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Vigorous spontaneous breathing has emerged as a promotor of lung damage in acute lung injury, an entity known as “patient self-inflicted lung injury”. Mechanical ventilation may prevent this second injury by decreasing intrathoracic pressure swings and improving regional air distribution. Therefore, we aimed to determine the effects of spontaneous breathing during the early stage of acute respiratory failure on lung injury and determine whether early and late controlled mechanical ventilation may avoid or revert these harmful effects. A model of partial surfactant depletion and lung collapse was induced in eighteen intubated pigs of 32 ±4 kg. Then, animals were randomized to (1) SB‐group: spontaneous breathing with very low levels of pressure support for the whole experiment (eight hours), (2) Early MV-group: controlled mechanical ventilation for eight hours, or (3) Late MV-group: first half of the experiment on spontaneous breathing (four hours) and the second half on controlled mechanical ventilation (four hours). Respiratory, hemodynamic, and electric impedance tomography data were collected. After the protocol, animals were euthanized, and lungs were extracted for histologic tissue analysis and cytokines quantification. SB-group presented larger esophageal pressure swings, progressive hypoxemia, lung injury, and more dorsal and inhomogeneous ventilation compared to the early MV-group. In the late MV-group switch to controlled mechanical ventilation improved the lung inhomogeneity and esophageal pressure swings but failed to prevent hypoxemia and lung injury. In a lung collapse model, spontaneous breathing is associated to large esophageal pressure swings and lung inhomogeneity, resulting in progressive hypoxemia and lung injury. Mechanical ventilation prevents these mechanisms of patient self-inflicted lung injury if applied early, before spontaneous breathing occurs, but not when applied late.

A 2-year-old polytraumatized male cat was admitted to a teaching hospital for correction of a defective inguinal herniorrhaphy. Upon arrival, the cat showed signs of neuropathic pain, including allodynia and hyperalgesia. Analgesic therapy was initiated with methadone and metamizole; however, 24 h later, the signs of pain continued. Reparative surgery was performed, and a multimodal analgesic regimen was administered (methadone, ketamine, wound catheter and epidural anesthesia). Postoperatively, the cat showed signs of severe pain, assessed using the UNESP-Botucatu multidimensional composite pain scale. Rescue analgesia was initiated, which included methadone, bupivacaine (subcutaneous wound-diffusion catheter) and transversus abdominis plane block. Because the response was incomplete, co-adjuvant therapy (pregabalin and electroacupuncture) was then implemented. Fourteen days after admission, the patient was discharged with oral tramadol and pregabalin for at-home treatment. Neuropathic pain is caused by a primary lesion or dysfunction in the nervous system and is a well-described complication following trauma, surgical procedures such as hernia repair, and inadequate analgesia. The aims of this report are to: (1) describe a presentation of neuropathic pain to highlight the recognition of clinical signs such as allodynia and hyperalgesia in cats; and (2) describe treatment of multi-origin, severe, long-standing, ‘mixed’ pain (acute inflammatory with a neuropathic component). The patient was managed using multiple analgesic strategies (multimodal analgesia), including opioids, non-steroidal anti-inflammatory drugs, locoregional anesthesia, co-adjuvant drugs and non-pharmacological therapy (electroacupuncture).