ICU · infectious-diseases
Pneumonia in the Immunocompromised Patient — Comprehensive ICU Management
Also known as Pneumonia in the immunocompromised host · Opportunistic pneumonia · Pulmonary infiltrates in the cancer patient · Pneumonia in transplant recipients · Pneumonia in haematological malignancy · Invasive pulmonary aspergillosis · Pneumocystis jirovecii pneumonia · CMV pneumonitis
Pneumonia in the immunocompromised host (non-HIV) — haematological malignancy, stem-cell/solid-organ transplant, prolonged steroids, cytotoxic chemotherapy, biologics. The pathogen spectrum is dictated by the SPECIFIC IMMUNE DEFECT: (1) NEUTROPENIA (post-chemo, <0.5 x 10^9/L) - Pseudomonas aeruginosa, other gram-negative bacilli, invasive pulmonary aspergillosis, Candida, mucositis-related viridans streptococci; (2) T-CELL DEFECT (transplant calcineurin inhibitors, fludarabine, alemtuzumab) - Pneumocystis jirovecii (PCP), CMV, Legionella, Nocardia, Cryptococcus, mycobacteria; (3) B-CELL / HUMORAL DEFECT (CLL, myeloma, post-rituximab) - encapsulated bacteria — Streptococcus pneumoniae, Haemophilus influenzae; (4) PROLONGED STEROIDS (20 mg/day prednisone 4 weeks) - PCP, Nocardia, Aspergillus. The intensivist's task: (1) classify the immune defect, (2) get a diagnostic BAL EARLY (galactomannan for Aspergillus, (1-3)-beta-D-glucan for PCP/fungal, CMV PCR, respiratory virus panel, bacterial + fungal + mycobacterial culture), (3) start BROAD EMPIRIC THERAPY — anti-pseudomonal beta-lactam + empiric antifungal (caspofungin for Candida, voriconazole for suspected mould) + ganciclovir if CMV likely + co-trimoxazole if PCP possible + reduce immunosuppression, (4) prefer NIV over intubation (lower VAP/mortality), (5) prophylaxis — co-trimoxazole (PCP), posaconazole (Aspergillus), valganciclovir (CMV). Mortality 20-50% — far higher than immunocompetent CAP. Early appropriate (pathogen-directed) therapy is the single biggest modifiable determinant of survival.
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- The PATHOGEN SPECTRUM follows the IMMUNE DEFECT — neutropenia -> Pseudomonas/Aspergillus; T-cell defect -> PCP/CMV/Nocardia; B-cell defect -> S. pneumoniae/H. influenzae; steroids -> PCP/Nocardia/Aspergillus. Classify the defect BEFORE choosing empiric therapy
- Get a diagnostic BAL EARLY — do not sit on empiric therapy. Send the full panel: bacterial/fungal/mycobacterial culture, galactomannan (Aspergillus), (1-3)-beta-D-glucan (PCP/fungal), CMV PCR, respiratory virus panel, Nocardia, PCP PCR/immunofluorescence
- Invasive pulmonary aspergillosis in neutropenia — voriconazole FIRST-LINE, check BAL galactomannan (OD index >=1.0) and CT HALO SIGN (nodule with ground-glass halo = angioinvasion)
- CMV pneumonitis 1-4 months post-transplant or during rejection treatment — ganciclovir is commonly the first-line antiviral; diagnose on BAL CMV PCR + cytopathic effect (owl's-eye inclusions)
- Prefer NIV over intubation for hypoxaemic respiratory failure — immunocompromised patients who are intubated have high VAP and mortality; early NIV reduces both
- Reduce immunosuppression if possible (balance against graft rejection / GVHD) — the 'net state of immunosuppression' must come down for any antimicrobial to work
Meet the patient
A 60-year-old man is day 90 after an allogeneic stem-cell transplant for AML, on tacrolimus and prednisolone for grade II skin graft-versus-host disease. Co-trimoxazole prophylaxis was stopped two weeks ago for neutropenia. He arrives with five days of dry cough and breathlessness, an oxygen saturation of 88 percent on room air, and a chest film that looks almost normal.[2][5]
The two questions that decide his next hour are the two that decide every case in this territory: what immune defect does he have right now? (the defect names the likely pathogen) and have I sampled the lung? (because empiric therapy alone kills these patients). Hold those two questions and the rest slots into place.[2]
References18ShowHide
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