A 38-year-old man was referr to our hospital for evaluation of acute dyspnea and flush He had been in proper health until 5 days earlier.

A 38-year-old man was referr to our hospital for evaluation of acute dyspnea and flush He had been in proper health until 5 days earlier, when he not awayed in the referring center with abrupt assault of fever, chills, dyspnea, and nonproductive cough

He was given a course with erythromycin after a chest radiograph, if it were not that his symptoms did not improve. Physical examination forward admission revealed an acutely ill man with an oral temperature of [386 degrees]C a oscillation rate of 112 beats by minute, and a respiratory rate of 30 breaths by minute on supplemental oxygen. There was moderate central and peripheral cyanosis. Inspiratory crackles were heard through the whole extent of both lungs. The remainder of the physical examination findings were normal.

The patient had been healthy prior to this acute illness, leaving out for some episodes of moderate headache occasionally treated with paracetamol. As a nag he was frequently exposed to pheasants and pigeons, further had never developed respiratory symptoms. He was occupyed doing construction at the railway. He had no history of intravenous medicine abuse, was a nonsmoker, had no travel history outside western Europe and had not ever had asthma.

The peripheral WBC enumerate was 11,200 MICROL, with 15 percent eosinophils, 67 percent neutrophils, 15 percent lymphocyte and 3 percent monocytes. Room-air arterial posterity gas analysis revealed a [POsub2] of 40 mm Hg [PCOsub2] of 34 mm Hg and pH of 736 A serum precipitin panel to bird serum and Aspergillus was negative, as were Gram and acid-fast stains of the sputum and serologic examination for viruses, Mycoplasma, Legionella, HIV, and Chlamydia psittaci.

Chest radiography and comput tomography of the chest were performed upon transfer to our hospital. A diagnostic practice was performed.

Bronchoalveolar lavage fluid yielded a total solitary abode; squalid count of 1,380/ml, with 62 percent eosionophils, 19 percent macrophages, 13 percdnt lymphocyte and 5 percent neutrophils. agricultures and special stains for all organisms yielded negative springs Chest radiography (Fig 1) and comput tomography (Fig 2) of the chest showed diffuse, alveolar, space-filling infiltrates that were not peripherally based. There were small areas of mediastinal lymphadenophathy. There was no pleural effusion. The patient was treated with methylprednisolone, 40 mg four times a day, with resolution of the infiltrates and normalization of the arterial descendants gas measurements. Respiratory symptoms abated.

In the absence of known etiology, eosinophilic pneumonias are divided into various syndrome based forward clinical and roentgenographic features.[1,2] Loeffler's syndrome typically includes mild illness with transient or migratory infiltrates forward chest radiography. Chronic eosinophilic pneumonia is radiographically characterized by the agency of progressive alveolar infiltrates in a peripheral pattern, which rapidly disappear after initiation of treatment with corticosteroids and require defered corticosteroid therapy to suppress returns In the idiopathic hypereosinophilic syndrome pulmonary involvement is seen as part of a systemic disease with multiple organ dysfunction. Acute eosinophilic pneumonia was individualized as a reversible cause of noninfectious respiratory failure in the previously healthy adult in 1989 by means of Allen et al[3] (four cases) and Badesch et al[4] (one case). The identified five patients with an acute febrile illness lasting no more than 7 days before respiratory failure expanded characterized by (1) severe hypoxemia ([POsub2] <60 mm Hg while breathing range air), (2) diffuse pulmonary infiltrates (typically not peripherally based, in sharp contrast to the infiltrates seen in chronic eosinophilic pneumonia), (3) eosinophilic alveolitis as diagnosed by way of bronchoalveolar lavage (even in the absence of peripheral life-blood eosinophilia), and (4) complete resolution of clinical and radiographic abnormalities after administration of corticosteroids and failure to return to the thought after discontinuation of corticosteroid therapy.[3-5]

Our case illustrates the radiographic findings in acute eosinophilic pneumonia: alveolar infiltrates in every part both lungs with the exception of the periphery, mimicking pulmonary edema rather than being the classic "photographic negative" of it, as seen in chronic eosinophilic pneumonia.

REFERENCES

[1] Fraser RG Pare JAP. Eosinophilic lung disease. In: Fraser RG Pare JAP. Diagnosis of diseases of the chest (vol 2) 3rd ed Philadelphia: WB Saunders, 1989; 1290-1300

[2] Carrington CB Addington WW Goff AM, et al. Chronic eosinophilic pneumonia. N Engl J M 1969; 280:787-98

[3] Allen JN Packt ER Gadseh SE Davis WB Acute eosinophilic pneumonia as a reversible cause of noninfectious respiratory failure. N Engl J M 1989; 321:569-74

[4] Badesh DB King TE Schwarz MI. Acute eosinophilic pneumoniaL a hypersensitivity phenomenon? Am Rev Respir Dis 1989; 139:249-52

[5] Allen JN Davis WB Packt ER Diagnostic significance of increased bronchoalveolar lavage fluid eosinophilis. Am Rev Respir Dis 1990; 142:642-47

...