Abstract

Infectious endocarditis refers to the colonization of cardiac valve endocardium by

virulent microorganisms. It is a rare condition that can lead to rapid and significant

morbidity and mortality if not efficiently diagnosed and treated. Infectious endocarditis is

the inflammation of the endocardium, the inner lining of the heart, as well as the valves

that separate each of the four chambers within the heart. It is primarily a disease

caused by bacteria and has a wide array of manifestations and sequelae. Without early

identification and treatment, a myriad of intracardiac and far-reaching extracardiac

complications can develop. Therefore, careful evaluation, including a thorough history

and physical exam, can help diagnoses cases and guide management, limiting mortality

and morbidity. This case presents a 35-year old male who has infectious endocarditis

which shows complications leading to the formation of a valvular heart disease and

cardiac dysrhythmia. The patient’s presenting signs correlates to the disorder.

Numerous managements were given to the patient and after weeks of stay in the

hospital, patient was discharged and had the disorder managed promptly.
 Objectives

This study aims to provide knowledge regarding infective endocarditis and its

course of treatment. The disease condition is fairly common and it is important for

everyone to know how can this disease be managed using the resources present in the

community. Furthermore, with this study, it can show how the disease can be managed

in the nursing side and how to alleviate the manifestations of an individual in order to

provide comfort and relief.

 Significance of the Study

Infectious endocarditis is the inflammation of the endocardium, the inner lining of

the heart, as well as the valves that separate each of the four chambers within the

heart. It is primarily a disease caused by bacteria and has a wide array of

manifestations and sequelae. Without early identification and treatment, a myriad of

intracardiac and far-reaching extracardiac complications can develop. Therefore, careful

evaluation, including a thorough history and physical exam, can help diagnoses cases

and guide management, limiting mortality and morbidity. This case has been chosen as

a case study because of several reasons: one of which is its prevalence. This disease is

fairly common among adults than in children and studying this case makes the citizens

of Balamban knowledgeable on how the disease is being developed and how it can be

prevented. The next reason is that this case is fatal if left untreated, thus it is imperative

and timely for the citizens of Balamban to know what are the risk factors in acquiring the

disease and what should be done to prevent it from developing complications.

 METHODOLOGY

Patients Profile:

Name: Mr. F.A.M

Address: Cebu City

Sex: male

Age: 35 years old

Race: Filipino

Weight:80.1 kgs

Height:168.5 kgs

Religion: Roman Catholic

Birthdate: October 16, 1987

Civil Status: married with 2 kids

Date and time of admission: May 20, 2023

Admitting diagnosis: Infective endocarditis cardiac dysrhythmia afib in RVR NYHA

class3.

Nursing History:

A case of patient F.A.M, 35 years old, male, married, from Cebu City, came to

VSMMC with complaints of bipedal edema. Seven months prior to admission, onset of

fever, weight loss and diarrhea. Patient had undergone HIV and Hepatitis B test and it
came negative; patient also undergone sputum test for TB but it turned out negative. 6

months prior to admission, noted body malaise, sought consult BMA done showing

unremarkable results. 3 months prior to admission, patient experienced bipedal edema

(+) and shortness of breath; the patient undergone echocardiography which revealed

infective endocarditis.

Gordon’s Typology on Functional Health Pattern

1. Health Perception/ Health Management – The patient claimed that he is not

healthy because he is constantly admitted in the hospital for a period of time already,

but stated he is used to it already. Patient was very eager to listen to advices and

accept health teachings related to his disease. The patient was very compliant to

medications that are ordered by the doctors, and are willing to undergo procedures that

is needed for his treatment.

2. Nutritional – Metabolic Patterns – The patient was under DAT with aspiration

precaution diet. The patient eats the food that was served in the hospital. The doctor

also limited his oral fluid intake to 1 liter per day. The patient is 5’6 in height and weighs

77 kilograms. Patient is overweight according to his BMI.

3. Elimination – The patient voided 5-6 x a day. But previously, the patient can void

1-2 x per day prior to admission. The patient’s urine color is yellowish. There was no

pain felt during urination. The patient recently had difficulty in defecation.

4. Activity – Exercise – The patient had a difficulty in ambulating because he has

exertional dyspnea. He doesn’t exercise because he gets tired easily. He can only

perform very limited activities. Previously before admission he has sedentary lifestyle.
5. Cognitive – Perceptual – The patient’s 6 senses is intact including pain

perception. Patient has a good cognitive functions such as he knows his language,

intact memory and have good decision making.

6. Sleep – Rest Pattern – The patient usually slept at 11pm and woke up at 7am

before admission, he usually consumed 8 hours of sleep. During admission, the patient

usually sleeps at 8pm and wakes up at 8am and took naps 2-3 hours in the afternoon.

7. Self perception/ self concept- The patient is satisfied about his image. He has

a good self-esteem. He likes grooming with the help of his wife. He is contented with his

personality. The patient’s disease condition is his only concern.

8. Roles and relationship patterns- Patient is a husband and a father of 2 kids.

He is the bread winner of his family. His wife accompanied him to the hospital. His sister

and his mother took care of his children at home.

9. Sexuality and reproduction pattern- The patient claimed that he is not sexually

active for about 8 months due to his health condition because he easily gets tired. He

loss his libido.

10. Coping and Stress tolerance pattern- The patient take a nap when he is tired.

If he is stressed he take a deep breath a think have a fresh air. He listens and cooperate

with the health care team because he wants faster recovery.

11. Values/ belief- The patient is still very faithful to God, he never blamed God of

his situation. He prays always to God and have faith in him. He still believes that God

will heal him.

 Course in the Ward

On June 1, 2023, the patient was transferred from the Emergency Department to

the ICU with an admitting diagnosis of Infective Endocarditis. Patient was awake,

coherent, with the following vital signs: Temperature of 38.6 degrees Celsius, Pulse of

104 beats per minute, Respiratory rate of 22 cycles per minute, BP of 160/100 mmHg,

weight of 80.1kg, abdominal girth of 104cm. Patient was hooked with PNSS 1L at KVO

rate, with IJ catheter attached. Patient was on complete bed rest with toilet privileges.

Patient was on DAT with strict aspiration precaution and limit of oral fluid intake to 1L

per day. Patient’s medications include paracetamol 500mg 1 tab PO OD PRN for fever;

furosemide 40mg ½ tab PO OD hold if systolic BP <100mmHg; spironolactone 25mg 1

tab PO OD; amiodarone 200mg 1 tab PO OD; sacubitril + valsartan 50mg ½ tab BID for

BP >140/90mmHg; ceftriaxone 2grams IV q24hrs; vancomycin 1gram IV q12hrs;

digoxin 0.25mg ½ tab OD. Patient’s vitals signs were monitored every hour including

intake and output monitoring in absolute figure. Patient was scheduled to undergo

cardio angiogram for valve replacement. Patient was eventually discharged without

concurring complications showing signs of an improved activity levels and gradual

reduction of the edema size in the lower extremities, which shown improvement than

during the admission manifestations.

 Discussion of the Case

Infectious endocarditis is the inflammation of the endocardium, the inner lining of

the heart, as well as the valves that separate each of the four chambers within the

heart. It is primarily a disease caused by bacteria and has a wide array of

manifestations and sequelae. Without early identification and treatment, a myriad of

intracardiac and far-reaching extracardiac complications can develop. Therefore, careful

evaluation, including a thorough history and physical exam, can help diagnoses cases

and guide management, limiting mortality and morbidity.

Etiology

The vast majority of infectious endocarditis cases stem from gram-positive streptococci,

staphylococci, and enterococci infection. Together, these three groups account for 80%

to 90% of all cases, with Staphylococcus aureus specifically responsible for around 30%

of cases in the developed world. In addition to various streptococci species, other

common colonizers of the oropharynx, such as the HACEK organisms (Haemophilus,

Actinobacillus, Cardiobacterium, Eikenella, and Kingella) can less frequently be the

culprit bacteria. Numerous other bacteria have been previously identified as well but

comprise only about 6% of total cases. Finally, fungal endocarditis represents only

about 1% of cases but can be a typically fatal complication of systemic Candida and

Aspergillus infection in the immunocompromised population. (Barnett, 2016)

Risk factors and the environmental setting of bacterial acquisition, healthcare

versus community, provide hints towards the underlying infectious etiology. The

definition of nosocomial infections remains controversial, but in general, healthcare-

related cases emerge in the setting of early prosthetic valve endocarditis (typically
defined as occurring within the first 60 days since surgery) or following recent vascular

catheterization, hemodialysis, hospitalization, or extra-cardiac operative procedures. In

these situations, S. aureus represents the predominant pathogen, responsible for

around 50% of nosocomial infections. The less virulent coagulase-negative

staphylococci, such as S. epidermidis, stereotypically stem from indwelling vascular

devices or recently implanted prosthetic valves. Enterococcal infection emerges with

similar frequency in both nosocomial and non-nosocomial infections, comprising about

15% and 18% of cases, respectively. (Hill, et. al, 2007)

Community-acquired infections tend to develop in the setting of

immunosuppression, intravenous drug use, poor dentition, degenerative valve disease,

and rheumatic heart disease. Intravenous drug use, which underlies almost 10% of

infectious endocarditis cases, suggests repeated inoculation with skin flora such as S.

aureus and S. epidermidis, with S. aureus demonstrating a predilection for healthy,

native tricuspid valves. While fairly uncommon in healthcare-related infections, viridans

group streptococci underlie about 20% of community-acquired infections (Murdoch, et.

al, 2009). Classically, infections with Streptococcus gallolyticus (bovis) organisms

should raise suspicion for underlying colon carcinoma (Abdulamir, et. al, 2011)

Prevalence of the disease

Infectious endocarditis is a rare condition with an estimated yearly incidence of 3

to 10 cases per 100,000 people (Cahill, et. al, 2016). Historically, this disease process

has demonstrated a predilection for males, with a male to female ratio of nearly 2 to 1.

The average age of infectious endocarditis patients is now greater than 65 years old.

This preponderance for the elderly likely corresponds to the increased prevalence of
predisposing factors such as prosthetic valves, indwelling cardiac devices, acquired

valvular disease, hemodialysis, and diabetes mellitus within this demographic (.

Although previously a major risk factor, rheumatic heart disease now underlies less than

5% of all cases in the modern antibiotic era. Recreational intravenous drug use

represents a growing risk factor that now accounts for about 10% of all infectious

endocarditis cases (Murdoch, et. al, 2009).

Disease process

The intact, healthy endocardium is typically resistant to bacterial seeding.

Overall, the development of infectious endocarditis requires prodromal endocardial

injury followed by a period of bacteremia. The preliminary endocardial disruption may

emerge secondary to turbulent flow around diseased valves or from the direct

mechanical trauma caused by catheter or electrode insertion. In the setting of

intravenous drug use, repetitive valvular barrage by co-injected particulate matter

generates the necessary injury (Cahill, et. al, 2016). As evidenced by the predilection for

vegetations to form on the ventricular surface of the aortic valve and the atrial surface of

the mitral valve, hemodynamics plays an important role in the pathogenesis. The

vegetations are localized immediately downstream from regurgitant flow, leading to the

hypothesis that hypoperfusion of the intima predisposes these areas to endocardial

injury. Furthermore, infectious endocarditis is more common with high turbulence

lesions such as a small ventricular septal defect with a jet lesion or stenotic valves;

presumably, the high-pressure flow creates more local damage than defects associated

with large surface areas or low flow (Rodbard, 1964). The damaged endocardium

serves as a nidus for platelet aggregation and activation of the coagulation cascade,
which fosters the formation of a sterile, non-bacterial thrombotic vegetation (Durack et.

al, 1973).

Subsequent bacteremia then allows for colonization of the vegetation. The

necessary bacteremia can stem from an established, distant source of infection or

emerge transiently secondary to intermittent hematogenous inoculation of oral flora from

dental/gingival manipulation. Although the minimum bacterial burden remains unknown,

experimental models have precipitated cases of infectious endocarditis with slow 1 mL

infusions of 106 colony-forming units of bacteria (Veloso, et. al, 2013). Even in the

setting of endocardial injury and bacteremia, pathogenesis still requires a virulent

organism capable of binding to and facilitating platelet-fibrin deposits. For instance,

three S. aureus proteins (clumping factors A, B, and serine-aspartate repeat protein)

have been found to independently mediate platelet aggregation. In theory, expanding

the originally sterile platelet-fibrin deposits protects pathogens from the host’s immune

response and allows the vegetation to grow (O’Brien, et. al, 2002).

Clinical Presentation of the Disease

Mature vegetations consist of an amalgamation of inflammatory cells, fibrin,

platelets, and erythrocyte debris. The initial platelet-fibrin clot provides a nidus for

bacterial adherence and further platelet aggregation. Confocal laser scanning

microscopic analysis of infected valve tissue demonstrates bacterial biofilms embedded

with platelet collections. In a self-revolving fashion, platelets facilitate bacterial

colonization, which in turn propagates further bacterial aggregation through the binding

of surface proteins (Jung, et. al, 2012). In the acute setting, vegetations remain
avascular; however, once healing commences, neovascularization, fibroblasts, and

fibrosis may start to emerge in the affected valve.

Both the gross and histologic appearance of valvular tissue will vary based on

the infecting organism. Virulent pathogens such as S. aureus characteristically generate

an inflammatory milieu predominated by neutrophils and large bacterial colonies. A

macroscopic evaluation may demonstrate friable tissue with frank destruction. The

inflammation associated with less virulent organisms such as viridans group

streptococci involves more mononuclear cell infiltration (Liesman, et. al, 2017).

The staining of histologic samples will often demonstrate focal bacterial colonies.

Although rarely culture-positive following initiation of antibiotic therapy, valve tissue

Gram staining remains positive in over 60% of cases undergoing active treatment

(Morris, et. al, 2003). In the case of strep and staph endocarditis, hematoxylin and eosin

staining will reveal basophilic cocci. Although typically used for fungal identification, the

Grocott-Gomori methenamine silver stain will highlight the contours of streptococci and

provide increased sensitivity for detecting bacteria in valve tissue than Gram staining.

Periodic acid-Schiff staining also offers greater sensitivity than Gram staining and best

accentuates the foamy macrophages characteristic of Tropheryma whipplei endocarditis

(Liesman, et. al, 2017).

In regard to prosthetic valve endocarditis, one study found that the associated

inflammatory cells remain relegated to the vegetation on the surface of the valve cusp.

Compared to the inflammatory response that characterizes degenerative valve

calcification, prosthetic valve endocarditis primarily involves neutrophilic infiltrates rather

than macrophages and lymphocytes (Lepidi, et. al, 2006).

 Clinically, infective endocarditis may present with a myriad of signs and

symptoms, and clinicians should consider this diagnosis in any patient with risk factors

who present with fever or sepsis of unknown origin (Cahill, et. al, 2016). Patients will

often describe the insidious onset of fevers, chills, malaise, and fatigue that generally

prompts medical evaluation within the first month. Fever, typically defined as a

temperature over 38.0 degrees C (100.4 degrees F), was found in over 95% of all

patients (Murdoch, et. al). However, immunosuppression, old age, antipyretic use, or

previous antibiotic courses may prevent manifestation and lower the frequency of this

finding. Other nonspecific symptoms indicative of systemic infection such as anorexia,

headache, and generalized weakness may also be present. Symptoms that help

localize to the cardiopulmonary system such as chest pain, dyspnea, decreased

exercise tolerance, orthopnea, and paroxysmal nocturnal dyspnea occur less commonly

and should raise concern for underlying aortic or mitral valve insufficiency. In the event

of acute valvular incompetence, patients may present in extremis with abrupt onset of

the symptoms of heart failure.

History often reveals predisposing conditions and risk factors that aid with

diagnosis. Current or previous indwelling catheterization, intravenous drug use, recent

pacemaker placement, or history of prosthetic valves suggests predisposing

endocardial injury. The physician should also inquire about known degenerative valve

disease such as calcific aortic stenosis or mitral valve prolapse, which underlie about

30% of all cases (Nakagawa, et. al, 2014). Previously a major risk factor for infectious

endocarditis, rheumatic heart disease precedes the onset of less than 5% of infective
endocarditis cases in the developed world today. In the Philippines, diabetes mellitus

represents one of the most common comorbidities.

A thorough physical exam may identify stigmata that reinforce the diagnosis and

highlight complications of peripheral embolization. As discussed above, a fever will often

be present, but tachypnea and tachycardia may also emerge in the setting of underlying

valvular insufficiency or systemic infection. Hypotension can similarly develop

secondary to either septic or cardiogenic shock in the event of acute valve perforation.

Although classically associated with infectious endocarditis, a new or worsening murmur

presents in less than 50% of all cases; nonetheless, identification will help localize valve

involvement. If severe mitral or aortic valve regurgitation develops, auscultation can

demonstrate bilateral pulmonary rales. The dermatologic exam may show the classic

immunologic and hemorrhagic cutaneous sequela of infectious endocarditis. However,

Osler nodes (painful subcutaneous nodules typically found on the palm), subungual

splinter hemorrhages, and Janeway lesions (painless hemorrhagic plaques on the

palms/soles) are each individually observed in less than 10% of all cases. The

abdominal exam can reveal splenomegaly or even localized peritonitis, which suggests

bowel perforation from mesenteric arterial occlusion. Intracerebral embolization can

present with focal motor or sensory deficits that correspond to the impacted vascular

territories.

Diagnosing the Disease

Most patients with endocarditis present with nonspecific symptoms such as

fatigue, fever, or chest pain. These symptoms correspond to multiple serious conditions,

and the workup must necessarily be broad. Patients with chest pain or dyspnea warrant
early consideration of other potentially life-threatening cardiopulmonary processes such

as acute coronary syndrome, pulmonary embolism, and pneumonia. Whereas those

appearing floridly septic should undergo rapid, guideline-directed evaluation following

validated protocols.

For those presenting primarily with chest pain or dyspnea, initial acquisition of a

12-lead electrocardiogram (ECG) is a rapid and inexpensive means to evaluate for

underlying ischemia, dysrhythmias, or structural disease that may be confounding the

diagnostic picture. The typical ECG in infectious endocarditis appears normal. ST-

elevation can be seen in infectious endocarditis but should be considered a marker of

myocardial infarction and handled consistent with ST-segment myocardial infarction

even in previously diagnosed cases of infectious endocarditis. A two-view chest X-ray

can reveal evidence of pulmonary abscesses, infiltrates, or pleural effusions. In the case

of severe left-sided valvular insufficiency, frank cardiopulmonary edema, cardiomegaly,

or cephalization of pulmonary vasculature may be appreciated. Investigating possible

pulmonary parenchymal disease, empyema, or arterial embolization may require more

advanced chest imaging such as a contrasted computed tomography (CT) scan or CT

angiogram. For patients with presentations concerning for myocardial ischemia or

myocarditis, cardiac biomarkers remain critical for elucidating underlying infarction.

In the acute setting, a broad laboratory workup is often indicated, given the

nonspecific presenting symptomatology. A complete blood count often demonstrates a

leukocytosis that points towards an underlying infectious process. Cases with more

subacute-chronic presentations may have normocytic anemia consistent with anemia of

chronic disease. Although nonspecific, inflammatory markers such as the erythrocyte

sedimentation rate (ESR) and c-reactive protein (CRP) are elevated in around 60% of

cases. A chemistry panel should be obtained to identify electrolyte derangements

requiring correction during the initial resuscitation.

Following exclusion of more immediately life-threatening etiologies, diagnosis of

infectious endocarditis anchors on both microbiologic and echocardiograph evidence of

infection. Diagnosis has long been predicated on the Modified Duke Criteria. Divided

into major and minor criteria, diagnosis requires satisfaction of either two major criteria,

one major and three minor criteria, or five minor criteria. The first major criterion

involves confirmation of bacteremia. More specifically, the Modified Duke Criteria

requires two separate blood cultures positive for typical pathogens such as viridans

group strep, S. gallolyticus, HACEK organisms, S. aureus, or community-acquired

enterococci in the absence of a primary focus. If other culprit pathogens are suspected,

blood cultures must remain persistently positive as defined by either two positive

cultures drawn more than 12 hours apart or positive results of all three or majority of 4

or more separate cultures (with first and last samples drawn one hour apart).

Additionally, a recent update by the American Heart Association (AHA) allows

satisfaction of this criterion with single positive blood culture for Coxiella burnetii or an

anti-phase 1 IgG antibody titer greater than or equal to 1:800.

The second major criterion involves sonographic evidence of endocardial

involvement. An echocardiogram must demonstrate a vacillating intra-cardiac mass

fixed to a valve, supporting structure, or implanted material. Initial evaluation with a

transthoracic echocardiogram (TTE) is common; however, the American Heart

Association (AHA) recommends obtaining a more sensitive and specific

transesophageal echocardiogram (TEE) if suspicion for infectious endocarditis remains

high despite a negative TTE (Class I, Level of Evidence B). Circumstances such as

comorbid chronic obstructive pulmonary disease, previous thoracic surgery, obesity, and

prosthetic valve involvement may hamper visualization via the transthoracic approach

and should prompt more expeditious attainment of a TEE.

Regarding the five minor criteria, these include the following:

 Predisposing conditions such as underlying valvular abnormalities, structural

heart disease, or intravenous drug use.

 Fever defined by a temperature greater than 38 degrees celsius.

 Evidence of vascular phenomena such as mycotic aneurysms, intracranial

hemorrhage, Janeway lesions, major arterial emboli, or septic pulmonary infarcts.

 Evidence of immunologic phenomena such as Osler’s nodes, Roth spots,

glomerulonephritis, or positive rheumatoid factor.

 Positive blood cultures that do not satisfy the aforementioned major criterion or

serologic evidence of infection consistent with infectious endocarditis.

Treatment and Management of the Disease

Effective treatment hastens endocardial vegetation eradication and limits or

prevents secondary complications. However, those presenting in extremis with acute

decompensated heart failure, septic shock, or stroke require stabilization and

resuscitation, prioritizing the tenets of airway, breathing, and circulation. Following initial

stabilization, subsequent treatment concentrates on prolonged bactericidal antibiotic

regimens and possible cardiothoracic surgical intervention.

 Antibiotic treatment duration and selection depend on the nature of the valve

involved and the resistance pattern of the infecting organism. In the case of native valve

endocarditis with penicillin-susceptible viridans group strep or S. gallolyticus, the

shortest proposed treatment regimen involves a two-week course of ceftriaxone 2 gm IV

every 24 hours plus gentamicin 3 mg/kg IV every 24 hours (Baddour, et. al, 2015).

[Class IIa, level of evidence B] For this same patient population, other possible

regimens include ceftriaxone 2 gm every 24 hours IV for four weeks or aqueous

penicillin G 12 to 18 million units every 24 hours via continuous IV drip or in 4 to 6

equally divided doses. In the case of prosthetic valve involvement, these same

pathogens typically require a minimum of a 6-week course of 24 million units of

penicillin G every 24 hours or ceftriaxone 2 gm with or without gentamicin 3 mg/kg every

24 hours.

Patients at risk for staphylococcal infection typically require more prolonged

antibiotic therapy. Patients with native valve methicillin-sensitive S. aureus (MSSA)

infections can receive 6-week courses of either nafcillin 2 gm every four hours or

cefazolin 2 gm every 8 hours. In cases of methicillin-resistant S. aureus (MRSA)

infections, a standard course involves vancomycin 15mg/kg every 12 hours or

daptomycin 8 mg/kg daily for 6-weeks. Of note, gentamicin dual therapy is no longer

recommended for MSSA or MRSA infections given the lack of clinical benefit and

associated renal toxicity (Hoen, et. al, 2013). Overall, therapy for prosthetic valve

staphylococcal infections is quite similar but requires augmentation with rifampin and

gentamicin. Prosthetic valve MSSA disease should receive gentamicin 3 mg/kg IV in 2

to 3 divided doses plus rifampin 900 mg IV in 2 to 3 equally divided doses every 24

hours for 2-weeks and 6-weeks, respectively, in addition to the above-described nafcillin

regimen. In addition to vancomycin, MRSA cases should receive this same course of

gentamicin and rifampin.

Since beta-lactam monotherapy does not possess bactericidal activity against

enterococci, both native and prosthetic valve enterococcal infections require

combination regimens. Examples include ampicillin or penicillin G plus an

aminoglycoside such as gentamicin for 4 to 6 weeks. Interestingly, a dual beta-lactam

regimen such as ampicillin plus ceftriaxone achieves appropriate bactericidal activity

against Enterococci faecalis and may be utilized. Of note, penicillin resistance warrants

combined vancomycin-gentamicin therapy; however, emerging penicillin, gentamicin,

and vancomycin resistance may require treatment with linezolid or daptomycin.

Overall, antimicrobial treatment guidelines remain ever-evolving and should be

routinely reviewed. To further guide and help develop appropriate antibiotic therapy

courses, early infectious disease consultation is encouraged. As an additional principle

of medical management, two blood cultures should be drawn every 24 to 48 hours to

ensure clearance of bloodstream infection and direct ongoing antimicrobial therapy.

In general, early surgical intervention, including valve repair versus replacement,

is indicated in the event of acute heart failure, extensive infection with localized

complications, and recurrent arterial embolization. Acute valvular compromise

manifesting with heart failure symptomatology typically warrants operative intervention

within 24 hours. However, AHA/ACC also recommends early surgical treatment before

completion of the initial antibiotic course in the event of an associated atrioventricular

block, paravalvular abscess, or presence of destructive infiltrative lesions. Prevention

and treatment of recurrent embolic events represent a major impetus for surgical

intervention. At this time, AHA/ACC also recommends early surgery if patients

experience recurrent embolic events or demonstrate large, mobile native valve

vegetations less than 10 mm, respectively. One large prospective cohort study found

the initiation of antimicrobial therapy alone decreased the incidence of stroke from 4.82

per 1000 patient days to 1.71 per 1000 patient days over one week. However, Kang and

colleagues found early surgical intervention within 48 hours significantly reduced the

overall in-hospital mortality (3% compared to 23% in the conventional therapy group) as

well as the 6-week risk of embolic events (0% compared to 21%). Today, this mortality

benefit means that almost half of all infectious endocarditis cases undergo some type of

surgery.

Complications

A host of intracardiac complications can stem from infective endocarditis. Acute

valvular incompetence can lead to symptoms of heart failure and occur in around one-

third of cases. This can occur secondary to acute valve perforation or from the

compromise of the chordae tendineae and papillary muscles. Mitral or tricuspid valve

regurgitation can lead to atrial enlargement and the subsequent emergence of atrial

fibrillation and other supraventricular dysrhythmias as well. Less commonly, intracardiac

abscesses (14%) and atrioventricular blocks (8%) emerge.

Peripheral embolization can also have far-reaching extracardiac complications.

Right-sided vegetation can lead to arterial emboli that manifest as disseminated

pulmonary abscesses, pneumonia, empyema, or focal regions of pulmonary infarctions.

Neurologic sequela constitutes the most severe and prevalent extracardiac

complications, impacting 15% to 30% of all cases. Potential complications include

ischemic stroke, intracranial hemorrhage, meningitis, intracerebral abscess, and

infective intracranial aneurysms. Ischemic strokes represent the vast majority of

neurologic complications and classically stem from cerebral artery occlusion from

embolized mitral/aortic vegetations. Septic embolization into the microcirculation of the

vasa vasorum can precipitate vessel wall degradation and subsequent mycotic

aneurysms, which typically only become symptomatic in the event of a rupture.

Less common complications include acute renal failure stemming from either

immune-mediated glomerulonephritis or focal infarction secondary to occlusive emboli.

Splenic infarcts and abscesses, especially in the setting of S. aureus infection, can also

occur from infected emboli. Acute mesenteric ischemia and subsequent bowel necrosis

and perforation is a feared complication of arterial embolization.

Prognosis

Prognosis can vary widely depending on the virulence of the infective pathogen,

the emergence of secondary complications, preexisting comorbidities, and the presence

of native versus prosthetic valve. The in-hospital mortality rate hovers around 18%, with

one-year mortality reaching up to 40%. In general, cases of prosthetic valve

endocarditis occurring within the first 60 days of surgery demonstrate the highest in-

hospital mortality rates (about 30%). A large, Japanese prospective cohort study found a

staphylococcal infection and heart failure to be the greatest predictors of in-hospital

mortality. Although nearly 50% of infectious endocarditis cases now undergo surgical

intervention, in of itself, the surgical intervention does not appear to elevate the in-

hospital mortality risk.

 NURSING CARE PLAN

NCP 1: Hyperthermia related to infective process of endocarditis

Nursing Goal: After 3 hours of nursing interventions, patient’s body temperature will be

stabilized within the normal limits.

Interventions Rationale

1. Assess the patient’s vital signs at To assist in creating an accurate

least every four hours. diagnosis and monitor effectiveness of

medical treatment, particularly the

antibiotics and fever-reducing drugs

administered

2. Remove excessive clothing, To regulate the temperature of the

blankets and linens. Adjust the environment and make it more

room temperature. comfortable for the patient.

3. Administer the prescribed antibiotic Use the antibiotic to treat bacterial

and anti-pyretic medications. infection (endocarditis), which is the

underlying cause of the patient’s

hyperthermia. Use the fever-reducing

medication to stimulate the hypothalamus

and normalize the body temperature.

4. Offer a tepid sponge bath. To facilitate the body in cooling down and

to provide comfort.

5. Elevate the head of the bed. Head elevation helps improve the

expansion of the lungs, enabling the

 patient to breathe more effectively.

NCP 2: Decreased cardiac output related to valvular dysfunction from infective process

Nursing goal: After 4 hours of nursing interventions, patient will be able to maintain

adequate cardiac output.

Interventions Rationale

1. Assess the patient’s vital signs and To assist in creating an accurate

characteristics of heart beat at diagnosis and monitor effectiveness of

least every 4 hours. medical treatment.

2. Assess heart sounds via Heart murmur sounds is an important

auscultation. Observe for signs of sign of endocarditis. The presence of

decreasing peripheral tissue signs of decreasing peripheral tissue

perfusion such as slow capillary perfusion indicate deterioration of the

refill, facial pallor, cyanosis, and patient’s status which require immediate

cool, clammy skin. referral to the physician.

3. Administer the antibiotics as Antibiotics will treat the bacterial infection

prescribed. that caused the endocarditis.

4. Administer supplemental oxygen, To increase the oxygen level and achieve

as prescribed. Discontinue if SpO2 an SpO2 value of at least 94%.

level is above the target range, or

as ordered by the physician.

5. Educate patient on stress Stress causes a persistent increase in

management, deep breathing cortisol levels, which has been linked to

 exercises, and relaxation people with cardiac issues. Chronic

techniques. stress may also cause an increase in

adrenaline levels, which tend to increase

the heart rate, respiratory rate, and blood

sugar levels. Reducing stress is also an

important aspect of dealing with fatigue.

NCP 3: Fatigue related to decreased cardiac output

Nursing goal: After 4 hours of nursing interventions, patient will be able to show

increase activity levels gradually.

Interventions Rationale

1. Assess the patient’s understanding Using a quantitative scoring system, such

of fatigue for severity, variations in as 1 to 10, might help the patient define

severity over time, and aggravating the degree of fatigue they are

or relieving factors. experiencing. Using graphics or

descriptive words for more scoring

scales. The nurse can use this technique

to account for changes in the patient’s

fatigue level over time. It’s crucial to

determine whether the patient’s level of

fatigue is continuous or fluctuating over

time.

2. Determine the patient’s capacity to Fatigue can limit a patient’s capacity to

 carry out activities of daily living. participate in self-care.

3. Determine the patient’s dietary Fatigue might be a sign of protein-calorie

intake to ensure that the patient is deficiency, vitamin deficiency, or iron

getting enough energy to meet the deficiency.

required metabolic needs.

4. Assess the patient’s likelihood of These will encourage active participation

experiencing relief from fatigue, in the planning, implementation, and

willingness to participate in fatigue- evaluation of fatigue-relieving therapy

reduction techniques, and level of management. Social support will be

family and social support. critical in assisting the patient in

implementing adjustments that will reduce

weariness.

5. Determine and monitor the Decreased oxygenation is indicated by a

patient’s oxygen saturation, WBC pulse oximetry value of 92 percent or

count, and ABG levels as indicated below, decreased PaO2, and increased

and report any deviation from the PaCO2. Infection is indicated by

normal values. increased WBC count.

6. Examine the patient’s usual Increased physical exertion will require

degree of physical activity and additional oxygen demand. However,

movement. decreased exercise may lead to fatigue,

the two should be balanced.

7. Examine the patient’s sleeping Changes in the patient’s sleep pattern

patterns for quality, amount, time it could be a factor in the emergence of

takes to fall asleep, and how the fatigue. Fatigue can be exacerbated by a
 feeling upon waking up, as well as variety of reasons, including sleep loss,

any changes in the mental mental discomfort, pharmacological side

processes or actions. effects, and the progression of CNS

disease.

8. Limit the patient’s exposure to In the patient’s physical environment,

ambient stimuli, especially at times bright lighting, noise, visitors, numerous

when the patient is supposed to be distractions, and litter can inhibit

resting or sleeping. relaxation, disrupt rest or sleep, and lead

to fatigue.

9. Assist the patient in creating a A schedule that alternates periods of

daily exercise and rest regimen. activity with periods of relaxation can let

Stress the need of taking frequent the patient do their preferred activities

breaks in between activities. without becoming fatigued and the patient

will be able to restore adequate oxygen

levels.

10. Assist the patient in prioritizing Setting priorities is an example of an

daily activities and role energy conservation technique that

responsibilities. allows the patient to focus available

energy on the most important tasks. The

patient’s mood and sense of emotional

wellness can improve as a result of

achieving targeted goals.

11. Determine the patient nutritional To offer energy resources, the patient will

status and encourage the patient require a well-balanced diet of fats,

 to take an adequate dietary carbohydrates, proteins, vitamins, and

requirement. minerals.

12. Encourage the patient to express Recognizing that living with fatigue is

feelings regarding the effects of physically and emotionally difficult for the

fatigue. patient, thus, aids in coping.

13. Provide relaxing diversional This strategy makes beneficial use of

activities for the patient like nervous energy and may help to reduce

listening to music or using one’s anxiety.

phone.

14. Plan with the patient on how to Weakness might make it nearly

save energy by sitting and splitting impossible for a patient to complete

activities of daily living into activities of daily living. It is important that

manageable tasks. As needed, someone will be with the patient to

advise the significant other to protect them from injury during activities.

assist the patient with movement

or self-care tasks.

Conclusion

Based on the study, it is safe to conclude that infective endocarditis is fairly

manageable if managed on its earlier stage. Although the patient showed signs of
systemic manifestations as evidenced by presence of bipedal edema, after careful

management and treatment, patient’s manifestations slowly regresses with patient

showing signs of an improved energy levels, which is a sign of an adequate cardiac

output.

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Pathophysiology

Predisposing factors Etiology

Precipitating factors
-Lifestyle
Bacterial infiltration in
the endocardium -Increase fat intake
-Hypertension
-Undiagnosed hypertension
-Unrepaired congenital heart
disorders

-Diabetes mellitus

-Post-GAHBS infection Endothelial erosion

caused by bacterial
 Diagnostic Exams/Laboratory Exams
Laboratory/ Date Normal Value Significance of the
Actual Result
Diagnostic Test Performed (Reference) Result
Complete Blood January WBC: 21, 110/ cu.mm 4,500-  Increase in the

Count 29, 2023 11,000/cu.mm number of WBC

count indicates

two reasons:

fibrotic conditions

and infection

which is present

in infective

RBC: 1.77 x 1012/ 4.0-6.0 x 1012 endocarditis.

cu.mm /cu.mm  Decrease in RBC

count indicates an

impairment in the

RBC production in

the body due to a

current disease

Hemoglobin: 9 g/dL 12-16 g/dL process.

 Low levels of

hemoglobin in

infective

endocarditis is a

result of the

presence of

vegetation in the

heart valves

which leads to a

poor circulation of

blood. With this

action there is a

reduction in the

levels of

circulating oxygen

Hematocrit: 28% 36-48 % as well.

 Low levels of
 Platelet count: 177,000/ 150,000- hematocrit is an

cu. mm 450,000/cu.mm indication of a

poor perfusion

status which is

Differential count: 40-60 common in

Neutrophil: 74 infective

endocarditis.

 High levels of

neutrophils

10-40 indicate a current

Lymphocyte: 12 infection is

happening in the

body.

 Low levels of

2-7 lymphocytes is an

Monocyte: 11 indication of a

concurring

bacterial infection.

 Increased levels

of monocytes

indicate a active

phagocytic

activity has

occurred.

Culture and June 12, Moderate growth of P.  Culture and

sensitivity 2023 aeruginosa and extended sensitivity result

spectrum beta lactamase reflects the

producing Klebsiella organism present

that causes the

infection.

Normally,

pathogenic

bacteria should
 not be present if

there is no

current infection

that is happening.

Blood Chemistry June 10, Serum Albumin: 3.5-5.2 g/dL  Low levels of

2023 2.90g/dL albumin in the

blood indicates

infection as

bacteria is able to

increase the

permeability of

the vascular walls

which makes

albumin leaks out

in the tissue

spaces. Edema

commences when

albumin is low in

the blood stream.

Electrocardiography June 20, Impression: ---  Atrial fibrillation

2023  Atrial occurs in infective

Fibrillation endocarditis as a

result of the

vegetation

present in the

heart valves.

Ultrasound(Abdomen June 2, Impression: ---  Ascites in infective

) 2023  Splenomegaly endocarditis

 Reactive indicates right

cholecystitis sided heart

 Ascites involvement.

Splenomegaly

results from a
 backflow of the

blood from the

right side of the

heart.

Echocardiography

Figure 1 Echocardiography result with Vegetation