 40 mm Hg in systolic BP that is unresponsive to a crystalloid fluid challenge of 20 to 40 mL/kg.

Learning Outcome 2

Describe evidence-based prevention strategies for ventilator associated pneumonia (VAP), central venous catheter site infections, and surgical site infections.

1. Hospital-acquired infections are associated with increased lengths of hospital stay as well as increased costs. Therefore, nurses and other health care providers need to be vigilant about utilizing evidence-based practices to prevent nosocomial infections.

2. Prevention of ventilator associated pneumonia (VAP)

• Airway infection that develops at least 48 hours after a patient is intubated

• VAP prolongs illness and hospitalization.

• VAP results in more time on the ventilator and more ICU days.

• VAP is the leading cause of death from hospital-acquired infections.

• Occurrence of VAP can be reduced by implementing evidence-based practices or bundles.

• Early recognition and treatment of VAP is also very important.

3. Prevention of VAP

• The institute of health care improvement (IHI) recommends implementation of the ventilator bundle (a series of interventions related to ventilator care that, when implemented together, will achieve significantly better outcomes than when implemented individually):

• American Association of Critical Care Nurses Endotracheal Tube and Oral Care

|Washed Hands, and don personal protective equipment. |

|Ensure that endotracheal tube is connected to ventilator using a swivel adapter. |

|Support the endotracheal tube and tubing as needed. |

| If suctioning is clinically indicated hyperoxygenate and Suction endotracheal tube. |

|Loosen and remove old tape and ties. |

|If patient is nasally intubated, clean around endotracheal tube using saline-soaked gauze or cotton swabs .Proceed to step 8. |

|If patient is intubated orally, remove bite-block or oropharyngeal airway (acting as bite-block). Proceed to step 8. |

|Perform oral hygiene, using Pediatric toothbrush or Adult (soft) toothbrush at least twice a day. Gently brush patient's teeth to |

|clean and remove plaque from teeth. (Level IV: Limited clinical studies to support recommendations.) |

|In addition to brushing twice daily, use oral swab with 1.5% hydrogen peroxide solution to clean mouth every 2 to 4 hours. With |

|each cleansing, applying a mouth moisturizer to the oral mucosa and lips to keep tissue moist. (Level IV: Limited clinical studies |

|to support recommendations.) |

|Suction oral cavity/pharynx frequently. |

|Move oral tube was to the other side of the mouth. Replace bit-block or oropharyngeal airway (to act as bite-block) along the |

|endotracheal tube if necessary to prevent biting, minimize pressure areas on lips, tongue, and oral cavity. |

|Ensured proper tube cuff inflation using minimal leak volume or minimal occlusion volume. |

|Reconfirm tube placement, and note position of tube at teeth or naris (common tube placement at teeth is 21 cm for women and 23 cm |

|for men). |

|Secure the endotracheal tube in place (according to institutional standard) ( to prevent inadvertent dislodgment of the tube) |

|Patient Monitoring and Care |

|Keep the head of the bed elevated at least 30 degree unless contraindicated. |

|Suctioning endotracheal tube if clinically indicated. |

|The nurse monitored the amount, type and color of secretions. |

|If patient is nasally intubated, the nurse monitor for nasal drainage. |

|Assesses the oral cavity and lips at least every 8 hours, and perform oral care (as outline in step 8 and 9) every 2 to 4 hours and|

|as needed. |

|With oral care, assess for buildup of plaque on teeth or potential infection related to oral abscess. |

|Reconfirm tube placement, and note position of tube at teeth or naris. Retape or secure endotracheal tube every 24 hours and as |

|needed for soiled or loose securing devices. |

•

4. Prevention of central venous catheter–related infections

Central venous catheters (CVCs) are being used more frequently in patient care. Compared to peripherally inserted catheters, CVCs carry a significantly greater risk of infection, accounting for nearly 90% of catheter-related bloodstream infections. The IHI advocates the use of the central line bundle, a group of evidence-based interventions for patients with intravascular catheters that, when implemented together, result in better outcomes than when implemented individually.

5. Prevention of catheter-related infections

The central line bundle includes:

• Hand hygiene

• Maximal barrier precautions upon insertion of CVCs

• Chlorhexidine skin antisepsis

• Optimal catheter site selection

• Daily review of line necessity and removal of the CVC as early as possible

6. Prevention of surgical site infections

• Surgical site infections are common, and patients who develop them are 60% more likely to spend time in the ICU, more time in the hospital, and are twice as likely to die than those who do not develop surgical site infections.

• Two methods are advocated for the prevention of surgical site infections:

• Administration of an appropriate antibiotic for an appropriate length of time

• Clipping rather than shaving the surgical site

Learning Outcome 5

Compare and contrast the use of three vasoactive medications in the management of septic shock.

❖ Vasopressors’ usefulness in septic shock

• Vasopressors used without inadequate fluid resuscitation can worsen organ perfusion by promoting severe vasoconstriction.

• May increase BP and perfusion to some organs at expense of others (intestines/kidneys).

• Choice of drug varies according to institution and physician.

1. Dopamine

• Increases MAP by increasing stroke volume and heart rate.

• Effect begins within 2 to 5 minutes.

• With moderate to high doses, it will increase heart rate and cause pronounced vasoconstriction.

• Should be administered via large peripheral vein or CVC because extravasation may cause severe irritation, necrosis, or sloughing of tissue.

2. Norepinephrine

• Results in a significant increase in MAP with little change in heart rate or cardiac output.

• More effective than dopamine at reversing hypotension in septic shock patients resistant to fluid resuscitation.

• Effect begins within 1 to 2 minutes of IV administration.

• Should be administered via CVC because of risk associated with extravasation.

3. Vasopressin

• Increases MAP without increasing cardiac index or heart rate.

• Effect should be noticed within 1 hour of beginning continuous infusion of vasopressin @ 0.04 units/min.

• Some studies indicate that it decreased cardiac output in patients with septic shock.

• At high doses, it has caused arrhythmias, bradycardia, hypertension, MI, and abdominal cramping.

• Overdose may cause water intoxication.

Learning Outcome 7

Evaluate methods used to reduce fever in a febrile patient.

Concepts for Lecture

Most patients with sepsis are febrile and may experience discomfort from fever or from the efforts of health care providers to reduce the fever. Uncomplicated fever is an important immunologic defense mechanism. Therefore, attempts are only made to actively reduce a fever in specific situations, which include:

• Severely elevated fever

• The patient is very uncomfortable

• The patient has a neurological disorder

• The patient is post cardiac arrest

• The patient is at risk for or is compromised by the fever

Fever is most often treated when it exceeds 39◦C (102◦F).

1. Interventions for fever

• Use of antipyretic drugs

o Acetaminophen

o Ibuprofen

• External cooling (hypothermia) blanket

o Continual assessment of core temperature

o Should be turned off when the patient’s temperature is about 1◦C above desired

Learning Outcome 8

Explain the process of disseminated intravascular coagulation.

1. DIC is not a common complication of hospitalized patients. However, it occurs in as many as 30–50% of patients with sepsis. Sepsis is the most common cause of DIC, but other precursors to DIC include:

• Trauma

• Burns

• Obstetrical complications

• Emboli

• Immunological disorders—transfusion reactions, rheumatoid arthritis, and lupus

• Malignancies

• Shock accompanied by acidosis

2. Disseminated intravascular coagulation (DIC)

• Systemic activation of the coagulation cascade

• Extrinsic pathway activated by massive tissue destruction.

• Intrinsic pathway activated by endothelial cell injury.

• Excess production of thrombin activates fibrinogen, which ( fibrin.

• Fibrin deposits in microcirculation (obstruction of blood vessels and tissue ischemia.

• As fibrin deposits are formed, platelets and coagulation factors are consumed and the patient begins to bleed.

• Bleeding may increase as clots are lysed and fibrin degradation products (anticoagulants) are released.

• Results in both thromboses and hemorrhagic complications.

• [DIC progression]

• [pic]

3. Assessment of the patient with DIC

• Patients may present with either signs of bleeding or symptoms from systemic microemboli.

• Signs of systemic microemboli:

o Cyanosis and/or gangrene, especially of the digits; patient may complain of pain.

o Diminished pulses

o Change in level of consciousness or CVA

o Signs of renal failure and pain at the costovertebral angle

o Abdominal pain and diminished or absent bowel sounds may indicate an ileus or a bowel infarction.

• Signs of bleeding:

o Oozing or bleeding from IV sites, arterial lines, urinary catheters, surgical sites, gastrointestinal tract, and mucous membranes (gums)

o Ecchymoses on the palate, gums, and skin

o Hemoptysis caused by bleeding in the lungs

o Hematuria

4. Diagnosis of DIC

Based on presence of underlying disorder that leads to DIC, clinical presentation, and laboratory values

• Assessment: laboratory findings in DIC

• Platelet count:

o Normal value is 150,000–400,000.

o 50,000 or less is suggestive of DIC.

o A drop of 50% from baseline is also suggestive of DIC.

• Fibrin degradation products

o Normal value is less than 10 mcg/mL.

o 40 mcg/mL or greater (or rising values) suggests DIC.

• D-dimer:

o Normal value is less than 250 ng/mL.

o May result any time a large clot is being dissolved.

o Less sensitive than fibrin degradation products (FDPs).

• Fibrinogen:

o Normal value is 200–400 mg/dL.

o Value less than 100 or falling values suggest DIC.

• Prothrombin time:

o Normal value is 11–12.5 seconds.

o Any elevation suggests DIC.

• Activated partial thromboplastin time:

o Normal value is 30–40 seconds.

o Prolonged values suggest DIC.

o Critical values are greater than 70 seconds.

5. Management of DIC

• Identify and treat the underlying disorder or the trigger for DIC.

• Restore the balance of clot formation, dissolution, and inhibition.

o Platelet replacement

o Cryoprecipitate(a precipitate such as from blood plasma, which separates out on freezing and thawing) (for fibrinogen < 100 mg/dL)

o Fresh frozen plasma (contains clotting factors)

• Heparin to decrease consumption of clotting factors and slow the process of DIC

6. Management of DIC

• Support organ perfusion and function.

o IV fluids to maintain adequate vascular volume and tissue perfusion

o Administration of packed red blood cells if indicated by low hemoglobin

7. Management of DIC

• Support organ perfusion and function.

o Monitor hemodynamics: blood pressure, heart rate, CVP or PAWP, and oxygen saturation at least every 2 hours or more often.

o Notify the physician if the heart rate changes more than 10% from baseline or if the MAP drops below a specified level (usually 65 to 70 mm Hg).

8. Management of DIC

• Assessment of organ integrity

o Glasgow Coma Scale for neurological screening

o Urine output measured every 2 hours; daily serum creatinine

o Assess adequacy of peripheral perfusion (pulses, sensations, movement, capillary refill, and warmth).

9. Management of DIC

• Prevention of injury

• Avoid unnecessary invasive devices

• Assure hemostasis at discontinued IV sites by holding pressure for 3 to 5 minutes

Nursing Diagnosis: Infection related to microorganism invasion into the body.

Long Term Goals: The patient will have negative cultures following antibiotic therapy; temperature < 100°F; HR 60-100 beats/min; and  MAP >70 mmHg.

|Outcome/ Short Term |Planning/Interventions |Rationale |Evaluation |

|Patient-Centered Goals | | | |

|The patient will be free |Wash hands before and after each patient care |To decrease risk of |*Patient’s temperature is  |

|of infection as evidenced|activity. |nosocomial infection or |< 100°F; cultures remain |

|by negative cultures. | |transmission of |negative. |

|Blood glucose will | |infection. |*The infection is not |

|remain  | | |transmitted to other |

|< 150 mg/dL. | | |patients on the unit. |

|  |Obtain blood, sputum, urine and wound cultures |To locate and identify |*Positive cultures will |

| |upon initial suspicion of onset of sepsis. |the source of infection. |emerge within 24-48 hours |

| | | |for identification of |

| | | |offending organism. |

|  |Use strict aseptic technique when handling |To decrease risk of |*The patient remains free of|

| |invasive lines and equipment. |nosocomial infection. |signs or symptoms of line |

| | | |infections; Afebrile. |

|  |Initiate broad spectrum antibiotics early and |Broad spectrum |*The patient will have |

| |change to narrow spectrum when culture results |antibiotics are intended |negative cultures after |

| |are known. |to work against a wide |treatment with appropriate |

| | |array of organisms, |antimicrobial treatment. |

| | |however, it is most | |

| | |prudent to utilize a | |

| | |narrow spectrum | |

| | |antibiotic for treatment | |

| | |once the specific | |

| | |organism has been | |

| | |identified. | |

Date: Nursing Care Plan

Patient Initials:            

Nursing Diagnosis:            Decreased cardiac output related to abnormal inflammation,

Long Term Goals: The patient will experience hemodynamic stability as evidenced by thrombosis and fibrinolysis MAP >65mmHg; HR 60-100 beats/min; CVP 8-12.

|Outcome/ Short Term |Planning/Interventions |Rationale |Evaluation |

|Patient-Centered Goals | | | |

|The patient will exhibit |Assess patient’s HR, BP and hemodynamic |Hemodynamic parameters reveal |*HR remains 60-100 |

|signs of adequate perfusion: |parameters every hour and after |information about adequacy of |beats/min. |

|    * MAP > 65 mmHg |interventions. |fluid volume status and tissue|*MAP > 65 mmHg. |

|    *CVP 8-12.  |  |perfusion. |*CVP 8-12. |

|    *HR 60-100 beats/min.    |Obtain serum lactate levels. |Serum lactate levels can be  | |

| | |indicative of decreased tissue| |

| | |perfusion (and organ | |

| | |dysfunction). | |

|The patient will exhibit |Administer fluid resuscitation to |Fluid replacement should occur|*The patient will maintain |

|signs of improvement in |maintain MAP > 65 mmHg and CVP 8-12. |prior to treatment with |MAP > 65 mmHg. |

|cardiac output: | |vasopressors. | |

|    *MAP > 65 mmHg. | | | |

|    *HR 60-100 beats/min. | | | |

|  |Administer vasopressors if necessary to |Norepinephrine or dopamine via|MAP > 65 mmHg. |

| |maintain MAP > 65 mmHg. |a central line are first | |

| | |vasopressors of choice (to | |

| | |increase vascular tone and BP)| |

| | |followed by epinephrine. | |

|  |Administer drotrecogin alfa (XIGRIS) |To reduce mortality; It |*The patient has capillary |

| |therapy for patients at high risk of |reduces development of |refill < 3 seconds. |

| |death. |microthrombi. |*Skin is warm, dry and |

| | | |pink. |

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Visual Map Infection, Sepsis, and Disseminated Intravascular Coagulation

Visual Map Septic Shock and Disseminated Intravascular Coagulation

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