Airway Obstruction – e.g., Foreign Body

• Valve Action
• By-pass valve action occurs when the foreign body allows air to pass during both inspiration and expiration.
• Check valve phenomenon occurs when air can enter the lung during inspiration, due to widening of the bronchus, but cannot escape during expiration. The net effect is alveolar hyperinflation
• Ball-valve action: air can leave but not enter, resulting in atelectasis
• Stop-valve phenomenon occurs when the airway is completely blocked, during both inspiration and expiration.
• Atelectasis: collapse, or change in condition from complete to incomplete pulmonary expansion
• Resulting from acute bronchial obstruction
• Edema and capillary congestion occurs and alveoli can be flooded by edema fluid.
• Subsequently, acute post-obstructive infection is followed by chronic, organizing pneumonia, abscess formation, fibrosis of alveoli fibrous obliteration of both bronchi and bronchioles (bronchiolitis obliterans), traction on bronchial walls weakened by chronic infection Þ bronchiectasis.
• Resulting from chronic bronchial obstruction due to tumor or pneumothorax Þ compression of alveolar tissue.
• allows the bronchial tree to remain patent and secretions to drain from the lung.
• hypoxia Þ interstitial edema and increased lymph flow Þ fibrosis of alveolar septa, pleura and peribronchial CT.
• chronically collapsed lungs Þ chronic infection Þ fibrosis, which will prevent complete expansion of lungs.

• Definition: "permanent enlargement of airspaces accompanied by destruction of respiratory tissue"
• disruptive pulmonary emphysema: loss of alveolar septal tissue and corresponding enlargement of airspaces.
• Interstitial fibrosis is not seen histologically unless it is the result of additional lung injury.
• Pathogenesis: a protease-antiprotease imbalance Þ enzymatic destruction of the lung structural protein, elastin.
• Cigarette smoke facilitates this by recruiting neutrophils which decrease elastase, inhibition of a -1antitrypsin, directly damaging lung tissue and inhibiting elastin synthesis
• Destruction of alveoli Þ ß lung elastic recoil and ß # of tethered airways Þ closure of airways at Ý lung volume
• Subgross Anatomy of the Lung
• bronchi are cartilage-containing conducting air tubes
• bronchioles are smaller, non-cartilaginous airways
• terminal bronchiole is the most distal bronchiole completely lined by respiratory epithelium
• respiratory bronchioles arise from terminal bronchioles 3 generations at a time and alveoli in their walls
• alveolar ducts arise from respiratory bronchioles, are almost completely lined by alveoli; duct lining epithelium is usually inconspicuous by light microscopy
• alveoli arise from Alveolar ducts by forming open clusters of air sacs
• pulmonary acinus is the region of lung supplied by a single terminal bronchiole
• secondary lobule = five to ten acini, considered to be the smallest radiographically identifiable unit of lung
• Anatomic Classification of Emphysema: classified anatomically into 4 subtypes, which are distinct entities.
• Centriacinar (centrilobular) emphysema:
• involves the proximal-portion of the acinus surrounding the respiratory bronchioles.
• is usually more severe in the upper lung zones, associated mostly with male smokers.
• severe centriacinar emphysema can look panacinar but has a rim of normal alveoli surrounding affected area.
• Panacinar (panlobular) emphysema results from non-selective destruction of the entire acinus.
• May be found throughout lung but normally prominent in lower lung zones.
• Associated with centriacinar, women and men, alpha-1-antitrypsin deficiency (more common in lower lobe), unilateral pulmonary transradiancy (Swyer-James syndrome) and bronchial atresia
• Paracicatricial (irregular) emphysema: Dilated airspaces are often seen on the edge of pulmonary scars, probably due to traction on surrounding lung tissue by contracting fibrous scar; incidental finding but significant in TB.
• Paraseptal (distal acinar) emphysema: involves the periphery of the acinus adjacent to pleura, interlobular septa, or bronchovascular bundles.
• most frequently associated with spontaneous pneumothorax in young persons and most prominent in apex.
• often complicated by subpleural bullae
• Emphysematous Bullae: may be found in combination with any of the four anatomic subtypes of emphysema.
• Bulla = an enlarged airspace due to emphysema, usually greater than 1 cm. in diameter, located immediately adjacent to the visceral pleura due to air-trapping in distensible, emphysematous lung.
• 'bullous emphysema' especially prominent bullae, but is not an anatomic variant.
• "bleb" is a small bulla, interstitial air cysts which result from dissection of air into interstitial connective tissue.
• As the bulla expands, the supplying bronchioles may be converted to check valves, which impede the escape of air. If giant bullae compress adjacent normal lung, surgical excision may be indicated. Rupture Þ pneumothorax.
• Pulmonary Vascular Changes in Emphysema
• Micro: small pulmonary arteries and arterioles show Ý medial smooth muscle, abnormal muscle which extends into normally non-muscular arteries, and longitudinal muscle bundles in the intimaÞ ß lumen and tone
• The strongest stimulus for this arterial muscularization in emphysema appears to be chronic hypoxia
• Right ventricular hypertrophy correlates most with persistent hypoxemia and emphysema severity not anatomic class.
• Extensive pulmonary capillary bed destruction is likely not the primary cause of pulmonary HTN due to reserve capacity.

• Chronic bronchitis is a clinically defined syndrome of chronic excessive mucus production in the airways not due to known specific causes such as bronchiectasis or tuberculosis.
• Pathology: hallmark is bronchial mucous gland enlargement
• Micro: chronic inflammation of the airway wall, a thickened bronchial basement membrane, and squamous metaplasia and goblet cell hyperplasia of the surface epithelium.
• Reid index = ratio of the bronchial mucus gland layer to bronchial wall thickness (from perichondrium to BM)
• an indicator of mucus gland hypertrophy. An index > 0.4 is consistent with mucus gland hypertrophy.
• Chronic bronchitis is usually accompanied by emphysema but alone, can produce respiratory failure and death
• Inflammatory changes in small airways Þ airflow obstruction
• Mucus overproduction and mucus gland hypertrophy
• Causes: cigarette smoking, air pollution (NO₂ and SO₂), and infection.
• may not only obstruct airways but provide a culture medium for bacterial growth Þ Infection Þ mucus production
• Airflow obstruction may be produced by mucus plugging of airways or impingement on the bronchial lumen by hyperplastic glands or an edematous bronchial wall, but is not usually present in fatalities of bronchitis
• "asthmatic bronchitis" hyper-reactive airways and smooth muscle hyperplasia accompany mucus over-production

Small airway (<2mm) disease – contributes to airflow obstruction in COPD of any type

• In emphysema, inflammation of non-respiratory bronchioles Þ ß in the mean caliber of bronchioles
• Micro: chronic inflammation, fibrosis, tortuosity, goblet and squamous cell metaplasia and mucus plugging.
• The most detrimental lesions are bronchiolar inflammation, squamous metaplasia, and peribronchial fibrosis.
• respiratory bronchiolitis: pigmented macrophages stuck in lumen of respiratory bronchioles (emphysema in situ)
• enzymes released from macrophages could injure septal tissue and produce centriacinar emphysema.

• Pathology of status asthmaticus: mucus plugging of bronchi and alveolar hyper-inflation, but not emphysema.
• Micro: mucous plugging in both bronchi and bronchioles.
• in intraluminal exudate: eosinophils, Charcot-Leyden crystals and fragments of epithelium=creola bodies
• edematous bronchial wall with a polymorphous inflam. infiltrate largely of eosinophils, plasma and mast cells
• partially denuded bronchial epithelium with regenerative changes and Ý in goblet cells; Elevated Reid index
• Ý Basement membrane and bronchial smooth muscle layer.
• Usually in asthma, the pulmonary arteries do not show hypertensive vascular changes

• Definition: permanent, abnormal dilatation of bronchi caused by destruction of their walls
• most is acquired after birth, although rare instances of congenital bronchiectasis exist
• Pathogenesis
• Atelectasis and bronchial obstruction Þ inflammation and destruction of bronchial wall Þ dilatation
• Can also result from primary direct bronchial wall injury following a pulmonary infection, often in the remote past (e.g.TB, purtussis, viral pneumonia: Respiratory syncytial virus, adenovirus, measles and influenzal pneumonia)
• Cystic fibrosis (CF) Þ Chronic pulmonary disease Þ chronic or recurrent infections and mucus hypersecretion.
• mucus hypersecretion is due to exocrinopathy in CF and early life pulmonary infection (Pseudomonas aeruginosa).
• immotile cilia syndrome characterized by abnormal anatomy and function of respiratory cilia
• includes Kartagener's syndrome characterized by bronchiectasis and chronic sinusitis and sometimes situs inversus. Dynein deficiency Þ ciliary dysfunction Þ mucus stasis and infection.
• Deficiencies of IgA or a 1-antitrypsin or congenital anomalies Þ chronic or recurrent lung infections
• Pathology
• Gross: dilated bronchi which extend almost to the pleural surface. 3 morphological types on bronchography:
• saccular bronchiectasis airways dilate progressively in a fusiform manner
• Cylindrical bronchiectasis, airway caliber is dilated, but remains nearly uniform from hilum to periphery.
• Varicose bronchiectasis: alternately dilated and narrowed segments of bronchi, looks like links of sausage
• this anatomic classification bears little relevance to clinical presentation or pathogenesis.
• Micro: bronchial mucosa is focally ulcerated or replaced by metaplastic squamous epithelium
• is extensive chronic inflammation of bronchial wall with fibrosis, atrophy and destruction of cartilage and muscle
• Peribronchial lymphoid hyperplasia often prominent when caused by viral infection = follicular bronchiectasis
• Fibrous obliteration of both bronchi and bronchioles leads to obstructive pneumonia in the surrounding lung.
• Inflammatory changes of Pulmonary vasculature in bronchiectasis
• Destruction of the alveolar capillary bed initially Þ locally decreased pulmonary blood flow.
• Stimulate increased flow through the bronchial arteries which become enlarged and tortuous.
• Precapillary shunts between bronchial and pulmonary circuits likely occur in granulation tissue formed in air way.
• Þ overworking of left ventricle Þ LVH Þ Ý pulmonary HTN changes in arteries Þ cor pulmonale
• Hemoptysis (common symptom) is thought to be due to rupture of small vessels in the inflamed bronchial tissue.