Bronchomalacia is a term for weak cartilage in the walls of the bronchial tubes, often occurring in children under a day. Bronchomalacia means floppiness of some part of the bronchi. Patients present with noisy breathing and/or wheezing. There is collapse of a main stem bronchus on exhalation. If the trachea is also involved the term tracheobronchomalacia (TBM) is used. If only the upper airway the trachea is involved it is called tracheomalacia (TM). There are two types of bronchomalacia. Primary bronchomalacia is due to a deficiency in the cartilaginous rings. Secondary bronchomalacia may occur by extrinsic compression from an enlarged vessel, a vascular ring or a bronchogenic cyst. Though uncommon, idiopathic (of unknown cause) tracheobronchomalacia has been described in older adults. Cause
Bronchomalacia can best be described as a birth defect of the bronchus in the respiratory tract. Congenital malacia of the large airways is one of the few causes of irreversible airways obstruction in children, with symptoms varying from recurrent wheeze and recurrent lower airways infections to severe dyspnea and respiratory insufficiency. It may also be acquired later in life due to chronic or recurring inflammation resulting from infection or other airway disease. Diagnosis
Classification
Primary Bronchomalacia
Secondary Bronchomalacia

Primary bronchomalacia
Primary Bronchomalacia is classified as congenital. Primary Bronchomalacia is caused by a deficiency in the cartilaginous rings. Primary airway malacia was defined as airway malacia in otherwise normal infants. Secondary bronchomalacia
Secondary Bronchomalacia is acquired. Secondary Bronchomalacia may occur by extrinsic compression from an enlarged vessel, a vascular ring or a bronchogenic cyst.
Evans syndrome is an autoimmune disease in which an individuals immune system attacks their own red blood cells and platelets, the syndrome can include immune neutropenia. These immune cytopenias may occur simultaneously or sequentially.Its overall phenotype resembles a combination of autoimmune hemolytic anemia and immune thrombocytopenic purpura. Autoimmune hemolytic anemia is a condition in which the red blood cells that normally carry oxygen are destroyed by an autoimmune process. Immune thrombocytopenic purpura is a condition in which platelets are destroyed by an autoimmune process. Platelets are a component of blood that contribute to the formation of blood clots in the body to prevent bleeding. The syndrome was first described in 1951 by R. S. Evans and colleagues. Signs and symptoms
The symptoms of Evans syndrome vary between patients depending on which blood cells are affected. If red blood cells are attacked, symptoms may include weakness and fatigue, paleness or jaundice, shortness of breath, lightheadedness, and/or a fast heartbeat. If platelets are attacked, symptoms may include increased bruising, prolonged nosebleeds, increased bleeding from minor cuts, and/or Petechiae. In the less common instance that white blood cells are attacked, symptoms may include increased proneness to infection, fevers, and/or mouth sores.It has been variously reported that between 7.8% and 23% of patients who have autoimmune hemolytic anemia, will also have thrombocytopenia and thus Evans syndrome. The two cytopenias may occur together or sequentially. Causes
Although Evans syndrome seems to be a disorder of immune regulation, the exact pathophysiology is unknown, but a gradual loss of self-tolerance is postulated.