Acute Interstitial Pneumonia

　　Although acute interstitial pneumonia has been categorized as idiopathic pulmonary interstitial pneumonia (IIP) at present, due to its clinical and pathological manifestations being almost identical to ARDS, and its etiology being unclear at the time of onset, some believe that its onset is closely related to acute viral infection, but it is limited by the current detection technology that cannot detect the virus. The relationship between viruses and IIP has always been one of the hotspots in the study of the etiology of the disease, with adenovirus and EB virus being the most studied.

　　Acute interstitial pneumonia often complicates with spontaneous pneumothorax and right heart failure, and attention should be paid to treatment.

　　1. Spontaneous pneumothorax

　　Sudden chest pain, dyspnea, and disappearance of breath sounds may indicate spontaneous pneumothorax, possibly accompanied by symptoms such as expectoration or hemoptysis.

　　2. Right heart failure

　　Right heart failure may present with distended jugular veins, positive hepatojugular reflux sign.

　　The onset of this disease is acute (within a few days to a few weeks), presenting with fever, cough, and dyspnea, followed by acute interstitial pneumonia respiratory failure, resembling idiopathic acute respiratory distress syndrome of unknown cause. The average age of onset is 49 years, with no significant gender difference. The mortality rate is extremely high (>60%), with most deaths occurring within 1-2 months. More than half of the patients have a sudden onset of fever and dry cough, and sputum with pus may be produced when secondary infection occurs. The patients then experience chest tightness, fatigue, and progressive worsening of dyspnea, which may be accompanied by cyanosis, wheezing, chest tightness or a band-like sensation, and acrocytes (toes) appear quickly.

　　Acute interstitial pneumonia with unknown etiology cannot be prevented. However, smokers have an increased risk of developing idiopathic pulmonary fibrosis, and this risk increases with the number of smokers.

　　Prevention of acute interstitial pneumonia with known etiology should focus on monitoring various personnel working in environments with large amounts of dust, long-term exposure to刺激性 gases such as chlorine, ammonia, carbon dioxide, formaldehyde, and various acid mists, radioactive damage, and bird owners, among others. Regular pulmonary function tests, blood gas analysis, and routine X-ray examinations should be conducted to detect the disease early and treat it promptly. In addition, inhalation of various microorganisms, particles, allergens of heterologous proteins, and harmful irritating gases can also cause lung damage.

　　Acute interstitial pneumonia (AIP) is a rare, rapidly progressive, fulminant lung injury. Generally, the diagnosis of this disease requires the following examinations:

　　1. Laboratory examination

　　Laboratory examination does not have specificity. The peripheral blood white blood cell count may be elevated, with a mild increase in eosinophils in a few cases. Red blood cells and hemoglobin increase secondary to hypoxia. Erythrocyte sedimentation rate (ESR) is often accelerated, reaching up to 60mm/h. Serum protein electrophoresis shows increased α2 or γ globulins, IgG and IgM are often elevated, while IgA is less frequently elevated. Blood gas analysis shows type I respiratory failure, occasionally type II.

　　2. Light Microscopy

　　In the early (exudative) stage of the lesion (within about 1 week after lung injury), the alveolar septum becomes diffusely thickened due to vascular dilation, matrix edema, and infiltration of inflammatory cells, with lymphocytic infiltration being predominant, as well as plasma cells, monocytes (or macrophages), neutrophils, and a few fibroblasts. The alveolar epithelium proliferates and metaplasia forms columns, widening the alveolar septum. The inner side of the alveolar cavity is normal or contains some proteinaceous material and cell exudate.

　　3. Electron Microscopy

　　Type I alveolar epithelial cell loss, local to extensive detachment of the basal membrane of alveolar epithelial cells, and edema and necrosis of type II alveolar epithelial cells and capillary endothelial cells. The mixture of cell fragments, fibrin, red blood cells, and surfactant-like substances is distributed along the surface of the alveoli, especially in the areas of hyaline membrane formation under the microscope. Scattered inflammatory cells, especially macrophages, lymphocytes, and plasma cells, are present in the alveolar space. A large number of fibroblasts, a small number of inflammatory cells, and scattered primitive parenchymal cells are distributed around the edematous matrix and varying amounts of collagen and elastic fibers in the interstitium.

　　4. Other Auxiliary Examinations

　　X-ray chest films show diffuse, bilateral lung shadows, and CT scans show bilateral symmetrical patchy opacities. These changes are similar to those of acute respiratory distress syndrome (ARDS).

　　Patients with this disease should eat more fruits and drink more water; avoid salty, spicy, greasy, and hot foods. It is not advisable to eat sweet and warm fruits such as apricots, peaches, oranges, plums, etc., to prevent heat and phlegm; do not add flavorings such as pepper, chili, Sichuan pepper, and mustard to the diet; and avoid smoking and drinking.

　　The disease responds well to adrenal cortical hormones and should be used early, in large doses, and for a long period. Prednisone is administered continuously for 3 months, and the dosage is gradually reduced after the condition stabilizes. The duration of maintenance should be determined according to the development of the disease, but the course of treatment should not be less than 1 year. If the disease recurs and worsens during the dose reduction process, the dosage should be increased again to control the condition. If the condition is severe, shock therapy can be used: intravenous injection of methylprednisolone, and then switching to oral administration after the condition stabilizes. In addition, there are reports of satisfactory efficacy through the combined use of immunosuppressants such as methylprednisolone, cyclophosphamide, and vincristine.