Back pain and dyspnoea in a middle aged diabetic male

Q1: What is the unifying diagnosis?

Pulmonary valve endocarditis (with septic pulmonary emboli and evidence of early right ventricular failure) secondary to S aureus spinal osteomyelitis.

The spinal osteomyelitis is the likely substrate for the endocarditis rather than vice versa as symptoms of back pain preceded cardiopulmonary symptoms by several weeks.

It is unclear whether the initial presentation elsewhere was with septic pulmonary emboli secondary to pulmonary valve endocarditis mimicking pneumonia, which was then partially treated, or whether he acquired S aureus bacteraemia secondary to an intravascular catheter with subsequent development of osteomyelitis and endocarditis: a murmur was noted at the initial presentation but one set of blood cultures was negative.

The chest radiograph shows bilateral basal infiltrates due to septic pulmonary emboli. Magnetic resonance imaging of the thoracic spine showed evidence of disc infection at the D9/D10 level, with abnormal enhancement extending into the paravertebral spaces anteriorly and laterally. A transthoracic echocardiogram shows a large vegetation attached to the pulmonary valve by a stalk. In addition, pulmonary artery pressure was raised at 45 mm Hg, there was moderate tricuspid regurgitation and paradoxical septal motion.

Q2: How does right sided endocarditis (RSE) usually present?

Presentation is usually with fever and symptoms caused by septic pulmonary emboli, which occur in 60%–100% of patients.¹ These include pleuritic chest pain (present in 60% of intravenous drug users (IVDUs) with RSE²), cough, dyspnoea, and haemoptysis. The chest radiograph is abnormal in three quarters of patients at presentation.³ Abnormalities include infiltrates, often multiple and appearing sequentially with a predilection for the lower lobes, cavitation, pleural effusion, and empyema.⁴ Tricuspid and pulmonary valve dysfunction is usually well tolerated haemodynamically so that pleuropulmonary rather than cardiac features usually dominate the presentation.

While these features are likely to prompt consideration of the diagnosis in IVDUs, the diagnosis may not be considered in non-addicted patients. In one series of 29 non-IVDUs eventually proved to have RSE, an average of nine months elapsed between onset of symptoms and diagnosis. Multiple admissions were common, positive blood cultures tended to be either disregarded as contaminants or ascribed to pulmonary events, and misdiagnoses such as pneumonia, malignancy, and vasculitis were frequent.⁵

Q3: What risk factors are recognised for right sided endocarditis in non-IVDUs?

The majority of these patients have chronic underlying medical conditions.⁵ Predisposing factors include congenital heart disease (whereas the majority of IVDUs with RSE have a structurally normal heart), inadequately treated sepsis, and indwelling vascular catheters (central lines, pacemakers, pulmonary artery catheters, etc).

Q4: What is the likelihood of endocarditis in cases of S aureus bacteraemia?

Eighty per cent of cases of S aureus bacteraemia are community acquired. With no other obvious primary source of bacteraemia, one third of these patients have underlying endocarditis.⁶ Nosocomially acquired cases are on the increase and usually occur in the context of intravenous cannulae/indwelling vascular devices.⁷ Factors known to increase the chance of underlying endocarditis in patients with S aureus bacteraemia include absence of an alternative primary site of infection, community acquisition, and metastatic sequelae.⁸ The incidence of endocarditis resulting in intravenous catheter related S aureus bacteraemia is thought to be <5%–10%.⁶ However, many cases may be overlooked: a recent study examining the utility of early transoesophageal echocardiography in patients with S aureus bacteraemia (the majority of whom acquired it nosocomially) has demonstrated that vegetations are frequently identified in cases where endocarditis is not suspected clinically.⁹ These cases often affect the right side of the heart at sites of endocardial injury induced by the catheters, commonly in the absence of pre-existing valvular disease.⁷ In one series of 142 consecutively necropsied patients, 55 of whom had undergone pulmonary artery catheterisation during their final hospitalisation, right sided endocardial lesions (subendocardial haemorrhages and thrombi) were identified in over half of the 55 cases, with evidence of endocarditis in 7%. Endocardial lesions were found in only 3% of the non-catheterised patients.¹⁰

Q5: What is the relationship between back pain and endocarditis?

Musculoskeletal symptoms are a common but under-appreciated feature of endocarditis: in one series of 192 cases, 44% of patients had musculoskeletal manifestations (including back pain, arthralgias, arthritis, and myalgias), and were the sole presenting feature in 15%. In the majority, musculoskeletal symptoms were present for some time before diagnosis and responded rapidly to treatment of the endocarditis. The incidence of back pain in this series was 12.5%, with disc space infection identified in just under a quarter of these.¹¹ In another series of 108 patients with endocarditis, 30% had musculoskeletal manifestations with back pain an important feature in 13 of the 108 (in whom four cases of vertebral osteomyelitis were identified). In this study, patients presenting with musculoskeletal symptoms were diagnosed significantly later and had a significantly higher mortality, presumably because of delays in initiation of treatment.¹²

Severe back pain may therefore be the predominant presenting complaint in a significant minority of cases of endocarditis and factors such as localised myositis, emboli, and immunological mechanisms have been cited to explain its presence in the absence of evidence of osteomyelitis or disc space infection.^{11  12}

Discussion

RSE accounts for approximately 5%–10% of all cases of endocarditis and is predominantly a disease of IVDUs.⁴ The incidence is increasing both in this group and in non-addicted patients (the latter because of increasing use of intravascular catheters).S aureusaccounts for the majority of cases in IVDUs¹³; in the series of non-IVDUs cited earlier S aureus, Streptococcus bovis, and candida were the commonest organisms identified.⁵  

 

Pulmonary valve endocarditis is rare. In one combined series of 351 cases of endocarditis (both left and right sided) in IVDUs, isolated pulmonary valve endocarditis was found in only 1% of cases. A further 1% had combined involvement of the pulmonary and tricuspid valves.¹⁴ In another series of 132 IVDUs with RSE, involvement of the pulmonary or pulmonary and tricuspid valves occurred in five cases.¹³ As with tricuspid endocarditis, typical mucocutaneous features are unusual and a murmur may not be audible at presentation (In one series, a murmur was absent at the time of hospitalisation in 28% of a series of IVDUs with RSE.¹³) Diagnosis may therefore be difficult and the true incidence is probably underestimated.^{4  15} Although transoesophageal echocardiography is superior to transthoracic echocardiography in the detection of valvular vegetations in left sided endocarditis, improved diagnostic accuracy has not been shown in tricuspid valve endocarditis.¹⁶ The situation is less clear for pulmonary valve endocarditis, though transoesophageal echocardiography may offer advantages over transthoracic echocardiography.^{15  17} As with tricuspid valve endocarditis, prognosis is favourable with a high response rate to medical treatment.⁴

S aureus is the second commonest cause of native valve endocarditis, accounting for 30% of total cases and has an increasing incidence (though it accounted for fewer than 10% of cases in the preantibiotic era¹⁸). It is the commonest cause of nosocomially acquired endocarditis and the commonest causative organism in IVDUs.² It is notable in that it commonly presents as an acute rather than a subacute illness and frequently affects normal valves. (In a series of 106 cases, half of the non-IVDUs had no underlying cardiac disease; only one case of pulmonary valve involvement was identified.¹⁹) In addition, suppurative complications (such as myocardial abscess formation) are common with metastatic localisations occurring in 40% of cases.² In a series from Denmark (where necropsy rates are high) over half of cases of S aureusendocarditis were not suspected clinically and only diagnosed at postmortem examination.²⁰

This case illustrates the fact that the correct diagnosis of RSE is rarely initially considered because of a presentation that is dominated by pleuropulmonary symptoms, an oversight particularly likely in non-IVDUs in whom a high index of suspicion is required. The case also illustrates the propensity for S aureus to metastasise and reinforces the importance of immediately considering the possibility of endocarditis in any patient with S aureus bacteraemia, particularly if community acquired, even in the absence of signs of cardiac disease. Clinicians should remain mindful that musculoskeletal symptoms are common in endocarditis, may dominate the clinical picture in a significant minority of patients, and may lead the unwary away from the true diagnosis.

The patient was treated with a prolonged course of intravenous antibiotics. He remains well at follow up with improvement in his exertional dyspnoea and gradual resolution of his back pain.

Final diagnosis

Pulmonary valve endocarditis secondary to S aureus spinal osteomyelitis.

Factors predisposing to RSE and learning points are shown in boxes 1 and 2.

Acknowledgements

We are grateful to Sharon Lynn, senior cardiac technician at Queen Mary's Hospital, for providing a photograph of the echocardiographic appearance of the pulmonary valve.

References