- Email: [email protected]
Medical Complications Following Gastric Surgery
Medical Complications Following Gastric Surgery JOHN A. HIGGINS, M.D.
WHEN, IN THE COURSE OF DUODENAL ULCER, evidence develops of severe or recurrent hemorrhage, pyloric obstruetion, acute perforation, or chronic, intractable pain, the physician usually resorts to surgical management of these complications. In the great majority of cases, patients so treated will undergo resection of two-thirds to three-fourths of the stomach, with gastrojejunostomy to re-establish gastrointestinal continuity. After a reasonable period of postoperative convalescence, most of these patients will have returned to good health with essentially normal digestive function; and most will not be bothered again by ulcer disease. Reports from large surgical centers generally agree that 85 to 90 per cent of patients thus treated obtain a good to excellent functional result. This evaluation is influenced, of course, by the personality of the subject and personal jUdgment of the reviewer, as well as by more objective evidence of disturbed function and by the length of ~he follow-up investigation. Within that minority of patients considered to have an unsatisfactory result, further ulceration or stomal malfunction will develop in perhaps one-third, who thus will become candidates for additional surgical procedures. Among the remaining patients-approximately 5 to 10 per cent of all those surgically treated-some complication of the gastrectomy will develop that is regarded generally as being within the therapeutic realm of the internist. These may be listed in the following categories: (1) the dumping syndrome or early postprandial symptoms, (2) loss of weight, (3) the malabsorption syndrome, (4) anemia, and (5) late postprandial symptoms. Obviously, there may be an interrelationship among the subdivisions. In most studies concerned with the efficacy of surgical management, only the dumping syndrome is regarded as a reason to consider the result functionally unsatisfactory. DUMPING SYNDROME
The indelicate but descriptive term dumping was coined by C. L. Mix, a Chicago surgeon, in 1922, following his fiuoroscopic observations of a
979
980
JOHN
A.
HIGGINS
woman who had had gastroenterostomy. The term has since come to be applicd to the complex of symptoms experienced in the early postprandial period by many persons who have had gastric surgical procedures of various types. The complex is often described as having two distinct components: the intestinal portion, including abdominal fullness, bloating, epigastric discomfort, hyperperistalsis, and nausea; and the vasomotor manifestations, such as weakness, tachycardia, palpitation, flushing, sweating, and lightheadedness. The development of these unpleasant effects can be prevented by keeping a recumbent position while eating or can be relieved by lying down after eating. Credit for early efforts to determine the physiologic derangements resulting in the dumping syndrome generally goes to Machella, who in 1949 demonstrated that the symptoms could be reproduced by the introduction of various hypertonic solutions into the jejunum or by distention of the jejunum with a balloon. He postulated that osmotic forces caused a rapid influx of fluid into the jejunum and that the resulting distention produced the symptom complex. A significant flaw in this reasoning was pointed out by Machella himself when he noted that the most prominent feature of experimentally produced jejunal distentionabdominal pain-is not usually present with the dumping syndrome. Despite this and other inadequacies in his explanation, Machella's technique of introducing hypertonic solutions directly into the jejunum remains the standard method of producing these symptoms for physiologic investigation. Failure to elicit the vasomotor manifestations by mechanical distention of the jejunum led to the search for other abnormalities. Reactive hypokalemia was endorsed briefly as the explanation for the syndrome, but now has been rejected generally as an inconstant and usually insignificant development. Roberts and co-workers focused attention on the systemic effects of the transfer of significant amounts of fluid from the plasma to the intestinal lumen. They measured changes in the circulating blood volume following the production of symptoms with hyperosmotic solutions, and in symptomatic patients they noted what were regarded as significant decrcases in blood volume. Normal controls did not show similar changes. Since this initial report, other studies3 , 9, 15, 18, 19 have appeared which support or reject the importance of alterations in blood volume. Chief support for the opponents of this concept comes from the nearly unanimous agreement that the correlation between the degree of bloodvolume lowering and the production of dumping symptoms is not necessarily a close one. Transfer of fluid into the intestinal lumen during the postprandial period is normal, but in the gastrectomized patient it usually is more sizable and more sudden. In both normal and gastrectomized persons, the volume of the circulating plasma decreases by about 10 to 15 per cent after they stand up. Together with the osmotic
M edical Complications Follouing Gastric Surgery
981
effeets of a meal, this is thought to provide a sufficient stimulus for vasomotor symptoms in susceptible persons. The nature of this individual susceptibility has been the focal point of most recently reported investigations. Clinically, the incidence of postoperative dumping seems higher in patients who, besides presenting organic evidences of their uleer disease, are tense and anxious and who are regarded as being gastrointestinal or vascular hyper-reactors. Therefore possible disturbances in factors influencing the autonomic nervous system have received the most attention. Attempts to demonstrate increased levels of circulating vasodilating or vasoconstricting substances such as histamine or serotonin have not been rewarding. Le Quesne and associates demonstrated the produetion of vasomotor symptoms in some subjects by applying pneumatie cuffs to the thighs, thus trapping a portion of the circulating blood in the legs. Persons who were sensitive to such cuffiing were, by and large, also those who experienced symptoms when challenged with a hypertonic test meal. Further, this study 5 pointed to the strong positive correlation between the amount of the fall in plasma volume and the slope of the rise of the blood sugar concentration following the ingestion of hypertonic glucose after gastrectomy. Subcutaneous administration of insulin prior to the test caused a deerease of the hyperglycemic response, and a concomitant lessening of the decline in plasma volume was noted. No correlation could be found between the influence upon the blood sugar and the extent to which the plasma volume was affected, but the symptoms produced by the test meal were distinctly lessened in all cases. On the basis of these observations, a primary defect in carbohydrate metabolism has been postulated, with assignment of more secondary importance to the disturbances of motility. This metabolic defect, of indeterminate cause, produces a decrease in the rate of removal from the blood of glucose absorbed from the intestine. The resulting sustained hyperglycemia interferes with diffusion processes, thereby slowing the further absorption of sugar from the bowel. This, in turn, causes the retention of osmotically active material within the lumen and the further shift of plasma water into the gut, increasing the fall in plasma volume and stimulating intestinal motility by increasing intraluminal volume. Gastric emptying is enhanced, more hypertonic material is brought to the jejunum, and a vicious cycle is developed. The therapeutic effect of insulin is presumed to be due to its influence upon the rate of removal of glucose from the circulation. Read has presented the hypothesis that the dumping syndrome is the result of direct hyperosmotic effects upon the bowel and other organs. Intravenous injection of hypertonic solutions can produce a state of vasodilatation, and the ensuing symptomatology is similar to that experienced with dumping. The syndrome is mimicked also by the effects of intravenous administration of acetylcholine or mecholyl.
982
JOHN
A.
HIGGINS
Powerful tissue cholinesterascs that rapidly destroy acetylcholine prevent its accumulation in identifiable amounts, but it is probable that the hyperosmotic stimulus aets only in a cholinergic-like manner. Other studies4 • 11 emphasize the importance of an alteration of vasomotor reaction in response to hyperosmolarity by demonstrating that the blood flow in some of the lesser circulatory pathways is altered during the experimental production of dumping. Mesenteric and renal blood flow may be increased, as are the skin temperature and the circulation to the digits. Thus an altered circulatory response may result in the pooling of significant quantities of blood in the splanchnic and cutaneous vessels, and this may have a decisive influence in the development of symptoms. The medical management of the dumping syndrome takes into account the apparent importance of osmotic influences. Generally patients who experience enough disability to justify the inconvenience are advised to resort to more frequent and smaller meals, thus reducing the mechanical stress on the gastrointestinal system. Most patients, by the time that they seek medical advice, have discovered that their discomfort is aggravated by eating simple carbohydrates, the most osmotically active elements in the diet. In addition, they have learned that prompt relief is afforded by lying down after a meal. A diet high in protein and fat and low in carbohydrates, with no simple sugars whatever, is usually best suited for the greatest number, although individual preferences are often important. Additional benefit, which often is striking, can be gained by closely restricting the fluid intake at mealtime. This apparently has some influence in slowing gastric emptying and retarding the otherwise immediate osmotic effects. The use of drugs has been disappointing for the most part, although occasionally antispasmodic preparations may give spectacular benefit. Hobsley and Le Quesne, on the basis of observations they had made with the use of insulin, have treated a few patients with small doses of subcutaneous insulin once or twice a day before meals. Preliminary results are reported to be encouraging. Inasmuch as the initiating step in the production of dumping symptoms is the rapid emptying of the gastric remnant, various surgical maneuvers to delay this process have been advocated. Variable success has been reported. Some surgeons6 have found it helpful to convert the anastomosis from gastrojejunal to gastroduodenal; othersl are content to limit the diameter of the stoma carefully to approximately 1 em. There has been little enthusiasm for attempts to enlarge the gastric capacity by interposing a segment of colon between the stomach and jejunum. LOSS OF WEIGHT
The majority of patients who undergo subtotal gastrectomy experience loss of weight in the early postoperative period, and some are unable to
Medical Complications Following Gastric Surgery
983
regain it subsequently. It is not unusual for this reduction to equal 10 to 15 per cent of the preoperative body weight; and in a small number of cases, failure to regain to near normal levels constitutes a major problem. As might be expected, the loss of weight tends to be greatest in those patients who have had the most severe early postprandial symptoms. Reduction of food intake to avoid the unpleasant consequences of eating is the single most important cause of weight problems in gastrectomized patients. Proper management of the dumping syndrome usually results in significant weight increases among this group. MALABSORPTION SYNDROME
A much smaller group of patients present as nutritional problems, not because of dumping symptoms but because of significant malabsorption of dietary constituents. Diarrhea is not necessarily the predominant complaint in these cases. In many of them, careful quantitative analyses of stool fat yields slightly abnormal values; but usually this loss amounts to only a few hundred calories a day. There are many possible causes for inefficient intestinal absorption in the patient with a gastrojejunal anastomosis. Very likely the principal factor is intestinal hurry, which moves diet elements well below the optimal absorptive zones before adequate digestion can occur. After gastrectomy, the normal secretory stimuli to hepatic and pancreatic cells are disrupted so that the response is relatively poor and the mixing of food and digestive enzymes in the efferent jejunal loop may be inadequate. In the occasional patient in whom significant malabsorption does occur, some benefit may result from the use of exogenous bile salts and pancreatic extracts. It has been demonstrated 17 that a meal high in carbohydrates increases steatorrhea-probably because the osmotic effects of such a diet produce hypermotility. On the other hand, the postgastrectomy steatorrhea of some patients may be favorably influenced by ingestion of 0.1 N hydrochloric acid before meals. This effeet is thought to result from pancreatic stimulation via the secretin pathway. Reports 8 • 16 have described villose atrophy, mucosal thickening, and other histologic abnormalities in the jejunal mucosa of patients with postgastrectomy steatorrhea. In the great majority of cases, however, the mucosa is normal under the light microscope; and it is doubtful that structural alterations are significant in malabsorption following gastrectomy. ANEMIA
Probably close reeheeking after the usual gastric resection for duodenal ulcer will reveal development of some degree of anemia in most
984
JOHN
A.
HIGGINS
cases. Nearly always this is relatively mild hypochromic anemia of the iron-deficiency type. In the postoperative state iron absorption, as measured by Fe59 uptake, is adversely affected. Investigation has shown that gastrectomized persons absorbed less than one-third as much of labeled organic iron compounds as did subjects with similar levels of anemia who had not had surgical treatment. 7 In another study,2 the rate of incorporation of radioiron into the hemoglobin molecules of patients following a Polya type of gastrojejunostomy was little more than onc-twentieth of the rate found in a matching group of anemic patients without operation. The fact that iron absorption may be significantly reduced after a gastroduodenostomy argues against the opinion that bypassing the duodenum is the sole cause of disturbed postgastrectomy iron absorption. The resulting hypochlorhydria or achlorhydria may provide an additional influence by removing the effect of hydrochloric acid in reducing ferric iron to its absorbable ferrous state. In the usual clinical situation, anemia develops too rapidly to be the result of defective iron absorption alone. Therefore the additional factor of chronic occult blood loss has been suggested. This is often difficult to demonstrate, but frequently the possibility of slight bleeding from irritated tissues around the stoma cannot be excluded. Be that as it may, the anemia nearly always responds to ordinary doses of inorganic iron salts. These seem best tolerated when taken at times other than mealtime, and many suggest that a bedtime dose is helpful. Macrocytic or megaloblastic anemia appears rarely after the usual subtotal gastrectomy, but more frequently as the degree of resection approaches 100 per cent. Nearly all patients who survive total gastrectomy long enough experience this complication. It is readily controlled by adequate replacement of vitamin B 12 • LATE POSTPRANDIAL SYMPTOMS
Late postprandial symptoms, occurring two or three hours after a meal, can be attributed confidently to hypoglycemia. The symptoms are similar to those resulting from hypoglycemia in other situations and can be prevented or relieved by oral or intravenous administration of sugar. The cause of this reaction has not been explained to complete satisfaction, but probably it is related to an excessive insulin response to the preceding hyperglycemia. CONCLUSIONS
Despite these apparent hazards of the surgical management of ulc:er disease, it is a rare patient whose postgastrectomy symptoms cannot be
Medical Complications Following Gastric Surgery
985
controlled reasonably well by appropriate medical management. K evertheless, the surgeon and internist will reduce significantly the number of unhappy and disappointed postoperative patients if they will adhere closely to rather rigid criteria in the selection of surgical candidates. For relief from a truly dangerous or incapacitating ulcer complication, moderate dumping symptoms are a relatively small price to pay. REFERENCES 1. Abbott, W. E., Krieger, Harvey, and Levey, Stanley: Technical Surgical Factors Which Enhance or Minimize Postgastrectomy Abnormalities. Ann. Surg. 148: 567-591 (Oct.) 1958. 2. Choudhury, M. R., and Williams, J.: Iron Absorption and Gastric Operations. Clin. Se. 18: 527-532, 1959. 3. Duthie, H. L.: Partial Gastrectomy for Peptic Ulcer: Six Years After. Scot. M. J. 5: 127-134 (Mar.) 19GO. 4. Hinshaw, D. B., Joergenson, E. J., Davis, H. A., and Stafford, C. E.: Peripheral Blood Flow in Blood Volume Studies in the Dumping Syndrome. Arch. Surg. 74: 686-693 (May) 1957. 5. Hobsley, M., and Le Quesne, L. P.: The Dumping Syndrome. n. Cause of the Syndrome and the Rationale of Its Treatment. Brit. M. J. 1: 147-151 (Jan. 16) 1!)60. 6. IIlingworth, C. F.: Post-gastrectomy Syndromes: A Review. Gut 1: 183-192 (Sept.) H)60. 7. Iron Defieipncy Anemia Following Partial Gastreetomy. Nutrition Rev. 17: 2()7-:~Ol (Oct.) Hl59. 8. Joske, R. A., and Blackwell, J. B.: Alimentary Histology in the Malabsorption Syndrome Following Partial Gastrectomy. Lancet 2: 379-382 (Sept. Hl) 1959. 9. Le Quesne, L. P., Hobsley, M., and Hand, B. H.: The Dumping Syndrome. 1. Faetors Responsible for the Symptoms. Brit. M ..J. 1: 141-147 (Jan. 16) 1960. 10. Machella, T. E.: The Mechanism of the Post-gastrectomy "Dumping" Syndrome. Ann. Surg. 130: 145-159 (Aug.) 1949. 11. Mathews, D. H., Lawrence, \Valter, Jr., Poppel, W. J., Vanamee, Parker, and Randall, H. T.: Changes in Effective Circulating Volume During Experimental Dumping Syndrome. Surgery 48: 185-1!)3 (July) 1960. 12. Mix, C. L.: "Dumping Stomach" Following Gastrojejunostomy. S. Clin. North America 2: 617-622 (June) 1922. 13. Head, R. C.: The Nature of the Dumping Syndrome. Minnesota Med. 44: 5664 (Feb.) 1961. 14. Hoberts, Kathleen, E., Handall, H. T., Farr, H. W., Kidwell, A. P., McNeer, G. P., and Pack, G. T.: Cardiovascular and Blood Volume Alterations Resulting from Intrajejunal Administration of Hypprtonic Solutions to Gastrectomized Patients: The Relationship of These Changes to the Dumping Syndrome. Ann. Surg. 140: 631-640 (Nov.) 1954. 15. Seott, H. W., Jr., Weidner, M. G., Jr., Shull, H. J., and Bond, A. G.: The Dumping Syndrome. n. Further Investigations of Etiology in Patients and Experimental Animals. Gastroenterology 37: 194-199 (Aug.) 1959. 16. Shiner, M., and Doniach, 1.: Histopathologic Studies in Steatorrhea. Proc. World Congress Gastroenterology and Fifty-ninth Annual Meeting of the American Gastroenterological Association, Washington, D. C., May 25 through 31, 1958, pp. 586-607. 17. Vanamee, Parker, Lawrence, WaIter, Jr., Levin, Sam, Peterson, Ann S., and Handall, H. T.: Further Observations on Postgastrectomy Steatorrhea:
986
JOHN
A.
HIGGINS
The Effect of High Carbohydrate Intake and of Hydrochloric Acid Administration on Fat Absorption. Ann. Surg. 150: .517-527 (Sept.) Hl59. 18. Webber, B. M., Bender, M. A., and Moore, G. E.: Dumping Syndrome: An Evaluation of Some Current Etiologie Concepts. New England J. Med. 256: 285289 (Feb. 14) 1957. 19. Weidner, M. G., Jr., Scott, H. W., Jr., Bond, A. G., and Shull, H. J.: The Dumping Syndrome. I. Studies in Pati(mts After Gastric Sllfgery. Gastroenterology 37: 188-193 (Aug.) 1959.
WHEN, IN THE COURSE OF DUODENAL ULCER, evidence develops of severe or recurrent hemorrhage, pyloric obstruetion, acute perforation, or chronic, intractable pain, the physician usually resorts to surgical management of these complications. In the great majority of cases, patients so treated will undergo resection of two-thirds to three-fourths of the stomach, with gastrojejunostomy to re-establish gastrointestinal continuity. After a reasonable period of postoperative convalescence, most of these patients will have returned to good health with essentially normal digestive function; and most will not be bothered again by ulcer disease. Reports from large surgical centers generally agree that 85 to 90 per cent of patients thus treated obtain a good to excellent functional result. This evaluation is influenced, of course, by the personality of the subject and personal jUdgment of the reviewer, as well as by more objective evidence of disturbed function and by the length of ~he follow-up investigation. Within that minority of patients considered to have an unsatisfactory result, further ulceration or stomal malfunction will develop in perhaps one-third, who thus will become candidates for additional surgical procedures. Among the remaining patients-approximately 5 to 10 per cent of all those surgically treated-some complication of the gastrectomy will develop that is regarded generally as being within the therapeutic realm of the internist. These may be listed in the following categories: (1) the dumping syndrome or early postprandial symptoms, (2) loss of weight, (3) the malabsorption syndrome, (4) anemia, and (5) late postprandial symptoms. Obviously, there may be an interrelationship among the subdivisions. In most studies concerned with the efficacy of surgical management, only the dumping syndrome is regarded as a reason to consider the result functionally unsatisfactory. DUMPING SYNDROME
The indelicate but descriptive term dumping was coined by C. L. Mix, a Chicago surgeon, in 1922, following his fiuoroscopic observations of a
979
980
JOHN
A.
HIGGINS
woman who had had gastroenterostomy. The term has since come to be applicd to the complex of symptoms experienced in the early postprandial period by many persons who have had gastric surgical procedures of various types. The complex is often described as having two distinct components: the intestinal portion, including abdominal fullness, bloating, epigastric discomfort, hyperperistalsis, and nausea; and the vasomotor manifestations, such as weakness, tachycardia, palpitation, flushing, sweating, and lightheadedness. The development of these unpleasant effects can be prevented by keeping a recumbent position while eating or can be relieved by lying down after eating. Credit for early efforts to determine the physiologic derangements resulting in the dumping syndrome generally goes to Machella, who in 1949 demonstrated that the symptoms could be reproduced by the introduction of various hypertonic solutions into the jejunum or by distention of the jejunum with a balloon. He postulated that osmotic forces caused a rapid influx of fluid into the jejunum and that the resulting distention produced the symptom complex. A significant flaw in this reasoning was pointed out by Machella himself when he noted that the most prominent feature of experimentally produced jejunal distentionabdominal pain-is not usually present with the dumping syndrome. Despite this and other inadequacies in his explanation, Machella's technique of introducing hypertonic solutions directly into the jejunum remains the standard method of producing these symptoms for physiologic investigation. Failure to elicit the vasomotor manifestations by mechanical distention of the jejunum led to the search for other abnormalities. Reactive hypokalemia was endorsed briefly as the explanation for the syndrome, but now has been rejected generally as an inconstant and usually insignificant development. Roberts and co-workers focused attention on the systemic effects of the transfer of significant amounts of fluid from the plasma to the intestinal lumen. They measured changes in the circulating blood volume following the production of symptoms with hyperosmotic solutions, and in symptomatic patients they noted what were regarded as significant decrcases in blood volume. Normal controls did not show similar changes. Since this initial report, other studies3 , 9, 15, 18, 19 have appeared which support or reject the importance of alterations in blood volume. Chief support for the opponents of this concept comes from the nearly unanimous agreement that the correlation between the degree of bloodvolume lowering and the production of dumping symptoms is not necessarily a close one. Transfer of fluid into the intestinal lumen during the postprandial period is normal, but in the gastrectomized patient it usually is more sizable and more sudden. In both normal and gastrectomized persons, the volume of the circulating plasma decreases by about 10 to 15 per cent after they stand up. Together with the osmotic
M edical Complications Follouing Gastric Surgery
981
effeets of a meal, this is thought to provide a sufficient stimulus for vasomotor symptoms in susceptible persons. The nature of this individual susceptibility has been the focal point of most recently reported investigations. Clinically, the incidence of postoperative dumping seems higher in patients who, besides presenting organic evidences of their uleer disease, are tense and anxious and who are regarded as being gastrointestinal or vascular hyper-reactors. Therefore possible disturbances in factors influencing the autonomic nervous system have received the most attention. Attempts to demonstrate increased levels of circulating vasodilating or vasoconstricting substances such as histamine or serotonin have not been rewarding. Le Quesne and associates demonstrated the produetion of vasomotor symptoms in some subjects by applying pneumatie cuffs to the thighs, thus trapping a portion of the circulating blood in the legs. Persons who were sensitive to such cuffiing were, by and large, also those who experienced symptoms when challenged with a hypertonic test meal. Further, this study 5 pointed to the strong positive correlation between the amount of the fall in plasma volume and the slope of the rise of the blood sugar concentration following the ingestion of hypertonic glucose after gastrectomy. Subcutaneous administration of insulin prior to the test caused a deerease of the hyperglycemic response, and a concomitant lessening of the decline in plasma volume was noted. No correlation could be found between the influence upon the blood sugar and the extent to which the plasma volume was affected, but the symptoms produced by the test meal were distinctly lessened in all cases. On the basis of these observations, a primary defect in carbohydrate metabolism has been postulated, with assignment of more secondary importance to the disturbances of motility. This metabolic defect, of indeterminate cause, produces a decrease in the rate of removal from the blood of glucose absorbed from the intestine. The resulting sustained hyperglycemia interferes with diffusion processes, thereby slowing the further absorption of sugar from the bowel. This, in turn, causes the retention of osmotically active material within the lumen and the further shift of plasma water into the gut, increasing the fall in plasma volume and stimulating intestinal motility by increasing intraluminal volume. Gastric emptying is enhanced, more hypertonic material is brought to the jejunum, and a vicious cycle is developed. The therapeutic effect of insulin is presumed to be due to its influence upon the rate of removal of glucose from the circulation. Read has presented the hypothesis that the dumping syndrome is the result of direct hyperosmotic effects upon the bowel and other organs. Intravenous injection of hypertonic solutions can produce a state of vasodilatation, and the ensuing symptomatology is similar to that experienced with dumping. The syndrome is mimicked also by the effects of intravenous administration of acetylcholine or mecholyl.
982
JOHN
A.
HIGGINS
Powerful tissue cholinesterascs that rapidly destroy acetylcholine prevent its accumulation in identifiable amounts, but it is probable that the hyperosmotic stimulus aets only in a cholinergic-like manner. Other studies4 • 11 emphasize the importance of an alteration of vasomotor reaction in response to hyperosmolarity by demonstrating that the blood flow in some of the lesser circulatory pathways is altered during the experimental production of dumping. Mesenteric and renal blood flow may be increased, as are the skin temperature and the circulation to the digits. Thus an altered circulatory response may result in the pooling of significant quantities of blood in the splanchnic and cutaneous vessels, and this may have a decisive influence in the development of symptoms. The medical management of the dumping syndrome takes into account the apparent importance of osmotic influences. Generally patients who experience enough disability to justify the inconvenience are advised to resort to more frequent and smaller meals, thus reducing the mechanical stress on the gastrointestinal system. Most patients, by the time that they seek medical advice, have discovered that their discomfort is aggravated by eating simple carbohydrates, the most osmotically active elements in the diet. In addition, they have learned that prompt relief is afforded by lying down after a meal. A diet high in protein and fat and low in carbohydrates, with no simple sugars whatever, is usually best suited for the greatest number, although individual preferences are often important. Additional benefit, which often is striking, can be gained by closely restricting the fluid intake at mealtime. This apparently has some influence in slowing gastric emptying and retarding the otherwise immediate osmotic effects. The use of drugs has been disappointing for the most part, although occasionally antispasmodic preparations may give spectacular benefit. Hobsley and Le Quesne, on the basis of observations they had made with the use of insulin, have treated a few patients with small doses of subcutaneous insulin once or twice a day before meals. Preliminary results are reported to be encouraging. Inasmuch as the initiating step in the production of dumping symptoms is the rapid emptying of the gastric remnant, various surgical maneuvers to delay this process have been advocated. Variable success has been reported. Some surgeons6 have found it helpful to convert the anastomosis from gastrojejunal to gastroduodenal; othersl are content to limit the diameter of the stoma carefully to approximately 1 em. There has been little enthusiasm for attempts to enlarge the gastric capacity by interposing a segment of colon between the stomach and jejunum. LOSS OF WEIGHT
The majority of patients who undergo subtotal gastrectomy experience loss of weight in the early postoperative period, and some are unable to
Medical Complications Following Gastric Surgery
983
regain it subsequently. It is not unusual for this reduction to equal 10 to 15 per cent of the preoperative body weight; and in a small number of cases, failure to regain to near normal levels constitutes a major problem. As might be expected, the loss of weight tends to be greatest in those patients who have had the most severe early postprandial symptoms. Reduction of food intake to avoid the unpleasant consequences of eating is the single most important cause of weight problems in gastrectomized patients. Proper management of the dumping syndrome usually results in significant weight increases among this group. MALABSORPTION SYNDROME
A much smaller group of patients present as nutritional problems, not because of dumping symptoms but because of significant malabsorption of dietary constituents. Diarrhea is not necessarily the predominant complaint in these cases. In many of them, careful quantitative analyses of stool fat yields slightly abnormal values; but usually this loss amounts to only a few hundred calories a day. There are many possible causes for inefficient intestinal absorption in the patient with a gastrojejunal anastomosis. Very likely the principal factor is intestinal hurry, which moves diet elements well below the optimal absorptive zones before adequate digestion can occur. After gastrectomy, the normal secretory stimuli to hepatic and pancreatic cells are disrupted so that the response is relatively poor and the mixing of food and digestive enzymes in the efferent jejunal loop may be inadequate. In the occasional patient in whom significant malabsorption does occur, some benefit may result from the use of exogenous bile salts and pancreatic extracts. It has been demonstrated 17 that a meal high in carbohydrates increases steatorrhea-probably because the osmotic effects of such a diet produce hypermotility. On the other hand, the postgastrectomy steatorrhea of some patients may be favorably influenced by ingestion of 0.1 N hydrochloric acid before meals. This effeet is thought to result from pancreatic stimulation via the secretin pathway. Reports 8 • 16 have described villose atrophy, mucosal thickening, and other histologic abnormalities in the jejunal mucosa of patients with postgastrectomy steatorrhea. In the great majority of cases, however, the mucosa is normal under the light microscope; and it is doubtful that structural alterations are significant in malabsorption following gastrectomy. ANEMIA
Probably close reeheeking after the usual gastric resection for duodenal ulcer will reveal development of some degree of anemia in most
984
JOHN
A.
HIGGINS
cases. Nearly always this is relatively mild hypochromic anemia of the iron-deficiency type. In the postoperative state iron absorption, as measured by Fe59 uptake, is adversely affected. Investigation has shown that gastrectomized persons absorbed less than one-third as much of labeled organic iron compounds as did subjects with similar levels of anemia who had not had surgical treatment. 7 In another study,2 the rate of incorporation of radioiron into the hemoglobin molecules of patients following a Polya type of gastrojejunostomy was little more than onc-twentieth of the rate found in a matching group of anemic patients without operation. The fact that iron absorption may be significantly reduced after a gastroduodenostomy argues against the opinion that bypassing the duodenum is the sole cause of disturbed postgastrectomy iron absorption. The resulting hypochlorhydria or achlorhydria may provide an additional influence by removing the effect of hydrochloric acid in reducing ferric iron to its absorbable ferrous state. In the usual clinical situation, anemia develops too rapidly to be the result of defective iron absorption alone. Therefore the additional factor of chronic occult blood loss has been suggested. This is often difficult to demonstrate, but frequently the possibility of slight bleeding from irritated tissues around the stoma cannot be excluded. Be that as it may, the anemia nearly always responds to ordinary doses of inorganic iron salts. These seem best tolerated when taken at times other than mealtime, and many suggest that a bedtime dose is helpful. Macrocytic or megaloblastic anemia appears rarely after the usual subtotal gastrectomy, but more frequently as the degree of resection approaches 100 per cent. Nearly all patients who survive total gastrectomy long enough experience this complication. It is readily controlled by adequate replacement of vitamin B 12 • LATE POSTPRANDIAL SYMPTOMS
Late postprandial symptoms, occurring two or three hours after a meal, can be attributed confidently to hypoglycemia. The symptoms are similar to those resulting from hypoglycemia in other situations and can be prevented or relieved by oral or intravenous administration of sugar. The cause of this reaction has not been explained to complete satisfaction, but probably it is related to an excessive insulin response to the preceding hyperglycemia. CONCLUSIONS
Despite these apparent hazards of the surgical management of ulc:er disease, it is a rare patient whose postgastrectomy symptoms cannot be
Medical Complications Following Gastric Surgery
985
controlled reasonably well by appropriate medical management. K evertheless, the surgeon and internist will reduce significantly the number of unhappy and disappointed postoperative patients if they will adhere closely to rather rigid criteria in the selection of surgical candidates. For relief from a truly dangerous or incapacitating ulcer complication, moderate dumping symptoms are a relatively small price to pay. REFERENCES 1. Abbott, W. E., Krieger, Harvey, and Levey, Stanley: Technical Surgical Factors Which Enhance or Minimize Postgastrectomy Abnormalities. Ann. Surg. 148: 567-591 (Oct.) 1958. 2. Choudhury, M. R., and Williams, J.: Iron Absorption and Gastric Operations. Clin. Se. 18: 527-532, 1959. 3. Duthie, H. L.: Partial Gastrectomy for Peptic Ulcer: Six Years After. Scot. M. J. 5: 127-134 (Mar.) 19GO. 4. Hinshaw, D. B., Joergenson, E. J., Davis, H. A., and Stafford, C. E.: Peripheral Blood Flow in Blood Volume Studies in the Dumping Syndrome. Arch. Surg. 74: 686-693 (May) 1957. 5. Hobsley, M., and Le Quesne, L. P.: The Dumping Syndrome. n. Cause of the Syndrome and the Rationale of Its Treatment. Brit. M. J. 1: 147-151 (Jan. 16) 1!)60. 6. IIlingworth, C. F.: Post-gastrectomy Syndromes: A Review. Gut 1: 183-192 (Sept.) H)60. 7. Iron Defieipncy Anemia Following Partial Gastreetomy. Nutrition Rev. 17: 2()7-:~Ol (Oct.) Hl59. 8. Joske, R. A., and Blackwell, J. B.: Alimentary Histology in the Malabsorption Syndrome Following Partial Gastrectomy. Lancet 2: 379-382 (Sept. Hl) 1959. 9. Le Quesne, L. P., Hobsley, M., and Hand, B. H.: The Dumping Syndrome. 1. Faetors Responsible for the Symptoms. Brit. M ..J. 1: 141-147 (Jan. 16) 1960. 10. Machella, T. E.: The Mechanism of the Post-gastrectomy "Dumping" Syndrome. Ann. Surg. 130: 145-159 (Aug.) 1949. 11. Mathews, D. H., Lawrence, \Valter, Jr., Poppel, W. J., Vanamee, Parker, and Randall, H. T.: Changes in Effective Circulating Volume During Experimental Dumping Syndrome. Surgery 48: 185-1!)3 (July) 1960. 12. Mix, C. L.: "Dumping Stomach" Following Gastrojejunostomy. S. Clin. North America 2: 617-622 (June) 1922. 13. Head, R. C.: The Nature of the Dumping Syndrome. Minnesota Med. 44: 5664 (Feb.) 1961. 14. Hoberts, Kathleen, E., Handall, H. T., Farr, H. W., Kidwell, A. P., McNeer, G. P., and Pack, G. T.: Cardiovascular and Blood Volume Alterations Resulting from Intrajejunal Administration of Hypprtonic Solutions to Gastrectomized Patients: The Relationship of These Changes to the Dumping Syndrome. Ann. Surg. 140: 631-640 (Nov.) 1954. 15. Seott, H. W., Jr., Weidner, M. G., Jr., Shull, H. J., and Bond, A. G.: The Dumping Syndrome. n. Further Investigations of Etiology in Patients and Experimental Animals. Gastroenterology 37: 194-199 (Aug.) 1959. 16. Shiner, M., and Doniach, 1.: Histopathologic Studies in Steatorrhea. Proc. World Congress Gastroenterology and Fifty-ninth Annual Meeting of the American Gastroenterological Association, Washington, D. C., May 25 through 31, 1958, pp. 586-607. 17. Vanamee, Parker, Lawrence, WaIter, Jr., Levin, Sam, Peterson, Ann S., and Handall, H. T.: Further Observations on Postgastrectomy Steatorrhea:
986
JOHN
A.
HIGGINS
The Effect of High Carbohydrate Intake and of Hydrochloric Acid Administration on Fat Absorption. Ann. Surg. 150: .517-527 (Sept.) Hl59. 18. Webber, B. M., Bender, M. A., and Moore, G. E.: Dumping Syndrome: An Evaluation of Some Current Etiologie Concepts. New England J. Med. 256: 285289 (Feb. 14) 1957. 19. Weidner, M. G., Jr., Scott, H. W., Jr., Bond, A. G., and Shull, H. J.: The Dumping Syndrome. I. Studies in Pati(mts After Gastric Sllfgery. Gastroenterology 37: 188-193 (Aug.) 1959.