Gastric Function After Fundoplication




© Springer International Publishing Switzerland 2017
Christophe Faure, Nikhil Thapar and Carlo Di Lorenzo (eds.)Pediatric Neurogastroenterology10.1007/978-3-319-43268-7_31


31. Gastric Function After Fundoplication



Samuel Nurko 


(1)
Center for Motility and Functional Gastrointestinal Disorders, Children’s Hospital Boston, 300 Longwood Ave, Boston, MA 02155, USA

 



 

Samuel Nurko



Keywords
FundoplicationGastric accommodationRetchingChildrenGastric emptyingGastric dysfunction


Fundoplication is one of the most common operations performed in children [15]. It is a very successful operation to control gastroesophageal reflux, but it can be associated with significant postoperative symptoms that may limit its effectiveness [14, 68]. The problems and symptoms after fundoplication seem to cluster in two main types: (a) esophageal or (b) gastric [6]. In this chapter we focus mainly on describing gastric function after fundoplication, and therefore on the later symptoms.


Effect on Gastric Sensorimotor Function


Fundoplication reduces the volume of the stomach and uses most of the proximal stomach to create a wrap around the lower part of the esophagus that results in an increase in LES pressure and in the esophagogastric junction contractile integral of 26.3 % [2, 4, 5, 810]. The surgery can have a major impact on gastric function, and may explain some of the postoperative symptoms that can be encountered [11]. There have been a few studies that have evaluated gastric accommodation, sensation, and emptying in children and adults after fundoplication. Mousa et al. [5] studied gastric compliance and gastric sensory function before and after Nissen fundoplication in children. They performed barostat studies in 13 children before surgery and repeated the test after surgery in 8. After fundoplication, patients had significantly higher minimal distending pressure values, reduced gastric compliance, and significantly higher pain scores. These indicate that gastric compliance was reduced, and presumably that lead to stimulation of visceral afferents and the heightened perception they noted. Zangen et al. [12] showed that in 12/14 children there was a decrease in gastric volume capacity that produced retching.

Findings of abnormal gastric accommodation have also been reported in adults. In a case controlled study proximal gastric function was studied with the use of barostat in 12 adult patients that underwent fundoplication and compared with 12 controls [13]. They found that there was no difference between groups in compliance during fasting. However the adaptive relaxation in the fundoplication group was significantly less than that in controls after ingestion of a liquid meal [13]. They also showed that the fundal wrap is not afunctional and is still able to accommodate to pressure increments, that the stomach relaxation after a meal occurs normally, but that in the patients there was a decrease in receptive relaxation. Similar findings related to accommodation were reported by Vu et al. [14] who studied with a barostat 12 adult patients before and after Nissen fundoplication and compared the results with the findings on 12 healthy adults and 12 adults with GERD who did not undergo surgery. The sensation of fullness was increased in the postoperative patients. Again post-Nissen patients had normal compliance, but reduced postprandial gastric accommodation and accelerated gastric emptying.

Other less invasive methods that indirectly assess gastric function have also been used to study gastric function after surgery. By using single photon emission computed tomography with three-dimensional analysis, Bouras et al. [15] showed that patients post-fundoplication had a postprandial/fasting gastric volume ratio that was lower than in healthy controls, again suggesting impaired gastric accommodation. By using the water load test Remes-Troche et al. [16] found that asymptomatic subjects after surgery had higher scores for bloating, nausea, and abdominal pain compared to controls. They found that patients with dyspeptic symptoms after fundoplication had a significantly lower drinking capacity and higher symptoms scores than controls, including patients that were asymptomatic after fundoplication [16]. Their scores were similar than those of patients without surgery and functional dyspepsia, while the scores of asymptomatic fundoplication patients were similar than those of healthy controls [16].

Visceral hypersensitivity has been associated with abnormal gastric accommodation and hyperalgesia, and cofactors of this hypersensitivity are likely to be wall tension and the function of visceral afferents [17]. Therefore it is possible that patients who do not develop dyspeptic symptoms after fundoplication may have a nearly normal gastric function [16].

The exact mechanism by which these changes in accommodation occur is not clear. There may be alterations in the proximal gastric wall function, the abnormalities may be secondary to vagal dysfunction, or to the mechanical effects of the fundoplication per se [5, 8, 11, 18]. A recent meta-analysis showed that rates of adverse results involving dysphagia, gas-bloat syndrome, inability to belch, and reoperation due to severe dysphagia were significantly higher after laparoscopic Nissen as compared with Toupet fundoplication, suggesting the type of gastric manipulation has an effect on prognosis [1]. The proximal gastric wall seems to work normally as gastric compliance, tone and volume waves have been found to be normal [13, 14]. It is then possible that surgical manipulation itself could impair autonomic pathways affecting the gastric sensorimotor function and that changes in postprandial relaxation after reflux surgery could result from alterations in neurohormonal control [11, 18]. Vagal nerve function after fundoplication has been evaluated by using different methods. By using sham-feeding-stimulated pancreatic polypeptide (PP) test before and after surgery Devault et al. [18] showed that 5/12 with normal testing before the surgery developed evidence of vagal dysfunction after surgery. Interestingly here was no correlation between PP tests and the development or worsening of symptoms after surgery. In another study that evaluated vagal function by seeing PP response to insulin-induced hypoglycemia, Vu et al. found that 11 of their 12 patients responded normally [14]. Given the information described above it appears that the reduced gastric accommodation is probably mechanical in origin [13, 14].


Effects on Gastric Emptying


Patients with GERD frequently have delayed gastric emptying [14]. It has been reported that fundoplication may accelerate gastric emptying for both solids and liquids [13, 14, 19]. More rapid gastric emptying after the creation of a fundoplication is attributed to the loss of accommodation in the stomach, thereby preventing the fundus from expanding to contain the liquid portion of the meal [20]. An acceleration of gastric emptying after Nissen in children has not been consistently found. Mousa et al. [5] found no significant change in emptying for both solids and liquids after surgery, although their patients had normal emptying before the surgery.

A fast gastric emptying after surgery can produce some of the postoperative symptoms that can be encountered [4, 7, 18]. Diarrhea , which can occur in up to 18 % of patients [18], has been correlated with rapid gastric emptying. An exaggerated fast gastric emptying for liquids may produce dumping syndrome [4, 7, 18]. Even though this occurrence is more frequent when a pyloroplasty has been performed, it has been shown to occur also in children and adults in which no pyloroplasty was done. The pathophysiology of dumping syndrome in children is multifactorial, although its incidence and severity appear to be proportional to the rate of emptying [21]. Fonskalrud et al. [3] described a postoperative transient dumping syndrome in 0.9 % of 7467 fundoplications (0–5 %), and in a prospective study of 50 pediatric patients, Samuk et al. [22] reported dumping diagnosed by testing in 30 %. One of the main problems with dumping syndrome is the postprandial hypoglycemia. The mechanisms responsible for that are not fully understood but are thought to involve reduced postprandial gastric relaxation and accelerated emptying, resulting in the precipitous emptying of hyperosmolar, carbohydrate-containing solutions from the stomach into the upper small bowel [3] and subsequent hyperglycemia. Although the occurrence of postprandial hyperglycemia has been blamed for the later hypoglycemia, recent studies have suggested it is most likely related to abnormal glucagon release [23].


Effects on Antroduodenal Motility and Gastric Myoelectrical Activity


The effect of fundoplication on antroduodenal motility has not been clearly established. No prospective studies that have measured antroduodenal motility before and after fundoplication have been reported, but studies of children and adults with postoperative problems have shown abnormal antroduodenal motility [11, 12, 24]. In one study it was shown that 25 of 28 symptomatic children after fundoplication had abnormalities. The most common abnormality found was an absence of the migrating motor complex in 12, while 6 had postprandial hypomotility; other nonspecific abnormalities included clustered, retrograde and tonic contractions [24]. Similar motility abnormalities have been described in adults [11].

In another study of 14 patients with food refusal after fundoplication, an abnormal antroduodenal manometry was found in 9 patients, suggesting that abnormal motility after surgery does not occur in all patients with symptoms. Therefore, it is unclear if the abnormalities were present before the operation or are a result of it. Given that the abnormalities found were similar to those seen in chronic intestinal pseudo-obstruction, and that not all children with problems postoperatively have motility dysfunction, it is likely the abnormalities seen in children probably predated the operation, suggesting that those children had a more generalized gastrointestinal dysfunction, and not only gastroesophageal reflux. The presence of preoperative gastric myoelectric dysfunction has also been shown. Richards et al. measured gastric myoelectric activity before and after fundoplication with the use of surface electrogastrography in 27 children (17 neurologically impaired and 10 neurologically normal) [25]. They found abnormal gastric electrical activity before surgery in 65 % of the neurologically impaired as compared with 20 % of the neurologically normal group. After surgery an abnormal myoelectrical activity developed in 6 (3 in each group), and in 4 the study deteriorated.


Relation of Postoperative Symptoms to Gastric Dysfunction


It has been reported that up to a third of patients may develop symptoms after fundoplication [5]. The problems and symptoms after fundoplication seem to cluster in two main types: (a) esophageal or (b) gastric [6]. Symptoms commonly seen after antireflux surgery include dysphagia, inability to belch, early satiety, bloating, dyspepsia, gas-bloat syndrome, retching, pain, feeding refusal, diarrhea, and dumping [4, 7, 12, 18]. The cause of dysphagia is multifactorial and can often be corrected with esophageal dilation and occasionally repeated surgery [2, 7]. Loots et al. studied 10 children before and after fundoplication with gastric emptying, and esophageal manometry/impedance studies [2]. They found that peristaltic contractions were unaltered. Complete lower esophageal sphincter relaxations decreased after fundoplication (92 % [76–100 %] vs. 65 % [29–91 %], P = 0.038). Four (40 %) patients developed postoperative dysphagia, which was transient in 2. In those patients, preoperative gastric emptying was delayed compared with patients without postoperative dysphagia, 96 min (71–104 min) versus 48 min (26–68 min), P = 0.032 [2], again suggesting that abnormal gastric emptying may play a role [2].

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Aug 29, 2017 | Posted by in GASTROENTEROLOGY | Comments Off on Gastric Function After Fundoplication

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