Annals of Burns and Fire Disasters - vol. XIII - n. 2 - June 2000


Fadaak H.A.

Division of Plastic Surgery, King Fahd Hospital of the University, AI-Khobar, Saudi Arabia

SUMMARY. Gastrointestinal (G1) ulceration complicated by haemorrhage used to be a potentially lethal complication of major thermal injury. Prophylactic treatment with antacids or H2-receptor blockers has dramatically reduced the incidence in many burn units. Early enteral feeding has recently been shown to be an effective additional measure in stress ulcer prophylaxis. Our experience with stress ulcer prophylaxis at the King Fahd Hospital of the University Burns Unit (Saudi Arabia) in the management of 1040 patients over 14 yr is described in this paper. The overall mortality was 5.38% (56 cases). Of the total admissions, nine patients developed G1 bleeding (0.86%). The group with significant burns, i.e. burns in more than 20% total body surface area, suffered GI bleeding in 3.28% of cases. The commonest presentation was melaena during the terminal stages of septicaemia. Surgical intervention to control bleeding was required in two out of the nine cases. Of the seven other patients who died owing to thermal injury, massive bleeding was directly responsible for death in only one patient. While septicaemia is a risk factor, it seems that prophylaxis with H2-receptor antagonists and early enteral feeding significantly reduced the incidence of bleeding in this series.


Gastrointestinal (G1) ulceration complicated by haemorrhage used to be potentially lethal after major burn injury. It has been documented that patients with severe burns experience stress gastritis within 72 h of major burn injury. GI erosions occur within 5 h of injury in 80% of all patients with severe burns. These erosions cause only minor upper bleeding, but within 72 h many of these may progress to frank GI ulcerations (Curling's ulcer) resulting in major haemorrhage.This sequence of events was frequently seen in the patients when no ulcer prophylaxis - either antacids or H2-receptor antagonists - was used.The incidence of GI bleeding in burn patients shows variations in different parts of the world. In Great Britain only 18 cases of alimentary bleeding were seen in a study cohort comprising 32,500 patients.The incidence in the rest of Europe appears to be the same, while in North America the incidence is much higher in some burn units.
Prophylactic treatment with antacids or H2-receptor antagonists has dramatically reduced the incidence of GI bleeding in many burn units. Early enteral feeding has been shown to be an effective additional measure in stress ulcer prophylaxis.
Although the literature is replete with publications on the subject, reports are scarce from the developing countries.
Our experience at the King Fahd Hospital of the University Burns Unit in Saudi Arabia over the past 14 yr confirms that the adoption of early feeding along with stress ulcer prophylaxis lowers the incidence of GI haemorrhage.

Materials and methods

Between May 1983 and April 1997 1040 burn patients were admitted to the burns unit of this hospital. Adequate resuscitation was achieved in all patients using the Parkland formula. In patients with burns in 30% total body surface area (TBSA) or more, prophylactic treatment for stress ulcers was initiated with 30 mI aluminium hydroxide orally or by nasogastric tube every 4 h. This regime was followed in the unit during the first three yr. As soon as cimetidine (an H2-receptor antagonist) became available, this drug replaced aluminium hydroxide at a dosage of 200 mg three times a day followed by 400 mg at night administered intravenously soon after admission for one week and continued orally for another 3-6 weeks.
Since 1990 early enteral feeding has been encouraged from the day of admission. When a high calorie intake is indicated Ensure-Plus is instilled through a Silastic feeding tube. Early tangential excision is carried out on day 5 if the patient's condition is stable. Prophylactic antibiotics are not prescribed unless indicated (mainly before surgical intervention, in children with deep burns, and in otherwise compromised patients).
GI bleeding was diagnosed when blood was evidenced in the stool or gastric aspirate. No routine use was made of endoscopy or tests for occult blood in the stool since bleeding copious enough to necessitate urgent control measures is usually clinically obvious.


The study cohort comprised 1040 patients seen over a 14-yr period. Of these, 274 (26.34%) presented 20% or more TI3SA involved in the thermal injury. The overall mortality rate was 5.38% (56 deaths out of the 1040 admissions. A higher mortality (20.43%) was found in the cohort with a TBSA involvement of 20% or more. The occurrence of gross GI bleeding was seen in only nine out of the initial 490 patients in the first phase of the study. Since 1990 no GI bleeding has been observed in this series. Patients presenting a burn area of 20% or more made a significant contribution to this complication (3.28%). One of these patients presented on admission a perforation of a bleeding duodenal ulcer.
Six of the nine patients presented with different degrees of melaena during the terminal stages of septicaemia and/or renal failure. All six died of septicaemia, terminal multiorgan failure, and disseminated intravascular coagulopathy. The remaining three cases had only haematemesis. Gastroscopy and colonoscopy were not utilized routinely and were performed in only three cases.
Surgical intervention to control bleeding was attemptedin two cases. A 35-yr-old woman with 60% deep burns developed mas sive lower GI bleeding two months after admission. Exploration revealed a caecal ulcer, for which a right hemicolectomy was performed. The second patient to undergo exploration was a 6-yr-old boy with 30% burns and inhalation injury who on day 4 post-burn developed upper GI bleeding necessitating laparotomy. Exploration revealed "kissing ulcers" in the duodenum, the anterior part of which had perforated. In another patient, a 30-yr-old male (45% flame burn), endoscopy revealed a bleeding pyloric diverticulum. Massive GI bleeding was the direct cause of death in only one patient out of the seven who died (Table 1). Consent for autopsy was not granted in these cases.

Causes of death

Number of patients
Microbial sespis 4
Multi-organ failure 2
G1 haemorrhage 1
Table I - Causes of death in patients with G1 haemorrhage
Site of bleeding Number of patients
Unknow (melaena) 5
Caecal ulcer (melaena) 1
Duodenal ulcer 1
Duodenal diverticum erosion 1
Gastric erosion 1
Table II - Source of bleeding in patients with G1 haemorrhage


GI bleeding in the burn patient during the first three days of the resuscitation period is explained by initial hypotension, hypoxia, and resultant mucosal ischaemia. Bleeding associated with the onset of sepsis usually occurs late, between 10 days to 2 weeks following thermal injury. Pruitt et al. reported an 11.7% incidence of Curling's ulcer in 323 autopsies performed in 2772 burn patients treated in their unit. Pruitt's review reported that the incidence of haemorrhage was 64% and that of perforation 12%.
Sepsis was identified as an important factor in the aetiology of stress ulcer complications. Yang et al7'reported that 574 of 4684 patients developed burn wound sepsis and that 10.8% of this cohort manifested GI bleeding, compared with only 0.3% of the non-septic patients. Six of the nine cases in the present series with bleeding had septicaemia and presented melacna late in the course of their management. These six patients died of septicaemia and multi-organ failure. Inadequate volume replacement in the presence of hypovolaemia and shock with or without sepsis is known to cause ischaemia of the bowel mucosa,8-14 as also described by Desai et al. Autopsy showed that over 50% of patients succumbing to thermal injury had ischaemic lesions in the small and large intestine. The lesions varied from superficial mucosal loss to fullthickness necrosis. Eighty per cent of patients demonstrating such lesions were septicaemic with the enteric group of pathogens at the time of their demise. Translocation of enteric pathogens through the cornpromised mucosal barrier is believed to be the main factor in the genesis of septicaemia and multi-organ failure in thermally injured patients Early and vigorous fluid resuscitation plays an important role in the prophylaxis of ischaemic mucosal injury.
Early enteral feeding has been proposed as an effective additional measure in stress ulcer prevention. The presence of food in the gut has been shown to stimulate mucosal proliferation, probably as a result of both humoral and nutritional mechanisms. Improved mucosal integrity has also been demonstrated in burn patients fed early.These findings suggest that early enteral feeding may help to diminish the incidence and severity of bacterial translocation by improving or preventing breach of the mucosal barrier. Support to the gut is thus best ensured by maintaining adequate splanchnic blood flow and by early, aggressive enteral feeding.
The low incidence of GI bleeding in the present series (0.86%) was due to prophylaxis with antacids and cimetidine, as is well established in the literature. It is significant that since 1990 - when early enteral feeding was initiated in this unit - not a single case of GI bleeding has been observed in any subsequent admissions, confinning our belief .
GI bleeding was seen, manifesting itself more than 10 days post-burn, mostly from the lower GI tract, in association with sepsis probably due to ischaemia of the bowel mucosa rather than to peptic acid erosion. Two patients in this series had to be operated upon for the diagnosis and control of bleeding.
Our experience in the management of 1040 burn patients over a period of 14 yr thus confirms that prophylaxis for stress ulcers in burn patients reduces GI complications, including bleeding. Initially antacids were used and later, when H2-receptor antagonists became available, were added to the regime. We have continued to use H2-receptor antagonists in our burn unit. We endorse early enteral feeding in these patients as an additional measure for ulcer prophylaxis. This regime has been in use since 1990 and has been very rewarding: not one case of bleeding from the gut in burn patients has been encountered since initiation of this line of management.


RESUME. L'ulcération gastro-intestinale compliquée par l'hémorragie une fois reprèsentait une complication potentiellement mortelle des lésions therrniques importantes. Le traitement prophylactique avec les antiacides on les bloquants des rècepteurs H2 a réduit dramatiquement l'incidence dans un grand nombre d'unité des brùlures. Récemment l'alimentation entérale précoce s'est démontrée une mesure supplémentaire efficace dans la prophylaxie de l'ulcére de stress. L'Auteur décrit son experience dans la prophylaxie de l'ulcére de stress à l'Unité de Brùlures de I'Hépital Roi Fahd de l'Université (Arabie Saoudite) dans la gestion de 1040 patients pendant une période de 14 ans. La mortalité complessive était de 5,38% (156 cas). Sur tous les patients hospitalisés, neuf ont dèveloppdè une hémorragie gastro-intestinale (0,86%). Le groupe qui présentait les brùlures significatives, c'est-ir-dire dans an moins 20% de la surface corporelle, prèsentait une condition d'hèmorragie dans 3,28% des patients. La pathologie la plus commune ètait la mèlaena pendant les phases terminales de la septicémie. L'intervention chirurgicale pour régler I'hémorragie été necessaire dans deux des
neuf cas examinés. Des autres sept patients qui sont morts à cause des lésions thermiques, Fhèmorragie massive 6tait directement responsable dans un seul cas. Tant que la septicdmie constitue un facteur de risque, il semble que la prophylaxie avec les antagonistes au recepteur H2 et I'alimentation entérale précoce ont réduit en maniée significative l'incidence de l'hémorragie dans la série étudiée.


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Acknowledgement. The author would like to thank Prof. Dilip Mitra
for his useful editorial suggestions and advice.

This paper was received on 14 December 1999.

Address correspondence to:
Dr Hussein A. Fadaak; Assistant Professor and Consultant
Head of Division of Plastic Surgery, King Fabd Hospital of the University
P.O. Box 2903, Al-Khobar 31952, Saudi Arabia.


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