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Hepatic Artery Embolization for Bleeding and Tumors
0039-6109/89 $0.00
Liver Surgery
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Hepatic Artery Embolization for Bleeding and Tumors
Melvin E. Clouse, MD*
TRAUMA
The liver is the third most commonly injured abdominal organ, surpassed only by the small bowel and spleen. The majority of injuries occur in male adolescents and young adults. The relative incidence of blunt or penetrating wounds depends on the geographic location and population sampled. Associated injuries are very common.' The injuries may be simple laceration, in which case manual compression or ligation will stop the bleeding, or deeper tears that require surgical hemostasis. Approximately 30 per cent of patients have more serious, deep lacerations or avulsion fractures of a portion of the liver. Most of the deaths are secondary to exsanguination in the latter group. 2, 34, 61 The fatality rate depends on the mechanism of injury and the degree of trauma. Blunt injuries are generally more damaging to the liver than a simple penetrating wound because of the shearing forces within the liver.2, 34, 60 Active hemorrhage at operation is associated with an increased mortality rate. Approximately 50 per cent of liver wounds will have stopped bleeding before surgery, but others continue to hemorrhage from small intrahepatic arteries and veins. 34, 38 Preoperative studies usually involve u1trasound or computed tomography (CT) because of their depiction of global anatomy and ability to evaluate the retroperitoneum and other abdominal organs. Preoperatively, arteriography is necessary to define arterial anatomy, as approximately 18 per cent of patients have a replaced right hepatic artery from the superior mesenteric artery, 39 In 1976, Cho and associates 9 showed that the hepatic artery could be safely embolized and suggested embolization as a treatment for liver trauma, The same year, Walter and coworkers 62 reported successful control of massive hematobilia after liver biopsy. Bass and Crosier' performed transcatheter hepatic artery occlusion for pseudoaneurysm soon thereafter. Since that time, hepatic artery embolization has become a standard treatment of liver hemorrhage from a variety of lesions, including those related to trauma, pseudoaneurysms (Fig. lA), hematobilia, or arteriovenous fistulas secondary to either trauma or iatrogenic injury. 25, 32, 51, 54, 55, 57 The technique can be performed safely, and embolization of the cystic artery and
*Professor,
Department of Radiology, Harvard Medical School, and Chairman, Department of Radiology, New England Deaconess Hospital, Boston, Massachusetts
Surgical Clinics of North America-Vol. 69. No.2, April 1989
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Figure 1. See legend on opposite page
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Figure 1. Massive upper gastrointestinal bleeding in a 16-year-old female patient. A, The hepatic arteriogram demonstrates a large pseudoaneurysm with contrast medium filling the common bile duct. B, Hepatic arteriogram 2 weeks after operative ligation of the right hepatic artery. Note filling of the aneurysm via intrahepatic collaterals (open arrow) from the middle hepatic artery branch and disruption of a branch of the right hepatic artery (solid arrow) producing the false aneurysm. C, Superior mesenteric artery injection opacifies a large collateral that is filling the aneurysm. D, Catheter within the false aneurysm via percutaneous transhepatic placement (arrow). Note coils in aneurysm and contrast filling the bile ducts. E, Hepatic artery injection 5 days after percutaneous embolization demonstrates continued filling of false aneurysm by intrahepatic collaterals. F, Superior mesenteric injection demonstrates filling of aneurysm from a second source. Note disruption of the artery (arrow). G, Hepatic artery injection after embolization with small Gelfoam pledgets soaked in absolute ethanol; note absence of filling in aneurysm. H, Superior mesenteric artery injection after embolization of collateral with small pledgets of Gelfoam soaked in absolute ethanol. There has been no further bleeding.
gallbladder necrosis can be avoided if large pledgets are used. The technique can be performed from the brachial or the femoral artery with 5-F or 6-F catheters. Embolic materials should be placed peripherally and as selectively as possible to avoid the problems of rebleeding from collateral vessels that occur with central occlusion whether it be by coils (radiologic) or ligatures (surgical). In most instances, surgical ligation of the hepatic artery should not be the primary therapy because the method can cause rebleeding of intrahepatic collateral vessels or collateral vessels in the hepatoduodenal ligament and inferior or superior phrenic arteries (Fig. IB and C). A variety of materials, including Gelfoam pledgets, polyvinyl alcohol, cyanoacrylates, and Gianturco coils, have been used. 3 • 4.11.12.29.37 Our technique has been to use Gelfoam pledgets soaked in alcohol to control bleeding from very small peripheral hepatic arteries. The pled gets should be cut to the approximate size of the appropriate feeding vessel, with pledgets ranging from 0.3 to 2.0 mm in diameter. For false aneurysms in a larger hepatic artery, Gianturco coils are very effective, because they can be placed distal as well as proximal to the false aneurysm, occluding both inflow and outflow and allowing for intrahepatic arterial collaterals to supply the embolized segment of the liver (Fig. 2). Performed judiciously, embolization can be done with little if any morbidity and mortality and is the preferred method for treating hemorrhage both preoperatively and postoperatively (approximately 3.5 per cent of patients will rebleed postoperatively"').
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Figure 2. Embolotherapy with Gianturco coils. A, Arterial phase of hepatic arteriography showing the placement of a biliary drainage catheter through the right hepatic artery. B, Hepatic arteriogram 5 days after left hepatectomy for metastatic tumor shows the false aneurysm of right hepatic artery. C, Hepatic arteriogram after the placement of Gianturco coils on either side of the false aneurysm. There was no further bleeding.
The treatment of hematobilia has usually required operative intervention. The problem is usually caused by blunt trauma, percutaneous biliary drainage or biopsy, postoperative hemorrhagic pancreatitis, abscesses, or vasculitis. B• 31. 41. 49 The pseudoaneurysm usually associated with hematobilia can be demonstrated by diagnostic celiac and superior mesenteric arteriography. It is much more difficult to control bleeding from a pseudoaneurysm if there has been operative ligation of the proper hepatic artery (Fig. 1). In these instances, a direct puncture of the aneurysm under fluoroscopic control, leaving a catheter directly in the false aneurysm, is the method of choice. Multiple Gianturco coils and other embolic material can then be placed directly into the false aneurysm to secure thrombosis. In those instances where occlusion of the pseudoaneurysm has not been accomplished primarily by direct puncture and placement of embolic material, embolization of collateral vessels can usually be accomplished by using superselective catheterization for those arteries in the hepatoduodenal ligaments primarily from the pancreatic arcade, collaterals from the left hepatic artery, or from the phrenic arteries. Lackgren and associates recently suggested that hepatic artery embolization is the treatment of choice for hematobilia in children. 31
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PORTAL HYPERTENSION
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The selection of therapy-for bleeding in portal hypertension remains controversial and is based on multiple factors, including the basic pathogenic mechanism of portal hypertension in the individual patient, the status of the patient as defined by Child's classification, the elective or urgent nature of operation, the hemodynamic stability of the patient at the time of bleeding, clotting factors, the site of the block in the portal system, and the caliber and anatomic relations of those veins available for anastomosis in the portal system. Additional factors include the presence or severity of ascites, encephalopathy, age of patient, site of bleeding (esophageal or gastric), severity of associated hypersplenism, and operative and radiologic expertise available at a given institution. Shunting procedures achieve the best long-term control of bleeding, but they can precipitate encephalopathy. Nonshunting procedures do not induce encephalopathy but are usually associated with a high rate of rebleeding. The logical approach is to assess the patient for the above factors clinically. Selective splenic and mesenteric arteriography is performed with filming in the venous phase to determine the patency and location of the portal system prior to shunting or percutaneous transhepatic portography and sclerosis of varices. Selective hepatic arteriography excludes the presence of hepatoma. Inferior vena cavography is usually performed to determine the position of the left renal vein in relation to the splenic vein, and hepatic wedge pressures are measured to determine the portal venous pressure. Patients who present with episodes of acute bleeding are usually treated initially with medical therapy including catheter tamponade and acute sclerotherapy by endoscopy. If the patient fails to respond, or if bleeding recurs, further therapy is required. Rebleeding after balloon tamponade appears in approximately 40 to 50 per cent of patients. 20, 48 The endoscopic injection of esophageal varices for sclerotherapy is an excellent method to control acute bleeding with a low morbidity and mortality rate (10 to 15 per cent). 15, 18, 19, 33, 36: 47,"",56 Complications include rebleeding and stricture related to the sclerotherapeutic agent. Temporizing and control of immediate bleeding can be achieved with intravenous or intra-arterial administration of vasopressin (Pitressin) in 56 to 58 per cent of the patients. 10, 26, 27 A more invasive technique but short of surgery is percutaneous transhepatic obliteration of esophageal varices by injecting sclerosing agents and embolic material into the coronary or short gastric veins. 5, 26, 35, 63," Widrich and Yune and their associates report an initial success rate of 70 to 95 per cent, with control of bleeding for 1 to 30 months. 63, . . Failures were related to ascites, severely cirrhotic liver, thrombosis of the portal vein, and difficult anatomy. However, the significant rebleeding rate and incidence of complications have diminished earlier enthusiasm for this technique. Nevertheless, in skilled hands and in well-selected patients, it can be helpful as a temporizing measure prior to various operative procedures for decompressing the portal system. In these instances; the portal vein is catheterized percutaneously and the catheter passed into the coronary vein with the injection of embolic material. We use absolute alcohol, Gelfoam pledgets soaked in absolute alcohol, or 3 per cent sodium tetradecyl sulfate (Sotradecol) followed by occlusion of the coronary vein with Gianturco coils. The short gastric veins can also be catheterized and injected to decompress esophageal varices temporarily, The objective is to occlude large and multiple small veins that are inflow channels to esophageal veins in the cardioesophageal area of the stomach (Fig. 3).
TUMORS Therapeutic arterial embolization of abdominal neoplasms, although still experimental, has become an integral part of the therapy for primary and secondary
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Figure 3. Obliteration of esophageal varices. A, Percutaneous transhepatic portal venogram; note large esophageal varices and spontaneous splenorenal venous shunting. B, Portal venogram after occlusion of varices with absolute ethanol and Gelfoam pledgets soaked in absolute ethanol with coil occlusion of the coronary vein.
liver neoplasms. Devascularization of hepatic neoplasms was initially achieved using Gelfoam pledgets and stainless steel Gianturco coilsY More recently, Chuang and associates have used 0.25-mm Ivalon particles for more peripheral embolization. 12 Our technique for hepatic arterial embolization is a modification of the Lunderquist technique using Gelfoam powder soaked in alcohol and mixed to a thick viscous consistency, which permits easy injection and exquisite control of the materiaP6 (A. Lunderquist; personal communication). The catheterization is through the left brachial artery. The catheter can be left in place for re-embolization and check of the results. 13. 64 A complete arterial map is obtained to determine anatomic variants and to locate the bulk of tumor tissue as well as to determine the patency of the portal system. The portal vein is the conduit for almost all metastatic neoplasms from the gastrointestinal tract to the liver and supplies 80 per cent of the required oxygen and nutrients of the normal liver. Both primary and metastatic hepatic neoplasms derive their blood supply and nourishment from the arterial circuit. Because of this differentiated perfusion, the hepatic artery is an ideal route for selective delivery of either chemotherapeutic agents or embolic material. 7 Only 80 per cent of the population is amenable to selective hepatic artery embolization, as approximately 18 per cent have the right hepatic artery arising from the superior mesenteric artery.39 In these instances, the replaced right hepatic artery can be catheterized via the transfemoral route and occluded with a Gianturco coil (Fig. 4). In those instances in which the left gastric artery arises from the left hepatic artery or the left hepatic artery supplies branches to the stomach, selective catheterization and occlusion of the gastric branch can be achieved prior to em bolization of the peripheral hepatic arteries. By this method, one can gain control of a single artery that supplies the entire liver, thereby accomplishing control of the hepatic blood flow. In certain instances, the gastroduodenal artery must be occluded with Gianturco coils to allow safe embolization of the hepatic artery without reflux of embolic material into either the right gastric artery or the duodenum or pancreas (Fig. 5). The rationale for peripheral artery embolization with Gelfoam is that primary
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Figure 4. Hepatic arteriography on a 44-year-old woman with colon cancer metastases to the liver. A, Right hepatic artery injection replaced from the superior mesenteric artery. B, Note coil in right hepatic artery replaced from the superior mesenteric artery (arrow). C, Injection of contrast medium into the common hepatic artery from the celiac trunk shows filling of arteries of both lobes of the liver.
and secondary tumors derive their blood supply and nutrition from the arterial circuit. 7 It is imperative to occlude small arteries and prevent re-establishment of collateral flow, which occurs with proper hepatic artery ligation whether by operative or radiologic means. The theoretical disadvantage of using Gelfoam powder is that it may be resorbed within 7 to 21 days.4 If the hepatic artery becomes recanalized, however, it serves as an excellent conduit for re-embolization. The indications for hepatic arterial embolization are unresectable tumor, no other effective treatment, and treatment failure with intra-arterial or intravenous chemotherapy or radiation. Immediately after embolization, no flow in the embolized hepatic artery should be demonstrated by angiography or radionuclide flow study. Computed tomography scanning is not helpful during the first 24 hours because tumor deposits will contain residual contrast medium from the embolization procedure. The CT follow-up is important and is performed at days 3 and 7 after embolization. The presence of gas
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Figure 5. Celiac artery injection after coil placement in the gastroduodenal artery (arrow). Note collaterals from dorsal artery filling the gastroduodenal and gastroepiploic artery.
within the tumor on day 2 does not indicate an abscess but rather excellent embolization and tumor necrosis; gas is almost always resorbed after 7 days. Bleeding time, prothrombin time, partial thromboplastin time, platelet count, serum uric acid, and a complete liver profile including bilirubin, alkaline phosphatase, aspartate transferase, and lactate dehydrogenase are obtained before embolization, daily for the first 3 days after embolization, and every other day for the next 9 days. To prevent urate nephropathy and renal failure after embolization, the patients are routinely prepared with allopurinol for 48 hours and given bicarbonates for alkalinization of the urine. Liver function tests become markedly elevated at 24 to 48 hours, peak at 72 hours, and return to pre-embolic levels after 6 to 9 days. The clotting factors have remained normal in all of our patients. Serum uric acid must be followed carefully because it may become markedly elevated secondary to tumor necrosis. Patients are therefore kept on allopurinol, probenecide, and diuretics. The possibility of gallbladder necrosis exists because the cystic artery arises from the hepatic artery. Gallbladder necrosis is probably more common than reported. 30, 40, 58 Gallbladder ultrasound examination should be performed prior to and 24 and 48 hours after embolization. If there is thickening of the gallbladder wall, a 99mTc-iminodiacetic acid scan should be performed and the patient followed closely for sepsis. For this reason, the patients are prepared approximately 3 hours prior to embolization with an antibiotic such as cefoperazone that is excreted in the bile. Complications may also arise from embolization to the left gastric artery and pancreas (Fig. 6). Postembolization syndrome consists of pain in the right upper quadrant, appearing almost immediately after embolization and perhaps lasting as long as 3 days, that requires intravenous meperidine or morphine every 3 to 6 hours. Nausea and vomiting may be pronounced but can be controlled with intramuscular prochlorperazine. Embolization for hypovascular tumor deposits such as colon cancer metastases, the most common metastatic tumor, is no longer performed at our institution, as the median survival time is not sufficiently increased. We do currently embolize the very vascular metastatic tumors and hepatomas. The most dramatic beneficial
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Figure 6. Hepatic artery embolization. A, CT scan in 56-year-old man 7 days after embolization for metastatic carcinoid tumor. Note gas in tumor consistent with extensive necrosis. B, -Tc-iminodiacetic acid scan 14 days after embolization because of pain in right upper quadrant and fever. The scan is positive for gallbladder necrosis and cholecystitis, with no filling of gallbladder even after 21 hours. C, Ultrasound scan of gallbladder showing thickened wall consistent with necrosis. Necrotic gallbladder removed at operation. D, Capillary phase of hepatic arteriogram 2 years later shows small tumor deposits throughout liver. Note the avascular area in the right upper lobe from embolization 2 years previously. E, CT scan prior to second embolization. Note the avascular area, which has diminished in size, corresponding to tumor embolized 2 years previously. F, Hepatic artery injection after second embolization showing absent arterial How to liver.
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Figure 7. Celiac arteriography after hepatic artery embolization in 55-year-old man with carcinoid tumor metastatic to the liver. Note extensive collaterals from pancreatic bed and hepatoduodenalligament (A), with filling of multiple metastatic deposits in the capillary phase (B).
effect occurs in the malignant hormone-secreting tumors, where the systemic effect of the hormone is more devastating than the tumor bulk. I. 14.42 We are currently following eight patients who have had embolization from one to four times over a period of 6 years, with excellent results. Embolization should be performed before collateral flow has been established because it may be impossible to superselect and interrupt collateral blood flow to the tumor on subsequent occasions if collaterals are well established and the main hepatic artery does not recanalize (Fig. 7). More recently, numerous articles have demonstrated the importance of chemo-
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Figure 8. CT scans of 72-year-old man with hepatoma. A, Superior segment of right lobe of liver (arrow). B, Completely replaced lateral segment of left lobe. C, Postembolization of liver with 10 ml of Ethiodol and 35 mg of doxorubicin to the lateral segment of left lobe and 5 ml of Ethiodol and 10 mg of doxorubicin to the superior segment of right upper lobe. D and E, Six days after embolization; note Ethiodol and gas in segment of right upper and left lobes consistent with tumor necrosis.
embolization, especially for hepatomas, using a variety of chemotherapeutic agents such as doxorubicin, mitomycin C, and cisplatin. 17• 24. 28. 44, 46, 52, 53, 59 The rationale is to decrease blood flow through the tumor, leaving the chemotherapeutic agent in contact with tumor cells for a longer time. This is accomplished by mixing the chemotherapeutic agent with Ethiodol followed by embolization with Gelfoam pledgets or powder. Ethiodol has also been reported to demonstrate angiographically small metastatic deposits in the liver. 43, 45, 65 Chemoembolization has been accom-
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plished without further morbidity and mortality and with significant improvement in 1- and 2-year survival rates (Fig. 8). TUMOR HEMORRHAGE Control of hepatic tumor hemorrhage by transcatheter embolization can be accomplished using a variety of agents such as Ethibloc, polyvinyl alcohol, or Gelfoam powder soaked on pads in alcohol. Excellent results have been reported from various institutions without increases in morbidity and mortality rates. 21-23 Hemorrhage is usually related to spontaneous rupture of hepatocellular carcinoma, which mayor may not erode through the liver capsule with subcapsular bleeding or frank hemorrhage into the peritoneal cavity. The objective in these instances is to prevent exsanguination, but the procedure may be combined with therapeutic chemoembolization. There has not been an increased morbidity relating to embolization to control bleeding. In a series of 17 patients reported by Hsieh and associates,23 11 patients died of their cancers at 16 to 386 days after embolization, and three patients were alive at 3, 7, and 15 months. There was no serious complication related to embolization.
REFERENCES 1. Ajani JA, Carrasco CH, Charnsanjavy C, et al: Islet cell tumors metastatic to the liver: Effective palliation by sequential hepatic artery embolization. Ann Intern Med 108:340344, 1988 2. Ali J: Abdominal trauma with special reference to hepatic trauma. Can J Surg 21:512515, 1978 3. Arnson SB, McMaster PRB, Moore TE, et al: Toxicity of cyanoacrylates. Arch Ophthalmol 82:342-349, 1970 4. Barth KH, Strandberg JD, White RI: Long-term followup of transcatheter embolization with autologous clot, Oxacel and Gelfoam in domestic swine. Invest Radiol 12:273-280, 1977 5. Bass EM, Crosier JH: Percutaneous control of post-traumatic hepatic hemorrhage by Gelfoam embolization. J Trauma 17:61-63, 1977 6. Bengmark S, Borjesson B, Hoevels J, et al: Obliteration of esophageal varices by PTP: A followup of 43 patients. Ann Surg 190:549-554, 1979 7. Breedis C, Young G: Blood supply to neoplasms in the liver. Fed Proc 8:351, 1949 8. Cerniak A, Thompson IN, Hemingway AP, et al: Hematobilia: A disease in evolution. Arch Surg 123:718-721, 1988 9. Cho KJ, Reuter SR, Schmidt R: Effects of experimental hepatic artery embolization on hepatic function. Am J Roentgenol 127:563-567, 1976 10. Chojkier M, Grossmann RJ, Alterbury CE, et al: A controlled comparison of continuous intraarterial and intravenous infusion of vasopressin in hemorrhage from esophageal varices. Gastroenterology 77:540-546, 1979 11. Chuang VP, Wallace S: Arterial occlusion and infusion in cancer patient. Semin Roentgenol 16:13-25, 1981 12. Chuang VP, Soo CS, Wallace S: lvalon embolization in abdominal neoplasms. AJR 136:729-733, 1981 13. Clouse ME, Ahmed R, Ryan RB, et al: Complications of long-term transbrachial hepatic arterial infusion chemotherapy. Am J RoentgenoI129:799-803, 1977 14. Clouse ME, Lee RGL, Duszlak EJ, et al: Hepatic artery embolization for metastatic endocrine-secreting tumors of the pancreas. Gastroenterology 85:1183-1186, 1983 15. Crafoord E, Frenckner P: New surgical treatment of varicose veins of the esophagus. Acta LaryngoI27:422-429, 1939 16. Ekelund L, Stigsson L, Jonsson N, et al: Transcatheter arterial embolization of normal livers and experimental hepatic tumors in rats. Acta Radiol Diagn 18:641-651, 1977
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17. Endoh F: Intra-arterial chemoembolization with albumin microspheres including mitomycin C in inoperable hepatic cancer. Nippon Geka Gakkai Zasshi 88:584-593, 1987 18. Fleig WE, Stange EF, Tue1j:enauer K, et aI: Emergency· endoscopic sclerotherapy for bleeding esophageal varices: A prospective study in patients not responding to balloon tamponade. Gastrointest Endosc 29:8-14, 1983 19. Galambos JT: Endoscopic sclerotherapy. Ann Intern Med 98:1009-1011, 1983 20. Hermann RE, Traul D: Experience with Sengstaken-Blakemore tube for bleeding esophageal varices. Surg Gynecol Obstet 130:879-885, 1970 21. Hirai K, Kawazoe Y, Yamashita K, et aI: Transcatheter arterial embolization for spontaneous rupture of hepatocellular carcinoma. Am J Gastroenterol 81:275-279, 1986 22. Hoevels J, Jaschke W: Control of hepatic tumor hemorrhage by transcatheter embolization with Ethibloc. Acta Radiol Diagn 29:15-19, 1988 23. Hsieh JS, Huang CJ, Huang YS, et aI: Intraperitoneal hemorrhage due to spontaneous rupture of hepatocellular carcinoma: Treatment by hepatic artery embolization. AJR 149:715-717, 1987 24. Itani K, Yoshikowa T, Tainaka K, et aI: Chemoembolization with degradable starch microspheres in malignant hepatic tumors. Gan to Kagaku Ryoho 14:388-395, 1987 25. Jander HP, Laws HL, Kogutt MS, et aI: Emergency embolization in blunt hepatic trauma. Am J Roentgenol 129:249-252, 1977 26. Johnson WC, Nabseth DC, Widrich WC, et aI: Bleeding esophageal varices: Treatment with vasopressin, transhepatic embolization and selective splenorenal shunting. Ann Surg 195:393-400, 1982 27. Johnson WC, Widrich WC, Ansell JE, et aI: Control of bleeding by vasopressin: A prospective randomized study. Ann Surg 188:369-376, 1977 28. Kanematsu T, Inokuchi K, Sugimachi K, et aI: Selective effects of lipiodized antitumor agents. J Surg Oncol 15:218-226, 1984 29. Kuntslinger F, Brunelle F, Chaumont P, et aI: Vascular occlusive agents. AJR 136:151156, 1981 30. Kuroda C, Iwasaki M, Tanaka T, et aI: Gallbladder infarction follOwing transcatheter arterial embolization: Angiographic study. Radiology 149:85-89, 1983 31. Lackgren G, Lorelius LE, Olsen L, et aI: Hematobilia in childhood. J Pediatr Surg 23:105-108, 1988 32. Lambeth W, Rubin BE: Nonoperative management of intrahepatic hemorrhage and hematoma follOwing blunt trauma. Surg Gynecol Obstet 148:507-511, 1979 33. Larson AW, Zweiban B, Gourdji M, et aI: Acute esophageal variceal sclerotherapy (EVS): Results of prospective control trial. Gastroenterology 86: 1153, 1984 34. Levin DC, Watson RC, Sos TA, et aI: Angiography in blunt hepatic trauma. Am J Roentgenol119:95-101, 1973 35. Lunderquist A, Vang J: Transhepatic catheterization and obliteration of the coronary vein in patients with portal hypertension and esophageal varices. N Eng) J Med 291:646649,1974 36. MacDougall BRD, Westaby D, Theodossi A, et aI: Increased long-term survival in variceal haemorrhage using injection sclerotherapy: Results of a controlled trial. Lancet 1:124127, 1982 37. Matsomoto T, Heisterkamp CA: Long-term study of isobutylcyanoacrylate tissue adhesive: Carcinogenicity and other untoward effects. Am Surg 35:825-827, 1969 38. Mays ET, Conti S, Fallahzedeh H, et aI: Hepatic artery ligation. Surgery 86:536-543, 1979 39. Michels NA: Blood Supply to the Upper Abdominal Organs with a Descriptive Atlas. Philadelphia, JB Lippincott, 1955 40. Miller FJ, Mineav ED: Transcatheter embolization: Major complications and their prevention. Cardiovasc Intervent Radiol 6:141-149, 1983 41. Mitchell SE, Shuman LS, Kaufman SL, et aI: Biliary catheter drainage complicated by hemobilia: Treatment by balloon embolotherapy. Radiology 157:645-652, 1985 42. Mitty HA, Warner RRP, Newman LH, et aI: Control of carcinoid syndrome with hepatic artery embolization. Radiology 155:623-626, 1985 43. Nakakuma K, Tashiro S, Hiraoka T, et aI: Hepatocellular carcinoma and metastatic cancer detected by iodized oil. Radiology 154:15-17, 1985 44. Nakamura H, Hashimoto T, Taguchi T, et aI: Chemoembolization. Gan to Kagaku Ryoho 14:1656-1663, 1987
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45. Ohishi H, Uchida H, Yoshimura H, et al: Hepatocellular carcinoma detected by iodized oil: Use of anticancer agents. Radiology 154:25-29, 1985 46. Ohmishi K, Sugita S, Nomura F, et al: Arterial chemoembolization with mitomycin C microcapsules followed by transcatheter arterial embolization for hepatocellular carcinoma. Am J Gastroenterol 82:876-879, 1987 47. Paguet KJ, Oberhammer E: Sclerotherapy of bleeding esophageal varices by means of endoscopy. Endoscopy 10:7-12, 1978 48. Pitcher J: Safety and effectiveness of the modified Sengstaken-Blakemore tube: A prospective study. Gastroenterology 61:291-298, 1971 49. Richardson A, Simmons K, Gutmann J, et al: Hepatic hematobilia: Nonoperative management in eight cases. Aust NZ J Surg 55:447-451, 1985 50. Rossi RL, Jenkins RL, Nielsen-Whitcomb FF: Management of complications of portal hypertension. Surg Clin North Am 65:231-262, 1985 51. Rubin BE, Katzen BT: Selective hepatic artery embolization to control massive hepatic hemorrhage after trauma. Am J Roentgenol 129:252-256, 1977 52. Sasaki Y, Imaoka S, Furtita M, et al: Regional therapy in the management of intrahepatic recurrence after surgery for hepatoma. Ann Surg 206:40-47, 1987 53. Sasaki Y, Imaoka S, Kasugai H, et al: A new approach to chemoembolization therapy for hepatoma using ethiodized oil, cisplatin and gelatin sponge. Cancer 60:1194-1203, 1987 54. Sclafani SJA, Nayaranaswamy T, Mitchell WG: Radiologic management of traumatic hepatic artery: Portal vein arteriovenous fistulae. J Trauma 21:576--580, 1981 55. Sclafani SJA, Shaftev GW, McCauley J, et al: Interventional radiology of hepatic trauma. J Trauma 24:256--262, 1984 56. Sivak MV Jr: Therapeutic endoscopy of the esophagus. Surg Clin North Am 62:807-820, 1982 57. Struyven J, Cremer M, Pirson P, et al: Post-traumatic bilhemia: Diagnosis and catheter therapy. AJR 138:746--747, 1982 58. Takayasu K, Moriyama N, Muramatsu Y, et al: Gallbladder infarction after hepatic artery embolization. AJR 144:135-138, 1985 59. Takayasu K, Shima Y, Muramatsu Y, et al: Hepatocellular carcinoma: Treatment with intraarterial iodized oil with and without chemotherapeutic agents. Radiology 162:345351, 1987 60. Trunkey DD, Shires GT, McClelland R: Management of liver trauma in 811 consecutive patients. Ann Surg 179:722-728, 1974 61. Walt AJ: The mythology of hepatic trauma: Or Babel revisited. Am J Surg 135:12-18, 1978 62. Walter JD, Passo BT, Cannon WB: Successful transcatheter embolic control of massive hematobilia secondary to liver biopsy. Am J Roentgenol 127:847-849, 1976 63. Widrich WC, Robbins AH, Nabseth DC: Transhepatic embolization of varices. Cardiovasc Intervent Radiol 3:298-307, 1980 64. Wirtanen GW: Percutaneous transbrachial artery infusion techniques. Am J Roentgenol 117:696--700, 1972 65. Yumoto Y, Jinno K, Tokuyama K, et al: Hepatocellular carcinoma detected by iodized oil. Radiology 154:19-24, 1985 66. Yune K, O'Connor KW, Klatte EL, et al: Ethanol thrombotherapy of esophageal varices: Further experience. AJR 144:1049-1053, 1985 Department of Radiology New England Deaconess Hospital 185 Pilgrim Road Boston, MA 02215
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Liver Surgery
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Hepatic Artery Embolization for Bleeding and Tumors
Melvin E. Clouse, MD*
TRAUMA
The liver is the third most commonly injured abdominal organ, surpassed only by the small bowel and spleen. The majority of injuries occur in male adolescents and young adults. The relative incidence of blunt or penetrating wounds depends on the geographic location and population sampled. Associated injuries are very common.' The injuries may be simple laceration, in which case manual compression or ligation will stop the bleeding, or deeper tears that require surgical hemostasis. Approximately 30 per cent of patients have more serious, deep lacerations or avulsion fractures of a portion of the liver. Most of the deaths are secondary to exsanguination in the latter group. 2, 34, 61 The fatality rate depends on the mechanism of injury and the degree of trauma. Blunt injuries are generally more damaging to the liver than a simple penetrating wound because of the shearing forces within the liver.2, 34, 60 Active hemorrhage at operation is associated with an increased mortality rate. Approximately 50 per cent of liver wounds will have stopped bleeding before surgery, but others continue to hemorrhage from small intrahepatic arteries and veins. 34, 38 Preoperative studies usually involve u1trasound or computed tomography (CT) because of their depiction of global anatomy and ability to evaluate the retroperitoneum and other abdominal organs. Preoperatively, arteriography is necessary to define arterial anatomy, as approximately 18 per cent of patients have a replaced right hepatic artery from the superior mesenteric artery, 39 In 1976, Cho and associates 9 showed that the hepatic artery could be safely embolized and suggested embolization as a treatment for liver trauma, The same year, Walter and coworkers 62 reported successful control of massive hematobilia after liver biopsy. Bass and Crosier' performed transcatheter hepatic artery occlusion for pseudoaneurysm soon thereafter. Since that time, hepatic artery embolization has become a standard treatment of liver hemorrhage from a variety of lesions, including those related to trauma, pseudoaneurysms (Fig. lA), hematobilia, or arteriovenous fistulas secondary to either trauma or iatrogenic injury. 25, 32, 51, 54, 55, 57 The technique can be performed safely, and embolization of the cystic artery and
*Professor,
Department of Radiology, Harvard Medical School, and Chairman, Department of Radiology, New England Deaconess Hospital, Boston, Massachusetts
Surgical Clinics of North America-Vol. 69. No.2, April 1989
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Figure 1. See legend on opposite page
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Figure 1. Massive upper gastrointestinal bleeding in a 16-year-old female patient. A, The hepatic arteriogram demonstrates a large pseudoaneurysm with contrast medium filling the common bile duct. B, Hepatic arteriogram 2 weeks after operative ligation of the right hepatic artery. Note filling of the aneurysm via intrahepatic collaterals (open arrow) from the middle hepatic artery branch and disruption of a branch of the right hepatic artery (solid arrow) producing the false aneurysm. C, Superior mesenteric artery injection opacifies a large collateral that is filling the aneurysm. D, Catheter within the false aneurysm via percutaneous transhepatic placement (arrow). Note coils in aneurysm and contrast filling the bile ducts. E, Hepatic artery injection 5 days after percutaneous embolization demonstrates continued filling of false aneurysm by intrahepatic collaterals. F, Superior mesenteric injection demonstrates filling of aneurysm from a second source. Note disruption of the artery (arrow). G, Hepatic artery injection after embolization with small Gelfoam pledgets soaked in absolute ethanol; note absence of filling in aneurysm. H, Superior mesenteric artery injection after embolization of collateral with small pledgets of Gelfoam soaked in absolute ethanol. There has been no further bleeding.
gallbladder necrosis can be avoided if large pledgets are used. The technique can be performed from the brachial or the femoral artery with 5-F or 6-F catheters. Embolic materials should be placed peripherally and as selectively as possible to avoid the problems of rebleeding from collateral vessels that occur with central occlusion whether it be by coils (radiologic) or ligatures (surgical). In most instances, surgical ligation of the hepatic artery should not be the primary therapy because the method can cause rebleeding of intrahepatic collateral vessels or collateral vessels in the hepatoduodenal ligament and inferior or superior phrenic arteries (Fig. IB and C). A variety of materials, including Gelfoam pledgets, polyvinyl alcohol, cyanoacrylates, and Gianturco coils, have been used. 3 • 4.11.12.29.37 Our technique has been to use Gelfoam pledgets soaked in alcohol to control bleeding from very small peripheral hepatic arteries. The pled gets should be cut to the approximate size of the appropriate feeding vessel, with pledgets ranging from 0.3 to 2.0 mm in diameter. For false aneurysms in a larger hepatic artery, Gianturco coils are very effective, because they can be placed distal as well as proximal to the false aneurysm, occluding both inflow and outflow and allowing for intrahepatic arterial collaterals to supply the embolized segment of the liver (Fig. 2). Performed judiciously, embolization can be done with little if any morbidity and mortality and is the preferred method for treating hemorrhage both preoperatively and postoperatively (approximately 3.5 per cent of patients will rebleed postoperatively"').
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Figure 2. Embolotherapy with Gianturco coils. A, Arterial phase of hepatic arteriography showing the placement of a biliary drainage catheter through the right hepatic artery. B, Hepatic arteriogram 5 days after left hepatectomy for metastatic tumor shows the false aneurysm of right hepatic artery. C, Hepatic arteriogram after the placement of Gianturco coils on either side of the false aneurysm. There was no further bleeding.
The treatment of hematobilia has usually required operative intervention. The problem is usually caused by blunt trauma, percutaneous biliary drainage or biopsy, postoperative hemorrhagic pancreatitis, abscesses, or vasculitis. B• 31. 41. 49 The pseudoaneurysm usually associated with hematobilia can be demonstrated by diagnostic celiac and superior mesenteric arteriography. It is much more difficult to control bleeding from a pseudoaneurysm if there has been operative ligation of the proper hepatic artery (Fig. 1). In these instances, a direct puncture of the aneurysm under fluoroscopic control, leaving a catheter directly in the false aneurysm, is the method of choice. Multiple Gianturco coils and other embolic material can then be placed directly into the false aneurysm to secure thrombosis. In those instances where occlusion of the pseudoaneurysm has not been accomplished primarily by direct puncture and placement of embolic material, embolization of collateral vessels can usually be accomplished by using superselective catheterization for those arteries in the hepatoduodenal ligaments primarily from the pancreatic arcade, collaterals from the left hepatic artery, or from the phrenic arteries. Lackgren and associates recently suggested that hepatic artery embolization is the treatment of choice for hematobilia in children. 31
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The selection of therapy-for bleeding in portal hypertension remains controversial and is based on multiple factors, including the basic pathogenic mechanism of portal hypertension in the individual patient, the status of the patient as defined by Child's classification, the elective or urgent nature of operation, the hemodynamic stability of the patient at the time of bleeding, clotting factors, the site of the block in the portal system, and the caliber and anatomic relations of those veins available for anastomosis in the portal system. Additional factors include the presence or severity of ascites, encephalopathy, age of patient, site of bleeding (esophageal or gastric), severity of associated hypersplenism, and operative and radiologic expertise available at a given institution. Shunting procedures achieve the best long-term control of bleeding, but they can precipitate encephalopathy. Nonshunting procedures do not induce encephalopathy but are usually associated with a high rate of rebleeding. The logical approach is to assess the patient for the above factors clinically. Selective splenic and mesenteric arteriography is performed with filming in the venous phase to determine the patency and location of the portal system prior to shunting or percutaneous transhepatic portography and sclerosis of varices. Selective hepatic arteriography excludes the presence of hepatoma. Inferior vena cavography is usually performed to determine the position of the left renal vein in relation to the splenic vein, and hepatic wedge pressures are measured to determine the portal venous pressure. Patients who present with episodes of acute bleeding are usually treated initially with medical therapy including catheter tamponade and acute sclerotherapy by endoscopy. If the patient fails to respond, or if bleeding recurs, further therapy is required. Rebleeding after balloon tamponade appears in approximately 40 to 50 per cent of patients. 20, 48 The endoscopic injection of esophageal varices for sclerotherapy is an excellent method to control acute bleeding with a low morbidity and mortality rate (10 to 15 per cent). 15, 18, 19, 33, 36: 47,"",56 Complications include rebleeding and stricture related to the sclerotherapeutic agent. Temporizing and control of immediate bleeding can be achieved with intravenous or intra-arterial administration of vasopressin (Pitressin) in 56 to 58 per cent of the patients. 10, 26, 27 A more invasive technique but short of surgery is percutaneous transhepatic obliteration of esophageal varices by injecting sclerosing agents and embolic material into the coronary or short gastric veins. 5, 26, 35, 63," Widrich and Yune and their associates report an initial success rate of 70 to 95 per cent, with control of bleeding for 1 to 30 months. 63, . . Failures were related to ascites, severely cirrhotic liver, thrombosis of the portal vein, and difficult anatomy. However, the significant rebleeding rate and incidence of complications have diminished earlier enthusiasm for this technique. Nevertheless, in skilled hands and in well-selected patients, it can be helpful as a temporizing measure prior to various operative procedures for decompressing the portal system. In these instances; the portal vein is catheterized percutaneously and the catheter passed into the coronary vein with the injection of embolic material. We use absolute alcohol, Gelfoam pledgets soaked in absolute alcohol, or 3 per cent sodium tetradecyl sulfate (Sotradecol) followed by occlusion of the coronary vein with Gianturco coils. The short gastric veins can also be catheterized and injected to decompress esophageal varices temporarily, The objective is to occlude large and multiple small veins that are inflow channels to esophageal veins in the cardioesophageal area of the stomach (Fig. 3).
TUMORS Therapeutic arterial embolization of abdominal neoplasms, although still experimental, has become an integral part of the therapy for primary and secondary
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Figure 3. Obliteration of esophageal varices. A, Percutaneous transhepatic portal venogram; note large esophageal varices and spontaneous splenorenal venous shunting. B, Portal venogram after occlusion of varices with absolute ethanol and Gelfoam pledgets soaked in absolute ethanol with coil occlusion of the coronary vein.
liver neoplasms. Devascularization of hepatic neoplasms was initially achieved using Gelfoam pledgets and stainless steel Gianturco coilsY More recently, Chuang and associates have used 0.25-mm Ivalon particles for more peripheral embolization. 12 Our technique for hepatic arterial embolization is a modification of the Lunderquist technique using Gelfoam powder soaked in alcohol and mixed to a thick viscous consistency, which permits easy injection and exquisite control of the materiaP6 (A. Lunderquist; personal communication). The catheterization is through the left brachial artery. The catheter can be left in place for re-embolization and check of the results. 13. 64 A complete arterial map is obtained to determine anatomic variants and to locate the bulk of tumor tissue as well as to determine the patency of the portal system. The portal vein is the conduit for almost all metastatic neoplasms from the gastrointestinal tract to the liver and supplies 80 per cent of the required oxygen and nutrients of the normal liver. Both primary and metastatic hepatic neoplasms derive their blood supply and nourishment from the arterial circuit. Because of this differentiated perfusion, the hepatic artery is an ideal route for selective delivery of either chemotherapeutic agents or embolic material. 7 Only 80 per cent of the population is amenable to selective hepatic artery embolization, as approximately 18 per cent have the right hepatic artery arising from the superior mesenteric artery.39 In these instances, the replaced right hepatic artery can be catheterized via the transfemoral route and occluded with a Gianturco coil (Fig. 4). In those instances in which the left gastric artery arises from the left hepatic artery or the left hepatic artery supplies branches to the stomach, selective catheterization and occlusion of the gastric branch can be achieved prior to em bolization of the peripheral hepatic arteries. By this method, one can gain control of a single artery that supplies the entire liver, thereby accomplishing control of the hepatic blood flow. In certain instances, the gastroduodenal artery must be occluded with Gianturco coils to allow safe embolization of the hepatic artery without reflux of embolic material into either the right gastric artery or the duodenum or pancreas (Fig. 5). The rationale for peripheral artery embolization with Gelfoam is that primary
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Figure 4. Hepatic arteriography on a 44-year-old woman with colon cancer metastases to the liver. A, Right hepatic artery injection replaced from the superior mesenteric artery. B, Note coil in right hepatic artery replaced from the superior mesenteric artery (arrow). C, Injection of contrast medium into the common hepatic artery from the celiac trunk shows filling of arteries of both lobes of the liver.
and secondary tumors derive their blood supply and nutrition from the arterial circuit. 7 It is imperative to occlude small arteries and prevent re-establishment of collateral flow, which occurs with proper hepatic artery ligation whether by operative or radiologic means. The theoretical disadvantage of using Gelfoam powder is that it may be resorbed within 7 to 21 days.4 If the hepatic artery becomes recanalized, however, it serves as an excellent conduit for re-embolization. The indications for hepatic arterial embolization are unresectable tumor, no other effective treatment, and treatment failure with intra-arterial or intravenous chemotherapy or radiation. Immediately after embolization, no flow in the embolized hepatic artery should be demonstrated by angiography or radionuclide flow study. Computed tomography scanning is not helpful during the first 24 hours because tumor deposits will contain residual contrast medium from the embolization procedure. The CT follow-up is important and is performed at days 3 and 7 after embolization. The presence of gas
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Figure 5. Celiac artery injection after coil placement in the gastroduodenal artery (arrow). Note collaterals from dorsal artery filling the gastroduodenal and gastroepiploic artery.
within the tumor on day 2 does not indicate an abscess but rather excellent embolization and tumor necrosis; gas is almost always resorbed after 7 days. Bleeding time, prothrombin time, partial thromboplastin time, platelet count, serum uric acid, and a complete liver profile including bilirubin, alkaline phosphatase, aspartate transferase, and lactate dehydrogenase are obtained before embolization, daily for the first 3 days after embolization, and every other day for the next 9 days. To prevent urate nephropathy and renal failure after embolization, the patients are routinely prepared with allopurinol for 48 hours and given bicarbonates for alkalinization of the urine. Liver function tests become markedly elevated at 24 to 48 hours, peak at 72 hours, and return to pre-embolic levels after 6 to 9 days. The clotting factors have remained normal in all of our patients. Serum uric acid must be followed carefully because it may become markedly elevated secondary to tumor necrosis. Patients are therefore kept on allopurinol, probenecide, and diuretics. The possibility of gallbladder necrosis exists because the cystic artery arises from the hepatic artery. Gallbladder necrosis is probably more common than reported. 30, 40, 58 Gallbladder ultrasound examination should be performed prior to and 24 and 48 hours after embolization. If there is thickening of the gallbladder wall, a 99mTc-iminodiacetic acid scan should be performed and the patient followed closely for sepsis. For this reason, the patients are prepared approximately 3 hours prior to embolization with an antibiotic such as cefoperazone that is excreted in the bile. Complications may also arise from embolization to the left gastric artery and pancreas (Fig. 6). Postembolization syndrome consists of pain in the right upper quadrant, appearing almost immediately after embolization and perhaps lasting as long as 3 days, that requires intravenous meperidine or morphine every 3 to 6 hours. Nausea and vomiting may be pronounced but can be controlled with intramuscular prochlorperazine. Embolization for hypovascular tumor deposits such as colon cancer metastases, the most common metastatic tumor, is no longer performed at our institution, as the median survival time is not sufficiently increased. We do currently embolize the very vascular metastatic tumors and hepatomas. The most dramatic beneficial
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Figure 6. Hepatic artery embolization. A, CT scan in 56-year-old man 7 days after embolization for metastatic carcinoid tumor. Note gas in tumor consistent with extensive necrosis. B, -Tc-iminodiacetic acid scan 14 days after embolization because of pain in right upper quadrant and fever. The scan is positive for gallbladder necrosis and cholecystitis, with no filling of gallbladder even after 21 hours. C, Ultrasound scan of gallbladder showing thickened wall consistent with necrosis. Necrotic gallbladder removed at operation. D, Capillary phase of hepatic arteriogram 2 years later shows small tumor deposits throughout liver. Note the avascular area in the right upper lobe from embolization 2 years previously. E, CT scan prior to second embolization. Note the avascular area, which has diminished in size, corresponding to tumor embolized 2 years previously. F, Hepatic artery injection after second embolization showing absent arterial How to liver.
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Figure 7. Celiac arteriography after hepatic artery embolization in 55-year-old man with carcinoid tumor metastatic to the liver. Note extensive collaterals from pancreatic bed and hepatoduodenalligament (A), with filling of multiple metastatic deposits in the capillary phase (B).
effect occurs in the malignant hormone-secreting tumors, where the systemic effect of the hormone is more devastating than the tumor bulk. I. 14.42 We are currently following eight patients who have had embolization from one to four times over a period of 6 years, with excellent results. Embolization should be performed before collateral flow has been established because it may be impossible to superselect and interrupt collateral blood flow to the tumor on subsequent occasions if collaterals are well established and the main hepatic artery does not recanalize (Fig. 7). More recently, numerous articles have demonstrated the importance of chemo-
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Figure 8. CT scans of 72-year-old man with hepatoma. A, Superior segment of right lobe of liver (arrow). B, Completely replaced lateral segment of left lobe. C, Postembolization of liver with 10 ml of Ethiodol and 35 mg of doxorubicin to the lateral segment of left lobe and 5 ml of Ethiodol and 10 mg of doxorubicin to the superior segment of right upper lobe. D and E, Six days after embolization; note Ethiodol and gas in segment of right upper and left lobes consistent with tumor necrosis.
embolization, especially for hepatomas, using a variety of chemotherapeutic agents such as doxorubicin, mitomycin C, and cisplatin. 17• 24. 28. 44, 46, 52, 53, 59 The rationale is to decrease blood flow through the tumor, leaving the chemotherapeutic agent in contact with tumor cells for a longer time. This is accomplished by mixing the chemotherapeutic agent with Ethiodol followed by embolization with Gelfoam pledgets or powder. Ethiodol has also been reported to demonstrate angiographically small metastatic deposits in the liver. 43, 45, 65 Chemoembolization has been accom-
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plished without further morbidity and mortality and with significant improvement in 1- and 2-year survival rates (Fig. 8). TUMOR HEMORRHAGE Control of hepatic tumor hemorrhage by transcatheter embolization can be accomplished using a variety of agents such as Ethibloc, polyvinyl alcohol, or Gelfoam powder soaked on pads in alcohol. Excellent results have been reported from various institutions without increases in morbidity and mortality rates. 21-23 Hemorrhage is usually related to spontaneous rupture of hepatocellular carcinoma, which mayor may not erode through the liver capsule with subcapsular bleeding or frank hemorrhage into the peritoneal cavity. The objective in these instances is to prevent exsanguination, but the procedure may be combined with therapeutic chemoembolization. There has not been an increased morbidity relating to embolization to control bleeding. In a series of 17 patients reported by Hsieh and associates,23 11 patients died of their cancers at 16 to 386 days after embolization, and three patients were alive at 3, 7, and 15 months. There was no serious complication related to embolization.
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45. Ohishi H, Uchida H, Yoshimura H, et al: Hepatocellular carcinoma detected by iodized oil: Use of anticancer agents. Radiology 154:25-29, 1985 46. Ohmishi K, Sugita S, Nomura F, et al: Arterial chemoembolization with mitomycin C microcapsules followed by transcatheter arterial embolization for hepatocellular carcinoma. Am J Gastroenterol 82:876-879, 1987 47. Paguet KJ, Oberhammer E: Sclerotherapy of bleeding esophageal varices by means of endoscopy. Endoscopy 10:7-12, 1978 48. Pitcher J: Safety and effectiveness of the modified Sengstaken-Blakemore tube: A prospective study. Gastroenterology 61:291-298, 1971 49. Richardson A, Simmons K, Gutmann J, et al: Hepatic hematobilia: Nonoperative management in eight cases. Aust NZ J Surg 55:447-451, 1985 50. Rossi RL, Jenkins RL, Nielsen-Whitcomb FF: Management of complications of portal hypertension. Surg Clin North Am 65:231-262, 1985 51. Rubin BE, Katzen BT: Selective hepatic artery embolization to control massive hepatic hemorrhage after trauma. Am J Roentgenol 129:252-256, 1977 52. Sasaki Y, Imaoka S, Furtita M, et al: Regional therapy in the management of intrahepatic recurrence after surgery for hepatoma. Ann Surg 206:40-47, 1987 53. Sasaki Y, Imaoka S, Kasugai H, et al: A new approach to chemoembolization therapy for hepatoma using ethiodized oil, cisplatin and gelatin sponge. Cancer 60:1194-1203, 1987 54. Sclafani SJA, Nayaranaswamy T, Mitchell WG: Radiologic management of traumatic hepatic artery: Portal vein arteriovenous fistulae. J Trauma 21:576--580, 1981 55. Sclafani SJA, Shaftev GW, McCauley J, et al: Interventional radiology of hepatic trauma. J Trauma 24:256--262, 1984 56. Sivak MV Jr: Therapeutic endoscopy of the esophagus. Surg Clin North Am 62:807-820, 1982 57. Struyven J, Cremer M, Pirson P, et al: Post-traumatic bilhemia: Diagnosis and catheter therapy. AJR 138:746--747, 1982 58. Takayasu K, Moriyama N, Muramatsu Y, et al: Gallbladder infarction after hepatic artery embolization. AJR 144:135-138, 1985 59. Takayasu K, Shima Y, Muramatsu Y, et al: Hepatocellular carcinoma: Treatment with intraarterial iodized oil with and without chemotherapeutic agents. Radiology 162:345351, 1987 60. Trunkey DD, Shires GT, McClelland R: Management of liver trauma in 811 consecutive patients. Ann Surg 179:722-728, 1974 61. Walt AJ: The mythology of hepatic trauma: Or Babel revisited. Am J Surg 135:12-18, 1978 62. Walter JD, Passo BT, Cannon WB: Successful transcatheter embolic control of massive hematobilia secondary to liver biopsy. Am J Roentgenol 127:847-849, 1976 63. Widrich WC, Robbins AH, Nabseth DC: Transhepatic embolization of varices. Cardiovasc Intervent Radiol 3:298-307, 1980 64. Wirtanen GW: Percutaneous transbrachial artery infusion techniques. Am J Roentgenol 117:696--700, 1972 65. Yumoto Y, Jinno K, Tokuyama K, et al: Hepatocellular carcinoma detected by iodized oil. Radiology 154:19-24, 1985 66. Yune K, O'Connor KW, Klatte EL, et al: Ethanol thrombotherapy of esophageal varices: Further experience. AJR 144:1049-1053, 1985 Department of Radiology New England Deaconess Hospital 185 Pilgrim Road Boston, MA 02215
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