Authors: La Brocca U et al.
Cureus 17(12): e98563, December 6, 2025
This case report describes a 78-year-old woman with severe acute respiratory distress syndrome (ARDS) due to a mixed etiology: chronic amiodarone pulmonary toxicity (APT) superimposed on Haemophilus influenzae pneumonia. Despite reaching a PaO2/FiO2 nadir of 58—meeting criteria for severe ARDS—she was successfully managed without intubation through high-flow nasal cannula (HFNC), high-dose corticosteroids, and a strategy of permissive hypoxemia.
The patient had been on long-term amiodarone (200 mg, five days/week for approximately 10 years), creating substantial cumulative exposure. She presented with dyspnea, bilateral infiltrates on chest X-ray, leukocytosis, elevated CRP, and a bronchoalveolar lavage positive for H. influenzae. Targeted ceftriaxone and standard dexamethasone were initiated.
Despite appropriate antibiotics, hypoxemia worsened. Re-evaluation of imaging—particularly comparison with a CT from 20 months earlier—revealed chronic basal ground-glass and reticular abnormalities consistent with underlying drug-induced pulmonary toxicity. The team escalated steroids to prednisone 160 mg/day, suspecting an acute inflammatory exacerbation of APT triggered by infection.
On day three, the patient’s PaO2/FiO2 fell to 58 while on HFNC at 60 L/min and FiO2 1.0. Oxygen saturation hovered around 85%, yet she remained alert, oriented, hemodynamically stable, and without signs of respiratory muscle fatigue. Although her ROX index strongly predicted HFNC failure, clinicians opted to delay intubation to avoid ventilator-associated pneumonia and other complications—especially given her high-dose steroid exposure.
Clinical improvement began by day five. Inflammatory markers declined, and follow-up CT on day 10 showed dramatic radiologic clearance of consolidations, unmasking an underlying interstitial pattern consistent with steroid-responsive APT. She was weaned off HFNC and discharged from the ICU without ever requiring invasive mechanical ventilation.
The authors emphasize several important themes:
• Amiodarone pulmonary toxicity can mimic or coexist with pneumonia, creating diagnostic ambiguity.
• Historical imaging comparison was pivotal in recognizing the mixed etiology.
• Severe hypoxemia (P/F < 60) does not mandate intubation if the patient remains clinically stable and the cause is rapidly reversible.
• “Treating the patient rather than the numbers” may be appropriate in carefully selected, closely monitored patients.
They caution, however, that permissive hypoxemia should not be generalized. Delayed intubation in non-reversible ARDS phenotypes is associated with increased mortality. Strict monitoring for neurological status, hemodynamics, and respiratory fatigue is essential.
Key Points
• Long-term amiodarone users with bilateral infiltrates should be evaluated for APT—even when infection is documented.
• Severe ARDS (P/F 58) was managed successfully with HFNC and high-dose prednisone.
• Permissive hypoxemia may be reasonable in hemodynamically stable patients with preserved mental status and reversible inflammatory pathology.
• Review of prior imaging can fundamentally alter management decisions.
• Noninvasive strategies must be individualized; delayed intubation can be harmful in other ARDS phenotypes.
This case challenges rigid oxygenation thresholds for intubation and highlights nuanced ICU decision-making in mixed inflammatory lung injury.
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