with Acute Respiratory Failure
PRESENTATION OF CASE
A 67-year-old man was transferred to this hospital with acute respiratory failure.
Four days before admission, the patient had visited his primary care physician because of a three-month history of chest congestion and cough productive of sputum that was initially clear but then became more opaque. His chestfelt tight when he breathed deeply, and deep inspirations triggered the cough. During the week before the physician visit, he had had slight nasal congestion, poor appetite, and decreased energy, but no fever, chills, nocturnal sweats, or postnasal drip. His physician obtained a chest radiograph, which showed increased markings at the base of the right lung; a computed tomographic (CT) scan of thechest was recommended. A combination inhaler
consisting of salmeterol and fluticasone was prescribed. Over the next 24 hours, severe pleuritic chest pain developed, with productive cough and severe shortness of breath. The patient went to the emergency department of another hospital.
On examination there, he was alert and afebrile, with a respiratory rate of 24 breaths per minute and somewhatlabored breathing. Pulse oximetry showed an oxygen saturation of 86 percent while he was breathing ambient air. Bilateral rales were heard on examination of the lungs — although chest pain prevented deep inspiration — but no wheezing. The remainder of the physical examination was unremarkable. A chest radiograph showed opacifications that now involved the left lower lobe, in addition to thosepreviously seen in the right middle and lower lobes. His white-cell count was 17,800 per cubic millimeter, with 74 percent neutrophils and 7 percent band forms; the hematocrit was 32.9 percent. The levels of serum electrolytes and cardiac enzymes and the results of tests of liver and renal function were all within normal ranges. He was admitted to the intensive care unit.
Two chest radiographs overthe next 24 hours showed progressive worsening of the opacifications to include both upper lobes. The patient’s respiratory rate increased, his dyspnea worsened, and his oxygen saturation dropped to 76 percent while he was breathing 100 percent oxygen with the use of a face mask; the trachea was intubated, and he was placed on ventilator support. Treatment with levofloxacin was begun, but as hiscondition deteriorated the antibiotic agents were changed to ceftriaxone and azithromycin, and he received two doses each of tetracycline and erythromycin.
A sputum culture grew normal flora, and two blood cultures showed no growth. He was transferred to the intensive care unit at this institution. The patient had a history of gastroesophageal reflux disease and chronic back pain, for which he tookesomeprazole and rofecoxib. He had had an appendectomy, bilateral inguinal hernia repairs, a transurethral resection of the prostate, and removal of benign colon polyps. He was married with two children. He was a retired engineer who had worked in a metal machine shop. He had no known toxic exposures, although he recalled a coworker becoming very ill from an undefined respiratory illness in the1970s. He had never smoked and rarely drank alcohol. He had not traveled outside the United States nor had he been in contact with anyone who had traveled recently. He swam regularly to help with his back pain. He had recently rewired his daughter’s attic, but had not been exposed to excessive dust or mold. He had no pets and did not hunt. His wife reported that several weeks before the onset ofthis illness, he had been exposed to bird droppings when he was changing an outdoor bird feeder and a gust of wind blew the droppings into his face. The temperature was 36.7°C, the blood pressure 113/54 mm Hg, and the pulse 79 beats per minute.
The oxygen saturation was 97 percent with the fraction of inspired oxygen at 0.5. On physical examination, he was a well-developed man, who was intubated...