Max is a 61-year-old retired police officer whom you've known for the past 4 years. He's never smoked, he watches his diet rigorously, and exercises 5 days a week. The only item of significance in his past medical history is a paroxysmal atrial fibrillation that developed after a routine inguinal hernia operation 6 years ago. Though he had a myocardial perfusion scan with stress test and an echocardiogram at the time, they showed no abnormalities, and no etiology for the arrhythmia was ever found. Initially, Max's cardiologist elected to treat the episodes with propaˇfenone and metoprolol, on an "as needed" basis. Over time, the palpitations became more frequent and the medications lost their effectiveness, so the patient underwent a successful cardiac ablation procedure that restored his rhythm to sinus.

Max presents to your office with a 6-week history of dizziness, hemoptysis, productive cough and shortness of breath. On examination, air entry seems good in all lung fields, with no adventitious sounds. You order a complete blood count and chest x-ray, and diagnose Max with a lower respiratory tract infection for which you start him on moxifloxacin 400 mg daily for 10 days. The white blood cell count comes back at 7.6 x 10⁹/L, the hemoglobin level 116 g/L. The chest x-ray is normal, other than showing old granulomatous disease.

Over the next week, Max takes a significant turn for the worse. Your previously fit patient continues to cough up blood and is now short of breath on minimal exertion. You order an urgent CT scan of the chest, which reveals an "extensive, patchy, ground-glass attenuation and septal thickening of the left upper lobe." You arrange for a respiratory consultation stat, after which Max undergoes a bronchoscopy with bronchoalveolar lavage.

The cytology results of the lavage are negative and there's no growth from cultures, including pneumocystis pneumonia and acid-fast bacilli. The patient continues to decline rapidly. What would you do next?

Why is Max's strength waning?