Atelectasis pathophysiology On the Web
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There are several types of atelectasis according to their underlying mechanisms or the distribution of alveolar collapse; resorption, compression, microatelectasis and contraction atelectasis. The exact pathogenesis of [disease name] is not fully understood.
It is thought that [disease name] is the result of / is mediated by / is produced by / is caused by either [hypothesis 1], [hypothesis 2], or [hypothesis 3].
[Pathogen name] is usually transmitted via the [transmission route] route to the human host.
Following transmission/ingestion, the [pathogen] uses the [entry site] to invade the [cell name] cell.
[Disease or malignancy name] arises from [cell name]s, which are [cell type] cells that are normally involved in [function of cells].
The progression to [disease name] usually involves the [molecular pathway].
The pathophysiology of [disease/malignancy] depends on the histological subtype.
- The exact pathogenesis of [disease name] is not fully understood.
- It is understood that [disease name] is the result of / is mediated by / is produced by / is caused by either [hypothesis 1], [hypothesis 2], or [hypothesis 3].
- [Pathogen name] is usually transmitted via the [transmission route] route to the human host.
- Following transmission/ingestion, the [pathogen] uses the [entry site] to invade the [cell name] cell.
- [Disease or malignancy name] arises from [cell name]s, which are [cell type] cells that are normally involved in [function of cells].
- The progression to [disease name] usually involves the [molecular pathway].
- The pathophysiology of [disease/malignancy] depends on the histological subtype.
Obstructive atelectasis: Most common type of atelectasis In case of obstruction from the trachea to the alveoli at any level, alveolar gas reabsorption may occur leading to diminished lung volume and subsequent atelectasis. The extent of atelectasis depends upon the level of obstruction: Lobar atelectasis: due to lobar bronchus obstruction Segmental atelectasis: leads to segmental bronchus obstruction
Causes of obstructive atelectasis: Foreign body Tumor Mucus plugs The rate and pattern of development of atelectasis depends on collateral ventilation and gas composition of inspired air. Non obstructive atelectasis: Non obstructive atelectasis may occur due to severe lung scarring caused by necrotizing pneumonias or granulomatous diseases (cicatrisation atelectasis) or infiltration (replacement atelectasis), extrinsic lung compression (due to thoracic space occupying lesions), diminished levels of surfactant (adhesive atelectasis presenting as ARDS), and passive atelectasis due to absence of contact between the parietal and visceral pleurae due to fluid (pleural effusion), air (pneumothorax), blood (hemothorax) etc.
Atelectasis of the upper lobe commonly occurs due to pneumothorax, whereas atelectasis of the middle and lower lobes occurs due to pleural effusion. Rounded atelectasis: This is a form of atelectasis that is characterized by formation of fibrous bands which adhere the lung to the pleura. There is a high association of rounded atelectasis in asbestosis due to the formation of fibrous pleural plaques. Mean age of presentation is 60 years. Middle lobe syndrome (Fixed or recurrent atelectasis of the lingula/right middle lobe): due to Sjogren’s syndrome Intraluminal or extraluminal obstruction (compression of the bronchi by adjacent structures) may result in middle lobe syndrome.
Non obstructive causes may also lead to atelectasis of the middle lobe.
Pathophysiology: The pathophysiology of obstructive and non-obstructive atelectasis is determined by several factors.
Obstructive atelectasis Bronchial obstruction leads to resorption of alveolar gas by the blood circulating in the alveolar capillary membrane. This leads to diminished lung volume and lung retraction. Perfusion of unventilated lung tissue leads to hypoxemia due to shunt formation. Following bronchial obstruction, complete collapse of the affected lung is prevented by secretions that fill up the spaces of the alveoli. The adjacent lung distends to prevent collapse of the part of the lung undergoing atelectasis. The mediastinum shifts towards the affected side. Diaphragmatic elevation of the diaphragm leads to flattening of the chest wall. Nonobstructive atelectasis This is primarily due to loss of contact between the parietal and visceral pleurae (due to pneumothorax or pleural effusion), leading to passive or relaxation atelectasis. While pneumothorax primarily affects the upper lobe, pleural effusions affect the lower lobes. Lung surfactant is composed of phospholipid dipalmitoyl phosphatidylcholine, which reduces alveolar surface tension. Absence or inactivation of surfactant leads to development of adhesive atelectasis. This can occur in case of ARDS, blunt trauma to the lung, alveolar collapse and radiation pneumonitis. Cicatrization atelectasis may develop due to scar formation in the lung parenchyma. Infiltration of the lung lobe by a tumor (bronchoalveolar carcinoma) may lead to replacement atelectasis. Patients with lower respiratory tract infections, PE and hypoventilation may develop obstruction of the small bronchus, leading to formation of small atelectatic areas within the lung. This may be due to respiratory stressors such as toxins, hyperoxia, hypoxia, ischemia leading to impaired surfactant production and impaired regional ventilation. Intrapulomary shunt formation and ventilation perfusion mismatch may arise to due to development of this platelike atelectasis. Postoperative atelectasis: Upper abdominal and thoracic procedures lead to postoperative atelectasis which may arise as a complication of surgery or anaesthesia leading to decreased surfactant activity and dysfunction of the diaphragm. This leads to atelectasis which is segmental and basilar in distribution.
- [Disease name] is transmitted in [mode of genetic transmission] pattern.
- Genes involved in the pathogenesis of [disease name] include [gene1], [gene2], and [gene3].
- The development of [disease name] is the result of multiple genetic mutations.
- On gross pathology, [feature1], [feature2], and [feature3] are characteristic findings of [disease name].
- On microscopic histopathological analysis, [feature1], [feature2], and [feature3] are characteristic findings of [disease name].