What Happens in (the) Vagus, Stays in (the) Vagus.

Many cardiothoracic operations put the nerves of the thorax at risk. In fact, nerve injuries are one of the most common reasons cited in malpractice cases brought against cardiothoracic surgeons. While all physicians learn about the nerves of the thorax during anatomy courses in medical school, little is written about avoiding injury to these important nerves in the cardiothoracic surgical literature. We have, therefore, embarked on an effort to collate information on the anatomy, function, and protection of these nerves, with which every cardiothoracic surgeon should be familiar. We will call this effort "The Nerve Protection Project." Acknowledging that the material to be covered is considerable, we will break the project into a series of editorials. The first installment in this series will address the anatomy and function of the vagus nerve and the protection of this nerve and its branches during cardiothoracic surgical operations, as they are in harm's way during many of these procedures.

Impact of vagus nerve integrity testing on surgical management in patients with previous operations with potential risk of vagal injury.

BACKGROUND: Thoracic and foregut operations can cause vagal nerve injury resulting in delayed gastric emptying or gastroparesis. However, the cause of gastroparesis in these patients is not always from a vagal injury. We hypothesize that vagal nerve integrity (VNI) testing may better define who has vagal nerve dysfunction. This information may change subsequent operations. The aim of this study was to evaluate the impact of VNI testing in patients with prior thoracic or gastric surgery. METHODS: From January 2014 to December 2017, patients who had previous operations with the potential risk of vagal injury and had VNI testing were reviewed. Excluded patients were those with no plan for a second operation or the second operation was only for gastroparesis. The main outcome was the percentage of operations altered due to the results of VNI testing. RESULTS: Twelve patients (eight females) were included. Ages ranged from 37 to 77 years. VNI results were compatible with vagal injury in eight patients (67%). VNI test results altered subsequent operative plans in 41.7% (5/12). Pyloroplasty was done in addition to fundoplication in two patients. Plans for hiatal hernia repair with or without redo-fundoplication in three patients were changed by an additional pyloroplasty in one patient and partial gastrectomy with Roux-en-Y reconstruction in two patients. All patients who had secondary surgery had resolution of symptoms and improvement in objective testing. CONCLUSION: The addition of VNI testing in patients with a previous potential risk of vagal nerve injury may help the surgeon select the appropriate secondary operation.

Tapia's Syndrome.

More than 100,000 general anesthetic procedures are conducted in United Kingdom every year for dental interventions, according to large survey of the National Health Services. 1 The risk of mortality has reduced considerably in the past few decades because of the use of safe and effective techniques. However, adverse effects still exist and are dependent on patient, environmental, and operator factors. We present an uncommon complication of intubation that merits due awareness.

Gastric hypomotility after second-generation cryoballoon ablation-Unrecognized silent nerve injury after cryoballoon ablation.

BACKGROUND: Few data are available on gastric hypomotility (GH) after cryoballoon pulmonary vein isolation. Also, the use of esophageal temperature monitoring for the prevention of endoscopically detected esophageal lesions (EDELs) is not well established. OBJECTIVE: The purpose of this study was to investigate GH and the impact of an esophageal probe on EDELs during second-generation cryoballoon ablation. METHODS: One hundred four patients with paroxysmal atrial fibrillation undergoing second-generation cryoballoon ablation under conscious sedation followed by esophagogastroscopy were prospectively included. Temperature probes were used in the first 40 (38.5%) patients, but not in the latter 64 (61.5%). Pulmonary vein isolation was performed with one 28-mm balloon using single 3-minute freeze techniques. RESULTS: Clinical and procedural characteristics were similar between the groups. Esophagogastroscopy 1.4 ± 0.5 days postablation demonstrated GH and EDELs in 18 (17.3%) and 9 (8.7%) patients. The incidence of GH was similar (7 of 40 vs 11 of 64; P = .967) between the groups, while that of EDELs was significantly higher in the former than in the latter group (8 of 40 vs 1 of 64; P < .0001). In multivariate analyses, the esophagus-right inferior pulmonary vein ostium distance (hazard ratio 0.870; 95% confidence interval 0.798-0.948; P = .002) was the sole predictor of GH, and the optimal cutoff for the prediction was 18.2 mm (sensitivity 88.1%; specificity 77.8%). The use of esophageal probes was the sole predictor of EDELs (hazard ratio 15.750; 95% confidence interval 1.887-131.471; P = .011). All collateral damage was asymptomatic and healed on repeat esophagogastroscopy at a mean of 2 ± 1 months postprocedure. CONCLUSION: Second-generation cryoballoon ablation is associated with an increased incidence of silent periesophageal nerve injury even using short freeze times, and anatomical information aids identifying high-risk populations. The use of esophageal probes increases the risk of EDELs.

Effect of Vagus Nerve Integrity on Short and Long-Term Efficacy of Antireflux Surgery.

OBJECTIVES: Vagus nerve injury is a feared complication of antireflux surgery (ARS) that may negatively affect reflux control. The aim of the present prospective study was to evaluate short-term and long-term impact of vagus nerve injury, evaluated by pancreatic polypeptide response to insulin-induced hypoglycemia (PP-IH), on the outcome of ARS. METHODS: In the period from 1990 until 2000, 125 patients with gastroesophageal reflux disease (GERD) underwent ARS at a single center. Before and 6 months after surgery, vagus nerve integrity testing (PP-IH), 24-h pH-monitoring, gastric emptying, and reflux-associated symptoms were evaluated. In 2014, 14-25 years after surgery, 110 patients were contacted again for evaluation of long-term symptomatic outcome using two validated questionnaires (Gastrointestinal Symptom Rating Scale (GSRS) and GERD-Health Related Quality of Life (HRQL)). RESULTS: Short-term follow-up: vagus nerve injury (PP peak ≤47 pmol/l) was observed in 23 patients (18%) 6 months after fundoplication. In both groups, a comparable decrease in reflux parameters and symptoms was observed at 6-month follow-up. Postoperative gastric emptying was significantly delayed in the vagus nerve injury group compared with the vagus nerve intact group. Long-term follow-up: patients with vagus nerve injury showed significantly less effective reflux control and a higher re-operation rate. CONCLUSIONS: Vagus nerve injury occurs in up to 20% of patients after ARS. Reflux control 6 months after surgery was not affected by vagus nerve injury. However, long-term follow-up showed a negative effect on reflux symptom control and re-operation rate in patients with vagus nerve injury.

Effect of atrial fibrillation ablation on gastric motility: the atrial fibrillation gut study.

BACKGROUND: Collateral damage to the vagal nerve and the upper gastrointestinal (UGI) system during atrial fibrillation ablation has not been systematically evaluated. METHODS AND RESULTS: We performed a prospective, observational study assessing the effect of atrial fibrillation ablation on the function of the vagus nerve/UGI system. All patients underwent esophageal manometry, gastric emptying study, and sham-feeding test (corresponding to esophageal, gastric, and small intestinal function evaluation, respectively) before ablation (baseline) and subsequently at 24 hours, 90 days, and 180 days after the procedure. In addition, UGI symptom assessment using the patient assessment of upper gastrointestinal disorders-symptom severity index (PAGI-SYM) questionnaire was performed at baseline and during each of the subsequent evaluations. Of the 27 patients enrolled in the study, 9 (33%) patients had abnormal UGI function at baseline; defined as at least one of the 3 abnormal tests. At 24 hours after the radiofrequency catheter ablation, 20 (74%) patients had at least 1 new abnormality on the UGI function tests (P<0.001). New onset esophageal dysmotility, delayed gastric emptying time, and abnormal sham-feeding tests were observed in 13 (48%), 13 (48%), and 9 (33%) patients, respectively. Mean PAGI-SYM scores increased from 7.78±6.6 at baseline to 15.56±13.4 (P=0.002) at 24 hours. New onset abnormalities persisted in 9 (33%) patients at 3 months and normalized in all patients at 6 months. CONCLUSIONS: Atrial fibrillation ablation results in functional impairment of the UGI system, including the esophagus, stomach, and small intestine. This impairment is transient and is probably mediated by the injury to the components of the vagal nerve. CLINICAL TRIAL REGISTRATION: URL: http://clinicaltrials.gov. Unique Identifier: NCT01396356.

Glossopharyngeal nerve and vagus nerve palsies associated with influenza vaccination.

We herein report the first case of glossopharyngeal nerve and vagus nerve palsies that appeared after an influenza vaccination. A 15-year-old boy developed dysphagia and dysarthria seven days after receiving an inoculation of the inactivated influenza vaccine. Massive intravenous immunoglobulin (IVIg) treatment was applied, as the patient's symptoms were considered to be immunological adverse effects of the influenza vaccine. He responded well to IVIg, and the symptoms immediately diminished. The mechanisms underlying the development of neurologic symptoms following vaccination are difficult to determine; however, providing immediate immunological treatment, such as IVIg, is effective and beneficial in countering these symptoms.

Clinical characteristics and management of periesophageal vagal nerve injury complicating left atrial ablation of atrial fibrillation: lessons from eleven cases.

INTRODUCTION: This study aimed to elucidate the clinical characteristics and management of periesophageal vagal nerve injury complicating the ablation of atrial fibrillation (AF). METHODS AND RESULTS: A total of 3,695 patients with drug-resistant AF underwent extensive pulmonary vein isolation at our institution. Either a nonirrigated or an irrigated ablation catheter was employed, with radiofrequency power of 25-40 W. Esophageal temperature was monitored in 3,538 patients: when the esophageal temperature reached 42°C radiofrequency delivery was stopped. A total of 11 patients (60 ± 11 years, 10 males) were diagnosed as having a periesophageal vagal nerve injury after the AF ablation. Symptoms included nausea, vomiting, bloating, constipation, and gastric pain, which occurred within 72 hours after the procedure. Gastrointestinal fluoroscopy and/or endoscopy revealed gastric hypomotility (10 patients) and pyloric spasm (1 patient). Intravenous erythromycin (3 mg/kg every 8 hours) was effective in relieving symptoms in 5 patients, and the patient with pyloric spasm underwent esophagojejunal anstomosis. Eight patients almost fully recovered within 40 days; however, 3 patients suffered from severe symptoms for 3-12 months. This complication occurred in 4 of the 157 patients (2.5%) who did not have esophageal temperature monitoring, and 7 of the 3,538 (0.2%) who did (P = 0.0007). The 3 patients with persistent severe symptoms received no esophageal temperature monitoring. CONCLUSION: The clinical course and severity of the periesophageal vagal nerve injury varied, but most patients finally recovered with conservative treatment. Radiofrequency delivery under esophageal temperature monitoring might reduce both the incidence and the severity of this complication.

Observation of vocal fold and pharyngeal paralysis after carotid endarterectomy using a magnifying laryngoscope.

BACKGROUND: Injury to the vagus nerve or one of its branches during carotid endarterectomy (CEA) can result in vocal fold paralysis (VFP), but the exact mechanisms and site of injury responsible for VFP after CEA are unclear. The aim of this study was to identify the site of nerve injury in patients with VFP after CEA using magnifying laryngoscopy. METHODS: We performed 96 consecutive CEA procedures in 87 patients over 5 years. After 56 CEA procedures, we examined vocal fold movements with a flexible nasolaryngoscope and detected VFP in 5 of 40 cases (9 %). At 6-8 weeks after CEA, these five patients also underwent magnifying laryngoscopy at another institution by a specialist in vocalization. RESULTS: We confirmed ipsilateral VFP and pharyngeal paralysis in three patients. The other two patients recovered from their nerve injuries spontaneously before the magnifying examination. CONCLUSIONS: VFP and pharyngeal paralysis were caused by damage to the recurrent laryngeal and pharyngeal nerves. Therefore, the probable site of nerve injury during CEA was near the inferior vagal ganglion of the vagus nerve trunk in our three patients.

Vernet's syndrome after carotid endarterectomy.

Unilateral paresis of cranial nerves IX to XI is defined as Vernet's syndrome. We retrospectively assessed cranial nerve symptoms from the clinical records of 143 carotid endarterectomy patients. A flexible nasolaryngoscope was used to examine vocal fold movements in 73 patients. If vocal fold paresis (VFP) was confirmed, the patient also underwent magnifying laryngoscopy (for correct diagnosis of injury to the glossopharyngeal and vagus nerves). It was found from clinical records that 8 patients (6%) were confirmed to have cranial nerve symptoms corresponding to Vernet's syndrome; 7 patients (9 %) had VFP on nasolaryngoscopy. In 2 patients, magnifying laryngoscopy confirmed ipsilateral VFP, pharyngeal paresis, pharyngeal wall hypesthesia, and ipsilateral pharyngeal wall swelling. These 2 patients also had symptoms of injury to the accessory nerve. Damage to cranial nerves IX to XI probably occurred in the parapharyngeal space, based on the existence of posterior pharyngeal wall edema or swelling after carotid endarterectomy.