A 70-year-old male with a known history of type 2 diabetes mellitus, hypertension, chronic kidney disease, and ischemic heart disease presented to the emergency department with 7-day history of gradual onset of shortness of breath, reduced effort tolerance, and lethargy. On further inquiry, there was loss of appetite for a month, but he denied any accompanying weight loss, and there was also no history of fever or night sweats. He admitted to vague abdominal and back pain that lasted for a week.
At the emergency department, he looked cachexic and dehydrated but was alert to time, place, and person. He was apyrexial with a pulse rate of 88 beats per minute and blood pressure of 131/72 mmHg, but tachypnoeic with a respiratory rate of 27 breaths per minute. The oxygen saturation, however, was maintained at 98% on room air. Respiratory examination revealed left-sided stony dullness up to the midzone on percussion with reduced air entry on the same side. Cardiovascular and gastrointestinal examinations were unremarkable.
Chest radiograph confirmed the presence of a left medium abundance pleural effusion (Figure 1).
 Table 1 summarizes the results of the blood investigations including hypercalcemia with a level of 3.03 mmol/L.
He was initially admitted to the ward for treatment with intravenous Augmentin and 0.9% saline hydration for presumed acute-on-chronic kidney injury as we did not have any baseline kidney function, but unfortunately his breathing deteriorated rapidly a day after admission. He became more tachypnoeic, and the arterial blood gases showed type 2 respiratory failure (pH, 7.32; pO2, 62 mmHg; pCO2, 50 mmHg; HCO3, 20; lactate, 3). In view of the worsening ventilation and his general medical condition, a decision was made to invasively ventilate him in the intensive care unit (ICU). In the ICU, his antibiotic was upgraded to intravenous piperacillin/tazobactam for presumed community-acquired pneumonia with pleural effusion and intravenous 0.9% saline 1000 mls over 24 hours for hydration was maintained.
Echocardiography demonstrated globally dilated severe hyperkinesia of the left ventricle and a severely impaired systolic function with a left ventricle ejection fraction of 20%. Because of this, the fluid balance was closely monitored to minimize the risk of pulmonary congestion.
His urine output remained good with an average of 100 mls/h equivalent to 1.4 mls/kg/h. Unfortunately, despite adequate hydration and a positive balance of 900 mls averaging over 3 days, his serum calcium continued to rise to 3.48 mmol/L.
Intravenous furosemide was also initiated as a forced diuresis measure, which also failed to bring the calcium down.
Further investigations for the cause of the pleural effusion included therapeutic and diagnostic left thoracocentesis, and blood tests for the cause of hypercalcemia were conducted during admission. The results are listed in Table 2.
To reduce the calcium, we decided to try him on subcutaneous denosumab at the dose of 120 mg, and his serum corrected calcium gradually improved to 2.40 mmol/L, as depicted in Table 3, after 4 days with no further drop in calcium thereafter.
At day 5, the pleural fluid analysis for rapid mycobacterium liquid culture and sensitivity test came back positive for Mycobacterium tuberculosis complex. The treatment for tuberculous pleural effusion with isoniazid, rifampicin, pyrazinamide, ethambutol, and pyridoxine (2HRZ/4HR) was subsequently commenced.
He was successfully extubated after 10 days in the ICU and was transferred to the general medical ward for further management. Unfortunately, he developed a severe concomitant hospital-acquired pneumonia complicated by respiratory failure that eventually led to multiorgan failure, cardiorespiratory arrest, and death.