Atelectasis is derived from the Greek words ateles and ektasis, meaning incomplete expansion. It is also referred to as collapse of the lung. Atelectasis is the loss of lung volume, either a part or all of a lung with or without mediastinal shift. This is in contrast to consolidation where the lung volume is normal. In clinical practice, there is often a combination of both. Atelectasis is common in the setting of anaesthesia and critical care. Atelectasis can be broadly classified into obstructive and non-obstructive, each having a particular radiological pattern. Obstructive atelectasis is by far the most common cause of lung collapse, in both adult and paediatric populations.

Air leaks can be defined as any extrusion of air from normal gas-filled cavities including the upper airway, sinuses, tracheobronchial tree, and gastrointestinal (GI) tract. Clinical conditions of relevance in anaesthesia and critical care include pneumothorax, pneumomediastinum, pneumopericardium, pneumoperitoneum, and subcutaneous emphysema. This review will cover those related to the chest; of these, pneumothorax is the most common serious complication. In critically ill patients, the diagnosis of pneumothorax is often complicated by other disease processes and the limitations of bedside imaging. Pneumothorax is the presence of air in the pleural cavity with associated lung collapse. It is classified into spontaneous (occurring without an obvious preceding event), traumatic (direct or indirect), and iatrogenic. Spontaneous is the commonest condition in general medicine and is sub-classified as: (i) primary spontaneous pneumothorax (PSP) occurring in the absence of obvious lung disease and (ii) secondary spontaneous pneumothorax (SSP) complicating a pre-existing lung disease. Most pneumothoraces occurring during anaesthesia and in the critically ill are classified into two categories: (i) pneumothorax secondary to barotrauma and (ii) traumatic pneumothorax as a result of thoracic injury from trauma, surgery, or other interventions.

The inner surface of the chest wall and the surface of the lungs are covered by the parietal and visceral pleura, respectively, with a 10– 24 mm separation normally between the two surfaces. This space is usually filled with a very small amount of fluid. However, large amounts (4–5 litres in an adult) of fluid can accumulate in the pleural space under pathological conditions. The parietal pleura has sensory innervation. Both pleural surfaces are mainly supplied by systemic arterial vessels. Lymphatic vessels from the parietal pleura drain to lymph nodes along the anterior and posterior chest wall; lymphatics from the visceral surface drain to the mediastinal lymph nodes. The pleural space typically contains a small amount of a colourless alkaline fluid (0.1–0.2 ml kg, pH 7.62), which has a low amount of protein (,1.5 g dl). Approximately 90% of accumulated fluid in the pleural space is drained by the venous circulation; the other 10% is absorbed by the lymphatics. A delicate balance between the oncotic and hydrostatic pressures of the pleural space regulates filtration and drainage of pleural fluid. Net absorption of pleural fluid is slightly greater than net filtration forces. In addition, lymphatic drainage from the parietal pleura can surpass the rate of fluid filtration in the pleural space. Chest wall and diaphragmatic movements also enhance absorption of pleural fluid by the vascular and lymphatic vessels. Excessive filtration of fluid can overwhelm these efficient absorptive mechanisms and lead to the formation of pleural effusion.