PJP Pneumonia

This 28 yo M with pmh of severe rheumatoid arthritis presents with shortness of breath and cough for 3 months. He has been treated as outpatient for presumed community acquired pneumonia but has failed to improve. He presents with worsening SOB.

On arrival, T 99.2, HR 108, BP 113/50, RR 20, SpO2 89%.

Exam: slightly increased WOB with tachypnea. Diffuse crackles. Otherwise unremarkable. No LAD, meningismus.

Labs: WBC 12.5, Hgb 11, PLT 309; BMP remarkable for HCO3 21, normal renal function. LDH 413. ABG 7.45/34/60/21 (A-a gradient 47)

Home meds: Methotrexate, abatacept, prednisone, percocet.

PJP Pneumonia

This is an immunocompromised patient with acute hypoxic respiratory failure due, subacute in onset, with a reticulonodular pattern on their CXR - makes you worry about PJP Pneumonia! But since this patient does not have HIV - why are they at risk? While there are no published guidelines on PJP ppx for most immunocompromised patients (other than HCT patients), a meta-analysis showed that patients with a greater than 6% chance of of PJP warrant ppx. For our purposes, the highest yield population in this group is the following: patients receiving a glucocorticoid dose >20mg/d for one month or longer who also have another cause of immunocompromise (hematologic malignancy or a second immunosuppressant medication). While we do not know the doses of the prednisone in this patient, the clinical picture suggests PJP in the setting of multiple immunosuppressants.

Interestingly, LDH is often used as a biomarker in PJP. This is only sensitive in the HIV-infected population! In the HIV-uninfected population, there are so many other causes of immunodeficiency that concurrently increase your LDH that it becomes significantly less sensitive.

The question asks what to start for treatment and treatment dosed bactrim is the correct answer - but this patient also warrants adjunctive glucocorticoids. This is based on the degree of respiratory compromise as seen on the ABG and A-a (Alveolar-arterial) gradient. A PO2 < 70 and A-a > 35 requires steroids. Steroids lessen the inflammatory response from the dying PJPs and improves morbidity and mortality.