Acute interstitial pneumonitis

Acute interstitial pneumonitis: Description, Causes and Risk Factors: Abbreviation: AIP. Acute interstitial pneumonitisAcute interstitial pneumonitis is characterized by the abnormal accumulation of cells and/or noncellular material within the walls of the alveoli (air sacs) of the lungs. This process results in thickening and stiffness of the normally elastic tissues of the lung, and thus interferes with normal breathing, so that patients with Acute interstitial pneumonitis often breathe in a rapid and shallow manner. While the mechanism of Acute interstitial pneumonitis remains elusive, recent studies have suggested possible pathogenetic mechanisms. Specifically, both natural killer cells and chemokines (any of various cytokines, produced during inflammation, that organize the leukocytes) such as interleukin-18 and interleukin-2 may play important roles in the evolution of acute cell injury into unremitting fibrosis specifically through abnormal wound repair. Risk Factors: Infections of the lungs.
  • Chronic autoimmune diseases: connective tissue diseases such as lupus, scleroderma, and rheumatoid arthritis.
  • Toxins in the environment (such as asbestos, silica dust).
  • Certain medications (particularly some drugs used as chemotherapy for cancers).
  • Radiation therapy to the chest.
Prevalence of AIP is estimated at 1 in 25,000. AIP occurs over a wide age range, with a mean age of approximately 50 years. There is no sex predominance or association with smoking. acute interstitial pneumonitis Cases of Acute interstitial pneumonitis have been researched by various researchers and research organizations to define the clinical and pathologic features and to determine the relationship to chronic interstitial pneumonia. Clinically, this disease differs from the chronic interstitial pneumonias by a sudden onset and a rapid course. An etiologic agent could not be identified in any case. The histologic hallmark was interstitial fibrosis and edema associated with type II pneumocyte hyperplasia. The fibrosis differed from that seen in the chronic interstitial pneumonias by extensive fibroblast proliferation and relatively little collagen deposition. Autoradiographic studies of tritiated thymidine (3H-TdR) uptake showed high labeling indices in interstitial cells and type II pneumocytes. Evidence of acute lung injury, including both endothelial and epithelial cell damage, was a prominent ultrastructural feature. These findings emphasize that Acute interstitial pneumonitis is a clinically and pathologically distinct form of interstitial pneumonia that should be separated from the group of chronic interstitial pneumonias. Symptoms: Symptoms may include: Shortness of breath.
  • Shallow and rapid breathing.
  • Wheezing and crackling sounds in lungs.
  • Cough.
  • Fever.
  • Cor pulmonale.
  • Cyanosis (A bluish discoloration of the skin and mucous membranes; a sign that oxygen in the blood is dangerously diminished.
  • Malaise.
  • Right-sided heart failure.
  • Clubbing.
  • Weight loss.
  • Increased gamma globulin levels in blood stream.
  • Brain and heart function issues as reduce in oxygen supply for long duration.
Diagnosis: The diagnosis of AIP is made in the appropriate clinical setting in a patient who has a clinical presentation compatible with acute respiratory distress syndrome (ARDS). The chest radiograph and high-resolution computed tomography (HRCT) scan manifestations of AIP are bilateral and sometimes patchy, and there are alveolar densities associated with areas of ground glass attenuation. Consolidation is seen in the majority of cases, but is not as common as ground glass attenuation. Lung biopsies from patients with AIP show histologic features of the acute and/or organizing phases of diffuse alveolar damage (DAD). The exudative phase shows edema, hyaline membranes, and microvascular thrombi. The organizing phase shows loose organizing fibrosis, mostly within alveolar septa, and type II pneumocyte hyperplasia, but without a clear etiology. Confirmatory diagnosis requires demonstration of diffuse alveolar damage on lung histopathology. Treatment: Generally, the primary focus of therapy is supportive care including supplemental oxygen and ventilatory support. Several reports have reported benefit from the use of glucocorticoids, in the treatment of AIP, but others contradict this finding. Alternative immunosuppressive therapies (e.g., vincristine, cyclophosphamide, cyclosporine, and azathioprine) and lung transplantation have been reported in case series of AIP, with limited success. Even with intensive treatment, including mechanical ventilation, the mortality from AIP remains high. Notably, survivors of AIP did not experience recurrence and enjoyed complete or near complete recovery of lung function. NOTE: The above information is educational purpose. The information provided herein should not be used during any medical emergency or for the diagnosis or treatment of any medical condition. DISCLAIMER: This information should not substitute for seeking responsible, professional medical care.


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