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Short Bowel Syndrome
Symposium on Gastrointestinal Surgery
Short Bowel Syndrome
Cornelius E. Sedgwick, M.D., and Anthony A. Goodman, MD.
Because of the ability of today's surgeons to resect longer lengths of intestine with good survival rates, the short bowel syndrome has been developing in increasing numbers of patients. This syndrome is characterized by diarrhea with impaired absorption of fats, vitamins, and other nutrients, ultimately leading to malnutrition, anemia and continued weight loss. In some instances, severe gastric hypersecretion also occurs ocasionally with the development of duodenal ulcer and its complications. It is of major importance to understand the physiology of these defects and the armamentarium available to the surgeon to help provide such patients with a stable and useful long-term survival after they are over the initial illness that leads to massive bowel resection.
CAUSES The disease that most often leads to massive bowel resection in elderly adults is infarction, secondary to mesenteric vascular disease, of both the occlusive and nonocclusive types. Strangulation following internal hernias occurred in all age groups and accounted for 0.6 per cent of 1252 cases in one series. 28 In children, mid gut volvulus is another leading cause, although this can occur in the adult also. Unrelenting regional enteritis accounts for a high percentage of instances of short bowel syndrome in young and middle-aged adults when the complications of regional enteritis cannot be managed medically and repeated resections are needed to save the patient from acute exacerbation. In a smaller group of patients, wide resection is required to deal with various forms of intra-abdominal malignancy, both related and unrelated to the gastrointestinal tract. Aganglionosis of the small intestine and meconium ileus account for a small number of instances in children. Finally, a number of patients are seen following blunt and penetrating abdominal trauma with disruption of the superior mesenteric vessels. Short bowel syndrome will be seen more frequently now, as surgeons perform shortcircuiting operations for obesity. Surgical Clinics of North America- Vol. 51, No.3, June 1971
675
676
CORNELIUS
E.
SEDGWICK AND ANTHONY A. GOODMAN
In mesenteric infarction, volvulus, and internal hernia, earlier diagnosis before infarction occurs may reduce the total length of resection required, but once nonviable bowel is present, the surgeon today has no avenue open to him but resection. Until intestinal transplantation is a reality, the surgeon must be prepared to deal with the more difficult problem of providing long-term survival after recovery from resection.
PHYSIOLOGY The extent of resection that produces symptoms of the short bowel syndrome is difficult to assess. Even the total length of the normal small intestine is a matter of dispute. Methods for measuring length vary from direct measurement of the antimesenteric border in vivo at surgery to measuring the resected specimen at necropsy. In vivo measurements are not readily reproducible, since the intestines may be in varying stages of relaxation or spasm, depending on anesthesia, the disease, and handling. These methods have put the total length from 300 cm. to 800 cm., with an average of about 650 cm. Blankenhorn et al. 4 passed radiopaque tubes and measured the length by roentgenogram at about 260 cm., but this method also depends upon such variables as the reefing of the bowel on the tube. In short, no completely acceptable method exists, but 600 cm. is generally regarded as a reasonable figure in the adult (classic anatomy texts estimate the length at 600 cm. at autopsy and 450 cm. in life)/ Approximately half the small intestine may usually be sacrificed before any special measures are needed to support and sustain normal nutrition. 26 From that point, the shorter the length of bowel that remains, the more difficult is the problem. Since the colon absorbs only water and electrolytes, it is usually believed that the length of colon is only of minor importance. However, some authors5 • 6.10,11 have stressed the importance of the intact ileocecal valve, since they believed this slows transit time and prevents colonization of the distal small intestine that occurs at the site of enterocolonic anastomoses. They believe a shorter totallength of small intestine may be tolerated when the ileocecal valve is intact than when it is not. The question then arises as to what is the minimal length of small intestine compatible with life. Most well-documented series of patients who have had several years of follow-up report a range from 20 to 60 cm. in conjunction with approximately half of the distal colon. 2, 8, 13, 16, 18,29,31 There is one report of a patient who survived for 1 year (out of the hospital) with all of the small bowel resected and only stomach, duodenum, and left colon intact.12 It is clear that patients with extremely short segments of small intestine (20 to 30 cm.) require intensive management and dietary control to permit a useful existence. The jejunum absorbs most sugars, amino acids, water-soluble vitamins, and proteins. These may be absorbed in the ileum as well. However, in the normal person very few of these are presented to the ileum. The ileum, on the other hand, has a unique function in its terminal portion of absorbing vitamin B 12 . Loss of terminal ileum, therefore, necessi-
677
SHORT BOWEL SYNDROME
tates life-long use of parenteral vitamin B 12 • Since vitamin B12 is also primarily absorbed in the ileum, steatorrhea and loss of fat-soluble vitamins (especially vitamin K) are problems in ileal resection. Other factors are also critical. When the ileum is resected, loss of bile salts, which are absorbed here, means inability to emulsify fats, leading to quantitative losses of these bile salts. Furthermore, calcium and magnesium are also lost. Soaps of fatty acids tend to be irritating to the intestinal mucosa and cause an increase in diarrhea; thus, steatorrhea increases in a vicious cycle. Finally, gastric hypersecretion (described later) causes diarrhea, just as it does in the Zollinger-Ellison syndrome, and the rapid transit time is further accentuated. All of this, and the fact that the jejunum has an inherently faster peristaltic rate than the ileum, combine to make ileal resection difficult to manage and less well tolerated by the patient. There are some natural compensatory changes, which take place over a period of months, that help in the patient's adjustment. 1O Villi have been seen to increase in height, and mucosal cell hyperplasia takes place. 21 All layers undergo hypertrophy, and gastric emptying slows somewhat, with the net result that overall absorptive processes become more efficient. The problem of gastric hypersecretion of acid was noted by several authors. 2o . 31 This is apparently caused by loss of some inhibitor substance that is secreted in response to the presence of substrate (primarily fats) in the lumen of the small intestine rather than the presence of a secretagogue. 15 • 23. 30 Hypersecretion begins within 24 hours ofresection,26 and the degree of hypersecretion seems to be directly proportional to the length of bowel resected. In some patients, vagotomy and pyloroplasty are required to control nutritional aspects and in some patients severe duodenal ulcer diathesis as well.
TREATMENT Medical Recovery usually falls into three phases. 22 The first phase of recovery for these patients is very much like that of any postoperative patient. Careful fluid and electrolyte replacement, management of infection, and general pulmonary therapy are required. After the first 10 to 14 days when the immediate postoperative problems have passed and the patient is taking oral feedings, a second phase begins that may last from 1 to 3 months, but actually overlaps the immediate postoperative period as well. This is the phase of weight loss and negative nutritional balance. It is at this time that diarrhea may be profuse, and severe weight loss may occur. Parenteral hyperalimentation has been of some help early in this phase, as patients can gain weight on the intravenous nutrients alone while they are gradually adapting to oral alimentation. The problems of the limited availability of large central veins and the continued threat of infection are the major drawbacks to prolonged intravenous hyperalimentation. Adjustments in electrolyte replacement and utiliza-
678
CORNELIUS
E.
SEDGWICK AND ANTHONY A. GOODMAN
tion of nutrients are now well worked out. The use of a pump to regulate 24 hour pump infusion has increased efficiency greatly in this regard. The major problem in oral alimentation is the control of steatorrhea Such antimotility drugs as diphenoxylate hydrochloride (Lomotil), codeine, and tincture of opium are used liberally. Transit time from mouth to terminal stoma is easily measured with powdered charcoal before and after the introduction of these various drugs so that a rough indication of their effectiveness may be obtained. Antacids are utilized to control hyperacidity. If hyperacidity is present, it may be of help to measure the pH of bowel contents at the ileostomy or rectum to determine the severity of the role of hypersecretion. Dietary long-chain fats are usually restricted (30 to 50 gm. per day) to decrease their deleterious effects discussed previously. Medium-chain triglycerides are commercially available and may help add less irritating high-caloric material to the diet. These are water soluble and are absorbed through the portal vein rather than the lacteals.:J2 The administration of oral bile salts has been advocated by some,but these may actually increase diarrhea because of their direct irritation on the colonic mucosa. Naturally, vitamins must be added to the diet. However, if the ileum has been resected, vitamin B12 will be required parenterally. Vitamin K should also be given when indicated by a falling prothrombin concentration. The nonresidue or space diets (Vi von ex) have also been used in these patients. They are tolerated well by some and poorly by others, and each patient must be assessed separately. Finally, because of both steatorrhea and diarrhea, levels of serum electrolytes to include calcium and magnesium should be monitored frequently in this phase and replaced as needed. 19 . 24. 25 For patients with ileostomies or other stomas, there is the problem of skin digestion. We have relied heavily on the help of our Stoma Clinic to provide early and continued care to keep ahead of these problems with individualized appliances for each patient. The use of karaya gum seals and other skin protectors has helped keep these patients comfortable and free from the extensive destruction that can occur when stomas are neglected and allowed to leak. The final phase, usually beginning after about 3 months, is that of nutritional adaptation. If the patient survives to this point. changes such as the slowing of peristalsis and intestinal hypertrophy begin to playa key role. The patient begins to gain weight and adapt to his new nutritional environment. The patient may, in some cases, begin to change to a more normal diet, and as is so often the case in medicine, he generally is the best judge of what he may be able to tolerate. Adrenocortical steroids have had some limited trial,14 but large series have not been reported. Surgical A number of patients will require further adjunctive surgery in order to return to a satisfactory existence. Vagotomy and pyloroplasty have already been mentioned in regard to control of gastric hypersecretion.
679
SHORT BOWEL SYNDROME
While hypersecretion causes diarrhea, vagotomy too may, by some as yet undetermined means, also increase diarrhea. There has been a great deal of clinical investigation and some clinical studies dealing with reversed intestinal segments and recirculating loops. The former is designed to cause functional partial intestinal obstruction, and therefore slow down transit time and allow better absorption. Recirculating loops allow food to pass over the same circuit several times and in effect provide more surface time for absorption. These attempts have met with varying degrees of success. For details of length of segment and so forth, the reader is referred to work of Altman and Ellison,! Baldwin-Price et al.,3 Gerwig and Ghaphery,9 and Venables et al. 27 The ultimate surgical treatment for this syndrome would be the transplantation of intestine from a human donorY Although this has been tried, at present it is not considered a realistic choice.
REFERENCES 1. Altman, D.P., and Ellison, E. H.: Massive intestinal resection: inadequacies of the recirculating loop. Surg. Forum 16:365-367,1965. 2. Anderson, C. M.: Long-term survival with six inches of small intestine. Brit. Med. J. 1 :419-422 (Feb. 13) 1965. 3. Baldwin-Price, H. K., Copp, D., and Singleton, A. 0., Jr.: Reversed intestinal segments in the management of anenteric malabsorption syndrome. Ann. Surg. 161 :225-230 (Feb.) 1965. 4. Blankenhorn D. H., Hirsch, J., and Ahrens, E. H., Jr.: Transintestinalintubation: technic for measurement of gut length and physiologic sampling at known loci. Proc. Soc. Exper. BioI. Med. 88 :356-362 (March) 1955. 5. Chen, K. M.: Massive resection of the small intestine. Surgery 65:931-938 (June) 1969. 6. Clayton, B. E., and Cotton, D. A.: A study of malabsorption after resection of the entire jejunum and the proximal half of the ileum. Gut 2: 18-22 (March) 1961. 7. Cunningham, D. J.: Manual of Practical Anatomy. 13th ed., London, Oxford University Press, 1966-1968. 8. Gibson, L. D., Carter, R., and Hinshaw, D. B.: Segmental reversal of small intestine after massive bowel resection. Successful case with follow-up examination. J.A.M.A. 182: 952-954 (Dec. 1) 1962. 9. Gerwig, W. H., Jr., and Ghaphery, A.: Experimental attempt to delay alimentary transit after small bowel exclusion. Arch. Surg. 87:34-41 (July) 1963. 10. Kaiser, M. H.: Malabsorption syndromes. In Bockus, H. L.: Gastroenterology. Vol. 2, 2nd ed., Philadelphia, W. B. Saunders Co., 1964, pp. 472-491. 11. Kalser, M. H., Roth, J. L., Tumen, H., and Johnson, T. A.: Relation of small bowel resection to nutrition in man. Gastroenterology 38:605-615 (April) 1960. 12. Kinney, J. M., Goldwyn, R. M., Barr, J. S., Jr., and Moore, F. D.: Loss of the entire jejunum and ileum, and the ascending colon. Management of a patient. J.A.M.A. 179:529-532 (Feb. 17) 1962. 13. Koeberle, E.: Resection de Deux Metres d' Intestin GriHe Suivie de Guerison. Gas Hebd. Med.18:55-58,1881. 14. Kogan, E., Schapira, E., Janowitz, H. D., and Adlersberg, D.: Malabsorption following extensive small intestinal resection including inadvertent gastro-ileostomy. In Aldersberg, D. (ed.): The Malabsorption Syndrome. New York, Grune & Stratton Inc., 1957, pp. 225-250. 15. Kosaka, T., and Lin, R. K. S.: Demonstration of the humoral agent in fat inhibition of gastric secretion. Proc. Soc. Exper. BioI. & Med 27:890-891 (Oct.-June) 1929-1930. 16. Leonard, A. S., Levine, A. S., Wittner, R., et al.: Massive small-bowel resections. Operative and dietary management. Arch. Surg. 95:429-435 (Sept.) 1967. 17. Lillehei, R. C., Idezuki, Y., Feemster, J. A., et al.: Transplantation of stomach, intestine, and pancreas: experimental and clinical observations. Surgery 62 :721-741 (Oct.) 1967. 18. May, A. G., Phillips, C. E., and Sherman, C. D.: Massive intestinal resection. Are adjunctive surgical procedures necessary? Arch. Surg. 92:344-348 (March) 1966.
680
CORNELIUS
E.
SEDGWICK AND ANTHONY A. GOODMAN
19. Mayo, H. W., Jr., and Duggan, J. J.: Postcolectomy enteritis: survival after extensive small bowel resection complicated by magnesium deficiency-case report. Ann. Surg. 157:92-96 (Jan.) 1963. 20. Osborne, M. P., Sizer, J., Frederick, P. L., et al.: Massive bowel resection and gastric hypersecretion. Its mechanism and a plan for clinical study and management. Amer. J. Surg. 114:393-397 (Sept.) 1967. 21. Porus, R. L.: Epithelial hyperplasia following massive small bowel resection in man. Gastroenterology 48:753-757 (June) 1965. 22. Pullan, J. M.: Massive intestinal resection. Proc. Roy. Soc. Med. 52:31-37 (Jan.) 1959. 23. Reul, G. J., and Ellison, E. H.: Effect of seventy-five percent distal small bowel resection on gastric secretion. Amer. J. Surg. 111 :772-776 (June) 1966. 24. Smith, W.O., Hammarsten, J. F., and Eliel, L. P.: The clinical expression of magnesium deficiency. J.A.M.A. 174:77-78 (Sept. 3) 1960. 25. Suter, C., and Klingman, W.O.: Neurologic manifestations of magnesium depletion states. Neurology 5 :691-699 (Oct.) 1955. 26. Spiro, H. M.: Clinical Gastroenterology. New York, The MacMillan Co., 1970, 1,011 pp. 27. Venables, C. W., Ellis, H., and Smith, A. D.: Antiperistaltic segments after massive intestinal resections. Lancet 2:1390-1394 (Dec. 24) 1966. 28. Wangensteen, O. H.: Intestinal Obstructions. 3rd ed., Springfield, Ill., Charles C Thomas, 1955, 838 pp. 29. Weinstein, M., Roberts, M., and Reynold, B.: Massive resection for ileitis: twelve-year follow-up of two patients. J.A.M.A. 171 :396-401 (Sept. 26) 1959. 30. Westerheide, R. L., Elliott, D. W., and Hardacre, J. M.: The potential of the upper small bowel in regulatory acid secretion. Surgery 58 :73-83 (July) 1965. 31. Winawer, S. J., Broitman, S. A., Wolochow, D. A., et al.: Successful management of massive small-bowel resection based on assessment of absorption defects and nutritional needs. New Eng. J. Med. 274:72-78 (Jan. 13) 1966. 32. Zurier, R. B., Campbell, R. G., Hashim, S. A., et al.: Use of medium-chain triglyceride in management of patients with massive resection of the small intestine. New Eng. J. Med. 274:490-493 (March 3) 1966.
Short Bowel Syndrome
Cornelius E. Sedgwick, M.D., and Anthony A. Goodman, MD.
Because of the ability of today's surgeons to resect longer lengths of intestine with good survival rates, the short bowel syndrome has been developing in increasing numbers of patients. This syndrome is characterized by diarrhea with impaired absorption of fats, vitamins, and other nutrients, ultimately leading to malnutrition, anemia and continued weight loss. In some instances, severe gastric hypersecretion also occurs ocasionally with the development of duodenal ulcer and its complications. It is of major importance to understand the physiology of these defects and the armamentarium available to the surgeon to help provide such patients with a stable and useful long-term survival after they are over the initial illness that leads to massive bowel resection.
CAUSES The disease that most often leads to massive bowel resection in elderly adults is infarction, secondary to mesenteric vascular disease, of both the occlusive and nonocclusive types. Strangulation following internal hernias occurred in all age groups and accounted for 0.6 per cent of 1252 cases in one series. 28 In children, mid gut volvulus is another leading cause, although this can occur in the adult also. Unrelenting regional enteritis accounts for a high percentage of instances of short bowel syndrome in young and middle-aged adults when the complications of regional enteritis cannot be managed medically and repeated resections are needed to save the patient from acute exacerbation. In a smaller group of patients, wide resection is required to deal with various forms of intra-abdominal malignancy, both related and unrelated to the gastrointestinal tract. Aganglionosis of the small intestine and meconium ileus account for a small number of instances in children. Finally, a number of patients are seen following blunt and penetrating abdominal trauma with disruption of the superior mesenteric vessels. Short bowel syndrome will be seen more frequently now, as surgeons perform shortcircuiting operations for obesity. Surgical Clinics of North America- Vol. 51, No.3, June 1971
675
676
CORNELIUS
E.
SEDGWICK AND ANTHONY A. GOODMAN
In mesenteric infarction, volvulus, and internal hernia, earlier diagnosis before infarction occurs may reduce the total length of resection required, but once nonviable bowel is present, the surgeon today has no avenue open to him but resection. Until intestinal transplantation is a reality, the surgeon must be prepared to deal with the more difficult problem of providing long-term survival after recovery from resection.
PHYSIOLOGY The extent of resection that produces symptoms of the short bowel syndrome is difficult to assess. Even the total length of the normal small intestine is a matter of dispute. Methods for measuring length vary from direct measurement of the antimesenteric border in vivo at surgery to measuring the resected specimen at necropsy. In vivo measurements are not readily reproducible, since the intestines may be in varying stages of relaxation or spasm, depending on anesthesia, the disease, and handling. These methods have put the total length from 300 cm. to 800 cm., with an average of about 650 cm. Blankenhorn et al. 4 passed radiopaque tubes and measured the length by roentgenogram at about 260 cm., but this method also depends upon such variables as the reefing of the bowel on the tube. In short, no completely acceptable method exists, but 600 cm. is generally regarded as a reasonable figure in the adult (classic anatomy texts estimate the length at 600 cm. at autopsy and 450 cm. in life)/ Approximately half the small intestine may usually be sacrificed before any special measures are needed to support and sustain normal nutrition. 26 From that point, the shorter the length of bowel that remains, the more difficult is the problem. Since the colon absorbs only water and electrolytes, it is usually believed that the length of colon is only of minor importance. However, some authors5 • 6.10,11 have stressed the importance of the intact ileocecal valve, since they believed this slows transit time and prevents colonization of the distal small intestine that occurs at the site of enterocolonic anastomoses. They believe a shorter totallength of small intestine may be tolerated when the ileocecal valve is intact than when it is not. The question then arises as to what is the minimal length of small intestine compatible with life. Most well-documented series of patients who have had several years of follow-up report a range from 20 to 60 cm. in conjunction with approximately half of the distal colon. 2, 8, 13, 16, 18,29,31 There is one report of a patient who survived for 1 year (out of the hospital) with all of the small bowel resected and only stomach, duodenum, and left colon intact.12 It is clear that patients with extremely short segments of small intestine (20 to 30 cm.) require intensive management and dietary control to permit a useful existence. The jejunum absorbs most sugars, amino acids, water-soluble vitamins, and proteins. These may be absorbed in the ileum as well. However, in the normal person very few of these are presented to the ileum. The ileum, on the other hand, has a unique function in its terminal portion of absorbing vitamin B 12 . Loss of terminal ileum, therefore, necessi-
677
SHORT BOWEL SYNDROME
tates life-long use of parenteral vitamin B 12 • Since vitamin B12 is also primarily absorbed in the ileum, steatorrhea and loss of fat-soluble vitamins (especially vitamin K) are problems in ileal resection. Other factors are also critical. When the ileum is resected, loss of bile salts, which are absorbed here, means inability to emulsify fats, leading to quantitative losses of these bile salts. Furthermore, calcium and magnesium are also lost. Soaps of fatty acids tend to be irritating to the intestinal mucosa and cause an increase in diarrhea; thus, steatorrhea increases in a vicious cycle. Finally, gastric hypersecretion (described later) causes diarrhea, just as it does in the Zollinger-Ellison syndrome, and the rapid transit time is further accentuated. All of this, and the fact that the jejunum has an inherently faster peristaltic rate than the ileum, combine to make ileal resection difficult to manage and less well tolerated by the patient. There are some natural compensatory changes, which take place over a period of months, that help in the patient's adjustment. 1O Villi have been seen to increase in height, and mucosal cell hyperplasia takes place. 21 All layers undergo hypertrophy, and gastric emptying slows somewhat, with the net result that overall absorptive processes become more efficient. The problem of gastric hypersecretion of acid was noted by several authors. 2o . 31 This is apparently caused by loss of some inhibitor substance that is secreted in response to the presence of substrate (primarily fats) in the lumen of the small intestine rather than the presence of a secretagogue. 15 • 23. 30 Hypersecretion begins within 24 hours ofresection,26 and the degree of hypersecretion seems to be directly proportional to the length of bowel resected. In some patients, vagotomy and pyloroplasty are required to control nutritional aspects and in some patients severe duodenal ulcer diathesis as well.
TREATMENT Medical Recovery usually falls into three phases. 22 The first phase of recovery for these patients is very much like that of any postoperative patient. Careful fluid and electrolyte replacement, management of infection, and general pulmonary therapy are required. After the first 10 to 14 days when the immediate postoperative problems have passed and the patient is taking oral feedings, a second phase begins that may last from 1 to 3 months, but actually overlaps the immediate postoperative period as well. This is the phase of weight loss and negative nutritional balance. It is at this time that diarrhea may be profuse, and severe weight loss may occur. Parenteral hyperalimentation has been of some help early in this phase, as patients can gain weight on the intravenous nutrients alone while they are gradually adapting to oral alimentation. The problems of the limited availability of large central veins and the continued threat of infection are the major drawbacks to prolonged intravenous hyperalimentation. Adjustments in electrolyte replacement and utiliza-
678
CORNELIUS
E.
SEDGWICK AND ANTHONY A. GOODMAN
tion of nutrients are now well worked out. The use of a pump to regulate 24 hour pump infusion has increased efficiency greatly in this regard. The major problem in oral alimentation is the control of steatorrhea Such antimotility drugs as diphenoxylate hydrochloride (Lomotil), codeine, and tincture of opium are used liberally. Transit time from mouth to terminal stoma is easily measured with powdered charcoal before and after the introduction of these various drugs so that a rough indication of their effectiveness may be obtained. Antacids are utilized to control hyperacidity. If hyperacidity is present, it may be of help to measure the pH of bowel contents at the ileostomy or rectum to determine the severity of the role of hypersecretion. Dietary long-chain fats are usually restricted (30 to 50 gm. per day) to decrease their deleterious effects discussed previously. Medium-chain triglycerides are commercially available and may help add less irritating high-caloric material to the diet. These are water soluble and are absorbed through the portal vein rather than the lacteals.:J2 The administration of oral bile salts has been advocated by some,but these may actually increase diarrhea because of their direct irritation on the colonic mucosa. Naturally, vitamins must be added to the diet. However, if the ileum has been resected, vitamin B12 will be required parenterally. Vitamin K should also be given when indicated by a falling prothrombin concentration. The nonresidue or space diets (Vi von ex) have also been used in these patients. They are tolerated well by some and poorly by others, and each patient must be assessed separately. Finally, because of both steatorrhea and diarrhea, levels of serum electrolytes to include calcium and magnesium should be monitored frequently in this phase and replaced as needed. 19 . 24. 25 For patients with ileostomies or other stomas, there is the problem of skin digestion. We have relied heavily on the help of our Stoma Clinic to provide early and continued care to keep ahead of these problems with individualized appliances for each patient. The use of karaya gum seals and other skin protectors has helped keep these patients comfortable and free from the extensive destruction that can occur when stomas are neglected and allowed to leak. The final phase, usually beginning after about 3 months, is that of nutritional adaptation. If the patient survives to this point. changes such as the slowing of peristalsis and intestinal hypertrophy begin to playa key role. The patient begins to gain weight and adapt to his new nutritional environment. The patient may, in some cases, begin to change to a more normal diet, and as is so often the case in medicine, he generally is the best judge of what he may be able to tolerate. Adrenocortical steroids have had some limited trial,14 but large series have not been reported. Surgical A number of patients will require further adjunctive surgery in order to return to a satisfactory existence. Vagotomy and pyloroplasty have already been mentioned in regard to control of gastric hypersecretion.
679
SHORT BOWEL SYNDROME
While hypersecretion causes diarrhea, vagotomy too may, by some as yet undetermined means, also increase diarrhea. There has been a great deal of clinical investigation and some clinical studies dealing with reversed intestinal segments and recirculating loops. The former is designed to cause functional partial intestinal obstruction, and therefore slow down transit time and allow better absorption. Recirculating loops allow food to pass over the same circuit several times and in effect provide more surface time for absorption. These attempts have met with varying degrees of success. For details of length of segment and so forth, the reader is referred to work of Altman and Ellison,! Baldwin-Price et al.,3 Gerwig and Ghaphery,9 and Venables et al. 27 The ultimate surgical treatment for this syndrome would be the transplantation of intestine from a human donorY Although this has been tried, at present it is not considered a realistic choice.
REFERENCES 1. Altman, D.P., and Ellison, E. H.: Massive intestinal resection: inadequacies of the recirculating loop. Surg. Forum 16:365-367,1965. 2. Anderson, C. M.: Long-term survival with six inches of small intestine. Brit. Med. J. 1 :419-422 (Feb. 13) 1965. 3. Baldwin-Price, H. K., Copp, D., and Singleton, A. 0., Jr.: Reversed intestinal segments in the management of anenteric malabsorption syndrome. Ann. Surg. 161 :225-230 (Feb.) 1965. 4. Blankenhorn D. H., Hirsch, J., and Ahrens, E. H., Jr.: Transintestinalintubation: technic for measurement of gut length and physiologic sampling at known loci. Proc. Soc. Exper. BioI. Med. 88 :356-362 (March) 1955. 5. Chen, K. M.: Massive resection of the small intestine. Surgery 65:931-938 (June) 1969. 6. Clayton, B. E., and Cotton, D. A.: A study of malabsorption after resection of the entire jejunum and the proximal half of the ileum. Gut 2: 18-22 (March) 1961. 7. Cunningham, D. J.: Manual of Practical Anatomy. 13th ed., London, Oxford University Press, 1966-1968. 8. Gibson, L. D., Carter, R., and Hinshaw, D. B.: Segmental reversal of small intestine after massive bowel resection. Successful case with follow-up examination. J.A.M.A. 182: 952-954 (Dec. 1) 1962. 9. Gerwig, W. H., Jr., and Ghaphery, A.: Experimental attempt to delay alimentary transit after small bowel exclusion. Arch. Surg. 87:34-41 (July) 1963. 10. Kaiser, M. H.: Malabsorption syndromes. In Bockus, H. L.: Gastroenterology. Vol. 2, 2nd ed., Philadelphia, W. B. Saunders Co., 1964, pp. 472-491. 11. Kalser, M. H., Roth, J. L., Tumen, H., and Johnson, T. A.: Relation of small bowel resection to nutrition in man. Gastroenterology 38:605-615 (April) 1960. 12. Kinney, J. M., Goldwyn, R. M., Barr, J. S., Jr., and Moore, F. D.: Loss of the entire jejunum and ileum, and the ascending colon. Management of a patient. J.A.M.A. 179:529-532 (Feb. 17) 1962. 13. Koeberle, E.: Resection de Deux Metres d' Intestin GriHe Suivie de Guerison. Gas Hebd. Med.18:55-58,1881. 14. Kogan, E., Schapira, E., Janowitz, H. D., and Adlersberg, D.: Malabsorption following extensive small intestinal resection including inadvertent gastro-ileostomy. In Aldersberg, D. (ed.): The Malabsorption Syndrome. New York, Grune & Stratton Inc., 1957, pp. 225-250. 15. Kosaka, T., and Lin, R. K. S.: Demonstration of the humoral agent in fat inhibition of gastric secretion. Proc. Soc. Exper. BioI. & Med 27:890-891 (Oct.-June) 1929-1930. 16. Leonard, A. S., Levine, A. S., Wittner, R., et al.: Massive small-bowel resections. Operative and dietary management. Arch. Surg. 95:429-435 (Sept.) 1967. 17. Lillehei, R. C., Idezuki, Y., Feemster, J. A., et al.: Transplantation of stomach, intestine, and pancreas: experimental and clinical observations. Surgery 62 :721-741 (Oct.) 1967. 18. May, A. G., Phillips, C. E., and Sherman, C. D.: Massive intestinal resection. Are adjunctive surgical procedures necessary? Arch. Surg. 92:344-348 (March) 1966.
680
CORNELIUS
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SEDGWICK AND ANTHONY A. GOODMAN
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