Congenital anomalies1- Agenesis or hypoplasia2- Tracheal & bronchial anomalies (atresia, stenosis, tracheoesophageal fistula)3- vascular anomalies.4- foregut cysts (abnormal detachment of primitive foregut) ,depending on wallstructure ,it classified into bronchogenic (most common), esophageal or entericcystBronchogenic cyst, 1-4cm in diameter, rarely connected to the tracheobronchialtree microscopically lined by respiratory epithelium with sq.metaplasia.5- pulmonary sequestration.presence of a discrete mass of lung tissue without any normal connection tothe airway system & with separate blood supply (not from pulmonary arteries butfrom aorta or its branches).- extralobar---- external to the lung anywhere in the thorax or mediastiunum.- intralobar---- within lung substance & usually associated with recurrentlocalized infection4
Atelectasis (collapse)Incomplete expansion of thelungs(neonatal) or to the collapse ofpreviously inflated lung (acquired oradult), producing relatively airlesspulmonary parenchymaTypes:1- Obstructive (resorption)2- Compression3- Contraction4- Patchy5
Acute respiratory distress syndrome (ARDS)Diffuse alveolar damage, shock lungIs a clinical syndrome caused by diffuse alveolar capillarydamageClinicallyrapid onset of severe life-threatening respiratoryinsufficiency& severe arterial hypoxemia that is refractory tooxygen therapy & may progress to extrapulmonarymultisystem organ failure9
Etiology:-1)pulmonary ARDS" (caused by direct lunginjury)2)"extra-pulmonary ARDS" (a remote effect ofinjury elsewhere).By:-* Infection (viral), sepsis* gas inhalation or liquid(gastric)aspiration.* drugs, chemicals, radiation.* trauma (head injury), sepsis.10
12Basic lesion is injury to alveolar type I pneumocytes& capillary endothelial cellsBy:-* O2 free radicals.* activated macrophages & neutrophils.loss of surfactant.
Pathology1st /acute (exudative) stageWhen the alveolar+/or endothelialcells are injured fluid leaks into theinterstitial spaces and alveolar airspaces -- this is Non-CardiogenicPULMONARY EDEMA.Later, with cell necrosis, FIBRIN isreleased into the alveoli, producingHYALINE MEMBRANES. Of coursethere is LOSS OF SURFACTANT, somany alveoli COLLAPSE.During this early stage, the patient isvery tachypneic and dyspneic13
2nd /Proliferative or organizing stageAs type I pneumocytes are destroyed,TYPE II PNEUMOCYTES DIVIDE toreplace them (regenerative epithelial hyperplasia" ).FIBROSIS ensues as the intra-alveolar hyaline membranesand the interstitial exudate organize14