infective endocarditis


in·fec·tious en·do·car·di·tis

, infective endocarditisendocarditis due to infection by microorganisms.

infective endocarditis

Acute endocarditis; bacterial endocarditis; subacute endocarditis Cardiology An infection of the endocardium which may involve the valves and extend to the myocardium, often occurring in Pts with underlying heart disease Sources of infection Transient bacteremia, common during dental, upper respiratory, urologic, and lower GI diagnostic and surgical procedures; IE may result in vegetations on valves, endocardium and the vascular intima, which may become dislodged and send clots to the brain, lungs, kidneys, or spleen Agents S viridans causes ±50% of IE, staphylococcus and group D streptococcus, Pseudomonas spp, Serratia spp Candida spp Clinical Sx develop slowly over months–subacute or abruptly; fever, fatigue, malaise, headache, night sweats, splinter hemorrhages under fingernails, heart murmurs due to vegetations especially on the mitral valve, splenomegaly, anemia Risk factors Congenital heart disease, ASD, PDA, etc; prior rheumatic heart disease; heart valve defects–eg, mitral insufficiency, prosthetic valves Prophylaxis Antiobiotics before surgery in in at-risk Pts. See Endocarditis.

in·fec·tious en·do·car·di·tis

, infective endocarditis (in-fek'shŭs en'dō-kahr-dī'tis, in-fek'tiv) Endocarditis due to infection by microorganisms.
OSLER'S NODES AS SEEN IN INFECTIVE ENDOCARDITIS

infective endocarditis

Abbreviation: IE
Endocarditis caused by any microorganism, esp. any species of streptococci or staphylococci, and less often by Haemophilus spp. or other HACEK bacteria (e.g., Actinobacillus actinomycetem comitans, Cardiobacterium hominis, Eikenella corrodens, or Kingella kingae), enteric bacteria, ricksettsiae, chlamydiae, or fungi. Traditionally, IE can be categorized as acute if the illness has a fulminant onset; catheter-related if the causative microorganism gains access to the heart from an indwelling line; culture-negative if echocardiograms reveal vegetations and other criteria for the disease are present, but the causative microbes have not been isolated in the laboratory; left-sided if it develops on the mitral or aortic valves; nosocomial if it occurs after 48 hr of hospitalization or an invasive surgical procedure; pacemaker-related if the disease occurs on an implanted pacemaker or cardioverter-defibrillator; prosthetic if it occurs on a surgically implanted heart valve; right-sided if it develops on the tricuspid or pulmonary valves; and subacute if it develops after several weeks or months of anorexia, low-grade fevers, and malaise. The incidence in the U.S. is about 2 to 4 cases per 100,000. Patients who are elderly or have a history of injection drug abuse, diabetes mellitus, immunosuppressing illnesses, aortic stenosis, mitral valve prolapse, or rheumatic heart disease are more likely than others to become infected.

Symptoms

Patients with subacute IE may have vague symptoms, including low-grade fevers, loss of appetite, malaise, and muscle aches. Acutely infected patients often present with high fevers, prostration, chills and sweats, stiff joints or back pain, symptoms of heart failure (esp. if the infection has completely disrupted a heart valve or its tethers), heart block (if the infection erodes into the conducting system of the heart), symptoms caused by the spreading of the infection to lungs or meninges (e.g., cough, headache, stiff neck, or confusion), stroke symptoms, symptoms of renal failure, rashes (including petechiae), or other findings. Signs of the illness typically include documented fevers, cardiac murmurs, or (more rarely) nodular eruptions on the hands and feet (Osler's nodes or Janeway lesions). Cottonwool spots may be seen on the retinas of some affected persons. See: illustration

Diagnosis

Blood cultures, esp. if persistently positive, form the basis for the diagnosis of endocarditis. Contemporary criteria for diagnosis also include visual confirmation of endocardial infection (vegetations) by echocardiography, the presence of several other suggestive anomalies (e.g., persistent fevers in a patient who is known to inject drugs or a patient with an artificial heart valve), infective emboli in the lungs or other organs; and characteristic skin findings. Occasionally, a patient who dies of a febrile illness may be found to have infective vegetations on the heart valves at autopsy.

Prognosis

Endocarditis is deadly in about 10% to 25% of patients. Death is most likely to occur in patients who suffer strokes resulting from infected fragments embolizing to the brain and in patients who suffer congestive heart failure. Patients with right-sided endocarditis have a better prognosis than patients with other forms of the disease.

Treatment

Many patients recover after treatment with prolonged courses of parenteral antibiotics. Some (e.g., those with heart failure or severely injured hearts) may not respond without surgery to replace damaged valves or débride abscesses within the myocardium.

Patient care

During the acute phase of treatment, patients are monitored for signs and symptoms of heart failure (e.g., dyspnea, orthopnea, crackles, dependent edema, changes in the heart murmur, and a postsystolic gallop), cerebral emboli (e.g., paralysis, aphasias, changes in mental status), and embolization to the kidney (e.g., decreased urine output, hematuria); lung involvement (e.g., dyspnea, cough, egophony, hemoptysis, pleuritic pain, or friction rub) or spleen involvement (e.g., left upper quadrant abdominal pain radiating to the left shoulder, abdominal rigidity); and peripheral vascular occlusion (e.g., numbness or tingling, changes in pulses, pallor, and coolness in an extremity). Blood cultures may be taken periodically to monitor the effectiveness of antibiotic therapy. Before the administration of antibiotics, a history of allergies is obtained. Treatment peak and trough drug levels are checked (e.g. when aminoglycoside or vancomycin is given) to maintain therapeutic levels and prevent toxicity. Supportive treatment includes bedrest, sufficient fluid intake to preserve hydration, and aspirin or acetaminophen for fever and aches.

Passive and active limb exercises are used to maintain muscle tone and quiet, diversional activities to prevent excessive physical exertion until a slow, progressive activity program that limits cardiac workload can be established.

Prophylaxis

The American Heart Association recommends that patients at high risk for endocarditis should receive prophylactic antibiotics prior to many procedures, including dental and periodontal cleanings and extractions, intraligamentary local anesthetic injections, tonsillectomy, adenoidectomy, bronchoscopy with rigid instrument, sclerotherapy for esophageal varices, esophageal stricture dilation, biliary tract procedures, barium enema or colonoscopy, surgery involving the respiratory or intestinal mucosa, prostate surgery, cystoscopy, and urethral dilation.

See also: endocarditis

Infective Endocarditis

DRG Category:216
Mean LOS:16.5 days
Description:SURGICAL: Cardiac Valve and Other Major Cardiothoracic Procedures With Cardiac Catheterization and With Major CC
DRG Category:218
Mean LOS:7.4 days
Description:SURGICAL: Cardiac Valve and Other Major Cardiothoracic Procedures With Cardiac Catheterization and Without CC or Major CC
DRG Category:219
Mean LOS:12.5 days
Description:SURGICAL: Cardiac Valve and Other Major Cardiothoracic Procedures Without Cardiac Catheterization and With Major CC
DRG Category:221
Mean LOS:5.6 days
Description:SURGICAL: Cardiac Valve and Other Major Cardiothoracic Procedures Without Cardiac Catheterization and Without CC or Major CC
DRG Category:307
Mean LOS:3.3 days
Description:MEDICAL: Cardiac Congenital and Valvular Disorders Without Major CC

Infective endocarditis (IE) is an inflammatory process that typically affects a deformed or previously damaged valve, which is usually the focus of the infection. Typically, endocarditis occurs when an invading organism enters the bloodstream and attaches to a sterile fibrin clot already present on the leaflets of the valves or the endocardium. The bacteria “innoculate” the clot, multiply, and form a projection of tissue that includes bacteria, fibrin, red blood cells, and white blood cells on the valves of the heart. This clump of material, called vegetation, may eventually cover the entire valve surface, leading to ulceration and tissue necrosis. Vegetation may even extend to the chordae tendineae, causing them to rupture and the valve to become incompetent. Most commonly, the mitral or aortic valve is involved. The tricuspid valve is mainly involved in intravenous (IV) drug abusers but is otherwise rarely infected. Infections of the pulmonary valve are rare.

IE can occur as an acute or a subacute condition. Generally, acute IE is a rapidly progressing infection, whereas subacute IE progresses more slowly. Acute endocarditis usually occurs on a normal heart valve and is rapidly destructive and fatal in 6 weeks if it is left untreated. Subacute endocarditis usually occurs in a heart already damaged by congenital or acquired heart disease on damaged valves and takes up to a year to cause death if it is left untreated.

Causes

Since the 1960s, the most common causes of IE have been nosocomial infections from IV catheters, IV drug abuse, and prosthetic valve endocarditis. IVs become infected at the insertion site, on the catheter itself, from another site in the body, or from the IV infusate.

The etiology of acute IE is predominantly bacterial. The two most common causes of bacterial endocarditis are staphylococcal and streptococcal infections (Box 1), and Staphylococcus aureus is the primary pathogen of endocarditis. Subacute IE occurs in people with acquired cardiac lesions. Possible ports of entry for the infecting organism include lesions or abscesses of the skin and genitourinary (GU) or gastrointestinal (GI) infections. Surgical or invasive procedures such as tooth extraction, tonsillectomy, bronchoscopy, endoscopy, colonoscopy, cystoscopy, transesophageal echocardiography, and prosthetic valve replacement also place the patient at risk.

Conditions Predisposing to Endocarditis
  • Rheumatic heart disease
  • Congenital heart disease (CHD; patent ductus arteriosus, ventricular septal defect, bicuspid aortic valve, Fallot’s tetralogy)
  • Prosthetic valve surgery
  • Parenteral drug abuse
  • Placement of intravascular foreign bodies (intravenous catheters, dialysis shunts, pacemakers, hyperalimentation catheters)
  • Mitral valve prolapse
  • Asymmetric septal hypertrophy
  • Marfan’s syndrome
  • Previous episodes of endocarditis
  • Skin, bone, and pulmonary infections

Genetic considerations

Heritable immune responses could be protective or increase susceptibility.

Gender, ethnic/racial, and life span considerations

The incidence of IE in infancy and childhood is low. Nearly all children infected have an identifiable predisposing lesion. Men over age 45 are at highest risk, males are affected three times more than females, and more than half the cases occur in people older than 60. There are no known racial or ethnic considerations.

Global health considerations

The incidence of IE in the United States, Western Europe, and other developed regions is approximately 13 cases per 100,000 persons per year. Less is known about the incidence in developing countries.

Assessment

History

A common finding of patients with preexisting cardiac abnormalities is a recent history (3 to 6 months) of dental procedures. Question the patient about the type of procedure performed and if bleeding of the gums occurred.

Patients with IE may have complaints of continuous fever (103°F to 104°F) in acute IE, whereas in the subacute form, temperatures are generally in the range of 99°F to 102°F. Other symptoms include chills (limited to acute IE), fatigue, malaise, joint pain, weight loss, anorexia, and night sweats.

Physical examination

The patient appears acutely ill. Observe for signs of temperature elevation, such as warm skin, dry mucous membranes, and alternating chills and diaphoresis. Inspect the conjunctivae, upper extremities, and mucous membranes of the mouth for the presence of petechiae, splinter hemorrhages in nailbeds, Osler nodes (painful red nodes on pads of fingers and toes), and joint tenderness. Palpate the abdomen for splenomegaly, which is present in approximately 30% of patients with IE. Auscultate the heart for the presence of tachycardia and murmurs. Approximately 95% of those with subacute IE have a heart murmur (most commonly mitral and aortic regurgitation murmurs), which is typically absent in patients with acute IE.

Psychosocial

Lengthy interventions, such as prophylactic antibiotic treatment, are generally required. Therefore, determine the patient’s ability to understand the disease, as well as to comply with prescribed long-term treatments.

Diagnostic highlights

General Comments: There are no specific serum laboratory tests or diagnostic procedures that conclusively identify IE, although some are highly suggestive of its presence. Special cultures or serologic tests may detect nonbacterial IE.

TestNormal ResultAbnormality With ConditionExplanation
Blood cultures and sensitivities (three to five sets of cultures over a 24–hr period)NegativePositive for microorganisms in 90% of patients but a high (50%) false-positive rate; continuous bacteremia for more than 30 min documented on blood culturesIf patients have been on antibiotics, they are less likely to have positive cultures; three sets of blood culture should be taken from separate sites over at least a 1-hr period before antibiotics are begun

Other Tests: Tests include complete blood count, computed tomography, M-mode and two-dimensional echocardiography, transesophageal echocardiogram, transthoracic echocardiogram, two-dimensional cardiac ultrasound Doppler, electrocardiogram, and rheumatoid factor.

Primary nursing diagnosis

Diagnosis

Infection related to the causative organism (streptococci, pneumococci, staphylococci, gram-negative bacilli, fungi)

Outcomes

Immune status; Knowledge: Infection control; Risk control; Risk detection; Nutritional status; Treatment behavior: Illness or injury

Interventions

Infection control; Infection protection; Medication prescribing; Nutritional management; Surveillance; Nutritional management; Infection control: Intraoperative

Planning and implementation

Collaborative

For persons at high risk for contracting IE, most physicians prescribe antibiotic therapy to prevent episodes of bacteremia before, during, and after invasive procedures. Procedures that are particularly associated with endocarditis are manipulation of the teeth and gums or GU and GI systems and surgical procedures or biopsies that involve respiratory mucosa.

Supportive treatment with oxygen, treatment of congestive heart failure, or management of acute renal failure with dialysis may be necessary. If the patient has developed endocarditis as a result of IV drug abuse, an addiction consultation is essential, with a possible referral to an appropriate treatment program. Surgical replacement of the infected valve is needed in those patients who have an infecting microorganism that does not respond to available antibiotic therapy and for patients who have developed infectious endocarditis in a prosthetic heart valve. (See Coronary Artery Disease, p. 282, for a full discussion of the collaborative and independent management of a patient following open heart surgery.)

Pharmacologic highlights

Medication or Drug ClassDosageDescriptionRationale
Penicillin G2 million units IV q 4 hr for 4 wkAntibioticTreats penicillin-susceptible streptococcal infections in subacute bacterial endocarditis; patients who are allergic to penicillin may receive vancomycin
Oxacillin; gentamicin, vancomycin, or tobramycin2 g IV q 4 hr; up to 5 mg/kg per day IV q 8 hrAntibioticTreats acute bacterial endocarditis; S. aureus and gram-negative bacilli are the most likely bacteria
Acetaminophen (Tylenol)650 mg as needed q 4–6 hrNonnarcotic analgesic; antipyreticRelieves joint and muscle achiness; controls fever

Other Drugs: Ceftriaxone at 2 g/day IV for 4 weeks; may also be given intramuscularly if problems occur with venous access problems and can be given once a day as an outpatient if the patient is stable. Other antibiotics are cefazolin and nafcillin.

Independent

During the acute phase of the disease, provide adequate rest by assisting the patient with daily hygiene. Provide a bedside commode to reduce the physiological stress that occurs with the use of a bedpan. Space all nursing care activities and diagnostic tests to provide the patient with adequate rest. During the first few days of hospital admission, encourage the family to limit visitation.

Emphasize patient education. Individualize a standardized plan of care and adapt it to meet the patient’s needs. Areas for discussion include the cause of the disease and its course, medication regimens, technique for administering IV antibiotics, and practices that help avoid and identify future infections.

If the patient is to continue parenteral antibiotic therapy at home, make sure that before he or she is discharged from the hospital, the patient has all the appropriate equipment and supplies that will be needed. Make a referral to a home health nurse as needed and provide the patient and family with a list of information that describes when to notify the primary healthcare provider about complications.

Evidence-Based Practice and Health Policy

Knirsch, W., & Nadal, D. (2011). Infective endocarditis in congenital heart disease. European Journal of Pediatrics, 170(9), 1111–1127.

  • In a population-based analysis of 34,279 children with CHD, investigators identified 185 cases of IE. The estimated incidence in this population was 6.1 cases per 1,000 children (95% CI, 5 to 7.5 cases).
  • The CHD most associated with IE risk was cyanotic CHD, which increased the likelihood of developing IE by 6.44 times (95% CI, 3.95 to 10.5).
  • Children who had undergone cardiac surgery during the previous 6 months were 5.34 times more likely to develop IE than those who had not (95% CI, 2.49 to 11.43). Children under age 3 were also 3.53 times more likely to develop IE than children ages 6 to 18 (95% CI, 2.51 to 4.96).

Documentation guidelines

  • Observations and physical findings regarding level of consciousness, degree of abdominal or chest pain, skin temperature, and color; presence of petechiae, splinter hemorrhages, Osler nodes, joint tenderness, abnormal vital signs, dyspnea, cough, and crackles or wheezing
  • Presence and characteristics of heart murmurs
  • Response to antibiotic therapy and antipyretics
  • Presence of complications: Signs of right- or left-sided heart failure, arterial embolization

Discharge and home healthcare guidelines

To prevent IE, provide patients in the high-risk category with the needed information for early detection and prevention of the disease. Instruct recovering patients to inform their healthcare providers, including dentists, of their endocarditis history because they may need future prophylactic antibiotic therapy to prevent subsequent episodes.

Be sure the patient understands all medications, including the dosage, route, action, and adverse effects. Make sure the patient understands the need to complete the course of antibiotic therapy. Explain the side effects that may occur during antibiotic administration (GI distress, yeast infection, sun sensitivity, skin rash). Encourage the patient to seek prompt medical attention if side effects occur. Make sure the patient or significant others can demonstrate the appropriate method of antibiotic administration. Instruct the patient on proper IV catheter site care as well as the signs of infiltration. Encourage good oral hygiene and advise the patient to use a soft toothbrush and to brush at least twice a day. Teach patients to avoid irrigation devices and flossing. Teach the patient to monitor and record temperature daily at the same time. Encourage the patient to take antipyretics according to physician orders. Instruct the patient to report signs of heart failure and embolization as well as continued fever, chills, fatigue, malaise, or weight loss.