Lung diseases can broadly be divided into those affecting (1) the airways, (2) the interstitium, and (3) the pulmonary vascular system. This division into discrete compartments is, of course, deceptively simple. In reality, disease in one compartment often causes secondary alterations of morphology and function in others.
Atelectasis, also known as collapse, is loss of lung volume caused by inadequate expansion of air spaces. It results in shunting of inadequately oxygenated blood from pulmonary arteries into veins, thus giving rise to a ventilation-perfusion imbalance and hypoxia. On the basis of the http://ebooksmedicine.net
Fig.13.1 Microscopicstructureofthealveolarwall.Notethatthebasementmembrane(yellow) isthinononesideandwidenedwhereitiscontinuouswiththeinterstitialspace.
underlying mechanism and the distribution of alveolar collapse, atelectasis is classified into three forms
Resorption atelectasis occurs when an obstruction prevents air from reaching distal airways. Any air present gradually becomes absorbed, and alveolar collapse follows. The most common cause of resorption collapse is obstruction of a bronchus. Resorption atelectasis most frequently occurs postoperatively due to intrabronchial mucous or mucopurulent plugs, but also may result from foreign body aspiration (particularly in children), bronchial asthma, bronchiectasis, chronic bronchitis, or intrabronchial tumor, in which it may be the first sign of malignancy.
Compression atelectasis is usually associated with accumulation of fluid, blood, or air within the pleural cavity. A frequent cause is pleural effusions occurring in the setting of congestive heart failure. Leakage of air into the pleural cavity (pneumothorax) also leads to compression atelectasis. Basal atelectasis resulting from a failure to breath deeply commonly occurs in bedridden patients, in patients with ascites, and during and after surgery.
Contraction atelectasis (or cicatrization atelectasis) occurs when local or diffuse fibrosis affecting the lung or the pleura hamper lung expansion.
Atelectasis (except when caused by contraction) is potentially reversible and should be treated promptly to prevent hypoxemia and superimposed infection of the collapsed lung.
The epidemiology and definition of acute respiratory distress syndrome (ARDS) are evolving. Formerly considered to be the severe end of a spectrum of acute lung injury, it is now defined as respiratory failure occurring within 1 week of a known clinical insult with bilateral opacities on chest imaging, not fully explained by effusions, atelectasis, cardiac failure, or fluid overload. It is graded based on the severity of the changes in arterial blood oxygenation. Causes are diverse; the shared feature is that all lead to extensive bilateral injury to alveoli.
Severe ARDS is characterized by rapid onset of life-threatening respiratory insufficiency, cyanosis, and severe arterial hypoxemia that is refractory to oxygen therapy. The histologic manifestation of ARDS in the lungs is known as diffuse alveolar damage (DAD). ARDS may occur in a multitude of clinical settings and is associated with primary pulmonary diseases and severe systemic inflammatory disorders such as sepsis. The most frequent triggers of ARDS are pneumonia (35%–45%) and sepsis (30%–35%), followed by aspiration, trauma (including brain injury, abdominal surgery, and multiple fractures), pancreatitis, and transfusion reactions. ARDS should not be confused with respiratory distress syndrome of the newborn; the latter is caused by a deficiency of surfactant caused by prematurity.
In ARDS, the integrity of the alveolar-capillary membrane is compromised by endothelial and epithelial injury. Most work suggests that ARDS stems from an inflammatory reaction initiated by a variety of pro-inflammatory mediators (