Factors associated with outcomes following microvascular decompression for the treatment of primary trigeminal neuralgia in adults: a systematic review and meta-analysis.

This study aimed to evaluate pain assessment strategies and factors associated with outcomes after microvascular decompression for the treatment of primary trigeminal neuralgia in adults. We conducted a systematic review and meta-analysis of English, Spanish, and French literature. We searched three databases, PubMed, Ovid, and EBSCO, from 2010 to 2022 and selected studies including patients with primary trigeminal neuralgia, clear pain assessment, and pain outcomes. Population means and standard deviations were calculated. Studies that included factors associated with postoperative outcomes were included in the meta-analysis. A total of 995 studies involving 5673 patients with primary trigeminal neuralgia following microvascular decompression were included. Patients with arteries compressing the trigeminal nerve demonstrated optimal outcomes following microvascular decompression (odds ratio [OR]= 0.39; 95% confidence interval [CI] = 0.19-0.80; X2 = 46.31; Dof = 15; I2 = 68%; P = < 0.0001). Conversely, when comparing arterial vs venous compression of the trigeminal nerve (OR = 2.72; 95% CI = 1.16-6.38; X2 = 23.23; Dof = 10; I2 = 57%; P = 0.01), venous compression demonstrated poor outcomes after microvascular decompression. Additionally, when comparing single-vessel vs multiple-vessel compression (OR = 2.72; 95% CI = 1.18-6.25; X2 = 21.17; Dof = 9; I2 = 57%; P = 0.01), patients demonstrated unfavorable outcomes after microvascular decompression. This systematic review and meta-analysis evaluated factors associated with outcomes following microvascular decompression (MVD) for primary trigeminal neuralgia (PTN). Although MVD is an optimal treatment strategy for PTN, a gap exists in interpreting the results when considering the lack of evidence for most pain assessment strategies.

Histopathological impact of SARS-CoV-2 on the liver: Cellular damage and long-term complications.

Coronavirus disease 2019 (COVID-19), caused by the highly pathogenic severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), primarily impacts the respiratory tract and can lead to severe outcomes such as acute respiratory distress syndrome, multiple organ failure, and death. Despite extensive studies on the pathogenicity of SARS-CoV-2, its impact on the hepatobiliary system remains unclear. While liver injury is commonly indicated by reduced albumin and elevated bilirubin and transaminase levels, the exact source of this damage is not fully understood. Proposed mechanisms for injury include direct cytotoxicity, collateral damage from inflammation, drug-induced liver injury, and ischemia/hypoxia. However, evidence often relies on blood tests with liver enzyme abnormalities. In this comprehensive review, we focused solely on the different histopathological manifestations of liver injury in COVID-19 patients, drawing from liver biopsies, complete autopsies, and in vitro liver analyses. We present evidence of the direct impact of SARS-CoV-2 on the liver, substantiated by in vitro observations of viral entry mechanisms and the actual presence of viral particles in liver samples resulting in a variety of cellular changes, including mitochondrial swelling, endoplasmic reticulum dilatation, and hepatocyte apoptosis. Additionally, we describe the diverse liver pathology observed during COVID-19 infection, encompassing necrosis, steatosis, cholestasis, and lobular inflammation. We also discuss the emergence of long-term complications, notably COVID-19-related secondary sclerosing cholangitis. Recognizing the histopathological liver changes occurring during COVID-19 infection is pivotal for improving patient recovery and guiding decision-making.

Validation of an equation for free calcium estimation: accuracy improves after adjustment for phosphate and CO2.

PURPOSE: Free calcium is the gold standard for diagnosis of calcium disorders, although calcium assessment is routinely performed by albumin-adjusted calcium. Our objective was to develop a novel-specific correction equation for free calcium employing serum total calcium and other analytes. METHODS: Retrospective single-center cohort study. A new equation for free calcium assessment was formulated from data of hospitalized patients (n = 3481, measurements = 7157) and tested in a validation cohort (n = 3218, measurements = 6911). All measurements were performed simultaneously from the same blood draw. RESULTS: Total CO2 and phosphate, in addition to albumin, were the principal factors associated to calcium misdiagnosis. A novel laboratory-specific prediction equation was developed: free calcium (mmol/L) = 0.541 + (total calcium [mmol/L] *0.441) - (serum albumin [g/L] *0.0067) - (serum phosphate [mmol/L] *0.0425) - (CO2 [mmol/L] *0.003). This new equation substantially improved adjusted R2 to 0.67 (95% CI 0.78-0.82, p < 0.001; Kendall's c-tau: 0.28, p < 0.001). Bland-Altman plots of estimated free calcium and free calcium showed a mean difference of - 0.0006 mmol/L (LOA + 0.126 to - 0.124). In validation cohort, the AUC-ROC curves for hypercalcemia and hypocalcemia diagnosis deploying the new equation were 0.88 (95% CI 0.86-0.89, p < 0.001) and 0.98 (95% CI 0.97-99, p < 0.001), respectively, which were superior to historical formulas for calcium. In univariate models, eGFR was associated with Ca-status misdiagnosis, yet this association disappeared when analysis was adjusted to phosphate and CO2. CONCLUSIONS: The novel equation proposed for prediction of free calcium could be useful when free calcium is not available. The conventional formulas misclassify many patients, in particular when phosphate or bicarbonate disturbances are present.