Interstitial Pneumonia: What Is It, Symptoms, Treatment

2024 Author: Rachel Wainwright | [email protected]. Last modified: 2024-01-15 19:51

Interstitial pneumonia: causes, symptoms, treatment

The content of the article:

Classification
Causes of pneumonia
Clinical picture

Possible changes in the lung structure
Diagnostics
Treatment
Complications
Forecast
Video

Interstitial pneumonia (interstitial pneumonia, idiopathic interstitial pneumonia) is an acute or chronic inflammatory lesion affecting the walls of the alveoli and connective tissue of the lung parenchyma, with possible intraalveolar exudation followed by a transition to fibrosis.

The interstitial form of pneumonia is characterized by a long course and changes in the pulmonary structure.

This form of pneumonia is characterized by a long severe course, often progressive fibrous and sclerotic lung transformation. The disease often leads to a decrease in the quality of life and disability of patients. Usually occurs in adults over 40. In younger people or in children, idiopathic pneumonia is rare.

Classification

The main classification of pneumonia includes the following forms:

focal;
focal drain;
segmental;
share;
interstitial.

Interstitial pneumonia has its own classification, standing out as a separate group of interstitial lung diseases (IBD):

idiopathic pulmonary fibrosis, or common interstitial pneumonia;
nonspecific interstitial pneumonia;
cryptogenic organizing pneumonia;
acute interstitial pneumonia, or diffuse alveolar injury;
respiratory bronchiolitis associated with interstitial lung disease (respiratory bronchiolitis);
desquamation (desquamative, macrophage) interstitial pneumonia;
lymphocytic (lymphoid) interstitial pneumonia.

Idiopathic pulmonary fibrosis is more common in older men, other types are more common in female patients aged 25–55, and the nonspecific and desquamative form sometimes occurs in children.

With all these forms of the disease, respiratory failure develops to one degree or another, in which gas exchange suffers.

Causes of pneumonia

The reasons for the development of the disease are unknown. An assumption is made about the involvement of a violation of immunological homeostasis, where the triggering factor is an agent that, having penetrated the body, leads to the production of antibodies.

Legionella can be the causative agent of pneumonia

The development of an interstitial form of pneumonia can be provoked by infections: mycoplasma, chlamydia, legionella, rickettsia, pneumococcus, respiratory viruses, cytomegalovirus, herpes simplex virus, and some types of dust.

The risk group includes smokers or previously smokers, HIV-positive people and patients with autoimmune diseases. There is a link between collagenoses and cryptogenic organizing pneumonia.

So, interstitial damage can occur against the background of the following diseases:

rheumatoid arthritis;
scleroderma;
polymyositis, or dermatomyositis;
mixed connective tissue diseases;
asbestosis;
chronic hypersensitivity pneumonitis;
radiation pneumonitis;
drug-induced lung damage.

Clinical picture

The disease can have a flu-like onset: fever, unproductive cough, and shortness of breath appear. At first, shortness of breath is noted only during physical exertion, then at rest. There are pains in the chest, there may be episodes of sudden shortness of breath at night. Rapid fatigue, general weakness, poor sleep, loss of appetite and weight loss appear.

At the onset of the disease, shortness of breath and cough appear.

Symptoms in most patients worsen significantly within 7-14 days and progress to the development of respiratory failure.

With different forms, there may be signs of the disease that are different in severity.

The interstitial lymphocytic form has an imperceptible onset with a slow increase in cough, shortness of breath, general weakness, muscle and joint pain. Fever and bloody sputum are often absent. With the onset of respiratory disorders, cachexia, primary pulmonary hypertension, can develop. Cor pulmonale with lymphoid form can form in a period from 2 months to 2 years.

Hammen-Rich syndrome, or acute interstitial pneumonia, develops with the clinic of influenza and acute respiratory distress syndrome. There is a lightning-fast course of the disease with rapidly progressive respiratory failure and a high percentage of deaths.

Possible changes in the lung structure

The interstitial form of pneumonia is characterized by various pathological changes in the pulmonary structure.

Interstitial pneumonia can lead to pathological changes in lung tissue

Changes in the lung structure depending on the form of pneumonia:

Pathology form	Features:
Normal (idiopathic) form	There is a violation of the architecture of the lungs, fibrosis with "cellular" changes. Fibroblast foci, temporal heterogeneity of fibrous changes are determined histologically
Non-specific form	Variable interstitial inflammation and fibrosis are characteristic. Changes become homogeneous, with rare fibroblastic foci in the histological material
Organizing form	Pulmonary architectonics is preserved, in the lower parts of the airways there is a patchy spread of polypoid granulation tissue
Diffuse alveolar lung injury	Diffuse thickening of alveolar septa, organization of alveoli, hyaline membranes is determined
Respiratory bronchiolitis	Morphological changes include bronchocentric accumulation of alveolar macrophages, minimal inflammation and fibrosis
Desquamation form	A uniform lesion of the lung parenchyma is characteristic, a large number of macrophages is determined in the lumen of the alveoli, the lesion of the interstitium is minimal
Lymphoid form	Characterized by pronounced lymphocytic infiltration of the interstitium associated with peribronchial lymphoid follicles

Diagnostics

The main diagnostic methods include:

clinical blood test;
X-ray examination of the chest organs;
high resolution computed tomography;
microscopic, cytological and bacteriological examination of sputum;
histological examination of lung biopsy.

The disease is diagnosed by a doctor if there are complaints, symptoms and a corresponding x-ray picture.

During an objective examination of the patient with auscultation of the lungs, soft crepitus is heard: first in the basal segments of the lungs, then along all the pulmonary fields and in the apex of the lungs.

High-resolution computed tomography of the lungs is performed to confirm the diagnosis

There is hard breathing, wet or dry fine bubbling rales in the lungs. Above the affected area with percussion, the shortening of the sound is determined.

The study of the function of external respiration by conducting spirometry and various functional breathing tests reveals impaired ventilation and disorders of the diffusion capacity of the lungs, for example, in the lymphoid form, changes of the restrictive type are noted with a sharp and extremely sharp decrease in lung volumes.

A clinical blood test and microbiological studies are carried out for the purpose of differential diagnosis with bacterial pneumonia or tuberculosis, since in most cases there are no specific changes in interstitial pneumonia.

Clinical blood test is of great diagnostic value

Chest X-ray shows diffuse bilateral opacification of pulmonary fields or progressive diffuse ground-glass changes and consolidation. The images show a diffuse lesion, a thickening of the bronchial wall, focal or diffuse changes like ground glass or a linear increase in the pulmonary pattern are determined. Later, bronchiectasis appears (irreversible expansion of the bronchus).

With severe fibrosis, a decrease in the volume of mainly the lower lobes of the lungs is determined.

But in most cases, a biopsy is required, since the examination data are not always specific or the diagnostic capabilities are often limited. It is the histological analysis that is decisive in making the final diagnosis.

Timely diagnosis has a positive effect on prognosis.

Treatment

The effectiveness of treatment depends on several indicators: the degree of prevalence of lung damage, the presence of concomitant diseases and complications, the general condition of the human body.

Smoking cessation plays an important role in treatment

A mandatory item in treatment is smoking cessation, especially with desquamative form and respiratory bronchiolitis.

In the lymphoid form, azathioprine or cyclophosphamides are prescribed in combination with a glucocorticoid drug. The initial daily dose of prednisone is 1 mg / kg of body weight. Treatment is carried out on average for 6 months.

Colchicine, D-penicillamine, interferon gamma-1b are used as additional antifibrotic agents. An increase in the effectiveness of therapy is noted when N-acetylcysteine is added to anti-inflammatory drugs.

With the development of hypoxia, oxygen therapy is necessary, with the development of pulmonary hypertension, the use of vasodilators. The development of infections or purulent complications requires the appointment of antibacterial and antifungal drugs, depending on the sensitivity of the pathogenic pathogen.

Patients with interstitial lung lesions are closely monitored at all times.

Against the background of cytostatic therapy, regular urine tests are required

When taking cytostatics during the first month, it is necessary to take a general urine test weekly. Then the analysis is repeated once every 2–4 weeks. When using Cyclophosphamide, urinalysis is necessary to diagnose hematuria.

Patients with lymphoid pneumonia are regularly vaccinated against influenza and pneumococcal infection.

Complications

With timely diagnosis and early treatment started, the disease can progress slowly, without the development of complications.

One of the possible complications is a lung abscess

But with a severe course, the presence of concomitant pathology or inadequate therapy, pulmonary and extrapulmonary complications of the disease are possible:

pleurisy;
pulmonary destruction;
lung abscess;
pneumothorax;
pyopneumothorax;
infectious toxic shock;
cardiovascular insufficiency;
respiratory distress syndrome;
pneumosclerosis;
DIC syndrome.

Forecast

The outcome of pneumonia depends on the prevalence of the pathological process, the presence of complications, the timing of the initiation of therapy and the state of the body. Clinical improvement and stabilization of patients' condition during treatment is observed in 70% of cases, and in 30% - patients have a ten-year survival rate.

With a critical decrease in gas exchange processes and the development of severe respiratory failure, the prognosis is poor. Supportive therapy is underway. With the development of pneumosclerosis and cardiovascular insufficiency, life expectancy is 3-5 years.