Gastric bezoars

INTRODUCTION — A bezoar is an agglutination of ingested material that is insoluble or indigestible in the gastrointestinal tract. Gastric bezoars are rare, cause nonspecific symptoms, and are usually found incidentally in patients undergoing upper gastrointestinal endoscopy or imaging [1]. This topic will review the epidemiology, pathogenesis, clinical manifestations, diagnosis, and management of gastric bezoars. In patients with pharmacobezoars, the toxicity of the underlying ingested pharmaceutical agent must also be considered as decontamination may be required. The specific management of pharmacobezoars is discussed in detail separately. (See "Gastrointestinal decontamination of the poisoned patient".)    

EPIDEMIOLOGY

Classification based on composition — Bezoars are classified according to their composition (table 1) [2-12].

●Phytobezoars – Phytobezoars, composed of vegetable matter, are the most common type of bezoar. The diospyrobezoar, composed of persimmon fruit, accounts for the majority of cases.

●Trichobezoars – Trichobezoars are composed of hair.

●Pharmacobezoars – Pharmacobezoars are composed of ingested medications (eg, extended-release nifedipine, theophylline, enteric-coated aspirin, sodium alginate, and sucralfate).

●Other – Bezoars may be composed of a variety of other substances (eg, tissue paper, shellac, fungus, Styrofoam cups, cement, vinyl gloves, polyurethane, and rarely, milk curd).

Prevalence and risk factors — Gastric bezoars are rare, with an estimated incidence of 0.3 percent on upper endoscopy [1]. Most adults with phytobezoars are males between the ages of 40 and 50 years, while trichobezoars are typically seen in females in their 20s [13]. In rare cases, a gastric trichobezoar has a long tail and extends throughout the small bowel to the cecum (also known as Rapunzel syndrome), which occurs almost exclusively in young girls [14-17].

Risk factors in patients with gastric bezoars include the following:

●Prior gastric surgery – An underlying anatomic abnormality may predispose to the formation of gastric bezoars [13]. Among patients with gastric bezoars, 70 to 94 percent have had gastric surgery and 54 to 80 percent have undergone vagotomy and pyloroplasty (image 1) [18-20].

●Altered gastric motility – Patients with gastroparesis appear to be at increased risk of formation of gastric bezoars due to impairment in the grinding mechanism of the stomach and the interdigestive migrating motor complex [21,22]. (See 'Pathogenesis' below.)

●Medications – Use of anticholinergic agents and opiates can alter gastric motility. Other medications include those with an insoluble carrying vehicle (eg, enteric-coated aspirin and nifedipine) or high hygroscopy, defined as the ability to attract and retain water (eg, psyllium and wheat dextrin).

●Other – Dehydration, inadequate chewing, and high fiber diets may also contribute to the risk of bezoar formation. Diabetes mellitus has been associated with an increased risk of gastric bezoars. Diabetic gastroparesis decreases motility and precipitates bezoar formation. Trichobezoars form in patients with trichotillomania (or hair pulling disorder) and are often associated with psychiatric comorbidities. (See "Skin picking (excoriation) disorder and related disorders".)

PATHOGENESIS — Gastric bezoars usually result from ingestion of indigestible material in patients with impairment in the grinding mechanism of the stomach and the interdigestive migrating motor complex [23]. Although it was initially thought that delayed gastric emptying was the underlying cause of all bezoars, studies have found that many patients have normal or accelerated gastric emptying, suggesting that the composition of the ingested material plays an important role in the pathogenesis. As an example, patients with diospyrobezoar form bezoars without gastric dysfunction. The unripe persimmon fruit contains high concentrations of a soluble tannin called shibuol, which forms a coagulum when mixed with gastric acid [19]. It is also hypothesized that proline-rich proteins secreted from the parotid and submandibular glands have a high affinity for binding tannins and promote bezoar formation [24]. (See "Pathogenesis of delayed gastric emptying", section on 'Motor functions of the stomach regions'.)

Trichobezoars form in patients with trichotillomania and trichophagia. They begin as retained hairs between the gastric folds; the hair is then denatured by gastric acid, becomes black due to oxidation, and combines with food to form an enmeshed mass. Trichobezoars subsequently become colonized by bacteria resulting in halitosis.

Once formed, bezoars grow by the continuing ingestion of food rich in cellulose and other indigestible materials, matted together by protein, mucus, and pectin.

CLINICAL MANIFESTATIONS

Clinical features — Affected patients remain asymptomatic for many years, and symptom onset is insidious. The most common symptoms include abdominal pain, nausea, vomiting, early satiety, anorexia, and weight loss [13]. Gastrointestinal bleeding due to concurrent gastric ulcers is a common presentation in patients who have previously undergone surgery [13]. The ulcers may be due to peptic ulcer disease due to prolonged exposure to gastric acid because of decreased motility or pressure necrosis. Although many bezoars become quite large, gastric outlet obstruction is an uncommon presentation [25].

Physical examination is unremarkable in most patients with a gastric bezoar except for an occasional abdominal mass or halitosis. Patients with trichobezoars may have patchy areas of alopecia. The hair shafts are typically of different length due to different points of breakage or pulling at different times. (See "Evaluation and diagnosis of hair loss", section on 'Nonscarring alopecia'.)

Imaging findings — Bezoars are usually an incidental finding on imaging in patients undergoing evaluation for nonspecific symptoms. Abdominal radiograph with (image 1) or without barium (image 2), abdominal ultrasound, or computed tomography (CT) scan may show the bezoar as a mass or a filling defect [26,27]. While phytobezoars are generally impervious to barium, trichobezoars tend to absorb barium. On ultrasound a gastric bezoar appears as an intraluminal mass with a hyperechoic arc-like surface and a marked acoustic shadow. On CT, gastric bezoars have the appearance of a low-density intraluminal mass containing air bubbles and exhibit a characteristic mottled appearance. Abdominal CT has the highest sensitivity for gastric bezoars and has the advantage of detecting both gastric and small intestinal bezoars [28].

Complications — Bezoars have been associated with small bowel obstruction, and more rarely, with gastrointestinal perforation, peritonitis, protein-losing enteropathy, steatorrhea, pancreatitis, intussusception, obstructive jaundice, appendicitis, constipation, and pneumatosis intestinalis [29-32]. (See "Gastric outlet obstruction in adults", section on 'Clinical manifestations'.)

DIAGNOSIS — The diagnosis of a gastric bezoar is usually made incidentally on imaging or upper endoscopy performed for evaluation of a patient with abdominal pain or nausea and vomiting. The CT appearance of a low-density intraluminal gastric mass containing air bubbles exhibiting a characteristic mottled appearance supports the diagnosis of a gastric bezoar.

Upper gastrointestinal endoscopy can establish a definitive diagnosis and allows for samples to be obtained to determine the composition of the gastric bezoar but should not be performed in patients with an obstruction. Endoscopically, a gastric bezoar has the appearance of a dark brown, green, or black ball of amorphous material in the fundus or antrum of the stomach (picture 1).

MANAGEMENT

Patients with bowel obstruction or severe bleeding — Patients with obstruction or severe bleeding require urgent intervention with surgery (algorithm 1) . (See 'Severe symptoms, resistance, or refractory to chemical dissolution' below and 'Surgery' below.)

Patients without obstruction or severe bleeding

Assess bezoar characteristics — In patients without obstruction or severe bleeding, the choice of treatment of gastric bezoars is based on the severity of symptoms and the characteristics of the bezoar. Feasibility of chemical dissolution is based on the composition, consistency, and size of the bezoar (algorithm 1).

●Phytobezoars, the most common bezoars, are amenable to chemical dissolution.

●Trichobezoars are resistant to chemical dissolution and require endoscopic or surgical removal. Endoscopic removal of an intact trichobezoar (weighing <55 g) has been reported, however, fragmentation of larger trichobezoars requires repeated introduction of the endoscope increasing the risk of pressure ulceration and perforation.

●Bezoars composed of vinyl gloves are resistant to chemical dissolution but are amenable to endoscopic removal if the gloves are soft and pliable. Surgery is required if they have become hardened and matted [10,17,33].

●In patients with pharmacobezoars, the toxicity of the underlying ingested pharmaceutical agent must also be considered as decontamination may be required. The management of pharmacobezoars is discussed in detail, separately. (See "Gastrointestinal decontamination of the poisoned patient".)    

Patients with severe symptoms and bezoars that are resistant or refractory to chemical dissolution require endoscopic therapy or surgery.

Adjuvant therapy with prokinetics — Prokinetics (eg, metoclopramide 10 mg orally before meals and at bedtime) used in conjunction with endoscopic therapy and chemical dissolution may decrease the time to dissolution of a gastric bezoar by enhancing contractions of the gastrointestinal tract and increasing their frequency. In one study, nine patients treated with adjunctive therapy required a mean of 1.2 courses of endoscopic therapy, while 15 patients treated with endoscopic therapy alone required 1.9 courses of treatment [34].  

Mild to moderate symptoms and chemical dissolution feasible

Choice of agent — Chemical dissolution involves administration of an agent to degrade the gastric bezoar. As compared with endoscopic therapy or surgery, chemical dissolution has the advantage of being noninvasive and inexpensive. However, a potential complication of chemical dissolution therapy is that partially dissolved bezoars may cause small bowel obstruction up to six weeks later [35,36]. Several agents have been used for chemical dissolution. However, there are no randomized trials comparing these agents.

●Coca-Cola – We administer Coca-Cola via gastric lavage (3000 mL over a 12-hour period) or advise oral consumption of the same amount in patients without nausea or vomiting [37-41]. The mechanism of Coca-Cola's action may be related to its low pH, the mucolytic effect of its high sodium bicarbonate content, and the CO₂ bubbles, which enhance dissolution.

Coca-Cola has the advantage of being widely available, inexpensive, well tolerated, and easy to administer. However, additional endoscopic therapy may be needed. In a systematic review of 24 observational studies that included 46 patients, administration of Coca-Cola alone resulted in resolution of phytobezoars in 23 (50 percent) patients [42]. Of the 23 patients with partial dissolution with Coca-Cola, concomitant endoscopic therapy resulted in dissolution in 19 patients (41 percent) and only four patients (9 percent) required surgery. (See 'Endoscopic therapy' below.)

Other agents have been tried with success in small series, but their use is limited by their efficacy, side effects, and/or availability. These include [43]:

●Acetylcysteine – Acetylcysteine has been administered via nasogastric tube (15 mL of acetylcysteine in 50 mL of water, twice daily) and endoscopically (30 mL of acetylcysteine in 30 mL of saline solution) for chemical dissolution of gastric bezoars [44,45]. However, success rates are low (50 percent) [46,47].

●Cellulase – Cellulase tablets or solutions have been used to degrade the cellulose and hemicellulose found in plant fiber and phytobezoars. Reported success rates range from 83 to 100 percent [43,48]. However, cellulase preparations are not readily available for use in many countries and are expensive.

●Papain – Papain is given in the form of Adolph's Meat Tenderizer, 1 teaspoon in 120 mL of water before each meal, or Papase, two (10,000 unit) tablets with each meal [49]. The use of papain is limited by side effects. In one series that included 36 patients with phytobezoars treated with papain and cellulase, papain was successful in treating 13 of 15 (87 percent) patients and cellulase was successful in 19 of 19 (100 percent) [48]. Adverse effects in the papain group included gastric ulcers and esophageal perforation, while no adverse effects were reported in the patients treated with cellulase.

Assess resolution — We perform a repeat upper endoscopy 24 hours later to assess for dissolution. In bezoars that have failed to dissolve with chemical dissolution, endoscopic fragmentation can be attempted at that time (algorithm 1). (See 'Endoscopic therapy' below.)

Severe symptoms, resistance, or refractory to chemical dissolution

Endoscopic therapy — Endoscopic therapy involves fragmenting the bezoar with water jet, direct suction through a large channel (6 mm) endoscope, forceps, or snares. The fragments can then be cleared with the endoscope or by using a large bore nasogastric tube (eg, Ewald tube), or allowed to pass through the gastrointestinal tract [48].

A variety of other methods have been described in case reports when the above techniques have failed, including use of the Nd:YAG laser, monopolar diathermy knife, and mechanical, electrohydraulic, or extracorporeal lithotripsy, injection of enzyme solutions or Coca-Cola, and a combination of methods using double-channel endoscopes [39,50-58]. The use of electrocautery or argon plasma coagulation should be avoided if the composition of the bezoar is unclear [59].

Surgery — Surgical management is generally reserved for patients in whom both chemical dissolution and endoscopic fragmentation cannot be safely performed or fails (algorithm 1). If a gastrotomy or enterotomy is performed to remove bezoars, the remainder of the small bowel and stomach should be examined to exclude other retained bezoars [60].

PREVENTION OF RECURRENCE — Up to 20 percent of patients have recurrent bezoars [18,48]. To prevent recurrence, patients should be encouraged to increase water intake, modify their diet (eg, avoid persimmons, stringy vegetables, and high-fiber foods), chew their food carefully, and underlying psychiatric comorbidities should be addressed. Patients without a clear predisposing etiology should also be evaluated for an underlying gastric motility disorder. (See "Gastroparesis: Etiology, clinical manifestations, and diagnosis", section on 'Evaluation'.)

SUMMARY AND RECOMMENDATIONS

●Epidemiology – Gastric bezoars result from the accumulation of foreign ingested material in the form of masses or concretions. Gastric bezoars are rare, with an estimated incidence of 0.3 percent on upper endoscopy.

•Bezoars are classified according to their composition. The major types are phytobezoars, trichobezoars, and pharmacobezoars.

-Phytobezoars, composed of vegetable matter, are the most common type of bezoar.

-Trichobezoars are composed of hair.

-Pharmacobezoars are composed of ingested medications.

●Pathogenesis – Gastric bezoars usually result from ingestion of undigestible material in patients with impairment in the grinding mechanism and the interdigestive migrating motor complex. Bezoars grow by the continuing ingestion of food rich in cellulose and other indigestible materials matted together by protein, mucus, and pectin. (See 'Pathogenesis' above.)

●Clinical manifestations – Affected patients remain asymptomatic for many years, and develop symptoms insidiously. The most common complaints include abdominal pain, nausea, vomiting, early satiety, anorexia, and weight loss. Gastrointestinal bleeding due to concurrent gastric ulcers is a common presentation in patients who have previously undergone surgery. (See 'Clinical manifestations' above.)

●Diagnosis – Bezoars are usually discovered as an incidental finding on imaging performed for evaluation of nonspecific symptoms. Abdominal radiograph with or without barium, abdominal ultrasound, or computed tomography scan may show the bezoar as a mass or a filling defect. Upper gastrointestinal endoscopy is required to establish the diagnosis and to obtain samples to determine the composition of the bezoar. (See 'Diagnosis' above.)

●Management – Therapy for bezoars should be tailored to the composition of the concretion and to the underlying pathophysiologic process (algorithm 1). In patients with pharmacobezoars, the toxicity of the underlying ingested pharmaceutical agent must be considered and decontamination may be required. The management of pharmacobezoars is discussed separately. (See "Gastrointestinal decontamination of the poisoned patient" and 'Management' above.)

•In patients with mild symptoms due to gastric phytobezoars, we suggest initial treatment with chemical dissolution rather than initial endoscopic therapy (Grade 2C). We administer Coca-Cola for chemical dissolution. (See 'Choice of agent' above.)

•In patients with bezoars that fail to dissolve with chemical dissolution, are resistant to chemical dissolution (trichobezoars), or moderate to severe symptoms due to large bezoars, we suggest endoscopic therapy rather than surgery (Grade 2C). (See 'Endoscopic therapy' above.)

•We suggest metoclopramide in conjunction with chemical dissolution and endoscopic therapy (Grade 2C). (See 'Adjuvant therapy with prokinetics' above.)

•Surgery should be reserved for selected patients with gastric bezoars if chemical dissolution and endoscopic fragmentation cannot be performed or fail and for patients with complications such as obstruction and significant bleeding. (See 'Surgery' above.)

●Prevention of recurrence – Up to 20 percent of patients have recurrent bezoars. In order to prevent recurrence, patients should be encouraged to increase water intake, modify their diet, chew their food carefully, and seek psychiatric evaluation if needed. Patients should also be evaluated for an underlying motility disorder. (See 'Prevention of recurrence' above and "Gastroparesis: Etiology, clinical manifestations, and diagnosis", section on 'Evaluation'.)

ACKNOWLEDGMENT — The UpToDate editorial staff acknowledges Moises Guelrud, MD, who contributed to an earlier version of this topic review.