A 31-year-old female, a mother of 2, originally from Mtubatuba in KwaZulu-Natal, presented to the King Edward VIII Hospital Acute Medical Unit with a 2-month history of progressive dyspnoea (New York Heart Association (NYHA) grade 4)   and generalised body swelling. She reported that her abdomen became enlarged within a few days before her presentation.
She reported no chest pain, palpitations, constitutional symptoms, nor rheumatic heart disease as a child. She was HIV-infected, diagnosed in 2019, and was currently on a tenofovir, emtricitabine, and efavirenz fixed-dose regimen of anti-retroviral therapy (ART). She also reported a previous history of pulmonary TB infection diagnosed on sputum testing in 2012, for which she had completed 6 months of anti-TB therapy. She reported no prior hospital admissions and related that she had regular menses, no history of pregnancy losses, nor a current or previous hormonal contraceptive history. She is of sober habits with no use of traditional or herbal treatment.
On examination, she was clinically fluid overloaded. She had mild pallor, no jaundice, no clubbing, and was acyanotic. She had minimal lower limb swelling - grade 1. She had no stigmata of advanced HIV infection or had any features consistent with chronic liver disease. She had distended pulsatile neck veins, with a markedly raised JVP (confirmed by a positive abdominal-jugular reflex) to the angle of the jaw - with notable CV waves. She was tachycardic (112 beats/min) with a pulse that was irregularly irregular in rhythm, consistent with atrial fibrillation (AF). Her blood pressure was within normal limits. She had a right-sided S3 gallop (possible pericardial knock) with a grade 3/6 pansystolic murmur of tricuspid regurgitation at the left sternal boarder with no clinical signs of pulmonary hypertension (no loud pulmonic component of second heart sound (P2), no parasternal heave and no loud P2). She was in respiratory distress with a tachypnoea (24 breaths/min); however, maintaining an oxygen saturation of 96% on room air. No crepitations were heard on auscultation of her chest. Her abdomen was grossly distended with ascites (notably out of proportion to the lower limb peripheral oedema) together with a tender right upper quadrant. At this point, we entertained a differential diagnosis that explored the presentation of disproportional ascites to peripheral oedema.
Our considerations therefore included the following:
right heart failure (RHF) secondary to post-TB bronchiectasis with cor pulmonale,
CP,
intra-abdominal malignancy or disseminated TB,
restrictive cardiomyopathy,
hepatic outflow obstruction,
chronic liver disease,
superior vena cava syndrome, and
right atrial myxoma.
Laboratory investigations (Table 1) revealed liver function tests, suggesting a predominantly infiltrative pattern.
Her chest radiograph showed patchy lower lobe pulmonary opacification with small bilateral pleural effusions - not amenable to pleurocentesis, with no pericardial calcifications being noted (Figure 1).
Her echocardiogram showed right atrial dilation with evidence of a thrombus, with mild to moderate tricuspid regurgitation. The cardiac contractility was mildly impaired with a significant septal bounce. The IVC appeared to be dilated with a spontaneous echo-contrast noted. There was respiratory variation, with a preserved left ventricular ejection fraction of 47%.
The abdominal ultrasound confirmed gross ascites with hepatomegaly measuring 16 cm with no focal lesions. The portal vein diameter was 1.2 cm (reference range = 0.7-1.5 cm). A Doppler ultrasound of the IVC and HV showed notable sludging, suggesting a thrombus within the aforementioned vessels.
A computed tomography (CT) scan of the abdomen and chest confirmed CP - pericardial thickening and calcifications were demonstrated. The right atrium was enlarged with early reflux into the IVC which was attributed to the features of RHF (arrows in Figure 2).
The final diagnosis made was that of an HIV-infected patient on ART with a previous history of treated pulmonary TB now presenting with features suggestive of:
CP with a possible BCS (acute 2-week history of rapidly enlarging abdomen with sludge/thrombus in both HV and IVC) associated with AF.
The patient was continued on ART and started on anti-coagulation in the form of Clexane  60 mg BD subcutaneous and warfarin 5 mg daily orally once the AF was detected. She was also commenced on anti-TB treatment before referral to the cardiothoracic department.