Emphysema Congenital Unilateral

Emphysematous lung disease in historical retrospective

Pulmonary emphysema is a pathological condition in which the cells of the walls of the alveoli fill with fluid. This change in the lung is caused by either functional or morphological defects of the bronchial tree (impaired patency). There can be many reasons: a congenital malformation or exposure to harmful factors on a newborn or adult.

General information

**Emphysema is a condition where there is not enough room in the lungs to fill with air** because the alveoli - the structures where the blood is oxygenated and carbon dioxide is produced - expand and begin to merge with each other. This process can cause chest pain, cough reflex, shortness of breath and other unpleasant symptoms. However, all this can be avoided if you perform proper breathing exercises and adhere to a healthy lifestyle.

*There are 2 types of emphysema:* congenital and acquired. Congenital emphysema occurs during embryonic development of the lungs and persists into adulthood. It manifests itself in the form of an increase in the airiness of the lung tissue, which creates additional stress on the heart and creates risks for the patient. The causes of this form of the disease include gene mutations, endocrine pathology, hereditary predisposition, etc. Acquired emphysema usually appears in adults as a consequence of other diseases. The most common pathologies that can cause emphysema are chronic obstructive bronchitis, bronchial asthma, pneumonia, interstitial lung diseases, and heart failure. Treatment of pulmonary emphysema begins with conservative methods: treatment of the underlying disease, prevention and general therapy, including



Pulmonary emphysema is a chronic inflammatory process in the lung tissue, characterized by an increase in air space in its lobules and destruction of the walls of the alveoli. Emphysema is based on a violation of the elasticity of the pulmonary walls, leading to disruption of the barrier functions of the mucous membrane.