The endoscopic diagnosis of colonic tuberculosis

8. 9. 10. 11. 12.

13. 14. 15.

phragm in the adult: review of the literature and report of a case. Ann Surg 1967;165:632-6. Ahmed MY, Kepkay, DL, Beck IT, McCorriston JR. Congenital duodenal diaphragm in an adult: diagnosis by endoscopy. Gastrointest Endosc 1972;18:120-1. Cooperman AM, Adachi M, Rankin GB, Sivak M. Congenital duodenal diaphragms in adults. A delayed cause of intestinal obstruction. Ann Surg 1975;182:739-42. Naylor RG, Juler GL. Congenital causes of duodenal ulcers in adults. Arch Surg 1976;111:658-62. Parker HW, Stewart ET, Geenan JE, Hogan WJ. Double duodenal diaphragms in an adult: endoscopic, radiographic and operative findings. Gastroenterology 1976;71:663-6 Turnbull A, Kussin S, Bains M. Radiographic and endoscopic features of a congenital duodenal diaphragm in an adult. A case report and review of the literature. Gastrointest Endosc 1980;26:46-8. Lehur PA, Poisson J, Lamontagne L, Haddad H. Congenital diaphragm of the duodenum in an adult: a case report. Can J Surg 1983;26:559-60. Airan B, Yadav K, Yadav RVS. Congenital incomplete duodenal diaphragm with prediaphragmatic duodenal ulcer. Am J GastroenterolI979;72:426-7. Killebrew LH, Kukora JS. Adult duodenal webs. A difficult

The endoscopic diagnosis of colonic tuberculosis Pedro E. Morgante, MD Miguel A. Gandara, MD Estaban Sterle, MD

The relatively few cases of intestinal tuberculosis that still occur in the western world continue to present a challenge in differential diagnosis from other more frequent inflammatory and neoplastic bowel diseases. None of the reported clinical manifestations and radiographic findings in intestinal tuberculosis are specific,1-3 and, in the past, the diagnosis was generally established by laparotomy.1-3 Surgical intervention in combination with antituberculous drug therapy was the treatment of choice. 2 In the last decade, however, numerous reports have clearly shown the value of the less invasive colonoscopic biopsy for bacteriological and/or histological confirmation ofprimary or secondary intestinal tuberculosis. 4- 11 It is also evident now that antituberculous chemotherapy alone is highly successful in the vast majority of cases. 1,3-6,8,12-14 We describe two cases of colonic tuberculosis, one of recent onset and the other of prolonged evolution, both studied by colonoscopy (Olympus model CF, type HM) and successfully treated with antituberculous drugs alone.

From the Department of Gastroenterology, Guemes Hospital, Buenos Aires, Argentina. Reprint requests: Pedro E. Morgante, MD, Guemes Hospital, Casilla de Correo 276, Correo Central, Buenos Aires, Argentino.

VOLUME 35, NO.2, 1989

diagnosis. Arch Surg 1983;118:875-7. 16. Deitch EA, Hamar TJ. Congenital duodenal diaphragm in the adult. Report of two cases with associated prepyloric and duodenal ulcerations. Am Surg 1981;363-5. 17. Cregan P, Hollinshead J, Smith R, Gillett D. Congenital duodenal diaphragm in an adult. Aust NZ J Surg 1981;51:74-6. 18. Morton JJ, Jones TB. Obstructions about the mesentery in infants. Ann Surg 1936;104:864-91. 19. Venu RP, Geenen JE, Hogan WJ, et at. Endoscopic electrosurgical treatment for strictures of the gastrointestinal tract. Gastrointest Endosc 1984;30:97-100. 20. Gertsch Ph, Mosimann R. Endoscopic laser treatment of a congenital duodenal diaphragm in an adult. Gastrointest Endosc 1984;30:253-4. 21. Jex RK, Hughes RW. Endoscopic management of duodenal diaphragm in the adult. Gastrointest Endosc 1986;32:416-9. 22. Brandt LJ, Boley SJ, Daum F, et at. Endoscopic resection of an obstructing antral web in an infant. Dig Dis 1978;5(suppl):6586. 23. Al-Kawas FH. Endoscopic laser treatment of an obstructing antral web. Gastrointest Endosc 1988;34:349-51. 24. Berr E, Rienmueller R, Sauerbruch T. Successful endoscopic transection of a partially obstructing antral diaphragm. Gastroenterology 1987;89:1147-51.

CASE REPORTS Case 1

A 24-year-old Caucasian female was admitted with a 38day history of early evening fever (39 to 40·C), chills, profuse nightsweats, and diarrhea that was watery and mild during the fIrst 30 days and then became bloody and severe (8 to 10/day) for the last 8 days. Laboratory data showed a white blood count of 9600, hemoglobin of 10 g/dl, and fIrst hour sedimentation of 120 mm. Stool examination for ova and parasites was negative, and liver function tests were also negative. A tuberculin test of 12-mm induration to PPD was documented. Chest radiograph showed no abnormalities. Conventional antidiarrheic treatment was ineffective. Barium enema showed "aphthoid" ulcerations 15 in the transverse and descending colon. Colonoscopy revealed, at the level of the sigmoid colon, the presence of multiple and relatively small (2 to 5 mm), rounded, white plaques surrounded by a congested halo (Fig. 1A), as well as rounded small erosions (4 to 6 mm in diameter) also surrounded by congested halos. The intervening mucosa had a normal aspect. Biopsy specimens taken from the mucosal plaques only showed fibrinoid deposits with mononuclear cell infIltrates. The examination of the descending colon showed multiple rounded (-1.5 em in diameter) and longitudinally oriented oblong ulcers (0.3 x 2.0 em). These ulcers were covered by a fIbrinopurulent exudate that was readily removed by a jet wash, revealing a rather smooth ulcer base with moderately elevated mucosal margins (Fig. 1B). These ulcerative lesions became more abundant toward the splenic flexure where the intervening mucosa was congested. Biopsy specimens from the base and margins of the ulcers again showed diffuse mononuclear cell infiltrates and a moderate number of acid-fast bacilli. The endoscopic examination was interrupted at the splenic flexure due to the patient's discomfort. Two days after combined treatment with rifampin, 115

Figure 1. A, Aphthoid lesions in the sigmoid colon of patient in Case 1 showing fibrinoid exudate surrounded by a congested halo. B, Two ulcers (arrows) in the descending colon showing smooth bases covered by fibrinopurulent exudate. The borders are moderately elevated, but the surrounding mucosa (upper left) show a normal vascular network. Figure 2. A, Pseudopolypoid formation (lower right) in the ascending colon of patient in Case 2. The elevated mucosal fold seen in the upper part of the photograph is a portion of the margin of the large ulcer shown in B. B, Large ulcer in the ascending colon showing a base formed by granulomatous tissue which also erodes part of the elevated margin seen in the lower part of the photograph.

isoniazid, and ethambutol, all of the patient's symptoms disappeared. A complete endoscopic examination and a barium enema performed 1 year after the initiation of treatment showed no abnormalities. Case 2

A 39-year-old Caucasian female was admitted with a 14month history of passage of pasty, greasy stools, diffuse crampy abdominal pain, fever (39.5 to 40.0°C), chills, profuse nightsweats, and 20-kg weight loss. She had been presumptively diagnosed as having typhoid fever and was unsuccessfully treated over the past 8 months. Past medical history indicated that she had similar diarrheic episodes at age 36 and melena at age 37. She underwent cholecystectomy for cholelithiasis at age 33 and a partial thyroidectomy for a hyperfunctioning goiter at age 29. Primary pulmonary tuberculosis was diagnosed and treated at age 9. The patient had lived her entire life in a rural area and had habitually ingested unpasteurized cow's milk since early childhood. Physical examination on admission revealed a mass of im116

precise contour in the right middle and lower abdominal quadrants. Laboratory workup showed a white blood count of 6400; hematocrit, 36%; hemoglobin, 10.8 gjdl, serum albumin, 2.67 gjdl; first hour sedimentation rate, 80 mm; and a fecal fat content of 20 gjday (Van de Kamer's procedure). Stool analysis for ova and parasites was negative. Liver function tests were normal. The analysis of the sputum for Mycobacterium tuberculosis (smear and culture) was negative. Chest x-ray did not show any active or healed lesions attributable to tuberculosis. A PPD was positive at ll-mm induration. Proctosigmoidoscopy was normal. A barium enema showed cecal constriction as well as ulcerative and constricting lesions in the ascending colon. Colonoscopic examination of sigmoid, descending, and transverse colon was unremarkable. In the proximal segment of the ascending colon, there was a pseudopolypoid formation (Fig. 2A) adjacent to an elevated smooth mucosal fold which on further examination was found to be part of the elevated margin of a large and deep ulcer (Fig. 2B). This round ulcer had a diameter of about 2.5 cm and a white, markedly granular base which showed some irregular spotty GASTROINTESTINAL ENDOSCOPY

vascularization. Part of the elevated margin of the ulcer was eroded by the same granular tissue. The colonic mucosa surrounding the ulcer was practically normal, but next to the inferior border of the ulcer there was a stricture that precluded the introduction ofthe colonoscope into the proximal ascending colon and cecum. Biopsy specimens taken from the base of the ulcer showed confluent granulomas with central caseating necrosis, a few Langhans giant cells, closely aggregated epithelioid cells, and lymphocytic peripheral rims. Although no acid-fast bacilli were seen in the histological sections or were recovered from the tissue culture, the patient was treated with rifampin, isoniazid, and ethambutol. Three months after initiation of therapy the patient was asymptomatic, regained weight, and the colonoscopy, which then included an examination of the cecum, showed no abnormalities. However, a barium enema still revealed a moderately reduced cecal lumen. DISCUSSION

The two cases presented here reinforce the concept that colonoscopic biopsy is currently the diagnostic procedure of choice in patients with colonic tuberculosis and provide further evidence that antituberculous chemotherapy alone may be highly efficacious, even in advanced intestinal tuberculosis of long duration. 4-14 In the absence of active pulmonary tuberculosis, particularly in nonendemic areas, tuberculosis is rarely considered in the differential diagnosis of inflammatory bowel disease. This was in fact the situation with our patients. In any case, whether tuberculosis is suspected or not, the value of colonoscopy as the less invasive technique to establish the correct diagnosis is quite evident. Although the strict diagnostic confirmation of intestinal tuberculosis would require the demonstration of M. tuberculosis, either hominis or bovis, in the biopsy specimens, it may suffice in practice to observe caseating or even noncaseating granulomata in association with clinical manifestations and endoscopic lesions suggestive of intestinal tuberculosis. Acid-fast bacilli were not visualized or recovered from colonoscopic biopsies in 30 to 50% of reported cases of intestinal tuberculosis.7,9,14,16 Antituberculous chemotherapy trials, even in cases with questionable endoscopic, histological, and bacteriological findings, would appear now justified in view of the reported successful outcomes in analogous circumstances. The protean morphological features of colonic tuberculosis may mimic the lesions produced by other infectious and noninfectious causes. For example, the aphthoid lesions observed in our Case 1, and radiologically detected by others in colonic tuberculosis,15 have been also reported in amebiasis,17 Behcet's disease/ 8 Yersinia enterocolitis,19 and the early stages of Crohn's disease. 2o- 23 Noncaseating granulomas sometimes found in intestinal tuberculosis 3,9,l1 are commonly observed in granulomatous colitis of Crohn's disease. 24 Nevertheless, certain endoscopic differences VOLUME 35, NO.2, 1989

between Crohn's disease and colonic tuberculosis may provide at least some diagnostic and therapeutic orientation. For instance, the "cobblestoning" of Crohn's disease 25 is seldom seen in colonic tuberculosis. Further colonoscopic experience in intestinal tuberculosis will most probably help to delineate more precisely the differential endoscopic aspects with other common intestinal diseases. ACKNOWLEDGMENT

The authors are indebted to Eduardo A. Porta, MD, Professor of Pathology of the School of Medicine, University of Hawaii for help in the preparation of the manuscript.

REFERENCES 1. Tabrisky J, Lindstrom RR, Peters R, et al. Tuberculous enteritis, review of a protean disease. Am J GastroenteroI1975;63:4957. 2. Boundurant RE, Reid D. Ileocecal teberculosis. Am J Gastroenterol 1975;63:58-65. 3. Schulze K, Warner HA, Murray D. Intestinal tuberculosis: experience at a Canadian teaching institution. Am J Med 1977;63:735-45. 4. Aoki G, Nagasako K, Nakae Y, et al. The fibercolonoscopic diagnosis of intestinal tuberculosis. Endoscopy 1975;7:113-21. 5. Bretholz A, Strasser H, Knoblauch M. Endoscopic diagnosis of ileocecal tuberculosis. Gastrointest Endosc 1978;24:250-1. 6. Franklin GO, Mohapatra M, Perrillo RP. Colonic tuberculosis diagnosed by colonoscopic biopsy. Gastroenterology 1979; 76:362-4. 7. Sakai Y. Colonoscopic diagnosis of the intestinal tuberculosis. Mat Med Polona 1979;11:275-8. 8. Breiter JR, Hajjar J-J. Segmental tuberculosis of the colon diagnosed by colonoscopy. Am J Gastroenterol 1981;76:369-73. 9. Bhargava DK, Tando HD, Chawla TC, et al. Diagnosis of ileocecal and colonic tuberculosis by colonoscopy. Gastrointest Endosc 1985;31:68-70. 10. Radhakrishnan S, Nakib H, Shaikh H, et al. The value of colonoscopy in schistosomal, tuberculous, and amebic colitis: two-year experience. Dis Colon Rectum 1986;29:891-5. 11. Zyngier FR, Liberal MHT, Dechoum A. Tuberculous colitis manifested by skip-lesions of the colon. Gastrointest Endosc 1986;32:375. 12. Kita R, Kim E, Yukawa K, et al. Treatment of the intestinal tuberculosis. Gastroenterol Jpn 1977;12:363-7. 13. Tishler JMA, Tuberculosis of the transverse colon. Am J Radiol 1979;133:229-32. 14. Hoshini M, Shibata M, Goto N, et al. A clinical study of tuberculous colitis. Gastroenterol Jpn 1979;14:299-305. 15. Carr-Locke DL, Finlay DB!. Radiological demonstration of colonic aphthoid ulcers in a patient with intestinal tuberculosis. Gut 1983;24:453-5. 16. Wig KL, Chikara NL, Gupta SP, et al. Ileocecal tuberculosis with particular reference to isolation of Mycobacterium tuberculosis: with a note on its relation to regional ileitis (Crohn's disease). Am J Resp Dis 1961;84:169-78. 17. Weinfeld A. The roentgen appearance of intestinal amoebiasis. Am J RadioI1966;96:311-22. 18. Smith GE, Kime LR, Picher JL. The colitis of Behcet's disease: a separate entity? Am J Dig Dis 1973;18:897-100. 19. Vantrappen G, Agg HO, Ponette E, et al. Yersinia enteritis and enterocolitis: gastrointestinal aspects. Gastroenterology 1977;72:220-7. 20. Simpkins KC. Aphthoid ulcers in Crohn's colitis. Clin Radiol 1977;28:601-8. 21. Hunt RH, Waye JD. Colonoscopy. London: Chapman & Hall, 1981. 22. Morson BC. The early histological lesions of Crohn's disease.

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Proc R Soc Med 1972;65:71. 23. Rickert RR, Carter HW. The gross light microscopic and scanning electron microscopic appearance of the early lesions in Crohn's disease. Scanning Electron Microsc 1977;2:179-86.

Percutaneous endoscopic gastrostomy button malfunction with severe cough Arun Sanyal, MD Patricia A. Jefferson, RN Donald F. Kirby, MD, FACP

Percutaneous endoscopic gastrostomy (PEG) has proven to be a significant addition in the care of patients who require long-term enteral nutrition. However, some patients may inadvertently pull the gastrostomy tube out. In addition, some PEG tubes have been reported to migrate into the stomach leading to gastric outlet obstruction. l Finally some patients are disturbed by the catheter protruding from their abdomen. The PEG button was introduced as a solution to some of these problems. 2 As experience with this device increases, new problems are likely to be encountered. We report two cases of PEG button malfunction due to repeated failure of the antireflux valve to function properly during severe coughing episodes in patients with pulmonary disorders. CASE REPORTS Case 1

A 66-year-old man with squamous cell carcinoma of the right tonsil extending to his mandible and metastasizing to the ipsilateral cervical lymph nodes in March 1987 was given 6000 rads of radiation therapy and chemotherapy with meth0trexate. Despite treatment, the local tumor mass kept growing and he was unable to handle his secretions and to swallow. A tracheostomy was performed followed by PEG tube (20 French) placement in July. His PEG tube care and feedings were performed according to our usual protoco1. 3 In October the PEG tube fell out and was replaced with a Foley catheter, which, because of problems with gastric migration, was replaced with a PEG button in November. Soon afterward, his PEG dressings were frequently found soaked with gastric secretions. It was noticed that the flap and plug on the PEG button would pop open each time the patient coughed, causing spillage of the intragastric contents and severe skin excoriation. Despite using several attachment devices and finally a clamp, which was put between the skin and the flap between feedings, the problem could not be resolved satisfactorily. At this time the PEG button was removed, and endoscopy was performed to place a SacksFrom the Divisions of Gastroenterology and Nutritional Support, Medical College of Virginia and McGuire VA Medical Center, Richmond, Virginia. Reprint requests: D. F. Kirby, MD, Box 711, MCV Station, Richmond, Virginia 23298-0711. 118

24. Robbins SL, Cotran RS, Kumar V. Pathologic basis of disease. Philadelphia: WB Saunders, 1984. 25. Lockhart-Mummery HE, Morson BC. Crohn's disease of the large intestine. Gut 1964;5:493-509.

Vine PEG tube. He has done well since then with rapid healing of the skin about his abdominal wound. Case 2

A 66-year-old man was seen in November 1986 for progressive dementia. Physical examination revealed a cachetic male with findings compatible with multi-infarct dementia. Attempts to feed him ended in aspiration and a PEG tube was placed. Following transfer to a nursing home, he was lost to follow-up until June 1987 when his PEG tube fell out. A Foley catheter was used to replace it, but repeated migration of the Foley catheter into his stomach occurred. In October 1987 the Foley catheter was removed and a Sacks-Vine PEG replacement tube was inserted. The same problem was noted with this tube and a PEG button was inserted in December. Soon afterward, we observed that each time the patient coughed, the PEG button flew open spewing gastric contents despite various attempts to keep the PEG button secure. Because of a problem with excoriation of the abdominal skin, the PEG button was removed and endoscopy was performed to place a Sacks-Vine PEG tube. He has had no further problems. DISCUSSION

The PEG button (Fig. 1) consists of a flange which lies flush with the skin. There is a central opening which leads to a short tube with a mushroom-type tip. After placement the mushroom tip lies in the stomach, and the flange is flush with the skin. The opening is occluded by a plug attached to the flange. There is a one-way valve in the tube that was designed to prevent Outer plug---\

Anti-reflu x valve "'2~~~~=j1

Figure 1. The PEG button components. GASTROINTESTINAL ENDOSCOPY