A BAT call is received for a 42-year-old man presenting with acute shortness of breath. He was discharged against medical advice two weeks earlier with acute hepatitis C–related liver failure and Streptococcus mitis bacteraemia, while receiving benzylpenicillin and gentamicin.

On arrival, he is deeply jaundiced, hypotensive (BP 90/74), tachycardic (HR 105) and hypoxic (SpO₂ 90% on room air). He has bilateral crepitations, a loud systolic murmur, pedal oedema and ascites. Right arm injection sites show tracking cellulitis.

He is commenced on BiPAP, GTN infusion, IV frusemide (40 mg), benzylpenicillin and gentamicin. Bedside glucose is “low”, and he receives 25 mL of 50% glucose.

This is his Xray:

 

His bloods come back : WCC 54 x 10^ 9/L , Hb 104 g/L, platelets 22 x 10 ^9/L,CRP 130, electrolytes are normal, creatinine 179 µmol/L, bilirubin 530µmol/L.

You are asked to do an ECHO to look for bacterial endocarditis. This is his parasternal right inflow tract which shows the RV, the RA and the tricuspid valves (posterior and anterior leaflets)

There is a tricuspid valve vegetation. This is better appreciated in slow motion flopping in and out of the right ventricle and atrium.

How is this view achieved? This view is essentially a parasternal long axis view with the probe tilted inferiorly and towards the patient’s right hip

This is his PSAX view

Note the D shaped ventricle indicating high RV pressures.  The tricuspid valve vegetation is not clearly viewed in this clip.

This is his focused right ventricular  4CV  view. To obtain this view angle the probe medially from the usual 4CV.

In slow motion the large vegetation can be clearly visualised flopping into the right ventricle and back into the right atrium with cardiac contractions. With breathing note the B lines that come into view due to his pulmonary oedema.

His classic 4CV shows an enlarged RV. The RV should be 2/3 of the size of the LV. If it the same size as the LV then it is moderately dilated, if larger than the LV it is severely dilated

He is admitted to ICU. His blood cultures come back positive for Staphyloccocus aureus in 2 bottles and alpha haemolytic strep in one of 2  bottles. He unfortunately does not recover from his sepsis, cardiac and liver failure and dies 5 days later in ICU.

Discussion

Right sided endocartitis is less common than left sided endocarditis comprising 5 -10 % of all bacterial endocarditis.

The following is a summary of an excellent review in the Annals of Cardiothoracic Surgery (1)

  • 90 % of right sided endocarditis involves the tricuspid valve
  • Both right and left sided endocarditis are strongly associated with IVDU but pacemaker leads, defibrilator leads and vascular access for dialysis are also major risk factors.
  • Infection from IVDU predominantly affects the TV (50 -60% of cases) for reasons that are not clear
  • Cardiac implantable electronic device infection (CIED)  is an increasing cause of TV infective endocarditis. However in most instances the CIED infection is localised to the device pocket and does not lead to infection of the TV. Lead echo densities are very common and indistinguishable from infective endocarditis vegetations but most of the time they are not infectious
  • Staphylococcus aureus is the predominant causative organism in  TV infective endocarditis occurring in 60 -90% of cases irrespective of risk factors

Diagnosis

  • Patients present with fever and bacteraemia
  • Multiple septic pulmonary emboli cause chest pain, cough and occasionally hemoptysis
  • Systemic emboli are rare and indicate left sided involvement or paradoxical emboli
  • Right heart failure is rare  and caused by increased pulmonary pressure combined with severe TR or TV obstruction from huge vegetations
  • Pulmonary septic emboli can cause pulmonary infarcts and pulmonary abscesses and be complicated by pneumothorax and empyema
  • The modified Duke’s criteria for diagnosing endocarditis may be difficult to determine in TV infective endocarditis.  First, the right heart has many echocardiographically anomalous anatomic features that may be difficult to distinguish from vegetations; second, septic emboli are pulmonary, as opposed to systemic, and clinically less obvious until they cause pulmonary infarcts and abscesses; third, early pulmonary radiographic findings may be mistaken for pneumonia (1).

Treatment

  • Most patients are successfully treated with antibiotics
  • 5 -16% require surgical intervention. Surgery is considered mainly for failed medical treatment, large vegetations and septic pulmonary emboli and less often for TV regurgitation and heart failure. Valve repair (debridement and repair) is advocated over valve replacement especially in patients who are IVDUs
  • Patients with concomitant left sided involvement have a worse prognosis than those with right sided infective endocarditis alone
  • Patients with isolated right ventricular tricuspid valve infective endocarditis have a 0 – 15% operative mortality and excellent survival

Teaching point : It is helpful knowing how to examine the right heart by using different views other than the standard BELS views. These include the parasternal right inflow tract view and the focused right ventricular 4CV

References

  1. Ann Cardiothorac Surg. 2017 May; 6(3): 255–261. doi: 10.21037/acs.2017.03.09 PMCID: PMC5494428 PMID: 28706868 Tricuspid valve endocarditis
    Syed T. Hussain,1 James Witten,2 Nabin K. Shrestha,3 Eugene H. Blackstone,1,4 and Gösta B. Petterssoncorresponding author1