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Splenic infarction after histoacryl injection for bleeding gastric varices
BRIEF REPORTS Splenic infarction after histoacryl injection for bleeding gastric varices Pin-Nan Cheng, MD Bor-Shyang Sheu, MD Chiung-Yu Chen, MD Ting-Tsung Chang, MD Xi-Zhang Lin, MD
Gastric varix bleeding is a serious but relatively common complication in cirrhotic patients. Treatment is difficult not only because of the gastric intertwining venous network but also its isolated location in the cardia and fundus. The disappointing results with sclerosing agents in this situation have led to the introduction of tissue adhesive injection. A 93% success rate for initial hemostasis was achieved with N-butyl cyanoacrylate injection.1 The reported complications of this treatment include injection site ulcers, fever, chest pain, and thrombosis of the portal venous system.2 Splenic infarction as a complication had not been reported. CASE REPORT A 20-year-old Chinese man with panhypopituitarism who was receiving regular growth hormone and thyroid hormone replacement therapy presented with acute hematemesis and melena. He was found to be positive for hepatitis B surface antigen and had evidence of liver cirrhosis on sonogram and CT. There was no jaundice, ascites, or encephalopathy found on physical examination. Endoscopy showed small esophageal varices and a tumorlike gastric varix located on the greater curvature of the cardia. The source of bleeding was thought to be a gastric varix. The bleeding was stopped by injection of 2 mL of a mixture of equal amounts of N-butyl2-cyanoacrylate (Histoacryl; B. Braun, Melsungen, Germany) and Lipiodol (Laboratoire Guerbet, France). Three subsequent successful injection sessions were performed at 3- to 4-week intervals. Despite the periodic endoscopic injection therapy for the gastric varix, one episode of massive hematemesis occurred. With the aim of eradicating the gastric varix, one additional session of Histoacryl injection therapy was undertaken about 2
Figure 1. A large, tumor-like varix in the cardia of the stomach was found during the last endoscopy before splenic infarction. The overlying ulceration of varix was induced by previous histoacryl injection. weeks after the third injection treatment. A tumorous gastric varix with ulceration caused by the prior injection was observed at endoscopy before treatment (Fig. 1). Immediately after this last injection session, the patient experienced persistent left upper quadrant pain; 4 hours later he developed a fever of 40° C. An abdominal x-ray film showed opacification of the gastric varix and the branches of the short gastric veins leading to the splenic hilum (Fig. 2A). CT demonstrated a large, wedge-shaped and several small infarctions in the spleen (Fig. 2B). During the patient’s hospitalization, white cell and platelet counts rose from 3400 to 8100/mm3 and 20,000 to 155,000/mm3, respectively, within 14 days. Despite negative blood cultures, the patient was given ceftazidime and an aminoglycoside in addition to supportive treatment measures. A sonogram was performed every 1 to 2 days to monitor for signs of further complications including localized fluid accumulation, change in splenic size, or air within the splenic infarction. The fever and abdominal pain gradually subsided. The remainder of the hospital course was uneventful, and the patient was discharged on day 17. The white cell count at discharge was 4000/mm3, and the platelet count was 88,000/mm3. Follow-up CT at day 45 after the event revealed persistent multiple filling defects in the spleen (Fig. 3). The patient has remained asymptomatic during his 5 months of follow-up outpatient visits.
DISCUSSION From the Division of Gastroenterology, Department of Internal Medicine, National Cheng Kung University Hospital, Tainan, Taiwan. Reprint requests: Xi-Zhang Lin, MD, Division of Gastroenterology, Department of Internal Medicine, National Cheng Kung University Hospital, 138 Sheng-Li Rd., Tainan 704, Taiwan. Copyright © 1998 by the American Society for Gastrointestinal Endoscopy 0016-5107/98/$5.00 + 0 37/4/91248 426
GASTROINTESTINAL ENDOSCOPY
After the introduction of Histoacryl injection for treatment of gastric varices by Soehendra et al.3 in 1986, fever, chest pain, ulceration, recurrent bleeding,1 and portal and splenic vein thrombosis2 were reported as complications. Splenic infarction resulting from Histoacryl injection, to our knowledge, has not been reported. VOLUME 48, NO. 4, 1998
Splenic infarction after histoacryl injection for bleeding gastric varices
P-N Cheng, B-S Sheu, C-Y Chen, et al.
Figure 3. Abdominal CT 45 days after the splenic infarction reveals persistent Lipiodol retention in splenic venules and unresolved hypodense areas in spleen. Perisplenic fluid accumulation and air in the spleen were not identified.
Figure 2. A, Plain x-ray film of the abdomen showing opacification of the gastric varix and short gastric veins with branches (arrows) that are confluent to the splenic hilum. B, CT showing wedge-shaped hypodense area in the spleen compatible with infarction and opacification of splenic hilar venules (arrow), secondary to Lipiodol retention.
Splenic infarction can occur when the splenic vasculature becomes compromised.4 It is possible that the injected tissue adhesive agent reached into the spleen as a result of centrifugal blood flow in this patient with increased portal pressure and that it may have caused damage to the splenic vasculature. The volume of the agent injected, the speed of the injection, and the partial obliteration of the varix may have been contributing factors. Additionally, the previous treatments may have resulted in obstruction in the neighboring network of veins. VOLUME 48, NO. 4, 1998
This could have resulted in the back flow of the Histoacryl into the spleen. Splenic infarction usually has a benign and selflimited clinical course. However, periodic ultrasonography is required to detect complications such as liquefaction, subcapsular hemorrhage, rupture, and pneumoperitoneum.5 Only 7% of patients with splenic infarction will need splenectomy because of sepsis, abscess, or persistent pain.4 An adverse, long-term outcome of splenic infarction with regard to the spleen’s function in blood cell sequestration has yet to be seen in this patient. In summary, injection of the tissue-adhesive agent Histoacryl into gastric varices is a safe procedure despite reported complications. Our case of splenic infarction is a new complication that may be preventable by slower injection of Histoacryl into a previously treated gastric varix. REFERENCES 1. Oho K, Iwao T, Sumino M, Toyonaga A, Tanikawa K. Ethanolamine oleate versus butyl cyanoacrylate for bleeding gastric varices: a nonrandomized study. Endoscopy 1995;27:349-54. 2. Shim CS, Cho YD, Kim JO, Bong HK, Kim YS, Lee JS, et al. A case of portal and splenic vein thrombosis after histoacryl injection therapy in gastric varices [abstract]. Endoscopy 1996;28:461. 3. Soehendra N, Nam VC, Grimm H, Kempeneers I. Endoscopic obliteration of large oesophageal gastric varices with bucrylate. Endoscopy 1986;18:25-6. 4. Jaroch MT, Broughan TA, Hermann RE. The natural history of splenic infarction. Surgery 1986;100:743-50. 5. Goerg C, Schwerk WB. Splenic infarction: sonographic patterns, diagnosis, follow-up, and complications. Radiology 1990;174:803-7. GASTROINTESTINAL ENDOSCOPY
427
Gastric varix bleeding is a serious but relatively common complication in cirrhotic patients. Treatment is difficult not only because of the gastric intertwining venous network but also its isolated location in the cardia and fundus. The disappointing results with sclerosing agents in this situation have led to the introduction of tissue adhesive injection. A 93% success rate for initial hemostasis was achieved with N-butyl cyanoacrylate injection.1 The reported complications of this treatment include injection site ulcers, fever, chest pain, and thrombosis of the portal venous system.2 Splenic infarction as a complication had not been reported. CASE REPORT A 20-year-old Chinese man with panhypopituitarism who was receiving regular growth hormone and thyroid hormone replacement therapy presented with acute hematemesis and melena. He was found to be positive for hepatitis B surface antigen and had evidence of liver cirrhosis on sonogram and CT. There was no jaundice, ascites, or encephalopathy found on physical examination. Endoscopy showed small esophageal varices and a tumorlike gastric varix located on the greater curvature of the cardia. The source of bleeding was thought to be a gastric varix. The bleeding was stopped by injection of 2 mL of a mixture of equal amounts of N-butyl2-cyanoacrylate (Histoacryl; B. Braun, Melsungen, Germany) and Lipiodol (Laboratoire Guerbet, France). Three subsequent successful injection sessions were performed at 3- to 4-week intervals. Despite the periodic endoscopic injection therapy for the gastric varix, one episode of massive hematemesis occurred. With the aim of eradicating the gastric varix, one additional session of Histoacryl injection therapy was undertaken about 2
Figure 1. A large, tumor-like varix in the cardia of the stomach was found during the last endoscopy before splenic infarction. The overlying ulceration of varix was induced by previous histoacryl injection. weeks after the third injection treatment. A tumorous gastric varix with ulceration caused by the prior injection was observed at endoscopy before treatment (Fig. 1). Immediately after this last injection session, the patient experienced persistent left upper quadrant pain; 4 hours later he developed a fever of 40° C. An abdominal x-ray film showed opacification of the gastric varix and the branches of the short gastric veins leading to the splenic hilum (Fig. 2A). CT demonstrated a large, wedge-shaped and several small infarctions in the spleen (Fig. 2B). During the patient’s hospitalization, white cell and platelet counts rose from 3400 to 8100/mm3 and 20,000 to 155,000/mm3, respectively, within 14 days. Despite negative blood cultures, the patient was given ceftazidime and an aminoglycoside in addition to supportive treatment measures. A sonogram was performed every 1 to 2 days to monitor for signs of further complications including localized fluid accumulation, change in splenic size, or air within the splenic infarction. The fever and abdominal pain gradually subsided. The remainder of the hospital course was uneventful, and the patient was discharged on day 17. The white cell count at discharge was 4000/mm3, and the platelet count was 88,000/mm3. Follow-up CT at day 45 after the event revealed persistent multiple filling defects in the spleen (Fig. 3). The patient has remained asymptomatic during his 5 months of follow-up outpatient visits.
DISCUSSION From the Division of Gastroenterology, Department of Internal Medicine, National Cheng Kung University Hospital, Tainan, Taiwan. Reprint requests: Xi-Zhang Lin, MD, Division of Gastroenterology, Department of Internal Medicine, National Cheng Kung University Hospital, 138 Sheng-Li Rd., Tainan 704, Taiwan. Copyright © 1998 by the American Society for Gastrointestinal Endoscopy 0016-5107/98/$5.00 + 0 37/4/91248 426
GASTROINTESTINAL ENDOSCOPY
After the introduction of Histoacryl injection for treatment of gastric varices by Soehendra et al.3 in 1986, fever, chest pain, ulceration, recurrent bleeding,1 and portal and splenic vein thrombosis2 were reported as complications. Splenic infarction resulting from Histoacryl injection, to our knowledge, has not been reported. VOLUME 48, NO. 4, 1998
Splenic infarction after histoacryl injection for bleeding gastric varices
P-N Cheng, B-S Sheu, C-Y Chen, et al.
Figure 3. Abdominal CT 45 days after the splenic infarction reveals persistent Lipiodol retention in splenic venules and unresolved hypodense areas in spleen. Perisplenic fluid accumulation and air in the spleen were not identified.
Figure 2. A, Plain x-ray film of the abdomen showing opacification of the gastric varix and short gastric veins with branches (arrows) that are confluent to the splenic hilum. B, CT showing wedge-shaped hypodense area in the spleen compatible with infarction and opacification of splenic hilar venules (arrow), secondary to Lipiodol retention.
Splenic infarction can occur when the splenic vasculature becomes compromised.4 It is possible that the injected tissue adhesive agent reached into the spleen as a result of centrifugal blood flow in this patient with increased portal pressure and that it may have caused damage to the splenic vasculature. The volume of the agent injected, the speed of the injection, and the partial obliteration of the varix may have been contributing factors. Additionally, the previous treatments may have resulted in obstruction in the neighboring network of veins. VOLUME 48, NO. 4, 1998
This could have resulted in the back flow of the Histoacryl into the spleen. Splenic infarction usually has a benign and selflimited clinical course. However, periodic ultrasonography is required to detect complications such as liquefaction, subcapsular hemorrhage, rupture, and pneumoperitoneum.5 Only 7% of patients with splenic infarction will need splenectomy because of sepsis, abscess, or persistent pain.4 An adverse, long-term outcome of splenic infarction with regard to the spleen’s function in blood cell sequestration has yet to be seen in this patient. In summary, injection of the tissue-adhesive agent Histoacryl into gastric varices is a safe procedure despite reported complications. Our case of splenic infarction is a new complication that may be preventable by slower injection of Histoacryl into a previously treated gastric varix. REFERENCES 1. Oho K, Iwao T, Sumino M, Toyonaga A, Tanikawa K. Ethanolamine oleate versus butyl cyanoacrylate for bleeding gastric varices: a nonrandomized study. Endoscopy 1995;27:349-54. 2. Shim CS, Cho YD, Kim JO, Bong HK, Kim YS, Lee JS, et al. A case of portal and splenic vein thrombosis after histoacryl injection therapy in gastric varices [abstract]. Endoscopy 1996;28:461. 3. Soehendra N, Nam VC, Grimm H, Kempeneers I. Endoscopic obliteration of large oesophageal gastric varices with bucrylate. Endoscopy 1986;18:25-6. 4. Jaroch MT, Broughan TA, Hermann RE. The natural history of splenic infarction. Surgery 1986;100:743-50. 5. Goerg C, Schwerk WB. Splenic infarction: sonographic patterns, diagnosis, follow-up, and complications. Radiology 1990;174:803-7. GASTROINTESTINAL ENDOSCOPY
427