Doctors (trainee registrars) and med students often casually mention “bacterial endocarditis” or “SBE” (subacute bacterial endocarditis) when discussing a diagnosis of fever or vague chest pain or a cardiac murmur. It appears that the terms are mentioned more to show that the speaker knows that there is something called endocarditis or SBE but does not necessarily understand what the terms mean or when the diagnosis should be applied.
So what is endocarditis?
Infective endocarditis (IE) refers to infection of the endocardial surface of the heart; it usually refers to infection of one or more heart valves or infection of an intracardiac device.
When does the endocardium become infected? With a smooth healthy endocardium and blood flowing rapidly over it in the heart during the pulsatile pumping the chances of bacteria attaching themselves to the inner surface of the heart are remote.
- Something goes wrong inside the heart. In a developing country there is usually the presence of a congenital heart defect which may or may not have been surgically corrected or the presence of valvular heart disease like mitral regurgitation, aortic stenosis or aortic regurgitation etc usually caused by rheumatic fever which is still significantly prevalent in the third world and may or may not have been corrected by putting in a prosthetic valve. The prosthesis can get infected.
- In a developed country the placement of an intracardiac device like a pacemaker may be the risk factor which leads to IE.
- Bacteria are forced into the circulation i.e. through the intravenous use of drugs for recreational purposes (I am talking about drug addiction), prolonged use of IV catheters, use of immunosuppressant drugs as in a renal transplant, glomerulonephritis, cancer chemotherapy or treatment of hematological malignancy.
- Bacteria are spread by septic emboli in the systemic circulation and metastasise to other organs the origin being a septic vegetation in the heart.
- Septic emboli (up to 25 percent of patients) cause infarction of kidneys, spleen, brain, and other organs if the vegetation is on the left side of the heart.
- In right-sided endocarditis (common among intravenous drug users), septic pulmonary emboli may be seen.
- Metastatic infection (such as vertebral osteomyelitis, septic arthritis, psoas abscess) may occur.
So when should you introduce endocarditis into the diagnosis when discussing a case?
The patient has undiagnosed fever (short duration and of acute onset if the patient can afford early access to medical care or prolonged fever of several weeks duration if the patient reaches the hospital late). There is malaise, night sweats, weight loss, arthralgia so you may think of rheumatic fever, myalgia, cough, pleuritic chest pain The fever is accompanied by one or more of the points below:
- The existence of a valvular heart lesion or congenital heart lesion of which you have hopefully taken the history.
- The presence of an implanted cardiac device like a pacemaker.
- Previous surgery for putting in a prosthetic cardiac valve. Ask the patient they are unlikely to forget such a major event.
- Previous history of bacterial endocarditis.
- Recent angioplasty and stenting (rare cause but the potential of bacteria getting in is there).
- Septic emboli like an abcess in the kidneys, spleen or lungs (in drug users)
- IE can present with cardiac complications (up to 50 percent of patients) such as valvular insufficiency, heart failure.
- IE can cause neurologic complications (up to 40 percent of patients). So a young patient can present with an embolic stroke, intracerebral hemorrhage, brain abscess. Check out the heart for the presence of vegetations.
- History of intravenous drug abuse.
- Prolonged use of IV line for nutrition or chemotherapy. Do an echocardiogram to exclude IE if the patient starts running fever.
- Use of immunosuppressive drugs.
- Recent toothache and history of dental procedure.
- Skin lesions recognised as occurring in endocarditis. These are not commonly seen as most patients have been put on antibiotic treatment before they have had time to develop but they are the ones that students remember. Frankly I haven’t seen a Roth spot or a Janeway lesion in 47 years of practice. They are not essential to diagnosis i.e even if they are not present a diagnosis of IE can be made.
- Janeway lesions – Non-tender erythematous macules on the palms and soles
- Osler nodes – Tender subcutaneous violaceous nodules mostly on the pads of the fingers and toes, which may also occur on the thenar and hypothenar eminences.
- Roth spots – Exudative, edematous hemorrhagic lesions of the retina with pale centers.
What is the difference between Janeway lesions and Osler nodes? The former are non-tender and the latter are tender and painful.
Where can you see a Roth spot? In the retina so don’t say you have seen one until you have used an ophthalmoscope.
Please do not mention Janeway lesions or Osler nodes when doing the GPE (general physical examination) because these are rarely seen in IE and are unlikely to be seen in the general patient population who do not have IE.
What are you going to find when you examine the patient?
- Cardiac murmurs are observed in approximately 85 percent of patients.
- Cutaneous manifestations such as petechiae or splinter hemorrhages are much more common than Janeway lesions or Osler nodes. Petechiae are observed in 20 to 40 percent of patients; they may be present on the skin (usually on the extremities) or on mucous membranes such as the palate or conjunctivae. Splinter hemorrhages consist of non-blanching linear reddish-brown lesions under the nail bed.
- The patient may present with a complication of IE so look for the manifestations of complications listed above. Or a complication may occur during the course of the disease so you will need to concomitantly investigate for IE, cardiac failure, brain abscess, embolic stroke, kidney abscess or splenic abscess. Remember splenic abscesses are uncommon and tend to occur in infective endocarditis, brucellosis and fungal infections.
Plan your investigations to find the organism causing the IE, finding the vegetations which are the source of emboli, investigations of the organs where the septic emboli have lodged, looking for the disability and damage in the heart.
Modified Duke Criteria.
Major criteria for the diagnosis of IE include:
- Presence of vegetations on echocardiogram
- The presence of a cardiac abscess.
- Two positive blood cultures taken 12 hours apart for organisms known to cause IE Staphylococcus aureus, Viridans streptococci, Streptococcus gallolyticus (formerly S. bovis), including nutritional variant strains (Granulicatella spp and Abiotrophia defectiva), HACEK group: Haemophilus spp, Aggregatibacter (formerly Actinobacillus actinomycete comitants), Cardiobacterium hominis, Eikenella spp, and Kingella kingae, Community-acquired enterococci, in the absence of a primary focus.
- 3-4 cultures positive for skin contaminants taken 1 hour apart.
- Single culture positive for Coxiella burnetii or positive IgG antibody titre>1:800.
- New regurgitant murmur (not change in an old murmur)
- Rupture of a prosthetic valve.
Minor criteria include:
- Predisposition: Intravenous drug use or presence of a predisposing heart condition (prosthetic heart valve or a valve lesion associated with significant regurgitation or turbulence of blood flow)
- Fever: Temperature ≥38.0°C (100.4°F)
- Vascular phenomena: Major arterial emboli, septic pulmonary infarcts, mycotic aneurysm, intracranial hemorrhage, conjunctival hemorrhages, or Janeway lesions.
- Immunologic phenomena: Glomerulonephritis, Osler nodes, Roth spots, or rheumatoid factor
- Microbiological evidence: Positive blood cultures that do not meet major criteria OR serologic evidence of active infection with organism consistent with IE.
You need proof of bacterial growth as a major criterion plus two major clinical criteria or one major and three minor clinical criteria or five minor clinical criteria. If a definite diagnosis of another cause of the fever is made then the diagnosis of IE is rejected.
I am putting down the conclusion of the POET trial for the effect of oral treatment of IE. So you do not need to keep the patient in the hospital for 6 weeks of IV therapy.
Partial Oral versus Intravenous Antibiotic Treatment of Endocarditis. The POET trial.
In patients with endocarditis on the left side of the heart who were in stable condition, changing to oral antibiotic treatment was noninferior to continued intravenous antibiotic treatment. (Funded by the Danish Heart Foundation and others; POET ClinicalTrials.gov number, NCT01375257.)