Atelectasis - as incidious as ever.

A telectasis is a commonly encountered pathophysiologic condition. The word atelectasis is derived from two Greek words, i.e., ateles and ektasis, which mean "incomplete" and "extension," respectively. Consequently, atelectasis means incomplete extension. From a respiratory therapy standpoint, atelectasis is described and viewed as collapsed or unventilated alveoli. Collapsed alveoli can occur in a lung segment, lobe, or whole lung. Respiratory therapists frequently attempt to prevent and to reverse atelectasis with hyperinflation (lung expansion) and bronchial hygiene therapy. Nonetheless, ascertaining the presence of atelectasis and determining the efficacy of therapeutic interventions indicated for its treatment sometimes presents an enigma. This article will present the different types of atelectasis, signs and symptoms of this condition, and forms of treatment. The following forms of atelectasis will be addressed: (1) absorption (obstructive), (2) adhesive, (3) compressive, and (4) cicatricial.

Absorption (Obstructive) Atelectasis

Absorption atelectasis is likely to occur whenever an airway obstruction occurs anywhere between the trachea and alveoli. For example, an obstruction in either the medial or lateral segment of the right middle lobe tends to result in the reabsorption of gas in a portion of the right middle lobe. When the obstruction develops in either of those segments, the air trapped distal to the obstruction continues exchanging with the mixed-venous blood flowing through the pulmonary capillaries in that region. Gas exchange there will continue until equilibrium is established with the nonventilated alveoli in the right middle lobe and the pulmonary capillary blood servicing that lobe. Eventually, gas volume in those gas exchange units will decrease, leading to alveolar collapse. Gas tensions in the atelectatic alveoli will eventually equal those of mixed-venous blood, i.e., PO2 40 mm Hg and PCO2 46 mm Hg. Complete obstruction of the bronchus leading to the right middle lobe will cause the entire lobe to experience absorption atelectasis. Generally speaking, obstruction of a larger bronchus tends to produce lobar atelectasis. On the other hand, obstruction of a smaller bronchus will likely produce segmental atelectasis. The pattern of atelectasis typically depends on the extent of collateral ventilation, which is provided by the pores of Kohn and the canals of Lambert.

The nature of the obstruction can also vary. It may be caused by a mucous plug, aspirated foreign body, an intraluminal neoplasm, an extraluminal neoplasm compressing the bronchial wall, inflammatory process (e.g., fungal infection), lymphadenopathy, or a malpositioned endotracheal tube.

Absorption atelectasis often develops from denitrogenation in patients who have low ventilation-perfusion ratios (maldistribution of ventilation), and are administered supplemental oxygen. For example, whenever anyone breathes an elevated FIO2, nitrogen is washed out from the lungs. When a patient with maldistribution of ventilation inspires an FIO2 greater than room air, the amount of nitrogen washed out of the lungs will depend on the FIO2.Whatever the degree of denitrogenation, the process occurs minutes. The denitrogenation causes the poorly ventilated alveoli to collapse. Ordinarily, alveoli rely on nitrogen to act as a filler gas to maintain adequate alveolar distending pressure. Patients with COPD are susceptible to this denitrogenation process.

Adhesive Atelectasis

Pulmonary surfactant is a physiologic molecule that is produced by alveolar type II cells. Pulmonary surfactant is responsible for preventing alveoli from collapsing during exhalation. When pulmonary surfactant is inactivated, alveoli collapse. Acute respiratory distress syndrome (ARDS) is an example of a pulmonary condition associated with inactivation of surfactant. Therefore adhesive atelectasis tends to occur with ARDS, as lung surface tension increases. When an infant is born at or before 28 weeks' gestation, the infant frequently lacks pulmonary surfactant because of pulmonary immaturity, and is unable to establish a functional residual capacity. Consequently, the infant experiences alveolar collapse at the end of every expiration. Each ensuing inspiration requires extremely forceful (-90 to -100 cm H2O) inspiratory efforts. Respiratory distress syndrome is also characterized by adhesive atelectasis. Treatment generally includes surfactant replacement therapy and positive pressure mechanical ventilation.

Compressive Atelectasis

Compressive atelectasis develops with any space-occupying lesion such as pneumothorax, hemothorax, pleural effusion, or abdominal distention. Any space-occupying lesion impinges upon the lungs and literally forces air out of the compressed region. The amount of air forced out depends on the volume of the pleural space being occupied by the fluid or lesion. For example, a small pleural effusion may not compress a significant area of the lung, thereby imposing little interference with pulmonary function and gas exchange. Conversely, a sizeable pleural effusion may compress an entire lobe or lung. Treatment of compression atelectasis involves either the evacuation of the fluid (liquid or air) in the pleural space, or the removal the lesion or mass responsible for compressing the lung.

Cicatricial Atelectasis

Post-infectious scarring following tuberculosis and necrotizing pneumonia are frequent causes of cicatricial pneumonia. This form of atelectasis is also a sequela of severe pulmonary fibrosis and chronic granulomatous disease.

Signs and Symptoms of Atelectasis

Basically, the size of the atelectatic area and the rapidity with which atelectasis develops determine the magnitude of the signs and symptoms of this condition. Generally speaking, patients who develop atelectasis will exhibit shortness of breath and increased respiratory rate. Impaired oxygenation and decreased lung compliance account for the shortness of breath and the increased respiratory rate. Patients with atelectasis will also have tachycardia, which is associated with impaired oxygenation and the increased work of breathing.

During physical examination of the chest, inspection often reveals decreased chest wall expansion, use of accessory muscles of ventilation, and, depending on the size of the atelectatic area, tracheal and mediastinal shift toward the affected region. Auscultation will demonstrate breath sounds that are either diminished or absent over the atelectatic region signifying underventilation or lack of air entry. Late inspiratory crackles may be heard indicating air passing through partially obstructed airways and inflating atelectatic alveoli. Percussion over the atelectatic region provides a dull percussion note. Palpation displays decreased tactile fremitus and also decreased chest wall expansion.

Radiographic features likewise vary according to the amount of lung that becomes atelectatic. However, radiographic presentations differ according the location of the atelectatic region. Nonetheless, common anteroposterior radiographic findings include (1) increased opacification, (2) mediastinal/tracheal shift toward the ipsilateral (affected) side, (3) hilar displacement, (4) elevation of the hemidiaphragm on the ipsilateral side, (5) compensatory hyperinflation of the contralateral lung, (6) crowded pulmonary vasculature, and (7) fissure displacement toward the affected region. A frequent radiographic presentation is obliteration of soft tissue boundaries. For example, when right middle lobe atelectasis occurs, the right heart border becomes obliterated because the right middle lobe and the heart reside in the same plane. Furthermore, the densities of the two anatomic structures become similar, causing the two structures to appear radiographically as one continuous feature. When the right middle lobe is normal, the anteroposterior chest film will demonstrate a distinct right heart border because the density of the air-filled right middle lobe differs from that of the blood-filled heart. This phenomenon is called the silhouette sign.

Lateral chest radiography helps appreciate the movement of oblique fissures. For instance, forward movement of the oblique fissure in left upper lobe atelectasis becomes apparent on a lateral chest radiograph. The oblique fissure, for example, migrates backward when the lower lobe is atelectatic.

Treatment of Atelectasis

The fact that atelectasis produces alveoli that are perfused, but not ventilated constitutes capillary shunting. These alveoli have a ventilation-perfusion value equal to zero, and the hypoxemia produced by capillary shunting is not amenable to oxygen therapy. Hyperinflation therapy, including positive pressure ventilation, plays an important role in the treatment of atelectasisis. The application of positive pressure to the airways is intended to re-inflate the collapsed alveoli, thereby increasing the patient's functional residual capacity, reducing the capillary shunt, and improving oxygenation. Bronchial hygiene therapy is a crucial adjunct to prevent atelectasis related to obstruction caused by increased secretions

Diligence in the application of respiratory therapy protocols such as hyperinflation therapy, bronchial hygiene, and oxygen therapy often reverses atelectasis within minutes to hours.

by Bill Wojciechowski, MS, RRT

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William Wojciechowski, MS, RRT, is chair and associate professor in the department of cardiorespiratory care at the University of South Alabama, Mobile.