Although dysphagia occurs in all patients in the early postoperative period following fundoplication, the majority of patients are able to swallow normally at late follow-up. A small number of patients experience dysphagia which is persistent and sufficiently severe to require further operative intervention.

Our attitude is to carefully monitor patients during the first 3 months, with a careful evaluation of the evolution of dysphagia and weight monitoring. Endoscopic dilation is proposed in the case of severe grade dysphagia. It is repeated in the case of partial response. Persists of dilatation, dysphagia recurs quickly, a new radiological assessment is carried out looking for any expansion of the lower esophagus, and persisting narrowing of the GEJ, which testifies to the importance of the obstacle to the evacuation. If this is the case, a re-intervention is programmed. The most common causes of this complication are a tight closure of the pillars of the diaphragm, or a too-tight valve. If there is no sign of suffering of the esophagus and the state of nutrition is maintained, the conservative attitude can be continued on the basis of the importance of discomfort described by the patient. A fairly common cause of this persistent dysphagia, without worrying radiological sign, is the “twisted” fundoplication. This technical error is usually associated with the technique of Nissen without mobilization of gastric fundus and consists in a phenomenon of rotation (twist) of the esophagus on its axis, caused by a tension of the gastric fundus. Response to dilatation is usually very low, and reoperation is habitually necessary.

The later onset of dysphagia in the postoperative course is usually caused by an anatomical change of the antireflux mechanism, the valve and/or the cruroplasty. Usually these anatomical abnormalities are easily detected by radiology or endoscopy. Intrathoracic migration of the valve, slippage of the valve on the stomach, diaphragmatic fibrosis and paraesophageal hernia are the most common causes, and all can be corrected only by a surgical approach [41–44].

The normal mechanism of ventilation of the stomach occurs mainly during transient relaxations of LES, not associated with swallowing. They are caused by gastric distension which provokes a vagovagal reflex leading to a steep drop in the pressure of the LES [45]. Concomitantly, coordinated events inhibit the contraction of the pillars of the diaphragm and cause a longitudinal contraction of the esophagus and aboral displacement of the LES. This mechanism may overcome the gastric valve effect and allow draining air through the GEJ. Fundoplication, essentially ensuring the length of the subdiaphragmatic zone of high-pressure, reduces cranial displacement and relaxation of the LES in response to axial stretch and vagal nerve stimulation [19], thereby air venting. Both partial and 360° fundoplication alter the belching pattern by reducing gastric belches and increasing supra-gastric belches [46]. The first serve to vent ingested air from the stomach, whereas the latter are esophageal belches that do not allow air ventilation from the stomach. Consequently, fundoplication reduces air venting, which causes gas-related symptoms. Postoperative gas-related symptoms are demonstrated to be common after fundoplication.

The so-called gas bloat syndrome is characterized by abdominal bloating, epigastric pain, and difficulty belching. Frequent bowel movements and excessive flatus may be related symptoms. In the long-term, decreased belching ability, increased rectal flatulence and bloating were reported by up to 70, 95.5, and 79.2 % patients, respectively [47]. However, there is a very high variability in the definition and how to quantify this problem. In addition, incidence of post-fundoplication symptoms should be compared with the preoperative incidence of the same symptoms. “Wind-related” symptoms may appear, improve or disappear following laparoscopic fundoplication, confirming that some of these symptoms are part of the spectrum of reflux symptomatology [48–51]. In a recent randomized trial comparing Nissen fundoplication and medical therapy, bloating and flatulence were reported by 40 vs 28 %, and 57 vs 40 %, respectively [52]. In a similar randomized trial, heartburn, regurgitation, and belching were reported less frequently in the group randomized to surgery than among those randomized to medication, with no significant differences in ‘difficulty swallowing,’ ‘wind from the bowel,’ and nausea [51]. Moreover, some patients with gastro-esophageal reflux develop the habit of air-swallowing [48]. This entails subconscious repetitive swallowing, presumably in response to the regurgitation of gastric content into the esophagus. Long-term sequential follow-up study demonstrated a significant reduction in the incidence of dysphagia and flatulence, in contrast to the results for abdominal bloating [6]. There was no significant difference in the incidence of side effects between partial and total fundoplication [6, 53].

Some authors suggest that the relative risk of one of these problems occurring is in part determined by the type of fundoplication performed. The incidence of these side effects are discordant, some reporting lower rates for partial fundoplication, others reporting similar rates [6, 40, 46, 54]. The rates of inability to belch (7.8 vs. 15.7 %) and gas bloating (22.5 vs. 35.9 %) by a recent meta-analysis comparing 270° and 360° fundoplication [40, 55] and the prevalence of increased flatulence were also similar to the results of the only randomized trial that compared increased flatulence after 270° and 360° LPF (67.2 vs. 74.6 %) [47]. Long-term follow-up of partial anterior vs Nissen did not demonstrate any difference after 10–15 years [6, 56].

Despite this disparity in reports, the treatment of “wind-related” side effects, when troublesome for the patient, is difficult. Implementing changes in diet and allowing sufficient time for “wind-related” symptoms to improve will result in a satisfactory outcome in many patients.

There are few published reports describing the outcome of endoscopic or surgical revision primarily for troublesome “wind-related” side effects. Indication for surgical redo is considered in 4–5 % of patients [42, 57]. Conversion to a lesser degree of fundoplication was associated with a good outcome in the small numbers of patients in one study [58]. These results were not confirmed in others reports [44, 59].

Early satiety, nausea, vomiting and bloating and diarrhea are recognized side effects of anti-reflux surgery.

They can be part of the gas-bloat syndrome, resulting from the inability to vent gas from the stomach to the esophagus, they can also be caused by alterations in gastric emptying or result from vagal injury. Gastric emptying becomes normal or accelerated after surgery in the majority of patients with symptoms suggesting a delay in gastric emptying (20–40 % of patients with GERD) [60–62]. Yet, if severe, this delay may contribute to reflux or promote reflux disease and was identified as a factor for unsatisfactory results after antireflux surgery [63]. Some surgeons combine fundoplication with gastric drainage, commonly pyloroplasty, when pathological delayed gastric emptying has been objectified [64–66]. Postoperative gastroparesis can also be caused by eso-gastric surgery (19 %) and vagal damage [67]. Actual incidence of vagal damage after antireflux surgery is completely unknown [68]. Vagus dysfunction, measured indirectly by the response of plasma PP to insulin-induced hypoglycemia, has been identified in 10 % of patients after partial fundoplication, without impact on gastric emptying and symptomatology [60, 68]. The vast majority of patients show signs of gastroparesis during the first 3 to 6 months after surgery, in the form of early satiety, bloating, and flatulence. After 1 year, these symptoms have improved 90 % of the patients [69]. The finding of postoperative symptoms suggesting delayed gastric emptying among patients with antireflux operations followed for >1 year was usually associated with delayed gastric emptying pre-operatively [70]. The impact of vagal dysfunction/injury on the side effects can be extrapolated from the experience of reoperation after failed fundoplication/recurrent hiatal hernia. Indeed, redo procedures require extensive dissection at the gastroesophageal junction due to major anatomic disturbances and may lead to vagal nerve injury. In this particular context, delayed gastric emptying appears not as a significant complication [42, 57]. Moreover, uni- or bilateral vagotomy is performed by some surgeons to increase the length of the esophagus in case of short esophagus. No impact on gastric emptying was observed in a series of 150 patients operated for complex para-esophageal hernias and hiatal hernia recurrence [71].

The primary objectives in gastroparesis treatment are decreasing symptoms and improving nutrition. The severity of gastroparesis dictates management. Mild to moderate gastroparesis can be managed medically with dietary modifications, nutritional supplements, pro-motility agents, and anti-emetics.

A spasm of pylorus may be the cause of gastroparesis. Endoscopic treatment (dilatation balloon or intrasphincteric injection of botulinum toxin) can be discussed. Pneumatic dilation results remain uncertain. In addition, studies did not highlight clear therapeutic benefit of intrasphincteric injection of botulinum toxin [72]. Gastric electrical stimulation demonstrated significant subjective and objective improvement up to 10 years after device placement in patients with severe gastroparesis [73].

Surgical indications remain exceptional. In major gastric stasis, with daily symptoms and important nutritional impact, a surgical treatment should be discussed only when all other options have failed. If the motor disorder is strictly limited to the stomach, partial or subtotal gastrectomy may be considered [74].

New onset diarrhea may occur in up to 33 % of post-fundoplication cases and is typically mild, low in volume, and worse after meals [75, 76]. The cause of post-fundoplication diarrhea is thought to be a result of vagal injury, small bowel bacterial overgrowth, rapid gastric emptying, and reduced gastric relaxation or exacerbation of underlying irritable bowel syndrome, and attributing diarrhea to a specific etiology can be quite difficult. Reports noted that as many as 33–66 % of patients who underwent antireflux surgery had pre-existing irritable bowel syndrome and stressed the value of obtaining a comprehensive preoperative gastrointestinal history in patients undergoing laparoscopic antireflux surgery [75, 77]. Diarrhea responds favorably to antimotility drugs, antibiotics for small bowel overgrowth, or cholestyramine [67]. Severe or uncontrollable diarrhea occurred in the minority of patients [78]. Surgical procedures should be reserved for patients presenting with complex clinical situations, mixing gas-bloating, altered gastric emptying or dumping syndrome, in whom medical treatment fails [77, 78].