- Email: [email protected]
Cholesterol embolism after colonoscopy: a case report
Brief Reports
the combined antegrade-retrograde endoscopic rendezvous technique to facilitate dilation. The reason for recurrent complete obstruction was unclear; our hypothesis was that it may have been related to previous scarring from the antecedent anastomotic leak, compounded by diversion colitis in the excluded colon. The loop ileostomy provided access for antegrade colonoscopy in this situation. Therefore, this previously described endoscopic technique in the foregut can be used for appropriate cases of complex colonic obstruction. REFERENCES 1. Bueno R, Swanson SJ, Jaklitsch MT, Lukanich JM, Mentzer SJ, Sugarbaker DJ. Combined antegrade and retrograde dilation: a new endoscopic technique in the management of complex esophageal stricture. Gastrointest Endosc 2001;54:368-72. 2. McGrath K, Brazer S. Combined antegrade and retrograde dilation: a new endoscopic technique in the management of complex esophageal stricture [comment]. Gastrointest Endosc 2002;56:163. 3. Baumgart DC, Veltzke-Schlieker W, Wiedenmann B, Hintze RE. Successful recanalization of a completely obliterated esophageal stricture by using an endoscopic rendezvous maneuver. Gastrointest Endosc 2005; 61:473-5. 4. Viriglio C, Consentino S, Favara C, Russo V, Russo A. Endoscopic treatment of postoperative colonic strictures using an achalasia dilator: short-term and long-term results. Endoscopy 1995;27:219-22. 5. Oz MC, Forde KA. Endoscopic alternatives in the management of colonic strictures. Surgery 1990;108:513-9. 6. Weinstock LB, Schatz BA. Endoscopic abnormalities of the anastomosis following resection of colonic neoplasm. Gastrointest Endosc 1994; 40:558-61.
7. Luchtefeld MA, Milsom JW, Senagore A, Surrell JA, Mazier WP. Colorectal anastomotic stenosis. Results of a survey of ASCRS membership. Dis Colon Rectum 1989;32:733-6. 8. Ravo B. Colorectal anastomotic healing and intracolonic bypass procedure. Surg Clin North Am 1988;68:1267-94. 9. Dineen MD, Motson RW. Treatment of colonic anastomotic strictures with ‘‘through the scope’’ balloon dilators. J R Soc Med 1991;84:264-6. 10. Kozarek RA. Hydrostatic balloon dilation of gastrointestinal stenosis: a national survey. Gastrointest Endosc 1986;32:15-9. 11. Hagiwara A, Sakakura C, Shirasu M, Torri T, Hirata Y, Yamagishi H. Sigmoidofiberscopic incision plus balloon dilation for anastomotic stricture after anterior resection of the rectum. World J Surg 1999;23: 717-20. 12. Dieruf LM, Prakash C. Endoscopic incision of a postoperative colonic stricture. Gastrointest Endosc 2001;53:522-4. 13. Guan YS, Sun L, Li X, Zheng XH. Successful management of a benign anastomotic colonic stricture with self-expanding metallic stents: a case report. World J Gastroenterol 2004;10:3534-6. 14. Piccinni G, Nacchiero M. Management of narrower anastomotic colonic strictures. Case report and proposal technique. Surg Endosc 2001;15:1227.
Division of Gastroenterology, Hepatology and Nutrition, Department of Medicine (N.K.); Division of Surgical Oncology, Department of Surgery (J.R.); Division of Gastroenterology, Hepatology and Nutrition, Department of Medicine, University of Pittsburgh Medical Center (K.M.), Pittsburgh, Pennsylvania, USA. Reprint requests: Neeraj Kaushik, MD, UPMC Presbyterian, M2, C Wing, 200 Lothrop St, Pittsburgh, PA 15213. Copyright ª 2006 by the American Society for Gastrointestinal Endoscopy 0016-5107/$32.00 doi:10.1016/j.gie.2005.10.022
Cholesterol embolism after colonoscopy: a case report `, MD, Cristiana Rollino, MD, Carlo Tomasini, MD, Roberta Di Placido, MD, Franco Apra Giulietta Beltrame, MD, Michela Ferro, MD, Giacomo Quattrocchio, MD, Carlo Massara, MD, Francesco Quarello, MD Turin, Italy
GI tract (GI bleeding,2 abdominal pain, intestinal infarction, pancreatitis), retina, lungs, spleen, muscle. Several organs can be involved concomitantly in the catastrophic form, which is often fatal. We describe the case of a patient who is atherosclerotic and who presented with catastrophic AED a few hours after a colonoscopy.
This report concerns the case of a patient affected with severe atherosclerosis and aortic aneurysm, who developed a cholesterol embolism within a few hours of a colonoscopic procedure. We hypothesize that aortic traumatism may have been caused during this procedure by compression of the abdomen. Atheroembolic disease (AED) is a multisystem disease that is a complication of atherosclerosis and can occur spontaneously or as a result of a radiologic or surgical procedure involving arterial vessels.1 The most frequently involved organs are the following: skin (‘‘blue toe,’’ livedo reticularis), kidneys (acute, subacute, or chronic renal failure),1 central nervous system,
In October 2004, a 68-year-old man (body mass index, 23.7 kg/m2), who was suffering from vascular disease (myocardial infarctions in 1987 and 1991, peripheral
730 GASTROINTESTINAL ENDOSCOPY Volume 63, No. 4 : 2006
www.giejournal.org
CASE REPORT
Brief Reports
Figure 1. Blue toe in the right foot.
vasculopathy), developed acute postinfectious glomerulonephritis. This was ascertained by a renal biopsy (which also showed arterio/arteriolosclerotic damage). An abdominal echography showed an aortic aneurysm of 50 56 mm. In February 2005, he complained of right flank and iliac pain. Serum creatinine was 3.8 mg/dL (reference range: 0.5-1.2 mg/dL); aspartate aminotransferase (AST), 9 U/L (!32 U/L); alanine aminotransferase (ALT), 8 U/L (!31 U/L); alkaline phosphatase (ALP), 150 U/L (!240 U/L); gammaglutamyltranspeptidase (g GT), 12 U/L (10-49 U/L); amylase, 202 U/L (28-100 U/L); lactate dehydrogenase (LDH), 645 U/L (240-480 U/L); white blood cell count, 12,240/mm3 (4-10 103/mL); Hb, 7.5 g/dL (12.5-16 g/dL); platelets, 122,000/ mm3 (150-450 103/mL); C3, 179 mg/dL (90-180 mg/dL); and C4, 45 mg/dL (10-40 mg/dL). The patient received 2 blood transfusions. His abdominal US was unchanged. A colonoscopy showed sigma diverticulitis and 3 polyps of less than 1-cm diameter in the left colon. Biopsy specimens of the transverse colon revealed congestive mucosa but no signs of cholesterol embolism. A few days later, the colonoscopy was repeated for polypectomy. In the afternoon, the patient developed intense abdominal pain, with abdominal distention. Blood pressure was 130/90 mm Hg; oxygen saturation (SO2), 99%; and heart rate, 65 beats/min. Laboratory examinations showed AST, 3300 U/L; ALT, 1630 U/L; ALP, 1240 U/L; gGT, 165 U/L; LDH, 14,880 U/L; amylase, 104 U/L; leukocytes, 33,000/mm3 (4-10 103/mL); Hb, 8.8 g/dL; D-dimer 17 mcg/mL (!0.5 mcg/mL); antithrombin III (AT III) 66% (80%-120%); international normalized ratio, 3.2; partial thromboplastin time, 45 seconds. US showed liver enlargement. An echoDoppler showed no thrombosis of the portal vein. An electrocardiogram (ECG) showed lateral ischemia; right precordial leads excluded right myocardial infarction (troponin increased slightly between the second and the ninth day after colonoscopy). An echocardiography showed diffuse hypokinetic areas, unchanged ischemic extent, ejection fraction of 25%, pulmonary arterial pressure of 65 mm Hg, biatrial dilation, and dilation of both ventricles.
CT of the abdomen and the thorax showed hepatic engorgement; regular suprahepatic and portal veins; celiac trunk, hepatic, and mesenteric arteries; no dilation of biliary ways; enlargement of the spleen; atheromasia of aorta, iliac, and femoral arteries; aortic aneurysm (5.6 cm, extending for 10 cm); and no signs of pulmonary embolism. Viral hepatitis markers were negative; C-reactive protein, 14.9 mg/dL; C3, 67 mg/dL; C4, 8 mg/dL (5 days after colonoscopy). The following day, dialysis was started because of oliguria. The patient developed blue toe in the right foot (Fig. 1); a skin biopsy revealed cholesterol crystals (Fig. 2). There was no evidence of cholesterol crystals at the fundus oculi examination, nor at the second colon biopsy. The patient’s general condition worsened, and he died a few days later.
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Volume 63, No. 4 : 2006 GASTROINTESTINAL ENDOSCOPY 731
Figure 2. Cholesterol emboli at skin biopsy (H&E, orig. mag. 100).
Figure 3. Longitudinal abdominal echography scan. Relationship between the colonoscope in the transverse colon and the aorta in a man with 2.2-cm aorta diameter.
Brief Reports
DISCUSSION This patient, who was suffering from an aortic aneurysm, developed severe abdominal pain, along with a marked increase in LDH and liver enzymes, shortly after a colonoscopy. The absence of abdominal free air and the suddenness in the increase in liver enzymes after the colonoscopy ruled out the hypothesis of septic liver involvement after intestinal perforation. Thrombosis of the portal axis was not confirmed by echo-Doppler, while embolic disease from the celiac trunk, thrombosis of the suprahepatic veins, and a pulmonary embolism were excluded by CT. There were no acute clinical or ECG signs of myocardial infarction, and troponin increase was delayed from the onset. Because of development of blue toe (Fig. 1) and C3 hypocomplementemia, a cutaneous biopsy was performed. This showed a cholesterol embolism (Fig. 2), even though no previous signs of AED had been evident (no eosinophilia, livedo reticularis, blue toe; negative colon biopsy; normal serial C3 detections), in spite of severe atherosclerosis. We suggest that the colonoscopy and the subsequent onset of AED are closely related for 2 reasons: the timing, with only a 2- to 3-hour gap between the procedure and the development of clinical manifestations, and the fact that it was impossible to prove other pathologic conditions to justify all the clinical symptoms. AED has never, to our knowledge, been reported as a complication of colonoscopy.3 The possibility that the passage of the endoscopic instrument in the transverse colon caused aortic traumatism was investigated: we performed echo-Doppler during a colonoscopy performed on a patient with an aorta of 22-mm diameter. Close contact between the colonoscope and the vessel was not documented (Fig. 3). We could assume that aortic traumatism was generated by abdominal compression. Insufflated transverse colon itself can become very rigid. In our patient, abdominal compression was maintained to aid progression of the instrument across the bowel lumen in relation to the difficulty in performing the procedure because of sigma diverticulitis. This hypothesis is particularly interesting, because a recent publication4 suggests the need of an external
732 GASTROINTESTINAL ENDOSCOPY Volume 63, No. 4 : 2006
straightener to obtain better abdominal compression to improve colonoscopy. Cholesterol embolism was systemic in this patient and affected his liver (elevation of hepatic enzymes), bowel (clinical signs and LDH elevation), muscle (weakness and LDH elevation), skin, brain (confusion), and heart (delayed increase in the troponin curve, possibly because of cholesterol embolic myocardial involvement with cardiac failure and secondary liver engorgement). No relationship can be hypothesized between AED and the previous acute glomerulonephritis. This case serves as a reminder that colonoscopy should be performed with particular caution in patients suffering from aortic aneurysm.
REFERENCES 1. Scolari F, Ravani P, Pola A, et al. Predictors of renal and patient outcomes in atheroembolic renal disease: a prospective study. J Am Soc Nephrol 2003;14:1584-90. 2. Case records of the Massachusetts General Hospital. Weekly clinicopathological exercises. Case 24-1998. A 76-year-old woman with cardiac and renal failure and gastrointestinal bleeding. N Engl J Med 1998;339:329-37. 3. Lieberman DA, Weiss DG, Bond JH, et al. Use of colonoscopy to screen asymptomatic adults for colorectal cancer. Veterans Affairs Cooperative Study Group 380. N Engl J Med 2000;343:162-8. 4. Catalano F, Catanzaro R, Branciforte G, et al. Colonoscopy technique with an external straightener. Gastrointest Endosc 2000;51:600-4.
Department of Nephrology and Dialysis, S. Giovanni Bosco Hospital (C.R.); Department of Dermatology, University of Turin (C.T.); Department of Gastroenterology, S. Giovanni Bosco Hospital (R.D.P.); High Dependency Unit, S. Giovanni Bosco Hospital (F.A.); Department of Nephrology and Dialysis, S. Giovanni Bosco Hospital (G.B., M.F., G.Q., C.M., F.Q.), Turin, Italy. Reprint requests: Cristiana Rollino, MD, Nefrologia, Ospedale S. G. Bosco, P.za Donatore di sangue 3, 10154 Torino, Italy. Copyright ª 2006 by the American Society for Gastrointestinal Endoscopy 0016-5107/$32.00 doi:10.1016/j.gie.2005.11.017
www.giejournal.org
the combined antegrade-retrograde endoscopic rendezvous technique to facilitate dilation. The reason for recurrent complete obstruction was unclear; our hypothesis was that it may have been related to previous scarring from the antecedent anastomotic leak, compounded by diversion colitis in the excluded colon. The loop ileostomy provided access for antegrade colonoscopy in this situation. Therefore, this previously described endoscopic technique in the foregut can be used for appropriate cases of complex colonic obstruction. REFERENCES 1. Bueno R, Swanson SJ, Jaklitsch MT, Lukanich JM, Mentzer SJ, Sugarbaker DJ. Combined antegrade and retrograde dilation: a new endoscopic technique in the management of complex esophageal stricture. Gastrointest Endosc 2001;54:368-72. 2. McGrath K, Brazer S. Combined antegrade and retrograde dilation: a new endoscopic technique in the management of complex esophageal stricture [comment]. Gastrointest Endosc 2002;56:163. 3. Baumgart DC, Veltzke-Schlieker W, Wiedenmann B, Hintze RE. Successful recanalization of a completely obliterated esophageal stricture by using an endoscopic rendezvous maneuver. Gastrointest Endosc 2005; 61:473-5. 4. Viriglio C, Consentino S, Favara C, Russo V, Russo A. Endoscopic treatment of postoperative colonic strictures using an achalasia dilator: short-term and long-term results. Endoscopy 1995;27:219-22. 5. Oz MC, Forde KA. Endoscopic alternatives in the management of colonic strictures. Surgery 1990;108:513-9. 6. Weinstock LB, Schatz BA. Endoscopic abnormalities of the anastomosis following resection of colonic neoplasm. Gastrointest Endosc 1994; 40:558-61.
7. Luchtefeld MA, Milsom JW, Senagore A, Surrell JA, Mazier WP. Colorectal anastomotic stenosis. Results of a survey of ASCRS membership. Dis Colon Rectum 1989;32:733-6. 8. Ravo B. Colorectal anastomotic healing and intracolonic bypass procedure. Surg Clin North Am 1988;68:1267-94. 9. Dineen MD, Motson RW. Treatment of colonic anastomotic strictures with ‘‘through the scope’’ balloon dilators. J R Soc Med 1991;84:264-6. 10. Kozarek RA. Hydrostatic balloon dilation of gastrointestinal stenosis: a national survey. Gastrointest Endosc 1986;32:15-9. 11. Hagiwara A, Sakakura C, Shirasu M, Torri T, Hirata Y, Yamagishi H. Sigmoidofiberscopic incision plus balloon dilation for anastomotic stricture after anterior resection of the rectum. World J Surg 1999;23: 717-20. 12. Dieruf LM, Prakash C. Endoscopic incision of a postoperative colonic stricture. Gastrointest Endosc 2001;53:522-4. 13. Guan YS, Sun L, Li X, Zheng XH. Successful management of a benign anastomotic colonic stricture with self-expanding metallic stents: a case report. World J Gastroenterol 2004;10:3534-6. 14. Piccinni G, Nacchiero M. Management of narrower anastomotic colonic strictures. Case report and proposal technique. Surg Endosc 2001;15:1227.
Division of Gastroenterology, Hepatology and Nutrition, Department of Medicine (N.K.); Division of Surgical Oncology, Department of Surgery (J.R.); Division of Gastroenterology, Hepatology and Nutrition, Department of Medicine, University of Pittsburgh Medical Center (K.M.), Pittsburgh, Pennsylvania, USA. Reprint requests: Neeraj Kaushik, MD, UPMC Presbyterian, M2, C Wing, 200 Lothrop St, Pittsburgh, PA 15213. Copyright ª 2006 by the American Society for Gastrointestinal Endoscopy 0016-5107/$32.00 doi:10.1016/j.gie.2005.10.022
Cholesterol embolism after colonoscopy: a case report `, MD, Cristiana Rollino, MD, Carlo Tomasini, MD, Roberta Di Placido, MD, Franco Apra Giulietta Beltrame, MD, Michela Ferro, MD, Giacomo Quattrocchio, MD, Carlo Massara, MD, Francesco Quarello, MD Turin, Italy
GI tract (GI bleeding,2 abdominal pain, intestinal infarction, pancreatitis), retina, lungs, spleen, muscle. Several organs can be involved concomitantly in the catastrophic form, which is often fatal. We describe the case of a patient who is atherosclerotic and who presented with catastrophic AED a few hours after a colonoscopy.
This report concerns the case of a patient affected with severe atherosclerosis and aortic aneurysm, who developed a cholesterol embolism within a few hours of a colonoscopic procedure. We hypothesize that aortic traumatism may have been caused during this procedure by compression of the abdomen. Atheroembolic disease (AED) is a multisystem disease that is a complication of atherosclerosis and can occur spontaneously or as a result of a radiologic or surgical procedure involving arterial vessels.1 The most frequently involved organs are the following: skin (‘‘blue toe,’’ livedo reticularis), kidneys (acute, subacute, or chronic renal failure),1 central nervous system,
In October 2004, a 68-year-old man (body mass index, 23.7 kg/m2), who was suffering from vascular disease (myocardial infarctions in 1987 and 1991, peripheral
730 GASTROINTESTINAL ENDOSCOPY Volume 63, No. 4 : 2006
www.giejournal.org
CASE REPORT
Brief Reports
Figure 1. Blue toe in the right foot.
vasculopathy), developed acute postinfectious glomerulonephritis. This was ascertained by a renal biopsy (which also showed arterio/arteriolosclerotic damage). An abdominal echography showed an aortic aneurysm of 50 56 mm. In February 2005, he complained of right flank and iliac pain. Serum creatinine was 3.8 mg/dL (reference range: 0.5-1.2 mg/dL); aspartate aminotransferase (AST), 9 U/L (!32 U/L); alanine aminotransferase (ALT), 8 U/L (!31 U/L); alkaline phosphatase (ALP), 150 U/L (!240 U/L); gammaglutamyltranspeptidase (g GT), 12 U/L (10-49 U/L); amylase, 202 U/L (28-100 U/L); lactate dehydrogenase (LDH), 645 U/L (240-480 U/L); white blood cell count, 12,240/mm3 (4-10 103/mL); Hb, 7.5 g/dL (12.5-16 g/dL); platelets, 122,000/ mm3 (150-450 103/mL); C3, 179 mg/dL (90-180 mg/dL); and C4, 45 mg/dL (10-40 mg/dL). The patient received 2 blood transfusions. His abdominal US was unchanged. A colonoscopy showed sigma diverticulitis and 3 polyps of less than 1-cm diameter in the left colon. Biopsy specimens of the transverse colon revealed congestive mucosa but no signs of cholesterol embolism. A few days later, the colonoscopy was repeated for polypectomy. In the afternoon, the patient developed intense abdominal pain, with abdominal distention. Blood pressure was 130/90 mm Hg; oxygen saturation (SO2), 99%; and heart rate, 65 beats/min. Laboratory examinations showed AST, 3300 U/L; ALT, 1630 U/L; ALP, 1240 U/L; gGT, 165 U/L; LDH, 14,880 U/L; amylase, 104 U/L; leukocytes, 33,000/mm3 (4-10 103/mL); Hb, 8.8 g/dL; D-dimer 17 mcg/mL (!0.5 mcg/mL); antithrombin III (AT III) 66% (80%-120%); international normalized ratio, 3.2; partial thromboplastin time, 45 seconds. US showed liver enlargement. An echoDoppler showed no thrombosis of the portal vein. An electrocardiogram (ECG) showed lateral ischemia; right precordial leads excluded right myocardial infarction (troponin increased slightly between the second and the ninth day after colonoscopy). An echocardiography showed diffuse hypokinetic areas, unchanged ischemic extent, ejection fraction of 25%, pulmonary arterial pressure of 65 mm Hg, biatrial dilation, and dilation of both ventricles.
CT of the abdomen and the thorax showed hepatic engorgement; regular suprahepatic and portal veins; celiac trunk, hepatic, and mesenteric arteries; no dilation of biliary ways; enlargement of the spleen; atheromasia of aorta, iliac, and femoral arteries; aortic aneurysm (5.6 cm, extending for 10 cm); and no signs of pulmonary embolism. Viral hepatitis markers were negative; C-reactive protein, 14.9 mg/dL; C3, 67 mg/dL; C4, 8 mg/dL (5 days after colonoscopy). The following day, dialysis was started because of oliguria. The patient developed blue toe in the right foot (Fig. 1); a skin biopsy revealed cholesterol crystals (Fig. 2). There was no evidence of cholesterol crystals at the fundus oculi examination, nor at the second colon biopsy. The patient’s general condition worsened, and he died a few days later.
www.giejournal.org
Volume 63, No. 4 : 2006 GASTROINTESTINAL ENDOSCOPY 731
Figure 2. Cholesterol emboli at skin biopsy (H&E, orig. mag. 100).
Figure 3. Longitudinal abdominal echography scan. Relationship between the colonoscope in the transverse colon and the aorta in a man with 2.2-cm aorta diameter.
Brief Reports
DISCUSSION This patient, who was suffering from an aortic aneurysm, developed severe abdominal pain, along with a marked increase in LDH and liver enzymes, shortly after a colonoscopy. The absence of abdominal free air and the suddenness in the increase in liver enzymes after the colonoscopy ruled out the hypothesis of septic liver involvement after intestinal perforation. Thrombosis of the portal axis was not confirmed by echo-Doppler, while embolic disease from the celiac trunk, thrombosis of the suprahepatic veins, and a pulmonary embolism were excluded by CT. There were no acute clinical or ECG signs of myocardial infarction, and troponin increase was delayed from the onset. Because of development of blue toe (Fig. 1) and C3 hypocomplementemia, a cutaneous biopsy was performed. This showed a cholesterol embolism (Fig. 2), even though no previous signs of AED had been evident (no eosinophilia, livedo reticularis, blue toe; negative colon biopsy; normal serial C3 detections), in spite of severe atherosclerosis. We suggest that the colonoscopy and the subsequent onset of AED are closely related for 2 reasons: the timing, with only a 2- to 3-hour gap between the procedure and the development of clinical manifestations, and the fact that it was impossible to prove other pathologic conditions to justify all the clinical symptoms. AED has never, to our knowledge, been reported as a complication of colonoscopy.3 The possibility that the passage of the endoscopic instrument in the transverse colon caused aortic traumatism was investigated: we performed echo-Doppler during a colonoscopy performed on a patient with an aorta of 22-mm diameter. Close contact between the colonoscope and the vessel was not documented (Fig. 3). We could assume that aortic traumatism was generated by abdominal compression. Insufflated transverse colon itself can become very rigid. In our patient, abdominal compression was maintained to aid progression of the instrument across the bowel lumen in relation to the difficulty in performing the procedure because of sigma diverticulitis. This hypothesis is particularly interesting, because a recent publication4 suggests the need of an external
732 GASTROINTESTINAL ENDOSCOPY Volume 63, No. 4 : 2006
straightener to obtain better abdominal compression to improve colonoscopy. Cholesterol embolism was systemic in this patient and affected his liver (elevation of hepatic enzymes), bowel (clinical signs and LDH elevation), muscle (weakness and LDH elevation), skin, brain (confusion), and heart (delayed increase in the troponin curve, possibly because of cholesterol embolic myocardial involvement with cardiac failure and secondary liver engorgement). No relationship can be hypothesized between AED and the previous acute glomerulonephritis. This case serves as a reminder that colonoscopy should be performed with particular caution in patients suffering from aortic aneurysm.
REFERENCES 1. Scolari F, Ravani P, Pola A, et al. Predictors of renal and patient outcomes in atheroembolic renal disease: a prospective study. J Am Soc Nephrol 2003;14:1584-90. 2. Case records of the Massachusetts General Hospital. Weekly clinicopathological exercises. Case 24-1998. A 76-year-old woman with cardiac and renal failure and gastrointestinal bleeding. N Engl J Med 1998;339:329-37. 3. Lieberman DA, Weiss DG, Bond JH, et al. Use of colonoscopy to screen asymptomatic adults for colorectal cancer. Veterans Affairs Cooperative Study Group 380. N Engl J Med 2000;343:162-8. 4. Catalano F, Catanzaro R, Branciforte G, et al. Colonoscopy technique with an external straightener. Gastrointest Endosc 2000;51:600-4.
Department of Nephrology and Dialysis, S. Giovanni Bosco Hospital (C.R.); Department of Dermatology, University of Turin (C.T.); Department of Gastroenterology, S. Giovanni Bosco Hospital (R.D.P.); High Dependency Unit, S. Giovanni Bosco Hospital (F.A.); Department of Nephrology and Dialysis, S. Giovanni Bosco Hospital (G.B., M.F., G.Q., C.M., F.Q.), Turin, Italy. Reprint requests: Cristiana Rollino, MD, Nefrologia, Ospedale S. G. Bosco, P.za Donatore di sangue 3, 10154 Torino, Italy. Copyright ª 2006 by the American Society for Gastrointestinal Endoscopy 0016-5107/$32.00 doi:10.1016/j.gie.2005.11.017
www.giejournal.org