Esophageal Calibration with Soft Orogasrtric Tube During Laparoscopic Nissen Fundoplication may Reduce Postoperative Transient Dysphagia

Gastroesophageal reflux is the most common benign disorder of the esophagus and laparoscopic Nissen fundoplication has become the standard surgical treatment for its treatment. In our area, where the use of bougie calibration is debatable, postoperative dysphagia is encountered often after this surgery although it is usually not permanent. The aim of this study was to investigate the effect of using a soft silicone tube 39 F in diameter for esophageal calibration during laparoscopic Nissen fundoplication on the incidence of postoperative dysphagia. We divided cases scheduled to undergo laparoscopic Nissen fundoplication between January 2009 and November 2010 into two groups, each consisting 25 patients. Esophageal calibration with a 39 F silicone orogastric tube was used for the first group while there was no operative calibration in the second group. The surgical duration was recorded; the presence and severity of the postoperative dysphagia was calculated by using a dysphagia severity scoring system during the 1-year postoperative follow-up. The dysphagia severity scores were significantly lower in group 1 than group 2 on the postoperative second day and at the end of the first week and first month. We did not find a significant difference at the end of the 6-month and first year. There was also no significant difference regarding surgery duration. The use of a soft orogastric tube 39 F in diameter for esophagus calibration during laparoscopic Nissen fundoplication has significantly decreased the incidence of postoperative transient dysphagia without affecting the duration of surgery. Although dysphagia gradually resolves in the majority of patients, a safe and easy calibration method for its prevention is worth developing, and we believe that the use of our method in larger series could be beneficial.     

Preoperative scoring system for predicting early adjacent vertebral fractures after Balloon Kyphoplasty

BackgroundAdjacent vertebral fracture (AVF) is a major complication following Balloon Kyphoplasty (BKP). There is no scoring system for predicting AVF using only preoperative elements. The purposes of this study were to develop a scoring system for predicting early AVF after BKP based on preoperative factors and to investigate the appropriate surgical indication for BKP.MethodsOf 220 patients who underwent BKP at a single institution since 2011, 65 patients over the age of 60 who had undergone a standing whole spine X-ray preoperatively were enrolled. Factors affecting the occurrence of early AVF were examined. A scoring system was created consisting of the factors exhibiting significant differences, and the correlation between the total score and the incidence of early AVF was investigated.ResultsTwenty of the 65 patients (30.8%) had early AVF. In a univariate analysis, age, previous vertebral fracture, pelvic tilt, and Local kyphosis significantly influenced early AVF. In a multivariate logistic regression analysis, age had an odds ratio of 1.136 (95% CI 1.001–1.289), previous vertebral fractures 4.181 (1.01–17.309), and Local kyphosis 1.103 (1.021–1.191). The scoring system was set as follows: ①Age (<75 years: 0 points(P), 75years≦: 1P), ②The number of previous vertebral fractures (0: 0 P, 1: 1P, 2: 2P, 3 or more: 3P), and ③Local kyphosis (<10°: 0P, 10°≦: 1P). There was a correlation between the total score and the incidence of early AVF (r = 0.812, 1P = 0.05). The incidence of early AVF was 6.4% (2 cases/31 cases) for a score of ≦1P and 54.5% (18 cases/33 cases) for a score of ≧2P.ConclusionsThere was a correlation between the total score and the incidence of early AVF. A score of 1 point or less may represent the appropriate surgical indication for BKP.     

An updated review on pathophysiology and management of burning mouth syndrome with endocrinological,psychological and neuropathic perspectives

Burning mouth syndrome (BMS) is a chronic oro‐facial pain disorder of unknown cause. It is more common in peri‐ and post‐menopausal women, and sex hormone dysregulation is believed to be an important causative factor. Psychosocial events often trigger or exacerbate symptoms, and persons with BMS appear to be predisposed towards anxiety and depression. Atrophy of small nerve fibres in the tongue epithelium has been reported, and potential neuropathic mechanisms for BMS are now widely investigated. Historically, BMS was thought to comprise endocrinological, psychosocial and neuropathic components. Neuroprotective steroids and glial cell line–derived neurotrophic factor family ligands may have pivotal roles in the peripheral mechanisms associated with atrophy of small nerve fibres. Denervation of chorda tympani nerve fibres that innervate fungiform buds leads to alternative trigeminal innervation, which results in dysgeusia and burning pain when eating hot foods. With regard to the central mechanism of BMS, depletion of neuroprotective steroids alters the brain network–related mood and pain modulation. Peripheral mechanistic studies support the use of topical clonazepam and capsaicin for the management of BMS, and some evidence supports the use of cognitive behavioural therapy. Hormone replacement therapy may address the causes of BMS, although adverse effects prevent its use as a first‐line treatment. Selective serotonin reuptake inhibitors (SSRIs) and serotonin and noradrenaline reuptake inhibitors (SNRIs) may have important benefits, and well‐designed controlled studies are expected. Other treatment options to be investigated include brain stimulation and TSPO (translocator protein 18 kDa) ligands.     

Feasibility and mid- to long-term results of endovascular treatment for portal vein thrombosis after living-donor liver transplantation

PURPOSEWe aimed to evaluate mid- to long-term results of endovascular treatment for portal vein thrombosis (PVT) after living-donor liver transplantation (LDLT).METHODSThirty cases (14 males, 16 females; age range, 0.67–65 years) who underwent endovascular treatment including thrombolysis, angioplasty, stent placement, and/or collateral embolization for PVT after LDLT from 2001 to 2017 were retrospectively reviewed. Clinical and procedural data were collected and analyzed regarding the patency of the PVT site at the last follow-up date (PVT-free persistency) using Log-rank test. Results were considered statistically significant at p < 0.05.RESULTSMedian follow-up was 120 months. The technical success rate was 80% (n=24). Patency rates at 1 week and 1, 3, 6, 12, 36, and 60 months were 73%, 59%, 55%, 51%, 51%, 51%, and 51% for primary patency and 80%, 70%, 66%, 66%, 66%, 61%, and 61% for assisted patency after secondary endovascular treatment. PVT-free persistency rates regarding the subgroups were as follows: children under 12 years vs. adults, 50% vs. 68% (p = 0.42); acute vs. nonacute, 76% vs. 46% (p = 0.10); localized vs. extensive, 90% vs. 50% (p = 0.035); transileocolic approach vs. percutaneous-transhepatic approach, 71% vs. 54% (p = 0.39); and thrombolysis-based treatment vs. non-thrombolysis-based treatment, 71% vs. 44% (p = 0.12), respectively. Among technically successful cases, PVT-free persistency rate was 94% for those with hepatopetal flow in the peripheral portal vein vs. 17% for those without hepatopetal flow (p < 0.001). The only major complication occurring was pleural hemorrhage (n=1). Minor complications (i.e., fever) occurred in 18 patients (60%).CONCLUSIONIn conclusion, mid- to long-term portal patency following endovascular treatment was approximately 50%–60% in PVT patients after LDLT. PVT site patency over three months after the first endovascular treatment, localized PVT, and hepatopetal flow in the peripheral portal vein were identified as key prognostic factors for mid- to long-term portal patency.

Portal vein thrombosis (PVT) is a vascular complication of living-donor liver transplantation (LDLT), with an estimated incidence of up to 4% (1, 2). The risk of vascular complications, including PVT, is higher in LDLT compared with conventional deceased-donor liver transplantation, because of the smaller vessels, insufficient vessel length for reconstruction, neointimal proliferation, and higher risk of twisting and kinking of the vascular pedicle (3) due to smaller graft size than in deceased-donor liver transplantation. PVT after LDLT can lead to graft failure and the need for retransplantation or death (2), making immediate treatment crucial.Endovascular-based treatment is one option for treating PVT. The utility of target-focused thrombolysis, balloon angioplasty, and stent placement to restore portal flow has been reported previously (4–10). However, the efficacy of endovascular treatment after LDLT has only been presented in some case reports (11, 12) and the mid- to long-term outcomes remain unclear.The purpose of this study was to evaluate the technical success, feasibility, and mid- to long-term results of endovascular treatment for PVT after LDLT in our institution.