Management of antacid impactions in hemodialysis and renal transplant patients

Management of Antacid Impactions in Hemodialysis and Renal Transplant Patients

John P. Welch,

MD, Hartford,

Robert T. Schweizer,

Connecticut

MD, Hartford,

Stanley A. Bartus, MD, Hartford,

Connecticut

Connecticut

Fecal impaction is a common problem among renal transplant and hemodialysis patients which is related to inactivity, dehydration, persistent uremia and ingestion of analgesics, ion-exchange resins and nonabsorbable antacids. Accompanying factors such as atherosclerosis, immunosuppression and uremic ulceration of the colon may predispose to colonic perforations in these patients. Despite this, there are f’ew report,s in the English literature of fecal impacticIn and its complications in either hemodialysis patients or renal transplant recipients. This study was undertaken to assess the complications of fecal impaction in hemodialysis and renal transplant patients, with particular emphasis on the causal role of high-dose antacids. Clinical

Material

Hetween 1973 and 1979, approximately 250 persons were tre.sted in the outpatient chronic hemodialysis program at Hartford Hospital, Hartford, Connecticut; 180 patients underwent renal transplantation. In a retrospective review of medical records covering the same time span, we identified 10 cases of fecal impaction and bowel obstruction, +ometimes accompanied by perforation, in 6 hemodialysis and 4 renal transplant patients. The patients ranged in age from 38 to 63 years (average :iO) (Table I). The transplant patients were on the average a decade younger than the hemodialysis patients. Only three patients were women. All patients were receiving antacids as often as every 2 hours when intestinal obstruction was clinically manifest. Most were also ingesting constipating medications such as ferrous sulfate, analgesics or antihypertensive agents. All transplant recipients were From the Department of Surgery. Hartford Hospital, Hartford, Connecticut and the University of Connecticut School of Medicine, Farmington, Connectcut. Reprint requests should be addressed to John P. Welch, MD, 85 Jefferson Street, Hartford, Connecticut 06106. Presented at the 60th Annual Meeting of the New England Surgical Society. Whitefield, New Hampshire, September 28-30, 1979.

Volume 139, April 1990

maintained on prednisone and Imuran@. The sites of intestinal obstruction or perforation corresponded to points of antacid impactions and were usually confined to the colon. In the transplant recipients most impactions were located in the proximal colon, whereas the distal colon was usually involved in the hemodialysis patients. Most patients had clinical evidence of bowel obstruction. All reported abdominal pain and constipation. Some had abdominal tenderness, abdominal distention, vomiting or fever. Abdominal roentgenograms invariably demonstrated considerable impacted stool in the colon, the small bowel or both. Most patients with proximal colon impactions had radiographic evidence of small bowel obstruction. A variety of radiologic findings accompanied colonic impactions (Figure l), including cecal distention (Figure 2), widespread retroperitoneal air (Figure 3) and free extravasation of contrast material from the colon during the contrast enema (Figure 3). Patients were initially treated with stool softeners and laxatives by mouth, saline enemas, and on occasion, longtube intubation of the small bowel with insertion of stool softeners and laxatives through the tube. Three patients (all with obstruction in the ascending colon or small bowel) were managed successfully in this manner alone, one of whom underwent incidental colonoscopy. Most patients managed medically alone were in the transplant group. Six patients required operative intervention 1 to 6 days after the inception of abdominal pain. One patient underwent two separate operations in 5 years, one for deflation of a long-tube balloon that was impacted at the ileocecal valve (case I). In another patient a large rectal concretion was disimpacted successfully with the use of general anesthesia. Outcome

Three patients (all in the hemodialysis group) died in the hospital (30 percent). All three had perforation of the colon at sites of ulceration. Microscopic views of the resected bowel showed disease localized to the points of ulceration and perforation, apparently

561

Welch et al

caused by pressure necrosis due to the antacid impactions. All patients undergoing resection had firm, whitish concretions in the vicinity of the perforation or obstruction. None were taking steroids at the time of perforation, and other factors such as diverticulitis, foreign bodies, carcinoma, chronic inflammatory bowel disease or recent trauma could not be implicated. Two of the perforations were in the sigmoid colon and the third was in the cecum near the site of multiple large ulcerations. Case I. A 46 year old man was admitted to Hartford Hospital on May 27, 1973 to undergo a cadaveric renal transplant for end-stage renal disease secondary to chronic nephritis. Medications at the time of admission included AldomeP and Colace@. After operation he developed acute tubular necrosis, but renal function later improved. He complained of nausea and vomiting 1 week postoperatively; an abdominal roentgenogram showed partial small bowel obstruction and considerable fecal material in the right colon. Laxatives and enemas failed to improve the clinical picture, and a Kaslow tube was passed with slow progression. During the next several weeks gastrointestinal function gradually improved, but the patient had several rejection*episodes. The long tube failed to move beyond the ileocecal valve. The inflated air bag became impacted and

Figure 1. Large antacid impaction of the ascending colon (arrow). Some dilatation of the small bowel loops is also seen.

562

had to be removed through an enterotomy. The patient was subsequently discharged on medications including prednisone, Imurane, Riopane and Gelusile. He was readmitted to the hospital on September 30,1978 because of crampy abdominal pain. In the interim, the kidney transplant had been rejected and he had undergone chronic hemodialysis therapy. He denied any bowel movements in the week before admission. He had been ingesting codeine for relief of bone pain due to renal osteodystrophy. The abdomen appeared distended and tympanitic but nontender. The bowel sounds were hypoactive. No impaction was palpable by rectal examination. Abdominal roentgenograms showed large amounts of stool from the ascending colon to the splenic flexure, but air was seen in the more distal colon and rectum. No airfluid levels were present in the small intestine. The hematocrit was 21 percent, the white cell count 5,20O/mms (without a left shift), and the serum amylase and potassium levels were normal. An electrocardiogram showed lateral wall ischemia. The patient was managed with long tube intubation, multiple enemas and instillation of cathartics and stool softeners. Subsequently he passed flatus and some liquid stool, but repeat radiographs continued to show a large oval fecal mass in the region of the splenic flexure (Figure 2). The long tube finally passed into the small intestine, but when cecal dilatation occurred he was taken to the operating room. Dense adhesions between the splenic flexure and the spleen necessitated resection of the spleen as well as the colon containing the impaction. The proximal and distal colon were exteriorized. The resected segment of colon contained a 7 by 4 cm hard green fecalith resembling an egg. There was congestion of the serosal surface, and several ulcers were noticeable on the mucosal surface, the largest measuring 2 by 1.5 cm. The sharply demarcated ulcers had the appearance of stercoral ulcerations. Microscopic sections demonstrated extensive edema of the

Figure 2. Case i, a 5 1 year old hemodiaiysis patient. The lateral decubitus view demonstrates an egg-shaped concretion near the spienic fiexure (arrow). Cecai diiatation is present.

The American Journal of Surgery

Intestinal Acid Impactions

C’ommrnt: This case demonstrates the failure of medical management of an impaction situated in the left colon. Without operation, perforation of the cecum or of the splenic flexure probably would have occurred. Case II. A 59 year old man who had been undergoing hemodialysis for 5 years entered the hospital on February 17, 1977 with a 24 hour history of abdominal pain, bloody

bowel wall and multiple mucosal ulcerations but no perforation. The postoperative course was complicated by a pericolostomy wound infection. The patient was discharged several weeks later on continued hemodialysis treatments. Intestinal continuity was reestablished several months later. He has had no recurrence of gastrointestinal symptoms since i.hat time.

Figure 3. Case II, a 59 year old hemodialysis patient. A, abdominal roentgenogram demonstrates retroperitoneal air ( white arrow). Pneumomediastinum is also visible (black arrow). 6, barium enema view. Free extravasation of contrast material is seen from the mid-descending colon into the retroperitoneum (black arrow). Note the large impaction adjacent to the perforation ( white arrow).

I

TABLE Age

Antacid

Impactions:

(yr)

& Sex

Antacid

Summary

of Clinical

Site of Obstruction

Course in 10 Patients Operative Complication

Treatment Transplant

46M

Amphojel@

Right colon

41M 42M

Amphojel Amphojel

Small bowel Right colon

45M

Amphojel

Right colon

Group

Long tube, laparotomy Long tube Long tube, colonoscopy Long tube Hemodialysis

__-.~--

Survived Survived Survived

Amphojel Basaljel@ Basaljel

Splenic flexure Rectum Left colon

Left colectomy Disimpaction Left colectomy

.38F

Basaljel, Kayexalatee Basaljel

Sigmoid colon Right colon*

Hartmann procedure Right colectomy

Amphojel. Kayexalate

Entire

Enemas,

:jlM f‘,SF

l

colon

Survived

~~. Group

51M 63F 59M

l

Outcome

cathartics

Wound

infection .

Myocardial infarction Sepsis

Survived Survived Died

(?)

Subphrenic abscess, pneumonia

Died Died Survived

” Perforation.

Volume 139, April 1980

563

Welch et al

diarrhea, fever and vomiting. He had previously had a hiatus hernia with bleeding, hyperparathyroidism and hepatosplenomegaly. He had also been hospitalized 4 years earlier for lower abdominal pain of uncertain cause. Medications included Basaljele, ferrous sulfate and Percodan@. He appeared chilled and anxious. The blood pressure was 122/70 mm Hg, pulse 80 and temperature 100.6°F by mouth. He had diffuse abdominal tenderness, especially in the left lower quadrant, where a discrete mass was palpable. Bilateral, nontender, reducible inguinal hernias were present. Some dark blood was noted on rectal examination but no mass could be appreciated. The hematocrit was 23 percent and the white blood count 6,600/mm3, with 85 neutrophils and five band forms. The plain abdominal roentgenogram showed little gas in the distal colon, but there was no proximal dilatation. The following day his temperature had decreased and the abdominal pain was less marked. Bowel sounds were still audible. The left lower quadrant mass remained moderately tender. A repeat chest x-ray and abdominal film suggested free mediastinal air and retroperitoneal air. A barium enema clearly demonstrated free extravasation from the medial aspect of the mid-descending colon into the retroperitoneum (Figure 3). Considerable stool was apparent adjacent to the perforation, and no definite diverticula were seen. Laparotomy disclosed a perforation of the medial surface of the descending colon partially walled off by loops of small intestine. It appeared that rock-hard fecal matter had eroded through the wall of the colon. Once the colon was resected, a descending colostomy and mucous fistula were constructed and the abdomen was irrigated with profuse amounts of saline, Bacitracinm and Kantrex@ solution. Irrigating catheters were left in place during the postoperative period. The gross specimen showed a 4 cm perforation and marked dilatation of the colon secondary to the large fecal impaction. Microscopically, there was focal ulceration of the bowel and bowel necrosis at the midpoint of the stercoral ulceration. Although the postoperative course was generally smooth and dialysis treatments were begun, the patient was found unexpectedly dead in bed on March 7, 1977. Comment: Free perforation of the colon was not diagnosed clinically until the radiographs were seen. However, an index of suspicion led to early diagnosis in this case.

Comments Fecal impaction is a frequent occurrence among chronic&y ill patients. The topic, however, is scantily or infrequently touched on in the literature. Fecal impaction

accounts

for about 1

percent of mechanical

intestinal obstructions in large reviews [I]. In selected groups such as immunosuppressed or fragile hemodialysis patients, the potential complications of fecal impaction are of great importance and can be catastrophic. Fecal impactions are classically found in the sigmoid colon and rectum, varying in consistency from putty-like to rock-hard [2], but they have been described in the cecum or the small bowel [3,4]. A 564

firm, irregular mass termed a fecaloma or stercoroma is formed within the intestinal tract over a prolonged period of time as a function of the intestinal motility and the nature of its contents. These may grow to giant size [5] and require hospitalization or even operation for removal. Pressure caused by the impaction may cause formation of a stercoral ulcer [6 71. Most patients with fecal impactions have a long history of constipation. A variety of conditions may contribute to the constipation and subsequent fecal impaction including foreign bodies, decreased mucous output by the colon, strictures due to inflammatory disease, poor muscle tone, mechanical obstruction from inflammatory or neoplastic disease, previous barium enema, accumulated digested food around fecal matter, megacolon, certain medications such as sympathetic blocking agents, opiates, sedatives or anticholinergics, altered neuromuscular reflexes in the intestine, hypothyroidism, hypokalemia, inactivity or bed rest, dehydration, inflammatory anal disease, adhesions, abdominal abscesses or tumors, and psychic and environmental factors [5,7-g]. Calculi that sometimes form in the inactive intestinal tract contain mineral salts such as calcium phosphate or calcium carbonate IlO]. High-dose antacids in the liquid or tablet form [ II] can also cause intestinal obstruction. Aluminumcontaining antacids such as aluminum hydroxide lead to constipation that is usually controlled by simultaneous treatment with magnesium-containing antacids and stool softeners. Fecal concretions of fatty acid salts of aluminum may be seen [12]. The earliest reports of antacid-induced fecal impactions were in patients with bleeding duodenal ulcer. Havens [I31 reported a large globular mass of inspissated material mixed with blood in the cecum. There was an abundant semisoft material resembling putty in the small intestine and numerous firm masses in the distal colon. This patient had received a constant drip of aluminum hydroxide and water for 7 days previously. Brearley [14] also surmised that antacids were responsible for two cases of perforation of the pelvic colon. Perlman [15] described a patient with a completely obstructing antacid fecaloma in the sigmoid colon and a perforation of the proximal colon at a site of impending infarction. The patient died after laparotomy when the greatly distended and friable proximal colon was inadvertently perforated. A second patient had findings similar to those in Havens’s case. He developed massive bleeding from a tube cecostomy, presumably due to a stercoral ulcer produced by the cecal mass. Brettschneider et al ]16] treated two patients with The American Journal of Surgery

Intestinal Acid Impactions

mechanical small bowel obstruction, both of whom had operative manipulation of the impactions into the colon. One had a 5 by 6 cm concretion occluding the ileocecal valve. The other had tenacious fecal matter in the terminal ileum and right colon; 13 percent of the concretion was composed of inorganic residue including aluminum oxide (46 percent), ferric oxide (25 percent), magnesium oxide (7 percent) and siiica oxide (2 percent). The remainder of the mass wils c.omposed of water; no barium was present. Antacids such as aluminum hydroxide have been a mainstay in the treatment of hemodialysis and renal transplant patients. They buffer gastric hyperacidity [ 171, which is a concern because chronic renal failure and high-dose corticosteroids potentiate the development of peptic ulcer disease [18,19]. Aluminum-containing antacids are particularly effective in binding phosphates in the gastrointestinal tract., thus lessening the risks of hyperphosphatemia, metastatic calcification and renal osteodyst,rophy accompanying chronic renal failure. Magnesiumcontaining antacids are not constipating but have caused magnesium intoxication and associated neurologic and cardiovascular effects [20]. Magnesium-containing agents are sometimes substituted in part for the aluminum-containing substances [2,1]. Calcium carbonate is a constipating agent that may precipitate hypercalcemia in the chronic hemodialys: s patient [22]. The risk of gastrointestinal complications such as duodenal ulcer, perforated diverticulitis, pancreatitis, appendicitis or antacid impactions approaches 10 to 15 percent in most centers [23]. The clinical experience with intestinal obstruction due to antacid impactions is summarized in Table II [24-311. In this group, antacids were considered the principal instigating fact.ors in the formation of the fecal concretions, which were not analyzed chemically. Two further reports of hemodialysis cases suggest that antacids contributed to the stercoral perforation of the otherwise-normal colon [21,32]. Seventy-five percent of antacid impactions were localized t.o the rignt colon and only 25 percent were situated in the left colon (Table II). This distribution is unlike that of the pretransplant era, when most fecal impactions were limited to the sigmoid colon or rectum [26,33]. Inhibition of vagal activity in the uremic patient may explain in part this peculiar anatomic distribution [26,34]. In the present series, impactions in the transplant group were localized to the small bowel or proximal colon, whereas the hemodialysis patients had a predominance of left-sided colonic impactions. Fifty-three percent of patients with antacid impactions in the literature were operated on with a hospital mortality Volume

139,

April

1980

of 44 percent, compared with a mortality of 50 percent in the present series. No patients managed medically in our group or in other reports died from the effects of intestinal obstruction during the same hospitalization. Patients with chronic renal failure are at particular risk of developing perforation from antacid impactions. Abnormalities of the gastrointestinal tract such as mucosal edema and hemorrhage, ulceration and perforation are seen, although the incidence is probably decreased by hemodialysis [3537]. Atherosclerosis and secondary hyperparathyroidism may compromise the blood supply to the colon [24], especially after shifts of intravascular volume during hemodialysis. The incidence of diverticulosis is increased in the presence of uremia [38]. Hypomotility of the gastrointestinal tract is common, and peristalsis may be further aggravated by electrolyte shifts. The decrease in tissue strength seen in uremic patients [38] increases the risk of perforation after stercoral ulceration. Vigorous enemas in a constipated patient may directly cause colon perforation or intramural hematomas after hemodialysis with heparinization. Most reports of antacid impactions concern transplant patients, where the dangers of immunosuppression, postoperative ileus, operative injury to the bowel or irradiation are added to the pathophysiologic derangements of chronic renal failure. There are several recent reports of ischemic colitis in transplant patients [39-431. Opportunistic infection is enhanced by immunosuppression, especially in cadaveric kidney recipients who generally have more episodes of rejection [44]. Corticosteroids cause lymphoid depletion in the lymphatic patches of the colon and thinning of the bowel wall, thus hindering containment of localized perforations [45]. Severe gastrointestinal complications may be masked by corticosteroid therapy and attributed to rejection episodes [34]. Candida or cytomegalovirus may cause gastrointestinal ulceration [46,47] or may colonize existent ulcers [48]. Perforated sigmoid diverticulitis is a distressing problem [34,39,44,49]. In recent reviews the incidence of colon perforation in transplant patients is 0.7 percent and the operative mortality is 75 to 90 percent [23,34]. Aggressive medical management is usually successful in preventing or treating antacid impactions. Townsend et al [31] noted no complications from the use of up to 240 ml/day of aluminum hydroxide suspension in 150 hemodialysis and renal transplant patients. Carson et al [50] stated that antacids were not responsible for any of 13 colon perforations in their transplant patients. When impaction of the ascending colon is diagnosed, we recommend the 565

Welch et al

TABLE II

Previous Reports of Antacid Impactions in Renal Transplant and Hemodialysis Patients

Age W) Author

& Sex

Site

Medication

Perforation

Treatment

Pathology

Outcome

Transplant Group Aguilo et al

[ 241

36M

Sigmoid colon

Aguilo et al

[ 241

20F

Rectum

Aguilo et al

[ 241

41M

Small bowel

Berger et al

[ 251

4M

Small bowel & right colon Right colon

Antacids Aluminum hydroxide Aluminum hydroxide

Yes

No

Hartmann procedure Hartmann procedure (1) Colotomy, jejunotomy; (2) Hartmann procedure Hypaque enema

No

Hypaque enema

NA

No

Hypaque enema

NA

Survived

No No No No

NA NA NA NA

Survived Survived NA Survived

No Yes

Medical Medical NA Enterotomy, disperse fecal mass Long tube Resection, colostomy

NA “Pressure necrosis”

Survived Died

Resection, colostomy Enterotomies, break up concretions Disperse concretions

5 cm tear

Died

Long concretion in jejunum and ileum Concretions distal I/.. small bowel “Inflamed colon”

Survived

Bernstein et al [ 261 Bernstein et al [ 261 Julien et al [ 271 Penn et al [ 281

49NA 30NA NA 10M

Right colon Right colon Cecum Right colon

Aluminum hydroxide Aluminum hydroxide Aluminum hydroxide Antacids Antacids NA Antacids

Penn et al [ 281 Thompson et al [ 291

17F 43M

Right colon Right colon

Antacids Antacids

Berger et al [ 251 Berger et al

12F

[ 251

Right colon

Yes

No

Survived colon 7 cm tear Obstructed proximal jejunum and sigmoid; necrotic colon NA

Survived Died

Survived

Hemodialysis Group Ghose et al

[ 301

Townsend et al [ 3 I]

49F

Sigmoid colon

Amphojel

Yes

27F

Small bowel

Kayexalate, Amphojel

No

Townsend et al

[ 3 71

37M

Small bowel

Amphojel

No

Townsend et al

[ 3 7]

66M

Sigmoid colon

Amphojel

No

Break up concretions

Died

Survived

NA = not available.

early use of long-tube intubation for intestinal decompression and deposition of stool softeners and cathartics. Other causes of intestinal obstruction such as adhesions, intraabdominal abscess or volvulus should not be managed medically if suspected [9,18,27]. A variety of enemas has been suggested to break up the impaction [2,15]. Penn et al [28] used a series of enemas containing Colace, olive oil, trypsin and soap suds, supplemented by administration of magnesium sulfate, milk of magnesia, castor oil and acetylcysteine through a Cantor tube. The hyperosmolar effect of Hypaquee enemas has been successful in a few patients after transplantation, just as Gastrografine is useful in management of meconium ileus [25]. Low impactions require manual disimpaction and calcified impactions generally require hospitalization since enemas are ineffective in dissolving them [2]. The use of a dental irrigating unit has been

566

suggested for low impactions [51]. Patients with colon impaction who do not respond to enemas, laxatives and stool softeners should undergo operation because of the dangers of stercoral perforation [6,40] (case II) or closed-loop obstruction associated with a competent ileocecal valve (case I). Once colon ischemia or perforation is suspected, operation should not be delayed, since mortality increases rapidly as time elapses between the perforation and laparotomy [28,38,52]. Since abdominal findings may be subtle in the immunosuppressed patient [45], contrast studies with water-soluble media such as Hypaque may be valuable in making the diagnosis [29] (case II). If the colon appears viable and the antacid concretion is movable, the impaction should be milked more distally if possible. As an alternative, the masses may be moved into the small intestine and removed through an enterotomy [31]. The thick consistency of the impaction makes suction

The American Journal of Surgery

Intestinal

removal difficult [ 151. In the case of impacted concretions (case I) or colonic necrosis or perforation (case II), primary resection with colostomy, or the Hartmann procedure in the case of more distal perforations, is recommended. Diverting colostomy and drainage alone is usually fatal in the presence of perforation [44,X)]. Anastomosis should be avoided in the unprepared colon or in the presence of contamination [44]. Postoperative peritoneal lavage may be of benefit [38,52]. The danger of antacid impactions may be prevented by several precautionary measures. Antacid regimens may be altered to include higher doses of nonconstipating agents such as magnesium hydroxide [24,31]. We routinely administer stool softeners such as Colace to hemodialysis patients, and the addition of sorbitol to liquid aluminum hydroxide improves the palatability of the antacid and decreases constipation. Control of gastric hyperacidity with cimetidine permits a reduction in the frequency of antacid administration, previously given as often as every hour in transplant patients [19]. Enemas, digital disimpaction and straining at stool are potentially dangerous in these patients, especially if diverticular disease is also present. Dehydration should be avoided during hemodialysis [al], and medications contributing to ileus should be scrupulously avoided if possible. In patients undergoing transplantation, preoperative bowel preparations should be optimal. In the postoperative period, ileus, hypotension, dehydration and inactivity should be eliminated as much as possible. If bowel distention does occur, reduction of immunosuppressive drugs should be considered 1421. Colon resection should be done before renal transplantation in patients with symptomatic diverticular disease [44,50]. An effort should be made to enlighten patients and dialysis unit personnel about the considerable risks of intes tinal obstruction precipitated by antacid impactions. Summary

Ten cases of intestinal obstruction caused by antacid impactions in renal transplant and hemodialysis patients are added to 16 reports in the literature. In six instances, operative intervention was necessary because of failure of vigorous medical therapy. Three patients who died had perforation of the colon at sites of stercoral ulceration due to firm antacid impactions. Aggressive medical and surgical management of constipation and fecal impaction is recommended. The outlook is grim once colonic perforation has occurred.

Volume 139, April 1980

Acid

Impactions

References 1. Smith GA, Perry JR Jr, Yonehiro EG. Mechanical intestinal obstructions. A study of 1252 cases. Surg Gynecol Obstet 1955; 100:651-60. 2. Andrews NL. Impactions of the rectum and colon. Am Surg 1955; 21:693-5. 3. Printz JH, Hoffman JS, Khazei Ii. Multiple stercoraceous ulcers of the colon associated with huge fecalomas and perforation: case report, Am Surg 1961; 27:714-8. 4. Walker AJ. Cecal fecalith. A report on two cases. Br J Surg 1948; 3655-8. 5. Abella ME, Fernandez AT. Large fecalomas. Dis Colon Rectum 1967; 10:401-4. 6. Grinvalsky HT. Bowerman Cl. Stercoraceous ulcers of the colon. Relatively neglected medical and surgical problem. JAMA 1959; 171:1941-6. 7. Bauer JJ, Weiss M, Dreiling DA. Stercoraceous perforation of the colon. Surg Clin North Am 1972; 52:1047-53. 8. Jones FA, Godding EW. eds. Management of Constipation. Oxford: Blackwell, 1972:158-g. 9. Gurll N, Steer M. Diagnostic and therapeutic considerations for fecal impaction. Dis Col Rectum 1975; 18:507--11. 10. Harland D. A case of multiple calculi in the large intestine with a review of the subject of intestinal calculi. Br J Surg 1953; 41209-l 1. 11. Potyk D. Intestinal obstruction from impacted antacid tablets. N Engl J Med 1970; 283:134-5. 12. Harvey SC. Gastric antacids and digestants. In: Goodman L, Gilman A, eds. The Pharmacological Basis of Therapeutics. 5th ed. New York: MacMillan, 1975: 962. 13. Havens WP. Intestinal obstruction caused by colloidal aluminum hydroxide. JAMA 1939; 113:1564-5. 14. Brearley R. Spontaneous perforation of the colon due to alkaline medication. Br Med J 1954; 1:743. 15. Perlman DM. Intestinal obstruction due to fecal impaction: report of two cases in patients with bleeding duodenal ulcer. Mil Med 1962; 127:471-5. 16. Brettschneider L, Monafo W, Osborne DP. Intestinal obstruction due to antacid gels. Complication of medical therapy for gastrointestinal bleeding. Gastroenterology 1965; 49: 291-4. 17. Hastings PR, Skillman JJ, Bushnell LS. Silen W. Antacid titration in the prevention of acute gastrointestinal bleeding. A controlled, randomized trial in 100 critically ill patients. N Engl J Med 1978: 298:1041-4. 18. Hadjiyannakis EJ, Smellie WAB. Evans DB, Calne RY. Gastrointestinal complications after renal transplantation, Lancet 1971; 2:781-5. 19. Schweizer RT, Bartus SA. Gastroduodenal ulceration in renal transplant patients. Conn Med 1978; 42:85-8. 20. Alfrey AC, Terman DS, Brettschneider L. Hypermagnesemia after renal homotransplantation. Ann Intern Med 1970; 73: 367-71. 21. Lipschutz DE, Easterling RE. Spontaneous perforation of the colon in chronic renal failure. Arch Intern Med 1973; 132: 758-9. 22. Ginsburg DS, Kaplan EL, Katz Al. Hypercalcemia after oral calcium-carbonate therapy in patients on chronic hemodialysis. Lancet 1973; 1:1271-4. 23. Lee HM, Madge GE, Mendez-Picon G, Chatterjee SN. Surgical COf?IpkatiOns in renal transplant recipients. Surg Clin North Am 1978; 58:285-304. 24. Aguilo JJ, Zincke H. Woods JE. Buckingham JM. Intestinal perforation due to fecal impaction after renal transplantation. J Urol 1976; 116:153-5. 25. Berger M, Schuessler JS, Carvajal HF, Lorentz WE Jr, Travis LB, Tyson KRT. Obturator intestinal obstruction following renal altotransplantation: relief with hyperosmolar enemas. Surgery 1974; 75:746-g. 26. Bernstein WC, Nivatvongs S, Tallent MB Cotonic and rectal

567

Welch et al

27.

28.

29.

30.

31.

32.

33.

34.

35.

36.

37.

38. 39.

40.

41.

42.

43.

44.

45.

46.

47.

48.

566

complications of kidney transplantation in man. Dis. Colon Rectum 1973; 16:255-63. Julien PJ, Goldberg HI, Margulis AR, Belzer FO. Gastrointestinal complications following renal transplantation. Radiology 1975; 117137-43. Penn I, Brettschneider L, Simpson K, Martin A, Starzl TE. Major colonic problems in human homotransplant recipients. Arch Surg 1970; 100:61-5. Thompson WM, Seigler HF. Rice RP. lleocolonic perforation. A complication following renal transplantation. Am J Roentgen01 Rad Ther Nucl Med 1975; 125723-30. Ghose MK, Sampliner JE, Cohn P. Spontaneous colonic perforation. A complication in a hemodialysis patient. JAMA 1970; 214:145. Townsend CM Jr, Remmers AR Jr, Sarles HE, Fish JC. Intestinal obstruction from medication bezoar in patients with renal failure. N Engl J Med 1973; 288:1058-g. Bartolomeo RS, Calabrese PR, Taubin HL. Spontaneous perforation of the colon. A potential complication of chronic renal failure. Dig Dis 1977; 22:656-7. Laxer A, Conte M, Solitare GB. Stercoraceous perforation of the cecum: report of two cases. Dis Colon Rectum 1975; 18:410-2. Archibald SD, Jirsch DW, Bear RA. Gastrointestinal complications of renal transplantation. 2. The colon. Can Med Assoc J 1978; 119:1301-9. Jaffe RH, Laing DR. Changes of the digestive tract in uremia. A pathologic anatomic study. Arch Intern Med 1934; 53: 851-64. Massry SG, Sellers AL, eds. Clinical Aspects of Uremia and Dialysis. Springfield, Illinois: Charles C Thomas, 1976: 199. Thoroughman JC, Peace RJ. Abdominal surgical emergencies caused by uremic enterocolitis: report of 12 cases. Am Surg 1959; 25:533-g. Guice K. Rattazzi LC, Marchioro TL. Colon perforation in renal transplant patients. Am J Surg 1979; 138:43-8. Sawyerr 01, Garvin PJ. Codd JE, Graff RJ, Newton WT, Willman VL. Colorectal complications of renal allograft transplantation. Arch Surg 1978; 113:84-6. Perloff LJ, Chon H, Petrella EJ. Grossman RA, Barker CF. Acute colitis in the renal allograft recipient. Ann Surg 1976; 183: 77-83. Powis SJA, Barnes AD, Dawson-Edwards P, Thompson H. fleocolonic problems after cadaveric renal transplantation. Br Med J 1972; 1:99-101. Demling RH, Salvatierra 0 Jr, Belzer FO. Intestinal necrosis and perforation after renal transplantation. Arch Surg 1975; 110:251-3. Arvanitakis C, Malek G, Uehling D, Morrissey JF. Colonic complications after renal transplantation. Gastroenterology 1973; 64:533-8. Misra MK. Pinkus GS, Birtch AG. Wilson RE. Major colonic diseases complicating renal transplantation. Surgery 1973; 73:942-8. Warshaw AL, Welch JP, Ottinger LW. Acute perforation of the colon associated with chronic corticosteroid therapy. Am J Surg 1976; 131:442-6. Aldrete JS, Sterling WA, Hathaway BM, Morgan JM, Diethelm AG. Gastrointestinal and hepatic complications affecting patients with renal allografts. Am J Surg 1975; 129:11524. Sutherland DER, Chan FY, Foucar E, Simmons RL, Howard RJ, Najarian JS. The bleeding cecal ulcer in transplant patients. Surgery 1979; 86:386-98. Goodman ZD, Boitnott JK, Yardley JH. Perforation of the colon

49. 50.

51. 52.

associated with cytomegalovirus infection. Dig Dis Sci 1979; 241378-80. Hognestad J, Flatmark A. Colon perforation in renal transplant patients. Stand J Gastroenterol 1976; 11:289-92. Carson SD, Krom RAF, Uchida K. Yokota K, West JC, Weil R III. Colon perforation after kidney transplantation. Ann Surg 1978; 188:109-13. Korn ER. Use of a dental irrigating unit in the treatment of fecal impactions. Gastrointest Endosc 1972; 19:88. Faro RS, Cony RJ. Management of surgical gastrointestinal complications in renal transplant recipients. Arch Surg 1979; 114:310-2.

Discussion Richard E. Wilson (Boston, MA): I enjoyed reading Dr. Welch’s paper and recommend his encyclopedic bibliography to anyone interested in this important problem. I support his statements. This concept applies not only to transplant and dialysis patients but also to many bedridden and disabled persons. Such patients will die of perforation because they have no previous inflammatory disease and no walling off of the leak. Frequently, these patients are receiving steroids or have other types of immunodepression; it is easy for them to develop widespread peritonitis, for which resection and double-barreled colostomy, as mentioned by Dr. Welch, is the treatment of choice. I think this is really part of the problem of diverticulitis, which may often be a sequel to chronic impaction. If we do not find perforation, then we go on to conservative management. It is frequently difficult to diagnose a colonic leak short of obtaining a barium enema. No bowel preparation is carried out, and we instruct the radiologist that we are only interested in viewing the left and sigmoid colon and that no compression is to be used. With the use of this approach, several patients have survived this insult. John P. Welch (closing): We have also seen several patients with serious colonic complications such as ischemit colitis or acute diverticulitis with perforation in our renal transplant program. My real purpose, however, was to emphasize a practical approach to a common but perhaps neglected problem that is shared by most renal transplant and hemodialysis centers. In the recent surgical literature there are numerous discussions of gastrointestinal complications in such patients, including perforated peptic ulcer disease or perforated sigmoid diverticulitis, yet the danger of fecal impaction sometimes goes unrecognized. Fecal impaction represents a life-threatening complication in hemodialysis and renal transplant patients, and antacid concretions may play at least a contributing role in many instances. While most general surgical patients with fecal impactions or stercoral perforations are not ingesting high-dose antacids, the same treatment principles emphasized in this report apply to them as well.

The American Journal of Surgery