Sepsis Nursing Treatment & Medications

Septicemia

 

Septicemia is a systemic inflammatory response to an infection that causes circulatory dysfunction.  When infections become blood borne and spread throughout the body, capillaries become more permeable, hypotension occurs, coagulation increases, and immune mediators are released. Infections leading to sepsis are usually bacterial but can also be fungal or viral. The term sepsis is often used interchangeable with septicemia and refers to a bloodstream infection. Sepsis can occur with or without organ dysfunction, depending on severity. Sepsis can be further classified as follows:

  • Systemic Inflammatory Response (SIRS): Infection in conjunction with the systemic inflammatory response syndrome.
    • Temperature > 38 C
    • Heart rate > 90 bpm
    • Respiratory rate > 20 bpm
    • WBC > 12,000/mm3
  • Severe Sepsis: Sepsis complicated by organ dysfunction.
  • Septic Shock: Sepsis causing acute circulatory collapse resulting in refractory hypotension unrelieved by intravenous volume resuscitation.

Sepsis is typically associated with a causative condition primarily from the skin, abdomen, lungs, or urinary tract, such as bowel perforation, pneumonia, pyelonephritis, renal abscess, or urosepsis related to a urinary tract obstruction.

CAUSES & PREVELANCE

Sepsis, or septic shock, is associated with direct introduction of pathogenic microorganisms. The most common iatrogenic sources are central or peripheral venous catheters, catheter-associated urinary tract infections (CAUTI), surgical site infections (SSI), and ventilator-associated pneumonia (VAP). Despite only accounting for 2% of hospitalizations in 2008, sepsis caused 17% of all in-hospital deaths. In a hospital setting, 50% of all sepsis cases start as an infection in the lungs. No definitive source is found in 1/3 to ½ of all documented cases.

The rate of hospitalization for septicemia has more than doubled since 2000. The sharp rise in cases has been attributed to microbial resistance due to increased use of antibiotics, greater use of invasive procedures, an aging population with more chronic illnesses, immunosuppressive drugs, chemotherapy, transplantation, increasing microbial resistance to antibiotics, and greater awareness of sepsis resulting in more frequent and accurate medical diagnosis and coding.

PATHOPHYSIOLOGY

The pathophysiology of sepsis is complex and related to the pathogen and its virulence and the patient’s immune status. Sepsis is characterized by a systemic inflammatory response resulting in systemic vasodilatation, hypotension, increased cardiac output and eventual end-organ damage caused by limited oxygen extraction by the tissues. The primary effects come from endogenous cytokine release (i.e. tumor necrosis factor, interleukins) and the inflammatory cascade in response to circulating bacterial products. Impaired pulmonary, hepatic, or renal function may result from excessive cytokine release. Disordered coagulation results in activation of the clotting cascade and a reduction in the natural inhibitors of clotting, such as activated protein C. Once initiated, the process is self-perpetuating without regard to the initial infection. Microcirculatory blood flow is impeded by an increase in thrombosis formation and reduced fibrinolysis (clot breakdown), microcirculatory ischemia, and eventual multiple organ dysfunction (MODS).

The stages of sepsis can be divided as follows:

  • Infectious insult
  • Initial systemic response
  • Overwhelming systemic response
  • Anti-inflammatory reaction
  • Immunomodulatory failure

EPIDEMIOLOGY & PROGNOSIS

Septicemia can quickly become life threatening if not recognized early and treated aggressively. Patients hospitalized for septicemia have twice the average length of stay versus patients hospitalized for other conditions and are eight times more likely to die during their hospitalization. Approximately 30-70% of patients with septic shock die. Patients who survive severe sepsis are more likely to have permanent organ damage including cognitive impairment and physical disability.

Several prognostic assessments exist to stratify sepsis outcomes. Lactate levels have been shown to be directly proportional mortality rate. The APACHE II scale can help classify the severity of the disease by calculating a score based on physiological measurements including: arterial pH, potassium, creatinine, hematocrit, and Glasgow coma scale. Without progression to septic shock, approximately 20-35% of patients still do not survive.

SIGNS & SYMPTOMS

bacterial_infections

Taking an accurate patient history is important in determining the potential source of sepsis. This will help guide essential antimicrobial therapy. Due to the vague nature and systemic progression of sepsis, it is difficult to determine the source without reviewing all systems and performing a thorough physical assessment. Most signs and symptoms relate to hypotension, coagulopathy, infection, and hypoperfusion of organs. The following are general signs and symptoms and special considerations:

  • Fever > 38 C or < 36 C
  • HR > 90 bpm
  • RR > 20 bpm
  • WBC > 12,000/mm3
  • Shaking or chills
  • Altered mental status
  • Oliguria: < 0.5 mL/kg/hour
  • Warm skin with dilatation of the superficial vessels
  • Cold skin with inadequacy of organ perfusion

ASSOCIATED CONDITIONS

  • IV line infection:
    • Almost always central line site vs. peripheral or arterial lines
    • Suspect if other potential sources are eliminated and patient has long-term IV line in place
  • Gastrointestinal or genitourinary infections:
    • Ileus: absent bowel sounds
    • History of pyelonephritis, renal abscess acute prostatitis, or prostatic abscess
    • Abdominal pain suggests pancreatitis or peritonitis
    • Right upper quadrant tenderness suggests gallbladder etiology
    • Right lower quadrant tenderness suggests appendicitis or Crohn’s complications
    • Left lower quadrant tenderness suggests diverticulitis
    • Abnormalities on rectal exam like severe tenderness suggest a prostatic abscess
    • Costovertebral angle tenderness suggests pyelonephritis
    • Elderly may have peritonitis without rebound tenderness of the abdomen
  • Urosepsis: Most common cause of sepsis in pregnancy secondary to obstructed urinary tract
  • Burns
  • Asplenia: No spleen
  • Gastrointestinal Disorders:
    • Intestinal obstruction
    • Gallbladder disease
    • Colon disease
    • Abscess
    • Liver disease
    • GI surgery
  • Ethanol abuse
  • Genitourinary Disorders:
    • Renal calculi
    • Pyelonephritis
    • Urinary tract obstruction
    • Acute prostatitis
    • Prostatic abscess
    • Renal insufficiency
    • GU catheters
  • Diabetes mellitus
  • Lung Disorders:
    • Empyema
    • Lower respiratory tract infection
    • Community-acquired pneumonia
    • Lung abscess
  • Immunocompromised
  • Bacterial endocarditis

DIAGNOSTIC STUDIES

  • Lactate: Marker for cellular hypoxia, normal 0.5-2.2 mmol/L, above 4.0 mmol/L = 27% mortality rate
  • Complete blood count: Anemia, elevated or low white blood cell count, or thrombocytopenia
  • Arterial blood gas: metabolic acidosis and arterial hypoxemia (PaO2/FiO2 < 300 mmHg)
  • Blood Glucose: Septic patients can have > 140 mg/dL without diabetes
  • Creatinine: > 0.5 mg/dL
  • Troponin T: > 0.1 ug/L in 85% of sepsis without coronary syndrome
  • Cultures: Blood, IV catheter tip, or urine cultures on admission before starting antibiotics to determine specific microbial target
  • Gram stain blood: Differentiate between gram positive and gram negative organisms
  • Urinalysis: Perform gram stain and culture
  • C-Reactive Protein: identify presence of inflammation and monitor response to treatment
  • Procalcitonin: Evaluate risk of developing system bacterial infection
  • Presepsin: Early risk stratification
  • Clotting screen: D-dimer and fibrinogen will reveal disseminated intravascular coagulation
  • Chest X-ray: Rule out pneumonia
  • Abdominal CT or MRI: Assess for peritonitis, abdominal abscesses, and renal pathology
  • Abdominal Ultrasound: Exam liver, gall bladder, pancreas, and biliary tract for obstruction
  • Thoracentesis: Patients with significant pleural effusions
  • Paracentesis: Patients with ascites
  • Swan-Ganz catheterization: Guides fluid management and reveals left ventricular dysfunction
  • Invasive investigation: Lumbar puncture, bronchoscopy, laparoscopy, lymph node biopsy

NURSE MANAGEMENT

  • ICU admission for monitoring and treatment
  • Lactate: Obtain initial serum level and regular follow-ups
  • Foley insertion: Monitor urine output closely to guide therapy and fluid replacement, goal > 0.5 mL/kg/hour
  • Intravenous antimicrobials: Cultures followed by broad-spectrum antibiotics given intravenously. Antivirals and antifungals may also be required. Once organism is isolated through lab cultures, the regimen may be targeted for the pathogen. Empirical combination therapy should not last longer than 3-6 days. Reducing to single therapy should be done as soon as the pathogen profile is known:
    • IV line infections: Line removal then meropenem or cefepime
    • MRSA: Linezolid, vancomycin, or daptomycin
    • Biliary tract infections: Imipenem, meropenem, piperacillin-tazobactam, or ampicillin-sulbactam
    • Abdominal and pelvic infections: Imipenem, meropenem, piperacillin-tazobactam, ampicillin-sulbactam, or tigecycline; clindamycin or metronidazole plus aztreonam, levofloxacin, or an aminoglycoside
    • Urosepsis: Aztreonam, levofloxacin, a cephalosporin, or an aminoglycoside
    • Enterococci: Ampicillin or vancomycin;
    • Vancomycin-resistant enterococcal urosepsis: Linezolid or daptomycin;
    • Community-acquired urosepsis: Levofloxacin, aztreonam, or an aminoglycoside plus ampicillin
    • Nosocomial urosepsis: Piperacillin, imipenem, or meropenem
    • Pneumococcal sepsis: Cephalosporins, carbapenem, or vancomycin
    • Sepsis of unknown origin: Meropenem, imipenem, piperacillin-tazobactam, or tigecycline; metronidazole plus either levofloxacin, aztreonam, cefepime, or ceftriaxone
  • Fluid Resuscitation:
    • Crystalloid 30 mL/kg: If hypotensive
    • Crystalloid 4-6 Liters total: Often required for septic shock
    • Colloids IV: Osmotic force may counteract third-spacing from increased capillary permeability, used only when unresponsive to isotonic crystalloids
    • Monitor fluid overload: dyspnea, crackles, JVD, pulmonary edema
  • Transfusions:
    • RBC transfusion: If patient’s hemoglobin falls below 7 g/dL
    • Platelet transfusion: Severe sepsis causes thrombocytopenia, transfuse < 20,000
    • FFP, Fibrinogen, or Cryoprecipitate: Consider with DIC, active bleeding, elevated PT, and decreased fibrinogen
  • External cooling: Fever control which may reduce vasopressor requirements
  • Enteral nutrition: Electrolyte and protein deficiencies are common, do not give parenterally, caution ileus
  • Vasopressors:
    • Indicated for hypotension that does not respond to initial fluid resuscitation
    • MAP > 65 mmHg: Administer fluids & vasopressors
    • CVP > 8 mmHg: Monitor central venous pressure to guide fluid resuscitation and vasopressors
    • ScvO2 = 70%: Monitor central venous oxygen saturation for cellular supply and demand
  • Supplemental oxygen: Monitor respiratory effort closely as respiratory failure is a risk
  • Dialysis: Patient may experience kidney failure
  • Monitor blood glucose: Goal < 150 mg/dL
  • DVT prophylaxis: heparin when not contraindicated, SCD’s
  • Asepsis: Maintain strict aseptic technique
  • Mechanical ventilation:
    • Acute Respiratory Distress Syndrome (ARDS) carries very poor prognosis
    • Tidal volume 5-8 mL/kg
    • Elongated inspiratory time
    • Sufficient PEEP
    • Peak pressure < 30 cmH2O

 

MEDICATIONS

– Norepinephrine

  • Trade Name: Levophed
  • Indication: Acute hypotension, sepsis, septic shock
  • Action: Increases blood pressure, cardiac output, and heart rate, beta-1 and alpha-adrenergic effects with moderate beta-2,
  • Class: Alpha/Beta adrenergic agonist
  • Considerations:
    • First line treatment of septic hypoperfusion unresponsive to fluids
    • 2-1.5 ug/kg/min up to 3 ug/kg/min due to alpha down-regulation in sepsis
    • Monitor blood pressure closely
    • Splanchnic (abdominal) perfusion can become compromised from prolonged administration
    • Caution IV site extravasation

– Dopamine

  • Trade Name: Intropin
  • Indication: Hypotension, low cardiac output, hypoperfusion of vital organs, raises mean arterial pressure in septic shock patients after fluid resuscitation has failed
  • Action: Endogenous catecholamine, stimulating dopaminergic and adrenergic receptors
  • Class: Inotropic agent
  • Considerations:
    • Low dose (1-5 mcg/kg/min) produces renal and mesenteric vasodilation
    • Moderate dose (5-15 mcg/kg/min) produces cardiac stimulation and renal vasodilation
    • High dose (20-50 mcg/kg/min) stimulates alpha receptors producing systemic vasoconstriction and increased mean arterial pressure
    • Use with caution in angina due to increased oxygen demand of heart
    • Always fluid resuscitate first
    • Prevent tissue damage at IV site by monitoring for extravasation

– Hydrocortisone

  • Trade Name: SoluCortef
  • Indication: Vasopressor-refractory shock or adrenal insufficiency secondary to cortisol stimulation test, improved survival of ARDS
  • Action: Controls or prevents inflammation by reducing rate of protein synthesis and suppressing migration of polymorphonuclear leukocytes and fibroblasts, reverses capillary permeability
  • Class: Corticosteroid, Glucocorticoid
  • Considerations:
    • High-dose corticosteroids should not be used with sever sepsis
    • Lower-dose (physiologic) steroids are beneficial for patient with adrenal insufficiency
    • Measuring cortisol levels before and 30 minutes after IV administration of ACTH can reveal adrenal insufficiency
    • Majority of patients with vasopressor-refractory sepsis benefit
    • Hydrocortisone 100 mg IV or Dexamethasone 10 mg IV

– Epinephrine

  • Trade Name: Adrenalin
  • Indication: Second-line agent for persistent hypotension despite fluid, norepinephrine, and dopamine administration, can be used in cardiac arrest
  • Action: Mainly alpha-adrenergic stimulation causing systemic vasoconstriction, strong beta-1 and beta-2 resulting in increased cardiac output, heart rate, and bronchial smooth muscle relaxation
  • Class: Alpha & Beta adrenergic agonist
  • Considerations:
    • Tachyarrhythmias and myocardial ischemia can result from strong beta-1 stimulation
    • Rapid increase in blood pressure can cause cerebral hemorrhage
    • May increase lactate and blood glucose levels
    • Gut ischemia from diversion of blood flow, must monitor bowels
    • 1-10 mcg/min IV infusion, titrate to effect

– Vasopressin

  • Trade Name: ADH, Vasostrict
  • Indication: Second-line agent for vasodilatory shock, should be used to supplement concurrent use of norepinephrine
  • Action: Endogenous peptide normally released from posterior pituitary that vasoconstricts without inotropic or chronotropic effects, stimulates peristalsis
  • Class: Antidiuretic hormone analog, Vasopressor
  • Considerations:
    • 03 U/min IV infusion added to norepinephrine as a therapy to treat unresponsiveness and reduce requirements for catecholamines
    • Restores effectiveness of catecholamine first-line agents
    • Increases renal perfusion and stimulates peristalsis

– Insulin

  • Trade Name: Humulin R, Novolin R
  • Indication: Glycemic control and avoidance further inflammatory response
  • Action: Reduces cytokine release, prevents polyneuropathy and myopathy, attenuates inflammation, and can decrease lactate formation
  • Class: Antidiabetic, Insulins
  • Considerations:
    • Previous recommendations were blood glucose levels 80-110 mg/dL but episodes of hypoglycemia negated any potential benefits
    • Recent sepsis-specific recommendations call for maintaining glucose level below 180 mg/dL
    • Administer in drip form according to ICU IV insulin infusion protocol
    • Insulin needs to be on connected to carrier line with fluid to infuse continuously
    • Blood glucose checks usually hourly

– Heparin

  • Trade Name: No trade name
  • Indication: Prevention of DVT or thrombosis-dominant disseminated intravascular coagulation (DIC)
  • Action: Inactivates factor Xa and inhibits conversion of Prothrombin to thrombin, inactivates factors IX, X, XI, and XII, and inhibits activation of factor VIII
  • Class: Anticoagulant
  • Considerations:
    • Only administer in the absence of active bleeding or thrombocytopenia
    • Caution creatinine clearance less than 30 mL/min
    • When contraindicated, use compression stockings or sequential compression devices
    • Also use in presence of inadequate perfusion to extremities or vascular skin infarctions
    • Weight-based dosing starting at 10 U/kg/hr with goal aPTT of 1.5-2.5 longer than patient’s pretreatment level

– Albumin

  • Trade Name: Albuminar, Alba
  • Indication: Hypovolemia and hypotension after substantial amounts of crystalloids have been administered
  • Action: Intravascular volume expansion through mobilization of fluids from interstitial spaces
  • Class: Volume expander
  • Considerations:
    • Increases circulating plasma volume by 3.5 times the volume infused within 15 minutes
    • Hemodilution lowers hematocrit and lowers blood viscosity
    • Monitor for signs of volume overload: dyspnea, JVD, crackles, pulmonary edema
    • Crystalloids should be given in 2-4 times greater quantity first
    • Results should be evident in CVP, PAOP, and urine output

– Phenylephrine

  • Trade Name: Vazculep
  • Indication: Second-line vasopressor for persistent hypotension despite maximal doses of norepinephrine and dopamine
  • Action: Strictly alpha-receptor agonist resulting in increased peripheral vascular resistance and blood pressure at the expense of cardiac output, heart rate and renal perfusion
  • Class: Alpha 1 agonist
  • Considerations:
    • 80-200 mcg/min IV infusion
    • Caution with cerebrovascular insufficiency and cardiovascular disease
    • Consider as first-line agent with tachycardia as it will reduce heart rate quickly and reliably while other catecholamine agents can exacerbate tachycardia
    • Extravasation can cause tissue ischemia
    • Reflex bradycardia should be considered in patients with low heart rates
    • Decrease in cardiac output can be detrimental in patients with hypermetabolic state like sepsis

Nurse Bullying – My co-worker stole my lunch money.

There is no need to try to make me feel inadequate, we are on the same team“.

This was the initial response from the most daring of new-graduate nurses to come through our ICU since I had joined the ranks.  I had only been working as an RN for about 6 months and knew the drill.  When the night shift nurses came on for report, you could expect a grilling about every last detail of your patient followed by admonishments, second-guessing, over-the-top interrogation, a few “gotcha’s” and plenty of eye rolling.  It was hard to tell as a new graduate nurse whether shift report followed by a room inspection was appropriate or not.  After all, bedside report has been promoted as a safety and continuity of care approach recently.  However, intimidation, poor teamwork, gossip, and pure bullying were also a big part of the experience for new nurses.  Although our unit had only a small number of nurses engaging in this behavior it made me wonder what other nurse’s experiences were like.

Having been in healthcare for over 10 years and being given the opportunity of attending graduate school, bedside nursing is no longer a part of my daily routine at work.  However, my curiosity surrounding nurse bullying has grown as I speak to nursing students about their fears regarding entering practice.  Work place incivility has taken a new role in the spotlight as an overarching issue that affects not only new nurses but veterans as well.  The problem has escalated to the point that in 2008 the Joint Commission issued a standard on intimidating and disruptive behaviors at work, citing concerns about patient care:

“Intimidating and disruptive behaviors can foster medical errors, contribute to poor patient satisfaction and to preventable adverse outcomes, increase the cost of care, and cause qualified clinicians, administrators and managers to seek new positions in more professional environments.  Safety and quality of patient care is dependent on teamwork, communication, and a collaborative work environment. To assure quality and to promote a culture of safety, health care organizations must address the problem of behaviors that threaten the performance of the health care team (Joint Commission, 2008).”

If the Joint Commission becomes involved, it is apparent that a significant problem exists.  For years, nurse bullying had been a silent issue that flew under the radar.  Nurses assumed that all professions experienced the phenomenon of “eating their young”.  Only with renewed focus on health care standards and containment of the costs of recruiting and training new nurses has the problem garnered new attention.

Bullying is the repeated and habitual use of force, threat, or coercion to abuse, intimidate, or aggressively dominate others.  The reason that nurses tend to bully one another is complicated.  Despite our large workforce numbers, nurses can be seen as an oppressed group within the hierarchy of the hospital.  Lateral violence takes place when nurses feel frustrated and unable to verbalize concerns to superiors for fear of punishment.  Sound familiar?  Often times, questioning physicians or supervisors within a strict practice model is met with opposition.  The inability to express feelings and concerns diminishes nurses’ self-esteem and fosters powerlessness.  In order to boost self-esteem, some nurses act out against other nurses because of lack of control over their own situation.  This, in turn, triggers the negative cycle which continues ad infinitum.

The toll on healthcare quality is immense.  With high nurse turnover, hospital staffing becomes a challenge and consistent training is threatened.  Studies estimate that 44% to 85% of nurses are victims of nurse bullying and up to 93% of nurses report witnessing lateral violence in the workplace (Jacobs & Kyzer, 2010; Quine, 2001).  In fact, one in three new graduate nurses considers quitting nursing altogether because of abusive or humiliating encounters (Townsend, 2012).

High staff turnover, absenteeism, poor performance, and patient safety issues related to inadequate teamwork and communication are preventable problems that can be attenuated with a sound approach to work place incivility.  The College of Physicians and Surgeons of Ontario and the Vanderbilt group (College of Ontario, 2008) have developed evidence-based suggestions to ameliorate workplace bullying:

  • Making expectations explicit by having a code of conduct supported by appropriate policies
  • Ensuring robust Board support for clinical leaders in implementation
  • Support and training for those dealing with disruptive and intimidating behavior
  • Screening for health and personal issues
  • Proactive surveillance systems
  • Dealing consistently and transparently with infringements
  • Dealing with lower level aberrant behavior early
  • Having a graduated set of responses (informal, formal, disciplinary, regulatory) depending on the severity of the incident
  • Making resources available to help those displaying and those affected by disruptive and intimidating behavior

Although it may appear that some nurses take self-righteous pleasure in other nurse’s mistakes, it is important to be assertive with co-workers rather than passive-aggressive.  Own your mistakes.  You will make many of them.  We all do.  Be humble, but also hold other people accountable for how they speak to you and treat you.  Don’t be afraid to have a professional conversation with someone who is being inappropriate.  We all fear conflict but you will have to confront people in a constructive manner.  Not just co-workers, doctors, and managers, but patients as well.  Most nurses dislike this part of the job but, unfortunately, it must be done.  These rare occasions can be a learning opportunity for both the offender and the recipient.  Escalating the matter to management is always an option, as well.  Workplace bullying can be overcome with both an organizational and personal approach.  In order to stop infighting amongst one another, we must advocate for our profession as a whole.  Only when nurses feel empowered within the health care model will we see improvement in lateral hostility among our ranks.  Until that time, remember what it was like to be a new graduate as you welcome the the next generation of nurses.  Strive to undo what may have been done to you and “be the change that you wish to see in the world.”

 

 

 

 

 

Jacobs, D., & Kyzer, S. (2010). Upstate AHEC lateral violence among nurses project. South Carolina Nurse, 17(1), 1.

Quine, L. (2001). Workplace bullying in nurses. Journal of Health Psychology, 6(1), 73-84.

Townsend, T. (2012) Break the Bullying Cycle. American Nurse Today.

College of Physicians and Surgeons of Ontario: Guidebook for managing disruptive physician behavior. Toronto, 2008, http://www.cpso.on.ca/uploadedFiles/downloads/cpsodocuments/policies/positions/CPSO%20DPBI%20Guidebook(1).pdf

Joint Commission: Behaviors that undermine a culture of safety. Sentinel Event Alert, July 9,2008:40, http://www.jointcommission.org/sentinel_event_alert_issue_40_behaviors_that_undermine_a_culture_of_safety/