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Emergency And Acute Medicine - Endocarditis
Basic Overview
Endocarditis is an inflammatory condition involving the endothelial lining of the heart. It most commonly affects native cardiac valves but may also involve prosthetic valves, the interventricular septum, chordae tendineae, mural endocardium, or intracardiac devices. The disease is defined by the formation of vegetations, which are thrombotic aggregates of fibrin and platelets that become colonized by microorganisms. Progressive bacterial growth enlarges these vegetations, disrupts normal blood flow, provokes inflammation, and may result in systemic embolization. The condition is almost always infectious in origin, typically bacterial. Rare noninfectious forms include nonbacterial thrombotic (marantic) endocarditis associated with hypercoagulable states and Libman–Sacks endocarditis related to systemic lupus erythematosus, both characterized by small sterile vegetations.
Epidemiologic Features
Endocarditis occurs more frequently in men, with incidence rates significantly higher than in women. Risk increases with advanced age, poor dental hygiene, and comorbid medical conditions. Structural heart disease, including rheumatic heart disease, mitral valve prolapse, aortic valve dysfunction, congenital heart defects, and prosthetic valves, predisposes patients due to altered intracardiac flow. Hemodialysis, diabetes, and indwelling intravascular catheters further increase risk. Intravenous drug use confers a particularly high risk and commonly involves right-sided valves. Septic embolization may lead to neurologic, pulmonary, splenic, renal, hepatic, or coronary complications, as well as mycotic aneurysm formation.
Causative Mechanisms
Most cases are due to bacterial infection. Common pathogens include Staphylococcus aureus, the most frequent cause across all populations and especially prevalent among intravenous drug users. Streptococcus viridans is a typical cause of native valve disease and originates from the oropharynx. Streptococcus bovis is associated with colonic polyps or gastrointestinal malignancy. Streptococcus pneumoniae may cause aggressive valvular destruction and heart failure. Staphylococcus epidermidis is frequently implicated in prosthetic valve infections. Enterococci are often linked to genitourinary or gastrointestinal instrumentation. Fungal causes, such as Candida or Aspergillus, occur primarily in immunocompromised patients or those with prosthetic valves. Culture-negative endocarditis may result from organisms such as Coxiella burnetii, Bartonella, or Brucella.
Clinical Presentation
Fever is the most common symptom, present in the majority of patients, though it may be absent in the elderly, those with chronic renal failure, heart failure, or severe debility. Constitutional symptoms include chills, sweats, rigors, malaise, and flulike illness. Cardiac findings often include a new or changing murmur and signs of heart failure. Embolic phenomena may cause neurologic deficits, stroke, or mycotic aneurysms. Cutaneous manifestations include petechiae, splinter hemorrhages, Osler nodes, and Janeway lesions. Splenomegaly, abdominal or back pain, arthralgias, and myalgias may also be present.
Diagnostic Assessment
Evaluation should focus on identifying risk factors in patients with unexplained fever. Multiple sets of blood cultures obtained before antibiotic administration are essential. Laboratory studies commonly show anemia, leukocytosis, elevated inflammatory markers, and microscopic hematuria. Electrocardiography may reveal arrhythmias or new conduction abnormalities. Chest radiography can demonstrate signs of heart failure or septic pulmonary emboli. Echocardiography is critical for diagnosis, with transesophageal echocardiography offering superior sensitivity for detecting vegetations, abscesses, and valvular dysfunction. Computed tomography may aid in identifying complications.
Differential Considerations
Conditions that may mimic endocarditis include rheumatic fever, atrial myxoma, acute pericarditis, myocardial infarction, aortic dissection with valvular involvement, thrombotic thrombocytopenic purpura, systemic lupus erythematosus, metastatic malignancy, septicemia, and cotton fever.
Initial Management Principles
Patients should be closely monitored for signs of heart failure or embolic complications. Early consultation with cardiology and cardiothoracic surgery is required for patients with severe valvular dysfunction, intracardiac abscess, prosthetic valve instability, persistent infection despite therapy, or large or fungal vegetations. Empiric intravenous bactericidal antibiotics should be initiated after blood cultures are obtained, with regimens tailored based on valve type, risk factors, and local resistance patterns.
Antimicrobial Therapy
Empiric treatment commonly includes combinations of penicillin, nafcillin, gentamicin, or vancomycin, adjusted once culture data are available. Prosthetic valve infections and intravenous drug use often require broader coverage, including rifampin. Resistant organisms may necessitate agents such as daptomycin or quinupristin–dalfopristin. Fungal endocarditis is treated with amphotericin B, and HACEK organisms respond well to ceftriaxone.
Disposition And Follow-Up
All patients with suspected or confirmed endocarditis require hospital admission. Individuals with hemodynamic instability, neurologic complications, or heart failure should be managed in a monitored or intensive care setting. There are no criteria for emergency department discharge.
Clinical Insights And Common Errors
Endocarditis should be strongly considered in any patient with fever and a new or changing murmur, even in the absence of known valvular disease. Health care exposure and indwelling devices are important risk factors. Failure to obtain adequate blood cultures before antibiotics or to recognize embolic and heart failure complications can delay diagnosis and worsen outcomes. All intravenous drug users presenting with fever should be admitted and evaluated for endocarditis.
Basic Overview
Endocarditis is an inflammatory condition involving the endothelial lining of the heart. It most commonly affects native cardiac valves but may also involve prosthetic valves, the interventricular septum, chordae tendineae, mural endocardium, or intracardiac devices. The disease is defined by the formation of vegetations, which are thrombotic aggregates of fibrin and platelets that become colonized by microorganisms. Progressive bacterial growth enlarges these vegetations, disrupts normal blood flow, provokes inflammation, and may result in systemic embolization. The condition is almost always infectious in origin, typically bacterial. Rare noninfectious forms include nonbacterial thrombotic (marantic) endocarditis associated with hypercoagulable states and Libman–Sacks endocarditis related to systemic lupus erythematosus, both characterized by small sterile vegetations.
Epidemiologic Features
Endocarditis occurs more frequently in men, with incidence rates significantly higher than in women. Risk increases with advanced age, poor dental hygiene, and comorbid medical conditions. Structural heart disease, including rheumatic heart disease, mitral valve prolapse, aortic valve dysfunction, congenital heart defects, and prosthetic valves, predisposes patients due to altered intracardiac flow. Hemodialysis, diabetes, and indwelling intravascular catheters further increase risk. Intravenous drug use confers a particularly high risk and commonly involves right-sided valves. Septic embolization may lead to neurologic, pulmonary, splenic, renal, hepatic, or coronary complications, as well as mycotic aneurysm formation.
Causative Mechanisms
Most cases are due to bacterial infection. Common pathogens include Staphylococcus aureus, the most frequent cause across all populations and especially prevalent among intravenous drug users. Streptococcus viridans is a typical cause of native valve disease and originates from the oropharynx. Streptococcus bovis is associated with colonic polyps or gastrointestinal malignancy. Streptococcus pneumoniae may cause aggressive valvular destruction and heart failure. Staphylococcus epidermidis is frequently implicated in prosthetic valve infections. Enterococci are often linked to genitourinary or gastrointestinal instrumentation. Fungal causes, such as Candida or Aspergillus, occur primarily in immunocompromised patients or those with prosthetic valves. Culture-negative endocarditis may result from organisms such as Coxiella burnetii, Bartonella, or Brucella.
Clinical Presentation
Fever is the most common symptom, present in the majority of patients, though it may be absent in the elderly, those with chronic renal failure, heart failure, or severe debility. Constitutional symptoms include chills, sweats, rigors, malaise, and flulike illness. Cardiac findings often include a new or changing murmur and signs of heart failure. Embolic phenomena may cause neurologic deficits, stroke, or mycotic aneurysms. Cutaneous manifestations include petechiae, splinter hemorrhages, Osler nodes, and Janeway lesions. Splenomegaly, abdominal or back pain, arthralgias, and myalgias may also be present.
Diagnostic Assessment
Evaluation should focus on identifying risk factors in patients with unexplained fever. Multiple sets of blood cultures obtained before antibiotic administration are essential. Laboratory studies commonly show anemia, leukocytosis, elevated inflammatory markers, and microscopic hematuria. Electrocardiography may reveal arrhythmias or new conduction abnormalities. Chest radiography can demonstrate signs of heart failure or septic pulmonary emboli. Echocardiography is critical for diagnosis, with transesophageal echocardiography offering superior sensitivity for detecting vegetations, abscesses, and valvular dysfunction. Computed tomography may aid in identifying complications.
Differential Considerations
Conditions that may mimic endocarditis include rheumatic fever, atrial myxoma, acute pericarditis, myocardial infarction, aortic dissection with valvular involvement, thrombotic thrombocytopenic purpura, systemic lupus erythematosus, metastatic malignancy, septicemia, and cotton fever.
Initial Management Principles
Patients should be closely monitored for signs of heart failure or embolic complications. Early consultation with cardiology and cardiothoracic surgery is required for patients with severe valvular dysfunction, intracardiac abscess, prosthetic valve instability, persistent infection despite therapy, or large or fungal vegetations. Empiric intravenous bactericidal antibiotics should be initiated after blood cultures are obtained, with regimens tailored based on valve type, risk factors, and local resistance patterns.
Antimicrobial Therapy
Empiric treatment commonly includes combinations of penicillin, nafcillin, gentamicin, or vancomycin, adjusted once culture data are available. Prosthetic valve infections and intravenous drug use often require broader coverage, including rifampin. Resistant organisms may necessitate agents such as daptomycin or quinupristin–dalfopristin. Fungal endocarditis is treated with amphotericin B, and HACEK organisms respond well to ceftriaxone.
Disposition And Follow-Up
All patients with suspected or confirmed endocarditis require hospital admission. Individuals with hemodynamic instability, neurologic complications, or heart failure should be managed in a monitored or intensive care setting. There are no criteria for emergency department discharge.
Clinical Insights And Common Errors
Endocarditis should be strongly considered in any patient with fever and a new or changing murmur, even in the absence of known valvular disease. Health care exposure and indwelling devices are important risk factors. Failure to obtain adequate blood cultures before antibiotics or to recognize embolic and heart failure complications can delay diagnosis and worsen outcomes. All intravenous drug users presenting with fever should be admitted and evaluated for endocarditis.
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