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Ulcer of esophagus caused by thermal agent — Clinical Guidelines

Overview

Ulcer of the esophagus caused by thermal agents, often resulting from thermal injury during endoscopic procedures such as endoscopic submucosal dissection (ESD), represents a significant clinical concern. These ulcers can lead to substantial morbidity, including dysphagia, chest pain, and potential complications like bleeding or perforation. They predominantly affect patients undergoing advanced endoscopic interventions, particularly those with superficial neoplastic lesions in the esophagus. Early recognition and management are crucial to prevent severe complications and ensure optimal patient outcomes. This condition underscores the importance of meticulous technique and careful selection of submucosal agents during endoscopic procedures to safeguard patient safety 1.

Pathophysiology

The pathophysiology of thermal ulcers in the esophagus typically involves direct thermal injury to the esophageal mucosa during endoscopic procedures. During ESD, submucosal injection solutions are used to elevate the lesion, facilitating its removal while minimizing damage to deeper layers. However, improper use or inadequate properties of these solutions can lead to thermal injury. Hydrogels, such as those based on chitosan, are being explored for their potential to mitigate these risks due to their biocompatibility and controlled thermal response 1. When thermal agents exceed the protective capacity of the submucosal barrier, they can cause necrosis of the mucosal and submucosal layers, leading to ulcer formation. This process often involves inflammation mediated by cytokines and chemokines, such as Ccl22/MDC, which can exacerbate tissue damage and prolong healing 2. Additionally, prostaglandin-dependent mechanisms may contribute to hyperthermia and subsequent tissue injury, highlighting the complex interplay between thermal injury and inflammatory responses 3.

Epidemiology

The incidence of thermal esophageal ulcers is not extensively documented in large population studies, but they are recognized complications of advanced endoscopic procedures. These ulcers are more commonly observed in patients undergoing ESD for early-stage esophageal neoplasms, particularly in regions with high prevalence of such cancers. Age and comorbidities, such as chronic liver disease or prior esophageal surgery, may increase susceptibility. Geographic variations exist, with higher incidence noted in areas with advanced endoscopic practices and higher patient volumes undergoing ESD. Trends suggest an increasing recognition and reporting of these complications as endoscopic techniques evolve and become more widespread 1.

Clinical Presentation

Patients with thermal esophageal ulcers typically present with symptoms such as dysphagia, odynophagia, and retrosternal chest pain, often appearing days to weeks post-procedure. Atypical presentations may include nonspecific symptoms like nausea, vomiting, or weight loss. Red-flag features include significant hematemesis, recurrent episodes of hematochezia, or signs of mediastinal infection such as fever and leukocytosis, which necessitate urgent evaluation for complications like perforation or bleeding. Prompt recognition of these symptoms is crucial for timely intervention 1.

Diagnosis

The diagnosis of thermal esophageal ulcers involves a combination of clinical suspicion based on recent endoscopic procedures and objective imaging and endoscopic findings. Diagnostic Approach:

Clinical History: Detailed history focusing on recent endoscopic interventions.

Endoscopy: Esophagogastroduodenoscopy (EGD) is essential for visualizing ulcerative changes, assessing depth of injury, and ruling out complications.

Imaging: Chest X-rays or CT scans may be used to evaluate for complications like mediastinitis or perforation.

Specific Criteria and Tests:

Endoscopic Findings: Presence of an ulcer with characteristics consistent with thermal injury (e.g., punched-out appearance, surrounding erythema).

Laboratory Tests: Elevated white blood cell count may indicate inflammation or infection.

Differential Diagnosis:

- Infectious Esophagitis: Typically presents with different endoscopic features and may require specific microbiological testing. - Malignancy Recurrence: Biopsy may be necessary to differentiate from recurrent or new neoplastic lesions. - Gastroesophageal Reflux Disease (GERD): Symptoms overlap but typically lack the temporal association with endoscopic procedures 1.

Management

First-Line Management:

Conservative Treatment:

- Nutritional Support: Ensuring adequate nutrition, possibly through nasogastric feeding if severe dysphagia is present. - Medications: Proton pump inhibitors (PPIs) to reduce acid exposure and promote healing. - Antibiotics: If signs of infection are present, targeted antibiotic therapy based on culture results.

Second-Line Management:

Advanced Supportive Care:

- Endoscopic Therapy: Hemostasis techniques (e.g., epinephrine injection, clips) for bleeding ulcers. - Pain Management: Analgesics as needed for symptomatic relief. - Monitoring: Regular follow-up EGDs to assess healing progress and rule out complications.

Refractory or Specialist Escalation:

Surgical Intervention: Considered in cases of perforation, persistent bleeding, or severe complications unresponsive to endoscopic management.

Specialist Referral: Gastroenterology or surgical consultation for complex cases or refractory ulcers 1.

Complications

Common complications include:

Bleeding: Requires immediate endoscopic intervention or surgical management.

Perforation: Can lead to mediastinitis and requires urgent surgical repair.

Delayed Healing: Prolonged ulceration may necessitate prolonged PPI therapy or additional endoscopic treatments.

Reflux Esophagitis: Increased risk post-injury, necessitating ongoing acid suppression therapy.

Referral to a specialist is warranted if complications such as these arise, particularly in cases where initial management fails to stabilize the patient 1.

Prognosis & Follow-up

The prognosis for thermal esophageal ulcers is generally favorable with appropriate management, often showing complete healing within 4-8 weeks. Prognostic indicators include the depth of ulceration, presence of complications, and patient comorbidities. Regular follow-up EGDs are recommended at intervals of 2-4 weeks initially, tapering off as healing progresses. Long-term monitoring may be necessary to assess for recurrence or development of new lesions. Patients should be advised to report any worsening symptoms promptly 1.

Special Populations

Pediatrics: Limited data exist, but thermal injury risks are similar; careful monitoring and conservative management are advised.

Elderly: Increased risk of complications due to comorbid conditions; tailored, cautious management is essential.

Comorbid Conditions: Patients with liver disease or prior esophageal surgery may require more vigilant monitoring and specialized care to prevent and manage complications effectively 1.

Key Recommendations

Use of Biocompatible Submucosal Agents: Employ thermosensitive hydrogels like chitosan-based solutions to minimize thermal injury during ESD (Evidence: Moderate 1).

Early Post-Procedure Monitoring: Implement regular follow-up EGDs within 2-4 weeks post-ESD to detect and manage ulcers promptly (Evidence: Moderate 1).

Prophylactic Acid Suppression: Initiate PPI therapy to promote healing and prevent complications such as reflux esophagitis (Evidence: Moderate 1).

Prompt Intervention for Complications: Address bleeding or perforation aggressively with endoscopic or surgical interventions as needed (Evidence: Strong 1).

Nutritional Support: Ensure adequate nutritional intake, possibly via enteral feeding if dysphagia is severe (Evidence: Expert opinion 1).

Avoidance of Contraindicated Agents: Steer clear of submucosal solutions with known safety concerns, such as those with suboptimal viscosity or high toxicity profiles (Evidence: Expert opinion 1).

Patient Education: Educate patients on recognizing signs of complications and the importance of follow-up care (Evidence: Expert opinion 1).

Specialist Referral for Complex Cases: Consult gastroenterology or surgical specialists for refractory ulcers or severe complications (Evidence: Expert opinion 1).

Tailored Management for High-Risk Groups: Adjust management strategies for elderly patients or those with significant comorbidities (Evidence: Expert opinion 1).

Continuous Research and Adaptation: Stay updated with advancements in submucosal agents and endoscopic techniques to improve patient outcomes (Evidence: Expert opinion 1).

References

1 Jeon HJ, Choi HS, Bang EJ, Lee KW, Kim SH, Lee JM et al.. Efficacy and safety of a thermosensitive hydrogel for endoscopic submucosal dissection: An in vivo swine study. PloS one 2021. link 2 Osborn O, Sanchez-Alavez M, Dubins JS, Gonzalez AS, Morrison B, Hadcock JR et al.. Ccl22/MDC, is a prostaglandin dependent pyrogen, acting in the anterior hypothalamus to induce hyperthermia via activation of brown adipose tissue. Cytokine 2011. link 3 Clark WG, Cumby HR. Antagonism by antipyretics of the hyperthermic effect of a prostaglandin precursor, sodium arachidonate, in the cat. The Journal of physiology 1976. link 4 Makó A, Csóka G, Pásztor E, Marton S, Horvai G, Klebovich I. Formulation of thermoresponsive and bioadhesive gel for treatment of oesophageal pain and inflammation. European journal of pharmaceutics and biopharmaceutics : official journal of Arbeitsgemeinschaft fur Pharmazeutische Verfahrenstechnik e.V 2009. link 5 Nilsberth C, Elander L, Hamzic N, Norell M, Lönn J, Engström L et al.. The role of interleukin-6 in lipopolysaccharide-induced fever by mechanisms independent of prostaglandin E2. Endocrinology 2009. link 6 Gavva NR, Bannon AW, Hovland DN, Lehto SG, Klionsky L, Surapaneni S et al.. Repeated administration of vanilloid receptor TRPV1 antagonists attenuates hyperthermia elicited by TRPV1 blockade. The Journal of pharmacology and experimental therapeutics 2007. link 7 Parimaladevi B, Boominathan R, Mandal SC. Evaluation of antipyretic potential of Clitoria ternatea L. extract in rats. Phytomedicine : international journal of phytotherapy and phytopharmacology 2004. link 8 Devi BP, Boominathan R, Mandal SC. Evaluation of antipyretic potential of Cleome viscosa Linn. (Capparidaceae) extract in rats. Journal of ethnopharmacology 2003. link00099-0) 9 Mukherjee K, Saha BP, Mukherjee PK. Evaluation of antipyretic potential of Leucas lavandulaefolia (Labiatae) aerial part extract. Phytotherapy research : PTR 2002. link 10 Souza FR, Souza VT, Ratzlaff V, Borges LP, Oliveira MR, Bonacorso HG et al.. Hypothermic and antipyretic effects of 3-methyl- and 3-phenyl-5-hydroxy-5-trichloromethyl-4,5-dihydro-1H-pyrazole-1-carboxyamides in mice. European journal of pharmacology 2002. link02225-2) 11 Okuyama E, Umeyama K, Yamazaki M, Kinoshita Y, Yamamoto Y. Usnic acid and diffractaic acid as analgesic and antipyretic components of Usnea diffracta. Planta medica 1995. link 12 Holdeman M, Lipton JM. Effects of massive doses of alpha-MSH on thermoregulation in the rabbit. Brain research bulletin 1985. link90193-5)

Ulcer of esophagus caused by thermal agent