Understanding Pharmacobezoars
Bezoars are indigestible masses that accumulate in the gastrointestinal tract, most commonly in the stomach. While some bezoars are made of hair (trichobezoars) or plant matter (phytobezoars), those composed of medications are called pharmacobezoars. This unusual complication is most likely to occur in patients with pre-existing risk factors that affect gastric motility or anatomy. Recognizing which medications can contribute to this risk is crucial for patient care and safety.
The Prime Culprit: Sucralfate
Among the various drugs implicated in pharmacobezoar formation, sucralfate is a key offender. This medication is a complex of aluminum hydroxide and sulfated sucrose used to treat and prevent ulcers. In the acidic environment of the stomach, sucralfate forms a thick, sticky, viscous gel that binds to the ulcer surface, creating a protective barrier. However, this same gelling property can cause problems.
In patients with risk factors like delayed gastric emptying, dehydration, or concurrent administration of enteral feeding, the sucralfate can aggregate and combine with other gastric contents to form a firm mass. Case reports have documented esophageal and gastric bezoars in critically ill, tube-fed patients receiving sucralfate. The putty-like substance formed can block the esophagus or stomach, leading to serious complications.
Other Medications Causing Bezoars
Beyond sucralfate, several other drug types and formulations are known to increase the risk of pharmacobezoar formation:
- Aluminum Hydroxide Antacids: Similar to the aluminum component in sucralfate, aluminum hydroxide gels can aggregate and contribute to the formation of pharmacobezoars.
- Extended-Release and Sustained-Release Medications: These drug formulations are designed with a polymer matrix, often cellulose acetate, that resists digestion and gradually releases the active ingredient over time. If gastric emptying is impaired, the undigested polymer shell can clump together, forming a bezoar. Examples include nifedipine XL, verapamil, and certain sustained-release formulations of other drugs.
- Enteric-Coated Medications: Enteric-coated tablets are covered with a protective layer to prevent dissolution in the stomach's acidic environment. If motility is compromised, this insoluble coating can build up and lead to bezoar formation, as seen with some enteric-coated aspirin products.
- Bulk-Forming Laxatives: Preparations containing hygroscopic fibers like psyllium or guar gum expand when they absorb water. In patients with insufficient fluid intake or reduced motility, these preparations can swell prematurely and congeal into a mass.
- Other Agents: Other reported culprits include cholestyramine, mesalamine, and enteral feeding formulas, particularly when combined with other risk factors.
Critical Risk Factors for Bezoar Formation
While certain medications are implicated, pharmacobezoar formation is heavily dependent on a patient's underlying health status and medication use. The following are crucial contributing factors:
- Impaired Gastrointestinal Motility: Conditions like gastroparesis (delayed stomach emptying), often associated with diabetes or other systemic illnesses, significantly increase risk. Critically ill patients, who are often dehydrated and have slowed bowel activity, are also highly susceptible.
- Anatomical Abnormalities: Prior gastrointestinal surgery, such as gastric bypass or partial gastrectomy, can alter the gut's normal anatomy and function, leading to delayed emptying.
- Polypharmacy: The concurrent use of multiple drugs, especially those that slow gastric motility, like opioids and anticholinergics, amplifies the risk.
- Reduced Gastric Acidity: A state of low stomach acid (hypochlorhydria) can affect the dissolution of certain medications, contributing to the formation of concretions.
- Dehydration: Inadequate hydration can worsen the situation, particularly with drugs that have hygroscopic (water-absorbing) properties.
Comparison of Common Pharmacobezoar Culprits
| Medication Type | Mechanism of Bezoar Formation | Common Risk Factors | Examples |
|---|---|---|---|
| Sucralfate | Forms a sticky, viscous gel in acidic environments that can combine with food or feed. | Delayed gastric emptying, critical illness, dehydration, concurrent enteral feeding. | Sucralfate suspension or tablets. |
| Extended-Release (ER/SR) Drugs | Undigestible polymer matrix (often cellulose acetate) aggregates in a low-motility gut. | Impaired gastric motility, anatomical changes from prior surgery. | Nifedipine XL, verapamil, venlafaxine XR. |
| Enteric-Coated Drugs | Insoluble polymer coating fails to dissolve properly and clumps together. | Delayed gastric emptying, altered gastric pH. | Enteric-coated aspirin. |
| Bulk-Forming Laxatives | Hygroscopic fibers absorb water and swell, potentially forming a mass without adequate fluid. | Inadequate fluid intake, poor GI motility. | Psyllium preparations, guar gum. |
Diagnosis and Management
Symptoms of a gastric bezoar can include nausea, vomiting, abdominal pain, early satiety, and unexplained weight loss. In many cases, bezoars are asymptomatic and discovered incidentally during imaging or endoscopy. If a bezoar is suspected, diagnosis is often confirmed via upper endoscopy, which allows for direct visualization of the mass.
Treatment depends on the size, location, and composition of the bezoar. Smaller pharmacobezoars may be chemically dissolved or broken down endoscopically. Larger or more obstructive masses may require endoscopic removal with specialized tools or, in rare cases, surgical intervention. Stopping the offending medication and addressing underlying risk factors are essential parts of the management strategy.
Prevention is Key
Preventing pharmacobezoar formation involves a combination of vigilant medication management and addressing patient risk factors. For patients at high risk, particularly those in intensive care or with impaired motility, careful consideration should be given to alternative drug formulations or different therapies. Maintaining adequate hydration and optimizing gastric emptying can also help. For patients on enteral tube feeding, proper flushing of the tube and awareness of potential drug-nutrient interactions, especially with sucralfate, is critical. Clinicians should remain mindful of the risk, especially when patients with gastrointestinal issues present with new or worsening symptoms.
For more detailed information, consult authoritative sources such as the National Institutes of Health (NIH) or the Merck Manual.
Conclusion
While relatively uncommon, pharmacobezoars are a serious complication that can result from the accumulation of certain medications. Sucralfate is a well-known agent with the potential to form a bezoar due to its gelling properties, but extended-release drugs, enteric-coated tablets, and bulk-forming laxatives are also implicated. The risk is significantly elevated in patients with delayed gastric emptying, polypharmacy, and other predisposing conditions. By understanding which drug causes gastric bezoar and recognizing the critical risk factors, healthcare providers can implement preventative strategies and ensure timely intervention for affected patients.
