BMC anesthesiology
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Comparative Study Observational Study
Impact of a goal directed fluid therapy algorithm on postoperative morbidity in patients undergoing open right hepatectomy: a single centre retrospective observational study.
Right hepatectomy is a complex procedure that carries inherent risks of perioperative morbidity. To evaluate outcome differences between a low central venous pressure fluid intervention strategy and a goal directed fluid therapy (GDFT) cardiac output algorithm we performed a retrospective observational study. We hypothesized that a GDFT protocol would result in less intraoperative fluid administration, reduced complications and a shorter length of hospital stay. ⋯ In patients undergoing open right hepatectomy with an established ERAS programme, use of GDFT was associated with less intraoperative fluid administration and reduced hospital length of stay when compared to Usual care. There were no significant differences in postoperative complications or mortality.
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Postoperative pulmonary complications (PPCs) increase morbidity and mortality of surgical patients, duration of hospital stay and costs. Postoperative atelectasis of dorsal lung regions as a common PPC has been described before, but its clinical relevance is insufficiently examined. Pulmonary electrical impedance tomography (EIT) enables the bedside visualization of regional ventilation in real-time within a transversal section of the lung. Dorsal atelectasis or effusions might cause a ventral redistribution of ventilation. We hypothesized the existence of ventral redistribution in spontaneously breathing patients during their recovery from abdominal and peripheral surgery and that vital capacity is reduced if regional ventilation shifts to ventral lung regions. ⋯ After abdominal surgery ventral redistribution of ventilation persisted up to the third postoperative day and was associated with decreased vital capacity. The peripheral surgery group showed only minor changes in vital capacity, suggesting a role of the location of surgery for postoperative redistribution of pulmonary ventilation.
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Sevoflurane, an inhalational general anesthetic, has become one of the most widely used inhalational anesthetics in surgery. However, previous studies have found that sevoflurane anesthesia can trigger an inflammatory response, resulting in secondary damage. Dexmedetomidine (DEX), a highly-selective α adrenergic receptor agonist, is widely used as an anesthetic adjuvant in the clinic. In this study we investigated whether DEX was able to suppress sevoflurane-induced neuroinflammation. ⋯ These data suggest that the PI3K/Akt/mTOR pathway contributes to sevoflurane-induced neuroinflammation and that activation of PI3K/Akt/mTOR signaling by DEX could help reduce the neuroinflammatory effects of sevoflurane.
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Randomized Controlled Trial
Comparison of volume-controlled ventilation mode and pressure-controlled ventilation with volume-guaranteed mode in the prone position during lumbar spine surgery.
During lumbar spine surgery, patients are placed in the prone position for surgical access. The prone position has various effects on cardiac and pulmonary function, including a decreased cardiac index (CI), decreased dynamic lung compliance (Cdyn), and increased peak inspiratory pressure (Ppeak). In this study, we compared the volume-controlled ventilation mode (VCV) and pressure-controlled ventilation with volume guaranteed mode (PCV-VG) based on hemodynamic and pulmonary variables in the prone position during lumbar spine surgery. ⋯ PCV-VG led to lower Ppeak and improved Cdyn values compared with VCV, showing that it may be a favorable alternative mode of mechanical ventilation for patients in the prone position during lumbar spine surgery.
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Dexmedetomidine (DEX) has been used as an anesthetic for decades. The present investigation aimed to elucidate the analgesic impact of DEX on 2,4,6-Trinitrobenzenesulfonic acid (TNBS)-induced chronic inflammatory visceral pain (CIVP) in rats. ⋯ DEX thus exhibited an analgesic effect on CIVP rats through the miR-34a-mediated HDAC2 pathway and suppressed visceral hypersensitivity.