![]() ![]() The air can be decompressed both retroperitoneally and intraperitoneally (pneumoperitoneum). When adequate air is accumulated in mediastinum, it is decompressed along cervical fascial planes into the subcutaneous tissues and subcutaneous emphysema is formed. Air can be introduced along the perivascular sheaths into the mediastinum and pneumomediastinum or pneumopericardium are present. When an overdistended alveolus ruptures, air is diffused into the perivascular adventitia, resulting in PIE. The two terms-barotrauma and volutrauma-reflect the two sides of the same phenomenon: the lung injury due to a large distending volume and/or to a high airway pressure ( 10- 19).Ĭlinical manifestations of barotrauma include pneumothorax, pulmonary interstitial emphysema (PIE), subcutaneous emphysema, pneumoperitoneum, pneumomediastinum or pneumopericardium, air embolisation, tension lung cysts, and hyperinflated left lower lobe. Volutrauma is the term that describes ultrastructural lung injury due to overdistention occurring during mechanical ventilation. Nevertheless, it seems that not only pressure, but high lung volume and lung hyperinflation as well, play a major role in barotrauma aetiology. According to the etymology, barotrauma refers only to high pressures. VALI and VILI can be divided into macrobarotrauma (the form of radiologically detected barotrauma) and microbarotrauma, with diffuse lung injury and possible injury of other organs due to release of inflammatory mediators-biotrauma. This is described as ventilator associated lung injury (VALI) or ventilator induced lung injury (VILI). The implementation of positive pressure ventilation predisposes an already affected lung-when certain limits are overcome-to injury. ![]() It is defined as the presence of extraalveolar air in locations, where it is not normally found in patients receiving mechanical ventilation ( 1- 9). Barotrauma must be considered as complication of the use of positive pressures in a tissue, where normal air movement is mainly passive. While human being is created, as other creatures, to breathe with a mechanism based on negative pressures, the patient on mechanical ventilation is ventilated with positive pressures, which is not physiological. These differences make the blood mass transfer toward the thorax, and results in pulmonary hypertension and consequent pulmonary barotraumas ( 5).Intubation and mechanical ventilation are common but aggressive therapeutic manoeuvres in anesthesia or in ICU setting. Also, in case of head-out water immersion, alveolar pressure is similar to atmospheric pressure, whereas extra-thoracic vascular pressure is similar to hydrostatic pressure. Relative pulmonary hypertension leads to an increased pressure gradient between the pulmonary capillaries and pulmonary parenchyma. The pressure difference causes blood circulation from the peripheral portion (extremities) to the central portion of the body (heart, lungs, and great vessels of the chest) and enlarges the venous return and cardiac preload ( 3 4). Additionally, the coldness induced by water increases this hemodynamic strain ( 1 2). During breath holding while swimming (including snorkeling), immersion in a reversed position causes a pressure difference between the thorax and lower extremities. In previous literature regarding alveolar hemorrhage as a complication of barotrauma caused by SCUBA diving, the increase in the intra-alveolar pressure due to breath holding in the water and the mechanism of barotrauma, which induced intra-alveolar hemorrhage, appeared to be similar to those seen in our case. His breath sounds were normal, without any crackle or abnormal sounds. Hemoptysis was his only complaint, and there were no other symptoms. Although he was fully conscious and lucid, he appeared to be acutely ill. His body temperature was within normal range, with no chills or other upper respiratory symptoms. He presented to the emergency department of our hospital with a pulse rate of 90 beats per minute and respiratory rate of 20 breaths per minute. He denied any accompanying aspiration of water or other respiratory symptoms, including shortness of breath. After snorkeling, he noticed blood-tinged sputum while coughing. Several hours before admission, he had been snorkeling in the late afternoon at a river for 1 hour, without any traumatic injury to his chest. He snorkeled about twice a year without any problems, and this was the first attack he had experienced. This was not his first attempt at snorkeling, and he had more than 5 years of snorkeling experience. He had been well before the current attack. He reported with approximately 20–30 mL of expectorated blood mixed with sputum. A healthy 54-year-old man with hemoptysis and a previous medical history of well-controlled hypertension (body weight, 74.5 kg height, 168 cm body mass index, 26.14 kg/m 2) visited our hospital. ![]()
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