- Email: [email protected]
Duodenoscopic view of cholesterol crystal embolization
mas that have just begun to invade the upper part of the submucosa. REFERENCES 1. Muto T, Kamiya J, Sawada T., et al. Small "flat adenoma" of the large bowel with special reference to its clinicopathological features. Dis Colon Rectum 1985;28:847-51. 2. Wolber RA, Owen DA. Flat adenomas of the colon. Hum Pathol 1991;22:70-4. 3. Adachi M, Muto T, Morioka Y, Ikegana T, Hara M. Flat adenoma and flat mucosal carcinoma (lIb type)-a new precursor of colorectal carcinoma? Dis Colon Rectum 1988;31:236-43. 4. Jaramillo E, Slezak P. The use of high resolution electronic video endoscopy, computerized image processing and chromoscopy to study the colorectal mucosa. Acta Endoscopica 1993;23: 59-62. 5. Macrae FA, St. John JB. Relationship between patterns of bleeding and hem occult sensitivity in patients with colorectal cancers or adenomas. Gastroenterology 1982;82:891-8. 6. Jaramillo E, Watanabe M, Witt H, Slezak P. Scanning immersion electronic video endoscopy: a new method to study the epithelial surface of the lower gastrointestinal tract. Acta Endoscopica 1993;23:163-9. 7. Karita M, Tada M, Okita K, Kodama T. Endoscopic therapy for early colon cancer: the strip biopsy resection technique. Gastrointest Endosc 1991;37:128-32.
8. Riddell RH. Management of colonic dysplasia and adenomas. In: Goldman H, Appelman HD, Kaufman N, eds. Gastrointestinal pathology. Baltimore: Williams and Wilkins, 1990:356-75. 9. Muto T, Bussey HJR, Morson BC. Pseudo-carcinomatous invasion in adenomatous polyps of the colon and rectum. J Clin Pathol 1973;26:25-31. 10. Kealy WF. Lymphoid tissue and lymphoid-glandular complexes of the colon: relation to diverticulosis. J Clin Pathol 1976;29: 245-9. 11. Rubio CA. Ectopic colonic mucosa in ulcerative colitis and in Crohn's disease of the colon. Dis Colon Rectum 1984;27:182-6. 12. Matsumoto T, Iida M, Kuwano Y, Tada S, Yao T, Fujishima M. Minute non -polypoid adenoma of the colon detected by colonoscopy: correlation between endoscopic and histologic findings. Gastrointest Endosc 1992;38:645-50. 13. Kazunori I, Masahiro T. Chromoscopy. In: Sivak MV, ed. Gastroenterologic endoscopy. Philadelphia: WB Saunders, 1987: 203-20. 14. Mitooka H, Fujimori T, Ohno S, et al. Chromoscopy of the colon using indigo carmine dye with electrolyte lavage solution. Gastrointest Endosc 1992;38:3~3-4. 15. bye A. Handbok i mikroskopi. Stockholm: Prisma, 1969:86-96 [in Swedish]. 16. Waye JD. Polyps large and small [Editorial]. Gastrointest Endosc 1992;38:391-2.
Duodenoscopic view of cholesterol crystal embolization Carlos Martin-de-Argila, Mayle M. Rivera, Victor V. Moreira, Clara Redondo, Gonzalo Garcia Y Otero, Antonio Candia,
MD MD MD MD MD MD
Cholesterol emboli can occasionally be released from ulcerated atheromatous plaques located in large arterial vessels and subsequently lodge in the systemic capillary bed. These microemboli may, in turn, give rise to a multisystemic disorder, which has been named cholesterol crystal embolization (CCE),l,2 Such a clinical condition was first described by Panum 3 in 1862; in 1945 Flory4 categorized its pathologic aspects. In necropsy studies the prevalence of CCE ranges from 3% and 4%5 to 17.6%.6 Gastrointestinal participation in CCE has been studied mainly through retrospective analysis of clinical series and occurs in nearly 10 % of all cases. In these cases, digestive hemorrhage seems to
Figure 1. Endoscopic photograph showing geographic whitish macules in second portion of duodenum.
From the Gastroenterology, Nephrology, and Pathology Departments, Ramon y Cajal Hospital, Madrid, and the Department of Medicine, Medical School of the University of Alcala de Henares, Alcala de Henares, Spain. Reprint requests: Dr. C. Martin-de-Argila, Concha Espina, 5, 28016 Madrid, Spain. 0016-5107/94/4003-0371$3.00 + 0 GASTROINTESTINAL ENDOSCOPY Copyright © 1994 by the American Society for Gastrointestinal Endoscopy 37/4/50098
VOLUME 40, NO.3, 1994
Figure 2. Endoscopic view of sessile polyps in the duodenal bulb.
371
poid duodenal lesions showed obliteration of small blood vessels by an intense inflammatory infiltration composed of eosinophils, multinucleated giant cells, and a few round cells surrounding cholesterol clefts (Fig. 3). Although fibrinoid necrosis was not present, the picture was similar to periarteritis nodosa. A biopsy specimen of the stomach and duodenum submitted 5 days later showed cholesterol emboli in both locations. At this time the histologic picture was similar except that eosinophils were less prominent. At autopsy multiple cholesterol emboli were seen, affecting mainly the brain, gastrointestinal tract, liver, spleen, pancreas, testes, kidneys, and thyroid. In these lesions, eosinophils were no longer present and the histologic picture was characterized by organized, fibrotic thrombus with occasional cholesterol crystals. Figure 3. Early vasculitic lesion (T) surrounding a cholesterol cleft (O). Giant cells are clearly seen (8). (H & E, original magnification X40.)
be the most common clinical presentation. 1 Although the endoscopic appearance of gastrointestinal involvement in CCE has been adequately described,2,7-9 a wide literature survey did not reveal a published endoscopic photograph. We herewith report a case of CCE presenting as an upper gastrointestinal hemorrhage. On UGI endoscopy distinct lesions were observed that later were confirmed by histologic study. CASE REPORT A 71-year-old man was admitted for a new onset of kidney failure. He had long-standing hypertension, which lately had been difficult to control. Multiple lacunar cerebral infarcts had been diagnosed 3 months before. He had intense asthenia, leg pain on exercise, and bilious vomiting during the 2 weeks before admission. Results of physical examination disclosed a blood pressure of 220/110 mm Hg, grade II hypertensive retinopathy, a periumbilical murmur, and a slight paresia of the right upper limb. Laboratory values were as follows: serum creatinine, 5.4 mg/dl (normal, <1.2); hemoglobin, 11.4 gm/dl; 11,650 leukocytes/mm3, with a normal differential count; proteinuria up to 15 gm/L in 24 hours, and 3 to 5 erythrocytes and numerous hyaline cylinders in urinary sediment. A renal biopsy specimen was consistent with nephroangiosclerosis. On the second hospital day, the patient presented with hematemesis without hemodynamic consequences. A UGI endoscopy was performed, which showed the presence of multiple geographic whitish macules, up to 5 mm in diameter, scattered throughout the first and second portions of the duodenum (Fig. 1) and several sessile polyps in the duodenal bulb, measuring 5 to 10 mm, covered by macroscopically normal mucosa (Fig. 2). Gastric mucosa was erythematous, and a slight thickening of fundal folds was observed. Digestive hemorrhage subsided with supportive treatment. After having entered a dialysis program, the patient died 10 days later from a cerebral hemorrhage. With regard to the pathologic study, sections of the poly372
DISCUSSION
CCE affects elderly men with long -standing atherosclerosis, hypertension, and renal insufficiency.! Although spontaneous cases have been described,4, 6, 10 vascular surgery, anticoagulation therapy, and angiographic procedures seem to be the most common precursors of CCE.!1-17 Symptoms, signs, and laboratory findings usually suggest a multisystemic disorder. In consequence, the antemortem diagnosis is only reached in about 30 % of all cases,l generally after a muscle, skin, or kidney biopsy. In most reported cases of CCE that present with upper digestive hemorrhage, the endoscopic lesions frequently have been sessile polyps in the first portion ofthe duodenum and in the colon and, less frequently, telangiectatic or angiodysplasia-like images. So far endoscopic documentation has not been described. 2, 7-9 In the present patient, in addition to sessile polyps, multiple geographic and whitish macules, with a diameter up to 5 mm, were observed throughout the duodenum (Fig. 1). From an endoscopic point of view, these whitish macular lesions have to be differentiated from xanthelasmas, which rarely are located in the duodenum. IS With regard to duodenal sessile polyps, the main differential diagnoses include hyperplastic/inflammatory polyps; gastric heterotopia; Brunner's gland hyperplasia; nodular duodenitis, either associ19 --24 or not lS to kidney failure; lymphoid hyperated 19 plasia; leiomyomas; lipomas; carcinoids; and adenomatous polyps. IS The present case illustrates the natural course of the lesion of CCE. The first duodenal biopsy specimen obtained 24 hours after the episode of hematemesis showed a vasculitic granulomatous lesion, with prominent eosinophilic and giant cell infiltration. This picture, similar to early lesions of experimental atheroembolic disease 25 rarely has been described in human beings. 26 Five days later the eosinophilic infiltrate was less prominent, and 10 days later (at autopsy) it was absent. GASTROINTESTINAL ENDOSCOPY
CCE should be suspected in patients with multisystemic disease, hypocomplementemia, thrombocytopenia, and eosinophilia, a syndrome previously considered diagnostic of complex-mediated vasculitis. 25 This report emphasizes the usefulness of gastrointestinal endoscopy and biopsy in these cases, mainly when an acute episode such as hematemesis appears. In such cases, the combination of whitish geographic macules and sessile polyps in the duodenum should evoke the diagnosis of CCE and prompt investigations to confirm it. REFERENCES 1. Fine MJ, Kapoor W, Falanga V. Cholesterol crystal embolization: a review of 221 cases in the english literature. Angiology 1987;38:769-84. 2. Francis J, Kapoor WN. Intestinal pseudopolyps and gastrointestinal hemorrhage due to cholesterol crystal embolization. Am J Med 1988;85:269-71. 3. Panum PL. Experimentelle Beitrage zur Lehre von der Embolie. Virchows Arch A Pathol Anat Physiol 1862;25:308-10. 4. Flory CM. Arterial occlusions produced by emboli from eroded aortic atheromatous plaques. Am J Pathol 1945;21:549-65. 5. Cross SS. How common is cholesterol embolism? J Clin Pathol 1991;44:859-61. 6. Gore I, Collins DP. Spontaneous atheromatous embolization. Am J Clin Pathol 1960;33:416-26. 7. O'Brian DS, Jeffers M, Kay EW, Hourihane D. Bleeding due to colorectal atheroembolism: diagnosis by biopsy of adenomatous polyps or of ischemic ulcer. Am J Surg PathoI1991;15:1078-82. 8. Bank S, Aftalion B, Anfang C, Altman H, Wise L. Acquired angiodysplasia as a cause of gastric hemorrhage: a possible consequence of cholesterol embolization. Am J Gastroenterol 1983; 78:206-9. 9. Korelitz BI. Atherosclerotic emboli. Dig Dis Sci 1985;30:506. 10. Kealy WF. Atheroembolism. J Clin Pathol 1978;31:984-9. 11. Feder W, Auerbach R. Purple toes: an uncommon sequela of oral coumarin drug therapy. Ann Intern Med 1961;55:911-7. 12. Bruns FJ, Segel DP, Adler S. Control of cholesterol emboliza-
Colonoscopic diagnosis and treatment of chronic chicken bone perforation of the sigmoid colon Paul R. Tarnasky, MD Michael K. Newcomer, MD M. Stanley Branch, MD
Impaction of an ingested foreign body in the colon is uncommon. We report a case of chicken bone perforation of the sigmoid colon, which was diagnosed and treated endoscopically. From the Department of Medicine, Division of Gastroenterology, Duke University Medical Center, Durham, North Carolina. Reprint requests: M. Stanley Branch, MD, Division of Gastroenterology, Duke University Medical Center, Box 3662, Durham, North Carolina 27710. 0016-5107/94/4003-0373$3.00 + 0 GASTROINTESTINAL ENDOSCOPY Copyright © 1994 by the American Society of Gastrointestinal Endoscopy
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tion by discontinuation of anticoagulant therapy. Am J Med Sci 1978;275:105-8. 13. Crussi FG, Lung as, Combs RG, Meade WHo Multiple atheromatous embolization after aortic surgery. Mich Med 1966;65: 627-33. 14. Drost H, Buis B, Haan D, Hillers JA. Cholesterol embolism as a complication of left heart catheterization: report of seven cases. Br Heart J 1984;52:339-42. 15. Harrington D, Amplatz K. Cholesterol embolization and spinal infarction following aortic catheterization. Am J Roentgenol Radium Ther Nucl Med 1972;115:171-4. 16. Lonni Y, Matsumoto K, Lecky JW. Postaortographic cholesterol (atheromatous) embolization. Radiology 1969;93:63-5. 17. Price DL, Harris J. Cholesterol emboli in cerebral arteries as a complication of retrograde aortic perfusion during cardiac surgery. Neurology 1970;20:1209-14. 18. Blackstone MO. Endoscopic interpretation: normal and pathologic appearance of the gastrointestinal tract. New York: Raven Press, 1984. 19. Franzin G, Muoio A, Ghidini 0, Tonon M, Fratton A. Rilievi morfofunzionali gastroduodenali nell'uremico in emodialisi periodica. Giorn Gastroent End 1979;2:39-41. 20. Feyrter F. Uber wucherungen der brunnerschen drusen. Virchows Arch 1934;293:509-26. 21. Franzin G, Musola R, Mencarelli R. Morphological changes of the gastroduodenal mucosa in regular dialysis uremic patients. Histopathology 1982;6:429-38. 22. Muoio A, Ghidini 0, Ancona G, et al. Gastroduodenal mucosal changes, gastric acid secretion and gastric levels following successful kidney transplantation. Transplant Proc 1979;11:127780. 23. Zukerman GR, Mills BA, Koehler RE, Siegel A, Harter HR, DeSchryver-Kecskemeti K. Nodular duodenitis: pathologic and clinical characteristics in patients with end-stage renal disease. Dig Dis Sci 1983;28:1018-24. 24. Margolis DM, Saylor JL, Giesse G, DeSchryver K, Harter H, Zukerman G. Upper gastrointestinal disease in chronic renal failure: a prospective evaluation. Arch Intern Med 1978;138: 1214-17. 25. Cosio FG, Zager RA, Sharma HM. Atheroembolic renal disease causes hypocomplementaemia. Lancet 1985;2:118-21. 26. Zak FG, Elias K. Embolization with material from atheromata. Am J M Sc 1949;218:510-5.
CASE REPORT
An 80-year-old woman was referred to our clinic for evaluation of chronic diarrhea and a positive fecal occult blood test. Her medical history was notable for peptic ulcer disease in the remote past, for which she had undergone a Billroth I gastrectomy. The history also included a total abdominal hysterectomy and appendectomy, and transient ischemic attacks. The patient reported altered bowel habits of 5 months' duration that were accompanied by intermittent crampy abdominal pain. She described frequent, low-volume, loose stools (four to eight movements per 24 hours) during the day and night. No melena, hematochezia, or fever was noted. Physical examination was remarkable for a documented 8-lb weight loss and brown stool that was positive for occult blood. Abdominal examination was negative for tenderness, rebound, guarding, or masses. A colonoscopy revealed severe diverticulosis, a fixed sigmoid loop, and colonic stenosis that prevented passage of a standard colonoscope beyond 30 cm. When an upper gastrointestinal endoscope was inserted per rectum beyond the
373
8. Riddell RH. Management of colonic dysplasia and adenomas. In: Goldman H, Appelman HD, Kaufman N, eds. Gastrointestinal pathology. Baltimore: Williams and Wilkins, 1990:356-75. 9. Muto T, Bussey HJR, Morson BC. Pseudo-carcinomatous invasion in adenomatous polyps of the colon and rectum. J Clin Pathol 1973;26:25-31. 10. Kealy WF. Lymphoid tissue and lymphoid-glandular complexes of the colon: relation to diverticulosis. J Clin Pathol 1976;29: 245-9. 11. Rubio CA. Ectopic colonic mucosa in ulcerative colitis and in Crohn's disease of the colon. Dis Colon Rectum 1984;27:182-6. 12. Matsumoto T, Iida M, Kuwano Y, Tada S, Yao T, Fujishima M. Minute non -polypoid adenoma of the colon detected by colonoscopy: correlation between endoscopic and histologic findings. Gastrointest Endosc 1992;38:645-50. 13. Kazunori I, Masahiro T. Chromoscopy. In: Sivak MV, ed. Gastroenterologic endoscopy. Philadelphia: WB Saunders, 1987: 203-20. 14. Mitooka H, Fujimori T, Ohno S, et al. Chromoscopy of the colon using indigo carmine dye with electrolyte lavage solution. Gastrointest Endosc 1992;38:3~3-4. 15. bye A. Handbok i mikroskopi. Stockholm: Prisma, 1969:86-96 [in Swedish]. 16. Waye JD. Polyps large and small [Editorial]. Gastrointest Endosc 1992;38:391-2.
Duodenoscopic view of cholesterol crystal embolization Carlos Martin-de-Argila, Mayle M. Rivera, Victor V. Moreira, Clara Redondo, Gonzalo Garcia Y Otero, Antonio Candia,
MD MD MD MD MD MD
Cholesterol emboli can occasionally be released from ulcerated atheromatous plaques located in large arterial vessels and subsequently lodge in the systemic capillary bed. These microemboli may, in turn, give rise to a multisystemic disorder, which has been named cholesterol crystal embolization (CCE),l,2 Such a clinical condition was first described by Panum 3 in 1862; in 1945 Flory4 categorized its pathologic aspects. In necropsy studies the prevalence of CCE ranges from 3% and 4%5 to 17.6%.6 Gastrointestinal participation in CCE has been studied mainly through retrospective analysis of clinical series and occurs in nearly 10 % of all cases. In these cases, digestive hemorrhage seems to
Figure 1. Endoscopic photograph showing geographic whitish macules in second portion of duodenum.
From the Gastroenterology, Nephrology, and Pathology Departments, Ramon y Cajal Hospital, Madrid, and the Department of Medicine, Medical School of the University of Alcala de Henares, Alcala de Henares, Spain. Reprint requests: Dr. C. Martin-de-Argila, Concha Espina, 5, 28016 Madrid, Spain. 0016-5107/94/4003-0371$3.00 + 0 GASTROINTESTINAL ENDOSCOPY Copyright © 1994 by the American Society for Gastrointestinal Endoscopy 37/4/50098
VOLUME 40, NO.3, 1994
Figure 2. Endoscopic view of sessile polyps in the duodenal bulb.
371
poid duodenal lesions showed obliteration of small blood vessels by an intense inflammatory infiltration composed of eosinophils, multinucleated giant cells, and a few round cells surrounding cholesterol clefts (Fig. 3). Although fibrinoid necrosis was not present, the picture was similar to periarteritis nodosa. A biopsy specimen of the stomach and duodenum submitted 5 days later showed cholesterol emboli in both locations. At this time the histologic picture was similar except that eosinophils were less prominent. At autopsy multiple cholesterol emboli were seen, affecting mainly the brain, gastrointestinal tract, liver, spleen, pancreas, testes, kidneys, and thyroid. In these lesions, eosinophils were no longer present and the histologic picture was characterized by organized, fibrotic thrombus with occasional cholesterol crystals. Figure 3. Early vasculitic lesion (T) surrounding a cholesterol cleft (O). Giant cells are clearly seen (8). (H & E, original magnification X40.)
be the most common clinical presentation. 1 Although the endoscopic appearance of gastrointestinal involvement in CCE has been adequately described,2,7-9 a wide literature survey did not reveal a published endoscopic photograph. We herewith report a case of CCE presenting as an upper gastrointestinal hemorrhage. On UGI endoscopy distinct lesions were observed that later were confirmed by histologic study. CASE REPORT A 71-year-old man was admitted for a new onset of kidney failure. He had long-standing hypertension, which lately had been difficult to control. Multiple lacunar cerebral infarcts had been diagnosed 3 months before. He had intense asthenia, leg pain on exercise, and bilious vomiting during the 2 weeks before admission. Results of physical examination disclosed a blood pressure of 220/110 mm Hg, grade II hypertensive retinopathy, a periumbilical murmur, and a slight paresia of the right upper limb. Laboratory values were as follows: serum creatinine, 5.4 mg/dl (normal, <1.2); hemoglobin, 11.4 gm/dl; 11,650 leukocytes/mm3, with a normal differential count; proteinuria up to 15 gm/L in 24 hours, and 3 to 5 erythrocytes and numerous hyaline cylinders in urinary sediment. A renal biopsy specimen was consistent with nephroangiosclerosis. On the second hospital day, the patient presented with hematemesis without hemodynamic consequences. A UGI endoscopy was performed, which showed the presence of multiple geographic whitish macules, up to 5 mm in diameter, scattered throughout the first and second portions of the duodenum (Fig. 1) and several sessile polyps in the duodenal bulb, measuring 5 to 10 mm, covered by macroscopically normal mucosa (Fig. 2). Gastric mucosa was erythematous, and a slight thickening of fundal folds was observed. Digestive hemorrhage subsided with supportive treatment. After having entered a dialysis program, the patient died 10 days later from a cerebral hemorrhage. With regard to the pathologic study, sections of the poly372
DISCUSSION
CCE affects elderly men with long -standing atherosclerosis, hypertension, and renal insufficiency.! Although spontaneous cases have been described,4, 6, 10 vascular surgery, anticoagulation therapy, and angiographic procedures seem to be the most common precursors of CCE.!1-17 Symptoms, signs, and laboratory findings usually suggest a multisystemic disorder. In consequence, the antemortem diagnosis is only reached in about 30 % of all cases,l generally after a muscle, skin, or kidney biopsy. In most reported cases of CCE that present with upper digestive hemorrhage, the endoscopic lesions frequently have been sessile polyps in the first portion ofthe duodenum and in the colon and, less frequently, telangiectatic or angiodysplasia-like images. So far endoscopic documentation has not been described. 2, 7-9 In the present patient, in addition to sessile polyps, multiple geographic and whitish macules, with a diameter up to 5 mm, were observed throughout the duodenum (Fig. 1). From an endoscopic point of view, these whitish macular lesions have to be differentiated from xanthelasmas, which rarely are located in the duodenum. IS With regard to duodenal sessile polyps, the main differential diagnoses include hyperplastic/inflammatory polyps; gastric heterotopia; Brunner's gland hyperplasia; nodular duodenitis, either associ19 --24 or not lS to kidney failure; lymphoid hyperated 19 plasia; leiomyomas; lipomas; carcinoids; and adenomatous polyps. IS The present case illustrates the natural course of the lesion of CCE. The first duodenal biopsy specimen obtained 24 hours after the episode of hematemesis showed a vasculitic granulomatous lesion, with prominent eosinophilic and giant cell infiltration. This picture, similar to early lesions of experimental atheroembolic disease 25 rarely has been described in human beings. 26 Five days later the eosinophilic infiltrate was less prominent, and 10 days later (at autopsy) it was absent. GASTROINTESTINAL ENDOSCOPY
CCE should be suspected in patients with multisystemic disease, hypocomplementemia, thrombocytopenia, and eosinophilia, a syndrome previously considered diagnostic of complex-mediated vasculitis. 25 This report emphasizes the usefulness of gastrointestinal endoscopy and biopsy in these cases, mainly when an acute episode such as hematemesis appears. In such cases, the combination of whitish geographic macules and sessile polyps in the duodenum should evoke the diagnosis of CCE and prompt investigations to confirm it. REFERENCES 1. Fine MJ, Kapoor W, Falanga V. Cholesterol crystal embolization: a review of 221 cases in the english literature. Angiology 1987;38:769-84. 2. Francis J, Kapoor WN. Intestinal pseudopolyps and gastrointestinal hemorrhage due to cholesterol crystal embolization. Am J Med 1988;85:269-71. 3. Panum PL. Experimentelle Beitrage zur Lehre von der Embolie. Virchows Arch A Pathol Anat Physiol 1862;25:308-10. 4. Flory CM. Arterial occlusions produced by emboli from eroded aortic atheromatous plaques. Am J Pathol 1945;21:549-65. 5. Cross SS. How common is cholesterol embolism? J Clin Pathol 1991;44:859-61. 6. Gore I, Collins DP. Spontaneous atheromatous embolization. Am J Clin Pathol 1960;33:416-26. 7. O'Brian DS, Jeffers M, Kay EW, Hourihane D. Bleeding due to colorectal atheroembolism: diagnosis by biopsy of adenomatous polyps or of ischemic ulcer. Am J Surg PathoI1991;15:1078-82. 8. Bank S, Aftalion B, Anfang C, Altman H, Wise L. Acquired angiodysplasia as a cause of gastric hemorrhage: a possible consequence of cholesterol embolization. Am J Gastroenterol 1983; 78:206-9. 9. Korelitz BI. Atherosclerotic emboli. Dig Dis Sci 1985;30:506. 10. Kealy WF. Atheroembolism. J Clin Pathol 1978;31:984-9. 11. Feder W, Auerbach R. Purple toes: an uncommon sequela of oral coumarin drug therapy. Ann Intern Med 1961;55:911-7. 12. Bruns FJ, Segel DP, Adler S. Control of cholesterol emboliza-
Colonoscopic diagnosis and treatment of chronic chicken bone perforation of the sigmoid colon Paul R. Tarnasky, MD Michael K. Newcomer, MD M. Stanley Branch, MD
Impaction of an ingested foreign body in the colon is uncommon. We report a case of chicken bone perforation of the sigmoid colon, which was diagnosed and treated endoscopically. From the Department of Medicine, Division of Gastroenterology, Duke University Medical Center, Durham, North Carolina. Reprint requests: M. Stanley Branch, MD, Division of Gastroenterology, Duke University Medical Center, Box 3662, Durham, North Carolina 27710. 0016-5107/94/4003-0373$3.00 + 0 GASTROINTESTINAL ENDOSCOPY Copyright © 1994 by the American Society of Gastrointestinal Endoscopy
37/4/54499
VOLUME 40, NO.3, 1994
tion by discontinuation of anticoagulant therapy. Am J Med Sci 1978;275:105-8. 13. Crussi FG, Lung as, Combs RG, Meade WHo Multiple atheromatous embolization after aortic surgery. Mich Med 1966;65: 627-33. 14. Drost H, Buis B, Haan D, Hillers JA. Cholesterol embolism as a complication of left heart catheterization: report of seven cases. Br Heart J 1984;52:339-42. 15. Harrington D, Amplatz K. Cholesterol embolization and spinal infarction following aortic catheterization. Am J Roentgenol Radium Ther Nucl Med 1972;115:171-4. 16. Lonni Y, Matsumoto K, Lecky JW. Postaortographic cholesterol (atheromatous) embolization. Radiology 1969;93:63-5. 17. Price DL, Harris J. Cholesterol emboli in cerebral arteries as a complication of retrograde aortic perfusion during cardiac surgery. Neurology 1970;20:1209-14. 18. Blackstone MO. Endoscopic interpretation: normal and pathologic appearance of the gastrointestinal tract. New York: Raven Press, 1984. 19. Franzin G, Muoio A, Ghidini 0, Tonon M, Fratton A. Rilievi morfofunzionali gastroduodenali nell'uremico in emodialisi periodica. Giorn Gastroent End 1979;2:39-41. 20. Feyrter F. Uber wucherungen der brunnerschen drusen. Virchows Arch 1934;293:509-26. 21. Franzin G, Musola R, Mencarelli R. Morphological changes of the gastroduodenal mucosa in regular dialysis uremic patients. Histopathology 1982;6:429-38. 22. Muoio A, Ghidini 0, Ancona G, et al. Gastroduodenal mucosal changes, gastric acid secretion and gastric levels following successful kidney transplantation. Transplant Proc 1979;11:127780. 23. Zukerman GR, Mills BA, Koehler RE, Siegel A, Harter HR, DeSchryver-Kecskemeti K. Nodular duodenitis: pathologic and clinical characteristics in patients with end-stage renal disease. Dig Dis Sci 1983;28:1018-24. 24. Margolis DM, Saylor JL, Giesse G, DeSchryver K, Harter H, Zukerman G. Upper gastrointestinal disease in chronic renal failure: a prospective evaluation. Arch Intern Med 1978;138: 1214-17. 25. Cosio FG, Zager RA, Sharma HM. Atheroembolic renal disease causes hypocomplementaemia. Lancet 1985;2:118-21. 26. Zak FG, Elias K. Embolization with material from atheromata. Am J M Sc 1949;218:510-5.
CASE REPORT
An 80-year-old woman was referred to our clinic for evaluation of chronic diarrhea and a positive fecal occult blood test. Her medical history was notable for peptic ulcer disease in the remote past, for which she had undergone a Billroth I gastrectomy. The history also included a total abdominal hysterectomy and appendectomy, and transient ischemic attacks. The patient reported altered bowel habits of 5 months' duration that were accompanied by intermittent crampy abdominal pain. She described frequent, low-volume, loose stools (four to eight movements per 24 hours) during the day and night. No melena, hematochezia, or fever was noted. Physical examination was remarkable for a documented 8-lb weight loss and brown stool that was positive for occult blood. Abdominal examination was negative for tenderness, rebound, guarding, or masses. A colonoscopy revealed severe diverticulosis, a fixed sigmoid loop, and colonic stenosis that prevented passage of a standard colonoscope beyond 30 cm. When an upper gastrointestinal endoscope was inserted per rectum beyond the
373