Inf-Endo-Carditis

Infective Endocarditis is caused by the invasion and colonization of endocardial structures by microorganisims with resulting inflammation. Microbial infections of the endocardium are characterized by fever, heart murmurs, anemia and endocardial vegetations; may result in valvular obstruction, myocardial abscess, or mycotic aneurysm. A variety of organisms are known to have an affinity for the endocardium and for cardiac valves. The course may be acute or subacute, and clinical finds vary (depending on host age and susceptibility, underlying or associated disease, and the organism involved).

The most common bacterial culprits are several strains of Streptococcus and Staphylococcus aureus.

Pathology

Infective endocarditis (IE) is a rare infection that takes place as a complication in varying percentages of bacteremic episodes. The ability of an organism to cause endocarditis is the result of these factors: 

• Predisposing structural abnormalities of the cardiac valve for bacterial adherence

• Adhesion of circulating bacteria to the valvular surface

• The ability of the adherent bacteria to survive on the surface and propagate as vegetation or systemic emboli. 

Certain bacteria, if present in the bloodstream, may colonize the initially sterile vegetation composed of fibrin and platelets; bacterial growth enlarges the vegetation, further impeding blood flow and inciting inflammation that involves the vegetation and adjacent endothelium. The true incidence of endocarditis complicating each of the bacterial species causing IE is difficult to estimate. About 20-30% of individuals with community-acquired staphylococcal bacteremia develop IE.

Heart of a patient who died from Acute Endocarditis caused by Staphylococcus aureus

Heart of a patient who died from Acute Endocarditis caused by Staphylococcus aureus

Local Consequences
s

Local consequences include formation of myocardial abscesses with tissue destruction and sometimes conduction system abnormalities. Severe valvular regurgitation may develop suddenly, causing heart failure and death (usually due to mitral or aortic valve lesions). Aortitis may result from spread of infection. Prosthetic valve infections are particularly likely to involve valve ring abscesses, obstructing vegetations, myocardial abscesses, and aneurysms manifested by valve obstruction, dehiscence, and conduction disturbances.

Systemic Consequences

Systemic consequences are related to embolization of infected material from the heart valve and, primarily in chronic infection, immune-mediated phenomena. Right-sided lesions typically produce septic pulmonary emboli, which may result in pulmonary infarction, pneumonia, or empyema. Left-sided lesions may embolize to any tissue, particularly the kidneys, spleen, and CNS. Mycotic aneurysms can form in any major artery. Cutaneous and retinal emboli are common.

Acute infective endocarditis may theoretically develop in any individual if host resistance is low, if the organism is highly virulent and if the bacterial invasion is sufficiently large.  Acute infective endocarditis usually affects individuals with previously normal valves and leads to death in a large percentage of patients. Intravenous drug abusers are susceptible to acute infective endocarditis.

Subacute infective endocarditis generally affects individuals with some preexisting propensity for valvular colonization. Rheumatic heart disease, congenital heart abnormalities, mitral valve prolapsed, calcified valves and prosthetic valves are important predisposing factors.

a | Pathogens gain (transient) access to the bloodstream as a result of health-care procedures, via a dentogen pathway, or by intravenous drug use. 

b | Pathogens can rapidly (within minutes) adhere via platelet fibrin deposition ('nonbacterial thrombotic endocarditis') to a mechanically injured valve surface (pre-existing valvular disease) or to an inflamed valve surface (without pre-existing valve disease). 

c | Some pathogen species, such as Staphylococcus aureus, obtain intracellular access to the valve endothelium, which adds to inflammation and aggressive tissue destruction by the pathogens. 

d | Proliferation of the pathogens on and in the endothelium leads to maturation of the vegetation on the valve. 
e | Consequently, embolization of vegetation particles and systemic haematogenous spreading of the pathogens often occurs, leading to complications such as ischaemic stroke, cerebral haemorrhage, meningitis or meningeal reaction, brain abscess, and mycotic aneurysm.

Preexisting cardiac disease may allow the formation of platelet-fibrin deposits on the valves because of abnormal or stagnant blood flow patterns. These deposits become the site of organism attachment. Antibodies against the invader may further assist attachment by causing organisms to clump together.

The diagnostic findings in both acute and subacute infective endocarditis are similar. They include large, bulky, bacteria vegetations hanging from the heart valves and adjacent endocardial surfaces.  In an addition to the risk of embolization, vegetations may cause erosion or perforation of the underlying valve leaflet. In acute forms, adjacent myocardium may be eroded and abscessed. Eventually, the valvular vegetations become fibrotic and calcified.

Both cases have similar signs and symptoms such as; low-grade fever, (<39° c), night sweats, fatigue, weight loss, flu-like symptoms, heart murmur, tachycardia, abdominal pain and acute arterial insufficiency in an extremity. Positive blood cultures may help confirm the diagnosis.

The interval between initiation of bacteremia and the onset of symptoms is less than 2 weeks in the majority of cases.

  Common Signs and Symptoms

·         Low-grade fever (<39°C)

·         Night sweats

·         Malaise

·         Shortness of breath

·         Paleness

·         Weight loss

·         Aching in joints and muscles

·         Tenderness in spleen

·         New or changed heart murmur

·         Petechia

·         Blood in urine

·         Abdominal pain

·         Tachycardia

·         Conjuctiva

·         Persistant cough

·         Splinter hemorrhages under the nails

·         Hemorrhagic retinal lesions (Roth’s spots)

·         Clubbing of fingers

·         Septic shock



Successful treatment requires:

1. Maintenance of high serum levels of an effective antibiotic. 
2. Surgical management of mechanical complications and resistant organisms.

Prevention measures that can be implemented include preventing pre-existing conditions that are related to the cardiovascular system. Examples include rheumatic heart disease, congenital heart abnormalities, mitral valve prolapsed, calcified valves and prosthetic valves.

According to an article published in 2013 on the National Institutes of Health Website, a nationwide study done (1998-2009) revealed interesting facts about Infective Endocarditis in the US.

The article “Infective Endocarditis in the U.S., 1998-2009: A Nationwide Study” has some invaluable information regarding this disease. According to this article that was published on the National Institutes of Health Website and examined Endocarditis hospitalization, bacteriology, co-morbidities, outcomes and costs. Furthermore, the article explains how hospital admissions for endocarditis rose from 25,511 in 1998 to 38976 in 2009 (12.7 per 100,000 population in 2009). The portion of patients with intra-cardiac devices rose from 13% to 18.9% while the share with drug use and/or HIV fell. Mortality remained stable at about 14.5% and cardiac valve replacement also remained at 9.6%. Staphylococcus aureus was the most common identified pathogen, increasing from 37.6% in 1998 to 49.3% in 2009, 53.3% of which were MRSA. Moreover, mean age rose from 58.6 to 60.5 years; elderly patients suffered higher rates of myocardial infarction and death, but slightly lower rates of Staphylococcus aureus infection and neurologic complications.

According to studies done between 1998 and 2009, a majority of patients hospitalized with endocarditis were male (57.7%). More than a third (36.4% were over 70 years of age. Most hospitalizations occurred in the Southern part of the country, the census region with the largest population. However, the Northeast had the highest rate per 100,000 population (15.8), the south had an intermediate rate (12.1) and both the Midwest and West, each had 10.3. Among the endocarditis patients, substance use and HIV were most common in the Northeast and least common in the Midwest.

The mean age of the endocarditis patients rose from 58.6 to 60.8 years. Cases with comorbid drug use, HIV (or both) fell from 4.8% to 1.5%, while the share with a diagnosis of drug use (narcotics, cocaine or amphetamines) fell from 9.7% to 4.7%. The proportion of patients with a pre-existing cardiac replacement, implant or indwelling device rose from 13.3% in 1998 to 18.9% in 2009.

Patients with S. aureus had significantly higher mortality (17.4%) than those with other (or no) specified causative organisms (11.3%), and higher rates of Central Nervous System infection (3.9% vs. 1.4%) and Acute Renal Failure (22.7% vs. 16.0%).

Other predictors of mortality included: any neurological complication (23.3%), especially stroke (28.5%); Acute Renal Failure (27.1%); and Myocardial Infarction (31.6%). Patients over 70 had the highest mortality (16.1%), while those 18–44 had the lowest (4.8%); 8.5% of children died. Mortality was not notably affected by HIV, pre-existing valvular abnormalities, or valve replacement during hospitalization, but was lower among patients with substance use (8.3%).

Current treatment recommendations

According to the Mayo clinic website, the main objective is to get rid of the infection and to then treat the complications. During the acute stage of the disease, antibiotics are started to reduce valve damage, in accordance to hospital protocol, which in most cases includes getting blood cultures before administration of antibiotics. Blood cultures are done to identify the bacteria in order to get the adequate class of antibiotics on board. That might require high doses of antibiotics that need to be administered at the hospital until the period of high fevers, other signs and symptoms such as chills and headaches, and initial antibiotic regimen have passed. Then the patient will be able to be discharged and continue antibiotic therapy from home. 

Functionality of the valves might have been impaired by the infection causing more complications such as regurgitation. Due to this and/or worsening complications, surgery might be indicated. Surgery is the next step if antibiotics are not on board in good time and the heart valves have been damaged. It is also an option turned too when the infection is persistent and reoccurring and/or if the infection is caused by a fungal infection. The heart valves might be repaired or completely replaced with an artificial valve.

Treatment Progression

With Infectious Endocarditis, it has been found that Congestive Heart Failure has had an impact on prognosis. CHF may develop acutely from perforation of a native or bioprosthetic valve leaflet, rupture of infected mitral chordae, valve obstruction by bulky vegetations, or sudden intracardiac shunts from fistulous tracts or prosthetic dehiscence.” It has also been found that patients who had mild CHF progressed to severe CHF during therapy.  This also predicts possible poor surgical outcome.

Not a side effect of the treatment but another complication seen with infectious endocarditis is the formation of emboli’s. Seen in almost half of the cases of the diseases, the emboli are usually found in the coronary arteries, lungs, extremities and other parts of the body. These emboli can form at any point in the infection process and treatment course, but are mostly seen within the first couple weeks of antibiotic therapy.

In regard to stopping treatment, the use of anticoagulants in patients with infectious endocarditis is controversial. This is because of the argument of preventing acute hemorrhagic transformation off embolic lesions. With the reintroduction of anticoagulants, strict monitoring of clotting times should be observed and caution should be taken when administering of these drugs.

Demographic, Other Patient, and Hospital Characteristics of Patients Hospitalized with Endocarditis, 1998–2009.

Characteristic	Percent
Age
<18	1.9
18–44	20.0
45–59	24.4
60–69	17.4
>69	36.4
Male	57.7
Race/ethnicity*
White	69.4
Black	17.1
Hispanic	8.4
Asian or Pacific Islander	2.0
Native American	0.6
Other	2.6
Insurance**
Private	24.2
Medicare	53.3
Medicaid	13.8
Self-pay/no charge	5.9
Other	2.9
Region
Northeast	24.4
South	36.2
Midwest	19.8
West	19.6
Mean income of zip code of patient’s residence
Poorest quartile	28.3
Second quartile	25.4
Third quartile	23.4
Wealthiest quartile	23.0

^*Information on patients’ race was not reported for 21.3% of patents.

^**Expected primary payer as indicated by hospital.

The Prime Suspects?

The incidence of endocarditis is approximately 5 to 7.9 cases per 100,000 persons per year in the United States and has been stable over time. Risk factors for IE include hemodialysis (7.9 %), intravenous drug use (9.8 %), degenerative valvular disease (mitral regurgitation in 43.4 %; aortic regurgitation in 26.3 %), and rheumatic heart disease (3.3 %). 
Furthermore, once the signs and symptoms are identified and medical procedures have been implements; there has been a consistently high survival rate except for the majority of geriatric population. Some of the factors that contribute to the morbidity and mortality of infective endocarditis in this era include cosmetic body piercings, unsterile tattoo parlors, more dental cavities, more cases of obesity, increase in cardio vascular cases and intravenous drug users.

Recent Study

A recent retrospective study was done in China to analyze the epidemiological and clinical featured 368 patients hospitalized with infective endocarditis in a period of 7 years (2005 to 2012).

•  6.8% had rheumatic heart disease
• 31.8% had congenital heart diseases
• 22.8% were post-percutaneous coronary intervention or operative endocarditis patients.
• 14.1% had developed IE without previous cardiac diseases
• Streptococci viridians were the most common causative organisms (27.6%), followed by coagulase-negative staphylococci (15.9%). 
• Fever and cardiac murmur were the most common clinical presentation. 
• Congestive Heart Failure patients had the most complications (87.8%).
• 80.9% IE cases were detected by echocardiography (this is important, in correlation to the lower positive rate of blood culture).
• In-hospital mortality rate was 6.7% mostly due to refractory congestion heart disease and sepsis.

Nursing Diagnoses Activity intolerance related to cardiac reserve. Decreased cardiac output r/t inflammation of lining of heart and change in structure of valve leaflets, increased myocardial workload. Ineffective health maintenance r/t deficient knowledge regarding treatment of disease, preventative measures against further incidence of disease. Risk for ineffective peripheral tissue perfusion. Risk for infection r/t disease causing agent. Nursing Plan Monitor and record patient’s ability to tolerate activity; note pulse rate, blood pressure, monitor pattern, dypsnea and use of accessory muscles. Monitor for symptoms of heart failure and decreased cardiac output; listen to heart sounds, lung sounds, not symptoms. Help client choose a healthy lifestyle and to have appropriate diagnostic screening tests.  Access client for pain presence routinely at frequent intervals (during activity & rest). Monitor food intake; record percentages of food eaten. Keep a 3 day food diary to determine actual intake. Consult dietitian if needed. Monitor vital signs at least three times daily or hourly if needed. Notify provider of any deviations from baseline. Check capillary refill, brachial, radial, dorsalis pedis, posterior tibial and popliteal pulses bilaterally.

My Nursing Care Plan

Nursing Diagnosis	Risk for infection r/t: - Spread of infecting organism into the blood and other sites associated with inadequate host defense. - Interruption in balance of usual endogenous microbial flora associated with administration of antimicrobial agents.
Desired Outcome	Client will not develop extrapulmonary infection or superinfectoin as evidenced by: Gradual return of vital signs to normal. Usual mental status. Absence of pericardial friction, precordial pain, and a pathologic murmur. Absence of joint pain and swelling. Absence of unusual drainage from body cavity. Absence of ulceration in mouth. Absence of stiff neck and headache. WBC and differencial counts returning toward normal range.
Nursing Action	Assess for and report signs and symptoms of an extrapulmonary infection or a superinfection: Increase in temperature and pulse. Change in mental status. Pericardial friction rub, precordial pain, or development of a pathologic murmur. Swollen, red, painful joints. White patches or ulcerated areas in the mouth. Stiff neck, headache. Elevated WBC level. Implement measures to prevent an extrapulmonary infection and/or a superinfection: Use good handwashing technique and encourage client to do the same. Maintain sterile technique during all invasive procedures. Change peripheral intravenous line sites according to hospital policy. Anchor catheters/tubings (reduction of  trauma to the tissues and the risk for introduction of pathogens). Instruct and assist client to perform good perineal care routinely and after each bowel movement. Reinforce importance of frequent oral hygiene. If signs and symptoms of an extrapulmonary infection or a superinfection occur: Prepare client for and/or assist with diagnostic tests (e.g. lumbar puncture, cultures, joint aspiration) if planned. Implement appropriate comfort measures for symptoms experienced. Administer antimicrobials as ordered.

The Center of Disease Control (CDC) and the National Institute of Health (NIH) websites have invaluable literature regarding IE. Furthermore, the websites are frequently updated and have the most current disease information that would be important for a nurse. The literature and medical journals on the NIH website are an essential tool of evidence-based practice. This information is important for nurses and other healthcare workers.

To get more information on the pathophysiology of Infective Endocarditis, visit these websites:
http://wwwnc.cdc.gov/eid/article/10/6/03-0848_article
http://www.nhlbi.nih.gov/health/health-topics/topics/endo
http://www.ncbi.nlm.nih.gov/books/NBK2208/
http://www.merckmanuals.com/professional/cardiovascular_disorders/endocarditis/infective_endocarditis.html
http://www.aafp.org/afp/2012/0515/p981.html
http://www.texasheart.org/HIC/Topics/Cond/endocard.cfm
http://www.utmb.edu/pedi_ed/core/cardiology/page_39.htm

References

Bor, D., Woolhandler, S., Nardin, R., Brusch, J., & Himmelstein, D. (n.d.). Infective Endocarditis in the U.S., 1998–2009: A Nationwide Study. Retrieved January 17, 2015, from http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3603929/
Copstead, L., & Banasik, J. (2010). Alterations in Cardiac Function. In Pathophysiology (3rd ed., pp. 484-485). St. Louis, Mo.: Saunders Elsevier.

EHS: Nursing Care Planning Guides - Care Planner: Diagnosis: Risk for infection: Extrapulmonary (e.g. bacteremia, pericarditis, endocarditis, meningitis, septic arthritis) and/or superinfection (e.g. candidiasis). (n.d.). Retrieved February 26, 2015, from http://www1.us.elsevierhealth.com/SIMON/Ulrich/Constructor/diagnoses.cfm?did=241

Endocarditis. (n.d.). Retrieved February 14, 2015, from http://www.mayoclinic.org/diseases-conditions/endocarditis/basics/treatment/con-20022403

Hoen, B. (n.d.). Epidemiology and antibiotic treatment of infective endocarditis: An update. Retrieved January 17, 2015, from http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1861255/

Infective Endocarditis. (2005, June 14). Retrieved February 14, 2015, from http://circ.ahajournals.org/content/111/23/e394.full#sec-40

Slipczuk, L., Codolosa, J., Davila, C., Romero-Corral, A., Yun, J., Pressman, G., & Figueredo, V. (n.d.). Infective Endocarditis Epidemiology Over Five Decades: A Systematic Review. Retrieved January 17, 2015, from http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3857279/figure/pone-0082665-g003/

Terpenning, M., Buggy, B., & Kauffman, C. (1987, October 1). Infective Endocarditis: Clinical Features In Young and Elderly patients. Retrieved February 7, 2015, from http://deepblue.lib.umich.edu/bitstream/handle/2027.42/26976/0000543.pdf?sequence=1

Wang, P., Lu, J., Wang, H., Yu, L., Xiong, C., Yang, Y., & Yu, L. (2014, January 1). Clinical characteristics of infective endocarditis: Analysis of 368 cases. Retrieved January 31, 2015, from http://www.ncbi.nlm.nih.gov/pubmed/24735626

Table 1 - Emerging Issues in Infective Endocarditis - Volume 10, Number 6-June 2004 - Emerging Infectious Disease journal - CDC. (n.d.). Retrieved January 17, 2015, from http://wwwnc.cdc.gov/eid/article/10/6/03-0848-t1

http://www.nature.com/nrcardio/journal/v11/n1/fig_tab/nrcardio.2013.174_F1.html

(n.d.). Retrieved January 24, 2015, from https://www.heart.org/idc/groups/heart-public/@wcm/@hcm/documents/downloadable/ucm_300297.pdf

(n.d.). Retrieved February 26, 2015, from http://www.clipartlord.com/wp-content/uploads/2014/04/nurse7.png

Endocarditis - Google Search. (n.d.). Retrieved January 31, 2015, from https://www.google.com/search?q=endocarditis&rlz=1C1CHFX_enUS589US589&es_sm=93&biw=1242&bih=567&source=lnms&tbm=isch&sa=X&ei=YODNVIXXG8ffoASvrIKQAw&ved=0CAYQ_AUoAQ