|Year : 2014 | Volume
| Issue : 1 | Page : 72-78
Upper gastrointestinal lesions and bleed in burn injuries: An endoscopic evaluation
Arige Subodh Kumar1, Gogulapati Venkata Sudhakar2
1 Department of Burns and Plastic Surgery, Gandhi Medical College, Hyderabad, Andhra Pradesh, India
2 Department of Burns and Plastic Surgery, Osmania Medical College, Hyderabad, Andhra Pradesh, India
|Date of Web Publication||15-Dec-2014|
Arige Subodh Kumar
13-6-457/29, Gayatri Nagar, Shivbagh, Gudi Malkapur, Hyderabad, Andhra Pradesh
Source of Support: None, Conflict of Interest: None
Upper gastrointestinal lesions are a known complication in burn injuries and are considered to be caused by acid-peptic digestion of gastric mucosa. Antacids and H2- receptor blockers are administered to neutralize the gastric secretions. The study aims to observe the incidence of upper gastrointestinal lesions, their natural course, the influence of the early oral feeds, oral Sucralfate and parenteral Ranitidine, the clinical and endoscopic incidence of the bleed. This study was undertaken on 92 patients having burns varying between 10% and 70% of body surface area and admitted within 24 h of the injury. Patients were divided randomly into three groups. Group I: Ranitidine at a dose of 50 mg intravenously twice a day was commenced from the time of admission and oral feeds after 24 h. Group II: Oral feeds, and sucralfate, 2 g at four hourly interval were administered from the time of admission. Group III: Oral feeds alone were given from the time of admission. Endoscopy was done at weekly interval, starting after 3 rd postburn day, after stabilization of the patient. Upper Gastrointestinal lesions were seen in 46% of patients, and they lasted up to 6 weeks while only 8% developed bleed. The lesions showed a direct proportionate relationship to the percentage of burn. Both Group I and Group III patients developed bleed, the incidence of which was more on endoscopy than the clinical manifestation. Group II patients did not have any bleed.
Keywords: Bleed, clinical manifestation, early oral feeds, endoscopy, erosions, Group I, Group II, Group III, Ranitidine, Sucralfate, TBSA (Total body surface area of burn injuries), ulcers, upper gastrointestinal lesions
|How to cite this article:|
Kumar AS, Sudhakar GV. Upper gastrointestinal lesions and bleed in burn injuries: An endoscopic evaluation. Indian J Burns 2014;22:72-8
|How to cite this URL:|
Kumar AS, Sudhakar GV. Upper gastrointestinal lesions and bleed in burn injuries: An endoscopic evaluation. Indian J Burns [serial online] 2014 [cited 2021 Jul 26];22:72-8. Available from: https://www.ijburns.com/text.asp?2014/22/1/72/147012
| Introduction|| |
Gastrointestinal lesions are a known complication in burn injuries. They are attributed due to the "stress response" a sequel of which is increased acid secretion and acid-peptic digestion of the gastric mucosa. Attempts at neutralizing gastric secretions are aimed by administering Antacids and H2 receptor blockers. This has become an accepted and established management protocol in burns, along with early enteral feeds. 
Conventional management of burn patients discourages oral feeding during the first 24 h, for fear of precipitating acute gastric dilatation.
Some of the patients have gastrointestinal bleeds, manifesting clinically as Melena or Hematemesis, which may be life-threatening.
There have been very few studies on the actual incidence of gastrointestinal lesions, effect of any of the treatment modalities on the occurrence of the lesions, the complications of the lesions, and the natural course of the lesions. 
Prospective, serial endoscopic evaluation is the only method to know the exact incidence  and behavior of these lesions, and the influence of medication on such lesions. It is for this reason the present study was contemplated.
Factors that have been implicated in the pathogenesis of "curling's ulcers" and stress ulcerations, include
- Changes in quality and quantity of gastric mucosubstance,
- Loss of integrity of the mucosal barrier,
- Reflux of bile acids and digestive enzymes,
- "Relative" acid hyper-secretion,
- Hypoproteinemia or negative nitrogen balance,
- Mucosal ischemia secondary to the opening of submucosal arteriovenous shunts, local vasoconstriction, or the development of microvascular thrombi
following disseminated intravascular coagulopathy has also been implicated.
Prevention of upper gastrointestinal bleeding in burn patients.
Gastrointestinal lesions can occur within 5 h of injury in patients with severe burns  Within 72 h, many of this progress to gastroduodenal ulcerations (curling's ulcer) resulting in major hemorrhage, or perforation. ,
The primary concern is "prevention and control" of major complications, as managing the established complications is a difficult proposition.
Effective resuscitation of shock at the earliest plays an important role in preventing ischemic mucosal injury.
Early oral or enteral feeding commencing within 6 h of burn injury is an effective additional measure in the prevention of stress-induced ulceration. , Early feeding diminishes the incidence and severity of bacterial translocation by maintaining the integrity of the mucosal barrier.
Use of antacids, and H2 receptor blockers has become an established practice in attempting to prevent the bleed. 
H2 receptor blockers viz., Ranitidine, administered at dosage of 150 mg twice daily orally for about 3-6 weeks, is normal practice today, with the idea of reducing the acid secretion through its action of blocking the Histamine H2 receptors on the Parietal cells of gastric mucosa.
Sucralfate is the basic aluminum salt of sucrose octasulfate. It is claimed to protect the mucosa and also enhance healing by stimulating epithelial regeneration. It is administered at a dosage of 2 g, at four hourly interval.
- To study the incidence of the upper gastrointestinal lesions and upper gastrointestinal bleed in patients with burn injuries.
- To study the clinical and endoscopic incidence of the bleed.
- To observe the influence of
- Early oral feeds,
- H2 receptor blockers,
- Sucralfate, in the prevention of lesions and bleed, as a complication.
- To study the natural course of these lesions.
| Materials and methods|| |
The study was conducted at Osmania General Hospital, Hyderabad, between February 2003 and December 2004, in the Department of Burns and Plastic surgery with the help of the Department of Gastroenterology, after the approval from the Ethics Committee.
A total of 92 patients with burn injuries ranging between 10% and 70% of body surface area, admitted within 24 h of injury, and having no other co-morbid conditions were divided randomly into three groups for the study.
Ranitidine at a dose of 50 mg intravenously twice daily was commenced from the time of admission and oral feeds after 24 h.
Oral feeds, and Sucralfate, 2 g at four hourly interval were administered from the time of admission.
Oral feeds were given from the time of admission, without either Ranitidine or Sucralfate.
Patients under 12 years, habitual alcoholics and smokers, pregnant women, patients with "facial or respiratory burns," chemical burns, electrical burns, those with past history of acid-peptic disease, or significant medical illnesses and patients admitted later than 24 h of sustaining burn injury were not considered for the study. Patients with chemical burns were excluded as they were few in number and often complicated with involvement of eyes, mouth etc., requiring interventions of other specialties like ophthalmology, etc. . Patients with electrical burns too were excluded as quite a few were requiring early surgeries like amputations.
Every patient, irrespective of the group, on admission, received intravenous fluids as per the Parkland formula. Crystalline pencillin at a dosage of 10 lakhs intravenously at six hourly interval was given for 7-10 days, but changed to the antibiotic based on sensitivity pattern at times of need such as fever or raised white cell counts. Pentazocin and Phenergan were given intravenously for analgesia, as per the standard protocol of the unit and were monitored continuously. Patients were subjected to serial upper gastrointestinal endoscopic study.
The first upper gastrointestinal endoscopy was done after stabilization of the patient usually around 3 rd or 4 th postburn day and the endoscopy was repeated at weekly intervals to observe the natural course of the lesions until complete healing of the lesions.
The findings of upper gastrointestinal endoscopy were noted, and if any patient complained of any Hematemesis or Melena, they were noted. All these patients with such complaints were immediately sent for endoscopy.
Upper gastrointestinal endoscopy revealed.
They are characterized by superficial epithelial necrosis above the muscularis mucosa.
They are characterized by mucosal infarction and necrosis extending below the muscularis mucosa. They appear as discrete, excavated lesions with a whitish base. The edges are smooth and regular, and symmetrically thickened folds typically radiate to the base of the ulcer.
Erosions were seen in 29 out of 92 patients (31.5%). [Table 1] shows the pattern of the erosions in the different groups.
Stomach was the most frequent site of erosions, followed by Duodenum and then the Esophagus and this pattern was the same in all three groups. [Table 2] and [Table 3] show the sites of erosions and in different groups respectively.
Ulcers were the other type of lesions and were seen in 15 out of 92 patients (16.30%).
[Table 4] shows the pattern of ulcers in the different groups.
Duodenum was the common site for ulcers in comparison to the esophagus and stomach, and this pattern was the same in all the three groups. [Table 5] and [Table 6] show the site of ulcers and in different groups, respectively.
Incidence of gastrointestinal lesions
Overall Incidence was 45.7% (42 out of 92). They were noted in all the three groups irrespective of the medication administered. [Table 7] shows the incidence of lesions in the different groups.
Healing of the lesions
The lesions once noted, lasted up to 6 weeks. They healed within 4 weeks period in all the patients in Group II, and the majority of patients in Group I and in Group III, but in some patients in Group I and in Group III, they took about 6 weeks to heal. [Table 8] shows the pattern of healing.
Relationship of lesions to body surface area of burns
Incidence of lesions was 30.3% (10 out of 33) for 11-30% total body surface area (TBSA), 50% (21 out of 42) for 31-50% TBSA, and 68.8% (11 out of 16) for 51-70% TBSA burns [Graph 1]. [Additional file 1]
Group-wise relationship between body surface area of burns and the lesions
The incidence of lesions in the Group I for burns between 11% and 30% TBSA was 20%, with the lesions developing in three out of 15 patients. The incidence was 43.8% with seven out of 16 patients for Burns between 31% and 50% TBSA. It rose to 60% in patients with TBSA between 51% and 70% with three out of five manifesting the lesions.
The incidence of the lesions in the Group II patients, for burns between 11% and 30% TBSA was 30% with the lesions developing in three out of 10 patients. The incidence was 75% with six out of eight patients for burns between 31% and 50% of TBSA, which was a rise and then the lesions rose to 80% with four out of five patients, developing them when they had burns between 51% and 70% TBSA.
In the Group III, the incidence of lesions was 50% with four out of eight patients developing them when they had burns between 11% and 30% TBSA, they was seen in 44.45% with eight out of 18 patients developing them when they had burns between 31% and 50% TBSA, and they rose to 67% with four out of seven patients showing them on Endoscopy when they had burns between 51% and 70% TBSA [Graph 2]. [Additional file 2]
The overall incidence of clinical and endoscopic bleed
The endoscopic bleed was higher than the clinical bleed in Group I and Group III. There was no bleed in Group II patients. [Table 9] and [Table 10] show the incidence of bleed on endoscopy, and that seen on clinical examination respectively. In Group III, 9.4% (three out of 32) Endoscopic bleed and 9.1% (three out of 33) of Clinical bleed was seen, (as one of the patients, with clinical bleed was not fit to undergo Endoscopy, while one case showed bleed on Endoscopy only, without any clinical bleed). Overall, the incidence of endoscopic bleed was 7.7% (seven out of 91), and that of the clinical bleed was 4.35% (four out of 92) [Graph 3]. [Additional file 3]
Incidence of upper gastrointestinal lesions and bleed
The lesions were found to develop in a larger number of patients compared with the bleed [Graph 4]. [Additional file 4]
Bleeding was seen from the erosions and ulcers and in Group I and Group III. Bleeding was more from the ulcers than the erosions in both Group I and Group III [Graph 5 [Additional file 5] and Graph 6 [Additional file 6]]. There was no bleeding in Group II. [Table 11] and [Table 12] show the patterns of bleeding from erosions and ulcers in the three groups.
Sites of the bleed
Four out of 23 patients with erosions (17.4%) in stomach and one out of four patients with erosions (25%) of the duodenum showed bleeding. Five out of ten patients with ulcers (50%) of the duodenum showed the bleed [Graph 7]. [Additional file 7]
| Discussion|| |
Gastointestinal lesions in the form of either erosions or ulcers were noted in all the three groups from the 3 rd day, irrespective of the modes adopted to prevent the lesions and the bleed. Erosions were seen in 31.5% of patients. The erosions were seen more commonly in Stomach, 79.3%, than the duodenum, which accounted for 13.8% and the esophagus which accounted for 6.9%. This reflects that acid-peptic digestion of the mucosa is a possibility and not just the ischemia. Gan reported the incidence as 100%. 
Ulcers were the other type of lesions and were seen in 16.30%. Ulcers were more commonly seen in duodenum 66.7%, than the esophagus which accounted for 26.7% and 6.7% were seen in the stomach. The incidence of ulcers reported by Gan was 27.6%,  Pruitt et al. reported it at 11.7%. 
The gastrointestinal lesions were seen in almost every alternate patient and the total incidence of the lesions on upper gastrointestinal endoscopy was 45.7% (42 out of 92). The incidence of the gastrointestinal lesions increased with the increase in TBSA of burns. This might be because of increase in the "stress response" to the injury and the ischemia and acid-peptic digestion of mucosa with increase in percentage of burn.
The incidence of the gastro intestinal lesions in Group I (Ranitidine) was less in comparison to the incidence in Group II (Sucralfate) and in Group III (early feeds only). This may be because of the protective effect of the H2 blockers in preventing the occurrence of the lesion, which may be by countering the "relative acid hyper-secretion." The incidence in Group II, was little higher than in Group III. It may be because patients advised to take liquid Sucralfate were not able to take early oral feeds to the same extent as in Group III.
In Group I, the endoscopic bleed was 11.1% and was higher than the clinical bleed which was 2.8%. In Group I, the bleeding was noticed in four cases on second postburn day in a 35% TBSA burn patient, fourth postburn day in a 47% TBSA burn patient, ninth postburn day in a 70% TBSA Burn patient, and on 20 th postburn day in a 46% TBSA Burn patient respectively. The cases which showed bleeding, were immediately put on intravenous Pantaprazole, oral liquid Sucralfate and received compatible blood transfusions. All the bleeds in Group I were minor in nature and were controlled by conservative means. The bleed that developed within a week's period, the causative agents could be ischemia and acidity, and septicemia could be another contributing reason for those that developed in the 2 nd and 3 rd week.
Bleed was not seen in Group II, suggesting that this drug has prophylactic effect, probably by coating the mucosal surface and the lesions and by preventing their further progression, though this drug did not prevent the lesions from developing.
In Group III, the clinical bleed was 9.1%, while the endoscopic bleed was 9.4%. The bleeding was noticed in four patients. One of the patients was taken away by his attenders in a moribund condition and was declared as absconded. The bleed was noticed on second postburn day (65% TBSA burns), seventh postburn day (56% TBSA burns), 7 th postburn day (65% TBSA Burns), and on 18 th postburn day (52% TBSA burns) respectively. One case, was not fit for endoscopy, following clinical bleed on 18 th postburn day, and the patient expired on 20 th postburn day. In another case, the bleed was seen only on endoscopy. It was controlled by conservative means, after the patient was put on intravenous Pantaprazole, oral liquid Sucralfate, and blood transfusion and the follow-up for the natural course of the lesions in this case was not considered.
Bleed was common from the ulcers (33.3%) in comparison to the erosions (17.2%) [Graph 7].
Bleed from duodenal lesions (42.9%) was more than that from the stomach (16.7%).
The overall incidence of clinical bleed was 4.35% and that of the endoscopic bleed was 7.7% [Graph 3]. The incidence of bleed in the study by Fadaak was 3.28%.  The low incidence of bleed might be due to the beneficial effects of liquid Sucralfate, H2 blockers, and the early oral feeds. The fact that endoscopic bleed is higher means, that sub-clinical bleeds do occur, which are not always manifest clinically, and if adequate protective measures are taken, they do not become full blown bleeds.
One patient having bled absconded, and two cases expired following bleed. The mortality in this study was 3.3%, assuming that the absconded patient too has expired, as he was quite moribund, when he was taken away by the attenders. The cases which expired were on eighth postburn day and 20 th postburn day. Septicemia might be a contributing factor in those who expired. Both were from Group III. This perhaps emphasizes that additional protective agents like H2 blockers, Sucralfate are needed. The other four cases with bleed responded to intravenous Pantaprazole, liquid Sucralfate and compatible blood transfusion.
The " P" values in the study are all larger than 0.05 and are not significant. A larger study might provide us with better information on whether the influence of the different drugs show statistical significance.
| Conclusions|| |
- Incidence of upper gastrointestinal lesions shows a direct proportionate relationship to the percentage of TBSA of burns. The incidence increased from 30.3% in 11% to 30% TBSA burn patients, to 50% in 31-50% TBSA burn patients to 68.8% in 51-70% TBSA burn patients.
- Upper gastrointestinal lesions appear within the first few days and are seen as early as 3 rd postburn day during first endoscopy and they last for nearly 6 weeks.
- Upper gastrointestinal bleed is much less when compared to the presence of the gastrointestinal lesions. The upper gastrointestinal lesions were seen in 46%, compared to the gastrointestinal bleed which occurred in <8% of patients.
- Bleed was more common from ulcers (33.3%) than the erosions (17.2). Bleed from duodenal lesions (42.9%) was more than that from the stomach (17.2%).
- The erosions were predominantly seen in the Stomach in all three groups. (77.8% in Group I, 75% in Group II, and 83.3% in Group III).
- The ulcers were predominantly seen in the duodenum in all the three groups. (75% in Group I, 66.7% in Group II, and 62.5% in Group III).
- Early oral feeds alone are not adequate, in preventing upper gastrointestinal bleed.
- H2 blockers have a limited role in preventing the lesions from developing. The belief that bleeds are prevented by these agents does not hold good. However, the bleeds that occurred were not life-threatening.
- Early feeds with Sucralfate have a role in preventing GI bleed, though it did not prevent the lesions from developing.
| References|| |
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Czaja AJ, McAlhany JC, Pruitt BA Jr. Acute gastroduodenal disease after thermal injury. An endoscopic evaluation of incidence and natural history. N Engl J Med 1974;291:925-9.
Gan YL. Acute stress mucosal lesion of the upper gastrointestinal tract after burn - a clinical and endoscopic analysis of 31 cases. Zhonghua Zheng Xing Shao Shang Wai Ke Za Zhi 1989;5:251-4, 315.
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[Table 1], [Table 2], [Table 3], [Table 4], [Table 5], [Table 6], [Table 7], [Table 8], [Table 9], [Table 10], [Table 11], [Table 12]