Case Study J.F. is a 50 year-old married homemaker with a genetic autoimmune deficiency; she

has suffered from recurrent bacterial endocarditis. The most recent episodes were a Staphylococcus aureus infection of the mitral valve 16 months ago and a Streptococcus mutans infection of the aortic valve 1 month ago. During this latter hospitalization, an ECG showed moderate aortic stenosis, moderate aortic insufficiency, chronic valvular vegetations, and moderate left atrial enlargement. Two years ago J..F. received an 18-month course of TPN for malnutrition caused by idiopathic, relentless N/V. she has also had CAD for several years, and 2 years ago suffered an acute anterior wall MI. In addition, she has a history of chronic joint pain.

Now, after being home for only a week, J.F. has been readmitted to your floor with endocarditis, N/V, and renal failure. Since yesterday she has been vomiting and retching constantly; she also has had chills, fever, fatigue, joint pain, and headache. As you go through the admission process with her, you note that she wears glasses and has a dental bridge. She is immediately started on TPN at 125 ml/hr and on penicillin 2 million units IV q4h, to be continued for 4 weeks. Other medications are furosemide 80 mg PO qd, amlodipine 5 mg PO qd, K-Dur 40 mEq PO qd (dose adjusted according to laboratory results), metoprolol 25 mg PO bid, and prochlorperazine (Compazine) 2.5 to 5 mg IVP prn for N/V.

Admission VS are 152/48 (supine) and 100/40 (sitting), 116, 22, 37.9 degrees Celsius. When you assess her, you find a grade II/VI holosystolic murmur and a grade III/VI diastolic murmur; 2+ pitting tibial edema but no peripheral cyanosis; clear lungs; orientation x3 but drowsy; soft abdomen with slight left upper quadrant (LUQ) tenderness; hematuria; and multiple petechiae on skin of arms, legs, and chest.

What is going on?Significance of orthostatic hypotension, wide

pulse pressure and tachycardia?Decreased cardiac output, aortic insufficiency

Significance of abdominal tenderness, hematuria, joint pain, and petechia?Indicates embolization.

EndocarditisInfection of the endocardial surface of the

heart.The endocardium is contiguous with the

valves and therefore inflammation from infective endocarditis (IE) affects cardiac valves.

Two types:Sub acuteAcute

EtiologyStaphylococcus aureus; MRSAStreptococcus viridansBartonella quintanaEnteroc0cciFungi- Candida AlbicansViruses

Staphylococcus aureus BacteremiaA study was conducted trying to identify the

leading risk factors for S. aureus infective endocarditis. The risk factors identified were: Presence of a valvular prosthesis, persistent fever,

and persistent bacteremiaMRSA and preexisiting valvular disorder were not

associated with S. aureus infective endocarditis (SAIE).

However, MRSA can increase the mortality rate of SAIE. (Hill et al., 2007)

PathophysiologyOccurs when blood flow

turbulence within the heart allows the causative organism to infect previously damaged valves or other endothelial surfaces

Vegetations adhere to valve surface or endocardiumCan break into circulation

and result in embolization.

Right versus Left sided Infective EndocarditisAccording to Thalme, Westling, Julander

(2006): Treatment for Left sided IE was longer than

Right sided (34 d vs. 28 d)Left-sided IE hospital mortality is significant

(13%) whereas in the study there were no mortalities with right sided IE.

Was thought that IVDA caused right sided IE however, the study found that IV drug use patient often with suspected IE suffers from left-sided IE which has a worse prognosis.

Risk Factors for EndocarditisPrior endocarditisProsthetic valvesAcquired valve diseaseCardiac lesionsRheumatic Heart DiseaseCongenital Heart DiseasePacemakersIV Drug Abuse (IVDA)Nosocomial bacteremiaIntravascular devices (PICCs, pulmonary artery

catheterCardiac catheters

Pacemakers and EndocarditisIn an article titled:

Pacemaker Endocarditis: Clinical Features and Management of 60 consecutive cases

- “This study shows that a majority of patients from an endocarditis during the first year after implantation of a pacemaker.” (Massoure, 2007)

- “Antibiotic prophylaxis should be recommended at the time of pacemaker implantation as most infections occur within the first year after implantation.” (Massoure, 2007)

Clinical Manifestations in relation to J.F.Primary manifestations

Fever Chills Weakness Malaise Fatigue Anorexia Arthralgia Myalgia Back pain Abdominal discomfort Weight loss HA Clubbing Oslers Nodes Janeway’s lesions Petechiae

Secondary due to embolization LUQ pain Splenomegaly Local tenderness and

abdominal rigidity Flank pain Hematuria Azotemia *Gangrene Hemiplegia Ataxia Aphasia Visual changes Change In level of

consciousness Pulmonary emboli (Right side)

Osler’s Nodes and Janeway’s Lesions

http://www.childrenshospital.org/cfapps/mml/viewBLOB.cfm?MEDIA_ID=1887

http://gsbs.utmb.edu/microbook/images/fig94_3.JPG

What do J.F.’s lab values mean?J.F.’s lab values: Na 138, K 3.9, Cl 103, BUN

85, Creatinine 3.9, glucose 185, WBC 6.7, Hct 27%, Hgb 9.0.

Her abnormal values and their indication:BUN & Creatinine = renal failureGlucose = stress from hospitalization and from

TPNHct &Hgb = anemia

Diagnostic StudiesBlood cultureH&PEchocardiographyECGCXRCardiac catheterization

Nursing Diagnoses Decreased cardiac output related to valvular

insufficiency as evidenced by heart murmurs, peripheral edema, and tachycardia.

Risk for imbalanced nutrition related to nausea and vomiting, use of TPN, and prior history of malnutrition

Decreased cardiac output related to valvular insufficiency as evidenced by heart murmurs, peripheral edema, and tachycardia. Maintains adequate tissue and organ perfusion throughout length

of stay Assess heart rate and blood pressure to assess for manifestations of

decreased cardiac output Assess skin color and temperature. Cold, clammy skin is secondary to

compensatory increase in sympathetic nervous system stimulation and low cardiac output and desaturation.

Elevate head of bed to reduce O2 demand Monitor intake and output hourly Monitor lab values closely to detect any irregular values.

Maintains normal cardiac output throughout length of stay and at home Administer stool softeners as needed. Straining for a bowel movement

further impairs cardiac output. Promote bed rest/activity limitaiton to decrease cardiac workland and O2

demand Administer antiobiotics prescribed to fight underlying cause of impaired

cardiac function Collaborate with home health nurse to set up IV therapy for patient at

home. Home health will have technical knowledge of IV maintenance.

Risk for imbalanced nutrition related to nausea and vomiting, use of TPN, and prior history of malnutrition Patient weighs within 10% of ideal body weight.

Monitor recorded intake for nutritional content and calories to evaluate nutritional status

Encourage exercise as tolerated. Metabolism and utilization of nutrients are enhanced by activity.

Weigh patient weekly. During aggressive nutritional support, patient can gain up to 0.5 pound/day.

Maintains lab values within normal limits Monitor laboratory values that indicate nutritional

well-being/deterioration Patient will be free of signs of malnutrition while in the

hospital. Monitor for signs of malnutrition such as: brittle hair, bruises,

dry skin, pale skin and conjunctiva, smooth red tongue. Watch for signs of infection because pts who are malnourished

are at an increased risk for infection.

Treatment for IEAntibiotic prophylaxis – used for high risk patients

before they undergo certain procedures such as : dental, GI, and GU procedures or who are undergoing drainage/removal of infected tissue, renal dialysis, or have ventriculoatrial shunts for hydrocephalus

Long-term antibiotic – regimens dependent on organism that it is eradicating. Penicillin is a common antibiotic used unless there are allergies. The regimen can take weeks to complete.

Acetaminophen, ibuprofen, fluid and rest are recommended to treat the fever that accompanies IE

Prevention of Infective Endocarditis Interesting article on American Heart Association website

regarding prevention of IE “The current practice of giving patients antibiotics prior to a

dental procedure is no longer recommended EXCEPT for patients with the highest risk of adverse outcomes resulting from BE (bacterial endocarditis)” (americanheart.org)

Patients at highest risk and therefore should be given prophylaxis antibiotics are those who have: Prosthetic cardiac valve Previous endocarditis Congenital heart disease Cardiac transplant recipient with cardiac valvular disease

PREVENTION OF BACTERIAL ENDOCARDITIS

Wallet CardThis wallet card is to be given to patients (or

parents) by their physician. Healthcare professionals: Please see back of card for

reference to the complete statement.Name:__________________________________________________________________________

Needs protection from BACTERIAL ENDOCARDITIS because of an existing heart

condition.Diagnosis:_______________________________________________________________________Prescribed by:____________________________________________________________________Date:___________________________________________________________________________

References American Heart Association. (2008). Endocarditis Prophylaxis Information.

Retrieved September 28, 2008, from http://www.americanheart.org/presenter.jhtml?identifier=11086

Hill, E.E., Vanderschueren, S., Verhaegen, J., Herugers, P., Claus, P., Herreods, M.C. and et al. (2007). Risk factors for Infective Endocarditis and outcome of patients with Staphylococcus aureus Bacteremia. Mayo Clinic Proc., 82(10), 1163-1169.

Massoure, P., Reuter, S., Lafitte, S., Laborderie, J., Bordachard, P., Clementy, J., et al. (2007). Pacemaker endocarditis: clinical features and management of 60 consecutive cases. Pacing & Clinical Electrophysiology, 30(1), 12-19.

Thalme, A., Westling, K., Julander, I. (2007). In-hospital and long-term mortality in infective endocarditis in injecting drug users compared to non-drug users: A retrospective study of 192 episodes. Scandinavian Journal of Infectious Diseases, 39, 197-204.

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