The acute eosinophilic pneumonia (AEP) is a disease of unknown etiology which is characterized by a rapid eosinophilic infiltration of the lung interstitium.
(See also overview of eosinophilic lung disease.)
The acute eosinophilic pneumonia (AEP) is a disease of unknown etiology which is characterized by a rapid eosinophilic infiltration of the lung interstitium. (See also overview of eosinophilic lung disease.) In contrast to chronic eosinophilic pneumonia AEP is an acute disease that is not usually repeated. Incidence and prevalence are unknown. AEP can occur at any age, but most commonly affects patients between 20 and 40 years with a sex ratio (m / w) of 2: 1. However, it could be an acute hypersensitivity reaction to an unidentified inhaled antigen in otherwise healthy individuals in the AEP. Cigarette smoking or other smoke exposure may be involved. Symptoms and complaints The AEP causes an acute febrile illness of short duration (typically <7 days). The symptoms is to nonproductive cough, dyspnea, malaise, myalgia, night sweats, and pleuritic chest pain. Among the findings include tachypnea, fever (often> 38.5 ° C) and bilateral basal inspiratory, not sounding RG and occasionally humming during forced expiration. often acute lung injury with artificial respiration occurs in patients with AEP. Rarely one can come to a distributive (hyperdynamic) shock. Diagnosis High-resolution CT (HRCT) Usually blood count, analysis of the pleural fluid and pulmonary function tests Bronchoscopy for obtaining a lavage and sometimes biopsy The diagnosis is used in patients with symptoms of acute pneumonia leading to respiratory failure and do not respond to antibiotics, suspected. Diagnosis is based on the routine examination findings and bronchoscopy confirmed. AEP is a diagnosis of exclusion and requires the absence of known causes of eosinophilic pneumonia (z. B. drug- and toxin-induced, in connection with worm and fungal infection, granulomatous eosinophilic with polyangiitis [Churg-Strauss syndrome], idiopathic hypereosinophilic syndrome, tumors). The blood count often is not significantly increased eosinophil numbers, unlike chronic eosinophilic pneumonia. BSG and IgE levels are nonspecific increased. In the chest X-ray only subtle reticular pattern propagation or frosted glass opacity can initially be seen, often with Kerley B lines. Isolated alveolar (ca. 25% of cases) or reticular (ca. 25% of cases) drawing proliferation may also be observed. Unlike the chronic eosinophilic pneumonia, which are not characteristic opacities localized in the lung periphery in AEP. small pleural effusions occur in two thirds of patients, often on both sides. The HRCT is always pathological with both sides present frosted glass opacity or reticular drawing reproduction. The study of the pleural fluid shows significant eosinophilia high pH. In lung function tests often finds a restriction of reduced CO diffusing capacity (DLCO). A bronchoscopy should be done occasionally to obtain a BAL for a biopsy. The BAL often provides high absolute and relative (> 25%) eosinophil numbers. The most common histopathological features in the biopsy include eosinophilic infiltration with acute and diffuse alveolar damage-organizing. However, biopsies are taken rarely in patients. Therapy Systemic corticosteroids The condition of some patients improved spontaneously. Most are administered p.o. with prednisone 40-60 mg treated 1 times daily. In patients with respiratory failure methylprednisolone is preferably 60-125 mg every 6 h. The prognosis is excellent; almost always the disease responds to corticosteroids, and a complete recovery is the rule. Pleural effusions develop slowly than parenchymal opacities.