Subacute Bacterial Endocarditis: making the diagnosis Illustration by Kevin A. Somerville/Phototake © Abstract: The presentation of endocarditis varies from patient to patient, making it a diffi cult infection to diagnose correctly. While some patients will develop symptoms acutely over days, it may take weeks or months for symptoms to develop as in the case of subacute bacterial endocarditis. By Kristen Luttenberger, RN, MSN, CCRN, APN; and Mary DiNapoli, RN, MSN, APN-c G was a 42-year-old man in optimal health who The records indicated normal S1S2 heart sounds with no men- worked full-time and was an active weight lifter, tion of murmur, rub, or gallop. Without any kind of signifi cant R hunter, and fi sherman. RG presented to the internist medical history noted, RG was sent home with a differential with complaints of malaise, shortness of breath, and low-grade diagnosis of bronchitis and viral syndrome and was prescribed fever for weeks. Upon exam, RG had “scattered crackles,” a an oral antibiotic and inhaler. A week later, family members temperature of 100.4º F, slight shortness of breath on exertion, brought RG to the ED due to the inability to walk from bilateral and diaphoresis. Otherwise, the physical exam was normal. lower extremity edema. Key words: Bacterial endocarditis, subacute bacterial endocarditis, prosthetic valve endocarditis www.tnpj.com The Nurse Practitioner • March 2011 31 Copyright © 2011 Lippincott Williams & Wilkins. Unauthorized reproduction of this article is prohibited. Subacute bacterial endocarditis: making the diagnosis Within the next few hours in the ED, RG became confused. pursue a protracted course of weeks to months, cures may The labs returned with a blood urea nitrogen of 45 mg/dL, cre- be produced with antibiotics alone, and a later mortality atinine of 3.3 mg/dL, aspartate aminotransferase-321 units/L, ensues (up to a year) if not treated.9 alanine aminotransferase-408 units/L, total bilirubin-2.4 ABE is characterized by more dramatic symptoms such mg/dL, and negative blood cultures masked by the weeklong as a continuous bacteremia, temperatures spiking over 102º therapy of oral antibiotics. RG developed multisystem organ F, frequent septic embolic complications (metastatic focus), failure from septic shock involving his kidneys, liver, and an acute and virulent organism attacking both damaged heart. A case of subacute bacterial endocarditis (SBE) turned and normal heart valves (more often normal), and a new acute, and a previously unknown bicuspid aortic valve from murmur with valvular destruction.6,8 Due to the dangers birth was the cause. of septic embolic phenomena, myocardial abscesses, valve Although this case ended well with an aortic valve re- destruction, sepsis, and diffi culty curing with antibiotics, placement, mitral valve repair, and a relatively full recovery, ABE is usually treated as a medical emergency requiring car- the lesson for NPs is that the vague symptoms of SBE can be diac valvular replacement. If untreated, an earlier mortality easily misdiagnosed leading to catastrophic results. ensues.8,9 (See Clinical differences between SBE and ABE). Nosocomial endocarditis (NE) is considered a hospital- ■ Defi nitions acquired form of ABE. It has similar characteristics in that it The history of endocarditis dates as far back 1723 where is acute, temperatures over 102º F, and affects normal heart Lazaire Riviere fi rst described gross autopsy fi ndings of the valves. NE is usually related to an intracardiac device placed disease.1 Then it was the Gulstonian lectures of 1885 where in the hospital setting such as temporary central venous cath- Sir William Osler (hence “Osler nodes”) drew a distinction eters, pulmonary artery catheters, and pacemakers. The im- between “simple” and “malignant” forms of the disease. The portance of the skin prep for the introduction of percutaneous “simple” form of endocarditis correlates to what now has central devices cannot be emphasized enough because MSSA become SBE and the “malignant” form is now characterized (methicillin-sensitive S. aureus) and MRSA (methicillin-resis- as an acute onset and fulminant course referred to as acute tant S. aureus) are the usual pathogens of cause.6 Sherwood infective endocarditis (IE) or acute bacterial endocarditis et al. compared outcomes of MSSA endocarditis with MRSA (ABE).2 It is worthy to note that many studies of diagnosis endocarditis and found no signifi cant difference.10 and treatment of endocarditis do not differentiate between Similarly, there is prosthetic valve endocarditis (PVE), acute and subacute disease process, and many principles which involves an infection of a prosthetic cardiac valve of diagnosis and management are identical.3 Some physi- or relating structure. In this situation patients would cian researchers also argue that the distinction between have bacteremia and cardiac vegetation on the prosthetic subacute and acute is not useful for clinical management structure. PVE is frequently caused by coagulase-negative and is arbitrary. The opinion is that the focus of diagnosis staphylococci (CoNS), which is a normal skin fl ora.8,11 The and clinical relevance should be on the causative organism importance of skin prep must be emphasized, along with involved (such as Staphylococcus aureus bacterial endocar- the practitioner’s ability to recognize the possibility of en- ditis).4,5 Some types of endocarditis are also not caused by docarditis in prosthetic valve patients with positive blood bacteria (that is, Haemophilus parainfl uenzae, fungi, culture cultures of CoNS. CoNS may not just be a skin contaminant negative), so using the word “bacteria” in diagnosis may be in these patients. misleading. Nonbacterial thrombotic endocarditis (NBTE) is char- In the literature, clear-cut definitions of SBE versus acterized with small sterile thrombi on the leafl ets of the ABE have been published by Burke A. Cunha, MD, Chief, cardiac valves that do not elicit any infl ammatory reaction Infectious Disease Division, Winthrop-University Hospital, but can become systemic emboli producing infarcts. NBTE Mineola, N.Y.6-8 In Dr. Cunha’s work, he characterizes SBE is usually seen in debilitated patients in a hypercoagulable by fever less than 102º F, a heart murmur, a continuous state, such as cancer or sepsis, and has been referred to as ma- bacteremia with possible aseptic emboli phenomenon, pri- rantic endocarditis in the past. Finally there is Libman-Sacks marily caused by viridian streptococci from the oral cavity, endocarditis, which is occasionally encountered in systemic an avirulent organism causing endocarditis in patients with lupus erythematosus (SLE). These vegetations are sterile preexisting valvular heart disease, and a variety of peripheral and may be encountered with a valvulitis in this disorder.9 manifestations. The majority of organisms responsible for SBE are avirulent/noninvasive pathogens of viridans strep- ■ Epidemiology tococci, which include S. sanguis, S. intermedius, S. sanguinis, Endocarditis accounts for approximately 1 case per 1000 S. anginosus, S. salivarius, S. mutans, and others.6-8 SBE may U.S. hospital admissions, with a range of 0.16 to 5.4 cases 32 The Nurse Practitioner • Vol. 36, No. 3 www.tnpj.com Copyright © 2011 Lippincott Williams & Wilkins. Unauthorized reproduction of this article is prohibited. Subacute bacterial endocarditis: making the diagnosis per 1,000 admissions.4 The American Heart As- sociation (AHA) places the annual incidence of Clinical differences between SBE and ABE IE in the United States at 10,000 to 20,000 new Symptoms SBE ABE 12 cases. Although the primary causes of endo- Anorexia + – carditis have varied, the incidence of the disease Myalgias/arthralgias +/– + has remained relatively the same over the past 30 Fatigue + – years. However, this epidemiology may possibly Dyspnea/cough – + vary due to changes in the diagnostic criteria Pleuritic chest pain/ hemoptysis – + of endocarditis and changes in defi nitions over Lumbar back pain + + time.4 Weight loss +/– – Endocarditis is more common in men and Headache +/– + the incidence increases with age due to the cur- Mental status changes +/– + rent, low incidence of acute rheumatic heart Acute confusional states – + disease.13,14 It is also more commonly involved Unexplained stroke + – with the mitral valve only (40%), followed by the Sudden unilateral blindness + – aortic valve only (36%), and followed by multi- Left upper quadrant pain Splenic Splenic abscess abscess valvular disease.15-17 Signs Rheumatic heart disease was the most com- Fever (° F) <102 >102 mon cause of endocarditis in the preantibiotic New heart murmur – +/– era. Nowadays about 75% of patients who de- Splenomegaly + – velop endocarditis have some type of underlying Petechiae + + structural heart disease (that is, congenital or Osler nodes + – calcifi cation). These include mitral regurgita- Janeway lesions – + tion; aortic valve disease, including stenosis and Splinter hemorrhages + +/– 17-19 regurgitation; and congenital heart disease. Roth spots + – Prosthetic valves (1% to 4% 1st year), prior his- Heart failure – + tory of endocarditis, invasive medical procedures, Laboratory tests drug use, healthcare-associated infections, soci- Anemia + – etal hazards as in body piercings, and some sys- Marked leukocytosis – + temic medical conditions (that is, HIV, end-stage Hematuria, proteinuria, RBC casts + – kidney disease, diabetes mellitus) are also among Microscopic hematuria + +/– risk factors.4,17 The majority of the time a right-