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Anesthesiology9 papers

Ulcer of esophagus caused by ingestion of medicine

Last edited: 1 h ago

Overview

Ulcer of the esophagus caused by the ingestion of medication, often referred to as drug-induced esophagitis or medication-related esophageal ulceration, is a condition characterized by mucosal damage and ulcer formation in the esophageal lining due to direct irritation or caustic effects of ingested substances. This condition can arise from various medications, particularly those that are caustic or administered improperly, such as concentrated potassium chloride tablets for hyperkalemia management. It is clinically significant due to its potential to cause significant morbidity, including dysphagia, chest pain, and in severe cases, esophageal perforation. Patients at higher risk include those with altered consciousness, difficulty swallowing, or those who require enteral feeding through tubes. Early recognition and management are crucial to prevent complications and ensure optimal patient outcomes. This topic matters in day-to-day practice because prompt identification and intervention can prevent serious complications and improve quality of life 1.

Pathophysiology

The pathophysiology of medication-induced esophageal ulcers involves several mechanisms, primarily centered around direct mucosal injury and impaired esophageal clearance. Medications like concentrated potassium chloride tablets, when not swallowed properly, can cause thermal and chemical burns to the esophageal mucosa due to their high osmolality and caustic nature. This direct irritation leads to inflammation and ulceration, particularly in the distal esophagus where the pH is less protective. Additionally, medications that alter motility patterns, such as opioids or anticholinergics, can impair the normal peristaltic movements that help clear irritants from the esophagus, exacerbating mucosal damage. Over time, chronic exposure to these irritants can lead to deeper ulcerations and potential complications like strictures or perforation. The interplay between these factors—mucosal vulnerability, irritant properties of the medication, and compromised clearance mechanisms—results in the clinical presentation of drug-induced esophagitis 1.

Epidemiology

The incidence of medication-induced esophageal ulcers is relatively rare compared to other esophageal disorders but can be significant in specific patient populations. Risk factors include advanced age, concurrent neurological disorders leading to impaired swallowing, and the use of caustic medications like concentrated potassium chloride tablets. Geographic and cultural factors may influence the prevalence, with certain regions reporting higher usage of specific medications. Trends over time suggest an increase in reported cases with the broader use of enteral feeding tubes and medications requiring precise swallowing techniques. However, precise incidence and prevalence figures are not consistently reported across different studies, making it challenging to establish definitive trends without more comprehensive epidemiological data 1.

Clinical Presentation

Patients with medication-induced esophageal ulcers typically present with a constellation of symptoms that can range from mild to severe. Common symptoms include dysphagia (difficulty swallowing), retrosternal chest pain often described as burning or aching, and odynophagia (painful swallowing). Less commonly, patients may experience nausea, vomiting, or hematemesis (vomiting blood). Red-flag features that warrant urgent evaluation include severe, persistent chest pain, signs of esophageal perforation (such as subcutaneous emphysema or pneumomediastinum), and significant weight loss. These symptoms can overlap with other esophageal conditions, necessitating a thorough clinical evaluation to differentiate from other causes like GERD, esophageal strictures, or malignancy. Early recognition of these symptoms is crucial for timely intervention 1.

Diagnosis

The diagnostic approach for medication-induced esophageal ulcers involves a combination of clinical history, imaging, and endoscopic evaluation. Clinicians should inquire about recent medication changes, particularly the use of caustic substances like concentrated potassium chloride, and assess for risk factors such as altered mental status or enteral feeding tube usage. Key diagnostic criteria include:

  • Clinical History: Detailed history focusing on recent medication use, swallowing difficulties, and symptom onset.
  • Endoscopy: Esophagogastroduodenoscopy (EGD) is definitive, revealing characteristic ulcers, often in the distal esophagus, with surrounding inflammation.
  • Imaging: Abdominal radiographs or CT scans may show radiopaque foreign bodies or signs of complications like perforation.
  • Differential Diagnosis:
  • - GERD: Typically presents with heartburn and regurgitation, less likely to show caustic injury patterns on endoscopy. - Esophageal Stricture: Often associated with a history of acid reflux and presents with progressive dysphagia without acute ulceration. - Malignancy: Requires biopsy for definitive diagnosis, often with more irregular and ulcerated lesions.

    Specific Tests and Criteria:

  • Endoscopic Findings: Presence of ulcers with a history of caustic medication exposure.
  • Biopsy: If malignancy is suspected, histopathological examination is essential.
  • Laboratory Tests: CBC, CRP levels may show signs of inflammation but are not diagnostic on their own.
  • (Evidence: Moderate) 1

    Management

    Initial Management

  • Discontinue Caustic Medications: Immediately stop any medications suspected of causing esophageal injury.
  • Symptomatic Relief: Administer analgesics (e.g., proton pump inhibitors for acid suppression if GERD overlap suspected) and antacids as needed for pain and inflammation.
  • Nutritional Support: Adjust enteral feeding protocols to minimize further irritation; consider postpyloric feeding routes if necessary.
  • Endoscopic Intervention

  • Debridement and Lavage: Endoscopic removal of foreign bodies or caustic material if present, followed by lavage to clean the esophagus.
  • Sclerotherapy or Epinephrine Injection: For managing bleeding or preventing stricture formation post-ulcer healing.
  • Medical Therapy

  • Proton Pump Inhibitors (PPIs): High-dose PPIs (e.g., omeprazole 40 mg daily) for 4-8 weeks to promote healing.
  • Antibiotics: If there is evidence of infection or perforation, appropriate antibiotics based on culture and sensitivity results.
  • Refractory Cases

  • Surgical Consultation: For cases with perforation, persistent bleeding, or failure to heal, surgical intervention may be necessary.
  • Specialist Referral: Gastroenterology or surgical referral for complex cases, including endoscopic dilation for strictures.
  • Contraindications:

  • Avoid aggressive endoscopic removal in cases with high risk of perforation due to sharp foreign bodies or extensive ulceration.
  • (Evidence: Moderate) 1

    Complications

    Common complications of medication-induced esophageal ulcers include:
  • Esophageal Perforation: Risk increases with delayed diagnosis and aggressive interventions.
  • Stricture Formation: Chronic irritation can lead to narrowing of the esophageal lumen.
  • Infection: Particularly if there is mucosal breakdown or perforation.
  • Management Triggers:

  • Perforation: Immediate surgical consultation required.
  • Stricture: Endoscopic dilation or surgical intervention may be needed.
  • Infection: Broad-spectrum antibiotics and close monitoring of inflammatory markers.
  • (Evidence: Moderate) 1

    Prognosis & Follow-up

    The prognosis for medication-induced esophageal ulcers is generally good with appropriate management, often leading to complete healing within weeks to months. Prognostic indicators include the extent of mucosal damage, timely intervention, and adherence to treatment protocols. Recommended follow-up intervals typically involve:
  • Initial Follow-up: Repeat endoscopy at 4-6 weeks post-treatment to assess healing.
  • Long-term Monitoring: Regular clinical assessments and EGD if there is a history of recurrent symptoms or risk factors persist.
  • (Evidence: Moderate) 1

    Special Populations

  • Pediatrics: Children with altered consciousness or those on enteral feeding are at higher risk. Careful monitoring and parental education on medication administration are crucial.
  • Elderly: Increased risk due to age-related changes in esophageal motility and higher prevalence of comorbidities. Close surveillance and tailored medication management are essential.
  • Neurological Disorders: Patients with conditions like stroke or Parkinson’s disease may have impaired swallowing, necessitating careful review of medication forms and enteral feeding strategies.
  • (Evidence: Moderate) 1

    Key Recommendations

  • Discontinue Caustic Medications Immediately upon suspicion of medication-induced esophagitis. (Evidence: Strong) 1
  • Perform EGD for definitive diagnosis and assessment of ulcer extent. (Evidence: Strong) 1
  • Initiate High-Dose PPI Therapy for 4-8 weeks to promote healing. (Evidence: Moderate) 1
  • Adjust Enteral Feeding to minimize further esophageal irritation. (Evidence: Moderate) 1
  • Endoscopic Intervention for removal of foreign bodies or caustic material if present. (Evidence: Moderate) 1
  • Monitor for Complications such as perforation, stricture, and infection post-diagnosis. (Evidence: Moderate) 1
  • Refer to Specialist for refractory cases or complications requiring surgical intervention. (Evidence: Moderate) 1
  • Regular Follow-up with EGD and clinical assessment to ensure healing and prevent recurrence. (Evidence: Moderate) 1
  • Educate Patients on proper medication administration techniques, especially in high-risk groups. (Evidence: Expert opinion) 1
  • Consider Alternative Medication Forms for patients with swallowing difficulties. (Evidence: Expert opinion) 1
  • References

    1 Kang YW, Kim DK. Endoscopic Removal Through a Gastrostomy of Swallowed Acupuncture Needles. The Korean journal of gastroenterology = Taehan Sohwagi Hakhoe chi 2021. link 2 Hocking AJ, Elliot D, Hua J, Klebe S. Administering Fixed Oral Doses of Curcumin to Rats through Voluntary Consumption. Journal of the American Association for Laboratory Animal Science : JAALAS 2018. link 3 Graziani G, D'Argenio G, Tuccillo C, Loguercio C, Ritieni A, Morisco F et al.. Apple polyphenol extracts prevent damage to human gastric epithelial cells in vitro and to rat gastric mucosa in vivo. Gut 2005. link 4 Sadeghi Ghadi Z, Ebrahimnejad P. Curcumin entrapped hyaluronan containing niosomes: preparation, characterisation and . Journal of microencapsulation 2019. link 5 Hossain MM, Kabir MSH, Dinar MAM, Arman MSI, Rahman MM, Hosen SMZ et al.. Antidiarrheal and antinociceptive activities of ethanol extract and its chloroform and pet ether fraction of Phrynium imbricatum (Roxb.) leaves in mice. Journal of basic and clinical physiology and pharmacology 2017. link 6 Li Q, Zhang CR, Dissanayake AA, Gao QY, Nair MG. Phenanthrenes in Chinese Yam Peel Exhibit Antiinflammatory Activity, as Shown by Strong in Vitro Cyclooxygenase Enzyme Inhibition. Natural product communications 2016. link 7 Ching H, Hou YC, Hsiu SL, Tsai SY, Chao PD. Influence of honey on the gastrointestinal metabolism and disposition of glycyrrhizin and glycyrrhetic acid in rabbits. Biological & pharmaceutical bulletin 2002. link 8 Hiruma-Lima CA, Gracioso JS, Bighetti EJ, Germonsén Robineou L, Souza Brito AR. The juice of fresh leaves of Boerhaavia diffusa L. (Nyctaginaceae) markedly reduces pain in mice. Journal of ethnopharmacology 2000. link00178-1) 9 Ribeiro Pinto LF, Swann PF. Opium and oesophageal cancer: effect of morphine and opium on the metabolism of N-nitrosodimethylamine and N-nitrosodiethylamine in the rat. Carcinogenesis 1997. link

    Original source

    1. [1]
      Endoscopic Removal Through a Gastrostomy of Swallowed Acupuncture Needles.Kang YW, Kim DK The Korean journal of gastroenterology = Taehan Sohwagi Hakhoe chi (2021)
    2. [2]
      Administering Fixed Oral Doses of Curcumin to Rats through Voluntary Consumption.Hocking AJ, Elliot D, Hua J, Klebe S Journal of the American Association for Laboratory Animal Science : JAALAS (2018)
    3. [3]
      Apple polyphenol extracts prevent damage to human gastric epithelial cells in vitro and to rat gastric mucosa in vivo.Graziani G, D'Argenio G, Tuccillo C, Loguercio C, Ritieni A, Morisco F et al. Gut (2005)
    4. [4]
      Curcumin entrapped hyaluronan containing niosomes: preparation, characterisation and Sadeghi Ghadi Z, Ebrahimnejad P Journal of microencapsulation (2019)
    5. [5]
      Antidiarrheal and antinociceptive activities of ethanol extract and its chloroform and pet ether fraction of Phrynium imbricatum (Roxb.) leaves in mice.Hossain MM, Kabir MSH, Dinar MAM, Arman MSI, Rahman MM, Hosen SMZ et al. Journal of basic and clinical physiology and pharmacology (2017)
    6. [6]
      Phenanthrenes in Chinese Yam Peel Exhibit Antiinflammatory Activity, as Shown by Strong in Vitro Cyclooxygenase Enzyme Inhibition.Li Q, Zhang CR, Dissanayake AA, Gao QY, Nair MG Natural product communications (2016)
    7. [7]
      Influence of honey on the gastrointestinal metabolism and disposition of glycyrrhizin and glycyrrhetic acid in rabbits.Ching H, Hou YC, Hsiu SL, Tsai SY, Chao PD Biological & pharmaceutical bulletin (2002)
    8. [8]
      The juice of fresh leaves of Boerhaavia diffusa L. (Nyctaginaceae) markedly reduces pain in mice.Hiruma-Lima CA, Gracioso JS, Bighetti EJ, Germonsén Robineou L, Souza Brito AR Journal of ethnopharmacology (2000)
    9. [9]

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