A 39-year-old man presented to the emergency department complaining of a 3-day history of shortness of breath and dry cough. He had no known significant co-morbidities and did not report any further associated symptoms. He reported that he was treated with antibiotics for a lower respiratory tract infection (LRTI) by a private physician in the previous 3 days with no improvement in symptoms. He was unsure of his HIV status and was not on antiretroviral therapy (ART).
His admission vitals were a blood pressure of 123/70 (82) mmHg, heart rate of 116 beats per minute, respiratory rate of 30 breaths per minute and a temperature of 36.9  C. On examination, he had no significant lymphadenopathy and was not found to have mucosal or skin lesions associated with advanced HIV. No other obvious stigmata of advanced HIV were noted. He was in severe respiratory distress with scattered bilateral predominantly basal crackles on auscultation. Wheezing was not present on auscultation. He had an oxygen saturation of 62% on a partial rebreather mask with an inspired oxygen fraction (FiO2) of 80%.
Laboratory investigations revealed a white cell count (WCC) of 14.5 x 109 cells/L, haemoglobin (Hb) of 11.6 g/L, platelets of 298 x 109 cells/L, urea of 6.3 mmol/L, creatinine of 108 mumol/L, C-reactive protein (CRP) of 102 mg/L and beta-d-glucan (BDG) of > 500 pg/mL. His admission blood gas showed a mixed respiratory and metabolic acidosis with type II respiratory failure and a markedly increased alveolar-arterial gradient (pH = 7.36, pCO2 = 34.7, pO2 = 64.8, HCO3 = 19.2, BE = -4.9, SpO2 = 96.9, Hb = 13.4, Lac = 4.4). His chest X-ray (CXR) showed diffuse bilateral alveolar infiltrates and granular opacities. A transthoracic echocardiogram performed at the time of admission showed normal left ventricular function, no evidence of pulmonary embolus and normal heart valves. Based on clinical suspicion, hypoxaemic respiratory failure with typical chest radiograph changes, the patient's normal echocardiogram, elevated BDG, and the relative absence of clinical signs usually associated with a multilobar pneumonia, the diagnosis of Pneumocystis pneumonia (PCP) was considered.
On the basis of his clinical condition and investigations, the patient was intubated, ventilated and admitted to the intensive care unit (ICU) for respiratory support. He was empirically started on treatment for partially treated community acquired pneumonia (CAP) (piperacillin and tazobactam and a macrolide) as well as PCP, on the basis of clinical case definition as suggested by the World Health Organisation (WHO), with high-dose intravenous trimethoprim-sulfamethoxazole (TMP-SMX) and high-dose intravenous corticosteroids (hydrocortisone). He consented to HIV testing on admission and was found to be HIV-infected with a CD4 count of 7 cells/muL. Additional sputum and blood investigations for Mycobacterium tuberculosis (TB) including TB culture (sputum and blood) and Auramine O stain, real-time polymerase chain reaction (PCR) (TB GeneXpert), sputum gram stain and bacterial culture and direct fluorescence antigen test for PCP were negative. Standard aerobic and anaerobic blood cultures yielded no pathogenic organisms.
The patient was intubated and ventilated for 3 days and spent a week in our unit. During this period, we adopted a lung protective ventilation strategy, permissive hypoxaemia as well as meticulous fluid management. Through his week-long admission, he had a cumulative fluid balance of -332 mL. Initial pre-admission ventilator settings of FiO2 = 1, PEEP = 14 and DeltaP = 8 were successfully weaned to FiO2 = 0.6, PEEP = 10 and DeltaP = 10 on day one of admission. We accepted oxygen saturations in the region of 70%-80% and PaO2 measurements in the region of 50 mmHg - 60 mmHg whilst maintaining tidal volumes of 4 mL/kg - 6 mL/kg. On day four of admission, despite oxygen saturations in the region of 80%, the patient was successfully extubated and placed on non-invasive ventilation (NIV). He required NIV (positive end expiratory pressure of 6 cm H2O and pressure support of 6 cm H2O) for a total of 3 days before being weaned onto oxygen supplementation with an FiO2 of 0.4. He maintained oxygen saturations in the region of 85%-90%. He was discharged to the ward on nasal cannula after a 7-day ICU stay.