A phantom tumour of the lung in a patient with heart failure was misdiagnosed as a lung mass.

Background
A phantom tumour of the lung is a rare but recognised radiographic finding, primarily observed in patients with fluid overload. It is characterised by an interlobular or encysted pleural effusion, usually located in the right-middle lung zone,1 although there have been reports of similar cases on the left side.2 It is predominantly observed in the transverse fissure, less commonly in the oblique fissure, and very rarely presents in both fissures simultaneously.3 Importantly, phantom tumours do not require specific interventions beyond the standard treatment for pleural effusions, which mainly involves the use of diuretics. One of the hallmark features of these tumours is their resolution following diuretic treatment, giving rise to the term ‘vanishing tumour of the lung’.1 4
In this report, we describe a case of a phantom lung tumour that was initially misdiagnosed as a malignant lung tumour.

Case presentation
Our patient is a man in his 70s with an established diagnosis of diabetes mellitus and hypertension, both of which are being managed with medication. He presented to the emergency department with a 10-day history of productive cough, producing sputum that was blackish and yellowish in colour. This was accompanied by a 3-day history of worsening shortness of breath, which had progressed to the point that he was unable to lie flat and experienced significant difficulty with routine daily activities. Additionally, he reported a 1-day history of left-sided chest pain, a 5-day history of epigastric pain, generalised fatigue, and unintentional weight loss of approximately 4 kg over a period of 3 months. The patient works as a driver and has a significant smoking history, having smoked 2–3 packs of cigarettes daily for approximately 40 years, before quitting 4 years ago.
On examination, the patient exhibited a blood pressure of 149/105 mm Hg, with a pulse rate of 88 beats per minute and a respiratory rate of 20 breaths per minute. Oxygen saturation was 98% on room air, and temperature was 36.3°C. Clinical findings revealed normal jugular venous pressure, mild bilateral pitting oedema, diminished breath sounds in the left lower lung lobe and basal crepitations on the right side.

Investigations
Complete blood count (CBC) showed WBC 6.6×10ˆ9 /L, RBC 4.1×10ˆ12 /L, and platelet count 220×10ˆ9 /L, all within normal limits. Venous blood gas analysis revealed a pH of 7.391, a pCO2 of 37 mmHg, a pO2 of 39 mmHg, a lactate of 1.00 mmol/L, and an HCO3 of 22.2 mmol/L. Laboratory tests revealed a haemoglobin level of 12.6 g/dL, normal renal and liver function tests, an elevated serum troponin level of 49 ng/L (normal<14 ng/L), and a Pro BNP level of 8583 pg/mL. Furthermore, an ECG showed no ischaemic changes but revealed left ventricular hypertrophy by voltage criteria, consistent with chronic pressure overload as illustrated in figure 1.
The echocardiogram demonstrated severe left ventricular systolic dysfunction, with an ejection fraction of 20% and global hypokinesia. There was a significant elevation in pulmonary artery pressure, accompanied by a left-sided pleural effusion. Right ventricular function was impaired, as indicated by a tricuspid annular plane systolic excursion of 16 mm and an RV S′ velocity of 9 cm/s (0.09 m/s). The right ventricular systolic pressure was significantly elevated at 67.83 mmHg, consistent with pulmonary hypertension. A chest X-ray (PA view) revealed a well-defined biconvex opacity measuring 5 by 4 cm in the right lung, as illustrated in figure 2. Given the patient’s characteristics, smoking history and reported weight loss, an initial diagnosis of a malignant lung tumour was considered, prompting the ordering of a CT thorax with contrast.
Furthermore, based on CT findings as demonstrated in figure 3, multilocular hypodensities were observed along the fissures of the right lung, suggestive of multilocular fissural effusions. Consequently, the patient was diagnosed with congestive heart failure accompanied by a phantom tumour, defined by localised fluid accumulation within the lung fissures as a result of the heart failure.

Differential diagnosis
Malignant lung tumour.

Transudate pleural effusions resulting from congestive heart failure or renal failure.

Exudates pleural effusions like parapneumonic pleural effusions, benign pleural effusions associated with asbestos exposure, and malignant pleural effusions.

Chylothorax, and fibrous tumours arising from the visceral pleura of the interlobar fissure.

Treatment
The treatment was initiated with a single intravenous dose of furosemide 80 mg, followed by a maintenance regimen of furosemide 20 mg twice daily for 7 days, along with restricted fluid intake.

Outcome and follow-up
The patient was hospitalised for 10 days and showed gradual improvement in his condition. Follow-up imaging after 7 days of diuretic therapy revealed that the chest X-ray opacities had resolved, as shown in figure 4. Moreover, a CT scan, seen in figure 5, displayed similar findings, confirming the diagnosis of a phantom tumour. He was discharged in stable condition, with outpatient cardiology follow-up arranged.

Discussion
Phantom tumours are most often seen as well-defined, homogeneous masses localised within the transverse fissure and, less frequently, in the oblique interlobar fissures. Due to the limited number of reported cases, the incidence is difficult to estimate. The phenomenon was first described by Stewart in 1928, who referred to it as ‘interlobar hydrothorax.5' Phantom tumours predominantly manifest in males, and, as illustrated in the current case, fluid accumulation has been reported primarily within the right hemithorax, with approximately 75% of reported cases occurring in the right transverse fissure and less frequently in the oblique fissure. Concurrent involvement of both fissures have been documented in about 20% of cases, while occurrences in the left hemithorax are relatively rare.6
In patients with congestive heart failure, elevated hydrostatic pressure in the right lung impedes venous and lymphatic drainage, leading to a greater likelihood of effusion on that side. Additionally, pleuritis may lead to closure of the pleural space, further restricting the distribution of fluid.7 While phantom tumours are usually located in the minor fissure, they may also be found in the major fissure, as demonstrated in this case.
The differential diagnosis of loculated pleural effusions within the fissure encompasses several conditions, including transudates resulting from left ventricular failure or renal failure, as well as exudates like parapneumonic pleural effusions, benign pleural effusions associated with asbestos exposure, and malignant pleural effusions. Furthermore, the differential should consider haemothorax, chylothorax, and fibrous tumours arising from the visceral pleura of the interlobar fissure.3

Conclusion
This case highlights the importance of considering and ruling out the possibility of a phantom lung tumour in any patient with congestive heart failure who presents with a visible lung mass on a chest X-ray. It demonstrates the effectiveness of conservative medical management, including loop diuretics and restricted fluid intake for treating localised interlobar effusion in the context of congestive heart failure. Furthermore, early identification of this condition is crucial to avoid misdiagnosis and to prevent unnecessary, invasive, and costly diagnostic procedures and treatments.

Learning points

The diagnosis of a phantom tumour of the lung is supported by the presence of fluid accumulation in the large pleural cavity.

Recognising this particular radiographic appearance is essential to prevent unnecessary investigations for potential pulmonary malignancies.

Treating the underlying condition usually leads to the resolution of the pseudotumour.