Atelectasis
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Atelectasis
Atelectasis refers to partial or complete collapse of the lung, i.e. failure of the lung to expand (inflate) completely. It is also termed as lung collapse.
History
The term atelectasis is derived from the Greek words ateles and ektasis, meaning incomplete expansion.
Atelectasis of the lung can be congenital (present since birth) or acquired (occurring after birth). Collapse of the lung may be acute (obstruction of bronchus by a foreign body) or chronic (compression by lymph nodes surrounding a bronchus, scarring due to repeated infections).
Frequency
The incidence and prevalence of atelectasis is not well known. However postoperative atelectasis and lobar atelectasis are the common types. There is no specific racial or sex predilection.
Causes
Atelectasis can occur due to obstructive or nonobstructive causes, leading to resorption of gas from alveoli.
Thus it can be caused by compression of lung due to pressure from outside, leading to loss of elastic recoil of the lung or due
to internal or external obstruction of the airway (bronchus), leading to collapse.
Acute, massive atelectasis usually occurs as a post-operative complication following surgical procedures in the abdomen or chest.
Obstructive type is the most common in which a bronchus is obstructed either internally or externally. Causes include, foreign body, tumor, granuloma, mucous plug, bronchial stricture, distortion, kinking; lung compression by fluid or air trapped in pleural space; bronchial compression by tumor, enlarged lymph node, aneurysm etc..
Depending on the type of the bronchus involved, atelectasis is termed as lobar (lobar bronchus) or segmental (segmental bronchus) atelectasis.
Nonobstructive atelectasis embraces in its fold many types depending upon the underlying pathology.
Passive atelectasis occurs when contact between the parietal and visceral pleurae is abolished by fluid (pleural effusion) or air (pneumothorax).
Compression atelectasis occurs due to pressure on the lung due to any space-occupying lesion of the thorax. Both passive and compression atelectasis force the air out of the alveoli.
Adhesive atelectasis follows a defect in the surfactant (due to decreased production or inactivation). Surfactant is a mixture of phospholipids and lipoproteins, covering the alveolar surface. It reduces the surface tension, and contributes to alveolar stability. Surfactant defect increases the alveolar surface tension leading to unstable alveoli and collapse. This can occur following conditions like; toxicity due to O2, drugs, or chemicals, adult or neonatal respiratory distress syndrome, pulmonary edema, pulmonary embolism, general anesthesia, and mechanical ventilation.
Cicatrization atelectasis follows severe scarring of lung. There is thus a reduction in lung volume as seen in granulomatous disease (tuberculosis) or necrotizing pneumonia.
Replacement atelectasis results in loss of lung volume as in tumorous conditions, occupying the alveoli of a lobe (alveolar cell carcinoma).
Pleural disease, as in asbestosis, causes fibrosis and adhesion of the visceral pleura to the lung causing rounded atelectasis.
Symptoms and signs
The symptoms of atelectasis vary, depending upon the cause, rapidity of development, extent of lung involvement, presence or absence of infection etc. In a slowly developing atelectasis as in middle lobe syndrome, there may be no or minimal symptoms. In acute and severe cases, there may be pain on the affected side, difficulty in breathing (dyspnea), cyanosis, hypotension, tachycardia, fever and sometimes shock. In diffuse atelectasis as in adult respiratory distress syndrome (ARDS), respiration is shallow and rapid, on auscultation there may be rhonchi, wheeze; hypoxia, acidosis and multisystem organ failure.
Chest expansion may be reduced or absent on the affected side. Trachea and mediastinum are pulled towards the affected side. There may be dullness on percussion, absent breath sounds or wet rales up on auscultation (due to fluid in the lung).
Diagnosis
Diagnosis is based on clinical and x-ray findings.
There is diminution of lung size (rib retraction and crowding, elevated diaphragm, deviated trachea and mediastinum, and compensatory increased distention of unaffected lung), airless dense opacification of the affected lobe (as seen in x-ray). Compensatory hyperinflation as evidenced by increased radiolucency can be seen in the normal lobe or unaffected lung.
Posterior-anterior and lateral chest x-rays are usually requested for. Radiographic appearance may vary from complete collapse to relatively normal-appearing lungs. In practice the involvement is more extensive than is suggested by the x-ray.
Bronchoscopy and CT scan of thorax may be more valuable in identifying the affected site and cause.
Pathophysiology
Following acute obstruction to bronchus, the capillary surrounding the alveoli absorbs the alveolar gas, causing airlessness, lung retraction and collapse. Despite blood perfusion, hypoxemia occurs, because there is no air in the lung to transfer the oxygen. Extensive alveolar hypoventilation may result in an effective right to left shunt of blood in the heart which also leads to hypoxia. The impaired breathing resulting from alveolar collapse also leads to hypoxia and pneumonia. Tissue hypoxia results in entry (transudation) of fluid in to the alveoli leading to pulmonary edema, which may prevent complete collapse of the atelectatic lung.
The reduced alveolar distention results in decreased surfactant production which propagates the atelectasis further. Mobilization of secretions may be inhibited by inflammatory lung disease leading to edema, with a need for tracheal intubation.
Distention of the unaffected surrounding area of the lung may partially compensate for the volume loss. When the lung loses air, it becomes stiff (less compliant) and increases the work of breathing (dyspnea). If the obstruction is relieved, air enters, and the lung may return to normalcy. But if obstruction persists, infection and inflammatory changes ensue, leading to fibrosis and bronchiectasis.
In non-obstructive case, changes in alveolar surface tension, lung-pleura pressure and alveolar size, cause inadequate regional ventilation and atelectasis. There is loss of negative pressure in the pleural space in case of pleural effusion or pneumothorax. In such cases the lung tends to recoil due to elastic property and becomes atelectatic.
Large doses of CNS depressants, high O2 concentrations during anesthesia, tight dressings, abdominal distention, and immobility of the body, all limit movement of thorax, diaphragm; ineffective clearance with accumulation of viscid bronchial secretions, suppressed cough reflex, shallow breathing due to pain- all resulting in acute massive collapse of lung that is commonly seen post-operatively. Similar mechanisms operate in atelectasis due to other causes like, CNS depressive disorders, thoracic cage abnormalities, pain, muscle spasm, and neuromuscular diseases.
Hyperosmolality of blood as in diabetic ketoacidosis also cause atelectasis, possibly by increasing the viscosity of respiratory secretions and obstruction due to mucus plugs.
Prevention
Adequate management of chronic bronchitis through antibiotics, bronchodilators to improve ventilation, bronchial toiletry to liquify thick sputum, suction to remove secretions, prohibition of smoking, judicious use of central nervous system depressant drugs, intermittent positive pressure breathing (IPPB), deep breathing exercises, respiratory physiotherapy, encouragement of cough and early movement would prevent development of atelectasis, in appropriate situations (e.g. post-operative patients, in those on mechanical ventilators etc).
Treatment
Acute atelectasis:
General measures include, -Appropriate positioning of the patient (with affected uppermost) to allow drainage of secretions, and comfort. -Encouragement of coughing, -Respiratory physiotherapy – active (deep breathing exercises), passive (percussion), -IPPB or an incentive spirometer to help ensure deep breaths and maintain/promote inflation of alveoli.
-If infection is suspected, a broad-spectrum antibiotic (e.g. ampicillin 500 mg po or 1 g parenterally q 6 h; for children, 50 to 100 mg/kg/day in divided doses q 6 to 8 h) should be given empirically at the outset. A 2nd generation cephalosporin, a newer macrolide (azithromycin or clarithromycin), or trimethoprim-sulfamethoxazole can also be used initially. Treatment is later modified according to the organism identified by culture and sensitivity.
Where ever possible the cause should be corrected.
Relief of obstruction depends on the type- urgent treatment e.g. removal of foreign body, mucus plug through bronchoscopy, or planned treatment e.g. surgical removal of a tumor, may allow the collapsed lung to re-inflate.
In case of recurrent atelectasis and in those on mechanical ventilation, apart from identification and correction of the underlying cause, oxygen maintenance, antibiotics, correction of hemodynamic (fluid) nutritional and metabolic derangements should be undertaken.
Surfactant level in amniotic fluid may be measured to judge the fetal lung maturity. This enables to identify the newborns at risk and treat them with surfactant.
In chronic cases the development of complications like fibrosis, bronchiectasis, infection etc., is proportional to the duration of the collapsed status of lung. Hence all appropriates measures towards removal of the cause and expansion of the collapsed lung should be undertaken at the earliest. In some instances even surgical removal of the affected part may be necessary to prevent recurrence.
Drugs
Apart from antibiotics, specific antituberculous, antifungal drugs may be needed depending upon the etiology.
Bronchodilators (beta adrenergic agonists like salbutamol, anticholinergics like ipratropium) may be necessary improve ventilation. Mucolytics like acetyl cysteine to liquify sputum may be more useful especially if directly applied via a bronchoscope.
Mortality/Morbidity
Mortality depends on the underlying cause and management. In postoperative atelectasis, the condition generally improves with good nursing care. The prognosis of lobar atelectasis secondary to endobronchial obstruction depends on the stage and treatment of the underlying malignancy.
Prognosis
Prognosis depends upon the cause, age of the patient, underlying complications and the management. It is usually good in case of post-operative atelectasis and poor in case of advanced cancer.
Author
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