Upper Gastrointestinal Bleeding Among Saudis: Etiology And Prevalence The Riyadh Central Hospital Experience Mohammed Al-Mofarreh, Facharzt; Yisa M. Fakunle, MD, FRCP (London); Mohammed Al-Moagel, Facharzt From the Department of Medicine, Riyadh Central Hospital, Riyadh. Address reprint requests and correspondence to Dr. Al-Mofarreh: Department of Medicine, Riyadh Central Hospital, P.O. Box 9789, Riyadh 11423, Saudi Arabia. Accepted for publication 8 October 1990. Fiberoptic esophagogastroduodenoscopic examination of 747 Saudi patients who presented with acute upper gastrointestinal (UGI) bleeding between January 1984G to December 1986G showed that ruptured esophageal varices, erosive gastritis, duodenitis and peptic ulcer disease were the most common findings. There were 515 males and 232 females (M:F2.2:1). Multiple lesions were detected in 83% of patients, emphasizing the need to anticipate more than one lesion at endoscopy in a patient with UGI bleeding. Sixty-seven patients (8.9%) gave a history of drug ingestion prior to the episode of bleeding; gastric and duodenal erosions were the most common lesions in these patients. No source of bleeding was apparent in 26 (3.5%) patients at the time of endoscopy. Endoscopy rather than barium studies has become established as the standard investigation in our patients with upper gastrointestinal bleeding. M Al-Mofarreh, YM Fakunle, M Al-Moagel, Upper Gastrointestinal Bleeding Among Saudis: Etiology and Prevalence the Riyadh Central Hospital Experience. 1991; 11(5): 547-550 Upper gastrointestinal (UGI) bleeding remains a common emergency worldwide. Its frequency is estimated at one in every 2,000 people per year in the UK [1]. Definitive diagnosis of the cause of bleeding relies largely on endoscopy, which is superior to barium studies in identifying the source of bleeding. Dronfield et al [2] and Stevenson et al [3] found double-contrast barium radiology is of equal diagnostic value in the identification of chronic ulcers. Endoscopy, however, has the added advantage of being performed with thepatients supine, thus avoiding the problems of postural hypotension. In addition, assessment of the site, rate of bleeding, and the causative pathology with histological confirmation as well as the option of intervention is unique to endoscopy. The etiology of UGI bleeding varies with the geographical area. In the US, esophageal varices and gastric erosions occur more frequently than in the UK where peptic ulcer accounts for the bleeding [3,4], InTurkey, duodenal ulcerwas the most common cause of bleeding in a series of 184 patients (32%), with UGI bleeding among 5,000 endoscopies spanning a period of five years [5]. Al-Moegel et al [6] reported that history of hematemesis was a common reason for the procedure in a series of 2,742 upper gastrointestinal endoscopies in Riyadh Central Hospital (RCH),Riyadh. Bleeding from rare causes such as fundal and duodenal varices has subsequently been reported by Al-Mofarreh (1986, 1987 and 1988) from the same center [7-9]. More recently, Laajam et al [10] reported their findings in 6,386 upper GI endoscopies over a 5 year period from two teaching hospitals also in the city of Riyadh: 424 (6.7%) had UGI bleeding. Esophageal varices 39%, duodenal ulcer 33.9%, and gastric erosions 3.7% accounted for 77% of cases with history of bleeding, while gastric cancer and carcinoma of the esophagus accounted for the remainder. Since the initial report by Al-Moagel [6], over 20,000 upper GI endoscopies have been performed in the gastrointestinal unit of RCH for a multiplicity of indications, prominent among which is UGI bleeding. In this report, we focus on the etiology and prevalence of UGI bleeding seen in this hospital over a period of three years
1404H to 1406H (January 1984G to December 1986G). Methods A Hematemesis/Melena Unit (HMU) was established in 1405H for the management of patients with hematemesis and/or melena. Hematemesis was defined as the vomiting of blood clot or coffee-ground material. Melena was defined as the passage of dark tarry stools. After initial resuscitation, and bearing in mind that endoscopic diagnosis falls rapidly after 24 hours as small lesions may heal or develop after the initial bleed [11], most of the endoscopies were done within 12 to 36 hours of admission. No sedation was given and most often a forward-view Olympus GF series was used. One instrument was kept for known HBsAG-positive patients. Endoscopic diagnosis of the lesions was based on macroscopic appearances using standard criteria [12]. If only a single lesion was found, it was considered the source of bleeding. In cases of multiple lesions, those which were actually bleeding or showing stigmata of recent bleeding (i.e., a clot or vessel or mucosal tears) were taken as the cause of bleeding. For the purpose of this analysis, the endoscopy reports and hospital records of all patients admitted with UGI bleeding in the years 1401H to 1406H were examined and information regarding age, sex, nationality, endoscopic findings, and history of drug ingestion were noted. The number of hospital admissions for the same period was also noted. Results Hospital admissions for the three-year period totaled 91,879 patients 7,706 upper GI endoscopies were performed during this period. There were 1,593 patients with UGI bleeding (1.7% of total hospital admission and 21% of upper GI endoscopies). Seven hundred forty-seven (46.9%) of these patients were Saudis. Figure 1 shows the age distribution of the Saudi patients. This pattern is similar to the overall age distribution of patients admitted to this hospital over the three-year period. The male to female ratio of 2.2:1 is also similar to that for the hospital population. A total of 1,617 lesions were observed in 747 patients, an average of 2.1 lesions per patient. Table 1 summarizes the frequencies of the lesions detected. Esophageal varices constituted the largest group. Gastritis and gastric erosions were the next common findings on endoscopy. Many of the patients with these lesions also had a history of non-steroidal anti-inflammatory drug (NSAID) ingestion prior to the symptoms of hematemesis and/or melena. Esophagitis, gastric ulcers, duodenal ulcers, and duodenal erosions occurred with decreasing frequency. Table 2 shows the multiplicity of lesions seen in our patients. Eighty-three patients had more than one lesion at endoscopy.
Table 1. Frequency of lesions seen at endoscopy in 747 Saudis with upper GI bleeding. Lesion found at endoscopy No. of lesions (%) Patients history of NSAIDs ingestion (%) Patients history of NSAIDs ingestion (%) Esophageal varices 321 19.3 23 7.4 Gastric erosions 236 14.6 38 16.1 Gastritis 241 14.9 24 9.9 Esophagitis, esoph erosions & Barrets esophagitis 206 12.7 18 8.7 Gastric ulcer 141 8.7 9 6.4 Duodenal ulcer 127 7.8 14 11.0 Duodenitis 104 6.4 12 11.5 Duodenal erosions 84 5.2 15 17.8 Hiatal hernia 62 3.8 - - Fundal varices 43 2.6 - - Esophageal ulcer 26 1.6 2 7.7 Mallory-Weiss 12 0.7 1 8.3 syndrome Carcinoma of stomach 12 0.7 - - Duodenal varices 4 0.2 - - Gastric polyp 4 0.2 - - Duodenal polyp 4 0.2 - - Carcinoma of esophagus 1 0.1 - - No abnormality detected 26 1.6 - - Discussion Riyadh Central Hospital, with a 1200-bed capacity, is the largest Ministry of Health hospital in the Kingdom of Saudi Arabia. Ninety-five percent of its admissions come from the city of Riyadh and suburbs, while the remainder are referred from other regions in the Kingdom. This study shows that UGI bleeding accounts for 1.7% of all admissions in this hospital, and 21% of all upper GI endoscopies. The most common finding at endoscopy was esophageal varices. This finding is in agreement with the report of Laajam et al [10], but differs in other respects. Mallory-Weiss syndrome, fundal varices and duodenal varices were noted in 12, 43 and 4 instances, respectively, in our series but were absent in their series. Most reports have quoted figures of 10% for patients with UGI bleeding with more than one lesion and some have suggested that more than 50% have multiple lesions [13]. Our series showed multiple lesions in 83% (Table 2), emphasizing that multiple lesions are the rule. To identify which lesion was the cause of bleeding, early endoscopy is advisable. Figure 1. Age distribution of 747 Saudi patients with hematemesis.
Table 2. Frequency of associated lesions at endoscopy in the eight leading endoscopic findings in patients with upper gastrointestinal tract bleeding Putative source of bleeding Gastric erosions Gastritis Associated lesions that might have bled Esophagitis Gastric ulcer Duodenal ulcer Duodenitis Esophageal varices 46 47 22 20 21 31 25 Gastric erosions - - - 7 7 7 3 Gastritis 14 - - 6 14 12 - Esophagitis 19 26-5 10 16 1 Gastric ulcer 13 - - - 4 4 - Duodenal ulcer 13 29 12 16-23 6 Duodenitis 6 14 7 4 12-2 Fundal varices 3 2 1-3 2 - Total 114 118 42 128 70 133 37 Fundal varices Reflux esophagitis frequently occurred in association with duodenal erosion, gastric erosion or ulcer; and the cause of bleeding was attributed to the lesion with active bleeding, or stigmata of recent bleeding. In 8.3% of patients, esophagitis and esophageal erosions were associated with hiatal hernia. There was history of drug ingestion, mostly NSAID (which in the majority of cases was aspirin) in 67 patients in this series. The association between UGI bleeding and aspirin has been described for over 25 years. Our finding supports this view. Corticosteroid therapy has also been implicated in UGI bleeding, but a review of 42 trials involving 5,000 patients who have been allocated corticosteroid therapy or placebo showed no more hemorrhage among patients as compared with controls [14]. A more recent review, however, estimated a 1.7-fold increase in peptic ulcerations during steroid therapy [15]. It is difficult to be certain about the exact contributions that the NSAID and corticosteroids have made to bleeding in our patients, in view of the multiplicity of lesions found, but a positive history of drug ingestion in patients presenting with UGI bleeding should alert the physician to give the patient appropriate advice. No definite diagnosis as to the etiology of bleeding could be made in six (3.5%) patients, even after repeated endoscopies. In one instance it was established that bleeding was self-induced (the patient intentionally injured his gum, swallowed the ensuing blood and subsequently vomited it out). It is possible that in the majority of these patients without a lesion at time of endoscopy, the lesions might have healed before the procedure as is known with Mallory-Weiss syndrome and erosions. Spiller and Parkins [16] have given a guide to the logical management of patients with obscure recurrent UGI bleeding. Duggan [17], who followed up 241 patients who had survived UGI bleeding for ten years, showed that those in whom no diagnosis was made had an excellent prognosis and were unlikely to be suffering from a serious undiagnosed disease. This evidence is reassuring, both to the doctor and to the patient. Esophageal varices and peptic ulcer disease (including gastroduodenitis) are the most common lesions found in our patients with upper gastrointestinal tract bleeding. Multiple lesions were often found at endoscopy. It is now our routine to perform endoscopy sooner, rather than later, after a bleed in order to identify actual bleeding lesions in our patients. References 1. Langman MJS. Upper gastrointestinal bleeding. In: Pounder RE, ed. Recent advances in gastroenterology. Edinburgh: Churchill and Livingstone, 1986;1-16. 2. Dronfield MW, Langman MJS, Atkinson M, et al. Outcome of endoscopy and barium radiology for acute gastrointestinal bleeding; controlled trial in 1,037 patients. Br Med J 1982;284:545-8. 3. Stevenson GW, Cox RR, Roberts CJC. A prospective comparison of double contrast barium meal examination and fibreoptic endoscopy in acute upper gastrointestinal bleeding. Br Med J 1976;2:723-4. 4. Gilbert DA, Silverstein FE, Tedesco FJ, et al. The national ASGE survey on upper gastrointestinal bleeding. Endoscopy in upper gastrointestinal bleeding. Gastrointest Endosc 1981;27:94-102. 5. Simsek H, Telatar H, Karacadag S, et al. Upper gastrointestinal endoscopy in Turkey: a review of 5000 cases. Gastrointest Endosc 1988;34:68-9.
6. Al-Moagel M, Al-Faraj M, Al-Mofarreh M. An endoscopy of the upper gastrointestinal tract in Riyadh Central Hospital. Proceedings of the Seventh Saudi Medicine Meeting, King Faisal University, Dammam, 3-6 August 1982. 7. Al-Mofarreh M, Al-Moagel M, Al-Faraj M, et al. Duodenal varices: report of 13 cases. Z. Gastroen-terologie 1986;24:673-80. 8. Al-Mofarreh M. Sclerotherapy of fundic varices: new approach? Z. Gastroenterologie 1987;8:525. 9. Al-Mofarreh M, Al-Moagel M, Neemat A, et al. Sclerotherapy of fundal varices: a new approach (abstract). Ann Saudi Med 1988;8(1):78 A. 10. Laajam MA, Al-Mofleh I, Al-Faleh FZ, et al. Upper gastrointestinal endoscopy in Saudi Arabia: analysis of 6386 procedures. Quart J Med 1988;249:21-5. 11. Foster DN, Miloszewski KJA, Losowsky MS. Stigmata of recent haemorrhage in diagnosis and prognosis of upper gastrointestinal bleeding. BrMed J 1978;1:1173-7. 12. Kasugai T, ed. Endoscopic diagnosis in gastroenterology. Tokyo: Igaku-Shoin, 1982. 13. Thomas GE, Cotton PB, Gast CG, et al. Survey of management in acute upper gastrointestinal haemorrhage J R Soc Med 1978;73:90-5. 14. Conn HO, Biltzer BL. Non-association of adrenocor-ticosteroid therapy and peptic ulcer. N Engl J Med 1976;294:473-9. 15. Messer J, Reitman D, Sacks HS, et al. Association of adrenocorticoid therapy and peptic ulcer disease. N Engl J Med 1983;309:21-4. 16. Spiller RC, Parkins RA. Recurrent gastrointestinal bleeding of obscure origin: report of 17 cases and a guide to logical approach to mangement. Br J Surg 1983;70:489-93. 17. Duggan JM. Ten-year follow up of gastrointestinal haemorrhage patients. Aust NZ J Med 1986;16:33-8.