Adult respiratory distress syndrome (ARDS) is a syndrome characterized clinically by the rapid onset of severe, life-threatening respiratory insufficiency. ARDS has also been called adult respiratory failure, shock lung, traumatic wet lung, pump lung, and diffuse alveolar damage (DAD). The initial and basic lesion in ARDS is diffuse damage to the alveolar wall. Protein-rich edema fluid then leaks into the alveolar spaces and combines with fibrin and dead cells to produce hyaline membranes that line the alveoli and are the characteristic histologic feature of ARDS. In the acute edematous stage, the lungs are congested (pulmonary congestion) and show pulmonary edema with interstitial inflammation. Collapsed, airless pulmonary parenchyma is called atelectasis and can also be seen in ARDS. These other changes, although present in ARDS, are not pathognomonic. In contrast, angioinvasive infiltrates of pleomorphic lymphoid cells are seen with lymphomatoid granulomatosis, a disease of middle-aged individuals that is characterized by an angiocentric and angioinvasive infiltrate of atypical lymphoid cells. Deposits of needle-like crystals from the membranes of eosinophils, called Charcot-Leyden crystals, can be seen in patients with asthma, while infiltrating groups of malignant cells having intercellular bridges characterize squamous cell carcinoma. Plexiform lesions within pulmonary aerioles are diagnostic of pulmonary hypeension Reference: Robbins & Cotran Pathologic Basis of Disease, 9edition.