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Fatal multiple systemic embolisms after injection of cyanoacrylate in bleeding gastric varices of a patient who was noncirrhotic but with idiopathic portal hypertension
BRIEF REPORTS
Fatal multiple systemic embolisms after injection of cyanoacrylate in bleeding gastric varices of a patient who was noncirrhotic but with idiopathic portal hypertension Giorgio Saracco, MD, Chiara Giordanino, MD, Navone Roberto, MD, David Ezio, MD, Todros Luca, MD, Stefania Caronna, MD, Patrizia Carucci, MD, Wilma De Bernardi Venon, MD, Claudio Barletti, MD, Mauro Bruno, MD, Claudio De Angelis, MD, Alessandro Musso, MD, Alessandro Repici, MD, Renzo Suriani, MD, Mario Rizzetto, MD Torino, Italy
Acrylates are widely used in many countries for the treatment of bleeding gastric varices.1 N-butyl-2-cyanoacrylate has recently been removed from the market and substituted with N-butyl-2-cyanoacrylate plus methacryloxysulpholane (Glubran 2; GEM, Viareggio, Italy), which has proven to have the same profile of tissue and blood compatibility and low toxicity. Adverse effects of cyanoacrylate include fever and abdominal discomfort; uncommon adverse effects are cerebral,2 pulmonary,3,4 splenic,5 and/or portal vein embolisms.6,7 To the best of our knowledge, this is the first report of a case of fatal systemic embolisms after obliteration of a bleeding gastric varix with undiluted Glubran 2 in a man who was noncirrhotic with idiopathic portal hypertension.
CASE REPORT A 30-year-old man with a medical history of persistent elevation of liver enzymes and chronic hepatitis of unknown origin was referred to our hospital with a suspected hemorrhagic relapse, 12 days after a gastric variceal bleeding had been medically treated in another hospital. The patient was pale, without symptoms of hepatic decompensation; blood pressure was 115/70 mm Hg, and cardiac pulse was normal. Results of laboratory tests were as follows: Hb, 10.0 g/dL (normal range, 13.5-17.5 g/dL); hematocrit, 30.4% (41%50%); white blood cell count, 2730/mL (4000-9000/mL); platelet count, 78.000/mL (150,000-400,000/mL); total protein, 6.4 g/dL (6.5-8.2 g/dL); albumin, 3.7 g/dL (3.8-5.0 g/dL); total bilirubin, 0.8 mg/dL (0.1-1.0 mg/dL); aspartate aminotransferase, 49 U/L (8-38 U/L); and alanine aminotransferase, 44 U/L (4-44 U/L). Upper endoscopy showed F2 esophageal varices according to Beppu et al8 (Table 1), without cherry red spots or red wale markings. A moderate volume of blood and a large fundal varix, isolated gastric varice (IGV) I according to Sarin and Kumar,9 with oozing bleeding was observed in the stomach. Endoscopic hemostasis was performed with Glubran 2 by using 2 mL of undiluted compound. The glue was www.giejournal.org
injected at 2 points into the gastric varix through a 21-gauge needle (Microvasive Endoscopy, Boston Scientific Corp, Natick, Mass). During endoscopy, the patient was slightly intolerant, despite mild sedation, with some episodes of coughing and vomiting. Immediately after the second injection, the patient became cyanotic and unconscious, with a sudden decline in blood oxygen saturation; the endoscope was removed, and the patient was intubated; despite mechanical ventilation, and pharmacologic and electric cardiac stimulation, the patient died. At postmortem the next day, the liver was atrophic, without evidence of cirrhosis; at histology, diffuse fibrosis and obliteration of the intrahepatic portal veins was observed, accompanied by nodular regenerative hyperplasia and focal dilatation of sinusoids. These findings, associated with the absence of known causes of liver fibrosis, suggested the diagnosis of hepatoportal sclerosis. The presence of esophageal and fundal varices was confirmed, but there was no sign of polymerized cyanoacrylate at the site of injection. Major arteries and veins were carefully explored but showed no abnormality. No heart malformation was found, except for a mild stenosis and hypoplasia of the ascending aorta. In particular, no interventricular or interatrial defects were found. Lungs were also carefully checked for vascular abnormality or macroscopic embolism, with no results. The diffuse presence of an eosinophilic, nonorganic substance was found in the hepatic arterial vessels (Fig. 1), heart, lungs, brain, spleen, and kidneys, suggestive of systemic embolisms of cyanoacrylate. In particular, the arterial microvasculature of the lungs was abnormal, showing diffuse dilatation (Fig. 2).
DISCUSSION Hepatoportal sclerosis is a distinct clinicopathologic syndrome of noncirrhotic portal hypertension characterized by sclerosis of the intrahepatic portal veins.10 Volume 65, No. 2 : 2007 GASTROINTESTINAL ENDOSCOPY 345
Brief Reports
TABLE 1. Classification of esophageal and gastric varices* Esophageal Size F1
Small, straight
F2
Enlarged, tortuous; occupy less than a third of the lumen
F3
Large, coil-shaped; occupy more than a third of the lumen
Color
White or blue
Presence of red signs Red wale marks
Longitudinal red streaks on varices
Cherry-red spots
Red, discrete, flat spots on varices
Hematocystic spots Red, discrete, raised spots
Figure 2. Dilated lung vessels completely obstructed by cyanoacrylate (H&E, orig. mag. 100).
Diffuse erythema
Various alternative names have been applied to this disorder, the most popular of which are idiopathic portal hypertension and noncirrhotic portal fibrosis.11,12 The
clinical presentation comprises manifestations of portal hypertension in the face of preserved liver function: bleeding from esophagogastric varices, splenomegaly, and thrombocytopenia from hypersplenism are common features. Endoscopic variceal obturation with acrylates has emerged in many countries in the world as the initial treatment of choice for acute gastric varices bleeding13; in our hospital, since 1992, undiluted cyanoacrylate has been injected into gastric varices to minimize the risk of embolisms. No clinical symptoms suggesting postprocedure embolisms were observed before this case; in particular, no clinically relevant episodes of glue embolization were observed in our patients after the advent of Glubran 2 in 1999. In this case, glue injection was performed as usual, slowly but continuously. The remaining vials of the lot used were all inspected visually, and the solution looked normal. Thus, a vascular malformation was suspected; spontaneous portosystemic splenorenal or gastrorenal shunts are more common in gastric varices (60%-85% of cases)14,15 than esophageal varices (17%-21% of cases).14 Moreover, systemic emboli may occur in patients with hepatopulmonary syndrome characterized by pulmonary microvasculature dilatation, with consequent right-to-left shunting. In our case, the postmortem histologic examination of the lungs confirmed our hypothesis, showing a diffuse dilatation of the arterial microvasculature. Thus, it is very likely that systemic embolization of Glubran 2 from the gastric varix occurred by means of the collateral gastrorenal circulation and through the arteriovenous pulmonary shunts to cause multiorgan infarction. Another possible explanation for the systemic embolism may be the transient patency of the foramen ovale caused by the episodes of coughing, inducing a temporary right-to-left shunt. In conclusion, we suggest that bleeding gastric varices that occur in juvenile portal hypertension of unknown
346 GASTROINTESTINAL ENDOSCOPY Volume 65, No. 2 : 2007
www.giejournal.org
Gastric GOV
In continuity with esophageal varices
GOV I
Along lesser curve (2-5 cm long)
GOV II
Along greater curve extending toward the fundus
IGV
Isolated
IGV I
In the fundus
IGV II
Elsewhere in the stomach
GOV, Gastroesophageal varice. *From Refs. 8 and 9.
Figure 1. Hepatic arterial vessel filled with eosinophilic nonorganic substance (H&E, orig. mag. 100).
Brief Reports
origin should be treated by cyanoacrylate injection with extreme caution because of the increased risk of systemic embolism related to the potential presence of right-to-left shunts. Balloon-occluded retrograde transvenous obliteration has been safely performed for the treatment of gastric varices.16 Indeed, this new radiologic technique may well represent a valid alternative to cyanoacrylate injection in this small subset of patients. DISCLOSURE The authors have no commercial associations that might be a conflict of interest in relation to this article. REFERENCES 1. Ryan BM, Stockburger RW, Ryan JM. A pathophysiologic, gastroenterologic, and radiologic approach to the management of gastric varices. Gastroenterology 2004;126:1175-89. 2. See A, Florent C, Lamy P, et al. Cerebrovascular accidents after endoscopic obturation of esophageal varices with isobutyl-2-cyanoacrylate in 2 patients. Gastroenterol Clin Biol 1986;10:604-7. 3. Roesch W, Rexroth G. Pulmonary, cerebral and coronary emboli during bucrylate injection of bleeding fundic varices. Endoscopy 1998;30:S89-90. 4. Hwang SS, Kim HH, Park SH, et al. N-butyl-2-cyanoacrylate pulmonary embolism after endoscopic injection sclerotherapy for gastric variceal bleeding. J Comput Assist Tomogr 2001;25:16-22. 5. Liu CH, Tsai FC, Liang PC, et al. Splenic vein thrombosis and Klebsiella pneumoniae septicemia after endoscopic gastric variceal obturation therapy with N-butyl-2-cyanoacrylate. Gastrointest Endosc 2006;63: 336-8. 6. Thakeb F, Salama Z, Salama H, et al. The value of combined use of N-butyl-2-cyanoacrylate and ethanolamine oleate in the management of bleeding esophagogastric varices. Endoscopy 1995;27:358-64.
7. Shim CS, Cho YD, Kim JO, et al. A case of portal and splenic vein thrombosis after Histoacryl injection therapy in gastric varices. Endoscopy 1996;28:461. 8. Beppu K, Inokuchi K, Koyanagi N, et al. Prediction of variceal hemorrhage by esophageal endoscopy. Gastrointest Endosc 1981;27:213-8. 9. Sarin SK, Kumar A. Gastric varices: profile, classification, and management. Am J Gastroenterol 1989;84:1244-9. 10. Mikkelsen WP, Edmondson HA, Peters RL, et al. Extra and intrahepatic portal hypertension without cirrhosis (hepatoportal sclerosis). Ann Surg 1965;162:602-18. 11. Boyer JL, Sen Gupta KP, Biswas SK, et al. Idiopathic portal hypertension. Comparison with portal hypertension of cirrhosis and extrahepatic portal vein obstruction. Ann Intern Med 1967;66:41-68. 12. Sarin SK. Non-cirrhotic portal fibrosis. Gut 1989;30:406-15. 13. Greenwald BD, Caldwell SH, Hespenheide EE, et al. N-2-butyl-cyanoacrylate for bleeding gastric varices: a United States pilot study and cost analysis. Am J Gastroenterol 2003;98:1982-8. 14. Watanabe K, Kimura K, Matsutani S, et al. Portal hemodynamics in patients with gastric varices. A study in 230 patients with esophageal and/or gastric varices using portal vein catheterization. Gastroenterology 1988;95:434-40. 15. Matsumoto A, Hamamoto N, Nomura T, et al. Balloon-occluded retrograde transvenous obliteration of high-risk gastric fundal varices. Am J Gastroenterol 1999;94:643-9. 16. Binmoeller KF, Borsatto R. Variceal bleeding and portal hypertension. Endoscopy 2000;32:189-99.
Department of Gastroenterology (G.S., C.G., T.L., S.C., P.C., W.D.B.V., C.B., M.B., C.D.A., A.M., M.R.), Molinette Hospital, Torino, Department of Pathology I (N.R., D.E.), University of Torino, Torino, Digestive Endoscopy Unit (A.R.), Humanitas Clinical Institute, Milano, Division of Gastroenterology (R.S.), Rivoli Hospital, Torino, Itlay. Reprint requests: Giorgio Saracco, MD, Department of Gastroenterology, Molinette Hospital, Corso Bramante 88, 10126 Torino, Italy. Copyright ª 2007 by the American Society for Gastrointestinal Endoscopy 0016-5107/$32.00 doi:10.1016/j.gie.2006.07.009
Gossypiboma diagnosed by upper-GI endoscopy Saroj K. Sinha, MD, DM, Harsh P. Udawat, MD, DM, Thakur D. Yadav, MS, Anupam Lal, MD, Surinder S. Rana, MD, DM, Deepak K. Bhasin, MD, DM Chandigarh, India
Gossypiboma (alternatively textiloma or cottonoids)1 denotes a mass of cotton or a sponge that is retained in the body after surgery. Its incidence is 1 in 100 to 5027 for all surgical interventions2,3 and 1 in 1000 to 1500 for intra-abdominal operations,4 the most common being gynecologic surgery, followed by thoracic,5 cardiovascular,6 orthopedic,7 neurosurgical,8 and soft tissue9 surgery. It can be diagnosed by plain abdominal x-ray films, US of the abdomen, contrast enhanced CT (CECT) of the abdomen, and during surgery. We are reporting a case in which a diagnosis of gossypiboma was made primarily by upper-GI
endoscopy. To the best of our knowledge, diagnosis of gossypiboma by upper-GI endoscopy has rarely been reported in the literature; the gossypiboma was removed by colonoscopy in 1 reported case.10
www.giejournal.org
Volume 65, No. 2 : 2007 GASTROINTESTINAL ENDOSCOPY 347
CASE REPORT A 38-year-old man presented with a dull aching pain in the right hypochondrium and right lumbar region for the last 4 months. It was mild, nonradiating pain, without any
Fatal multiple systemic embolisms after injection of cyanoacrylate in bleeding gastric varices of a patient who was noncirrhotic but with idiopathic portal hypertension Giorgio Saracco, MD, Chiara Giordanino, MD, Navone Roberto, MD, David Ezio, MD, Todros Luca, MD, Stefania Caronna, MD, Patrizia Carucci, MD, Wilma De Bernardi Venon, MD, Claudio Barletti, MD, Mauro Bruno, MD, Claudio De Angelis, MD, Alessandro Musso, MD, Alessandro Repici, MD, Renzo Suriani, MD, Mario Rizzetto, MD Torino, Italy
Acrylates are widely used in many countries for the treatment of bleeding gastric varices.1 N-butyl-2-cyanoacrylate has recently been removed from the market and substituted with N-butyl-2-cyanoacrylate plus methacryloxysulpholane (Glubran 2; GEM, Viareggio, Italy), which has proven to have the same profile of tissue and blood compatibility and low toxicity. Adverse effects of cyanoacrylate include fever and abdominal discomfort; uncommon adverse effects are cerebral,2 pulmonary,3,4 splenic,5 and/or portal vein embolisms.6,7 To the best of our knowledge, this is the first report of a case of fatal systemic embolisms after obliteration of a bleeding gastric varix with undiluted Glubran 2 in a man who was noncirrhotic with idiopathic portal hypertension.
CASE REPORT A 30-year-old man with a medical history of persistent elevation of liver enzymes and chronic hepatitis of unknown origin was referred to our hospital with a suspected hemorrhagic relapse, 12 days after a gastric variceal bleeding had been medically treated in another hospital. The patient was pale, without symptoms of hepatic decompensation; blood pressure was 115/70 mm Hg, and cardiac pulse was normal. Results of laboratory tests were as follows: Hb, 10.0 g/dL (normal range, 13.5-17.5 g/dL); hematocrit, 30.4% (41%50%); white blood cell count, 2730/mL (4000-9000/mL); platelet count, 78.000/mL (150,000-400,000/mL); total protein, 6.4 g/dL (6.5-8.2 g/dL); albumin, 3.7 g/dL (3.8-5.0 g/dL); total bilirubin, 0.8 mg/dL (0.1-1.0 mg/dL); aspartate aminotransferase, 49 U/L (8-38 U/L); and alanine aminotransferase, 44 U/L (4-44 U/L). Upper endoscopy showed F2 esophageal varices according to Beppu et al8 (Table 1), without cherry red spots or red wale markings. A moderate volume of blood and a large fundal varix, isolated gastric varice (IGV) I according to Sarin and Kumar,9 with oozing bleeding was observed in the stomach. Endoscopic hemostasis was performed with Glubran 2 by using 2 mL of undiluted compound. The glue was www.giejournal.org
injected at 2 points into the gastric varix through a 21-gauge needle (Microvasive Endoscopy, Boston Scientific Corp, Natick, Mass). During endoscopy, the patient was slightly intolerant, despite mild sedation, with some episodes of coughing and vomiting. Immediately after the second injection, the patient became cyanotic and unconscious, with a sudden decline in blood oxygen saturation; the endoscope was removed, and the patient was intubated; despite mechanical ventilation, and pharmacologic and electric cardiac stimulation, the patient died. At postmortem the next day, the liver was atrophic, without evidence of cirrhosis; at histology, diffuse fibrosis and obliteration of the intrahepatic portal veins was observed, accompanied by nodular regenerative hyperplasia and focal dilatation of sinusoids. These findings, associated with the absence of known causes of liver fibrosis, suggested the diagnosis of hepatoportal sclerosis. The presence of esophageal and fundal varices was confirmed, but there was no sign of polymerized cyanoacrylate at the site of injection. Major arteries and veins were carefully explored but showed no abnormality. No heart malformation was found, except for a mild stenosis and hypoplasia of the ascending aorta. In particular, no interventricular or interatrial defects were found. Lungs were also carefully checked for vascular abnormality or macroscopic embolism, with no results. The diffuse presence of an eosinophilic, nonorganic substance was found in the hepatic arterial vessels (Fig. 1), heart, lungs, brain, spleen, and kidneys, suggestive of systemic embolisms of cyanoacrylate. In particular, the arterial microvasculature of the lungs was abnormal, showing diffuse dilatation (Fig. 2).
DISCUSSION Hepatoportal sclerosis is a distinct clinicopathologic syndrome of noncirrhotic portal hypertension characterized by sclerosis of the intrahepatic portal veins.10 Volume 65, No. 2 : 2007 GASTROINTESTINAL ENDOSCOPY 345
Brief Reports
TABLE 1. Classification of esophageal and gastric varices* Esophageal Size F1
Small, straight
F2
Enlarged, tortuous; occupy less than a third of the lumen
F3
Large, coil-shaped; occupy more than a third of the lumen
Color
White or blue
Presence of red signs Red wale marks
Longitudinal red streaks on varices
Cherry-red spots
Red, discrete, flat spots on varices
Hematocystic spots Red, discrete, raised spots
Figure 2. Dilated lung vessels completely obstructed by cyanoacrylate (H&E, orig. mag. 100).
Diffuse erythema
Various alternative names have been applied to this disorder, the most popular of which are idiopathic portal hypertension and noncirrhotic portal fibrosis.11,12 The
clinical presentation comprises manifestations of portal hypertension in the face of preserved liver function: bleeding from esophagogastric varices, splenomegaly, and thrombocytopenia from hypersplenism are common features. Endoscopic variceal obturation with acrylates has emerged in many countries in the world as the initial treatment of choice for acute gastric varices bleeding13; in our hospital, since 1992, undiluted cyanoacrylate has been injected into gastric varices to minimize the risk of embolisms. No clinical symptoms suggesting postprocedure embolisms were observed before this case; in particular, no clinically relevant episodes of glue embolization were observed in our patients after the advent of Glubran 2 in 1999. In this case, glue injection was performed as usual, slowly but continuously. The remaining vials of the lot used were all inspected visually, and the solution looked normal. Thus, a vascular malformation was suspected; spontaneous portosystemic splenorenal or gastrorenal shunts are more common in gastric varices (60%-85% of cases)14,15 than esophageal varices (17%-21% of cases).14 Moreover, systemic emboli may occur in patients with hepatopulmonary syndrome characterized by pulmonary microvasculature dilatation, with consequent right-to-left shunting. In our case, the postmortem histologic examination of the lungs confirmed our hypothesis, showing a diffuse dilatation of the arterial microvasculature. Thus, it is very likely that systemic embolization of Glubran 2 from the gastric varix occurred by means of the collateral gastrorenal circulation and through the arteriovenous pulmonary shunts to cause multiorgan infarction. Another possible explanation for the systemic embolism may be the transient patency of the foramen ovale caused by the episodes of coughing, inducing a temporary right-to-left shunt. In conclusion, we suggest that bleeding gastric varices that occur in juvenile portal hypertension of unknown
346 GASTROINTESTINAL ENDOSCOPY Volume 65, No. 2 : 2007
www.giejournal.org
Gastric GOV
In continuity with esophageal varices
GOV I
Along lesser curve (2-5 cm long)
GOV II
Along greater curve extending toward the fundus
IGV
Isolated
IGV I
In the fundus
IGV II
Elsewhere in the stomach
GOV, Gastroesophageal varice. *From Refs. 8 and 9.
Figure 1. Hepatic arterial vessel filled with eosinophilic nonorganic substance (H&E, orig. mag. 100).
Brief Reports
origin should be treated by cyanoacrylate injection with extreme caution because of the increased risk of systemic embolism related to the potential presence of right-to-left shunts. Balloon-occluded retrograde transvenous obliteration has been safely performed for the treatment of gastric varices.16 Indeed, this new radiologic technique may well represent a valid alternative to cyanoacrylate injection in this small subset of patients. DISCLOSURE The authors have no commercial associations that might be a conflict of interest in relation to this article. REFERENCES 1. Ryan BM, Stockburger RW, Ryan JM. A pathophysiologic, gastroenterologic, and radiologic approach to the management of gastric varices. Gastroenterology 2004;126:1175-89. 2. See A, Florent C, Lamy P, et al. Cerebrovascular accidents after endoscopic obturation of esophageal varices with isobutyl-2-cyanoacrylate in 2 patients. Gastroenterol Clin Biol 1986;10:604-7. 3. Roesch W, Rexroth G. Pulmonary, cerebral and coronary emboli during bucrylate injection of bleeding fundic varices. Endoscopy 1998;30:S89-90. 4. Hwang SS, Kim HH, Park SH, et al. N-butyl-2-cyanoacrylate pulmonary embolism after endoscopic injection sclerotherapy for gastric variceal bleeding. J Comput Assist Tomogr 2001;25:16-22. 5. Liu CH, Tsai FC, Liang PC, et al. Splenic vein thrombosis and Klebsiella pneumoniae septicemia after endoscopic gastric variceal obturation therapy with N-butyl-2-cyanoacrylate. Gastrointest Endosc 2006;63: 336-8. 6. Thakeb F, Salama Z, Salama H, et al. The value of combined use of N-butyl-2-cyanoacrylate and ethanolamine oleate in the management of bleeding esophagogastric varices. Endoscopy 1995;27:358-64.
7. Shim CS, Cho YD, Kim JO, et al. A case of portal and splenic vein thrombosis after Histoacryl injection therapy in gastric varices. Endoscopy 1996;28:461. 8. Beppu K, Inokuchi K, Koyanagi N, et al. Prediction of variceal hemorrhage by esophageal endoscopy. Gastrointest Endosc 1981;27:213-8. 9. Sarin SK, Kumar A. Gastric varices: profile, classification, and management. Am J Gastroenterol 1989;84:1244-9. 10. Mikkelsen WP, Edmondson HA, Peters RL, et al. Extra and intrahepatic portal hypertension without cirrhosis (hepatoportal sclerosis). Ann Surg 1965;162:602-18. 11. Boyer JL, Sen Gupta KP, Biswas SK, et al. Idiopathic portal hypertension. Comparison with portal hypertension of cirrhosis and extrahepatic portal vein obstruction. Ann Intern Med 1967;66:41-68. 12. Sarin SK. Non-cirrhotic portal fibrosis. Gut 1989;30:406-15. 13. Greenwald BD, Caldwell SH, Hespenheide EE, et al. N-2-butyl-cyanoacrylate for bleeding gastric varices: a United States pilot study and cost analysis. Am J Gastroenterol 2003;98:1982-8. 14. Watanabe K, Kimura K, Matsutani S, et al. Portal hemodynamics in patients with gastric varices. A study in 230 patients with esophageal and/or gastric varices using portal vein catheterization. Gastroenterology 1988;95:434-40. 15. Matsumoto A, Hamamoto N, Nomura T, et al. Balloon-occluded retrograde transvenous obliteration of high-risk gastric fundal varices. Am J Gastroenterol 1999;94:643-9. 16. Binmoeller KF, Borsatto R. Variceal bleeding and portal hypertension. Endoscopy 2000;32:189-99.
Department of Gastroenterology (G.S., C.G., T.L., S.C., P.C., W.D.B.V., C.B., M.B., C.D.A., A.M., M.R.), Molinette Hospital, Torino, Department of Pathology I (N.R., D.E.), University of Torino, Torino, Digestive Endoscopy Unit (A.R.), Humanitas Clinical Institute, Milano, Division of Gastroenterology (R.S.), Rivoli Hospital, Torino, Itlay. Reprint requests: Giorgio Saracco, MD, Department of Gastroenterology, Molinette Hospital, Corso Bramante 88, 10126 Torino, Italy. Copyright ª 2007 by the American Society for Gastrointestinal Endoscopy 0016-5107/$32.00 doi:10.1016/j.gie.2006.07.009
Gossypiboma diagnosed by upper-GI endoscopy Saroj K. Sinha, MD, DM, Harsh P. Udawat, MD, DM, Thakur D. Yadav, MS, Anupam Lal, MD, Surinder S. Rana, MD, DM, Deepak K. Bhasin, MD, DM Chandigarh, India
Gossypiboma (alternatively textiloma or cottonoids)1 denotes a mass of cotton or a sponge that is retained in the body after surgery. Its incidence is 1 in 100 to 5027 for all surgical interventions2,3 and 1 in 1000 to 1500 for intra-abdominal operations,4 the most common being gynecologic surgery, followed by thoracic,5 cardiovascular,6 orthopedic,7 neurosurgical,8 and soft tissue9 surgery. It can be diagnosed by plain abdominal x-ray films, US of the abdomen, contrast enhanced CT (CECT) of the abdomen, and during surgery. We are reporting a case in which a diagnosis of gossypiboma was made primarily by upper-GI
endoscopy. To the best of our knowledge, diagnosis of gossypiboma by upper-GI endoscopy has rarely been reported in the literature; the gossypiboma was removed by colonoscopy in 1 reported case.10
www.giejournal.org
Volume 65, No. 2 : 2007 GASTROINTESTINAL ENDOSCOPY 347
CASE REPORT A 38-year-old man presented with a dull aching pain in the right hypochondrium and right lumbar region for the last 4 months. It was mild, nonradiating pain, without any