Although many surgical procedures originally associated with gastroparesis are less commonly performed nowadays, several more recently developed upper abdominal procedures may be complicated by the development of gastroparesis. Gastroparesis has been described in association with neurologic disorders ranging from Parkinson disease to muscular dystrophy, and its presence may have important implications for patient management and prognosis. Although scleroderma is most frequently linked with gastrointestinal motility disorder, gastroparesis has been linked to several other connective tissue disorders. The management of these patients presents several challenges, and is best conducted in the context of a dedicated and skilled multidisciplinary team.
Key points
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Fundoplication, bariatric procedures, and pancreatic surgeries are nowadays the surgical approaches most commonly complicated by gastroparesis.
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Virtually any neurologic disorder may be complicated by gastroparesis, and its development may affect nutrition and drug availability.
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Gastroparesis is a common feature of gastrointestinal involvement in scleroderma and other connective tissue disorders.
Postsurgical gastroparesis
Although acute gastroparesis may be a component of the ileus syndrome that can complicate many surgical procedures and of the acute pseudo-obstruction syndrome that may accompany severe sepsis and multiorgan failure, this review focuses on chronic manifestations of gastric dysmotility. In contrast to chronic gastroparesis, whose pathophysiology is often poorly understood, inflammatory processes seem fundamental to the inhibition of motility in the acute form.
Gastroparesis and other disorders of gastric sensorimotor function may complicate specific surgical procedures. In the important Olmstead County study of the community prevalence of gastroparesis, 7.2% of all cases of definite gastroparesis were related to prior gastrectomy or fundoplication. Rates of postsurgical gastroparesis vary widely depending on many factors, including the site and nature of the surgical procedure. For example, in their comprehensive review, Dong and colleagues noted that rates ranged from 0.4% to 5% following gastrectomy, from 20% to 50% after pylorus-preserving pancreaticoduodenectomy, and from 50% to 70% after cryoablation therapy for pancreatic cancer.
Vagotomy
Although vagotomy is infrequently performed nowadays in the management of acid-peptic disease, inadvertent vagal injury may complicate other interventions, rendering an understanding of the complex effects of vagotomy on gastric motor function still relevant. Receptive relaxation, a vagally mediated reflex, is impaired. As a consequence, the early phase of liquid emptying is accelerated. This acceleration causes rapid emptying of hyperosmolar solutions into the proximal small intestine and may result in the early dumping syndrome. By contrast, and as a consequence of impaired antropyloric function, the later phases of liquid and solid emptying are prolonged by vagotomy. Other motor effects of vagotomy include an impairment of the motor response to feeding (which contributes to the pathophysiologic mechanisms of postvagotomy diarrhea) and a suppression of the antral component of the migrating motor complex. The latter phenomenon is particularly prevalent among individuals who have symptomatic postvagotomy gastroparesis.
The now standard addition of a drainage procedure, such as a pyloroplasty or gastroenterostomy, has tended to negate the effects of vagotomy alone. In most patients, the net result of the combined procedure is little alteration in the gastric emptying of liquids or solids. Thus, prolonged postoperative gastroparesis (ie, lasting longer than 3–4 weeks) is, in fact, rare (<2.5% of patients after either vagotomy and pyloroplasty or vagotomy and antrectomy). Significant postoperative gastroparesis may occur, however, in patients who have a prior history of prolonged gastric outlet obstruction. In this circumstance, normal gastric emptying may not return for several weeks.
Longitudinal studies suggest that vagotomy-related gastroparesis tends to resolve over time, with one study suggesting gastric emptying rates in those who had undergone either a truncal or a highly selective vagotomy being similar by 12 months after the procedure.
Persisting postsurgical gastric motor dysfunction often presents a formidable management challenge. Therapeutic responses to prokinetic agents have proved particularly disappointing in this group. In these resistant cases, a completion gastrectomy may be the best alternative. It should be noted, however, that in one large series this approach was deemed successful in only 43% of patients.
Gastrectomy
Antral resection by removing the antral mill renders the stomach incontinent to solids and leads to accelerated emptying, and symptomatic “dumping” may occur in up to 50% of patients after Billroth I or II gastrectomy. Late dumping symptoms occur 90 to 120 minutes after a meal and are a consequence of reactive hypoglycemia. The accommodation reflex is impaired among symptomatic patients. By contrast, delayed gastric emptying sometimes occurs after a Billroth II gastrectomy as a result of a large atonic gastric remnant. Meng and colleagues reported a 6.9% frequency of gastroparesis among 563 patients who underwent radical gastrectomy for gastric cancer in their unit in Shanghai, China. Preoperative gastric outlet obstruction and the performance of a Billroth II anastomosis were the principal risk factors for the occurrence of gastroparesis. Of note, they documented a similar rate of gastroparesis (3.7%) among a smaller group of patients who underwent a laparoscopic gastrectomy. Laparoscopy-assisted, pylorus-preserving gastrectomy represents a less radical operative approach to early gastric cancer; gastric stasis is the most common complication of this procedure, occurring in 6.2% of cases. In one series, and in contrast to the aforementioned experience with this procedure following vagotomy, completion gastrectomy resulted in significant symptomatic improvement among subjects with postgastrectomy gastroparesis.
Roux-en-Y Syndrome
The creation of a Roux-en-Y gastroenterostomy may be associated with a specific clinical entity, the Roux syndrome. Severe symptoms of postprandial abdominal pain, bloating, and nausea many develop. Studies have variably described impaired gastric motor function and a functional obstruction within the duodenal Roux limb as a result of motor asynchrony. The latter can be revealed by manometry, but the status of these motility patterns in the pathophysiologic processes of this syndrome remains unclear.
Pancreatectomy
Pancreatectomy and pylorus-preserving pancreaticoduodenectomy, in particular, have been associated with a high incidence of postoperative gastric stasis. The principal predictor of gastric emptying delay after these operations is the occurrence of other postoperative complications. Operative technique seems, in general, to be of less importance, although there is a suggestion that an antecolic anastomosis may be associated with less emptying delay. Accordingly in what has been, perhaps, the largest series (N = 711) to date, Parmar and colleagues documented an overall rate of delayed gastric emptying following pancreaticoduodenectomy of 20%. The occurrence of gastroparesis did not seem to be influenced by such technical factors as pylorus preservation or whether the gastrojejunostomy was antecolic or retrocolic, but was associated with fistula formation, postoperative sepsis, and reoperation. These results contrast with those of a prior systematic review, which found that antecolic reconstruction was linked to lower rates of gastroparesis. Furthermore, others have suggested that the use of a Billroth II rather than a gastrojejunostomy for reconstruction following this procedure may reduce the risk of gastric emptying delay. Preoperative diabetes has been identified as an additional risk factor. Gastroparesis has also been reported following pancreas transplantation.
Antireflux Operations
The physiology of the lower esophageal sphincter and the proximal stomach are intimately related in health; it should come as no surprise, therefore, that a variety of antireflux procedures can influence gastric sensorimotor function. Fundoplication, as expected, affects sensorimotor function of the proximal stomach. Most, but not all, studies have demonstrated impaired relaxation of the proximal stomach, in response to meal ingestion, following this surgical procedure. Although the usual effect of fundoplication is to accelerate, rather than delay, gastric emptying, instances of gastroparesis have been described following antireflux surgery and endoscopic antireflux procedures. Given the high frequency with which the procedure is now performed, it should come as no surprise that Nissen fundoplication was the most common cause of postsurgical gastroparesis in the audit performed by the National Institute of Diabetes and Digestive and Kidney Diseases gastroparesis consortium. The pathophysiologic process leading to these occurrences is unclear. In some, postsurgical gastroparesis may represent the overt appearance of an unrecognized preoperative disorder; in others there is compelling evidence to incriminate vagal injury, which is especially likely in relation to redo procedures and may contribute to persistent gas-bloat symptoms. In rare instances, postfundoplication gastroparesis may be persistent and severe. Although gastric resection does not seem to offer much help for these unfortunate patients, some success has been reported with an approach that combines conversion to a partial fundoplication with a pyloroplasty.
Bariatric Surgery
Ardila-Hani and Soffer comprehensively reviewed the impact of bariatric (or metabolic) surgical procedures on gastrointestinal motor function. Esophageal problems were by far the most common. Gastric emptying did not appear to be affected by laparoscopic adjustable gastric banding and tended to accelerate following Roux-en-Y gastric bypass. However, instances of gastroparesis, at times severe and persistent, have been reported following the latter procedure. Salameh and colleagues, for example, described successful treatment of 6 patients with intractable gastroparesis following Roux-en-Y gastric bypass for morbid obesity using gastric electrical stimulation. In an uncontrolled trial, endoscopic injection of the pylorus with botulinum toxin A produced symptomatic improvement in a small series of patients with postvagotomy gastroparesis, which was thought to result from fundoplication in the vast majority.
Other Procedures
Virtually any procedure that could compromise the vagi or affect upper gastrointestinal motor function could result in gastroparesis. Clinically significant gastroparesis has, therefore, been reported not only in association with a wide range of gastric procedures but also in relation to esophageal resection, botulinum toxin injection for achalasia, lung transplantation, and even hepatic surgery. Sutcliffe and colleagues noted a 12% rate of gastric emptying delay following esophagectomy in their series; in another report, gastroparesis was more common after minimally invasive than open esophagectomy. Gastroparesis in relation to lung transplantation is especially ominous, as its presence preoperatively has been associated with an increased risk for the development of bronchiolitis obliterans syndrome. Though common before surgery, new-onset gastroparesis was documented in 6% of subjects after transplantation in one large series. In the lung transplant patient gastroparesis may trigger or exacerbate gastroesophageal reflux, from which these patients have no protection. For this reason there is a low threshold for the performance of fundoplication in this patient population, and gastric electrical stimulation has been added to address concomitant gastroparesis.
Although cholecystectomy, per se, has not been incriminated as a cause of gastroparesis, a prior cholecystectomy seems to negatively affect the natural history of both diabetic and idiopathic gastroparesis.
Postsurgical gastroparesis
Although acute gastroparesis may be a component of the ileus syndrome that can complicate many surgical procedures and of the acute pseudo-obstruction syndrome that may accompany severe sepsis and multiorgan failure, this review focuses on chronic manifestations of gastric dysmotility. In contrast to chronic gastroparesis, whose pathophysiology is often poorly understood, inflammatory processes seem fundamental to the inhibition of motility in the acute form.
Gastroparesis and other disorders of gastric sensorimotor function may complicate specific surgical procedures. In the important Olmstead County study of the community prevalence of gastroparesis, 7.2% of all cases of definite gastroparesis were related to prior gastrectomy or fundoplication. Rates of postsurgical gastroparesis vary widely depending on many factors, including the site and nature of the surgical procedure. For example, in their comprehensive review, Dong and colleagues noted that rates ranged from 0.4% to 5% following gastrectomy, from 20% to 50% after pylorus-preserving pancreaticoduodenectomy, and from 50% to 70% after cryoablation therapy for pancreatic cancer.
Vagotomy
Although vagotomy is infrequently performed nowadays in the management of acid-peptic disease, inadvertent vagal injury may complicate other interventions, rendering an understanding of the complex effects of vagotomy on gastric motor function still relevant. Receptive relaxation, a vagally mediated reflex, is impaired. As a consequence, the early phase of liquid emptying is accelerated. This acceleration causes rapid emptying of hyperosmolar solutions into the proximal small intestine and may result in the early dumping syndrome. By contrast, and as a consequence of impaired antropyloric function, the later phases of liquid and solid emptying are prolonged by vagotomy. Other motor effects of vagotomy include an impairment of the motor response to feeding (which contributes to the pathophysiologic mechanisms of postvagotomy diarrhea) and a suppression of the antral component of the migrating motor complex. The latter phenomenon is particularly prevalent among individuals who have symptomatic postvagotomy gastroparesis.
The now standard addition of a drainage procedure, such as a pyloroplasty or gastroenterostomy, has tended to negate the effects of vagotomy alone. In most patients, the net result of the combined procedure is little alteration in the gastric emptying of liquids or solids. Thus, prolonged postoperative gastroparesis (ie, lasting longer than 3–4 weeks) is, in fact, rare (<2.5% of patients after either vagotomy and pyloroplasty or vagotomy and antrectomy). Significant postoperative gastroparesis may occur, however, in patients who have a prior history of prolonged gastric outlet obstruction. In this circumstance, normal gastric emptying may not return for several weeks.
Longitudinal studies suggest that vagotomy-related gastroparesis tends to resolve over time, with one study suggesting gastric emptying rates in those who had undergone either a truncal or a highly selective vagotomy being similar by 12 months after the procedure.
Persisting postsurgical gastric motor dysfunction often presents a formidable management challenge. Therapeutic responses to prokinetic agents have proved particularly disappointing in this group. In these resistant cases, a completion gastrectomy may be the best alternative. It should be noted, however, that in one large series this approach was deemed successful in only 43% of patients.
Gastrectomy
Antral resection by removing the antral mill renders the stomach incontinent to solids and leads to accelerated emptying, and symptomatic “dumping” may occur in up to 50% of patients after Billroth I or II gastrectomy. Late dumping symptoms occur 90 to 120 minutes after a meal and are a consequence of reactive hypoglycemia. The accommodation reflex is impaired among symptomatic patients. By contrast, delayed gastric emptying sometimes occurs after a Billroth II gastrectomy as a result of a large atonic gastric remnant. Meng and colleagues reported a 6.9% frequency of gastroparesis among 563 patients who underwent radical gastrectomy for gastric cancer in their unit in Shanghai, China. Preoperative gastric outlet obstruction and the performance of a Billroth II anastomosis were the principal risk factors for the occurrence of gastroparesis. Of note, they documented a similar rate of gastroparesis (3.7%) among a smaller group of patients who underwent a laparoscopic gastrectomy. Laparoscopy-assisted, pylorus-preserving gastrectomy represents a less radical operative approach to early gastric cancer; gastric stasis is the most common complication of this procedure, occurring in 6.2% of cases. In one series, and in contrast to the aforementioned experience with this procedure following vagotomy, completion gastrectomy resulted in significant symptomatic improvement among subjects with postgastrectomy gastroparesis.
Roux-en-Y Syndrome
The creation of a Roux-en-Y gastroenterostomy may be associated with a specific clinical entity, the Roux syndrome. Severe symptoms of postprandial abdominal pain, bloating, and nausea many develop. Studies have variably described impaired gastric motor function and a functional obstruction within the duodenal Roux limb as a result of motor asynchrony. The latter can be revealed by manometry, but the status of these motility patterns in the pathophysiologic processes of this syndrome remains unclear.
Pancreatectomy
Pancreatectomy and pylorus-preserving pancreaticoduodenectomy, in particular, have been associated with a high incidence of postoperative gastric stasis. The principal predictor of gastric emptying delay after these operations is the occurrence of other postoperative complications. Operative technique seems, in general, to be of less importance, although there is a suggestion that an antecolic anastomosis may be associated with less emptying delay. Accordingly in what has been, perhaps, the largest series (N = 711) to date, Parmar and colleagues documented an overall rate of delayed gastric emptying following pancreaticoduodenectomy of 20%. The occurrence of gastroparesis did not seem to be influenced by such technical factors as pylorus preservation or whether the gastrojejunostomy was antecolic or retrocolic, but was associated with fistula formation, postoperative sepsis, and reoperation. These results contrast with those of a prior systematic review, which found that antecolic reconstruction was linked to lower rates of gastroparesis. Furthermore, others have suggested that the use of a Billroth II rather than a gastrojejunostomy for reconstruction following this procedure may reduce the risk of gastric emptying delay. Preoperative diabetes has been identified as an additional risk factor. Gastroparesis has also been reported following pancreas transplantation.
Antireflux Operations
The physiology of the lower esophageal sphincter and the proximal stomach are intimately related in health; it should come as no surprise, therefore, that a variety of antireflux procedures can influence gastric sensorimotor function. Fundoplication, as expected, affects sensorimotor function of the proximal stomach. Most, but not all, studies have demonstrated impaired relaxation of the proximal stomach, in response to meal ingestion, following this surgical procedure. Although the usual effect of fundoplication is to accelerate, rather than delay, gastric emptying, instances of gastroparesis have been described following antireflux surgery and endoscopic antireflux procedures. Given the high frequency with which the procedure is now performed, it should come as no surprise that Nissen fundoplication was the most common cause of postsurgical gastroparesis in the audit performed by the National Institute of Diabetes and Digestive and Kidney Diseases gastroparesis consortium. The pathophysiologic process leading to these occurrences is unclear. In some, postsurgical gastroparesis may represent the overt appearance of an unrecognized preoperative disorder; in others there is compelling evidence to incriminate vagal injury, which is especially likely in relation to redo procedures and may contribute to persistent gas-bloat symptoms. In rare instances, postfundoplication gastroparesis may be persistent and severe. Although gastric resection does not seem to offer much help for these unfortunate patients, some success has been reported with an approach that combines conversion to a partial fundoplication with a pyloroplasty.
Bariatric Surgery
Ardila-Hani and Soffer comprehensively reviewed the impact of bariatric (or metabolic) surgical procedures on gastrointestinal motor function. Esophageal problems were by far the most common. Gastric emptying did not appear to be affected by laparoscopic adjustable gastric banding and tended to accelerate following Roux-en-Y gastric bypass. However, instances of gastroparesis, at times severe and persistent, have been reported following the latter procedure. Salameh and colleagues, for example, described successful treatment of 6 patients with intractable gastroparesis following Roux-en-Y gastric bypass for morbid obesity using gastric electrical stimulation. In an uncontrolled trial, endoscopic injection of the pylorus with botulinum toxin A produced symptomatic improvement in a small series of patients with postvagotomy gastroparesis, which was thought to result from fundoplication in the vast majority.
Other Procedures
Virtually any procedure that could compromise the vagi or affect upper gastrointestinal motor function could result in gastroparesis. Clinically significant gastroparesis has, therefore, been reported not only in association with a wide range of gastric procedures but also in relation to esophageal resection, botulinum toxin injection for achalasia, lung transplantation, and even hepatic surgery. Sutcliffe and colleagues noted a 12% rate of gastric emptying delay following esophagectomy in their series; in another report, gastroparesis was more common after minimally invasive than open esophagectomy. Gastroparesis in relation to lung transplantation is especially ominous, as its presence preoperatively has been associated with an increased risk for the development of bronchiolitis obliterans syndrome. Though common before surgery, new-onset gastroparesis was documented in 6% of subjects after transplantation in one large series. In the lung transplant patient gastroparesis may trigger or exacerbate gastroesophageal reflux, from which these patients have no protection. For this reason there is a low threshold for the performance of fundoplication in this patient population, and gastric electrical stimulation has been added to address concomitant gastroparesis.
Although cholecystectomy, per se, has not been incriminated as a cause of gastroparesis, a prior cholecystectomy seems to negatively affect the natural history of both diabetic and idiopathic gastroparesis.
Parkinson disease and other neurologic disorders
As populations age the prevalence of neurologic disease in the community continues to increase, and consultations relating to gastrointestinal motility problems in the patient afflicted with a neurologic disorder become ever more common.
The high prevalence of gastroparesis and other disturbances of gut motor function in neurologic diseases is based on similarities in morphology and function between the neuromuscular apparatus of the gut and that of the somatic nervous system. First, it is now recognized that the enteric and central nervous systems share many similarities, both morphologic and functional. The basic organization of the enteric nervous system (ENS) (neurons, ganglia, glia, and ENS-blood barrier), and the ultrastructure of its components, are similar to those of the central nervous system (CNS), and almost all neurotransmitters identified within the CNS are also found in enteric neurons; the concept of ENS involvement in neurologic disease should not, therefore, come as a great surprise. Second, given the prevalence of dysfunction in the autonomic nervous system (an important modulator of enteric neuromuscular function) in several neurologic syndromes, in addition to the existence of several primary and secondary disorders of autonomic function, disturbed autonomic modulation of gut motor function may be an important contributory factor to symptomatology in some scenarios. Third, it is now evident that the gut has important sensory functions; though usually subconscious, gut sensation may be relayed to and perceived within the CNS. Sensory input is also fundamental to several reflex events in the gut, such as the viscerovisceral reflexes that coordinate function along the gut. However, the role of sensory dysfunction in the mediation of common symptoms, such as abdominal pain and nausea, in the patient with CNS disease with gastrointestinal manifestations has not been extensively investigated.