Case #024

A chest that sounds normal has no business belonging to a man who desaturates crossing the corridor and whose room-air PaO₂ is 62 mmHg. That mismatch, profound hypoxia against an unremarkable examination, is the classic tell of Pneumocystis, and it is what separates this from the bacterial pneumonia six weeks of cough might otherwise suggest. Oral candidiasis with weight loss and night sweats points to underlying immunosuppression, and a CD4 count below 200 cells/µL is the threshold at which Pneumocystis becomes a real risk. A raised LDH is sensitive though non-specific, and beta-D-glucan supports the diagnosis. Radiographically, bilateral perihilar interstitial shadowing without effusion, cavitation or lymphadenopathy fits, and helps separate this from tuberculosis, which typically shows upper zone changes with cavitation. Treatment should never wait on bronchoalveolar lavage, because organism burden persists for days after therapy starts, so a sample taken later still yields the diagnosis. High-dose trimethoprim-sulfamethoxazole for 21 days is the treatment, given intravenously at this severity. The PaO₂ of 62 mmHg also settles the second decision: below 70 mmHg, or with an alveolar-arterial gradient above 35 mmHg, adjunctive corticosteroids improve survival. The reason is counterintuitive. Killing the organism releases antigen and provokes an inflammatory deterioration around day three, so patients get worse on effective treatment; steroids blunt that and are started with the antibiotic rather than in response to it. The negative AFB smear matters too, since tuberculosis is the other diagnosis a CD4 of 84 invites and steroids without cover would be the wrong move there.