Type IV paraesophageal hiatal hernias are rare but carry a significant risk of life-threatening complications, including gastric volvulus, incarceration, and the involvement of other intra-abdominal organs. Pancreatic herniation and associated pancreatitis are exceedingly uncommon. We report the case of a 74-year-old woman with Barrett's esophagus, chronic obstructive pulmonary disease (COPD), and obesity who presented with nausea, vomiting, and abdominal pain after a recent increase in the dose of tirzepatide. Imaging demonstrated a massive type IV paraesophageal hernia with organoaxial gastric volvulus. Initial laparoscopic reduction was aborted due to dense adhesions and a foreshortened esophagus. She subsequently developed progressive herniation involving the stomach, colon, and pancreatic body and tail, and ultimately underwent delayed robotic-assisted repair. The patient's postoperative course was complicated by multiple recurrences, including episodes of volvulus, duodenal obstruction, and mild pancreatitis. She ultimately required open repair with mesh reinforcement and gastropexy after unsuccessful endoscopic detorsion. Despite temporary improvement, she later developed recurrent herniation and severe gastroparesis, likely secondary to injury to the vagal nerve. This report highlights the complexity of managing massive type IV paraesophageal hernias, particularly with multi-organ involvement and recurrence. Even with advanced surgical approaches, recurrence and long-term complications remain significant challenges.

Interstitial cells of Cajal (ICC) regulate gastrointestinal motility by generating electrical slow waves that orchestrate downstream calcium (Ca[2] [+]) waves and coordinate smooth muscle contractions. A reduced ICC number has been reported in diabetic gastroparesis patients and in mouse models of delayed gastric emptying (DGE). However, functional changes in ICC propagating across the gastric regions in intact stomach are not well understood. The aim of this study was to develop an imaging approach to visualize ICC Ca[2+] waves in mouse stomach and determine spatiotemporal changes in mice with DGE. Tamoxifen-treated B6.GCaMP5-KitCreERT2 female mice were used as non-diabetic controls (Non-Db), while mice treated with streptozocin to induce diabetes were categorized as having normal (Db-NGE) or delayed (Db-DGE) gastric emptying based on emptying of solids. The ICC Ca[2+] network was imaged from excised intact mouse stomachs and subsequently opened along the lesser curvature and pinned flat. ICC Ca[2+] waves typically propagated along the greater curvature from the fundus-corpus line toward the antrum. The propagation length of ICC Ca[2+] activity was significantly decreased in Db-DGE compared to Non-Db and Db-NGE and correlated to longer GE times. There was also a decrease in frequency, and the velocity was significantly faster in stomachs from Db-DGE compared to Non-Db and Db-NGE. All experimental groups exhibited similar proportions of aberrant Ca[2+] propagation patterns (e.g., retrograde waves), but ectopic initiation only occurred in Db-DGE stomachs. Thus, DGE is possibly driven by dysfunction in Ca[2+] activity in the ICC network that propagates rapidly over short distances, resulting in uncoordinated, non-phasic muscle activity. KEY POINTS: Dysfunction of the interstitial cells of Cajal (ICC) has been implicated in diabetic gastroparesis but the changes in spatiotemporal properties of ICC network activity are not known. We developed an ex vivo Ca[2+] imaging approach to visualize ICC network activity across the entire stomach and determined changes in ICC Ca[2+] activity in a diabetic mouse model of delayed gastric emptying (GE). Decreased frequency and increased velocity of ICC Ca[2+] activity was observed in stomachs of diabetic mice with delayed GE. Ectopic initiation was a key feature associated with delayed GE. The propagation length of ICC Ca[2+] activity was inversely correlated to GE times and significantly reduced in stomach preparations from diabetic mice with delayed GE.

Despite the availability of drugs which prevent vomiting, treatment gaps in controlling nausea and vomiting remain. New approaches are needed.

A Belgian Malinois dog developed advanced gastroparesis with gastric atony and progressive dilatation following surgical correction of gastric dilatation-volvulus. Following gastric dilatation-volvulus, the dog developed recurrent gastric distension, vomiting of undigested food and progressive weight loss. Imaging and endoscopy demonstrated a markedly enlarged, static stomach with a patent pylorus, refractory to prokinetic therapy. Exploratory laparotomy revealed global gastric atony, and a radical sleeve-type gastrectomy was performed. Histopathology identified interstitial fibrosis and sparsely distributed nerve plexuses. Although delayed gastric emptying persisted postoperatively on barium contrast study, the dog regained weight, tolerated liquid meals and remained clinically stable without further vomiting or dilatation at 12 months follow-up. Severe gastroparesis with chronic gastric dilatation can occur as a delayed complication of gastric dilatation-volvulus, likely related to truncal vagal injury. Sleeve-type gastrectomy might represent a salvage option for dogs with end-stage, medically refractory gastric atony.

Gastroparesis is a chronic gastrointestinal disorder characterized by delayed gastric emptying, often presenting with symptoms including nausea, vomiting, early satiety, and abdominal pain. Moreover, studies demonstrate higher rates of psychological distress among individuals with gastroparesis, compared with the general population; increasing evidence suggests that anxiety and depression contribute to symptom severity, reduced quality of life, and poorer treatment outcomes. Potential mechanisms underlying this seeming association include dysregulation of the gut-brain axis and the psychosocial burden of living with a chronic illness. Thus, this contemporary, mini review aims to integrate some current literature on the prevalence, pathophysiology, and clinical implications of anxiety and depression in patients with gastroparesis.

Delayed complications may occur up to weeks after atrial fibrillation (AF) ablation and are usually a consequence of initial injury during ablation and ongoing processes progressing to severe symptomatic but late-onset events. A structured clinical follow-up of patients to appraise for late complications is therefore imperative for all centers performing AF ablations. Late complications should also be reported when testing new ablation technologies. Red flag symptoms like fever, neurological events, and syncope but also delayed onset thoracic pain, dyspnea, exercise intolerance or gastrointestinal symptoms within the first months after AF ablation should trigger standardized diagnostic testing to evaluate for complications like esophageal injury/esophagoatrial fistula, gastroparesis, pulmonary vein stenosis (can become symptomatic even later), diaphragmatic paralysis, or late pericarditis/pericardial effusion. Whereas severe late complications are rare, the remote onset of associated symptoms warrants a high degree of awareness of all medical disciplines involved in the follow-up and also on the patient side to assure appropriate management without further delay. Indicative symptoms, incidences, and standardized management workflows for late complications like esophagoatrial fistula, gastroparesis, pulmonary vein stenosis, phrenic nerve injury/diaphragmatic palsy, and late pericarditis/pericardial effusion are discussed. Different imaging modalities have been used to clarify diagnosis and clinical relevance of these complications. Treatment options may range from wait-and-watch to emergency surgical interventions.