An Unusual Murder: Vasovagal Death From Atypical Stabbing to the Neck.

Fatalities due to stabbings are usually caused by large blood vessels or organs injuries resulting in hemorrhagic shock. Vagal inhibition from a stab to the neck is an undeniably exceptional event, infrequently described in the literature. In our case report, we describe one such fatality.The body of a deceased 38-year-old man was found near a public garden. According to a bystander, the victim had been assaulted by 2 individuals, sustaining a stab wound to the neck with a broken glass bottle. At the autopsy, there was a large, inverted L-shaped cut wound in the left cervical region, measuring approximately 4.5 × 3 cm. The carotid artery and the jugular vein, as well as their main branches, were uninjured. The trachea and bronchi contained no exudate or blood. There was a hematoma near the trunk of the vagus nerve and its branches.The cause of death was attributed to the deep stab wound to the neck via vasovagal inhibition and parasympathetic nervous system stimulation.

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.

Attempt of peripheral nerve reconstruction during lung cancer surgery.

BACKGROUND: Vagus nerve and recurrent laryngeal nerve (RLN) injury are not rare complications of lung cancer surgery and can cause lethal consequences. Until now, no optimal method other than paying greater attention during surgery has been available. METHODS: Four patients underwent lung surgery that involved RLN or vagus nerve injury. The left RLN or vagus nerve was cut off and then reconstructed immediately during surgery. Two patients underwent direct anastomosis, while the remaining two underwent phrenic nerve replacing tension-relieving anastomosis. RESULTS: All patients were able to speak immediately after recovery. No or minimal glottal gap was observed during laryngoscopy conducted on the second day after surgery. Most patients achieved full recovery of voice quality. CONCLUSIONS: Immediate reconstruction of RLN is technically feasible and can be carried out with satisfying short-term and long-term outcomes.

Neurotrophin expression and laryngeal muscle pathophysiology following recurrent laryngeal nerve transection.

Laryngeal palsy often occurs as a result of recurrent laryngeal or vagal nerve injury during oncological surgery of the head and neck, affecting quality of life and increasing economic burden. Reinnervation following recurrent laryngeal nerve (RLN) injury is difficult despite development of techniques, such as neural anastomosis, nerve grafting and creation of a laryngeal muscle pedicle. In the present study, due to the limited availability of human nerve tissue for research, a rat model was used to investigate neurotrophin expression and laryngeal muscle pathophysiology in RLN injury. Twenty-five male Sprague-Dawley rats underwent right RLN transection with the excision of a 5-mm segment. Vocal fold movements, vocalization, histology and immunostaining were evaluated at different time-points (3, 6, 10 and 16 weeks). Although vocalization was restored, movement of the vocal fold failed to return to normal levels following RLN injury. The expression of brain­derived neurotrophic factor and glial cell line-derived neurotrophic factor differed in the thyroarytenoid (TA) and posterior cricoarytenoid muscles. The number of axons did not increase to baseline levels over time. Furthermore, normal muscle function was unlikely with spontaneous reinnervation. During regeneration following RLN injury, differences in the expression levels of neurotrophic factors may have resulted in preferential reinnervation of the TA muscles. Data from the present study indicated that neurotrophic factors may be applied for restoring the function of the laryngeal nerve following recurrent injury.

The role of vagal nerve root injury on respiration disturbances in subarachnoid hemorrhage.

AIM: We examined whether there is a relationship between vagal nerve root injury and the severity of respiration disorders associated with subarachnoid hemorrhage (SAH). MATERIAL AND METHODS: This study was conducted on 20 rabbits. Experimental SAH was induced by injecting homologous blood into the cisterna magna. During the experiment, electrocardiography and respiratory rhythms were measured daily. After the experiment, any axonal injury or changes to the arterial nervorums of the vagal nerves were examined. All respiratory irregularities and vagal nerve degenerations were statistically analyzed. RESULTS: Normal respiration rate, as measured in the control group, was 30 ± 6 bpm. In the SAH-induced group, respiration rates were initially 20 ± 4 bpm, increasing to 40 ± 9/min approximately ten hours later, with severe tachypneic and apneic variation. In histopathological examinations, axon density of vagal nerves was 28,500 ± 5,500 in both control and sham animals, whereas axon density was 22,250 ± 3,500 in survivors and 16,450 ± 2,750 in dead SAH animals. The severity of axonal degeneration of vagal nerves was greater in the six dead animals than in the survivors. CONCLUSION: If vagal nerves are lesioned, the muscles of respiration are paralyzed and respiratory reflexes are disrupted. That the ischemic and mechanical factors created by SAH cause vagal nerve root injury and respiration disorders may be inevitable and fatal.

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.

Longitudinal voice outcomes following laryngeal reinnervation via vagus-to-recurrent laryngeal nerve anastomosis after vagal nerve sacrifice: a case series.

OBJECTIVE: This study aimed to describe longitudinal voice outcomes of vagus-to-recurrent laryngeal nerve anastomosis following operative vagal nerve sacrifice. METHODS: Two patients who underwent anastomosis were assessed by a multidisciplinary voice team at 1, 4, 9, 12, and 18 months after vagal sacrifice. RESULTS: Long-term changes in voice function based on auditory perceptual measures of voice quality and visual perceptual changes in glottal closure were observed and maintained for 18 months after vagus-to-recurrent laryngeal nerve anastomosis in 2 patients with proximal vagal nerve sacrifice. Patients achieved acceptable voice outcomes and elected not to undergo further treatment, which was supported by Voice Handicap Index scores. CONCLUSION: Gradual restoration of voice following operative vagal sacrifice can be achieved over an 18-month period using vagus-to-recurrent laryngeal nerve anastomosis and warrants further investigation in appropriately selected patients.

Factors associated with periesophageal vagal nerve injury after pulmonary vein antrum isolation.

BACKGROUND: Periesophageal vagal nerve injury is recognized as a rare complication in atrial fibrillation ablation procedures. We investigated the factors associated with the occurrence of symptomatic periesophageal vagal nerve injury after pulmonary vein antrum isolation. METHODS AND RESULTS: Overall, 535 consecutive patients who underwent sole pulmonary vein antrum isolation were included. Point-by-point radiofrequency applications were applied using irrigated-tip catheters under minimal sedation without esophageal temperature monitoring. In the initial 165 patients, the ablation settings for the posterior left atrium were a maximum energy of 25 to 30 W and a duration of 30 seconds. In the subsequent 370 patients, the power was additionally limited to 20 to 25 W at specific parts of the posterior left atrium where the ablation line transversed the esophagus. Symptomatic gastric hypomotility was found in 13 patients, and all were observed during the initial period (7.9%). No other collateral damage was observed. Logistic regression analysis revealed that the body mass index was the only independent predictor for identifying patients with gastric hypomotility (odds ratio 0.770; 95% confidence interval 0.643 to 0.922; P=0.0045) during the initial period. The prevalence of gastric hypomotility was significantly higher in the initial study period than subsequently (0 of 370, 0%; P<0.0001). All except for 1 patient recovered completely with conservative treatment within 4 months after the procedure. CONCLUSIONS: Periesophageal vagal nerve injury is more common collateral damage than direct esophageal injury in pulmonary vein antrum isolation procedures. Titrating the radiofrequency energy at specific areas where the ablation line transverses the esophagus and taking account of the body mass index might reduce occurrences not only of direct esophageal damage but also of periesophageal vagal nerve injury in pulmonary vein antrum isolation procedures.

Anatomical factors associated with periesophageal vagus nerve injury after catheter ablation of atrial fibrillation.

BACKGROUND: The periesophageal vagus nerve plexus controls the kinetics of the stomach, digestive tract, and gallbladder, and catheter ablation of atrial fibrillation (AF) can cause vagus nerve injury (VNI). We sought to clarify the incidence, clinical course, and anatomical factors related to periesophageal VNI. METHODS: The present study included 257 consecutive patients with AF (mean age, 62±11 years) who underwent catheter-based pulmonary vein isolation. With 64-slice computed tomographic images, the left atrium (LA)-esophageal contact length, LA diameter, and distances between each mediastinal structure were compared between patients with VNI and those without VNI. RESULTS: VNI occurred in 5 patients (1.9%), gastric hypomotility in 3 patients, and acalculous cholecystitis in 2 patients, within 3 days after ablation, and all patients recovered completely within 2 weeks. Compared with patients without VNI, those with VNI more frequently underwent ablation at the mitral isthmus (p=0.03) and inside the coronary sinus (p=0.03). On computed tomographic images, the esophagus was closer to the aorta than to the spine in 67% of patients and was defined as an aorta-sided esophagus. In patients with VNI, the distance from the LA to the spine or the descending aorta (in patients with an aorta-sided esophagus) was shorter (p=0.03), and the transverse LA-esophageal contact length was longer (p=0.01). CONCLUSION: Acalculous cholecystitis, as well as gastric hypomotility, can develop as a result of periesophageal VNI in patients undergoing AF ablation. The anatomical relationships among the LA, esophagus, spine, and descending aorta may influence the occurrence of VNI.

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.