Health Questions and Answers

Pill- Induced and Corrosive Injury of the Esophagus

Who is affected by pill-induced esophageal injury?
Anyone of any age who ingests caustic pills is susceptible to pill-induced injury. Reported cases range from ages 5-89. Women outnumber men by a ratio of 1.5:1. It is not uncommon for pills to stick in a normal esophagus during transit. One study showed that 36 of 49 normal subjects who assumed a supine position after swallowing a round, nonsticky barium tablet with 15 mL of water retained the tablet in the esophagus for 5-45 minutes. A more sticky gelatin tablet remained in the esophagus for more than 10 minutes in over one half of normal subjects who ingested the pill in a supine position. Esophageal dysmotility or structural abnormalities, such as rings or strictures, are clearly not required for pill-induced injury.

What factors contribute to esophageal retention of pills?
Esophageal clearance is determined by several factors, some of which can be modified to decrease the risk of pill-induced injury. Upright posture improves esophageal clearance of pills. The volume of water ingested with pills also affects clearance, although no study has identified the volume required to ensure passage through the esophagus. One study showed that 11 of 18 patients retained a barium pill swallowed with 15 mL of water compared with 3 of 18 who swallowed the pill with 120 mL of water. Other partially modifiable factors include structural abnormalities, such as rings or strictures, which can be dilated as needed. Abnormal esophageal motility is sometimes improved with pharmacologic agents, but motility is usually normal in patients with pill-induced injury. Taking the pill with inadequate fluid and lying down immediately afterward are often the only identifiable risk factors.

What are the risk factors for pill-induced injury?
Anyone who takes a caustic pill is at risk, but some patients are at particular risk for severe pill-induced esophageal injury, including those with structural abnormalities of the esophagus, both pathologic (stricture, tumor, ring) and physiologic (hiatal hernia, narrowing of the esophagus secondary to compression from the left atrium, aortic arch, left mainstem bronchus). Cardiac disease is a risk factor because of esophageal compression by a dilated left atrium and frequent use of inherently caustic medications (e.g., aspirin, potassium chloride, quinidine). Patients who have undergone thoracotomy are at increased risk because they are bedridden and may develop adhesions and fibrosis that trap the esophagus between the aorta and vertebral column, making it more susceptible to compression by an enlarged left atrium and thus decreasing esophageal clearance. Supine positioning during pill ingestion impairs esophageal clearance and places patients at risk. The stickiness of the pill surface, the inherent caustic nature of certain drugs, and the volume of liquid consumed with pills affect risk. Elderly patients and patients with underlying gastroesophageal reflux disease (GERD) are at increased risk. GERD may cause a more acidic environment; because many drugs, including nonsteroidal anti-inflammatory drugs (NSAIDs), are weak acids, their absorption into tissues is increased in an acidic environment.

Describe the typical presentation of patients with pill-induced injury.
The typical patient has no prior history of esophageal disease and presents with the sudden onset of retrosternal pain, which may have awakened the patient from sleep (particularly if pills were ingested with little liquid just before or while lying down) and may be exacerbated by swallowing. The pain may be mild or so severe that swallowing is impossible. The pain increases typically over the first 3-4 days before gradually subsiding. Painless dysphagia is uncommon (20%) and may suggest an alternative diagnosis. Less common symptoms and signs include dehydration, weight loss, fever, and hematemesis. Patients with preexisting esophageal problems, such as GERD, frequently present with worsening symptoms of heartburn, regurgitation, and dysphagia.

How is the diagnosis of pill-induced esophageal injury made?
The diagnosis of pill-induced esophageal injury may be suspected on the basis of history alone when typical symptoms suddenly appear soon after the ingestion of a pill known to cause esophageal injury. In a typical and uncomplicated case, an invasive diagnostic test may not be required, and the diagnosis can be made on the basis of history and physical exam. A diagnostic study is indicated when symptoms are severe, persist longer than 3-4 days, have atypical features, or suggest a complication (stricture, hemorrhage), or when the history suggests an alternative diagnosis (e.g., foreign body obstruction, infectious esophagitis in an immunocompromised host). Upper endoscopy is the most sensitive test; results are abnormal in almost all cases of pill-induced esophageal injury. In addition, it allows the most accurate assessment of alternative diagnoses, such as severe GERD, infectious esophagitis, or malignancy.

What does the typical pill-induced lesion look like at time of endoscopy?
The typical lesion of pill-induced esophageal injury is one or more discrete ulcers with normal surrounding mucosa. Ulcers range in size from pinpoint to circumferential lesions that may be several centimeters long. Most ulcers involve the mucosa only, but deeper penetration can occur and localized perforations have been reported. Ulcers may have local surrounding inflammation. Pill fragments have been seen in ulcer craters.

What are the potential complications of pill-induced esophageal ulcers?
Typical ulcers involve the mucosa only, but deeper lesions may occur. Torrential hemorrhage has resulted from erosions into vascular structures, including the left atrium. Cases with penetration to the mediastinum have been reported. Deep circumferential ulceration may result in formation of a circumferential fibrotic stricture, but this occurs in less than 10% of reported cases. Probably the true incidence of stricture formation is much less, because severe or atypical cases are more likely to be reported.

What pills are frequently implicated or particularly injurious?
Antibiotic pills are frequent offenders, accounting for more than one half of all reported cases of pill-induced esophageal injury because of the large number of prescriptions written and the caustic nature of the pills themselves. Doxycycline and tetracycline accounted for 293 of 454 reported cases of pill-induced esophageal injury in one recent review. Although frequent offenders, antibiotics rarely cause complicated injury to the esophagus. Patients with antibiotic-associated injury almost always present with acute, severe pain and local, circumscribed tissue injury due to mucosal ulceration. The ulceration is believed to be secondary to a single trapped pill.
Cardiac and vascular medications, including antihypertensives and anti-arrhythmics, compose a large group of caustic drugs. Quinidine alone has been reported in 13 cases of pill-induced injury; 7 of the 13 patients later developed strictures, making quinidine a particularly injurious substance. An unusual feature of quinidine-induced injury is its tendency to form profuse, irregular exudate that is sufficiently thick and adherent, appearing as a filling defect suggestive of carcinoma on barium swallow. On endoscopy the exudate can be washed away and has not been shown to be predictive of late fibrotic stricture formation.
Anti-inflammatory medications are relatively uncommon agents in pill-induced esophageal injury. A recent review reported only 71 cases of injury attributable to this class of drugs. In part because they are so widely prescribed, 22 different anti-inflammatory agents have been reported to cause injury, but approximately 45% of these reports are secondary to aspirin, Doleron, and indomethacin, with aspirin the single most common anti-inflammatory medicine to cause pill esophagitis. No hallmark lesion is associated with NSAIDs.

Do any new drugs on the market deserve special notice?
Alendronate sodium (Fosamax, Merck & Co., West Point, PA) is an oral aminobiphosphonate that inhibits osteoclast activity in the bones. It is used to treat and prevent osteoporosis in postmenopausal women. It can cause significant esophageal injury. The package insert for Fosamax advises how to administer the medication to maximize esophageal clearance. These factors include consuming 6-8 oz of water with the pill and staying upright for 30 minutes after taking the pill. In one study, a full 50% of patients who had complications with alendronate failed to follow these guidelines. The manufacturer advises that abnormalities of the esophagus that delay esophageal emptying and the inability to stand or sit upright for 30 minutes after ingestion are contraindications for prescription. Endoscopy reveals a classic esophageal lesion with Fosamax. Like quinidine, it causes a circumscribed ulceration covered by a thick, white, loosely adherent exudate. Histology confirms a leukofibrinous exudate similar to pseudomembranous colitis. Current data suggest that actual incidence of severe or serious esophageal injury is actually well under 1% of patients using alendronate. A newer bisphosphonate, risedronate, is now available for the prevention and treatment of osteoporosis and appears to have minimal gastrointestinal toxicity.

What other mechanisms have been proposed to explain pill-induced injury?
Animal studies have demonstrated that certain pills placed in direct contact with esophageal tissue can cause ulceration. This finding has been verified in humans by esophagogastroduodenoscopy (EGD), which revealed an esophageal ulcer containing a retained pill and circumscribed to the location of the pill. It is believed that pills must be inherently caustic to cause injury. Local acid burn is proposed for pills (e.g., doxycycline, tetracycline, ascorbic acid, ferrous sulfate) that produce an acidic solution with a pH <3 when dissolved in 10 mL of water. Phenytoin dissolved in 10 mL of saliva raises the pH to 10.4, suggesting that it may cause an alkaline burn. Other proposed mechanisms of injury include induction of gastroesophageal reflux (theophylline and anticholinergics) and production of localized hyperosmolarity capable of tissue desiccation and vascular injury (potassium chloride). Finally, some medications appear to be absorbed locally into the esophageal mucosa, causing toxic intramucosal concentrations (doxycycline, NSAIDs, alprenolol).

What are the postulated mechanisms of NSAID-induced injury?
Thirty million people use NSAIDs each day, and approximately 16% of patients report gastrointestinal side effects. Gastric injury is most common, although cases of esophageal injury are well documented. In one study, all patients with NSAID-induced esophageal injury, who were tested with 24-hour pH monitoring, had GERD. In the presence of GERD associated with a pH <4, NSAIDs may enter the mucosa and cause direct toxicity. NSAIDs may cause injury by inhibiting synthesis of mucosal prostaglandins. Prostaglandins are known to have a cytoprotective role in gastric mucosa, but it is unclear whether the same effect applies to esophageal mucosa. The role of the mucus and bicarbonate layer in protecting the esophagus is also unclear, but the deleterious effect of NSAIDs on the mucosal barrier of the stomach secondary to prostaglandin inhibition may also occur in the esophagus. Finally, NSAIDs may negatively affect lower esophageal sphincter pressure and function, thereby increasing GERD and potentiating their own absorption. Local acid injury may be caused by medications such as doxycycline, tetracycline, ascorbic acid, and ferrous sulfate. Each of these compounds has a pH of less than 3 when dissolved in distilled water or saliva.

Where are the areas of physiologic narrowing of the esophagus?
The normal esophagus has areas, generally minor, of external compression and narrowing at the sphincters. Pills may be more likely to hang up and cause injury in these areas. Degenerative arthritis of the cervical spine may cause external compression of the esophagus, which often worsens with age. The aortic arch and the left mainstem bronchus may cause compression of the esophagus. The left atrium varies in size, depending on underlying heart disease and may cause significant compression of the esophagus. Such compression is particularly troublesome because the medications often used to treat diseases associated with left atrial enlargement, such as potassium chloride in conjunction with diuretics and quinidine for atrial fibrillation, are particularly caustic agents.

Does alcohol consumption play a role in pill-induced esophageal injury?
Yes. Alcohol appears to act synergistically with caustic agents to induce esophageal injury. In one study, healthy volunteers took eight aspirin/day for 2 weeks. EGD showed no esophageal mucosal damage. After the same volunteers consumed a single dose of aspirin combined with alcohol, 33% had erythema and/or esophageal hemorrhage. Alcohol may affect the esophagus by interfering with esophageal clearance and thus prolonging aspirin contact with the mucosa. Alcohol is believed to decrease primary and secondary contractions of the esophagus.

What are the options for treating pill-induced esophageal injury?
Most cases of pill-induced injury heal without active intervention in 3 days to several weeks. Therapy starts with avoidance of the initial drug responsible for the injury and all other caustic drugs, when possible. When avoidance is not possible, every effort must be made to decrease the potential for reinjury by using elixir or other liquid preparations, administering medications in the upright position with at least 4 oz of liquid, and maintaining an upright posture for at least 10 minutes after ingestion.
Medications that buffer acid, decrease production of acid, or create a barrier coat for the esophagus are frequently prescribed (antacids, H2-blockers, sucralfate) but are of questionable value unless GERD contributes to symptoms. The use of topical anesthetics in various combinations (Bemylid-Benadryl, Mylanta, and lidocaine in equal parts) may decrease symptoms, but their use is limited by potential systemic toxicity.
Patients with such severe symptoms that they cannot eat or drink require hydration. If symptoms persist, they may require parenteral nutrition and analgesia. Other supportive measures may also be required for treatment of complications (e.g., blood products for hemorrhage and antibiotics for bacterial superinfection).
Acute inflammatory stenosis may resolve spontaneously, but chronic stricture formation may require repeated esophageal dilation. Strictures that prove to be recalcitrant to repeated dilation may require surgical correction, but this complication is rare.

Lye (sodium hydroxide) is a common caustic ingestion. How has its formulation changed over the past 30 years? How has this change affected the pattern of injury?
Before the 1960s caustic ingestion frequently involved solid or crystalline lye products with concentrations >50%. Such products were extremely corrosive and caused extensive damage on contact with the mucosa, but the immediate burning pain on contact with the oral mucosa often caused the victim to spit out the solid material. Injury was limited usually to the mouth, pharynx, and esophagus and rarely affected the stomach. Reports vary, but free esophageal perforation and mediastinitis were common complications. Such experiences led to the belief that lye injured the esophagus with relative sparing of the stomach compared with acids. This dictum did not hold true with concentrated liquid lye preparations, which can be swallowed more easily and quickly than solid lye. In the late 1960s such products were introduced as drain cleaners in concentrations of 25-36%. They caused devastating injury. Complications included respiratory compromise, esophageal and gastric perforations, septicemia, and death. Patients who survived often developed esophageal stricture as a later complication of ingestion. By the mid 1970s highly concentrated liquid products had been replaced in the United States by moderately concentrated (<10%) liquid drain cleaners. If ingested in sufficient quantity, such products are strong enough to cause severe esophageal and gastric injury, including visceral perforation. More often a smaller volume is ingested, and the patient recovers from the acute injury; later, however, strictures may develop. Caustic materials currently available for industrial usage are often much more concentrated than household products. Children occasionally encounter cleaning products containing highly concentrated lyes or acids, particularly around farms, construction sites, and swimming pools.

Do acute signs and symptoms predict the severity and extent of caustic injury?
Clinicians should be aware, when evaluating patients with caustic ingestion, that early signs and symptoms are not reliable indicators of the severity of caustic injury. Caustic agents (acids and crystalline lye) frequently cause immediate pain on contact with the mucosa of the oropharynx and may be expectorated before they are swallowed. Therefore, patients who ingest such agents may exhibit signs and symptoms of damage to the oropharynx with no injury to the esophagus. In contrast, lethal esophageal burns may occur with minimal evidence of oropharyngeal damage. Therefore, signs and symptoms of injury to the oropharynx do not reliably indicate the severity of damage to the esophagus or stomach. The distribution and severity of injury with acid or alkali depend as much on the physical characteristics of the product (solid versus liquid, volatility, titratable acid or base) as the volume ingested and the duration of exposure.

What is the mortality rate associated with caustic ingestion?
The mortality rate has decreased markedly over the past three decades from approximately 20% to 1-3%. The decreased mortality is due probably to improvements in supportive care (antibiotics and nutritional support), advances in surgery, anesthesia, and intensive care management as well as substitution of less concentrated alkali and acids for the highly concentrated products available in the 1950s and before.

What is the cancer risk to a patient with stricture after lye ingestion?
The association between esophageal cancer and caustic ingestion is strong. The expected incidence of esophageal carcinoma is higher in patients with caustic ingestion than in the general population. Approximately 1-7% of patients with carcinoma of the esophagus have a history of caustic ingestion. The latent period is long and in one study was on average 41 years. Currently, no screening is recommended after lye ingestion.

Should gastric lavage be performed on patients with caustic ingestion?
The answer is controversial. Patients most likely to benefit from gastric lavage present shortly after ingestion when a significant amount of caustic material may still be present in the stomach. In addition, patients with suspected coingestion of pills may benefit from lavage to decrease absorption. Such benefits must be weighed against the risks. Nasogastric intubation may induce retching and vomiting with recurrent exposure of the esophagus and oropharynx to caustics. Because the nasogastric tube may perforate the esophagus or stomach, strong consideration should be given to placement under fluoroscopic guidance. If the tube is placed, gastric contents should be aspirated before lavage. The stomach should be lavaged with cold water to dissipate any heat that is produced.

What is the role of endoscopic evaluation in patients with caustic ingestion?
Flexible upper endoscopy has a role in the early, emergent and later, subacute management of caustic ingestion. Patients in whom perforation (diagnosed either radiographically or clinically) requires surgical exploration should undergo complete upper endoscopy to identify the extent of disease. For example, in patients with a normal esophagus but injured stomach, surgery may be limited to the abdomen. The risk of upper endoscopy is acceptable once the decision to operate has been made.
If surgery is not indicated, endoscopy should still be performed to identify uninjured patients who do not require prolonged hospital observation and to define the severity of burns in injured patients. Timing of endoscopy is based on clinical suspicion of severe injury. If significant esophageal injury is unlikely, EGD should be performed promptly to provide rapid reassurance and to avoid hospital observation. More than 50% of patients with a history of caustic injury are found on endoscopy to have no injury. If internal injury is likely but signs of perforation are absent, a delay of 48-72 hours permits development of the inflammatory reaction (little inflammation may be present in the first 24 hours) and easier assessment of the true extent of injury. Although endoscopic evaluation identifies the location of the mucosal injury, it may not accurately predict the depth of invasion.

What is the role of corticosteroids in the treatment of caustic ingestion?
Patients in whom endoscopy demonstrates near-circumferential or circumferential esophageal burns are at risk for strictures. Since the 1950s, corticosteroids have been the mainstay of prophylaxis against stricture formation. The rationale for their use was based on animal studies showing that steroid therapy that begins within 24 hours after lye injury and continue for 6-8 weeks reduce the incidence of strictures by inhibiting formation of granulation tissue. This effect may be observed when corticosteroids are used as late as 4-7 days after caustic ingestion. Follow-up was short, however, and early death from septicemia was much more common in steroid-treated animals.
A prospective, randomized, controlled trial in children with caustic ingestion, performed by Anderson in 1990, showed that corticosteroids did not decrease stricture formation. The study, however, had a small number of patients and, although formation of esophageal stricture did not seem to be affected by corticosteroids, the need for total esophagectomy was decreased in the steroid-treated group (four vs. seven untreated patients).
Clearly there is no consensus. If steroids are to be used, they should be reserved for patients with circumferential esophageal burns, who are at greatest risk of stricture formation. The dosage and length of therapy for corticosteroids have not been defined. Prednisone, 1.5-2.0 mg/kg/day, with a tapering period of 2 months, has been recommended.

In patients with significant caustic ingestion and clinical evidence of impending airway compromise, corticosteroids may help to decrease inflammation of the bronchopulmonary tree. Dexamethasone (pediatric dosage = 0.5-1.0 mg/kg; adult dosage = 2.0-3.0 mg/kg) is given intravenously to patients who have a high probability of impending airway compromise and may need intubation, cricothyrotomy, or tracheostomy for treatment of airway obstruction.
The negative aspects of corticosteroids, including increased risk of infection and systemic side effects, must also be considered.

What is the role of antibiotics in the treatment of caustic ingestion?
Empiric antibiotic therapy is even less established. It was originally advocated because antibiotics reduced the early mortality rate in animals treated with steroids for esophageal burns. In addition, antibiotics were originally thought to decrease long-term stricture formation, but this effect has not been reproducible in animal or human studies. The patients most likely to benefit are those who are treated with corticosteroids and appear to be at increased risk of systemic infection. Gram-positive organisms are most commonly implicated, but broad-spectrum coverage is generally prescribed.
Empiric therapy has not been shown to be more efficacious than monitoring for clinical signs of infection and using broad-spectrum antibiotics at their first appearance. If empiric therapy is chosen, antibiotics may be stopped after 5-7 days of infection-free observation.

What is the role of computed tomography (CT) scanning?
Available data support CT scan with contrast as a predictor of the number of sessions of dilation that will be required to maintain a patent esophagus. Maximal esophageal wall thickness (>9 mm) in the area of the stricture was shown on multivariate analysis to be independently associated with the number of sessions of dilation required by the patient.

What factors contribute to the controversies associated with treatment of caustic ingestions?
Currently, many sources promote different invasive and noninvasive therapies for caustic ingestions. Fortunately, the number of severe caustic ingestions seems to be decreasing. Because of decreasing experience and ethical concerns about testing experimental therapies on humans, few well-controlled data are available to guide the clinician. Withholding therapy, however, is also an ethical concern.

What are the advantages and disadvantages of nasogastric intubation?
Advantages: Nasogastric tubes (NGTs) provide a mechanism to deliver adequate nutritional support and needed medications. They also allow the esophagus to rest and prevent wound trauma that may be associated with bolus food ingestion. Finally, NGTs maintain a lumen that can be used to assist dilation.
Disadvantages: NGTs may cause continuous irritation and inflammation of the healing esophagus and lead to increased fibrosis and stricturing.
Overall recommendation: A fluoroscopically placed, flexible NGT seems to be beneficial for the first 2 weeks in patients who are seriously ill and unlikely to maintain adequate nutrition.

What is the role of total parenteral nutrition (TPN)?
TPN has been advocated to allow complete esophageal rest and maintain maximal nutrition for healing. No prospective data support TPN in all patients. Clear candidates are patients at high risk of aspiration and patients in whom passage of an NGT is contraindicated because of the severity of esophageal injuries.

Why is prophylactic dilation controversial?
The final area of controversy is the use and timing of prophylactic dilation. Most agree that oral esophageal dilation is the cornerstone of stricture prophylaxis. Others argue that repeated trauma to esophageal mucosa from dilation causes increased fibrosis and encourages stricture formation. Prophylactic dilation of all patients with caustic ingestion clearly subjects some patients to unneeded, potentially hazardous procedures. No data are available to resolve this issue. Because strictures rarely manifest before the second week after ingestion, it seems wise to wait 10-14 days before beginning bougienage.

Last Updated: June 22, 2010

References
BIBLIOGRAPHY

  1. Anderson KD, Rouse TM, Randolph JG: A controlled trial of corticosteroids in children with corrosive injury of the esophagus. N Engl J Med 323:10, 1990.
  2. Bozymski EM, London JF: Miscellaneous diseases of the esophagus. In Sleisinger MH, Fordtran JS (eds): Gastrointestinal Diseases, 5th ed. Philadelphia, W.B. Saunders, 1993.
  3. Broor SL, Raju GS, Bore PP, et al: Long-term results of endoscopic dilation for treatment of corrosive esophageal strictures. Gut 34:1498-1501, 1993.
  4. Browne JD, Thompson JN: Caustic injuries of the esophagus. In Castell DO (ed): The Esophagus. Boston, Little, Brown and Company, 1992.
  5. Byrne WJ: Foreign bodies, bezoars, and caustic ingestions. Gastrointest Endosc Clin N Am 4:99-119, 1994.
  6. Gumaste VV, Pradyuman BD: Ingestion of corrosive substances by adults. Am J Gastroenterol 87:1-5, 1991.
  7. Kikendall JW: Caustic ingestion injuries. Gastroenterol Clin N Am 20:847-857, 1991.
  8. Kikendall JW: Caustic injury of the esophagus and stomach. In Current Therapy in Gastroenterology and Liver Disease, 3rd ed. Philadelphia, B.C. Decker, 1990.
  9. Kikendall JW, Johnson LF: Pill-induced esophageal injury. In Castell DO (ed): The Esophagus. Boston, Little, Brown and Company, 1995.
  10. Kochhar R, Ray JD, Sriram PVJ, et al: Intralesional steroids augment the effect of endoscopic dilation in corrosive esophageal strictures. Gastrointest Endosc 49:135-141, 1999.
  11. Lahoti D, Broor SL, Basu PP, et al: Corrosive esophageal strictures: Predictors of response to endoscopic dilation. Gastrointest Endosc 141:86-91, 1995.
  12. Lanza FL, Hunt RH, Thomson AB: Endoscopic comparison of esophageal and gastroduodenal effects of risedronate and alendronate in postmenopausal women. Gastroenterology 119:631-638, 2000.
  13. Loeb PM, Eisenstein AM: Caustic injury to the upper gastrointestinal tract. In Scharschmidt BF (ed): Gastrointestinal Diseases, 5th ed. Philadelphia, W.B. Saunders, 1993, pp 293-301.
  14. Minocha A, Greenbaum DS: Pill-esophagitis caused by nonsteroidal antiinflammatory drugs. Am J Gastroenterol 86:1086-1089, 1991.
  15. Ribeiro A, DeVault KR, Wolfe J, Stark ME: Alendronate-associated esophagitis: Endoscopic and pathologic features. Gastrointest Endosc 47:216-221, 1998.
  16. Semble EL, Wu WC, Castell DO: Nonsteroidal antiinflammatory drugs and esophageal injury. Semin Arthritis Rheum 19:99-109, 1989.
  17. Spechler SJ: Caustic ingestions. In Taylor MB (ed): Gastrointestinal Emergencies. Baltimore, Williams & Wilkins, 1990, pp 13-21.
  18. Taggart H, Bolognese MA, Lindsay R, et al: Upper gastrointestinal tract safety of risendronate: A pooled analysis of 9 clinical trials. Mayo Clin Proc 77:262, 2002.

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