Prosthetic Heart Valves


Practice Essentials

Bioprosthetic valves (see the image below) used in heart valve replacement generally offer functional properties (eg, hemodynamics, resistance to thrombosis) that are more similar to those of native valves. Implantation of prosthetic cardiac valves to treat hemodynamically significant aortic or mitral valve disease has become increasingly common.

The Hancock M.O. II aortic bioprosthesis (porcine)The Hancock M.O. II aortic bioprosthesis (porcine). Reproduced with permission from Medtronic, Inc.

Replacement of diseased valves with prosthetic heart valves reduces the morbidity and mortality associated with native valvular disease, but it comes at the expense of risking complications related to the implanted prosthetic device. Emergency medicine physicians must be able to rapidly identify patients at risk and begin appropriate diagnostic testing, stabilization, and treatment. Even when promptly recognized and treated, acute prosthetic valve failure is associated with a high mortality rate.

Essential update: Study finds equivalent patient survival rates for bioprosthetic and mechanical aortic valves

In a retrospective cohort analysis of 4253 patients who underwent primary isolated aortic-valve replacement, 15-year survival and stroke rates were equivalent with bioprosthetic and mechanical valves. For bioprosthetic valves, the risk of repeat surgery was greater but the incidence of major bleeding was lower. [12]

In propensity-matched comparisons, actuarial 15-year mortality rates were 60.6% with the bioprosthetic aortic valve and 62.1% with the mechanical valve. Cumulative 15-year stroke rates were 7.7% and 8.6% in the two groups, respectively. The reoperation rate was 12.1% in the bioprosthetic valve group at 15 years and 6.9% in the mechanical valve group, while major bleeding occurred in 6.6% of bioprosthesis patients and in 13.0% of the mechanical-valve group.

Signs and symptoms

Signs and symptoms of prosthetic heart valve malfunction depend on the type of valve, its location, and the nature of the complication. Presentations may include the following:

  • Acute prosthetic valve failure: Sudden onset of dyspnea, syncope, or precordial pain

  • Acute aortic valve failure: Sudden death; survivors have acute severe dyspnea, sometimes accompanied by precordial pain, or syncope

  • Subacute valvular failure: Symptoms of gradually worsening congestive heart failure; they also may present with unstable angina or, at times, may be entirely asymptomatic

  • Embolic complications: Symptoms related to the site of embolization (eg, stroke, myocardial infarction [MI], sudden death, or symptoms of visceral or peripheral embolization)

  • Anticoagulant-related hemorrhage: Symptoms related to the site of hemorrhage

A history of fever should raise the possibility of prosthetic valve endocarditis (PVE).

On physical examination, normal prosthetic heart valve sounds include the following:

  • Mechanical valves: Loud, high-frequency, metallic closing sound; soft opening sound (tilting disc and bileaflet valves); low-frequency opening and closing sounds of nearly equal intensity (caged ball valves)

  • Tissue valves: Closing similar to those of native valves, low-frequency early opening sound in the mitral position

Prosthetic heart valve murmurs noted include the following:

  • Aortic prosthetic valves: Some degree of outflow obstruction with a resultant systolic ejection murmur (loudest in caged ball and small porcine valves); low-intensity diastolic murmur (tilting disc and bileaflet valves)

  • Mitral prosthetic valves: Low-grade systolic murmur (caged ball valves); short diastolic murmur (bioprostheses and, occasionally, St. Jude bileaflet valves)

Additional findings may include the following:

  • Acute valvular failure: Evidence of poor tissue perfusion; hyperdynamic precordium and right ventricular impulse (50% of cases); absence of a normal valve closure sound or presence of an abnormal regurgitant murmur

  • Subacute valvular failure: Rales and jugular venous distention; signs of right-side failure; a new regurgitant murmur or absence of normal closing sounds; a new or worsening hemolytic anemia (may be the only presenting abnormality)

  • PVE (often obscure): Fever (97% of cases); a new or changing murmur (56% of cases); classic signs of native valve endocarditis; splenomegaly; congestive heart failure, septic shock, or primary valvular failure; systemic emboli

See Clinical Presentation for more detail.

Diagnosis

Laboratory studies that may be useful include the following:

  • Complete blood count

  • Blood urea nitrogen (BUN) and creatinine levels

  • Urinalysis

  • Blood culture

  • Prothrombin time (PT) or international normalized ratio (INR)

Imaging studies that may be helpful include the following:

  • Chest radiography: This can help in delineating the valvular morphology and determining whether the valve and occluder are intact; each of the most commonly used valve types has its own characteristic radiographic appearance

  • Echocardiography (2-dimensional, Doppler, transesophageal [the study of choice for a suspected prosthetic valve complication], transthoracic)

  • Cinefluorography: This may detect impaired occluder movement but often cannot readily determine the etiology

  • Computed tomography: A consensus statement from the Society of Cardiovascular Computed Tomography (SCCT) states that CT should be performed as part of the evaluation of all patients being considered for transcatheter aortic valve implantation (TAVI)/transcatheter aortic valve replacement (TAVR), except those in whom CT is contraindicated, [34and that the CT images should be interpreted with a member of the TAVI/TAVR team or reviewed with the operator before the procedure

See Workup for more detail.

Management

In patients with acute valvular failure, diagnostic studies must be performed simultaneously with resuscitative efforts.

Treatment approaches to primary valve failure include the following:

  • Emergency valve replacement

  • Concomitant adjunctive therapy

  • Afterload reduction and inotropic support

  • In selected cases, intra-aortic balloon counterpulsation

Treatment approaches to PVE include the following:

  • Intravenous antibiotics administered as soon as 2 sets of blood cultures are drawn

  • Cessation of warfarin until central nervous system involvement is ruled out and invasive procedures are determined to be unnecessary [5]

  • Consideration of anticoagulation

  • Consideration of emergency surgery in patients with moderate to severe heart failure or with an unstable prosthesis noted on echocardiography or fluoroscopy

Treatment approaches to thromboembolic complications include the following:

  • Anticoagulation (if it has not already been initiated or if the patient has a subtherapeutic INR)

  • Assessment of valve function

  • Note: US dabigatran prescribing information now includes a contraindication in patients with mechanical prosthetic valves [6]

Treatment approaches to prosthetic valve thrombosis include the following:

  • Surgery (historically the mainstay of treatment but associated with a high mortality)

  • Thrombolytic therapy (appropriate for selected patients with thrombosed prosthetic valves): Should always be performed in conjunction with cardiovascular surgical consultation

  • In cases of major anticoagulant-related hemorrhage, reversal of anticoagulation

See Treatment and Medication for more detail.

Background

Implantation of prosthetic cardiac valves to treat hemodynamically significant valvular disease has become an increasingly common procedure. It is estimated that 60,000-95,000 patients per year are undergoing heart valve replacement in the United States.

Bioprosthetic valves used in heart valve replacement generally offer functional properties (eg, hemodynamics, resistance to thrombosis) that are more similar to those of native valves. Implantation of prosthetic cardiac valves to treat hemodynamically significant aortic or mitral valve disease has become increasingly common.

Replacement of diseased valves reduces the morbidity and mortality associated with native valvular disease but comes at the expense of risking complications related to the implanted prosthetic device. These complications include primary valve failure, prosthetic valve endocarditis (PVE), prosthetic valve thrombosis (PVT), thromboembolism, and mechanical hemolytic anemia. In addition, because many of these patients require long-term anticoagulation, anticoagulant-related hemorrhage may occur.

Transcatheter approaches to aortic valve implantation have allowed patients previously felt to be poor operative risks to undergo valve replacement.

Emergency medicine physicians must be able to rapidly identify patients at risk and begin appropriate diagnostic testing, stabilization, and treatment. Even when promptly recognized and treated, acute prosthetic valve failure is associated with a high mortality rate.

More than 80 models of artificial valves have been introduced since 1950. In day-to-day emergency practice, however, it is necessary to be familiar with a few basic types. Prosthetic valves are either created from synthetic material (mechanical prosthesis) or fashioned from biological tissue (bioprosthesis). The choice of prosthesis is determined by the anticipated longevity of the patient and his/her ability to tolerate anticoagulation. [7]

Design Features

Three main designs of mechanical valves exist: the caged ball valve, the tilting disc (single leaflet) valve, and the bileaflet valve. The only Food and Drug Administration (FDA)–approved caged ball valve is the Starr-Edwards valve, shown in the image below.

Starr-Edwards Silastic ball valve mitral Model 612Starr-Edwards Silastic ball valve mitral Model 6120. Reproduced with permission from Baxter International, Inc.

Tilting disc valve models include the Medtronic Hall valve, shown in the image below, Omnicarbon (Medical CV) valves, Monostrut (Alliance Medical Technologies), and the discontinued Bjork-Shiley valves.

Medtronic Hall mitral valve. Reproduced with permiMedtronic Hall mitral valve. Reproduced with permission from Medtronic, Inc.

Bileaflet valves include the St. Jude (St. Jude Medical), shown in the image below, which is the most commonly implanted valve in the United States; CarboMedics valves (Sulzer CarboMedics); ATS Open Pivot valves (ATS Medical); and On-X and Conform-X valves (MCRI).

St. Jude Medical mechanical heart valve. PhotograpSt. Jude Medical mechanical heart valve. Photograph courtesy of St. Jude Medical, Inc. All rights reserved. St. Jude Medical is a registered trademark of St. Jude Medical, Inc.

Bioprosthetic (xenograft) valves are made from porcine valves or bovine pericardium. Porcine models include the Carpentier-Edwards valves (Edwards Lifesciences) and Hancock II and Mosaic valves (Medtronic); both valves are shown in the images below.

Carpentier-Edwards Duralex mitral bioprosthesis (pCarpentier-Edwards Duralex mitral bioprosthesis (porcine). Reproduced with permission from Baxter International, Inc.
The Hancock M.O. II aortic bioprosthesis (porcine)The Hancock M.O. II aortic bioprosthesis (porcine). Reproduced with permission from Medtronic, Inc.

Pericardial valves include the Perimount series valves (Edwards LifeSciences). Ionescu-Shiley pericardial valves have been discontinued. Stentless porcine valves have also come into use. They offer improved hemodynamics with a decreased transvalvular pressure gradient when compared with older stented models. These models include the Edwards Prima Plus, Medtronic Freestyle, and Toronto SPV valve (St. Jude Medical). [8]

Homografts or preserved human aortic valves are used in a minority of patients.

Two devices have been approved for transcatheter aortic valve implantation (TAVI): the SAPIEN XT valve (Edwards LifeSciences), made of bovine pericardium, and the CoreValve (Medtronic), made of porcine pericardium.

Indications for Bioprosthetic Valves

Aortic stenosis

The American College of Cardiology/American Heart Association (ACC/AHA) recommendations for aortic valve replacement in patients with valvular aortic stenosis (AS) are summarized in the list below. [9In most adults with symptomatic severe AS, aortic valve replacement (AVR) is the surgical treatment of choice. If concomitant coronary disease is present, AVR and coronary artery bypass graft (CABG) surgery should be performed simultaneously.

Successful AVR produces substantial clinical and hemodynamic improvement in patients with AS, including octogenarians. AVR should be performed in all symptomatic patients with severe AS regardless of left ventricular (LV) function, as survival is better with surgical treatment than with medical treatment.

ACC/AHA recommendations for AVR in AS are as follows (indication; class):

  • Symptomatic patients with severe AS; Class I

  • Patients with severe AS undergoing CABG surgery; Class I

  • Patients with severe AS undergoing surgery on the aorta or other heart valves; Class I

  • Patients with moderate AS undergoing CABG surgery or surgery on the aorta or other heart valves; Class IIa

  • Prevention of sudden death in asymptomatic patients with none of the findings listed under asymptomatic patients with severe AS; Class III

AVR is also recommended in asymptomatic patients with severe AS and the following:

  • LV systolic dysfunction; Class IIa

  • Abnormal response to exercise (eg, hypotension); Class IIa

  • Ventricular tachycardia; Class IIb

  • Marked or excessive left ventricular hypertrophy (LVH) (>15 mm); Class IIb

  • Valve area less than 0.6 cm2; Class II

The classes referred to above are defined as follows:

  • Class I - Conditions for which there is evidence and/or general agreement that the procedure or treatment is beneficial, useful, and effective

  • Class II - Conditions for which there is conflicting evidence and/or a divergence of opinion about the usefulness/efficacy of a procedure or treatment

  • Class IIa - Weight of evidence/opinion is in favor of usefulness/efficacy

  • Class IIb - Usefulness/efficacy is less well established by evidence/opinion

  • Class III - Conditions for which there is evidence and/or general agreement that the procedure/treatment is not useful/effective and in some cases may be harmful

Candidates for percutaneous aortic valve placement must have severe, symptomatic aortic stenosis with formal contraindications for conventional aortic valve surgery or other characteristics that would limit the patient's surgical candidacy because of excessive morbidity or mortality. The procedure should be offered to patients who would gain functional improvement from the procedure and not because they refuse conventional operation.

Aortic regurgitation

Under current ACC/AHA guidelines, aortic valve surgery is recommended for patients with chronic, severe aortic regurgitation (AR) when the patient is symptomatic. It is also recommended in the asymptomatic patient with chronic, severe AR who has a resting ejection fraction (EF) of 50% or less or left ventricular dilatation. Additional circumstances in which aortic valve surgery may be reasonable are listed below. [9Surgical treatment of AR usually requires replacement of the diseased valve with a prosthetic valve, although valve-sparing repair is increasingly possible with advances in surgical technique and technology.

ACC/AHA recommendations for AVR in AR are as follows (indication; class):

  • Symptomatic patients with severe AR, irrespective of LV systolic function; Class I

  • Asymptomatic patients with chronic, severe AR and LV systolic dysfunction (EF < 0.50) at rest; Class I

  • Patients with chronic, severe AR while undergoing CABG or surgery on the aorta or other heart valves; Class I

  • Asymptomatic patients with severe AR with normal LV systolic function (EF >0.50) but with severe LV dilatation (end-diastolic dimension >75 mm or end-systolic dimension >55 mm); Class IIa

  • Patients with moderate AR while undergoing surgery on the ascending aorta; Class IIb

  • Patients with moderate AR while undergoing CABG; Class IIb

  • Asymptomatic patients with severe AR and normal LV systolic function at rest (EF >0.50) when the degree of LV dilatation exceeds an end-diastolic dimension of 70 mm or end-systolic dimension of 50 mm, when there is evidence of progressive LV dilatation, declining exercise tolerance, or abnormal hemodynamic responses to exercise; Class IIb

  • Asymptomatic patients with mild, moderate, or severe AR and normal LV systolic function at rest (EF >0.50) when degree of dilatation is not moderate or severe (end-diastolic dimension < 70 mm, end-systolic dimension < 50 mm); Class III

Mitral stenosis

Valve replacement for mitral stenosis (MS) may be considered in patients who are candidates for surgical therapy when the valve is not suitable for valvotomy (either surgical or percutaneous). The recommendations for surgery in patients with mitral stenosis, according to the current ACC/AHA guidelines, are described below. [9]

Mitral valve surgery (repair if possible) is indicated in patients with symptomatic (New York Heart Association [NYHA] functional Class III–IV) moderate or severe MS under any of the following circumstances:

  • Percutaneous mitral balloon valvotomy is unavailable

  • Percutaneous mitral balloon valvotomy is contraindicated because of left atrial thrombus despite anticoagulation or because concomitant moderate to severe mitral regurgitation (MR) is present

  • The valve morphology is not favorable for percutaneous mitral balloon valvotomy in a patient with acceptable operative risk (Class I)

Symptomatic patients with moderate to severe MS who also have moderate to severe MR should receive mitral valve replacement (MVR) unless valve repair is possible at the time of surgery (Class I).

Mitral valve replacement is reasonable in patients with severe MS and severe pulmonary hypertension (pulmonary artery systolic pressure >60 mm Hg) who have NYHA functional Class I–II symptoms and who are not considered candidates for percutaneous mitral balloon valvotomy or surgical mitral valve repair (Class IIa).

Mitral regurgitation

Although more technically demanding, mitral valve repair is recommended over MVR in most patients with severe, chronic mitral regurgitation (MR) who require surgery. Patients should be referred to surgical centers experienced with mitral valve repair. If mitral valve repair is not feasible, MVR with preservation of the chordal apparatus is preferred, as this preserves LV function and enhances postoperative survival. [9]

Clinical Implementation of Bioprosthetic Valves

The ACC/AHA recommendations for selection of a prosthetic aortic valve include the following [7:

  • A mechanical prosthesis is recommended for AVR in patients with a mechanical valve in the mitral or tricuspid position (Class I)

  • A bioprosthesis is recommended for AVR in patients of any age who will not take warfarin or who have major medical contraindications to warfarin therapy (Class I)

  • A bioprosthesis is reasonable for AVR in patients aged 65 years or older without risk factors for thromboembolism (Class IIa)

  • Aortic valve re-replacement with a homograft is reasonable for patients with active prosthetic valve endocarditis (Class IIa)

  • A bioprosthesis might be considered for AVR in a woman of childbearing age (Class IIb)

In addition, according to the recommendations, patient preference is a reasonable consideration in the selection of aortic valve operation and valve prosthesis. A mechanical prosthesis is reasonable for AVR in patients younger than age 65 years who do not have a contraindication to anticoagulation. A bioprosthesis is reasonable for AVR in patients younger than 65 years who elect to receive this valve for lifestyle considerations after detailed discussions of the risks of anticoagulation versus the likelihood that a second AVR may be necessary in the future (Class IIa).

The ACC/AHA recommendations for selection of a prosthetic mitral valve include the following [9:

  • A mechanical prosthesis is recommended for MVR in patients with a mechanical valve in the mitral or tricuspid position (Class I)

  • A mechanical prosthesis is reasonable for MVR in patients younger than age 65 years with long-standing atrial fibrillation (Class IIa)

  • A bioprosthesis is reasonable for MVR in patients aged 65 years or older (Class IIa)

A bioprosthesis is reasonable for MVR in patients younger than age 65 years in sinus rhythm who elect to receive this valve for lifestyle considerations after detailed discussions of the risks of anticoagulation versus the likelihood that a second MVR may be necessary in the future (Class IIa).

Clinical Trial Evidence for Bioprosthetic Valves

In a Veterans Affairs study comparing bioprosthetic valves with mechanical valves, at 15 years, all-cause mortality after AVR was lower in patients who received a mechanical valve than in those who received a bioprosthetic valve (66% vs 79%, respectively). In the study, 575 patients at 13 VA medical centers undergoing single AVR (n = 394) or single MVR (n = 181) were randomized at the time of surgery to receive a Hancock porcine valve or a Bjork-Shiley spherical disc valve. Long-term survival and valve-related complications were compared. No significant difference in all-cause mortality was seen between the two MVR groups. [10]

Reoperation rate after AVR was higher with the bioprosthetic valve than with the mechanical valve (29 ± 5% vs 10 ± 3%). Valve-related deaths after AVR accounted for 41% of all deaths in the bioprosthetic group and 37% in the mechanical valve group; valve-related deaths after MVR were 57% and 44% of all deaths, respectively. Primary valve failure was significantly greater with bioprosthetic valves for AVR (bioprosthetic vs mechanical, 23 ± 5% vs 0 ± 0%) and for MVR (44 ± 8% vs 5 ± 4%).

Almost all the primary valve failures were in patients younger than age 65 years (18 of 20 patients in the AVR group and 20 of 21 patients in the MVR group). Bleeding occurred more frequently in patients with a mechanical valve than in those with a bioprosthesis (AVR, 51 ± 4% vs 30 ± 4%; MVR, 53 ± 7% vs 31 ± 6%). No statistically significant differences were seen between the two valve groups for systemic embolism, infective endocarditis, or valve thrombosis.

Similar results were seen in the Edinburgh heart valve trial, in which 533 patients (AVR, n = 211; MVR, n = 261; double valve replacement, n = 61) were randomized at the time of surgery to receive a Bjork-Shiley 60° spherical tilting disc valve (n = 267) or a porcine bioprosthesis (Hancock, n = 107; Carpentier-Edwards, n = 159). Long-term survival rates at 20 years were not significantly different between the 2 valve groups (mechanical 25.0 ± 2.7%, porcine 22.6 ± 2.7%). Major bleeding was more common in Bjork-Shiley patients than in bioprosthesis patients (40.7 ± 5.4% vs 27.9 ± 8.4%, respectively). No significant differences were seen in major embolism or endocarditis. [11]

Pathophysiology

Valve failure

Primary valve failure may occur abruptly from the tearing or breakage of components or from a thrombus suddenly impinging on leaflet mobility. More commonly, valve failure presents gradually from calcifications or thrombus formation. Bioprostheses are less thrombogenic than mechanical valves, but this advantage is balanced by their diminished durability when compared with mechanical valves. Although 30-35% of bioprostheses will fail within 10-15 years, it can be anticipated that most mechanical valves will remain functional for 20-30 years.

Stenosis or incompetence of prosthetic valves occurs and may be due to a tear or perforation of the valve cusp, valvular thrombosis, pannus formation, valve calcification, or stiffening of the leaflets.

Primary failure of mechanical valves may be caused by suture line dehiscence, thrombus formation, or breakage or separation of the valve components. Acute valvular regurgitation or embolization of the valve fragments may result.

When the mitral valve acutely fails, rapid left atrial volume overload causes increased left atrial pressure. Pulmonary venous congestion and, ultimately, pulmonary edema occur. Cardiac output is decreased because a portion of the left ventricular output is being regurgitated into the left atrium. The compensatory mechanism of increased sympathetic tone increases the heart rate and the systemic vascular resistance (SVR). This may worsen the situation by decreasing diastolic filling time and impeding left ventricular outflow, thereby increasing the regurgitation.

Acute failure of a prosthetic aortic valve causes a rapidly progressive left ventricular volume overload. Increased left ventricular diastolic pressure results in pulmonary congestion and edema. The cardiac output is reduced substantially. The compensatory mechanism of an increased heart rate and a positive inotropic state, mediated by increased sympathetic tone, partly helps to maintain output. However, this is hampered by an increase in SVR, which impedes forward flow. Increased systolic wall tension causes a rise in myocardial oxygen consumption. Myocardial ischemia in acute aortic regurgitation may occur, even in the absence of coronary artery disease.

Biological prosthetic valves often slowly degenerate over time, become calcified, or suffer from thrombus formation. These events result in the slowly progressive failure of the valve. The presentation is usually that of gradually worsening congestive heart failure, with increasing dyspnea. Alternatively, patients may present with unstable angina or systemic embolization, or they may be entirely asymptomatic.

The first TAVI device for use in the United States was approved in November 2011. Subsequently, not enough time has passed to gather data concerning longevity and use. Vascular complications and strokes related to the procedure are decreasing with improved delivery techniques and equipment. Complications related to the conduction system requiring permanent pacemaker implantation occur in 14% of patients. This risk is increased with the use of the CoreValve prosthesis. [12]

Prosthetic valve endocarditis

PVE occurring within 1 year of implantation (early PVE) usually is due to perioperative contamination or hematogenous spread. PVE occurring after 1 year (late PVE) is usually caused by hematogenous spread. [13]

The pathologic hallmark of PVE in mechanical valves is ring abscesses. Ring abscess may lead to valve dehiscence and perivalvular leakage. Local extension results in the formation of myocardial abscesses. Further extension to the conduction system often results in a new atrioventricular block. Valve stenosis and purulent pericarditis occur less frequently.

Bioprosthetic valve PVE usually causes leaflet tears or perforations. Valve stenosis is more common with bioprosthetic valves than with mechanical valves. Ring abscess, purulent pericarditis, and myocardial abscesses are much less frequent in bioprosthetic valve PVE.

Finally, glomerulonephritis, mycotic aneurysms, systemic embolization, and metastatic abscesses also may complicate PVE.

Epidemiology

Frequency

United States

Prosthetic valve thrombosis is more common in mechanical valves. With proper anticoagulation, the rate of thrombosis in all valves is within the range of 0.1-5.7% per patient-year. Caged ball valves have the highest rate of thromboembolic complications, and bileaflet valves have the lowest. Valve thrombosis is increased with valves in the mitral position and in patients with subtherapeutic anticoagulation.

Anticoagulant-related hemorrhagic complications of mechanical valves include major hemorrhage in 1-3% of patients per year and minor hemorrhage in 4-8% of patients per year.

Low-grade hemolytic anemia occurs in 70% of prosthetic heart valve recipients, and severe hemolytic anemia occurs in 3%. The incidence is increased with caged ball valves and in those with perivalvular leaks.

Primary valve failure occurs in 3-4% of patients with bioprostheses within 5 years of implantation and in up to 35% of patients within 15 years. Mechanical valves have a much lower incidence of primary failure.

PVE occurs in 2-4% of patients. The incidence is 3% in the first postoperative year, then 0.5% for subsequent years. The incidence is higher when valve surgery is performed in patients with active native valve endocarditis. The incidence is higher in mitral valves. Mechanical and biological valves are equally susceptible to early PVE, but the incidence of late PVE is higher for bioprostheses. Despite improvements in surgical techniques, no appreciable change in the incidence has been observed. [14]

Mortality/Morbidity

Acute failure of a prosthetic aortic valve usually leads to sudden or near-sudden death. Prompt recognition and treatment of acute prosthetic mitral valve failure can be lifesaving. [13]

PVE has an overall mortality rate of 50%. In early PVE, the mortality rate is 74%. In late PVE, the mortality rate is 43%. The mortality rate with a fungal etiology is 93%. The mortality rate for staphylococcal infections is 86%. PVE due to Staphylococcus has a mortality rate of 25-40%. [1314]

Fatal anticoagulant-induced hemorrhage occurs in 0.5% of patients per year.

Age

In children, bioprostheses rapidly calcify and, therefore, undergo rapid degeneration and valve dysfunction. Incidence of bioprosthetic failure is much higher in patients younger than 40 years. The incidence of having any prosthetic valve complication decreases with age.


Clinical Presentation


History

In patients with malfunctioning prosthetic valves, symptoms are dependent on the type of valve, its location, and the nature of the complication. With valvular breakage or dehiscence, failure often occurs acutely with rapid hemodynamic deterioration. Failure occurs more gradually with valve thrombosis, calcification, or degeneration.

Note the following:

  • Information about the type of valve is important; the potential for complications depends on valve type and position. Sources include a wallet-sized identification card (typically given to the patient at the time of surgery) and/or a review of medical records.

  • Review of the operative report may be useful. If the native valve annulus is described as being heavily calcified or infected, the chance of a perivalvular leak is greater.

  • Patients with acute prosthetic valve failure often present in extremis with the sudden onset of dyspnea, syncope, or precordial pain.

  • Patients with acute aortic valve failure often experience sudden death. Those surviving have acute severe dyspnea, sometimes accompanied by precordial pain, or syncope.

  • Patients with subacute valvular failure present with symptoms of gradually worsening congestive heart failure. This includes increasing dyspnea with exertion, orthopnea, paroxysmal nocturnal dyspnea, and fatigue. They also may present with unstable angina or, at times, be entirely asymptomatic.

  • Patients with embolic complications have symptoms related to the site of embolization. Stroke syndromes are the most common presentation, although patients may present with myocardial infarction (MI), sudden death, or symptoms of visceral or peripheral embolization.

  • Symptoms due to anticoagulant-related hemorrhage are related to the site of hemorrhage.

  • A history of fever should alert the physician's suspicion to the possibility of PVE.

Physical

Normal prosthetic heart valve sounds

Mechanical valves

Tilting disc and bileaflet valves have a loud, high-frequency, metallic closing sound. This frequently can be heard without a stethoscope. Absence of this distinct closing sound is abnormal and implies valve dysfunction. These valves also may have a soft opening sound. Caged ball valves (Starr-Edwards) have low-frequency opening and closing sounds of nearly equal intensity.

Tissue valves

Closing sounds are similar to those of native valves. A low-frequency early opening sound may present in the mitral position.

Valve failure/thrombosis

Muffled or absent normal prosthetic heart sounds may be a clue to valve failure or thrombosis.

Prosthetic heart valve murmurs

Aortic prosthetic valves

Because of their smaller orifice size, all aortic valves often produce some degree of outflow obstruction with a resultant systolic ejection murmur. Caged ball and small porcine valves produce the loudest murmurs. The intensity of the murmur increases with rising cardiac output. Tilting disc valves and bileaflet valves do not occlude their outflow tract completely when closed, allowing some back flow. This causes a low-intensity diastolic murmur. Suspect prosthetic aortic valve failure in a patient with a greater than 2/6 diastolic murmur. Caged ball and tissue valves cause no diastolic murmur since they completely occlude their outflow tract in the closed position. Consider any degree of diastolic murmur in these patients pathologic until proven otherwise.

Mitral prosthetic valves

Caged ball valves may cause a low-grade systolic murmur due to the turbulent flow caused by the cage projecting into the left ventricle. Consider any holosystolic murmur greater than 2/6 pathologic in a patient with an artificial mitral valve. Short diastolic murmurs may be heard with bioprostheses and, occasionally, with the St. Jude bileaflet valve. These are best heard at the apex with the patient in the left lateral decubitus position.

Acute valvular failure

Patients with acute valvular failure present with cardiogenic shock and severe hypotension.

  • Evidence of poor tissue perfusion is present, including diminished peripheral pulses, cool or mottled extremities, confusion or unresponsiveness, and decreased urine output.

  • A hyperdynamic precordium and right ventricular impulse is present in 50% of patients with acute valvular failure.

  • Absence of a normal valve closure sound or presence of an abnormal regurgitant murmur is an important clue to the presence of prosthetic valvular failure.

Subacute valvular failure

Patients with subacute valvular failure often present with signs of gradually worsening left-sided congestive heart failure, including the following:

  • Rales and jugular venous distention may be present.

  • Signs of right-sided failure, including hepatic congestion and lower extremity edema, may also be present.

  • Patients with subacute valvular failure may present with a new regurgitant murmur or absence of normal closing sounds.

  • A new or worsening hemolytic anemia may be the only presenting abnormality in patients with subacute valvular failure.

PVE manifestations

The clinical manifestations of PVE are often obscure. Note the following:

  • Fever occurs in 97% of patients with PVE.

  • A new or changing murmur is present in 56% of patients. Absence of a murmur does not exclude the diagnosis. Valvular dehiscence, stenosis, or perforation causes the murmur. They may not occur early in the course of the illness.

  • Signs considered classic for native valve endocarditis, including petechiae, Roth spots, Osler nodes, and Janeway lesions, often are absent in PVE.

  • Splenomegaly supports the diagnosis but is present in only 26% of early PVE cases and in 44% of late PVE cases.

  • PVE may present as congestive heart failure, septic shock, or primary valvular failure.

  • Systemic emboli may be the presenting symptom in 7-33% of cases of PVE. This is more common with fungal etiologies.

Thromboembolic complications

Patients with complications related to embolization present with signs related to the site of embolization. Stroke syndromes are the most common; however, patients may present with MI, sudden death, or visceral or peripheral embolization. Systemic embolization should alert the physician to suspect valve thrombosis or PVE.

Anticoagulant-related hemorrhage: Signs due to anticoagulant-related hemorrhage depend on the site of hemorrhage. [1516]

Causes

Prosthetic valve endocarditis (PVE) has been divided into 2 subcategories. These reflect differences in clinical features, microbial patterns, and mortality. Early PVE occurs within the first year of valve insertion, whereas late PVE occurs after the first year.

Early PVE is usually the result of perioperative contamination. Causative organisms include Staphylococcus epidermidis (25-30%), Staphylococcus aureus (15-20%), gram-negative aerobes (20%), fungi (10-12%), streptococci (5-10%), and diphtheroids (8-10%).

Late PVE is usually the result of transient bacteremia from dental or genitourinary sources, GI manipulation, or intravenous drug abuse. The causative organisms are similar to those causing native valve endocarditis. These include Streptococcus viridans (25-30%), S epidermidis (23-38%), S aureus (10-12%), gram-negative bacilli (10-12%), group D streptococci (10-12%), fungi (5-8%), and diphtheroids (4-5%). An increase in cases of PVE due to methicillin-resistant S aureus has been observed.

Multiple negative blood culture results are unusual with common pathogens but often are seen more commonly with infections by the Haemophilus aphrophilus, Actinobacillus actinomycetemcomitans, Cardiobacterium hominis, Eikenella corrodens, and Kingella kingae (HACEK) group; Serratia and Rickettsia species; as well as Aspergillus, Histoplasma, and Candida species.


Diagnostic Considerations

Other conditions to consider in patients with prosthetic heart valves include the following:

  • Hemolytic anemia

  • Thromboembolic disease

  • Cardiac conduction disturbances

Prepare patients with acute primary valve failure and severe hemodynamic compromise for surgery as quickly as possible. Delays in surgery to pursue diagnostic testing result in increased mortality.

Consider PVE in any patient with a prosthetic valve and a fever.

Pregnancy

Some debate exists concerning the most advantageous method of providing adequate anticoagulation in pregnant patients with mechanical prostheses. [18]

Warfarin increases the chance of spontaneous abortion and stillbirths and is associated with teratogenicity from 6-12 weeks gestation.

Current recommendations are to use heparin from 6-12 weeks and from 38-40 weeks gestation. Warfarin may be used for the remainder of pregnancy.

The American College of Obstetrics and Gynecology has recommended against using low molecular weight heparin in pregnancy.

Differential Diagnoses

Laboratory Studies

Complete blood count

Hemolysis may cause anemia. In this case, microscopic evidence of hemolysis should be present. A sudden increase in hemolysis may signal a perivalvular leak. [19]

A hematocrit lower than 34% is present in 74% of patients with PVE and is the most common hematologic finding.

A WBC count lower than 12,000 is present in as many as 54% of patients with PVE.

BUN/creatinine levels

Glomerulonephritis and acute renal failure may complicate PVE.

Urinalysis

Hematuria is present in 57% of patients with PVE.

Blood cultures

Culture results are positive in multiple samples in 97% of patients with PVE. Blood cultures should be held for 3 weeks. Multiple blood cultures should be taken.

Prothrombin time (PT)/international normalized ratio (INR)

Recommendations vary as to the target INR. The following is offered as a general guideline, but remember that therapy must be individualized.

Bioprosthetic valves

INR 2-3 for 3 months following implantation; anticoagulation may then be discontinued unless the patient has another indication, such as atrial fibrillation or development of prosthetic valve thrombosis.

Mechanical valves

Aortic valve INR is 2-3; mitral valve INR is 2.5-3.5; Patients with atrial fibrillation should be kept at the higher end of this range. [5In patients with low hemorrhage risk, low-dose aspirin is recommended in addition to warfarin. [5]

Nontherapeutic values should raise the suspicion of valve thrombosis or systemic embolization.

Procedures

Certain procedures may cause bacteremia and thereby increase the chance of PVE. The emergency physician must be up to date with the latest prophylaxis guidelines. See Deterrence/Prevention.

Chest Radiography

An overpenetrated anteroposterior chest radiograph helps to delineate the valvular morphology and whether or not the valve and occluder are intact. In more stable patients, a lateral chest film helps identify the valve position and type.

The following are descriptions of the radiographic appearance of the more commonly seen valves.

Starr-Edwards caged ball valve

The base ring is radiopaque, as is the cage.

There are 3 struts for the aortic valve, and there are 4 struts for the mitral or tricuspid valve

The silastic ball is impregnated with barium that is mildly radiopaque (but not in all models).

Bjork-Shiley tilting disc valve

Although the Bjork-Shiley tilting disc valve has been discontinued, many patients still have these valves implanted.

The base ring and struts are radiopaque. Two U-shaped struts project into base ring.

The edge of the occluder disc is also radiopaque.

Medtronic-Hall tilting disc valve

The base ring is radiopaque.

Radiopaque struts that project into base ring: 3 small ones and 1 large hook-shaped one.

The occluder disc is mildly opaque but often cannot be seen.

Alliance Monostrut valve

The occluder has a radiopaque rim; the base ring and two struts are radiopaque.

St. Jude medical bileaflet valve

Mildly radiopaque leaflets are best seen when viewed on end. These are seen as radiopaque lines when the leaflets are fully open.

The base ring is not visualized on most models. The valve may not be visualized on some radiographs.

CarboMedics bileaflet valves

The valve housing and leaflets are radiopaque and easily visible.

Carpentier-Edwards porcine valve

The tall serpiginous wire support is the only visualized portion.

Hancock porcine valve

The radiopaque base ring is the only visible part in some models.

Other models have radiopaque stent markers with or without a visible base ring.

Ionescu-Shiley bovine pericardial valve

The base ring and wide fenestrated stents are one piece.

Echocardiography

Acoustic shadowing originating from the components of the prosthetic valve can severely limit the image of the valve itself as well as any pathologic process such as regurgitant streams, vegetations, and thrombosis. This is especially true with valves in the mitral position.

Two-dimensional and Doppler echocardiography, while not as reliable, may demonstrate perivalvular leaks, vegetations, and inadequate valve/occluder movement.

Two-dimensional echocardiography and Doppler echocardiography can detect the presence of acute valvular regurgitation and grade the severity.

Transesophageal echocardiography has emerged as the imaging study of choice in patients with a suspected prosthetic valve complication. This applies especially to prosthetic mitral valves, where transthoracic Doppler is often insensitive. Adequately excluding prosthetic valve regurgitation with a transthoracic echocardiogram is difficult.

In cases where any significant suspicion of valvular stenosis or regurgitation exists, an unremarkable transthoracic echocardiogram is unlikely to be sufficient to adequately rule out a pathologic process.

Cinefluorography

Cinefluorography may detect impaired occluder movement but often cannot readily determine the etiology.

Electrocardiography

An atrioventricular (AV) block may indicate the presence of a myocardial abscess. A fever and new AV block is considered PVE until proven otherwise.

AV block may also complicate TAVI, although this usually occurs early in the postoperative period.

Atrial fibrillation is common in mitral valve replacement and may cause hemodynamic compromise.


Treatment & Management


Emergency Department Care

In patients with acute valvular failure, diagnostic studies must be performed simultaneously with resuscitative efforts.

Primary valve failure

Patients with valvular failure due to breakage or abrupt tearing of the components usually present with acute hemodynamic deterioration. They need emergent valve replacement. Adjunctive therapy may be initiated while these arrangements are being made. A less dramatic presentation of valvular failure may be seen in patients with valve thrombosis or in those with more gradual deterioration of bioprosthetic valves (see Thromboembolic complications).

Begin afterload reduction and inotropic support in order to reduce the impedance to forward flow and improve peripheral perfusion. If the mean arterial pressure is higher than 70 mm Hg, sodium nitroprusside may be used. If the mean arterial pressure is lower than 70 mm Hg, dobutamine alone or in combination with inamrinone may be used.

Avoid inotropic agents with vasoconstricting properties.

Intra-aortic balloon counterpulsation may be useful in cases of acute mitral regurgitation when the patient is in extremis and surgical facilities are not immediately available. Intra-aortic balloon counterpulsation is relatively contraindicated in the presence of an incompetent aortic valve.

Prosthetic valve endocarditis

Administer intravenous antibiotics as soon as 2 sets of blood cultures are drawn. Vancomycin and gentamicin may be used empirically pending blood cultures and determination of methicillin resistance.

Patients taking warfarin who develop PVE should stop until CNS involvement is ruled out and invasive procedures are determined to be unnecessary. [5]

Consider anticoagulation in PVE, since the incidence of systemic embolization is as high as 40%.

Consider emergency surgery in patients with moderate-to-severe heart failure or in patients with an unstable prosthesis noted on echocardiography or fluoroscopy.

Thromboembolic complications

Patients presenting with embolization need to be anticoagulated if they are not already taking anticoagulants or have a subtherapeutic INR.

Assessment of valve function is needed.

The RE-ALIGN trial evaluated the safety and efficacy of dabigatran in patients with bileaflet mechanical prosthetic heart valves (recently implanted or implanted more than 3 months prior to enrollment). Patients were randomized to dose-adjusted warfarin or dabigatran 150, 220, or 300 mg BID. The study was terminated early due to the occurrence of significantly more thromboembolic events and excessive major bleeding with dabigatran compared with warfarin. These data resulted in revision of the US dabigatran prescribing information to include a contraindication in patients with mechanical prosthetic valves. [6]

Prosthetic valve thrombosis

Note the following:

  • Surgery had historically been the mainstay of treatment but is associated with a high mortality rate.

  • Mortality rates of 18% have been reported in those with New York Heart Association (NYHA) class IV undergoing surgery for left-sided prosthetic valve thrombosis.

  • Thrombolytic therapy may be used to treat select patients with thrombosed prosthetic valves.

  • Thrombolytic therapy is currently recommended over surgery for right-sided prosthetic valve thrombosis. [5]

  • Thrombolytic therapy is recommended over surgery for small left-sided prosthetic valve thrombosis (thrombus area < 0.8 cm2). The use of heparin and serial echocardiography is also recommended in these cases to documents improvement and thrombus resolution. [5]

  • Thrombolytic therapy is recommended in large (=0.8 cm2) left-sided prosthetic valve thrombosis when contraindications to surgery are present. [5]

  • Contraindications to thrombolysis of left-sided prosthetic valve thrombosis include the presence of a large left atrial thrombus, ischemic CVA between 4 hours and 4-6 weeks ago, and very early postoperative state (< 4 d). [20]

  • Thrombolytic therapy should always be done in conjunction with cardiovascular surgical consultation.

  • Patients with major anticoagulant-related hemorrhage require reversal of their anticoagulation with fresh frozen plasma and vitamin K.

  • The time off anticoagulants should be as short as possible to avoid valve thrombosis.

  • Use of recombinant factor VIIa or prothrombin complex concentrate should not be used to reverse excessive anticoagulation in patients with prosthetic heart valves.

Based on findings from a retrospective study of 778 patients, Yaffee et al recommend extending established guidelines for blood conservation strategy (BCS) in routine cardiac surgeries to aortic valve replacement. [2122The investigators reported that implementing BCS (eg, limits on intraoperative hemodilution, tolerance of perioperative anemia, blood management education of the cardiac surgery team) may reduce the use of red blood cells (RBCs) during surgery—without increasing mortality or morbidity. [2122]

In their study, implementation of the strategy resulted in a 2.7-fold reduction in RBC transfusions as well as a 1.7-fold reduction in the incidence of major complications (eg, sepsis, respiratory failure, renal failure, death). [2122The incidence of RBC transfusion fell significantly from 82.9% before use of BCS to 68.0% after implementation of the strategy.

Transfusion of 2 or more units of RBC on the day of surgery was associated with mortality, prolonged intubation, postoperative renal failure, and an increased incidence of any complication. Factors that affected the risk of RBC transfusion included the following [2122:

  • Decreased risk: Isolated aortic valve replacement, minimally invasive approach, BCS

  • Increased risk: Older age, previous cardiac procedure, female sex, smaller body surface area

Consultations

In patients presenting with any degree of prosthetic valvular failure, early consultation with a cardiologist is recommended in order to perform and interpret an echocardiogram.

Consult a cardiothoracic surgeon early in cases of severe hemodynamic compromise.

Medication Summary

Antibiotics, vasodilators, inotropic agents, and anticoagulants are the therapeutic agents most commonly used in heart-valve complications.

Vasodilators

Class Summary

A significant portion of cardiac output is regurgitated through an incompetent valve in acute mitral or aortic valve failure. By increasing peripheral vascular resistance, catecholamines worsen this effect. Vasodilators reduce SVR, which may allow forward flow, improving cardiac output.

Nitroprusside (Nitropress)

Produces vasodilation and increases inotropic activity of the heart. Causes peripheral vasodilation by direct action on venous and arteriolar smooth muscle, reducing peripheral resistance. At higher dosages, may exacerbate myocardial ischemia by increasing heart rate.

Inotropic agents

Class Summary

These agents increase cardiac output. Agents used in the setting of acute valvular failure should not induce vasoconstriction, as this increases valve regurgitation.

Dobutamine (Dobutrex)

Produces vasodilation and increases inotropic state. At higher dosages, may cause increased heart rate, exacerbating myocardial ischemia. Synthetic direct-acting catecholamine and beta-receptor agonist. Compared with other sympathomimetic drugs, does not significantly increase myocardial oxygen demands, which is its major advantage compared with other direct-acting catecholamines.

Inamrinone (Inocor)

Formerly amrinone. Phosphodiesterase inhibitor with positive inotropic and vasodilator activity. Produces vasodilation and increases inotropic state. More likely to cause tachycardia than dobutamine and may exacerbate myocardial ischemia.

Anticoagulants

Class Summary

Patients receiving bioprosthetic valves should receive anticoagulants for 3 months. Lifelong anticoagulation is needed in patients with mechanical valves and in patients with atrial fibrillation. Any patients presenting with thromboembolic complications must be promptly anticoagulated if they do not have a therapeutic INR of 2.5-3.5.

Heparin

Augments activity of antithrombin III and prevents conversion of fibrinogen to fibrin. Does not actively lyse but is able to inhibit further thrombogenesis. Prevents reaccumulation of clot after spontaneous fibrinolysis.

Antibiotics

Class Summary

These agents are given to patients with prosthetic heart valves prior to performing procedures that may cause bacteremia (see Deterrence/Prevention).

Amoxicillin (Amoxil, Polymox, Trimox)

Derivative of ampicillin and has similar antibacterial spectrum, namely certain gram-positive and gram-negative organisms. Superior bioavailability and stability to gastric acid and has broader spectrum of activity than penicillin. Somewhat less active than that of penicillin against Streptococcus pneumococcus. Penicillin-resistant strains also resistant to amoxicillin, but higher doses may be effective. More effective against gram-negative organisms (eg, N meningitidis, H influenzae) than penicillin. Interferes with synthesis of cell wall mucopeptides during active multiplication, resulting in bactericidal activity against susceptible bacteria. DOC for prophylaxis in nonallergic patients undergoing dental, oral, or respiratory tract procedures. Patients must be able to take oral medications.

Ampicillin (Omnipen, Marcillin)

Broad-spectrum penicillin. Interferes with bacterial cell wall synthesis during active replication, causing bactericidal activity against susceptible organisms. Alternative to amoxicillin when unable to take medication orally.

For prophylaxis in patients undergoing dental, oral, or respiratory tract procedures. Coadministered with gentamicin for prophylaxis in GI or genitourinary procedures.

Azithromycin (Zithromax)

Acts by binding to 50S ribosomal subunit of susceptible microorganisms and blocks dissociation of peptidyl tRNA from ribosomes, causing RNA-dependent protein synthesis to arrest. Nucleic acid synthesis is not affected. Concentrates in phagocytes and fibroblasts as demonstrated by in vitro incubation techniques. In vivo studies suggest that concentration in phagocytes may contribute to drug distribution to inflamed tissues. Treats mild-to-moderate microbial infections.

Plasma concentrations are very low, but tissue concentrations are much higher, giving it value in treating intracellular organisms. Has a long tissue half-life.

Used in penicillin-allergic patients undergoing dental, esophageal, and upper respiratory procedures.

Cefazolin (Ancef)

First-generation semisynthetic cephalosporin that by binding to 1 or more penicillin-binding proteins arrests bacterial cell wall synthesis and inhibits bacterial replication. Poor capacity to cross blood-brain barrier. Primarily active against skin flora, including S aureus. Typically used alone for skin and skin-structure coverage. Regimens for IV and IM dosing are similar. Primarily active against skin flora, including staphylococcal species.

Ceftriaxone (Rocephin)

Third-generation cephalosporin with broad-spectrum, gram-negative activity; lower efficacy against gram-positive organisms; higher efficacy against resistant organisms. Bactericidal activity results from inhibiting cell wall synthesis by binding to one or more penicillin-binding proteins. Exerts antimicrobial effect by interfering with synthesis of peptidoglycan, a major structural component of bacterial cell wall. Bacteria eventually lyse due to the ongoing activity of cell wall autolytic enzymes while cell wall assembly is arrested.

Highly stable in presence of beta-lactamases, both penicillinase and cephalosporinase, of gram-negative and gram-positive bacteria. Approximately 33-67% of dose excreted unchanged in urine, and remainder secreted in bile and ultimately in feces as microbiologically inactive compounds. Reversibly binds to human plasma proteins, and binding has been reported to decrease from 95% bound at plasma concentrations < 25 mcg/mL to 85% bound at 300 mcg/mL.

Cephalexin (Keflex)

First-generation cephalosporin that inhibits bacterial replication by inhibiting bacterial cell wall synthesis. Bactericidal and effective against rapidly growing organisms forming cell walls.

Resistance occurs by alteration of penicillin-binding proteins. Effective for treatment of infections caused by streptococcal or staphylococci, including penicillinase-producing staphylococci. May use to initiate therapy when streptococcal or staphylococcal infection is suspected.

Used orally when outpatient management is indicated.

Clarithromycin (Biaxin)

Semisynthetic macrolide antibiotic that reversibly binds to P site of 50S ribosomal subunit of susceptible organisms and may inhibit RNA-dependent protein synthesis by stimulating dissociation of peptidyl tRNA from ribosomes, causing bacterial growth inhibition.

Used in penicillin-allergic patients undergoing dental, esophageal, and upper respiratory procedures.

Clindamycin (Cleocin)

Inhibits bacterial growth. Widely distributes in the body without penetration of CNS. Protein bound and excreted by the liver and kidneys.

Used in penicillin-allergic patients undergoing dental, oral, or respiratory tract procedures. Useful for treatment against streptococcal and most staphylococcal infections.

Semisynthetic antibiotic produced by 7(S)-chloro-substitution of 7(R)-hydroxyl group of parent compound lincomycin. Inhibits bacterial growth, possibly by blocking dissociation of peptidyl tRNA from ribosomes, causing RNA-dependent protein synthesis to arrest. Widely distributes in the body without penetration of CNS. Protein bound and excreted by the liver and kidneys.

Useful in penicillin-allergic patients who require antibiotic prophylaxis prior to dental, oral, gastrointestinal, or respiratory tract procedures.

Gentamicin

Aminoglycoside antibiotic for gram-negative coverage bacteria including Pseudomonas species. Synergistic with beta-lactamase against enterococci. Interferes with bacterial protein synthesis by binding to 30S and 50S ribosomal subunits.

Dosing regimens are numerous and are adjusted based on CrCl and changes in volume of distribution, as well as body space into which agent needs to distribute. Dose of gentamicin may be given IV/IM. Each regimen must be followed by at least trough level drawn on third or fourth dose, 0.5 h before dosing; may draw peak level 0.5 h after 30-min infusion.

Vancomycin (Vancocin)

Potent antibiotic directed against gram-positive organisms and active against Enterococcus species. Useful in the treatment of septicemia and skin structure infections. Indicated for patients who cannot receive or have failed to respond to penicillins and cephalosporins or who have infections with resistant staphylococci. Use creatinine clearance to adjust dose in patients with renal impairment.


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