[Results of emergency management of esophageal lesions related to caustic ingestion in children in the emergency department of the General Reference Hospital of Niamey (Niger)]. / Résultats de la prise en charge médico-chirurgicale en urgence des lésions œsophagiennes liées aux ingestions de produits caustiques chez l'enfant dans le service des urgences de l'Hôpital général de référence de Niamey (Niger).

Introduction: Caustic ingestion in children is a public health problem; it is mainly due to domestic accidents due to improper packaging and storage of caustic products. It is a medical and surgical emergency whose management is multidisciplinary. The lesions caused by the accidental ingestion of caustics can affect the functional and vital prognosis in 10% of cases. Methodology: A retrospective, descriptive study from January 2020 to December 2022 (2 years), carried out in the emergency department of the General Reference Hospital of Niamey (Niger). The study included patients less than 15 years old admitted for ingesting a caustic product. Results: Our study included 17 patients. The average age was 5 years, with age extremes of 2 to 11 years. We noted a male predominance with a sex ratio (M/F) of 2.4. Ingestion of caustic products was accidental in all cases. The caustic product was caustic soda in 59%. The average quantity of product ingested was 5 ml (2 ml to 20 ml). The average consultation time was 3 days (3 hours to 15 days). Clinically, dysphagia was the most functional sign, represented by 13 cases, or 76%. Regarding general signs, 3 patients (18%) were admitted with fever; blood pressure was normal in 15 patients (88%); and 2 patients (18%) were admitted in a state of shock. The respiratory rate was normal in 14 patients (82%). Four patients (24%) were admitted in a state of deterioration in the general condition associated with severe malnutrition and dehydration. On physical examination, 2 patients (12%) presented with abdominal defense at the epigastric level. Examination of the ENT sphere revealed benign buccopharyngeal ulcerations in 2 patients (12%). Esogastroduodenal fibroscopy was performed in 4 patients (24%). The caustic lesions observed in the esophagus were: Zargar stage I at 25%, stage Ila at 50%, and stage Illb at 25%. In the stomach, the lesions were Zargar stage I in 75% of cases and stage III in 25% of cases. An injected thoracic-abdominopelvic computed tomography (CT) was performed in 3 patients (18%). It revealed a lack of enhancement of the esophageal wall compatible with esophageal necrosis in one patient. An esophagogastroduodenal transit was performed in 8 patients (47%) admitted more than 72 hours after ingestion of the caustic. They showed esophageal stenoses longer than 3 cm in 3 patients, multiple esophageal stenoses in 2 patients, a single esophageal stenosis in 2 patients, and a single antropyloric stenosis in 1 patient. Therapeutically, all patients benefited from antiemetics to avoid vomiting and proton pump inhibitors. Intravenous antibiotic prophylaxis with third-generation cephalosporin was administered to 12 patients (71%). Corticosteroid therapy based on IV prednisolone at a dose of 1 g/1.73 m2 per day was used to limit or prevent stenoses in 9 patients (53%). Parenteral nutrition was administered to 7 patients (41%). Endoscopic dilations were performed in 2 patients (12%). Emergency surgical treatment was performed in 7 patients (41%): 3 patients underwent transitional feeding gastrostomies; in 3 others, esophagoplasties by colon transplant were performed, and 1 patient was treated by stripping of the esophagus associated with total gastrectomy. The postoperative course was marked by a leak of esocolic anastomosis in one patient for whom conservative treatment was performed with good progress. The average length of hospital stay was 5 days (1-32 days). Conclusion: Accidental caustic ingestions can have serious consequences. Preventing these accidents relies on raising public awareness of the dangers associated with improper storage of these products.

Drug-induced esophageal injuries with an atypical presentation mimicking acute coronary syndrome.

BACKGROUND: Pill-induced esophageal injury may cause severe complications if not diagnosed in a timely fashion. The condition is under-recognized and under-reported, and some patients present with atypical clinical or endoscopic features mimicking other common conditions. If the diagnosis is missed the patient will continue to take the offending drug, potentially worsening the illness. We present a case in which acute coronary syndrome was the initial working diagnosis leading to a delay in diagnosis of doxycycline-induced esophageal injury. The patient developed multiple esophageal ulcers and hemorrhage. CASE PRESENTATION: A 50-year-old male driver with a history of hypertension and dyslipidemia was brought to the emergency department with complaints of severe retrosternal chest pain, vomiting, diaphoresis and syncope. On initial evaluation, acute coronary syndrome was considered due to the clinical presentation and history of cardiovascular risk factors. Electrocardiogram and serum troponins were normal. On the second day of his admission, the patient developed odynophagia and bloody vomitus. Esophagogastroduodenoscopy revealed extensive esophageal ulcerations with hemorrhage. The patient was taking Doxycycline capsules for an acute febrile illness. Doxycycline is the oral medication most commonly reported to cause esophageal injury. Doxycycline was discontinued, and the patient was treated with intravenous omeprazole and oral antacid suspension. The patient improved, was discharged after 6 days of hospitalization, and reported resolution of all symptoms at an outpatient follow-up visit 3 weeks later. CONCLUSION: Medication-induced esophageal injury can present with atypical symptoms mimicking acute coronary syndrome. This condition should be included in the initial differential diagnosis of patients presenting with acute chest pain, especially those taking oral medications known to cause esophageal injury.

Ulceración esofágica por ingestión de doxiciclina / Doxycycline induced esophageal ulceration

La ulceración esofágica por ingestión de doxiciclina es una de las causas más frecuentes de lesión esofágica. Ha sido subdiagnosticada y escasamente reconocida en dermatología. El dolor retroesternal, la odinofagia de aparición brusca y el antecedente de ingesta de doxiciclina u otros fármacos son características que facilitan su diagnóstico. Puede presentar complicaciones serias, como hemorragias, estenosis y mediastinitis.

Esophageal ulceration due to ingestion of doxycycline is one of the most frequent causes of esophageal injury. It has been underdiagnosed and scarcely recognized in dermatology. Retrosternal pain, sudden odynophagia and a history of doxycycline or other drugs intake are some of the characteristics that lead to diagnosis. It may cause severe complications such as bleeding, stenosis and mediastinitis.

Metachronous Esophageal Ulcers after Immune-mediated Colitis Due to Immune Checkpoint Inhibitor Therapy: A Case Report and Literature Review.

Although cases of gastrointestinal toxicity of pembrolizumab have been reported, cases of acute immune-mediated colitis accompanied with metachronous esophageal disorders (esophagitis and ulcer) are rare. We herein report a case of acute colitis and metachronous esophageal ulcers due to an immune-related adverse event following concomitant pembrolizumab chemotherapy for lung adenocarcinoma. To our knowledge, there have so far been no reports of cases in which both acute immune-mediated colitis and metachronous esophageal ulcers developed. We therefore report the details of this case along with a review of the pertinent literature.

Anticholinergic, anti-depressant and other medication use is associated with clinically relevant oesophageal manometric abnormalities.

BACKGROUND: Medications can affect gastrointestinal tract motility. However, their effects on oesophageal motility in particular are often not as widely known or may be underestimated. AIM: To review the effect of existing medication use on high-resolution oesophageal manometry (HRM) in a 'real-world' setting. METHODS: Adult patients with upper gut symptoms and normal endoscopy or imaging who had HRM over a 22-month period were analysed. Achalasia and major disorders of peristalsis were excluded. All medications taken within 24 hours of the procedure were prospectively recorded and compared with HRM results, controlling for age, gender and proton pump inhibitor use. RESULTS: A total of 502 patients (323 female, mean age 51) were recruited. Of these, 41.2% had normal oesophageal HRM, while 41.4% had ineffective oesophageal motility (IOM) and 7.6% had oesophagogastric junction outflow obstruction (OGJOO). Serotonin/norepinephrine reuptake inhibitors (SNRI) and opioids were associated with significantly higher resting lower oesophageal sphincter pressure. Benzodiazepines and opioids were associated with elevated integrated relaxation pressure. SNRI and inhaled beta-agonists were associated with increased distal contractile index, whereas calcium channel blockers were associated with a lower distal contractile index. Odds ratio of being on anticholinergics was higher in IOM patients vs normal (3.6, CI 1.2-10.8). Odds ratio for anticholinergics, inhaled beta-agonists, anticonvulsants, SNRIs and opioids (trend) were all > 3 for OGJOO patients vs normal. CONCLUSION: Many medication classes are associated with abnormal HRM variables and diagnoses such as OGJOO and IOM; some of these associations are probably causal. These possible links should be taken into consideration during manometry interpretation.

Multiple esophageal ulcers due to tofacitinib 10 mg twice daily for ulcerative colitis.

A 26-year-old man was admitted to our institution for ulcerative colitis treatment. He used mesalamine, steroid, immunomodulators, and anti-TNFα anti-body, but it was difficult to maintain remission. We started induction therapy with tofacitinib (TOF) 10 mg twice daily. He maintained clinical remission but had chest pain 44 days after the start of TOF. Esophagogastroduodenoscopy showed multiple ulcers from middle to lower esophagus. Although rare, TOF induced esophageal ulcers were considered based on his clinical course and endoscopic findings.

Necrosis esofágica aguda secundaria a quimioterapia por cáncer de colon / Acute esophageal necrosis secondary to chemotherapy for colon cancer

La necrosis esofágica aguda es un trastorno clínico raro de etiología desconocida, incidencia baja y pronóstico generalmente malo. Presentamos un caso de esófago negro en paciente con vómitos copiosos, disfagia y mucositis, que estaba siendo tratado con quimioterapia con intención paliativa en el contexto de un adenocarcinoma de sigma metastásico. El diagnóstico se determinó mediante gastroscopia a consecuencia de hematemesis de sangre coagulada y heces melénicas durante el ingreso hospitalario. La esofagitis necrosante se ha relacionado clásicamente con algunos agentes infecciosos oportunistas y con el uso prolongado de determinados fármacos pero hasta ahora no existe bibliografía abundante que relacione este síndrome con la quimioterapia. El objetivo de este trabajo es analizar la evolución del paciente para poder determinar si el agente desencadenante de esta reacción adversa fue el tratamiento antineoplásico intravenoso

Acute esophageal necrosis is a rare clinical disorder of unknown etiology, low incidence and poor prognosis. We present a case of black esophagus in patient with copious vomiting, dysphagia and mucositis, who was being treated with palliative chemotherapy for metastatic sigmoid adenocarcinoma. The diagnosis was determined by gastroscopy as a result of hematemesis of coagulated blood and melenic stools during the patient’s hospital admission. Necrotizing esophagitis has been classically related to some opportunistic infectious agents and to the prolonged use of certain drugs, but until now there is no abundant bibliography that attributes this syndrome to chemotherapy. The objective of this work is to analyze the evolution of the patient in order to determine if the black esophagus was caused for the intravenous antineoplastic treatment

Opioid-Induced Esophageal Dysfunction: Differential Effects of Type and Dose.

OBJECTIVE: Data regarding opioid effects on esophageal function are limited. We previously demonstrated an association between chronic opioid use and esophageal motor dysfunction characterized by esophagogastric junction outflow obstruction, distal esophageal spasm, achalasia type III, and possibly Jackhammer esophagus. Our aim was to characterize the influence of different opioids and doses on esophageal dysfunction. METHODS: Retrospective review of 225 patients prescribed oxycodone, hydrocodone, or tramadol for >3 months, who completed high-resolution manometry from 2012 to 2017. Demographic and manometric data were extracted from a prospectively maintained motility database. Frequency of opioid-induced esophageal dysfunction (OIED, defined as distal esophageal spasm, esophagogastric junction outflow obstruction, achalasia type III, or Jackhammer esophagus on high-resolution manometry, was compared among different opioids. The total 24-hour opioid doses for oxycodone, hydrocodone, and tramadol were converted to a morphine equivalent for dose effect analysis. RESULTS: OIED was present in 24% (55 of 225) of opioid users. OIED was significantly more prevalent with oxycodone or hydrocodone use compared with tramadol (31% vs 28% vs 12%, P = 0.0162), and for oxycodone alone vs oxycodone with acetaminophen (43% vs 21%, P = 0.0482). There was no difference in OIED for patients taking hydrocodone alone vs hydrocodone with acetaminophen. Patients with OIED were taking a higher median 24-hour opioid dose than those without OIED (45 vs 30 mg, P = 0.058). DISCUSSION: OIED is more prevalent in patients taking oxycodone or hydrocodone compared with tramadol. There is greater likelihood of OIED developing with higher doses. Reducing the opioid dose or changing to tramadol may reduce OIED in opioid users.

Hepatocyte Growth Factor Facilitates Esophageal Mucosal Repair and Inhibits the Submucosal Fibrosis in a Rat Model of Esophageal Ulcer.

BACKGROUND/AIMS: Esophageal mucosal damage often causes scar tissue, leading to refractory stricture. The aim of this study was to clarify the effect of hepatocyte growth factor (HGF) on esophageal mucosal repair and fibrosis leading to stricture in a rat model of esophageal ulcer. METHODS: Esophageal ulcers were induced in rats by topical exposure of the lower esophageal serosa to acetic acid, followed by intraperitoneal administration of HGF (200 µg/day) using an osmotic pump for 7 days. The effect of HGF on esophageal mucosal injury was investigated macroscopically and microscopically. The effect of HGF on epithelial cell proliferation and the expression of genes closely associated with the development of fibrosis were also examined. RESULTS: The administration of HGF for 7 days led to a significant reduction in the ulcerative area and enhanced the proliferation of esophageal epithelial cells. HGF treatment significantly decreased the fibrosis, and subsequently attenuated not only the foreshortening but also the narrowing of the esophagus. The expression levels of tissue inhibitor of metalloproteinase (TIMP)-1, -2, and matrix metalloproteinase (MMP)-2, -9 were significantly decreased among rats treated with HGF. CONCLUSION: HGF facilitates the repair of esophageal mucosal injury and may also ameliorate the esophageal fibrosis, possibly through enhanced re-epithelization.

Oesophageal ulcer due to a herbal remedy.

Herbal-induced oesophageal lesions are rare. We report the case of an 85-year-old male who presented with cough and odynophagia. An upper endoscopy showed white deposit under the proximal oesophageal sphincter. Biopsy of the lesion revealed an oesophageal ulcer with adherent plant material and ruled-out candidiasis. At this point, the patient divulged self-preparation of an herbal remedy consisting of Aloe Vera pulp, whisky, honey, ginger and turmeric. Aloe Vera, ginger and turmeric are commonly used to sooth some gastroenterological symptoms in Complementary and Alternative Medicine. Incorrect extraction of Aloe Vera pulp and adding honey to it transformed the recipe into a sticky paste that may have injured the oesophageal mucosa. Follow-up showed that the cough and odynophagia subsided after discontinuing this herbal remedy.

Successful treatment of drug-induced esophageal ulcer in a patient with chronic heart failure: A case report.

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.

Acute oesophageal necrosis: a rare but potentially fatal association of cocaine use.

Acute oesophageal necrosis (AON), also known as 'black oesophagus', is a rare condition characterised by the necrosis of the oesophagus usually involving the distal part. It has been associated with various conditions, and the pathogenesis is thought to involve hypovolaemia combined with decreased function of oesophageal protective mucosal barriers and may be compounded by the effect of gastric secretions on oesophageal mucosa. The hallmark of this condition is characteristic circumferential black discolouration of the distal oesophagus that may extend proximally. We present a case of a man who presented with haematemesis associated with cocaine abuse. Oesophagogastroduodenoscopy confirmed black oesophagus. The patient was managed with intravenous fluids, packed red blood cell transfusions, proton pump inhibitors and sucralfate suspension; however, he failed to recover. We have also reviewed the previous reported cases of AON in association with cocaine use.

The effect of platelet-rich plasma on motility changes in experimental caustic esophageal burn.

BACKGROUND: Besides stricture formation, diminished esophageal motility after caustic esophageal burns also plays a role in the deterioration of the clinical course. In this study, we aimed to investigate the effect of caustic burn on the esophageal contractions and the effect of platelet-rich plasma (PRP) on these changes. METHODS: Twenty-one Wistar albino rats were divided into three groups [Sham operation (n = 8), caustic esophageal burn with NaOH (n = 6), PRP treatment after caustic burn (n = 7)]. After 3 weeks, esophagectomy was performed and contractions and EFS responses were evaluated in the organ bath. RESULTS: KCl- and acetylcholine-induced responses were reduced in the Burn group, but increased in Sham and PRP groups (p < 0.05). EFS responses were higher in Burn group compared to the other groups. Response with L-arginine was increased in Burn group, but decreased in PRP group. There was more decrease in the contraction in Sham and PRP groups compared to the Burn group after SNP (sodium nitroprusside) incubation (p < 0.05). L-NAME (Nω-Nitro-L-arginine methyl ester) did not change the EFS responses in the Burn group, but EFS responses were decreased significantly in Sham and PRP groups (p < 0.05). EFS responses were decreased in all groups, but more in the Sham and PRP groups after Y-27632 (Rho-kinase inhibitor) incubation (p < 0.05). CONCLUSIONS: For the first time, we demonstrated that both cholinergic and non-adrenergic non-cholinergic mechanisms are responsible for the altered motility in corrosive esophageal injury. Our results suggest that PRP treatment may be helpful in regulating the esophageal motility and decreasing altered contractions in corrosive burns. This effect may also contribute to the reduction of stricture formation, especially by reducing inappropriate contractions of the esophageal wall during the post-burn healing phase.