Rumination syndrome

INTRODUCTION — Rumination syndrome is a functional gastrointestinal disorder characterized by effortless regurgitation of ingested food into the mouth after most meals. The material is either spat out or re-swallowed [1]. Rumination syndrome is frequently misdiagnosed as gastroesophageal reflux disease or vomiting, resulting in a delay in diagnosis [2]. This topic will review the epidemiology, etiology, diagnosis, and management of rumination syndrome. An approach to patients with nausea and vomiting and the clinical manifestations, diagnosis and treatment of gastroesophageal reflux disease are discussed in detail separately. (See "Approach to the adult with nausea and vomiting" and "Approach to the infant or child with nausea and vomiting" and "Clinical manifestations and diagnosis of gastroesophageal reflux in adults" and "Medical management of gastroesophageal reflux disease in adults" and "Clinical manifestations and diagnosis of gastroesophageal reflux disease in children and adolescents" and "Management of gastroesophageal reflux disease in children and adolescents".)

EPIDEMIOLOGY

Prevalence — Rumination syndrome can affect children and adults [3]. In a study that surveyed 2163 children and adolescents, 110 (5 percent) fulfilled clinical criteria for rumination syndrome [4]. In these two studies, one from the United States [5] and the other which surveyed over 50,000 participants across 26 countries [6], the prevalence of rumination was 3.1 and 5.8 percent, respectively. In patients with fibromyalgia or eating disorders, the prevalence of rumination syndrome may be as high as 7 to 8 percent [7,8].

Associated conditions — Rumination syndrome has been associated with anxiety, depression, obsessive compulsive disorder, post-traumatic stress disorder, adjustment disorder, attention deficit-hyperactivity disorder, and constipation from a rectal evacuation disorder [2,9,10]. While some studies have suggested that rumination syndrome occurs predominantly among children and adults with development delay, this has not been substantiated by other studies [11-15].

PATHOPHYSIOLOGY — The pathogenesis of rumination syndrome is unclear, but unperceived abdominal wall activation in the postprandial period appears to be a key pathogenetic feature. The exact trigger for this abdominal wall activation is not well established; however, as there is overlap between rumination syndrome and functional dyspepsia [5], it is possible that rumination events occur in response to post-prandial dyspeptic symptoms.  

The retrograde flow of ingested gastric content into the mouth in patients with rumination syndrome occurs due to a combination of raised intra-abdominal pressure coupled with negative intrathoracic pressure, resulting in a permissive esophagogastric gradient. On postprandial esophageal high resolution impedance manometry, rumination follows gastric pressurizations exceeding 30 mmHg, which is associated with lower and upper esophageal relaxation at the time of gastric pressurization (figure 1). This indicates that raised intra-abdominal pressure alone cannot explain rumination and that upper and lower esophageal sphincter dysfunction also likely play a role [13]. (See "Esophageal multichannel intraluminal impedance testing" and "High resolution manometry".)

Typical findings during a gastroduodenal manometry include a characteristic spike pattern recorded simultaneously across all sensors termed the "R" wave (figure 1) [16]. This spike in intraluminal pressure is thought to occur due to activation of abdominal wall musculature. Postprandial activation of the abdominal wall has also been observed during electromyography recordings and correlate with regurgitation episodes (figure 1) [9,15]. One study suggested that the reflux of gastric content into the esophagus in rumination is preceded by an elevation of the gastroesophageal junction into the thorax creating a false hernia [17,18]. However, the significance of this observation remains unknown, particularly as it has also been described in healthy people during physical activity. The majority of patients with rumination syndrome appear to have normal gastric accommodation and emptying [19-21].

Given the now documented clinical overlap between rumination syndrome and functional dyspepsia [5,6], combined with the finding of low-grade duodenal inflammation in rumination characterized by increased eosinophils and intraepithelial lymphocytes (IELs) [22,23], it has been hypothesized that after nutrient exposure, duodenal inflammation may result in duodenogastric reflex responses inducing gastric (fundic) disaccommodation and abdominal wall activation that predispose to both rumination and dyspepsia [5].

CLINICAL MANIFESTATIONS — Rumination syndrome is characterized by rapid onset of regurgitation, usually within 10 minutes of finishing a meal. Episodes often persist for one to two hours after the meal, and the regurgitant consists of partially digested food that is recognizable in its taste to ingested food. Regurgitation is effortless and is often triggered by a sensation of discomfort (pressure, pain, burning) in the abdomen that is relieved by regurgitation.

Episodes are usually not preceded by retching. The material is consciously spat out or re-swallowed. Regurgitation occurs after most, if not all, meals. Patients often adapt their eating behaviors to compensate for this, and may avoid eating in social situations.

Patients frequently report associated dyspeptic symptoms including epigastric fullness or burning, and nausea [9,14], and the overlap between functional dyspepsia and rumination syndrome is nearly four times more likely than expected by chance [5]. Overt pain is rarely a feature. Weight loss has been observed in approximately 20 to 40 percent of patients [9,13,14]. Significant weight loss, electrolyte abnormalities, dental erosions, and malnutrition are rare in the absence of a co-existing eating disorder [24].

DIAGNOSIS

Overview of diagnostic approach — Rumination syndrome should be suspected in patients with effortless postprandial regurgitation without retching. The presence of "refractory GERD" characterized by regurgitation is suggestive of underlying rumination, which is more prevalent in younger female patients [25]. A clinical diagnosis of rumination syndrome requires the fulfillment of symptom-based diagnostic criteria and a limited evaluation to exclude a mechanical obstruction (table 1 and table 2). We perform high resolution impedance pH manometry to confirm the diagnosis of rumination syndrome. (See 'Diagnostic criteria' below and 'Evaluation' below.)

Diagnostic criteria — The following are the Rome IV criteria for rumination syndrome. In order to fulfill the Rome IV criteria, all of the following conditions must be met: adults and children (table 1 and table 2).

●Persistent or recurrent regurgitation of recently ingested food into the mouth with subsequent spitting or remastication and swallowing

●Regurgitation is not preceded by retching

Other clinical features that are not required but are supportive of the diagnosis of rumination syndrome include:

●Effortless regurgitation events are usually not preceded by nausea

●Regurgitant contains recognizable food that might have a pleasant taste

●Cessation of rumination when the regurgitated material becomes acidic

The diagnostic criterion is similar in children except that rumination should not occur during sleep and should not respond to standard medical therapy for reflux.

Evaluation

History and physical examination — History should focus on establishing whether the postprandial symptoms are vomiting (as often reported by patients) or regurgitation. Regurgitation, unlike vomiting, is effortless, may not be associated with nausea, and is not preceded by retching or heaving. Vomitus, unlike regurgitate, in patients with rumination syndrome, cannot voluntarily be kept in the mouth or re-swallowed. Patients with rumination syndrome often report a triggering event before the onset of the symptoms of rumination [3]. In children and adolescents with symptoms suggestive of rumination syndrome, an eating disorder should be excluded based on the history. (See "Eating disorders: Overview of epidemiology, clinical features, and diagnosis".)

Exclude mechanical obstruction — In patients with suspected rumination syndrome, we exclude a mechanical obstruction with upper gastrointestinal endoscopy and, if uncertain, CT/MR enterography. Upper endoscopy is usually normal in patients with rumination syndrome. In rare cases, patients may have evidence of esophagitis. We perform biopsies to exclude other disorders (eg, eosinophilic gastroenteritis, celiac disease, and H. pylori infection).

High resolution impedance pH manometry — Diagnostic findings of rumination syndrome on postprandial high resolution impedance manometry are reflux events extending to the proximal esophagus that are closely associated with an increase in gastric pressure to >30 mm Hg (figure 1) [26]. Normative values for conventional manometry have not been established.

Three rumination variants can be identified based on the pressure pattern on high resolution manometry:

●Primary rumination – Abdominal pressure increase is preceded by the retrograde flow

●Secondary rumination – An increase in abdominal pressure follows the onset of a reflux event

●Supragastric belch induced rumination – Supragastric belch immediately followed by a rumination event

Although data in children are limited, rumination patterns appear to be similar to adults [27]. A diagnostic cutoff for gastric pressure increase >25 mmHg, associated with retrograde bolus flow into the proximal esophagus, has been proposed as diagnostic cut off for rumination syndrome in children [28].

Other tests

●Duodenal biopsies – Although subtle increases in duodenal eosinophils and intraepithelial lymphocytes (IELs) have been found in rumination syndrome, not all cases have pathology, and disease cut-offs are not yet established [22,23].

●Gastroduodenal manometry – Gastroduodenal manometry was historically used to diagnose rumination syndrome, but is cumbersome, invasive, and is not widely available [16,21]. The hallmark of rumination on gastroduodenal manometry is a postprandial "R-wave" (figure 1). This spike in intraluminal pressure is thought to occur due to activation of abdominal wall musculature. (See 'Pathophysiology' above.)

●Gastric emptying study – Gastric emptying study, while frequently performed in patients with rumination syndrome, is not required for the diagnosis. The majority of patients with rumination syndrome have normal gastric emptying. In the author's clinical experience, the test often fails because the patient regurgitates the meal during the study period. (See 'Pathophysiology' above.)

●Ambulatory pH-impedance monitoring – One study found that patients with rumination had a higher number of non-acid reflux events after meals and a higher post-prandial symptom index, which in a small sample of patients had a sensitivity and specificity of 92 and 79 percent, respectively, for identifying rumination syndrome [25].

DIFFERENTIAL DIAGNOSIS — There are few other gastrointestinal disorders which present with frequent, effortless postprandial regurgitation.

●Achalasia – Some patients with achalasia and poor gastric accommodation have post-prandial regurgitation. However, the predominant symptom in patients with achalasia is dysphagia which is not a feature of rumination syndrome. Achalasia can be distinguished from rumination syndrome by esophageal manometry. (See "Achalasia: Pathogenesis, clinical manifestations, and diagnosis", section on 'Esophageal manometry' and 'High resolution impedance pH manometry' above.)

●Gastroesophageal reflux disease – Regurgitate in rumination syndrome lacks a sour, bitter, or acid taste reported in patients with gastroesophageal reflux disease (GERD). Unlike GERD, rumination syndrome episodes are not nocturnal. Medications that suppress gastric acid production, such as proton pump inhibitors, typically do not improve symptoms in patients with rumination syndrome. GERD can be distinguished from rumination syndrome by impedance pH manometry by detecting gastric straining preceding or during reflux events that extend to the proximal esophagus. (See 'High resolution impedance pH manometry' above.)

MANAGEMENT

General approach — A combination of interventions are typically used in clinical practice for the management of rumination syndrome. These include education, treatment of underlying mood disorder, and behavior modification with diaphragmatic breathing. We reserve the use of pharmacologic therapy with baclofen for patients with symptoms refractory to initial management.

Initial management

Education and treatment of associated mood disorder — An essential component of initial management of rumination syndrome includes education and reassurance. The aim of education is to enhance the patient's understanding of their disease and to encourage patients to take an active role in the management of their condition. A multidisciplinary approach, involving gastroenterologists and psychologists, is necessary, especially in patients with underlying depression, anxiety disorder and/or refractory symptoms. (See "Generalized anxiety disorder in adults: Management" and "Unipolar major depression in adults: Choosing initial treatment".)

Diaphragmatic (abdominal) breathing — The mainstay of therapy for rumination syndrome is diaphragmatic (abdominal) breathing (figure 2). Diaphragmatic breathing reduces postprandial intragastric pressure and increases esophagogastric junction zone pressure, restoring the gastroesophageal pressure gradient [13]. Using this technique, patients inhale by contracting the diaphragm and expanding the abdomen [29].

●Technique – Patients are instructed to place one hand on the abdomen and one on the chest (figure 2). We then instruct patients to slowly inhale through the nose, and during inhalation only the hand on the abdomen should rise, and the hand on the chest should move minimally. Patients then slowly exhale via the mouth. Each inhalation or exhalation should be slow and complete with a goal of six to eight respirations per minute. Patients are initially taught in the supine position [30]. Once they gain practice, the technique is re-enforced in semisupine or sitting position. Some patients require several sessions to learn the technique. We typically instruct patients to perform diaphragmatic breathing exercises immediately after a meal and continue for 10 to 15 minutes or longer until the sensation of regurgitation resolves. Diaphragmatic breathing can be combined with an electromyography or high resolution impedance manometry to provide visually guided biofeedback [9,13]. However, it is unclear if biofeedback improves effectiveness.

●Effectiveness – Diaphragmatic (abdominal) breathing may be effective in the treatment of rumination syndrome [2,10,14,15,31]. A randomized trial that included 24 patients with rumination syndrome confirmed by gastroduodenal manometry were assigned to either diaphragmatic breathing with biofeedback or premeal simethicone [9]. Patients in the diaphragmatic breathing group were trained to modulate abdominothoracic muscle activity using electromyographic guided biofeedback in three sessions over 10 days. Patients were instructed to perform diaphragmatic breathing exercises for five minutes before and after each meal. At 10 days, diaphragmatic breathing with biofeedback, but not placebo, resulted in a significant reduction in rumination episodes as compared with baseline (74 versus 1 percent). Postprandial abdominal symptoms decreased as compared with baseline, but there was no difference between groups. Patients in the placebo group who failed to improve during the 10 day period subsequently received diaphragmatic breathing training with biofeedback and were advised to continue exercises over time. Among 21 total patients who were trained in diaphragmatic breathing with biofeedback, there was a significant and progressive reduction in the number of daily rumination episodes over six months.

Refractory symptoms

Gamma-aminobutyric acid receptor agonist — We reserve the use of baclofen for patients with symptoms refractory to initial management. Baclofen is a gamma-aminobutyric acid agonist that raises lower esophageal sphincter tone and suppresses transient lower esophageal sphincter relaxations. Only two trials have evaluated the impact of baclofen on regurgitation in rumination syndrome. In an open label trial, 16 adult patients with clinically suspected rumination syndrome were treated with baclofen (10 mg three times daily) for one week. In 12 patients who completed the study, treatment with baclofen was associated with a significant reduction in the number of postprandial flow events and symptoms as compared with baseline [32]. In another randomized controlled trial, which included 21 adult patients of which 16 had with rumination syndrome and five predominantly supragastric belching, baclofen at a dose of 10 mg three times daily led to an approximately 50 percent reduction in regurgitation events during a post-prandial manometry, and 63 percent of patients reported improved symptoms using a visual analogue scale during the two-week study period [33]. However, long-term data on efficacy and tolerability are lacking. Baclofen crosses the blood-brain barrier and causes a variety of central nervous system-related side effects. Side-effects primarily include somnolence, confusion, dizziness, lightheadedness, drowsiness, weakness, and trembling. We usually begin by giving 5 to 10 mg at bedtime, which can be increased slowly to 10 mg three times daily while carefully monitoring for side effects.

Therapies of uncertain benefit — There are several approaches that have been used to treat patients with rumination syndrome that we do not recommend, due to lack of data demonstrating efficacy.

●Prokinetics – In one study in which 21 adults with rumination syndrome were treated with levosulpiride, a selective dopamine D2-receptor antagonist with prokinetic activity, in combination with supportive psychotherapy, over an eight-month period; 38 percent reported an improvement in symptoms [34]. There was no change in symptoms or worsening in 48 and 14 percent, respectively.

●Surgery – Nissen fundoplication and subtotal gastrectomy have been performed in patients with refractory rumination syndrome. However, the role of surgery, if any, in rumination syndrome remains unclear. While data from small case series have noted an improvement in symptoms, in the author’s clinical practice, many patients report refractory symptoms despite having undergone surgery [14,35,36]. (See "Surgical treatment of gastroesophageal reflux in adults", section on 'Fundoplication procedures'.)

●Other – In case reports, chewing gum has been associated with a reduction in the number of rumination episodes, but randomized trials are lacking [37,38].

PROGNOSIS — Few studies have reported long-term outcomes in patients with rumination syndrome, but limited data suggest that symptoms can recur. In a survey of 47 adolescents who had completed an intensive inpatient program at least one year prior for rumination syndrome symptoms, resolution occurred in 20 percent, but in 73 percent of responders rumination reoccurred to some degree [39].

SUMMARY AND RECOMMENDATIONS

●Epidemiology – Rumination syndrome is a functional gastrointestinal disorder characterized by effortless regurgitation of ingested food into the mouth after most meals. Rumination syndrome can affect both children and adults. It has been associated with anxiety, depression, and constipation secondary to a rectal evacuation disorder. The estimated prevalence of rumination syndrome is up to 6 percent in adults in the general population. (See 'Epidemiology' above.)

●Pathogenesis – The pathogenesis of rumination syndrome is unclear, but unperceived abdominal wall activation in the postprandial period appears to be a key pathogenetic feature. The retrograde flow of ingested gastric content into the mouth in patients with rumination syndrome occurs due to a combination of raised intra-abdominal pressure coupled with negative intrathoracic pressure, resulting in a permissive esophagogastric gradient. (See 'Pathophysiology' above.)

●Clinical features – Symptoms of rumination syndrome include rapid onset of regurgitation usually within 10 minutes of finishing a meal. The regurgitated material is similar to ingested food. Regurgitation is effortless and is not preceded by retching. The material is either spat out or re-swallowed. Regurgitation occurs after most, if not all, meals. Patients frequently report associated dyspeptic symptoms including epigastric fullness or burning, and nausea. (See 'Clinical manifestations' above.)

●Diagnosis – Rumination syndrome should be suspected in patients with effortless postprandial regurgitation without retching. A clinical diagnosis of rumination syndrome requires the fulfillment of Rome IV symptom-based diagnostic criteria (table 1 and table 2). A typical clinical history is diagnostic.  

High resolution impedance manometry testing is an adjunct for the clinical diagnosis. It serves to rule out achalasia, and postprandial evaluation can be used to objectively confirm rumination syndrome. Diagnostic findings of rumination syndrome on postprandial high resolution impedance manometry are reflux events extending to the proximal esophagus that are closely associated with an increase in gastric pressure to >30 mm Hg. (See 'Overview of diagnostic approach' above and 'High resolution impedance pH manometry' above.)

We perform an upper gastrointestinal endoscopy in patients with suspected rumination syndrome to rule out a structural esophagogastric disorder. While duodenal biopsies may be abnormal, disease cut-offs for increased eosinophils and intraepithelial lymphocytes (IELs) in rumination are not yet established.  

●Management – Initial management of rumination syndrome consists of education, treatment of underlying mood disorder, and behavior modification with diaphragmatic breathing. Diaphragmatic breathing reduces postprandial intragastric pressure and increases esophagogastric junction pressure, restoring the gastroesophageal pressure gradient. We reserve the use of baclofen for patients with symptoms refractory to initial treatment. (See 'Initial management' above and 'Refractory symptoms' above.)