Your browser doesn't support javascript.
loading
Show: 20 | 50 | 100
Results 1 - 2 de 2
Filter
Add more filters










Database
Language
Publication year range
1.
Surg Endosc ; 37(1): 510-517, 2023 01.
Article in English | MEDLINE | ID: mdl-36002681

ABSTRACT

BACKGROUND: Postoperative pulmonary complications (PPCs) are among the most common complications after liver resection. Although the application of laparoscopy has reduced the incidence of PPCs, the rate of PPCs after laparoscopic liver resection (LLR) remains high and the risk factors for the same are unclear. Therefore, this study aimed to determine the risk factors for PPCs after LLR. METHODS: In this multicenter study, 296 patients underwent LLR from January 2019 to December 2020. Demographic data, pathological variables, and perioperative variables were reviewed. Univariate and multivariate analyses were performed to identify the independent risk factors for PPCs. RESULTS: Of the 296 patients, 80 (27.0%) developed PPCs. Patients with PPCs had significantly increased total costs, operation costs, length of stays, and postoperative hospital stays. Multivariate analysis identified three independent risk factors for PPCs after LLR: smoking [Odds ratio (OR): 5.413, 95% confidence intervals (CI): 2.446-11.978, P = < 0.001], location of lesion in segment 7 or 8 (OR 3.134, 95% CI 1.593-6.166, P = 0.001), duration of liver ischemia (OR 1.038, 95% CI 1.022-1.054, P < 0.001), and presence of intraoperative hypothermia (OR 3.134, 95% CI 1.593-6.166, P < 0.001). CONCLUSION: Smoking, location of lesion in segment 7 or 8, duration of liver ischemia and intraoperative hypothermia were independent risk factors for PPCs which significantly increased the length of stays and burden of healthcare costs.


Subject(s)
Hypothermia , Laparoscopy , Liver Neoplasms , Humans , Hypothermia/complications , Hypothermia/surgery , Hepatectomy/adverse effects , Risk Factors , Retrospective Studies , Laparoscopy/adverse effects , Postoperative Complications/epidemiology , Postoperative Complications/etiology , Postoperative Complications/surgery , Liver , Ischemia/complications , Ischemia/surgery , Liver Neoplasms/surgery
2.
J Clin Anesth ; 37: 123-128, 2017 Feb.
Article in English | MEDLINE | ID: mdl-28235500

ABSTRACT

This study aimed to review research on the effects of nonsteroidal anti-inflammatory drugs (NSAIDs) on ß-endorphin. NSAIDs are commonly used as anti-inflammatory and analgesic drugs. They are well known for inducing peripheral analgesia by inhibiting cyclooxygenase (COX). However, an increasing number of studies have shown that NSAIDs have an analgesic effect not only in the periphery but also at the center. It means that a central analgesic mechanism of the action of NSAIDs exists besides the peripheral mechanism, and the central mechanism likely involves ß-endorphin. ß-Endorphin is one of the most prominent endogenous peptides, existing in the hypophysis cerebri and hypothalamus. It plays an irreplaceable role in the central and peripheral analgesia in the human body mainly through three mechanisms including three parts, the spinal cord, the supraspinal cord, and peripheries. ß-Endorphin plays an important role in the development of hyperalgesia. However, the specific signal transduction pathways between prostaglandin E2 or NSAIDs and ß-endorphin are still not quite clear. Whether NSAIDs can lead to the increased content of ß-endorphin in all patients after any operation needs further investigation. Further studies should determine the optimal dose when NSAIDs and opioid drugs are used together, and also explore the existence of one NSAID that has the potential to replace the traditional opioid drugs and can achieve adequate analgesia.


Subject(s)
Analgesia/methods , Anti-Inflammatory Agents, Non-Steroidal/pharmacology , Hyperalgesia/chemically induced , Pain/drug therapy , Prostaglandin-Endoperoxide Synthases/metabolism , beta-Endorphin/metabolism , Anti-Inflammatory Agents, Non-Steroidal/administration & dosage , Cyclooxygenase Inhibitors/administration & dosage , Cyclooxygenase Inhibitors/pharmacology , Dinoprostone/metabolism , Humans , Signal Transduction/drug effects
SELECTION OF CITATIONS
SEARCH DETAIL
...