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Pill-Induced Esophageal Injury: Endoscopic Features and Clinical Outcomes
Abstract
Pill-induced esophageal injury is a common but under-reported problem. The purpose of this study was to explore the clinical and endoscopic features, and the outcome of pill-related esophageal injury.
Endoscopy records for the period from January 1997 to June 2003 were searched for reports of esophageal pathology. The records of patients with pill-induced esophageal injury were evaluated.
A total of 92 patients with pill-induced esophageal injury were identified (33 men, 59 women; mean age 59, range 25-87). Common symptoms were odynophagia (n = 69, 75 %), chest pain (n = 55, 60 %), vomiting (n = 53, 58 %), dysphagia (n = 31, 33 %), and hematemesis (n = 14, 15 %). The endoscopic findings in the esophagus were: erythema in 76 patients (83 %), erosions in 53 patients (58 %), ulcers in 24 patients (26 %), seven of which were "kissing" ulcers, esophageal ulcer with bleeding in 17 patients (18 %), and esophageal strictures in seven patients (8 %). The causative pills were nonsteroidal anti-inflammatory drugs in 38 patients (41 %), tetracyclines in 20 patients (22 %), potassium chloride tablets in nine patients (10 %), alendronate in eight patients (9 %), and other drugs in 17 patients (18 %). Underlying diseases included diabetes in 60 patients (65 %), ischemic heart disease in 39 patients (42 %), and hypothyroidism in four patients (4 %). The mean hospital stay was 1.94 days; 14 patients (15 %) required injection of epinephrine 1 : 10,000 to control bleeding; and two patients died.
Pill-induced injury may present as erosions, kissing ulcers, and multiple small areas of ulceration with bleeding, mainly in the middle third of the esophagus. Advanced age, female gender, diabetes, and ischemic heart disease were common associations. The majority of patients made an uneventful recovery.
... Dysphagia means difficulty in swallowing is a common medical problem that has many causes, including esophageal injury [1][2][3][4][5][6][7][8]. Odynophagia means painful swallowing. ...
... It is very important to determine the offending drug which should be discontinued [14][15] or substituted with other formulations, such as crushed or liquid preparations, that reduce the duration of contact J Clin Gastro Hepatol Res between the drug and the esophageal mucosa. If the required offending drug is utmost importance then patient should be instructed on how to minimize the risk of injury when taking the medication [1][2][3][4][5][6][7][8][9][10][11][12][13][14][15][16]. ...
... The greater awareness of the condition in conjunction with preventive approaches will help in decreasing the incidence of medication-induced esophagitis [19]. Once medication-induced esophagitis has been resolved, preventing recurrence is always preferred over retreatment and entails educating patients on how to ingest their medications appropriately [1][2][3][4][5][6][7][8][9][10][11][12][13][14][15][16]. Ideally, medications should be swallowed with at least 8 oz of water. ...
Introduction: Dysphagia, or difficulty in swallowing, is a common medical problem that has many causes, including esophageal injury. Currently, more than 70 frequently used medications have been implicated in esophageal injury, and pill-induced Esophagitis should be considered in the differential diagnosis of dysphagia in individuals who take prescription and over-the-counter medications. Case Report: A 21-year old female, not a known case of any chronic illness presented with acute onset of dysphagia and odynophagia of one week duration. She gave history of taking analgesic tablet (Diclofenac and paracetamol combination) for headache in night in lying down position with sips of water and immediately she felt that this tablet has stucked in her food pipe. She was just on liquids for one week and after that reported in Medical Gastroenterology department. On history and clinical presentation, working diagnosis of pill induced Esophagitis was made and she was subjected to upper gastro-intestinal endoscopy which revealed healing ulcer with ragged ends and edematous mucosa in mid esophagus. She was put on syrup sucralfate two teaspoonfuls thrice daily and started accepting semi-solid diet after three days and solid diet after gap of one week without any dysphagia or odynophagia. Conclusion: It is proven fact that prevention is better than cure and stitch in time saves nine. Thus all precautions should be taken to prevent pill induced esophagitis. In case, it happens then early endoscopy and treatment is key for early recovery.
... A higher risk for the condition is present in older patients, since in them reduced salivary secretion is already present, as well as reduced esophageal motility or anatomical esophageal abnormalities (strictures due to chronic reflux, achalasia, compression by the enlarged heart) (ref. 15,29 ). Druginduced esophagitis is more common in women, and can as well occur in children 30 .The condition is more common with the administration of capsules 31 . ...
... Pill-induced esophagitis clinically manifests with sudden-onset dysphagia, odynophagia or retrosternal pain regardless of swallowing, while in rare cases bleeding from the esophageal lesion may occur 26 . The complaints usually occur within 3 days of drug intake 4,15 , and may also develop in a matter of hours or up to 10 days after taking the drug 32 . Concomitant gastroesophageal reflux disease may exacerbate pill-induced esophagitis 33 . ...
... The treatment of superimposed reflux is best accomplished using proton pump inhibitors twice a day, although there is no data that would suggest that the prevention of acid reflux accelerates symptom improvement or histological healing of pill-induced esophageal injury. The patients with serious odynophagia, which would abolish adequate oral intake, require parenteral nutrition and hydration until the disappearance of complaints and reinstitution of oral intake 4,15,26 . There is not any information concerning the question whether a repeated use of the drug that once induced esophagitis represents a higher risk if taken this time with proper caution. ...
Almost all drugs, including some plant-based compounds, can have adverse effects, about 10% of which are expressed at the level of the digestive tract and in some cases resemble gastrointestinal diseases. Most commonly manifest as difficult and/or painful swallowing, nausea, vomiting, diarrhea and constipation. In rare cases, lesions caused by medications may be complicated by bleeding, strictures and perforations and can manifest in all segments of the gastrointestinal tract (GIT). The diagnosis is made from a detailed medical history and clinical examination inter alia. and best confirmed by proximal or distal endoscopy.
... Oesophageal injury was seen more often in the female gender who used the capsule form of the medicine. Medication induced oesophageal injury is seen more frequently in female gender in case series of the literature [10][11][12] . In our study, female gender dominance is seen. ...
... Common clinical presentations are chest pain, painful swallowing and dysphagia reported with varying frequencies in the literatures 10,12,14 . In this study, the most frequent clinical presentation was chest pain 94.6% (35), next common was painful swallowing 78.4% (29), while hematemesis was an uncommon clinical presentation. ...
... Upper gastrointestinal endoscopy is the gold standard for diagnosis of medication-induced oesophageal injury. It allows the detection of the mucosal changes, taking biopsy sampling, and intervening in bleeding and other complications of the esophagus 10,12,16,26 . In the upper GI endoscopy, we found that most of the ulcers were located in the middle third of the esophagus (n-21), which is compatible with the literature 10,14 . ...
Medications can cause several complications in the esophagus and lead to medication-induced esophageal injury. This study was carried out among patients diagnosed as medication-induced esophageal injury from June 2015 to October, 2018 in the Department of Gastroenterology, Enam Medical College and Hospital, Savar, Dhaka to investigate clinical and endoscopic characteristics of medication-induced esophageal injury as well as outcome of these patients with treatment. Patients diagnosed as malignancy, viral or fungal esophagitis, esophageal varix, corrosive and sclerotherapy induced ulcer and GERD were excluded. Clinical and endoscopic characteristics of patients diagnosed as medication-induced injury were analyzed. After given treatment, clinical improvements as well as mucosal healing of oesophageal injury were noted. Thirty seven patients were diagnosed as medication-induced esophageal injury. Their median age was 40; 17 were males and 20 were females. Common symptoms were chest pain (94.6 %), odynophagia (78.4 %) and dysphagia (62.2 %). Symptoms appeared between 3 hours to 15 hours after ingestion of medication. Predisposing factors for 75.67% of the patients were related to taking the medicine with insufficient water or in recumbent position, or both. The main causative agents were antibiotics, Non-steroidal anti-inflammatory drugs (NSAIDs) and Alendronate sodium. Common diseases that required treatment with these drugs were various urinary system diseases, osteoporosis and migraine. During endoscopy, 25 had only ulcer, 7 had only erosion and 5 had both ulcer and erosion. Most of the ulcers and erosions were located at the middle third of the oesophagus with a rate of 70%, and 58.3% respectively. Appearance of the ulcer was oval, circular, kissing and geographical shaped and their sizes vary between 6 mm to 18 mm and single or multiple in numbers. All the patients were treated with proton pump inhibitors (PPIs) or sucralfate, and the causative drugs were discontinued. Symptoms resolution occurred within 5 to 12 days after treatment and mucosal healing were detected in all patients after 4 weeks who were performed endoscopy. Almost every kind of medication, particularly doxycycline, NSAIDs can cause oesophageal ulcer and erosion. It can be successfully treated with PPIs and discontinuation of the causative medication and prevented by warning patients about drinking water sufficiently and sitting up while taking the pill. Faridpur Med. Coll. J. Jan 2019;14(1): 2-7
... Over 100 different drugs have thus far been reported to cause drug-induced esophageal injuries (DIEIs). [1] DIEIs occur when caustic drugs dissolve in the esophagus and release their noxious contents. [1,2] The most-important patient-related risk factors for DIEIs are insufficient water consumption and recumbent position while taking medicines, which extend the drug-exposure time in the esophagus. ...
... [1] DIEIs occur when caustic drugs dissolve in the esophagus and release their noxious contents. [1,2] The most-important patient-related risk factors for DIEIs are insufficient water consumption and recumbent position while taking medicines, which extend the drug-exposure time in the esophagus. [3] The lesions are frequently located in the middle thoracic esophagus, where the aortic arch and left atrium (LA) physiologically constrict the esophageal lumen and probably delay the transit of medicines. ...
... However, these forms have disadvantages of increased local concentration of active pharmaceutical ingredients that injure susceptible tissues, particularly the esophagus, compared with liquid preparations. [1] Capsule forms of medicines such as doxycycline, tetracycline, and clindamycin can adhere to the esophagus and cause more serious injuries than the tablet forms. [3] Large pills such as those for clarithromycin, alendronate, and ibuprofen and sustained-release formulations of drugs such as ferrous sulfate and potassium chloride may be more commonly retained in the esophagus and more injurious than the standard preparations of the same medicines. ...
Rationale:
Although esophageal compression due to cardiomegaly may be a risk factor of drug-induced esophageal injuries (DIEIs), the causal relationship between the two conditions has not been fully demonstrated.
Patient concerns:
We present a case of a drug-induced esophageal ulcer caused by left atrial enlargement in a 44-year-old woman with end-stage hypertrophic cardiomyopathy. Upper gastrointestinal endoscopy showed a deep, circumferential ulcer in the middle thoracic esophagus. CT revealed that the esophagus was compressed between the enlarged left atrium (LA) and the vertebral body. In the upper gastrointestinal series, retention of contrast media was observed in the esophagus near the LA.
Diagnosis:
The ulcer was a result of potassium chloride retention in the esophagus, which was compressed by the enlarged LA.
Intervention:
After cessation of potassium chloride administration for 2 months, the ulcer healed and a stricture developed. Two years after the ulcer development, the patient underwent heart transplantation, and subsequent endoscopic balloon dilation was performed for the esophageal stricture.
Outcomes:
The patient's oral intake recovered completely without any ulcer recurrence.
Lessons:
The case demonstrated that esophageal compression by the enlarged LA caused a drug-induced esophageal ulcer. Preventive care and treatment measures for DIEIs, including an anatomical approach, should be considered for patients with LA enlargement.
... Esophageal lesions is more common in the middle third part of esophagus, although distal and proximal lesions may be involved in some cases. 11,12 Endoscopy is more sensitive than radiological examination although studies comparing both examination have not been performed. 3 ...
... Endoscopic views of drug-induced esophagitis 11A. A small ulcer (< 5 mm) in the lower third of the esophagus, with adjacent erythematous streaks, in a 25−yearold woman who had taken a tablet of doxycycline B. Desloughing and ulceration of the mid−esophagus, with areas of bleeding, in a 60−year−old businessman who had taken a clarithromycin C. Extensive whitish exudates with underlying desloughed mucosa in the upper esophagus in a 52−year−old man who had taken a tetracycline D. A vascular bleb was seen in the lower esophagus with a blood clot and active oozing from the surrounding area in a 74-year-old man who was taking aspirin and naproxen E.Areas of mucosal ulceration in the mid−esophagus facing each other (kissing ulcers) in 66−year−old woman who was taking potassium chloride tablets Endoscopic views of drug-induced esophagitis11 A. A small ulcer (< 5 mm) in the lower third of the esophagus, with adjacent erythematous streaks, in a 25−year-old woman who had taken a tablet of doxycycline B. Desloughing and ulceration of the mid−esophagus, with areas of bleeding, in a 60−year−old businessman who had taken a clarithromycin C. Extensive whitish exudates with underlying desloughed mucosa in the upper esophagus in a 52−year−old man who had taken a tetracycline D. A vascular bleb was seen in the lower esophagus with a blood clot and active oozing from the surrounding area in a 74-year-old man who was taking aspirin and naproxen E. Areas of mucosal ulceration in the mid−esophagus facing each other (kissing ulcers) in 66−year−old woman who was taking potassium chloride tablets F. An area of denudation of the proximal esophageal mucosa seen in a 68−year−old who had recently started taking alendronate tabletsF.An area of denudation of the proximal esophageal mucosa seen in a 68−year−old who had recently started taking alendronate tablets Barium esophagram of drug-induced esophagitis13 A. Double-contrast esophagram in a 26-year-old woman taking tetracycline who presented with dysphagia shows a radiolucent round filling defect with a thin rim of barium (arrow). The finding represents a superficial ulcer with surrounding edema B. Double-contrast esophagram (profile view) in a 59-year-old man taking clindamycin who presented with dysphagia shows an elongated, flat, plaquelike filling defect (arrow) consistent with an ulcer C. Barium esophagram in a 72-year-old woman taking alendronate who presented with dysphagia shows a cluster of linear erosions (arrows) in the mid esophagus Barium esophagram of drug-induced esophagitis13 ...
Esophageal injury could be caused by a various etiology, such as drug administration. Drug-induced esophagitis is a spectrum of esophageal lesions due to drugs that can cause complications of ulceration, perforation and stricture of the esophagus. More than one hundred drugs have been identified to cause damage to the esophageal wall, such as antibiotics, nonsteroidal anti inflammatory drugs (NSAID), alendronate, potassium chloride, anti-hypertension, quinidine, etc. Symptoms of drug induced esophagitis might appear as retrosternal pain, heartburn, odynophagia, dysphagia, weight loss, gastrointestinal bleeding, which also found in other cases of gastrointestinal lesions so they are often misdiagnosed in daily clinical practice. Endoscopic procedure is the first choice in diagnosis of drug-induced esophagitis. The lesion may appear as erosion, bleeding, ulcers, strictures, kissing ulcers, and residual drugs fragment on endoscopy. Management of drug-induced esophagitis are by stopping suspected drugs and educating about the proper drug administration. In severe cases, adequate fluid hydration and parenteral nutrition can be given. Sucralfat forms a protective layer in the area of the lesion, thus accelerates wound healing process. Acid-lowering agents can be considered in cases of reflux esophagitis. Therapeutic endoscopic may indicated in strictures cases, active bleeding due to esophageal ulcers, and retrieval remaining drug fragments that are lodged in the esophagus. While surgery should be reserved for patients with severe complications such as erosion of the mediastinal organs, heart and large blood vessels
... The most frequently implied drugs for this condition are doxycycline, tetracycline, non-steroid anti-inflammatory drugs, clindamycin, aspirin, potation chloride and alendronate sodium. [1,2] Risk factors for esophagitis after usage of drugs are taking gelatin-coated pills and capsules without sufficient amount of fluids, the quantity of the drug, and sleeping right after taking the drug. [3] Typical symptoms of medication-related esophagitis are retrosternal burning that occurs after taking drugs, pain that extends to the back and odynophagia. ...
... It was reported that ulcers that develop because of doxycycline and tetracycline are small, separate from each other, and they are located in the middle esophagus. [1,2] Our case was admitted with complaints of retrosternal burning, back pain and odynophagia. In the upper GIS endoscopy, an area surrounded by continuous hyperemic ulcers was observed to cover ¾ of the esophagus lumen. ...
... Endoscopy of our case demonstrated a typical esophageal ulcer at the mid-esophagus, which is consistent with medication-induced esophagitis [3,4,11,12]. The mid-esophagus is the most common site of injury due to its anatomical narrowing from aortic arch compression [2], and so pills may be easily retained in this area. ...
... The mid-esophagus is the most common site of injury due to its anatomical narrowing from aortic arch compression [2], and so pills may be easily retained in this area. Although a Kissing ulcer was observed in our patient, which is typical of an endoscopic finding, this has only been found in 8% of the patients undergoing endoscopy [12]. Conversely, among biopsy-proven histopathology, this has correlated with a kissing-ulcer in 77% of cases [13]. ...
Pill-induced esophagitis or esophageal ulcers are considered when patients have retrosternal chest pain or odynophagia following the ingestion of suspicious medications. Various drugs have been reported to induce esophageal ulcers. However, amoxycillin-clavulanic acid-induced esophagitis or esophageal ulcer has not been reported in literature. Hence, we report the case of a 30-year-old Thai male who presented with acute, severe odynophagia and retrosternal chest pain. He had a history of taking amoxycillin-clavulanic acid for 12 days. An esophagogastroduodenoscopy was performed and revealed geographic clean-based ulcers, with a kissing-ulcer appearance at the level of the mid-esophagus. A biopsy was taken and revealed inflamed granulation tissue and an ulcer with neither infection nor malignancy. Thus, the diagnosis of an amoxycillin-clavulanic acid-induced esophageal ulcer was made according to the clinicopathologic report.
... While it can occur at any age, it is more prevalent in elderly patients [37]. Polypharmacy, decrease in esophageal motility, and taking medication with insufficient amounts of water are factors most commonly associated with pill esophagitis in elderly [38]. Additionally, patients with cardiomegaly can develop esophageal compression from enlarged left atrium, placing them at increased risk for medication induced esophagitis. ...
... Additionally, patients with cardiomegaly can develop esophageal compression from enlarged left atrium, placing them at increased risk for medication induced esophagitis. Abid et al. found female gender, presence of diabetes, and ischemic heart disease, in addition to advanced age, to be associated with pill esophagitis [38]. The most commonly implied causative agents include nonsteroidal anti-inflammatory drugs (NSAID), aspirin, doxycycline, bisphosphonates, ferrous sulfate, and captopril. ...
Considering an increase in the life expectancy leading to a rise in the elderly population, it is important to recognize the changes that occur along the process of aging. Gastrointestinal (GI) changes in the elderly are common, and despite some GI disorders being more prevalent in the elderly, there is no GI disease that is limited to this age group. While some changes associated with aging GI system are physiologic, others are pathological and particularly more prevalent among those above age 65 years. This article reviews the most important GI disorders in the elderly that clinicians encounter on a daily basis. We highlight age-related changes of the oral cavity, esophagus, stomach, small and large bowels, and the clinical implications of these changes. We review epidemiology and pathophysiology of common diseases, especially as they relate to clinical manifestation in elderly. Details regarding management of specific disease are discussed in detail if they significantly differ from the management for younger groups or if they are associated with significant challenges due to side effects or polypharmacy. Cancers of GI tract are not included in the scope of this article.
... Oropharyngeal and esophageal dysphagia is common in people with Parkinson's disease [7,16,23]. With a third of respondents reporting difficulties swallowing pills, there is an increased risk of medicines entering the airway or becoming stuck in the throat or oesophagus [1,21,22]. This has severe health consequences [1,39]. ...
... With a third of respondents reporting difficulties swallowing pills, there is an increased risk of medicines entering the airway or becoming stuck in the throat or oesophagus [1,21,22]. This has severe health consequences [1,39]. In addition to the risk of asphyxiation or respiratory infection from aspirated materials, pill-induced oesophageal injury can occur when medicines get stuck and dissolve in the oesophagus [21,39]. ...
Medicine administration errors are twice as frequent in people with dysphagia than in those without. Medicine administration is particularly critical for people with Parkinson's disease where late, or missed doses reduce medicine effectiveness and impact on the quality of life. The aim of this study was to explore the current medicine administration practices of people with Parkinson's disease in New Zealand. A self-administered online survey was developed by an interprofessional group including people with Parkinson's disease (the primary stakeholders), speech-language pathologists and pharmacists. The survey was administered using a cross-sectional study design and asked respondents about self-reported swallowing difficulties [using Eating Assessment Tool (EAT-10)], medicine regimes and strategies used to swallow medicines. Seventy-one people with Parkinson's disease responded to the survey (69% male, mean age 72 years, mean years with Parkinson's disease 9 years). Respondents reported complex daily multi-medicine consumption (mean no. of pills 11, range 2-25). Analyses showed that 57% of respondents scored outside the normal range for EAT-10 (> 3) with 57% complaining of difficulties with pills. Many respondents admitted to missing medicines and requiring external reminders. Multiple strategies for swallowing pills were described including crushing tablets, using yoghurt or fruit juice, and swallowing strategies (such as head tilt, effortful swallow, chin down and altered pill placement in the mouth). Medicine administration is complex and challenging for people with Parkinson's disease. The development of educational packages for people with Parkinson's disease, their carers and health professionals is much needed.
... The most frequently implied drugs for this condition are doxycycline, tetracycline, non-steroid anti-inflammatory drugs, clindamycin, aspirin, potation chloride and alendronate sodium. [1,2] Risk factors for esophagitis after usage of drugs are taking gelatin-coated pills and capsules without sufficient amount of fluids, the quantity of the drug, and sleeping right after taking the drug. [3] Typical symptoms of medication-related esophagitis are retrosternal burning that occurs after taking drugs, pain that extends to the back and odynophagia. ...
... It was reported that ulcers that develop because of doxycycline and tetracycline are small, separate from each other, and they are located in the middle esophagus. [1,2] Our case was admitted with complaints of retrosternal burning, back pain and odynophagia. In the upper GIS endoscopy, an area surrounded by continuous hyperemic ulcers was observed to cover ¾ of the esophagus lumen. ...
... 26 Of 92 patients with pill-induced esophageal injury, NSAIDs were causative in 41% (38 of 92) of them. 27 The prevalence of esophagitis in patients with arthritis taking NSAIDs was 21%, 28 and a case-control study 29 indicated that, together with hiatal hernia, NSAID intake represents a significant (P 5 .021) risk factor (OR 1.87; 95% CI 1.10-3.19) ...
... At endoscopy, erosions, kissing ulcers, and multiple areas of ulceration with bleeding may be seen. 27 The presence of exudates with thickening of the esophageal wall suggests a chemical esophagitis. Moreover, 50% of patients with acute necrotizing esophagitis, a previously considered rare cause of upper gastrointestinal bleeding (UGIB), had taken NSAIDs. ...
Non-steroidal anti-inflammatory drugs (NSAIDs) can damage the gastrointestinal tract, causing widespread morbidity and mortality. Although mechanisms of damage involve the activities of prostaglandin-endoperoxide synthase 1 (PTGS1 or COX1) and PTGS1 (COX2), other factors are involved. We review mechanisms of gastrointestinal damage induction by NSAIDs, via COX-mediated and COX-independent processes. NSAIDs interact with phospholipids and uncouple mitochondrial oxidative phosphorylation, which initiates biochemical changes that impair function of the gastrointestinal barrier. The resulting increase in intestinal permeability leads to low-grade inflammation. NSAID's inhibition of COX enzymes, along with luminal aggressors, results in erosions and ulcers, with potential complications of bleeding, protein loss, stricture formation, and perforation. We propose a model for NSAID-induced damage to the gastrointestinal tract that includes these complex, interacting, and inter-dependent factors. This model highlights the obstacles for the development of safer NSAIDs.
... NSAIDs use is also associated with esophagitis and affected patients present with complaints of dysphagia, odynophagia, or abdominal pain [58]. Endoscopy showing damage to the mucosal lining of the esophagus and pill components adherent to the esophageal lining confirms the diagnosis [59]. ...
Non-steroidal anti-inflammatory drugs (NSAIDs) are commonly used for their anti-inflammatory, antipyretic, and analgesic properties. However, their use is often associated with gastrointestinal tract (GIT) side effects due to the inhibition of both cyclooxygenase (COX)-1 and COX-2 enzymes, leading to a decrease in gastroprotective prostaglandins (PG). To minimize these adverse effects, various approaches have been explored, including selective COX-2 inhibitors, NO-NSAIDs (nitric oxide-releasing NSAIDs), and dual COX/LOX (lipoxygenase) NSAIDs. However, the effects of these gastroprotective NSAIDs on the GIT and their efficacy remains uncertain. This review aims to provide an overview of the current understanding of the effects of traditional NSAIDs and gastroprotective NSAIDs on GIT. We discuss the underlying mechanisms of GIT damage caused by NSAIDs, including mucosal injury, ulceration, and bleeding, and the potential of gastroprotective NSAIDs to mitigate these effects. We also summarize recent studies on the efficacy and safety of various gastroprotective NSAIDs and highlight the limitations and challenges of these approaches. The review concludes with recommendations for future research in this field.
... Pill-induced esophagitis may present as erosions, kissing ulcers, and multiple small areas of ulceration with bleeding mainly in the middle third of the esophagus [33]. Treatment of pill-induced esophagitis consists of discontinuation of the offending drug and use of PPIs or sucralfate to hasten esophageal mucosal healing [34]. ...
Upper gastrointestinal endoscopy is the most important test used to diagnose esophageal disease. Proper insertion of the endoscope is essential for accurate examination of the esophagus. However, due to coughing or the gag reflex, esophageal examinations can be difficult. Further, when a central ridge is present in the middle of the pyriform sinus, careful approach is necessary. Chromoendoscopy of the esophagus includes acetic acid chromoendoscopy for Barrett’s esophagus and lugol’s iodine chromoendoscopy for squamous cell carcinoma. In recent times, electronic chromoendoscopy is widely used. In this chapter, diagnosis and treatment of various esophageal diseases including esophagitis, Barrett’s esophagus, adenocarcinoma, squamous cell carcinoma, diverticulum, inlet patch, hiatal hernia, polyps, subepithelial lesions, and varix are discussed.
... Bisphosphonates including alendronate are commonly prescribed osteoporosis medications and have also been described to cause pill oesophagitis, with the long-term risk of oesophageal stricture formation. 6 Apart from retrosternal pain, odynophagia and dysphagia, if left unrecognised, and offending medications are continued, oesophageal haemorrhage, strictures or even fatal oesophageal perforations can occur, albeit rarely. 4 We recommend that to limit this potential complication and its potential significant morbidity, prescribing physicians should counsel patients on the risk of pill oesophagitis and advise that the tablet not be taken immediately prior to lying down. ...
... Therefore, quite different drugs have been reported to cause esophageal injury. This type of injury, called pill esophagitis or injury to the esophagus caused by the pill, is common (3,10,11). However, it has not been sufficiently reported. ...
... Common symptoms for pill-induced esophagitis are odynophagia, chest pain, vomiting, dysphagia and, less frequently, hematemesis 11 . Perforation and fatal injuries have also been reported. ...
Several pathological conditions, other than gastro-esophageal reflux disease and its complications, can affect the esophagus. While some of these can present with unspecific lesions (i.e. ulcers and epithelial damage) and require clinico-pathological correlation for diagnosis (i.e. drug-induced esophagitis and corrosive esophagitis) other conditions show distinctive histological lesions which enable the pathologist to reach the diagnosis (i.e. some specific infectious esophagites and Crohn's disease). In this context eosinophilic esophagitis is the condition which has been increasingly studied in the last two decades, while lymphocytic esophagitis, a relatively new entity, still represents an enigma. This overview will focus on and describe histologic lesions which allow pathologists to differentiate between these conditions.
... По данным систематического обзора [22] имеются три основные патофизиологические гипотезы, связанные с возникновением НЯ на уровне пищевода после приема лекарственного средства: 1. Эзофагеальное раздражение из-за попадания таблетки в пищевод, преимущественно вследствие медленного прохождения. Это подтверждается тем наблюдением, что повреждение часто локализовано в средней или проксимальной трети пищевода [23]. ...
Treatment of osteoporosis is a difficult task due to the need for long-term medication and maximum safety. The main goal of osteoporosis treatment is to prevent bone fractures. According to the national clinical guidelines for the treatment of osteoporosis, nitrogen-containing bisphosphonates are among the first-line drugs for the prevention and treatment of this disease. The diversity in the side chain structure determines the strength with which bisphosphonates bind to hydroxyapatite, are distributed, and remain in bone tissue for a certain time after treatment has been completed. They are the drugs of choice as they have proven efficacy in reducing the risk of fractures, and at the same time an acceptable safety profile. Bisphosphonates are the most well-known and studied drugs, successfully used in all countries for the treatment of various forms of osteoporosis. When using oral forms of bisphosphonates, the most expected undesirable phenomenon is esophagitis. The development of new forms of well-known and proven medicines that reduce adverse events and increase adherence to treatment is extremely important and promising. Of the latest achievements in this regard, it should be noted a new form of alendronate-Binosto-effervescent soluble tablet, the use of which reduces the risk of irritating effects on the upper gastrointestinal tract.
... Injury of this type, called pill esophagitis or pill induced esophageal injury is common but unfortunately is under-reported. More than a hundred different medicines have been reported to cause esophageal injury [1]. This injury is a common cause of esophageal complaints such as severe odynophagia, dysphagia, bleeding and even perforation. ...
... In addition, medications such nonsteroidal anti-inflammatory drugs, tetracyclines, potassium, iron, and vitamin C tablets can cause pill-induced esophagitis that presents as acute esophageal dysphagia. These types of medications can cause mid-or distal esophageal ulceration and even a stricture [27]. ...
Functional dysphagia is an uncommon cause of dysphagia symptoms presenting a diagnostic and therapeutic challenge to clinicians. It is defined as a sensation of abnormal bolus transit in the absence of any mucosal, structural, or major functional abnormalities of the esophagus. The pathophysiology of functional dysphagia is multifactorial and includes esophageal hypersensitivity, abnormal central processing of esophageal stimuli, intermittent abnormal esophageal motor disorder, and psychological comorbidities. Diagnosis requires exclusion of structural, mucosal, and major esophageal motor disorders. This is accomplished with a careful history and physical examination, upper endoscopy with mucosal biopsies, and high-resolution esophageal manometry. Treatment of functional dysphagia includes lifestyle modifications and avoidance of triggers, neuromodulators, and management of psychological comorbidities. Nonpharmacologic management includes bougie dilation and in carefully selected patients botulinum toxin injections into the distal esophagus. Functional dysphagia remains an area of active research, and thus, the definition, epidemiology, diagnosis, and treatment are likely to continue and evolve in the future.
... Moreover, pills tend to lodge at areas of esophageal narrowing, such as the levels of the aortic arch, the left main bronchus, and the gastroesophageal junction [5]. Most cases of pill-induced esophagitis are self-limiting and heal without intervention over 3-10 days [6]. ...
We report an unusual case of severe chest pain caused by N -acetylcysteine-induced esophagitis. An 81-year-old Chinese man with a history of interstitial lung disease was admitted to our hospital with intermittent arrhythmia that began 5 days ago. The patient presented with complaints of cough, sputum, and shortness of breath. Cefminox injections and N -acetylcysteine tablets were prescribed to improve respiratory symptoms. The patient developed severe chest pain and odynophagia 4 hours after swallowing the N -acetylcysteine tablet while in the decubitus position. Upper gastrointestinal endoscopy revealed four discrete areas of ulcerations measuring approximately 1 cm at the midesophageal level. The distance between the foci and the incisors was approximately 24 cm. The patient continued the N -acetylcysteine orally, which was administered in powdered form with more water while in the upright position. Pantoprazole and hydrotalcite were also administered to the patient. The symptoms subsided, and a follow-up endoscopy after 20 days showed that the ulcers healed. This case highlights that seemingly safe drugs such as N- acetylcysteine can lead to severe chest pain if ingested inappropriately.
... 9 It has been suggested that mechanisms for the development of pill-induced esophagitis include direct irritant effects caused by contact of the medication with the esophageal mucosa leading to local acid burn or hyperosmolality or by disruption of the cytoprotective barrier. 10 Prolonged contact time between the offending compound and esophageal mucosa seems to increase the likelihood of injury. Ulcers are commonly located in the middle third of the esophagus, where the aortic arch may provide extrinsic compression of the esophagus and narrow its lumen. ...
Cases of pill-induced esophagitis can be associated with significant acute symptoms leading to hospitalization and have resulted in mediastinal penetration and hemorrhage. Clinicians often consider the diagnosis in patients taking classically associated medications. However, because many patients take dietary supplements, it is important to consider these as a potential etiology in a patient presenting with esophageal symptoms. We present a case of pill-induced esophagitis in a 40-year-old woman after the ingestion of l-arginine, selenium, and vitamin E supplements. Literature review revealed 6 cases of l-arginine-induced esophagitis reported, and no previous cases associated with vitamin E or selenium.
... S. Abid и соавт. (2005), оценивая причины развития 92 случаев лекарственного эзофагита, отметили, что прием НПВП был наиболее частой (41 %) причиной [11]. ...
Нестероидные противовоспалительные препараты (НПВП) являются каузальным фактором повреждения слизистой оболочки не только желудка и двенадцатиперстной кишки, но и пищевода, запуская механизмы развития гастроэзофагеальной рефлюксной болезни (ГЭРБ). Известно, что прием НПВП (включая низкие дозы аспирина) способен существенно увеличивать вероятность развития пептического эзофагита с риском образования язв, кровотечения или формированием стриктур. В последние годы увеличилось количество работ, посвященных поражениям пищевода и изучению механизмов развития ГЭРБ, возникающих на фоне приема НПВП (включая низкие дозы ацетилсалициловой кислоты) и других лекарственных средств. Проанализирована структура лекарственно-индуцированных поражений верхних отделов желудочно-кишечного тракта у пациентов, принимающих НПВП. Изучена частота и особенности поражений пищевода у больных с остеоартрозом крупных суставов, получающих лечение НПВП, и определены факторы, повышающие риск развития данной патологии. Выбран наиболее рациональный подход диагностики и первичной профилактики НПВП-индуцированного эзофагита с учетом рассмотренных факторов риска, что в большинстве случаев должно уменьшить частоту побочных эффектов НПВП-ассоциированных поражений пищевода. Вычленены основные направления в лечении НПВП-ассоциированных повреждений пищевода, а именно: изменение образа жизни, рациональное питание, изменение дозы и режима приема НПВП или перевод на селективный НПВП, современная фармакотерапия и хирургическое лечение. На клинических примерах пациентов с повреждениями пищевода и желудка, ассоциированными с длительным приемом НПВП и антитромбоцитарных средств, обсуждены меры профилактики и лечения этой категории пациентов с использованием ингибиторов протонной помпы и висмутсодержащих препаратов.
... Injury of this type, called pill esophagitis or pill induced esophageal injury is common but unfortunately is under-reported. More than a hundred different medicines have been reported to cause esophageal injury [1]. This injury is a common cause of esophageal complaints such as severe odynophagia, dysphagia, bleeding and even perforation. ...
... The endoscopic study of the esophagus can demonstrate erythema in 83% of cases, erosions in 58%, ulcers in 26% (hemorrhagic ulcers in 18% and "kissing type" ulcers in 8%) and stenoses in 8%. These lesions are mainly found in the middle third of the esophagus, which is the most common site of impaction of tablets, in 75.6% of cases, due to extrinsic compression of the esophagus by the aortic arch or the left atrium (43,44) . ...
BACKGROUND:
Gastroesophageal reflux disease (GERD) is a clinical condition that develops when the reflux of stomach contents causes troublesome symptoms and/or complications. Transient lower esophageal sphincter relaxation is the main pathophysiological mechanism of GERD. Symptoms and complications can be related to the reflux of gastric contents into the esophagus, oral cavity, larynx and/or the lung. Symptoms and other possible manifestations of GERD are heartburn, regurgitation, dysphagia, non-cardiac chest pain, chronic cough, chronic laryngitis, asthma and dental erosions. The proton pump inhibitor (PPI) is the first-choice drug and the most commonly medication used for the treatment of GERD. The most widespread definition of Refractory GERD is the clinical condition that presents symptoms with partial or absent response to twice-daily PPI therapy. Persistence of symptoms occurs in 25% to 42% of patients who use PPI once-daily and in 10% to 20% who use PPI twice-daily.
OBJECTIVE:
The objective is to describe a review of the current literature, highlighting the causes, diagnostic aspects and therapeutic approach of the cases with suspected reflux symptoms and unresponsive to PPI.
CONCLUSION:
Initially, the management of PPI refractoriness consists in correcting low adherence to PPI therapy, adjusting the PPI dosage and emphasizing the recommendations on lifestyle modification change, avoiding food and activities that trigger symptoms. PPI decreases the number of episodes of acid reflux; however, the number of “non-acid” reflux increases and the patient continues to have reflux despite PPI. In this way, it is possible to greatly reduce greatly the occurrence of symptoms, especially those dependent on the acidity of the refluxed material. Response to PPI therapy can be evaluated through clinical, endoscopic, and reflux monitoring parameters. In the persistence of the symptoms and/or complications, other causes of Refractory GERD should be suspected. Then, diagnostic investigation must be initiated, which is supported by clinical parameters and complementary exams such as upper digestive endoscopy, esophageal manometry and ambulatory reflux monitoring (esophageal pH monitoring or esophageal impedance-pH monitoring). Causes of refractoriness to PPI therapy may be due to the true Refractory GERD, or even to other non-reflux diseases, which can generate symptoms similar to GERD. There are several causes contributing to PPI refractoriness, such as inappropriate use of the drug (lack of patient adherence to PPI therapy, inadequate dosage of PPI), residual acid reflux due to inadequate acid suppression, nocturnal acid escape, “non-acid” reflux, rapid metabolism of PPI, slow gastric emptying, and misdiagnosis of GERD. This is a common cause of failure of the clinical treatment and, in this case, the problem is not the treatment but the diagnosis. Causes of misdiagnosis of GERD are functional heartburn, achalasia, megaesophagus, eosinophilic esophagitis, other types of esophagitis, and other causes. The diagnosis and treatment are specific to each of these causes of refractoriness to clinical therapy with PPI.
... In pill-induced esophagitis, ulcers are typically located at the level of the mid-esophagus when identified during esophagogastroscopy. 10 This site is commonly implicated as pills often ' lodged in narrow areas of the esophagus, leading to prolonged mucosal contact. This may result in mucosal inflammation, erosion, and ulceration, even in the absence of underlying esophageal disorders. ...
Pill-induced esophagitis is a rare cause of acute chest pain. Patients likely to be affected are those with underlying esophageal disorders, those who ingest medications without a sufficient amount of water, or adopt a supine position during or shortly after swallowing medication. Esophagitis secondary to ingestion of ascorbic acid pills is extremely rare. Here, we report a case of ascorbic acid-induced esophagitis in a middle-aged adult, with no known underlying pathological abnormalities of the esophagus. Diagnosis was made based on the history and endoscopic findings. The patient fully recovered and an esophageal ulcer healed after discontinuation of ascorbic acid.
Macrolides and tetracyclines are antibiotics that have a range of anti‐inflammatory properties beyond their microbial capabilities. Although these antibiotcs have been in widespread use, the long‐term safety profiles are limited. We performed a systematic review and meta‐analysis of randomized clinical trials (RCTs) that compared macrolides or tetracyclines with placeboes to provide long‐term safety information. We searched Medline and EMBASE from inception to October 2022 and identified studies that reported study‐drug‐related death, serious adverse events (SAEs), or withdrawal rates, and common adverse effects of each drug. Relative risk (RR) and number needed to harm (NNH) were calculated. Of the 52 RCTs included, there are 3,151 participants on doxycycline, 2,519 participants on minocycline, 3,049 participants on azithromycin, 763 participants on clarithromycin, 262 participants on erythromycin, and 100 participants on roxithromycin. There was no death related to any study drugs and rates of SAE were not significantly different from placebo in any drug. Overall withdrawal rates were slightly higher than placebo in doxycycline (RR, 1.30; 95% CI, 1.12‐1.52) and minocycline (RR, 1.29; 95% CI, 1.15‐1.46). Withdrawal rates due to adverse events were higher in doxycycline (RR, 2.82; 95% CI, 1.88‐4.22), minocycline (RR, 1.48; 95% CI, 1.09‐1.98), and azithromycin (RR, 1.53; 95% CI, 1.13‐2.08). Gastrointestinal (GI) disturbances are the most common tolerable adverse effects for every drug. Photosensitivity and rash are the second most common for doxycycline and minocycline. We found no evidence that long‐term use up to 2 years of macrolides or tetracyclines was associated with increased risk of SAEs.
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Endoscopy is a critical skill set for deployment of surgical teams at sea on certain platforms. There are multiple emergent indications for endoscopy, most commonly esophageal food impactions and gastrointestinal bleeding; however, as a diagnostic modality endoscopy is also critical to rapidly triage and evaluate the deployed patient to maintain mission readiness. Additionally, endoscopy can be utilized as an adjunct during various surgical procedures. Familiarity with the endoscopic equipment and pathologies diagnosed and managed endoscopically are important for the deployed surgical team. This chapter reviews the endoscopic equipment including basic setup, risks of endoscopy, fundamentals of endoscopic technique, troubleshooting steps during the difficult procedure, and presentation, diagnosis, and endoscopic and medical management of the most commonly encountered gastrointestinal (GI) pathologies at sea.KeywordsColonoscopyGastrointestinal hemorrhageDuodenumInflammatory bowel diseasesGastrointestinal endoscopyEsophagogastroduodenoscopyEGDEndoscopy equipmentEndoscopy techniqueCommon endoscopic findingsEndoscopic management of common diseasesForegut obstructionsMaritime surgerySurgery at sea
Objectives:
Dabigatran-induced oesophagitis has emerged in recent years. However, the incidence and clinical characteristics of patients with dabigatran-induced oesophagitis have not yet been clarified. The aim of this study was to examine the clinical characteristics of the disease.
Methods:
A retrospective analysis was undertaken of the literature on dabigatran-induced oesophagitis in Chinese and English from 2008 onwards.
Results:
There were 20 men (74.07%) and seven women (25.93%) in the study; their median age was 75 years (range 37-90). The main clinical symptoms were dysphagia (42.31%), odynophagia (26.92%), retrosternal pain (23.08%) and heartburn (23.08%). Endoscopy mainly showed sloughing mucosal casts (14 cases, 56%), ulcers (8 cases, 32%) and erosion (6 cases, 24%). The main injury sites were the mid to lower oesophagus (32%) and the mid oesophagus (32%). Withdrawal of dabigatran or giving the correct medication regimen resulted in rapid recovery of clinical symptoms from 1 day in some patients and up to 4 weeks, and mucosal recovery (2-5 weeks) in a median time of 3 weeks (range 0.29-48) in all patients.
Conclusions:
Oesophagitis is a rare complication of dabigatran with a good prognosis. Patients should be given proper medication instructions to prevent the occurrence of dabigatran-induced oesophagitis.
In recent decades, the number of cases developing drug-induced esophagitis (DIE) has reportedly been growing, which indicates the significance of detecting medicines capable of causing this adverse reaction. This study aims to provide an updated review on recent case reports of DIE, to evaluate the possible mechanism of this side effect, and to provide helpful management. Data was gathered through searches of three databases, namely PubMed, Medline, and Cochrane. Seven drug categories were evaluated: antibiotics, bisphosphonates, cardiovascular medicines, chemotherapeutic agents, non-steroidal anti-inflammatory drugs (NSAIDs), other medications, and supplements. According to the findings, retrosternal pain, heartburn, odynophagia, and dysphagia are typical symptoms of DIE, and in most cases, DIE is a self-limiting side effect which can be resolved by removing the causative agent and providing supportive therapy.
The esophagus is susceptible to a variety of environmental exposures and the effects of systemic and dermatological diseases. This chapter discusses causes of esophageal pathology. Esophageal perforation may also be attributed to foreign body ingestion, and in rare instances, may manifest following esophageal infection. Injury to the esophagus resulting in perforation or rupture is life threatening, and successful management depends on early diagnosis and prompt intervention. Elderly patients are at increased risk for pill esophagitis due to frequent use of high‐risk medications, decreased salivation, and a higher prevalence of esophageal dysmotility. For endoscopic therapy of strictures, balloon dilators may be preferable to bougienage to avoid damage to friable mucosa, and a preprocedural barium swallow may help plan the procedure by assessing angulation within the stricture. Because dilation carries an increased risk of esophageal trauma and perforation, fluoroscopy may be a valuable adjunct.
Gastrointestinal manifestations resulting from either prescribed medications or over the counter drugs are commonly encountered in clinical practice. Adverse drug events (ADEs) are often mistaken for a disease process or a syndrome, leading to multiple and unnecessary diagnostic studies, hospitalizations, and poor outcomes. The morbidity, mortality, and health care costs associated with adverse drug events, even restricted to the GI tract, are underestimated. The consequences of adverse effects may be asymptomatic or range from mild abdominal discomfort to fatal hemorrhage, perforation, and requirement for hospitalization, including surgery. Increased awareness and recognition of the intended and unacceptable effects of medications on the gastrointestinal tract and taking steps to withdraw the offending medication or revising the regimen will help improve outcomes. The Beers criteria, which are updated annually, provide a concise list of medications to avoid or use with caution in older adults. Polypharmacy is common in older adults and leads to adverse drug events due to drug-drug or drug-disease interactions. Appropriate deprescribing, referring to the timely discontinuation or decrease in dosage of offending drugs, may be the answer to polypharmacy in order to minimize adverse drug-related outcomes.
For both patients (i.e., pediatric and geriatric) the products should be age appropriate, an essential criterion for achieving efficient drug therapy. Some frequently reported problems associated with these formulations may include the inappropriateness of the product with different age-groups, imperfect labeling, incompatibility, and unacceptability of drugs, which are the primary concern for causing errors in pediatric populations. During formulation, some factors such as formulation components (active pharmaceutical ingredient and excipients), substances used in primary packaging, and employed devices should be considered for their suitability and safety. However, for both populations, the oral route is widely preferred for delivering drugs for efficient results. Further, recent clinical investigations advocate the suitability of minitablets if we consider swallow-ability and acceptability of formulation as compared to other traditional liquid products. This chapter provides deep insight into different oral products for pediatric and geriatric patients. It discusses various alternative novel formulations (e.g., minitablets and flexible oral formulations) over conventional solid and liquid products.
Objectives:
Esophagitis dissecans superficialis (EDS) is a desquamative disorder of the superficial esophageal epithelium with variable clinical characteristics. Endoscopically there is an appearance of superficial peeling of sheets of epithelium. Histologically there is two-toned epithelium with coagulative necrosis of the superficial epithelium. Currently, there is paucity of data regarding this condition in children.
Methods:
A ten-year retrospective search of the pathology information system was performed for cases with a pathologic diagnosis of EDS in a tertiary care pediatric center. Demographic data, clinical history, endoscopic findings and histopathologic reports were reviewed.
Results:
Thirteen patients (nine female; ages 3-18 years), were identified with histologic findings of EDS. Esophageal food impaction, dysphagia, vomiting, and abdominal pain were the most common presenting symptoms. Sixty-nine percentage of the patients had underlying comorbidities and 76% were on at least one medication chronically. Eosinophilic esophagitis (23%), inflammatory bowel disease (23%) and gastro-esophageal reflux disease (15%) were the most common associated diagnoses. Of the 13 patients, five had repeat endoscopies showing complete resolution of EDS with no complications.
Conclusions:
EDS is an under-recognized entity that endoscopists should be familiar with. In our series, the most prevalent associations were with food impaction and eosinophilic esophagitis. Contact injury and/or inflammation may precede the development of EDS. Pediatric EDS appears to be an incidental finding without significant morbidity or mortality.
The esophagus has a pearly white and smooth surface under which a network of small vessels is seen. Fungi and viruses are responsible for most cases of infectious esophagitis, and dual infections may be encountered. Bacterial, mycobacterial, and parasitic esophagitis are rarely encountered in esophageal biopsy material. The chronic regurgitation of gastroduodenal juice into the esophagus causes gastroesophageal reflux disease. There are several endoscopic classifications of gastroesophageal reflux disease. Eosinophilic esophagitis is a chronic, immunemediated or antigen‐mediated inflammatory condition characterized by symptomatic esophageal dysfunction and eosinophil predominant mucosal inflammation. Sloughing esophagitis is characterized by extensive superficial squamous mucosal necrosis or desquamation, associated with endoscopic plaques imparting a sloughing appearance to the mucosa. Graft versus host disease is an important complication of allogeneic stem cell transplantation, leading to considerable morbidity and mortality. The histological differential diagnosis includes lymphocytic esophagitis, eosinophilic esophagitis, certain infections, and pill esophagitis.
This chapter starts with a description of esophageal anatomy and how esophageal symptoms may develop. It addresses the effect that esophageal symptoms have on the patient's quality of life (QoL). The chapter discusses the most common symptoms that are attributed to the esophagus: dysphagia, odynophagia, heartburn, regurgitation, chest pain, globus, and extraesophageal symptoms. Patients with infectious esophagitis often present with odynophagia. Many patients seek care from pulmonologists and otolaryngologists for what are referred to as extraesophageal symptoms of gastroesophageal reflux disease. Esophageal disease is a significant source of symptoms for patients worldwide, and its impact on the health care system and QoL is significant. Esophageal disease is a significant source of patient symptoms worldwide, and symptoms result from a complex neurophysiologic response to the activation of a variety of nociceptors. Esophageal symptoms have accounted for significant healthcare utilization in the form of clinic visits, endoscopic procedures, medication usage, and surgical intervention.
This chapter presents an overview of the pathophysiology, etiologies, diagnosis, and management of patients with esophageal perforation. Boerhaave syndrome, or effort rupture of the esophagus, describes a spontaneous, longitudinal perforation of the left posterolateral aspect of the distal esophagus due to a sudden increase in intraesophageal pressure, combined with negative intrathoracic pressure and/or failure of the cricopharyngeal muscle to relax. Iatrogenic perforation can occur during endoscopic procedures, esophageal intubation, and surgery. The clinical manifestations of an esophageal rupture or perforation vary by its etiology. Urgent surgical management remains the mainstay of treatment for the majority of patients with esophageal perforations and rupture to limit ongoing mediastinal contamination and manage the perforation site. Although esophageal perforation traditionally required surgical management, a modern, multidisciplinary approach that might involve endoscopic, interventional radiology, and surgical approaches is increasingly used.
Drug-induced injury to the gastrointestinal tract is fairly common, often with important clinical consequences. An aging population, coupled with an ever-expanding drug industry, and availability of a bewildering array of both prescription and over-the-counter medications offer increasing opportunities to encounter unwarranted side effects from different medications. Several factors such as dose, mechanism of action, drug interactions, and the individual’s underlying health status can influence the type and severity of medication effects. Mucosal damage may occur due to direct physical injury or by altering mucosal immunity and local environmental milieu. Pathologic changes induced by medications are varied, often non-specific, and can mimic various diseases, including neoplasms. An awareness of the spectrum of pathologic changes induced by various drugs is important in establishing a temporal relationship and avoiding misdiagnosis.
Esophagitis frequently causes clinical symptoms, including dysphagia, odynophagia, and regurgitation, that compel patients to seek evaluation and treatment. The most common cause of these symptoms is esophageal inflammation related to reflux; however, causes of nonreflux esophagitis are an increasingly important diagnostic consideration. Nonreflux esophagitis remains relatively rare in clinical practice, but its incidence has seen a dramatic increase over the last two decades. In particular, there has been a rapid expansion in the incidence and prevalence of eosinophilic esophagitis. Other causes include infections esophagitis (fungal, viral, and tuberculous), medication-induced esophagitis, radiation esophagitis, and acute esophageal necrosis. This chapter outlines these causes and examines the clinical presentation, epidemiology, diagnostic work-up, and management of each distinct cause.
Gastrointestinal (GI) disorders are common in older adults. Age-related changes in gastrointestinal function and an increase in the prevalence of diseases that impact gastrointestinal function, including diabetes and polypharmacy, all play a role. US census data from 2005 revealed that approximately 50% of people over the age of 65 had at least one GI complaint severe enough to merit an annual medical visit [1]. In the United States, the number of residents aged 65 years or older will double from the current 47 million to more than 90 million in 2060 [2]. These demographic changes will result in an increasing number of GI disorders requiring care. Common GI problems seen in older adults include swallowing disorders, reflux disease, constipation, pill esophagitis, peptic ulcer disease, gallbladder disease, diverticular disease, nonalcoholic fatty liver disease, and GI cancers. In this chapter, we will address approaches which promote healthy aging by preventing, identifying, and treating common GI complaints in older adults.
This book concisely summarises non-neoplastic gastrointestinal (GI) pathology and provides histopathologists aiming to refresh or expand their knowledge with a practical approach to the interpretation of biopsies. It focuses on GI biopsies, but also covers the pathology of resections and other organs where appropriate. The editor and contributors bring their expertise as practicing diagnostic pathologists across Europe and the US. Examples of topics include inflammatory bowel disease, infections, vascular disorders, and inflammatory conditions specific to various anatomical sites. Fact sheets, practice points and tables facilitate rapid assimilation of information and enhance the reader's experience, and with additional access to the full online version, including expandable images on Cambridge Core, achieve accuracy every time. High-quality illustrations are also numerous, and references are relevant and reliable. This book is a practical, readable and up-to-date asset for any pathologist encountering GI biopsies.
This book concisely summarises non-neoplastic gastrointestinal (GI) pathology and provides histopathologists aiming to refresh or expand their knowledge with a practical approach to the interpretation of biopsies. It focuses on GI biopsies, but also covers the pathology of resections and other organs where appropriate. The editor and contributors bring their expertise as practicing diagnostic pathologists across Europe and the US. Examples of topics include inflammatory bowel disease, infections, vascular disorders, and inflammatory conditions specific to various anatomical sites. Fact sheets, practice points and tables facilitate rapid assimilation of information and enhance the reader's experience, and with additional access to the full online version, including expandable images on Cambridge Core, achieve accuracy every time. High-quality illustrations are also numerous, and references are relevant and reliable. This book is a practical, readable and up-to-date asset for any pathologist encountering GI biopsies.
The gastrointestinal (GI) tract is an extraordinary organ system consisting of different functional regions with varying functions. It serves as a digestive organ, taking in whatever is swallowed, converting it into nutrients, and discarding the waste. In general, the GI tract consists of four concentric layers progressing outward from the lumen, namely mucosa, submucosa, muscularis propria, and serosa or adventitia. Although the mucosal features vary significantly from one region to another, the other layers share many of the same features throughout the GI tract, albeit some differences do exist.
The use of prescription and over-the-counter medications is on the rise in the US population, especially among those aged 65 and over, with over 46% of the population taking at least 1 prescription medication. Given the frequency of medication use, and that the majority of these medications are taken orally, it has become increasingly relevant for pathologist examining endoscopically obtained gastrointestinal tract mucosal biopsies to consider and recognize patterns of mucosal injury associated with various drugs. Reports on injuries associated with certain classes of drugs can be scattered among different sources, making a comprehensive view of various injury patterns and the drugs known to cause them difficult to obtain. Herein, we provide a comprehensive overview of the drugs known to cause mucosal injuries in the tubular gastrointestinal tract organized by the organ involved and the prominent pattern of injury.
Drug-induced esophagitis has been increasingly recognized in the past few years, with the most severe injuries resulting from the ingestion of caustic alkali, usually accidentally in children. Esophageal injuries from acid occur more commonly in some developing countries. Numerous medications have been implicated in the production of esophageal injury, which occurs via systemic effects or by causing direct esophageal mucosal injury, with elderly patients in particular being at risk. More than 30 medications have now been implicated in causing drug-induced esophagitis.
As the portal to the gastrointestinal (GI) tract, the esophagus is susceptible to insults and injury from a variety of environmental exposures and to the effects of systemic and dermatological diseases. This chapter discusses several causes of esophageal pathology. The esophagus is the most common site of foreign body impaction in the GI tract, due to its proximal location and narrow caliber. Food is the most common cause of esophageal foreign body impaction (EFBI) in adults. Due to frequent use of high-risk medications, decreased salivation, and a higher prevalence of esophageal dysmotility, elderly patients are at increased risk for pill esophagitis. Pill esophagitis can largely be prevented with appropriate patient education. Once a corrosive injury has occurred, there is no role for inducing emesis, lavaging the esophagus, or using a neutralizing agent because these modalities have the potential to cause further mucosal damage.
A retrospective study of 55 patients with a benign esophageal stricture showed that in 11 patients (20%) the cause was a drug-induced lesion due to potassium chloride (3), tetracyclines (3), aspirin (2), vitamin C (1), phenytoin (1), and quinidine (1). Five of the 11 patients would have been diagnosed as having a reflux etiology of their stricture if 24-hour esophageal pH monitoring was not performed. Six patients responded to dilatation and five patients required resection or bypass. A prospective study of 18 asymptomatic volunteers showed a high incidence of esophageal lodgment of a radiolabeled medicinal capsule, with subsequent dissolution and release of the isotope. This occurred most frequently in elderly subjects and was reduced by increasing the volume of water chaser. The sites of lodgment correspond to the location of the observed strictures in the patient population. An in vitro study showed that, when the causative drugs were mixed with saliva, dissolution occurred within 60 minutes and was associated with significant changes in pH. These investigations show that drug-induced esophageal strictures are more common than previously appreciated, and can be confused with a reflux etiology. Diagnosis is suggested by a history of drug ingestion, location of the stricture, and a normal esophageal acid exposure on 24-hour pH monitoring. The severity of the esophageal injury is variable and requires dilatation to resection for therapy.
The oesophageal transit of six commonly used tablets and capsules containing barium sulphate was evaluated radiologically using fluoroscopy in 121 healthy volunteers. To determine the influence of the subject's position and the amount of water taken each subject swallowed three preparations while recumbent and standing and with 25 ml or 100 ml of water. Failure of swallowing (defined as oesophageal transit taking more than 90 seconds) occurred in 22% of 726 swallowings, but globus was complained of in only 33% of these. Sixty per cent of the volunteers had difficulty in taking one or more of the preparations. Many preparations adhered to the oesophageal membrane and started to disintegrate in the lower part of oesophagus. It is recommended that subjects should remain standing for at least 90 seconds after taking capsules or tablets and that all preparations should be taken with at least 100 ml of water. Small tablets are swallowed most easily. Liquid forms of medication (suspensions) should be considered for bedridden patients and those who have difficulty in swallowing.
In recent years, many case reports concerning esophageal injuries caused by drugs have been published. The primary cause has apparently been the delay in passage and the adherence of the caustic drugs on the esophageal mucosa. The authors report a case of esophageal ulceration caused by an analgesic in a 26-year-old male with no esophageal symptoms. A review of the literature shows that a variety of medications have been implicated; size, shape and improper ingestion of pills affect esophageal transit.
Alendronate sodium, an aminobiphosphonate used primarily to treat osteoporosis in postmenopausal women, is known to cause esophagitis. A 71-year-old woman experienced severe, acute esophagitis and severe stricture of the esophagus due to oral alendronate therapy. Unlike in previous cases, she had taken alendronate for 10 months before the onset of complications and the stricture proved resistant to dilation.
With the advance of gastrointestinal endoscopy, pill-induced esophagitis has been detected more frequently, but the association of mucosal dissection is rare. We reported a case of pill-induced esophagitis associated with mucosal dissection.
A 66-year-old male with combined valvular heart disease was admitted for cardiac surgery. Cefotiam hydrochloride tablet was administered for postoperative wound infection of cardiac surgery. Next morning severe odynophagia and retrosternal pain were occurred. Upper gastrointestinal endoscopy performed 2 days after onset of the symptom showed detached mucosa at the upper thoracic esophagus and acute esophagitis at middle and lower thoracic esophagus. Histological examination of the mucosa revealed that the esophageal mucosa was detached from the lamina propria. After the treatment for esophagitis, almost normal esophageal mucosa covered the esophagus without scarring or stricture.
The present case was diagnosed as cefotiam hydrochloride tablet induced esophagitis because of the onset of this disease. Mucosal dissection of the esophagus may be associated with both the esophagitis and bleeding tendencies caused by anticoagulant therapy.
Drug-induced esophagitis is an infrequently diagnosed but important cause of esophagitis. Damage to the esophageal mucosa
can be severe and cause esophageal strictures that may appear malignant by radiographic and endoscopic criteria. The diagnosis
requires a high index of suspicion and a careful review of the patient's drug history. Cessation of implicated drugs permits
resolution of esophageal inflammation. Two patients with drug-induced esophagitis simulating esophageal carcinoma are presented.
A review is presented of drugs which can damage the oesophagus. Only one case of non-fatal ulceration in the oesophagus provoked by indomethacine has been reported previously. The author reports a case in which administration of indomethacine to an elderly, debilitated, bed-ridden patient is presumed to have produced two oesophageal ulcerations with subsequent fatal haemorrhage. It is emphasized that ulcerogenic drugs should be administered with copious fluid, possibly prior to or during a meal. Ingestion shortly before bedtime is advised against. In patients with obstructive conditions in the oesophagus, drugs should be administered preferably in fluid form.
Most oral medications are administered as non-chewable tablets or capsules because these solid, compact pills are easily stored, transported, and consumed, and may be modified to regulate absorption. On occasion, tablets and capsules may lodge in the esophagus and dissolve therein, releasing their undiluted contents directly onto the esophageal mucosa. If the concentrated medication thus released is sufficiently caustic, the esophageal wall may be injured, either directly or through interaction with refluxed gastric contents. This process is known as pill-induced esophageal injury.
Etude portant sur 60 patients souffrant de polyarthrite rhumatoide ou d'arthrose. Realisation d'une endoxapie digestive haute chez tous les malades et d'une PHmetrie oesophagienne ambulatoire des 24 heures chez 6 patients. Frequence de l'atteinte oesophagienne (erosions, ulcerations, stenoses) lors d'un traitement par anti-inflammatoire non steroidien. Description clinico-biologique. Discussion sur la conduite therapeutique chez des patients atteint de polyarthrite et presentant ces lesions iatrogenes
Three cases of esophagitis caused by oral medication are reported: 2 were the result of prolonged use of quinidine tablets (producing focal subacute inflammation mimicking carcinoma in one and stricture in the other) and one occurred soon after ingestion of liquid KCl. Previous reports have implicated KCl tablets ("slow KCl"), tetracycline and doxycycline capsules, and ferrous sulfate tablets. The factors predisposing to this uncommon complication of oral medication are discussed. In all reported cases caused by KCl tablets, left atrial enlargement was present as the result of mitral stenosis.
We describe nine cases of esophageal injury associated with the ingestion of prescribed medications. Antibiotics were the most commonly implicated drugs. Odynophagia, retrosternal chest pain and dysphagia were the usual presenting symptoms. The typical endoscopic finding was that of discrete ulcers in the mid-esophagus. All patients recovered uneventfully with discontinuation of the offending drug and symptomatic treatment. Drug induced esophageal injury should be considered in patients presenting acutely with the above mentioned symptoms and having discrete esophageal ulcers on endoscopy.
Alendronate, an aminobisphosphonate and a selective inhibitor of osteoclast-mediated bone resorption, is used to treat osteoporosis in postmenopausal women and Paget's disease of bone. Aminobiphosphonates can irritate the upper gastrointestinal mucosa.
We describe three patients who had severe esophagitis shortly after starting to take alendronate and also analyze adverse esophageal effects reported to Merck, the manufacturer, through postmarketing surveillance.
As of March 5, 1996, alendronate had been prescribed for an estimated 475,000 patients worldwide, and 1213 reports of adverse effects had been received. A total of 199 patients had adverse effects related to the esophagus; in 51 of these patients (26 percent), including the 3 we describe in case reports, adverse effects were categorized as serious or severe. Thirty-two patients (16 percent) were hospitalized, and two were temporarily disabled. Endoscopic findings generally indicated chemical esophagitis, with erosions or ulcerations and exudative inflammation accompanied by thickening of the esophageal wall. Bleeding was rare, and stomach or duodenal involvement unusual. In patients for whom adequate information was available, esophagitis seemed to be associated with swallowing alendronate with little or no water, lying down during or after ingestion of the tablet, lying down during or after ingestion of the tablet, continuing to take alendronate after the onset of symptoms, and having preexisting esophageal disorders.
Alendronate can cause chemical esophagitis, including severe ulcerations, in some patients. Recommendations to reduce the risk of esophagitis include swallowing alendronate with 180 to 240 ml (6 to 8 oz) of water on arising in the morning, remaining upright for at least 30 minutes after swallowing the tablet and until the first food of the day has been ingested, and discontinuing the drug promptly if esophageal symptoms develop.
Since 1972, a number of publications, in particular in the Anglo-American literature, have reported the occurrence of drug-induced esophagitis. Among the causative agents under discussion, tetracyclines and their derivatives play a leading role. We now report on a case with the aim of describing the typical course and clinical symptoms, diagnosis and treatment of such ulcerative esophagitis, and also consider the pathophysiological basis for its development.
Drug-induced injury of the esophagus has become increasingly common in today's pill-oriented society. Antibiotics such as tetracycline and doxycycline are the most frequent offending agents. However, other oral medications such as potassium chloride, quinidine, and nonsteroidal antiinflammatory drugs (NSAIDs) also have been implicated in the development of this condition. Many patients are found to have small, superficial ulcers that are readily visualized on double-contrast barium studies, but some patients can have large ulcers or even strictures. The correct diagnosis often can be suggested on the basis of the clinical and radiographic findings without need for endoscopic evaluation. This article provides an overview of drug-induced esophageal injury and its radiographic manifestations.
Esophageal perforations, Mallory-Weiss tears, and esophageal hematoma involve traumatic injury to the esophagus. These can be iatrogenic, in particular due to esophageal instrumentation, but can also occur spontaneously. The remarkable increase in diagnostic and therapeutic endoscopy as well as esophageal surgery has made instrumentation the most common cause of esophageal perforation. In many instances, spontaneous perforations are associated with retching and vomiting, which causes a sudden increase in intraesophageal pressure. A high index of suspicion leading to rapid diagnosis and appropriate therapy are needed to optimize clinical outcomes. This article focuses on esophageal perforations, Mallory-Weiss tears, and esophageal hematomas, with emphasis on etiology, pathogenesis, clinical presentation, diagnosis, management, and prevention.