Mucosal healing after high dose pantoprazole in acute corrosive injury of esophagus

INTRODUCTION : The ingestion of corrosive agents is still an important public health issue in our country. The GIT injuries caused by caustic agents can range from minor to fatal, or can lead to chronic disease with poor quality of life. Corrosive agents with a pH level less than two or more than twelve can rapidly penetrate the layers of the oesophagus and result in necrosis and scar formation in the mucosa. Acidic agents produce coagulation necrosis and eschar formation that may limit tissue penetration and may even spare the oesophagus when the transit is rapid. On the other hand, Alkaline agents when ingested produce liquefaction necrosis and can cause serious oesophageal injury by penetrating to deep muscle layers. The basic histopathologic reaction of tissue subjected to caustic burn is the synthesis, deposition and remodelling of collagen. Following full-thickness injuries to the oesophageal wall, the normal oesophagus is replaced by dense connective tissue. Collagen overproduction has been estimated to cause stenosis in half of the patients suffering severe burns. Consequently, when treating caustic burn injuries, it is necessary to prevent stenosis by inhibiting collagen synthesis or changing the properties of the deposited collagen. The optimal management protocol in the treatment of severe caustic injury remains controversial. The main goal of medical treatment is to inhibit inflammatory reaction or stricture formation secondary to oesophageal burning. Stricture formation is thought to be overcome by suppressing fibroplasia and scarring. Many agents directed at wound healing and stricture prevention have been used in several experimental studies in past. Results of such treatment protocols including steroids, antibiotics, heparin, indomethacin, sucralfate, vitamin E, as well as total parenteral nutrition are all controversial in treatment of corrosive burns. Randomised control trials on the role of proton pump inhibitors in caustic injuries of GIT are lacking. A few experimental studies have investigated the relationship between proton pump inhibitors and corrosive burns and has shown that proton pump inhibitors can reduce inflammation in early phase of caustic injury. Proton pump inhibitors, by decreasing gastric acid secretion and thereby GER can prevent worsening of corrosive injury. In addition proton pump inhibitors has also been shown to have anti-inflammatory and antioxidant properties. A prospective study from turkey on 13 patients have showed that omeprazole can be used effectively in treatment of acute corrosive injury of esophagus. There are no studies from India which have attempted to assess the usefulness of proton pump inhibitors in treatment of acute corrosive injury of esophagus. This prompted us to study the usefulness of pantoprazole in the treatment of patients presenting with acute corrosive injury of the oesophagus. AIM OF THE STUDY : To study the efficacy of high dose pantoprazole in causing mucosal healing after acute corrosive injury of esophagus. CONCLUSION : Treatment of corrosive injury is controversial and there are no definitive protocols. Intravenous proton pump inhibitors are widely used in treatment of corrosive injuries despite lack of evidence. Our study has demonstrated that effective mucosal healing can be achieved by intravenous proton pump inhibitor infusion. Though majority of patients in our study had minor grade of injury, 27% of the patients included in the study had 2b and 3a injury. When analysis is confined to these patients, 53% showed improvement by 1 grade, 33.3% showed improvement by 2 grades and 13.3% did not show improvement. Therefore it is evident from above that high dose pantoprazole is also beneficial in patients with higher grade of injury and may prevent late complications in these patients. A larger randomised placebo controlled trial in patients with higher grade of oesophageal injury is needed to determine if high dose pantoprazole should form standard of care in treatment of patients with acute corrosive injury of oesophagus.