A 53-year-old woman presents with a 3-day history of generalized body fatigue, fever, weakness, and shortness of breath. The patient’s medical history is significant for achalasia but otherwise is noncontributory. At triage, the patient’s vital signs are taken. An electrocardiogram (ECG) shows atrial flutter. A chest radiograph reveals bibasilar infiltrates and bilateral pleural effusions, indicative of pneumonia. Complete blood cell count and complete metabolic panel results are within normal limits.
Because radiography shows infiltrates and the patient is having trouble breathing and is experiencing progressively worsening fever, chills, sweats, and rigors, she is admitted, treated with intravenous (IV) antibiotics, and monitored.
The patient converts to a normal sinus rhythm after admission but shortly thereafter goes into shock (Table 1). Her heart rate increases to 109 beats per minute, her blood pressure decreases, and her O2 saturation level drops to 92%, despite delivery of 4 liters of O2 per minute via nasal cannula. Collectively, these changes indicate systemic inflammatory response syndrome and hypoxic respiratory failure.
A second chest radiograph shows increasing interstitial and alveolar radiodensities in the lower lungs. The patient’s antibiotic regimen is changed to levofloxacin, piperacillin/tazobactam, and vancomycin. The patient is transferred to the intensive care unit (ICU) and placed on a ventilator. A pulmonologist is called to consult on the case. Cultures for Legionella antigens, influenza A and B, and methicillin-resistant Staphylococcus aureus are negative.
A CT scan of the chest, which is more sensitive and specific for aspiration pneumonia, empyema, and abscess than radiographs, shows diffuse alveolar and ground glass opacities, a common finding in early interstitial lung disease.1,2 Although cultures did not reveal any significant abnormal findings, a bronchoscopy recovers slightly sanguineous, cloudy fluid.
After the patient is on a ventilator for 10 days, sputum cultures are positive for Candida albicans infection, a common cause of nosocomial sinusitis and a common sequela of endotracheal intubation due to impairment of sinus drainage.3 A therapeutic thoracentesis is considered, but because the effusions remain stable, it is deemed unnecessary.
During the next 4 days of hospitalization, the patient continues to be febrile, with her temperature ranging from 37.5°C to 38°C, and her respiratory rate is 20 to 30 breaths per minute. However, chest radiographs show progressively decreasing bibasilar infiltrates.
After another 5 days of intubation, the respiratory therapy team attempts ventilator weaning, which initially fails. Her laboratory values show hypocalcemia, hypokalemia, and anemia. The following day, the patient appears more comfortable, more easily aroused, and a chest radiograph reveals considerably less bibasilar infiltrates. Due to these improvements, the respiratory team decides to reattempt ventilator weaning. Pulmonology provides continuous positive airway pressure ventilation, with gradual weaning from the pressure support to increase the likelihood of spontaneous breathing. Weaning from the ventilator is successful.
For the next 4 days, the patient continues IV antibiotics and daily chest radiographs to monitor her bibasilar infiltrates. At discharge, the patient is instructed to take oral antibiotics and practice breathing with a spirometer to increase her forced expiratory volume capacity. She follows up with the pulmonologist every 2 weeks for the next 2 months to monitor for the complete resolution of the bibasilar infiltrates and effusions on chest radiograph.
This article originally appeared on Clinical Advisor