MEDizzy - A 38-year-old woman is admitted to the medical ICU with

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Disorders of the Respiratory System and Critical Care Illness

A 38-year-old woman is admitted to the medical ICU with acute hypoxemic respiratory failure. She was well and healthy until 4 days prior when she abruptly began to feel ill with fevers, chills, bilateral pleuritic chest pain, and worsening shortness of breath. She has no signifcant past medical history but has suffered the recent death of her father following a car accident. In coping with his loss, she began smoking cigarettes again after a 15-year period of abstinence. She has been smoking up to two packs of tobacco daily. After she began to feel ill, she started taking acetaminophen and pseudoephedrine but otherwise takes no medications. Upon arrival in the emergency department, her oxygen saturation was 78% on room air. On a non-rebreather mask, the oxygen saturation increased to 92%. The vital signs are as follows: temperature 38.7°C (101.7°), heart rate 122 bpm, respiratory rate 28 breaths/min, and blood pressure 132/82 mmHg. She appears in moderate respiratory distress. There are bilateral difuse crackles. The cardiovascular examination shows regular tachycardia without murmur. The jugular venous pressure is not elevated, and no edema is present. The abdomen is soft and not tender. No hepatosplenomegaly is present. Extremity and neurology examinations are normal. Chest radiograph shows difuse bilateral infiltrates. Her echocardiogram shows normal left heart systolic and diastolic function. She is treated with ceftriaxone 1 g intravenously (IV) daily and azithromycin 500 mg IV daily. Over the course of the first 24 hours, the patient’s clinical condition continues to deteriorate. She remains febrile, and she requires intubation and mechanical ventilation. The patient’s ventilator is set on assist control with a rate of 28/min, tidal volume of 330 mL, fraction of inspired oxygen (FiO2) of 0.8, and positive end-expiratory pressure (PEEP) of 12 cmH2O. On these settings, her arterial blood gas values are pH 7.28, PaCO2 68 mmHg, and PaO2 62 mmHg. A bronchoalveolar lavage is performed. The cell count shows 58% neutrophils, 12% lymphocytes, and 30% eosinophils. What is the best approach to the treatment of the patient at this time?

ExplanationAcute eosinophilic pneumonia is an acute respiratory syndrome that often presents with a clinical picture that is difficult to differentiate from acute lung injury or acute respiratory distress syndrome (ARDS). Clinically, patients present with a prodrome of fevers, malaise, myalgias, night sweats, dyspnea, cough, and pleuritic chest pain. Physical examination may demonstrate high fevers, bibasilar rales, and rhonchi. The clinical course is frequently marked by rapid clinical progression to hypoxemic respiratory failure that requires mechanical ventilation. Chest radiography shows bilateral pulmonary infiltrates. This clinical picture clearly overlaps with infectious causes of respiratory failure and ARDS. However, the hallmark of acute eosinophilic pneumonia is the funding of >25% eosinophils in the bronchoalveolar lavage f uid. Acute eosinophilic pneumonia most frequently presents in individuals between the ages of 20 and 40 years and is more common in men. There is no epidemiologic link between the diagnosis and a prior history of asthma. However, several case reports have linked the development of acute eosinophilic pneumonia to the recent initiation of cigarette smoking or exposure to other environmental stimuli including dust. A bronchoalveolar lavage showing eosinophilia >25% is sufficient to establish the diagnosis of acute eosinophilic pneumonia. A surgical lung biopsy is not necessary. If performed, it would demonstrate eosinophilic infiltration with acute and organized difuse alveolar damage. Peripheral eosinophilia is not present acutely at disease onset but often becomes present between day 7 and day 30. Other organ failure is not present. The disease has a high degree of corticosteroid responsiveness and a good prognosis. Initiation of therapy with corticosteroids should not be delayed. Although there is no recommended dose of steroids for therapy, patients are often initiated on therapy with intravenous glucocorticoids with rapid improvement in hypoxemic respiratory failure. The expected clinical course is a complete resolution of clinical and radiographic features of the disease over several weeks without relapse upon tapering of steroids.