BackgroundAn inguinoscrotal hernia is defined as “giant” if descending below the midpoint of the inner thigh of a patient in upright position. In developed countries this is a rare entity. In the literature different surgical techniques have been reported so far to achieve a successful treatment.Case presentationWe present the case of a 63 year-old man suffering from a giant inguinoscrotal hernia, whom we treated using a combined open transabdominal and inguinal approach following an unsuccessful laparoscopic attempt. Meshes were placed in a premuscular position (Lichtenstein’s procedure) and in a preperitoneal position. In addition, a reconstruction of the abdominal wall by modified components separation technique was performed. During the early postoperative period no complications were registered. Intensive care treatment was not necessary. The patient was discharged on postoperative day 8 in an excellent condition. Six months after surgery a scrotal hematocele was diagnosed and operatively removed. After a follow-up of 1.5 years neither hernia recurrence, nor chronic groin pain were recorded. The patient reported to be sexually active. His quality of life improved notably.Additionally, a Medline and PubMed database research was performed to create an overall picture of the existing surgical treatment strategies. Included were patients with diagnosis of primary giant inguinoscrotal hernia according to the given definition. Emergency interventions and cases without details of the surgical approach were excluded.ConclusionsFirstly, this report describes a novel, successful surgical treatment of a giant inguinoscrotal hernia without administering preoperative progressive pneumoperitoneum therapy or visceral resection. Secondly, we summarize cases previously reported as a practical guide for possible surgical therapy approaches.

Background: Intraoperative nerve monitoring (IONM) of the recurrent laryngeal nerve (RLN) predicts the risk of vocal cord palsy (VCP). IONM can be used to adapt the surgical strategy in order to prevent bilateral VCP and associated morbidity. Controversial results have been reported in the literature for the effect of IONM on rates of VCP, and large multicentre studies are required for elucidation. Methods: Patients undergoing first-time thyroidectomy for benign thyroid disease between May 2015 and January 2019, documented prospectively in the European registry EUROCRINE ® , were included in a cohort study. The influence of IONM and other factors on the development of postoperative VCP was analysed using multivariable regression analysis. Results: Of 4598 operations from 82 hospitals, 3542 (77⋅0 per cent) were performed in female patients. IONM was used in 4182 (91⋅0 per cent) of 4598 operations, independent of hospital volume. Postoperative VCP was diagnosed in 50 (1⋅1 per cent) of the 4598 patients. The use of IONM was associated with a lower risk of postoperative VCP in multivariable analysis (odds ratio (OR) 0⋅34, 95 per cent c.i. 0⋅16 to 0⋅73). Damage to the RLN noted during surgery (OR 24⋅77, 12⋅91 to 48⋅07) and thyroiditis (OR 2⋅03, 1⋅10 to 3⋅76) were associated with an increased risk of VCP. Higher hospital volume correlated with a lower rate of VCP (OR 0⋅05, 0⋅01 to 0⋅13). Conclusion: Use of IONM was associated with a low rate of postoperative VCP.

Purpose Thyroid nodules in the pediatric population are more frequently associated with malignant thyroid disease than in adult cohorts. Yet, there is a potential risk of surgical overtreatment. With this single center study, an analysis of potential overtreatment for suspected malignant thyroid disease in children and young adults was aimed for. Methods In a period from 2005 to 2018, 155 thyroid operations in children and young adults performed at the University Medical Center Mainz, Germany, were analyzed (patient age 3-20 years, 117 female). Cases were categorized for preoperative diagnosis: non-malignant (group I, n = 45) and malignant thyroid disease (group II, n = 110). Postoperative parameters (histology, complication rates) were assessed and compared between groups. Results 91.1% of group I were histologically benign. 44.5% of group II harbored malignancy. Permanent hypoparathyroidism was documented in group I (2.7%) and in group II (1.4%, p = 1.000). Wound infections were absent in group I but observed in group II (0.9%, p = 1.000). Transient vocal cord palsy was recorded only in group I (2.3%, 2/85 vs. 0/177 nerves at risk, p = 0.104). Permanent vocal cord palsies were absent. Conclusion Preoperative diagnoses were correct in over 90% of group I and in nearly 45% of group II. The high proportion of carcinomas in group II ruled out the issue of potential overtreatment. The risk of severe postoperative complications was equally low in both patient groups.

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Cholinergic regulation of arterial luminal diameter involves intricate network of intercellular communication between the endothelial and smooth muscle cells that is highly dependent on the molecular mediators released by the endothelium. Albeit the well-recognized contribution of nitric oxide (NO) towards vasodilation, the identity of compensatory mechanisms that maintain vasomotor tone when NO synthesis is deranged remain largely unknown in the ophthalmic artery. This is the first study to identify the vasodilatory signalling mechanisms of the ophthalmic artery employing wild type mice. Acetylcholine (ACh)-induced vasodilation was only partially attenuated when NO synthesis was inhibited. Intriguingly, the combined blocking of cytochrome P450 oxygenase (CYP450) and lipoxygenase (LOX), as well as CYP450 and gap junctions, abolished vasodilation; demonstrating that the key compensatory mechanisms comprise arachidonic acid metabolites which, work in concert with gap junctions for downstream signal transmission. Furthermore, the voltage-gated potassium ion channel, Kv1.6, was functionally relevant in mediating vasodilation. Its localization was found exclusively in the smooth muscle. In conclusion, ACh-induced vasodilation of mouse ophthalmic artery is mediated in part by NO and predominantly via arachidonic acid metabolites, with active involvement of gap junctions. Particularly, the Kv1.6 channel represents an attractive therapeutic target in ophthalmopathologies when NO synthesis is compromised.