Upper Gastrointestinal Bleeding with Special Reference to Peptic Ulcer

Upper Gastrointestinal Bleeding with Special Reference to Peptic Ulcer

Vol. 57, No. 1 Printed in U.S.A. GASTROENTEROLOGY Copyright © 1969 by The Williams & Wilkins Co. CURRENT CLINICAL CONCEPTS Thomas R. Hendrix, M.D. ...

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Vol. 57, No. 1 Printed in U.S.A.

GASTROENTEROLOGY

Copyright © 1969 by The Williams & Wilkins Co.

CURRENT CLINICAL CONCEPTS Thomas R. Hendrix, M.D. Current Clinical Concepts Editor The Johns Hopkins University School of Medicine Baltimore, Maryland

UPPER GASTROINTESTINAL BLEEDING WITH SPECIAL REFERENCE TO PEPTIC ULCER J . E. DEVITT, M.D., C.M ., M .Sc., F.R.C.S.(EDIN.), F.R.C .S.(C) Department of Surgery , Ottawa Civic Hosp ital, University of Ottawa, Ottawa , Canada

ferent hospitals even if standardization of statistical data could be achieved. Unfortunately, attempts to "standardize" patients on the basis of volume of blood loss3 do not take into account the rate of loss which is just as important, or such factors as age, 1 ' 4 associated disease,5· 6 or the underlying gastrointestinal disorder. 7 Neither can there be standardization of the judgment necessary to decide that bleeding has continued long enough, vigorously enough, or recurred sufficiently to warrant operation, or that the patients' general condition justifies or contraindicates surgery. In any report it takes little retrospective effort to separate and discard the patients who do not have acute or chronic peptic ulcers. Conclusions may be reached which cannot be applied in practice when nonpeptic ulcer patients are not so easily separated and no patient can be discarded.8 In theory the ideal method of determining the best therapy is through prospective randomized clinical trials. 2 Few such trials have been reported, 8· 9 no doubt because of the time required to collect enough patients. But the management of a disorder as complex as upper gastrointestinal bleeding must surely be individualized so that, at best, a randomized clinical trial will only show that more patients need the one type of treatment while fewer patients require the other. At worst, well conducted trials may pro-

A disorder as protean in its presentation, cause, course, and complications as upper gastrointestinal bleeding can have no simple method of management. Its complexities make it difficult to compare the effects of different kinds of treatment. Most studies make a low death rate the chief objective. Unfortunately, factors of selection which authors may not recognize may be more important than therapy in determining any given mortality rate. 1 • 2 In a small series good luck may produce a high survival rate, and as good results are more frequently published than bad, a bias toward a particular form of treatment is possible, particularly if the therapy is that which is the current fad. Most reports are based on mass hospital statistics which depend on the unmeasurable and certainly variable accuracy with which physicians complete hospital charts. Methods of recalling and compiling data differ also; thus, there may be important differences in the criteria of diagnosis of bleeding or of ulcer. Differences in age, sex, and nutritional status of patients, geographical differences in peptic ulcer disease and causes of upper gastrointestinal bleeding, and variations in ease of admission to hospital of mild cases and in availability of medical personnel make it futile to compare results at difAddress requests for reprints to: Dr. J . E. Devitt, Department of Surgery, Ottawa Civic Hospital, University of Ottawa, Ottawa , Canada.

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duce statistically significant but clinically misleading ·results, the error being revealed only if the ' trial is continued. 10· 11 The remaining method of developing a ba~is therapy is to critically review the failures ' of therapy. By considering death of 'the patient as a failure of therapy, the clinical f~atures and the natural history of 12 13 may be determined. It th~ fat~l cases ' is also possible to identify, with all of the advantagtls of hindsight, common inadequacifs in the therapeutic program. In this way it should be possible to recognize th~ patients }Vith upper gastrointestinal bleeding who ar~ in danger of dying, and to plan and conduct a regimen of therapy that avoids the common pitfalls. Any hospital that critically reviews its deaths can do this. The approach suffers, however, from the absence of early reliable feedback that could confirm whether a change in management had produced a meaningful improvement.

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History of Fatal Bleeding Ulcer Usually, bleeding from a peptic ulcer is abrupt and it soon stops spontaneously.' · 13 ' 14 The classic case of fatal bleeding ulcer has four or five short lived, vigorous, self-limiting hemorrhages. 13 One occurs in the week before hospitalization and is recognized by the history of a melena stool 2 or 3 days earlier. The second bleed is more dramatic with hematemesis or fainting or more melena stools, and it results in admission to the hospital. Three bleeds of 1000 to 2000 cc occur in the. hospital at 12 to 48 hr intervals before death supervenes. The median day of defith is the sixth day after admission. 12 ' 13' 15 Usually, death results from the cardiovascular embarrassment that follows the repeated, inadequately replaced blood losses. It rarely results from abrupt exsanguination. These features tend to be true of other causes of upper gastrointestinal bleeding. In the spectrum of the problem there are some patients who die within a day of admission, or without obvious recurrent bleeding. In most of these cases, either

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the diagnosis of bleeding will not have been made12 or no treatment will have have been offered because of lack of time, the supervening of complications such as myocardial infarction, or intentional abandonment because of old age or other major illness. 13 Only a very few patients will continue to bleed so vigorously in the first 12 hr as to threaten exsanguination or aspiration. These few can be readily recognized, and there is sufficient time for appropriate intervention.

Clinical Features of Patients at Risk Age is of critical importance. Except in unusual circumstances, death is uncommon under age 55. 7 ' 13 The increasing mortality over age 55 is presumably due to the inability of the older patient to tolerate the repeated bouts of hypovolemia, rather than any difference in the ulcer or severity or frequency of recurrent hemorrhage.4 Provided that there are no associated serious disorders, under age 55 the main threat is that of surgical complications. Associated medical disorders result in high mortality rates. 6· 13 Although these diseases increase the surgical mortality rates, they probably increase the risk of nonoperative therapy even more, because of the patient's decreased ability to tolerate the repeated hypovolemic episodes.5· 16 The type of lesion is the third factor that influences mortality. Provided there are no special considerations, e.g., stress ulcers or coagulation disorders, death tends to be restricted to chronic ulcer patients. 4· 7 ' 13 A few patients, of course, do not give meaningful histories of dyspepsia suggestive of chronic ulcer, but this need not unduly influence the plan of therapy.1 7 Males are more common in most series of fatal bleeding but this probably only reflects the sex incidence of peptic ulcer disease. The history of a previous hemorrhage prior to the current bout of bleeding episodes does not worsen the prognosis. 4· 16 Indeed, the survival of a bleed in the past

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suggests a healthy or at least an adaptable cardiovascular system.

Identification of Inadequacies in Management In an earlier review 13 of 50 consecutive deaths from bleeding peptic ulcer, the management of each patient was critically assessed in an attempt to identify inadequacies, with all of the advantage of hindsight. All details were reviewed that were relevant to the nature of the presenting and subsequent hemorrhages, the rate and volume of blood given, and the response of the patient's pulse rate, blood pressure, urine output, and hemoglobin levels to the transfusions given. In addition, the indications for the timing and the preparation for surgery, the surgical technique, and the surgical complications were reviewed. The most common deficiency was in the technique of blood transfusion. The amount of blood required on admission to the hospital was regularly underestimated by one-half. There was frequently a delay in instituting transfusion. This was worst on the patient's arrival at the hospital when 2 to 4 hr frequently elapsed before blood was actually given. Too seldom was blood given rapidly (more than 1000 cc per hr), and then usually just as part of the immediately preoperative resuscitation. Not only was there a delay in returning the patient to a compensated state but, just as important, patients were seldom provided with a reserve for possible subsequent recurrent hemorrhages. 18 The failure to provide either the volume of blood or the rate at which it was required was considered the most important factor in the unsuccessful management of these patients. The second most common area of error was in the timing of surgical intervention. The reviewers considered the timing to be inappropriate in 33 of the 50 patients. In 21 patients operation was indicated and not done, in 8 it was indicated considerably earlier than when it was carried out, and in 4 it was performed earlier than appeared justifiable. Poor timing of surgery

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was more often the fault of the surgical consultant than the referring physician, The third area of weakness was in the technical surgery. Occasionally, patients were precipitously operated upon with no reasonable attempt to correct blood volume or water or electrolyte deficits. As in any operated series there were patients who bled from missed or retli.iqed uicers and deaths from fistulae and injuries to abdominal organs. 6 • 19 ' 20 Finally, it was evident that the experience gained from the f50 fatal cases was so widely distributed over 9 years and 85 doctors that there was little hope that lessons learned from one patient would be remembered when the next ,patient was encountered. Others2 • 21 have observed the tendency for experience with this disorder to be diffused both by time and the number of physicians and surgeons involved.

Suggested Plan of Therapy The problem, of course, is to identify those patients in whom the potehtial mortality of recurrent or cobt,i nued bleeding is greater than the mortality of operation. Both risks must be calculated for each patient because they . djffer widely with each individual and each situation. Neither can the long term motbidity be ignored. In general, surgery will more effectively reduce further peptic ulcer trouble 7 although perhaps leps effectively than we would all like. On the other hand, patients operated on for massive hemorrhage are more likely to have a lifetime of unwanted postgastric surgical phenomena. 22 ' 23 These risks will be far better estimated by an experienced team than they can ever be by occasional managers of patients with upper gastrointestinal bleeding. Based on the observed natural history of fatal bleeding ulcer and the clinical features of the high risk patients, the following regimen is proposed. Since 75% of patients will (if they have not already) stop bleeding spontaneously, and the remainder can be expected to survive the first recurrent hemorrhage in the

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hospital, there is no need for immediate surgery, provided the patient is adequately transfused·. Thus, regardless of the age or sex of the patient, the nature of the causative lesion, or the magnitude of the hemorrhage, the initial treatment is simply vigorous transfusion. The only important concern is the accurate estimate of the blood loss and its aggressive replacement, with monitoring of the central venous pressure, if necessary. Rapid transfusion is required to allow the patient the reserve to withstand further bleeding, if it occurs, as much as to assist recovery from the previous hemorrhage. Shock requires the personal presence of a responsible physician or surgeon, skilled in its management, for its duration. Through this period and for as long afterward as seems appropriate the following observations are required: hourly pulse and blood pressure; urine output (to monitor kidney perfusion and hence adequacy of functional blood volume) if necessary by indwelling catheter; hemoglobin or hematocrit, no more often than 12 hourly (to recognize unsuspected but usually compensated blood loss that will perforce be several hours old); where appropriate, central venous pressure; nursing reports on general condition, pallor, sweating, restlessness, or apprehension; the nature, timing, and volume of any hematemeses; and the nature, timing, and size of all bowel movements. Any abnormalities of these must be reported to the responsible doctor. If another significant hemorrhage occurs in hospital, it must be feared that the patient will have further recurrent bleeds which he will be unable to tolerate. Therefore, if he is over age 55 and has a chronic ulcer, emergency operation is indicated not, as a rule, to stop the bleed• ing, because it will have stopped usually, but to prevent further bleeding episodes in the current series. If there are associated general medical diseases that make the patient less tolerant of blood volume reduction, then operation is even more urgent. 5 ' 16 It is essential that a 1- or 2-hr

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period of intense resuscitation precede the operation. Since fatal hemorrhage is rare with acute ulcers or in patients under 55 years of age, patients without convincing histories of chronic ulcers, or under age 55, may be transfused through the first hospital recurrent hemorrhage, and not operated upon unless there is a second recurrent bleed. In this way some unnecessary operations may be avoided. Similarly, the rarity of fatal acute ulcers challenges the place of true "blind" gastrectomy. The two decisions of transfusion technique and need of surgery are based almost entirely on the nature of the bleeding and the patient's reaction to it. 17 Neither of these require or are helped by emergency X-ray investigation. 7 • 8 • 24 • 25 Barium studies are best delayed until the patient has been compensated and stable for 48 hr. When, because of the nature of the bleeding, surgery is indicated yet there is no confident clinical diagnosis, emergency endoscopy may be invaluable in identifying esophageal varices and acute gastric lesions. Although some deaths from operative injuries, fistulae, and retained ulcers are inevitable, their incidence must surely be reduced by restricting the surgery to only the highly experienced gastric surgeons. Only the development of a "hematemesis team" of physicians and surgeons to handle all patients with upper gastrointestinal bleeding in a hospital will avoid the errors of inexperience that are inevitable when exposure is limited to an annual or semi-annual case. Suture-ligation, vagotomy, and pyloroplasty is the operation of choice for bleeding ulcer, whether duodenal or gastric, only because it should have a lower mortality rate than gastrectomy. 26 Unfortunately, it is not always applicable, either because of technical infeasibility or the incidence of re-bleeding, 19 ' 27 to those very patients where the severity of the ulcer process makes gastrectomy the most hazardous.

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There will be situations in the spectrum of upper gastrointestinal bleeding where the suggested regimen will have to be adjusted. Earlier surgery will be desirable where obvious profuse bleeding continues, or if there_ is a shortage of available blood. Urgent elective surgery may be justifiable on the past history of suffering alone, the admitting hemorrhage serving only as an excuse to get on with the procedure now. Because bleeding usually stops spontaneously, gastric cooling should be restricted to desperate situations, but even then, it must be used for the patient's benefit rather than the physician's need to appear to be doing something. Bleeding stress ulcers associated with other major disorders require more urgent surgery than other acute ulcers. Finally, most large ulcers and all tumors will require some sort of resection to ensure lasting control of bleeding. Unfortunately, it is often difficult to show meaningful statistical improvement in results following theoretical improvement in type 19 or timing or even use of surgery. 7 - 9 · 2 1 One can only hope that this is due to lack of individualization of therapy and that the benefit is more than a reduction of strain on the blood bank and of the incidence of further peptic ulcer trouble. 7

What of the Future? Until peptic ulcers are prevented, the management of bleeding ulcer centers about three points: 1) the recognition of bleeding, its rate and volume, and the patient's response to it; 2) the recognition of the patient who will re-bleed in a lifethreatening form; and 3) the selection and execution of the operation most likely to prevent re-bleeding at the lowest risk to the patient. There must be no glib rules or formulae, as tempting as they may be, to obviate the need for thoughtful consideration. Only the concentration of experience through a hematemesis team is likely to improve the efficiency of coping with these dilemmas. At the very least, such a

team would improve the management of the shock and the pulmonary complications of respiratory failure, aspiration, and pulmonary edema. Indeed, it may be improvement in the management of these alone 6 • 28 that has accounted for any bettering of our results in recent years. REFERENCES 1. Jones, F. A. 1947. Haematemesis and melaena . Brit. Med . J. 2: 441- 446. 2. Chalmers, T. C. 1964. Mortality rate versus funeral rate in clinical medicine. Gastroent erology 46: 788-791. 3. Stewart, J . D., G. M. Sanderson, and C. E. Wiles. 1952. Blood replacement and gastric resection for massively bleeding peptic ulcer. Ann. Surg . 136: 742-751. 4. Lewin, D. C., and S. Truelove. 1949. Haematemesis. Brit. Med. J. 1: 383- 386. 5. Mitty, W. F., F. J . Breen, R. Wallace, and W. J. Grace. 1961. Factors influencing mortality in bleeding peptic ulcer. Amer. J . Dig. Dis. 6: 389- 394. 6. Foster, J. H. , D. F. Hickok, and J . E. Dunphy. 1963. Factors influencing mortality following emergency operation for massive upper gastrointestinal hemorrhage. Surg . Gynec . Dbstet. 117: 257- 262. 7. Jones, F. A. 1956. Hematemesis and melena. Gastroenterology 30: 166-190. 8. Read, R. C., H. C. Huekl, and A. P. Thai. 1965. Randomized study of massive bleeding from peptic ulceration . Ann. Surg. 162: 561- 577. 9. Enquist, I. F., K. E. Karlson, C. Dennis, S. M. Fierst, and G. W. Shagton. 1965. Statistically valid ten-year comparative evaluation of three methods of management of massive gastroduodenal hemorrhage. Ann. Surg . 162: 550-560. 10. Cole, M. P. 1968. Suppression of ovarian function in primary breast cancer, p. 146-156. In A. P . M . Forrest and P . B. Kunkler [ed.], Prognostic factors in breast cancer. E. and S. Livingstone, Ltd., Edinburgh. 11. Atkins, H. 1966. Carcinoma of the breast. Ann. Roy . Call. Surg . Eng. 38: 133-153. 12. Chalmers, T. C., N. I. Zamcheck, G. W. Curtens, and F. W. White. 1952. Fatal gastrointestinal hemorrhage: clinic-pathologic correlations in 101 patients. Amer. J. Clin . Path. 22: 634- 645. 13. Devitt, J . E., F. N . Brown, and W. G. Beattie. 1966. Fatal bleeding ulcer. Ann. Surg. 164: 840- 844. 14. Jones, F. A. and J. W. P. Gummer. 1968. Clini-

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cal gastroenterology, Ed. 2, p. 548-588. Charles C Thomas, Publisher, Springfield, lll. Meulengracht, E. 1947. Fifteen year experience with free feeding of patients with bleeding ulcer. Arch. Intern. Med . (Chicago) 80: 697-708. Coghill, N. F., and R. G. Willcox. 1960. Factors in the prognosis of bleeding gastric and duodenal ulcer. Quart. J. Med . 29: 575- 596. Banning, A. , A. Baron, A. Kopelman, K. L. Lam, and P. Warren. 1965. Bleeding peptic ulcer. Brit . Med . J. 2: 781-784. Gunz, F. W., I. D. Gebbie, and R. C. S. Dick. 1964. Treatment of acute gastroduodenal haemorrhage. Brit. Med. J . 1: 950-956. Kelley, H . G., G. N. Grant, and D. W. Elliott. 1963. Massive gastroduodenal hemorrhage. Arch. Surg. (Chicago) 87: 6- 12. Carruthers, R. K., G. R. Giles, C. G. Clark, and J . C. Goligher. 1967. Conservative surgery for bleeding peptic ulcer. Brit. Med . J . 1: 8082. Stafford, E. S. , W. F. Ballinger, G. D. Zuidema, and J . L. Cameron. 1967. Benign gastric ulcer with life-threatening hemorrhage. Ann. Surg. 165: 967- 976. Jordan, S. M., J . M . Ruffin, A. H. Aaron, F. Hollander, J . E. Thomas, W. Walters, F. D.

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Moore, A. Winkelstein, F. P . Brooks, and I. Lorge. 1952. Report of the committee on surgical procedures of the national committee on peptic ulcer of the American Gastroenterological Association. Gastroenterology 22: 297- 499. Tanner, N. C. 1954. Surgical aspects of gastric and duodenal ulceration. Postgrad. Med. J . 30: 124-131. Herrington, J. L. 1964. A more aggressive surgical attitude in the management of massively bleeding duodenal ulcer. Surgery 55: 349-350. Mouchet, A., J . Marquand, M. Guinarch'h, and M . Berlinski . 1968. A propos de 135 cas d'hemorragies gastro-duodenales massives. Ann. Chir. 22: 321-328. Foster, J. H. , D. F. Hickok, and J. E. Dunphy. 1965. Changing concepts in the surgical treatment of massive gastroduodenal hemorrhage. Ann. Surg. 161 : 968-976. Silen, W. , and F. D. Mear. 1964. Surgical treatment of bleeding duodenal ulcer: a plea for caution . Ann. Surg . 160: 778-779. Hampson, L. G., D. S. Mulder, G. L. Elias, and J . D. Palmer. 1968. The emergency surgical treatment of massively bleeding peptic ulcer. Arch. Surg. (Chicago) 97: 450-458.