Incomplete Expansion Of The Lung

Abstract

Atelectasis describes an incomplete expansion of lung tissue, which may be congenital or acquired. Congenital atelectasis is due to incomplete expansion of the lungs, including primary and secondary congenital atelectasis, whereas the most common causes of subsequently atelectasis are loss of air in lung tissue previously expanded or collapse of a lung or lung tissue. Several pulmonary and extrapulmonary conditions may cause atelectasis. Occlusion of the bronchial lumen is the most common crusade and may be due to airways inflammation and mucous plug, to increased viscosity of the bronchial mucus and to foreign bodies, amid other causes. In occlusion of the bronchial lumen, the air of the occluded lung tissue has gradually been captivated by the perfusing claret. Atelectasis may also occur during anesthesia. The middle right lobe is often the location of atelectasis caused by pulmonary infections equally bronchiolitis or airways inflammation during asthma and is often called center-lobe syndrome. Atelectasis may occur without clinical signs; patently chest radiography at end-inspiration is important for diagnosis. Multislice computed tomography may point to the diagnosis when plain 10-rays exercise not suffice, and magnetic resonance imaging is well suited for the diagnosis and follow-upwardly of atelectasis. Bronchography combined with diagnostic and therapeutic bronchoscopy may be diagnostic in selected cases. Breast physiotherapy is often the first-line treatment, but its efficacy is not however proven. Centre-lobe atelectasis has been associated with positive bacterial cultures; in such cases antibody handling may exist tried. Bronchoalveolar saline lavage with or without direct instillation of dornase alfa has been tried on rare occasions, and lobectomy has been tried in cases of persistent right-eye-lobe and left-lower-lobe syndrome non responding to intensive medical therapy. Stent placement has been tried in carefully selected patients, with biodegradable stents offering a new alternative.

Keywords

atelectasis, congenital, acquired, bronchial lumen occlusion, lung tissue pinch, atelectasis due to anesthesia, postoperative atelectasis, middle-lobe syndrome, strange torso, breast radiography, multislice computed tomography, magnetic resonance imaging, physiotherapy, antibiotic treatment, nebulized dornase alfa

The word atelectasis stems from two Greek words: ateles, meaning "imperfect," and ektasiz, significant "expansion." Atelectasis thus means imperfect expansion, and the word is used to describe incomplete expansion of a lung or lung tissue. After inventing the stethoscope in 1816, René Laennec was the get-go to describe atelectasis every bit a finding during an dissection in 1819. There are many causes of atelectasis, which is a common complication of both astute and chronic lung affliction affecting patients of all ages. It may be congenital or acquired. Congenital atelectasis is normally due to incomplete expansion of the lungs, including primary and secondary congenital atelectasis. The nearly common cause of atelectasis is loss of air in lung tissue that was previously expanded, thus resulting in the plummet of a lung or lung tissue.

Etiology and Pathogenesis

Several mechanisms associated with a multifariousness of pulmonary and extrapulmonary diseases may cause atelectasis. Pulmonary causes include obstruction of the bronchial lumen (the near mutual crusade) and increased surface tension of the fluid lining the respiratory tract and alveoli. Extrapulmonary causes include pinch of airways and lung tissue from exterior the lung and weakness of respiratory muscles in neuromuscular disease. Obstruction of the bronchial lumen by mucus may have several causes, such as airway inflammation and impaired clearance of airway mucus caused by increased mucous viscosity (cystic fibrosis), reduced ciliary function, or a weak cough reflex secondary to neuromuscular disease. Box seventy.i shows the causes of atelectasis.

Box 70.1

Causes of Atelectasis

Intraluminal Causes

Airways inflammation with increased bronchial mucus and formation of fungus plug due to
- Bronchial asthma
- Respiratory tract infection
  - Bronchiolitis, Pneumonia
- Bronchopulmonary dysplasia
- Cystic fibrosis (increased viscosity of the mucus)
- Chief and secondary ciliary dyskinesia (impaired mucociliary clearance)
- Immunodeficiency
- Tracheoesophageal fistula or esophageal atresia
Foreign body in the lower respiratory tract
- Nuts, plastics, other foreign bodies, misplaced tracheal tube

Compression of the Airways

Lobar emphysema
Lymph node enlargement
Vascular ring
Circuitous congenital heart disease (eastward.g., enlargement of left atrium compressing left main bronchus)

Bronchial Wall Involvement

Airway stenosis
- After aspiration or inhalation injury
- After intubation
- Consummate cartilaginous rings
Bronchiectasis
Tracheobronchomalacia
Bronchial tumor

Compression of Lung Tissue

Pneumothorax
Congestive heart failure with cardiac enlargement
Hemothorax
Chylothorax
Lung tumor

Surfactant Dysfunction

Respiratory distress syndrome of the newborn
Adult respiratory distress syndrome
Other

Chief Atelectasis

Congenital malformation

Pathogenic Mechanisms

Congenital pulmonary airway malformations may prevent the normal aeration of parts of the lungs at nascence due to lack of advice of the main bronchial tree with the affected parts of the lungs that have never been inflated, thus causing primary atelectasis. However, a secondary atelectasis may develop presently after birth if a congenital malformation occludes or narrows the bronchial lumen, thus presenting as a differential diagnosis to main atelectasis.

Secondary atelectasis is most oftentimes caused past collapse of normal lung tissue due to obstruction or alternatively due to compression of the bronchial lumen. The pores of Kohn form at three–iv years of age and function every bit collateral communications between neighboring alveoli; they ensure a more even ventilation/perfusion ratio in the lung, thereby playing a role in preventing atelectasis. At more proximal levels no such collateral communications exist, and occlusion of the bronchial lumen initially leads to air trapping in lung tissue peripheral to the occluded bronchus. The trapped air is gradually captivated, leading to atelectasis. Causes of obstruction or compression of the bronchial lumen are shown in Box seventy.1 .

The solubility of the trapped gases determines their absorption rate. The absorption of atmospheric air will take identify within hours, whereas oxygen is absorbed within minutes. Atelectasis therefore occurs more rapidly during ventilation with an increased inspired oxygen fraction and especially with 100% oxygen, compared with breathing normal air. This may partly explicate the increased hazard of atelectasis during anesthesia. The ventilation/perfusion ratio of the atelectatic tissue is regulated through the increased vascular resistance resulting from hypoxic vasoconstriction of the pulmonary vessels secondary to apoplexy of the bronchial lumen.

Atelectasis may be acquired past whatever process or procedure that occludes the bronchial lumen. Foreign bodies in the lower respiratory tract may lead to partial or complete occlusion of a bronchus, and complete occlusion will crusade atelectasis. With an initial incomplete apoplexy, the strange body may cause inflammation of the mucous membranes, with resulting mucosal swelling and increased respiratory secretions causing complete obstruction of the bronchial lumen and the development of atelectasis.

Misplaced endotracheal intubation may cause total collapse of i lung when the distal office of the tracheal tube is located in a principal bronchus (well-nigh often the right 1).

Inflammatory processes within the bronchial tree are among the almost common causes of obstruction of the bronchial lumen, including bronchial asthma (oft eosinophilic inflammation) and acute bronchiolitis due to respiratory syncytial virus infections. In asthma and bronchiolitis, the right eye lobe and the lingula are the most common locations of atelectasis, so common that this is given the proper name of middle-lobe syndrome. The finding of positive bacterial cultures from the respiratory tract in children with asthma and bronchiolitis with atelectasis and middle-lobe syndrome has led to a suggested function for bacterial infection in long-standing atelectasis of asthma and bronchiolitis.

Airway inflammation due to asthma, bronchiolitis, and other respiratory infections may cause increased bronchial secretions, mucosal edema, bronchial smooth muscle wrinkle, and devastation of bronchial epithelium with reduced ciliary office, leading to the retention of mucus within the bronchial lumen. Devastation of the bronchial epithelium may alter the airway surface liquid, with an event on surfactant function; it may thus enhance the tendency for bronchial collapse. In both bronchopulmonary dysplasia and respiratory distress syndrome of prematurity, abnormal surfactant function may contribute to the germination and persistence of atelectasis. Aspiration of meconium, acids, alkali and amniotic fluid also has this effect.

Many diseases increase the susceptibility of the respiratory tract to infection and lead to the accumulation of mucus, which predisposes to the development of atelectasis. These include immunodeficiency, chief ciliary dyskinesia (PCD), and cystic fibrosis.

Bronchial wall processes that narrow the bronchial lumen, including tracheobronchomalacia, vascular rings, tumors such as polyps, papillomas, and (rarely) bronchocentric carcinoma, may cause atelectasis in children. Bronchiectasis, usually caused past recurrent or long-standing airway inflammation, is often complicated by atelectasis.

Extrapulmonary processes may compress normal lung tissue and cause atelectasis without affecting the bronchi, as seen in some patients with congenital heart defects and likewise with pneumothorax or hemothorax. Rounded atelectasis, seen more often in adults than children, is generally asymptomatic and associated with chronic pleural disease, lung fibrosis, or pleural effusions. It consists of infolding of atelectatic lung tissue with claret vessels, pleura, and sometimes bronchi.

Atelectasis is mutual in neuromuscular diseases. Muscular hypotonia impairs ventilation because of reduced movement of respiratory muscles and causes difficulty in clearing bronchial secretions, thus increasing the private's susceptibility to respiratory infections and atelectasis. Hypoventilation may as well contribute to the development of atelectasis that is seen in children during anesthesia.

Clinical Manifestations

The symptoms and signs of atelectasis will depend on whether single or multiple lobes are involved, the underlying cause, and the age of the patient. In total-term newborn infants with respiratory distress, the presence of atelectasis when accompanied by situs inversus and the need for prolonged supplemental oxygen is highly predictive of a PCD diagnosis (run across Chapter 71 ). In this example, atelectasis caused by mucous plugging secondary to poor mucociliary clearance is most prevalent in the upper (75%) and heart (25%) lobes. Infants with bronchiolitis who develop lobar atelectasis are more likely to have severe affliction and require admission to the intensive intendance unit of measurement, while burnout and sudden severe deterioration may point the development of massive atelectasis affecting a whole lung. Preterm infants with bronchiolitis are at higher risk of developing atelectasis, and younger children in general are more at adventure of developing atelectasis than older children and adults owing to less well developed collateral ventilation effected by the pores of Kohn and the canals of Lambert. In children with asthma, acute deterioration of symptom control may exist due to the development of atelectasis affecting the correct middle lobe, so-chosen right-middle-lobe syndrome ( Fig. lxx.1 ). Similarly, an exacerbation of symptoms in children with cystic fibrosis or PCD may exist due to the evolution of atelectasis secondary to bacterial infection in the lower airways, causing increased product of mucus and cellular droppings with subsequent mucus plugging.

An episode of sudden paroxysmal cough with or without subsequent respiratory distress in a previously salubrious immature child accompanied by x-ray features of atelectasis may indicate the need for bronchoscopy to exclude an inhaled foreign body. Atelectasis may non crusade detectable abnormalities on clinical examination; thus the diagnosis must exist made radiologically. Simply more often than not clinical signs relate to the size of the atelectasis. There may be impaired oxygen saturation, decreased expansion of the chest on the affected side, dullness to percussion, and diminished or absent-minded breath sounds. If the atelectasis is fractional or airway obstacle is not complete, crackles may exist heard during inspiration and expiration. In some cases of significant or fifty-fifty whole-lung atelectasis, oxygen saturation may be normal, since alveolar hypoxia tin induce reflex vasoconstriction and thus minimize ventilation/perfusion mismatch. Paradoxically, intubation and mechanical ventilation of such patients with supplemental oxygen may cause a temporary deterioration in oxygen saturation due the abolition of the protective vasoconstrictive reflex, thus inducing intrapulmonary shunting and the perfusion of unventilated, atelectatic lung tissue that does not take part in gas exchange. Lung part in patients with atelectasis may be normal if the atelectasis is small-scale or demonstrate a restrictive pattern with a reduced FEV ₁and FVC, and a normal FEV _i/FVC.

Diagnosis

The prompt diagnosis of atelectasis in children is important, since early on detection and subsequent treatment may lead to an improved effect. Diagnosis is aided by an agreement of situations in which atelectasis is more likely to occur and the underlying pathophysiologic mechanisms. For example, postoperative atelectasis is not uncommon, especially in children undergoing cardiac surgery. All the same, since atelectasis is not e'er detectable clinically, it may be discovered unexpectedly, for case, during routine breast ten-ray in a child with a chronic underlying condition such as asthma or PCD. Flexible bronchoscopy has a part in the diagnosis of atelectasis when at that place is suspected airway obstruction due to, for example, strange-body inhalation, mucous plugging, endobronchial tuberculosis, airway malacia, external compression from a vascular ring, enlarged lymph nodes, or an enlarged heart. Information technology may also be therapeutic in cases of intraluminal obstruction.

The almost frequently used modality for the diagnosis of atelectasis is chest radiography. Frontal projection is always included, but sometimes lateral views are amend suited, as in atelectasis of the right heart lobe and the lower lobes. Oblique views may be of particular value in segmental atelectasis. Sometimes fluoroscopy is also used to delineate hard locations of increased opacification. Fluoroscopy may also be used to diagnose air trapping and mediastinal shift when a foreign trunk is suspected. In older children, notwithstanding, an x-ray at terminate-inspiration followed by another at finish-expiration will suffice. Because atelectasis results in volume reduction of the afflicted office of the lung, this may atomic number 82 to full general signs such as elevation of the diaphragm and narrowing of ipsilateral intercostal spaces ( Fig. lxx.2 ). Shift of the mediastinum and tracheal contours toward the afflicted side is quite mutual, only these general signs may be absent if emphysema develops in the ipsilateral lung or if the atelectasis occurs together with ipsilateral pleural effusion. Atelectasis of the right upper lobe is seen as a combination of increased opacity and volume reduction leading to elevation of the interlobar cleft ( Fig. seventy.iii ). A summary of major findings on chest radiography related to extent and location of the atelectasis is presented in Tabular array 70.1 .