Infective Endocarditis

This is one with beautiful classic signs that all medical students look for, but rarely actually see. We’ll perform a cardiovascular examination on a patient and stare at their hands for signs of infective endocarditis, regardless of what they come in with.

I saw a patient, Matilda (not real name), with infective endocarditis (IE) on the ward round and was told to have a listen to her heart at the end. She had a murmur which excited me very much. I get SUPER excited whenever I hear a murmur for some strange reason. It’s basically a whoosh which can point to a different diagnosis depending on its character and where it falls in regards to the heart sounds. At the moment, I can tell there is a whoosh but I’m not fully able to do much else. I misidentified the murmur as pan-systolic, when it was actually ejection systolic. I think I need to listen to more whooshes before I get the hang of it.


Here’s some of Matilda’s history, which I extracted from her notes:

PC: fever, generalised body aches, productive cough with white sputum

HPC: feverish for 9 days, given a course of amoxicillin by GP- initially improved and then redeveloped fever, denies chest pain

PMHx: congenital bicuspid aortic valve, aortic valve replacement, aortic dissection, aortic root replacement, pacemaker insertion following complete heart block, previous IE of aortic valve (i.e. lots and lots of risk factors) + hypertension, previous pulmonary embolisms, recent eczema flare up (likely portal of entry for infective agent).

DHx: Ramipril (ACE inhibitor), Bisoprolol (beta blocker), Carbocisteine (mucolytic)

SHx: ex-smoker, 22 pack years

O/E: sweaty and warm to touch, feeling cold, pulse rate-100 bpm, ejection systolic murmur, midline sternotomy scar (from previous heart surgery)

-no splinter haemorrhages/ Osler nodes/ Janeway lesions

-HR 105 bpm, T 39°C, RR 19, BP 149/56 mmHg

Investigations:

-Bloods: CRP, WBC and neutrophils raised

-Echocardiogram: no clear evidence of infective endocarditis

-Blood culture: positive for Methicillin-sensitive Staphylococcus aureus (MSSA)

Management:

-6 week course of IV antibiotics: Flucloxacillin, Gentamicin, Rifampicin


 

Infective Endocarditis

Definition: infection of the endocardium or vascular endothelium of the heart, mainly the heart valves, which may occur as acute infection (usually on normal valves) but more commonly runs an insidious course (usually on abnormal valves) and is known as subacute bacterial endocarditis (SBE).

Aetiology/ Risk factors:

-commonly caused by Staph. aureus (most common), Strep. viridans and enterococci (blood cultures -ve in 5-10%)

-culture negative endocarditis likely with: Coxiella burnetti, Chlamydia spp., Bartonella spp., Legionella

-usual cause is prior antibiotic therapy

-infection occurs on valves with a congenital or acquired defect (usually on the left side of the heart), on prosthetic valves (like Matilda), in association with a ventricular septal defect or persistent ductus arteriosus (due to turbulent flow), or on normal valves with virulent organisms such as Strep. pneumoniae or Staph. aureus.

Risk factors: aortic or mitral valve disease, IV drug users (tricuspid valve), coarctation, patent ductus arteriosus, VSD, prosthetic valves, dermatitis (eczema), organ transplantation, diabetes, post-op wounds, recent dental work & bacteraemia.

Epidemiology: incidence 16-22 per million per year (UK)

Symptoms:

-systemic features of infection: malaise, fever, night sweats, rigors, weight loss

-arthralgia (due to immune complex deposition in joints), myalgia

-confusion (particularly in elderly)

Signs:Image result for INFECTIVE ENDOCARDITIS osler nodes janeway lesions

-pyrexia, tachycardia

-signs of anaemia

-heart failure + new/changing heart murmurs due to valve destruction (causing obstruction & regurgitation)

-slight splenomegaly

-splinter haemorrhages, Roth’s spots (retinal haemorrhage with pale centre)

– Osler’s nodes (tender), Janeway lesions (non-tender)

-clubbing (rare, in long standing disease)

MNEMONIC: FROM JANE
Fever
Roth’s spots
Osler’s nodes
Murmur
Janeway lesions
Anaemia
Nail haemorrhage (splinter haemorrhages)
Emboli

ALWAYS CONSIDER INFECTIVE ENDOCARDITIS IN ANY PATIENT WITH A HEART MURMUR AND FEVER

Investigations:

-Blood cultures- before starting antibiotics. 3 sets. Special culture techniques and serological tests if blood cultures negative and unusual organisms suspected.

-Blood count- normochromic, normocytic anaemia, raised ESR/CRP, often leucocytosis/neutrophilia

-Urine dipstick- haematuria in most cases (acute glomerulonephritis-due to immune complex deposition)

-Echocardiogram- identify vegetations and underlying valvular dysfunction. Small vegetations may be missed, so as with Matilda, a normal echo does not exclude IE. (TOE is most sensitive)

-Chest X-ray- may show heart failure or evidence of septic emboli in right-sided IE

-ECG- may show myocardial infarction (emboli to coronary circulation) or conduction defects caused by abscesses (e.g. prolonged PR)

-Serum immunoglobulins increased + complement level decreased due to immune complex formation

Management:

-Duke classification for diagnosis

-Bacterial antibiotics- IV for first 2 weeks and by mouth for a further 2-4 weeks (at least 6 weeks in total for prosthetic valve IE)

   –Benzylpenicillin + gentamicin on clinical suspicion and then different ones depending on bacterial agent

-Consider valve replacement if: severe heart failure, early infection of prosthetic material, worsening renal failure, extensive valve damage

Complications:

-heart failure due to valve destruction

-intracardiac fistulae or abscesses

-aneurysm formation

-heart conduction abnormalities- e.g. aortic root abscess → PR prolongation → complete AV block

-vascular phenomena due to embolization of vegetations and metastatic abscess formation in the brain, spleen, kidney, heart and gut.

-Embolization from right sided endocarditis → pulmonary infarction + pneumonia

-glomerulonephritis + acute renal failure due to immune complex deposition (rare)

Prognosis: Fatal if untreated. Even when treated, 15-30% mortality

References: Kumar & Clark’s clinical medicine, Rapid Medicine, Cheese & Onion
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