Diagnostic utility of fecal calprotectin in patients presenting to the emergency department with suspected acute appendicitis.

BACKGROUND: Acute appendicitis (AA) is one of the most common diseases faced by the surgeon in the emergency department. In clinical practice, how to diagnose patients with AA accurately is still challenging. METHODS: We conducted a prospective study of 84 patients who presented in the emergency department with suspected AA and measured fecal calprotectin (FC) value. The final diagnosis of AA was independently determined without reference to the test results of FC. Then, we retrospectively analyzed the FC value for identifying AA. RESULTS: FC value in patients with AA were significantly higher than that in patients without AA (240.5 vs. 68.5 ug/g, P < 0.001). Receiver-operating characteristic analyses demonstrated FC value to be highly sensitive and specific for the diagnosis of AA, as indicated by an overall area under the curve (AUC) of 0.928 (500 times of boot strap estimated 95% CI, 0.855-0.972), with an optimal cut off point of 106 ug/g. FC levels in 26 patients with simple AA were significantly lower than it in the 14 patients with suppurative AA (206 vs. 304ug/g, P = 0.001). CONCLUSIONS: FC test provides a sensitive, convenient and economical method to help facilitate the diagnosis of AA in emergency department. Especially for hospitals without computed tomography equipment or patients who are not suitable to exposed to radiation, FC test is of great significance for improving the diagnostic accuracy of AA.

Comparison of the Level of Free Hexafluoro-isopropanol in Adults' Blood and the Incidence of Emergence Agitation After Anesthesia With Different Concentrations of Sevoflurane in Laparoscopic Gastrointestinal Surgery: A Randomized Controlled Clinical Trial.

PURPOSE: The aim of the study is to compare the free hexafluoro-isopropanol (HFIP) concentration in adults' blood and the incidence of emergence agitation (EA) after inhaled different concentrations of sevoflurane. METHODS: Sixty adult patients planning to undergo laparoscopic gastrointestinal surgery were randomly assigned to 3 groups. Each group received sevoflurane as the volatile anesthetic at different concentrations: 0.5 minimum alveolar concentration (MAC), 1.0 MAC, and 1.5 MAC. The use of sevoflurane was continued until the end of surgery. Venous blood samples were obtained at 30, 60, 120, and 180 minutes after starting the use of sevoflurane and subsequently at 60, 180, and 300 minutes after discontinuation of volatile anesthetic administration. Blood concentrations of sevoflurane and free HFIP were determined using gas chromatography. The recovery time and the incidence of EA at different time points were evaluated among the 3 groups. FINDINGS: Changes in the blood concentrations of sevoflurane and free HFIP during and after the use of sevoflurane were similar in all 3 groups. The peak blood concentration of free HFIP occurred 60 minutes after onset of sevoflurane anesthesia in all 3 groups (P < 0.05). The lowest level of free HFIP and the longest recovery time were found in the 1.5-MAC group (P < 0.05). No significant difference was found in the incidence of EA or moderate pain among the 3 groups during recovery. IMPLICATIONS: The generation of HFIP would be inhibited when the inhaled sevoflurane concentration increased to 1.5 MAC. However, the incidence of EA during recovery had nothing to do with the inhaled different sevoflurane concentrations (within 1.5 MAC) in adults. ChicCTR.org identifier: ChiCTR-IPD-17011558.

Neonatal anesthetic neurotoxicity: Insight into the molecular mechanisms of long-term neurocognitive deficits.

Mounting animal studies have demonstrated that almost all the clinically used general anesthetics could induce widespread neuroapoptosis in the immature brain. Alarmingly, some published findings have reported long-term neurocognitive deficits in response to early anesthesia exposure which deeply stresses the potential seriousness of developmental anesthetic neurotoxicity. However, the connection between anesthesia induced neuroapoptosis and subsequent neurocognitive deficits remains controversial. It should be noted that developmental anesthesia related neurotoxicity is not limited to neuroapoptosis. Early anesthesia exposure caused transient suppression of neurogenesis, ultrastructural abnormalities in synapse and alteration in the development of neuronal networks also could contribute to the long-term neurocognitive dysfunction. Understanding the mechanisms of developmental anesthetic neurotoxicity, especially by which anesthesia impairs brain function months after exposure, may lead to development of rational preventive and therapeutic strategies. The focus of present review is on some of those potential mechanisms that have been proposed for anesthesia induced cognitive decline.