14 research outputs found

    Spleen volumetry and liver transient elastography: Predictors of persistent posthepatectomy decompensation in patients with hepatocellular carcinoma

    No full text
    International audienceBackground Posthepatectomy decompensation remains a frequent and poor outcome after hepatectomy, but its prediction is still inaccurate. Liver stiffness measurement can predict posthepatectomy decompensation, but there is a so-called “gray zone” that requires another predictor. Because splenomegaly is an objective sign of portal hypertension, we hypothesized that spleen volumetry could improve the identification of patients at risk. Methods Patients with hepatocellular carcinoma who underwent hepatectomy in our tertiary center between August 2014 and December 2017 were reviewed. The primary endpoint was to determine if the spleen volumetry and liver stiffness measurement were independent predictors of posthepatectomy decompensation, and secondarily, to determine if they were synergistic through a theoretic predictive model. Results One hundred and seven patients were included. The median follow-up time was 3 months (3–5). Postoperative 90-day mortality was 4.7%. By multivariate analysis, liver stiffness measurement and spleen volumetry predicted posthepatectomy decompensation. The liver stiffness measurement had a cutoff point of 11.6 kPa (area under receiver operating curve = 0.71 confidence interval 95% 0.71–0.88, sensitivity 89%, specificity 47%). The spleen volumetry cutoff point was 381.1 cm3 (area under receiver operating curve = 0.78, 95% confidence interval 0.77–0.93, sensitivity 55%, specificity 91%). The spleen volumetry improved prediction of posthepatectomy decompensation, because use of the spleen volumetry increased sensitivity (from 62% to 97%) and the negative predictive value (from 96% to 100%) along with a negligible decrease in specificity (from 96.7 to 93.4) and positive predictive value (from 64% to 59%) (P = .003). Conclusion Spleen volumetry (andgt;380 cm3) and liver stiffness measurement (andgt;12 kPa) are non-invasive, independent, and synergistic tools that appear to be able to predict posthepatectomy decompensation. The importance of this finding is that these measurements may help to anticipate posthepatectomy decompensation and may possibly be used to direct alternative treatments to resection. © 2020 Elsevier Inc

    Efeito da hidrocortisona sobre a lesão de reperfusão e reparação da mucosa após isquemia venosa experimental no jejuno de eqüinos Effect of hydrocortisone on reperfusion injury and on mucosal repair after experimental venous ischemia in the equine jejunum

    No full text
    Os efeitos do succinato sódico de hidrocortisona (SSH) nas lesões de isquemia e reperfusão no jejuno foram estudados em 12 eqüinos submetidos a isquemia total arteriovenosa e venosa no jejuno. Após uma hora de isquemia, seis eqüinos receberam 4,0mg/kg/IV de SSH (grupo T) e os demais receberam placebo (grupo NT). Foram colhidas amostras para avaliação histomorfológica após uma e duas horas de isquemia e uma, duas e 12 horas de reperfusão, sendo as alterações quantificadas por meio de escores. Os escores para infiltração de neutrófilos, edema e hemorragia foram equivalentes entre os grupos T e NT. No segmento submetido a isquemia venosa o agravamento da lesão na mucosa durante a reperfusão foi significativo (P<0,05) apenas no grupo NT, indicando que o SSH atenuou a lesão de reperfusão no jejuno. Após 12 horas de reperfusão os escores para lesão na mucosa na isquemia arteriovenosa foram equivalentes entre os grupos T e NT. Na isquemia venosa os escores foram significativamente menores no grupo T (P<0,01), indicando que o tratamento com SSH acelerou a reparação das lesões. Estes resultados indicam que o SSH pode ser utilizado como tratamento adjuvante de afecções isquêmicas e de reperfusão no eqüino.<br>In order to evaluate the effect of hydrocortisone sodium succinate (HSS) for treatment of intestinal ischemia-reperfusion, 12 halothane-anesthetized horses were subjected to both venous and arteriovenous ischemia of the jejunum. After one hour of ischemia, HSS (4.0 mg/kg/IV) was administered to six animals (T group). The other six horses received saline (NT group). Biopsy specimens were obtained after one and two hours of ischemia, and one, two and 12 hours after reperfusion. These samples were evaluated to assess the degree of mucosal damage and infiltration of neutrophils, hemorrhage, and edema. The scores for neutrophil infiltration, edema and hemorrhage did not differ between T and NT groups in both models of ischemia. However, in the jejunum subjected to venous ischemia, the scores for mucosal lesion increased significantly (P<0.05) after two hours of reperfusion only in the NT group, indicating that HSS prevented reperfusion injury. The scores for mucosal damage were equivalent after 12 hours of reperfusion following arteriovenous ischemia in T and NT groups. In contrast, mucosal lesion due to venous ischemia were more severe in the NT group (P<0.01), indicating that intestinal repair was stimulated by HSS. These results indicate that HSS may be used as an adjuvant for treatment of intestinal isquemia and reperfusion lesions in the horse
    corecore