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Respiratory failure is probably the most common organ failure in patients with AP [6]. Pleural effusion, atelectasis, and pulmonary infiltrates are common radiological findings in patients with moderate‐to‐severe AP, but these are not directly correlated with the presence of hypoxemia [7,8]. In addition, there are cases with hypoxemia without these findings, so other mechanisms of lung injury have been proposed [4]. Several mediators and pathophysiological pathways are involved during the different phases of acute lung injury and acute respiratory distress syndrome. The initial exudative phase is characterized by diffuse alveolar damage, microvascular injury, and influx of inflammatory cells [4,7]. This phase is followed by a fibro‐proliferative phase with lung repair, type II pneumocyte hypoplasia, and proliferation of fibroblasts [4,7]. Proteases derived from polymorphonuclear neutrophils and various proinflammatory mediators and phospholipases seem to be involved, among others [4,7]. Contributing factors that promote pancreatitis‐associated acute lung injury may be found in the gut and mesenteric lymphatics [4,7].

Another important factor in the development of respiratory failure could be increased intra‐abdominal pressure (IAP), with subsequent abdominal compartment syndrome, mainly due to the restrictive effect on respiratory mechanics [9,10].

All patients admitted to hospital due to AP should be carefully observed, especially in the first 48 hours [11]. Hypoxemia may be an early event during the first 48 hours after presentation [12], but it may present later in the course of disease [7]. Older patients, smokers, or patients with preexisting pulmonary diseases have an increased risk of developing respiratory failure [8]. A direct relationship between necrosis extension on abdominal computed tomography (CT) and respiratory complications has been described [7]. If a patient develops respiratory failure, a complete evaluation should be performed, including arterial gasometry, chest imaging, and measurement of IAP. An abdominal CT scan may be useful as respiratory failure could be a consequence of local and systemic complications, such as intestinal ischemia, infected necrosis, or intestinal perforation,

The management of a patient with respiratory failure and hypoxemia includes adequate analgesia and medical or surgical treatment of intra‐abdominal hypertension [13]. Respiratory mechanics and oxygen saturation should be periodically monitored, and if there is no improvement the patient should be managed in an ICU setting [14]. Oxygen delivery is important, initially using noninvasive devices [15]. High‐flow nasal cannula therapy may offer relief to patients suffering from high work of breathing [16]. Noninvasive ventilation could be an option for treating acute respiratory distress syndrome, but should be applied with caution in the most severe cases, especially if abdominal distension is associated [17,18]. If invasive mechanical ventilation is required, protective mechanical ventilation is essential, avoiding high plateau pressures. Higher than recommended plateau pressures of 30 cmH₂O might be required in the setting of abdominal compartment syndrome. Taking normal IAP as 10 mmHg and abdominal–thoracic transmission of around 50% into account, 23 + (0.7 × IAP, in mmHg) might be an appropriate upper limit of plateau pressure [10,19].