159
FALSE CAROTID ANEURYSM
affords cerebral protection in the event of the subsequent development of contralateral occlusive extracranial cerebrovascular disease.
Acknowledgement
The authors thank Dr Raymond Garrick FRACP, neurologist, for his assistance in the preparation of the manuscript. References I. LORD R. S. A. (1986) Surgery of Occlusive Cerebrovascular Disease. C. V. Mosby. Missouri. 2. WELLING R. E., TAHAA., GOELT. er 01. (1983) Extracranial carotid artery aneurysms. Surgery 93, 319-23. H., WHEELER W. G . . NOONG.P. & D E 3. MCCOLLUMC. BAKEYM. E. (1979) Aneurysms of the extracranial carotid artery. Twenty-one years experience. Amer. J. Surg. 137, 196-200. 4. RHODE~ E. L., STANLEY J. C., HOFFMAN G. L., CRONENWAIT J. L. & FRYW. J. (1976) Aneurysms of the extracranial carotid mries. Arch. Surg. 111. 339-43. W. K. & HAYS R. J. (1972) False 5 . EHRENFELD
Ausr. N.Z. J. Surg. 1991.61.
6.
7. 8. 9. 10.
11.
12. 13. 14.
aneurysms afkr carotid endarterectomy. Arch. Sure. 104,288-91. SMITHR. B. 111, PERDUE G. D. JR, COLLIERR. H.er al. (1970) Post-operative false aneurysms of the carotid artery. Amer. Surg. 36, 335-41. L.C.. MOOREW. S. & HALLA. D. (1%9) BUSCAGLIA False aneurysm after carotid endarterectomy. JAMA 209. 1529. ANDERSON W. A. D. & S c m T. M. (1972) Synopsis of Parhology. 8th edn. C. V. Mosby, St Louis. PEYMAN G. A. (1980) Principles and Practice of Ophthalmology, Vol. 2. W. B. Saunders, Philadelphia. PLUMF. & POSNER J. B. (1980) The Diagnosis of Srupor and Coma. 3rd edn. F. A. Davis, USA. W. K., Lusev R. J.. F ~ L L.L D., EHRENFELD STOREYR. J. & WYUEE. J. (1982) Carotid plaque haemorrhage: its role in production of cerebral ischaemia. Arch. Surg. 117, 1479. DAVIS1.. Fmm R. S. & GAMELLIR. L. (1987) Clinical Surgery. C . V. Mosby, Missouri. SALMELA K. & AHONEN J. (1981) The effect of methylpdnisolone and vitamin A on healing tissue (I). Acra Chir. Scud. 147, 307. COOPER A. (1836) Account of the first successful operation performed on the common carotid artery for aneurysm in the year of 1808 with postmortem examination in the year 1821. Guys Hosp. Rep. 1,53.
159-161
BLEEDING CYSTIC ARTERY ANEURYSM: RARE CAUSE OF HAEMOBlLlA A. READ.*M. LANNAN,~ S. T. CHOU*AND 0. HENNESSY~ Departments of *Surgery, ?Radiology and $Pathology.Repatriation General Hospital, Heidelberg West, Victoria A case of a bleeding cystic artery aneurysm which presented with recurrent episodes of haemobilia is presented. The diagnosis was established at emergency visceral angiography and cholecystectomy was curative.
Key words: aneurysm, cystic artery, haemobilia.
Introduction
The majority of cases of upper gastrointestinal haemonhage are caused by peptic ulcer disease, bleeding varices and malignancy. Haemohage secondary to haemobilia is uncommon, but in recent years has been diagnosed and reported with increased frequency. Cystic artery aneurysms are
rare. When present, the diagnosis has usually been established at surgery or at post-mortem. These aneurysms may present with massive haemorrhage or be more obscure with episodes of haematemesis and or melaena. Case history A 7 1 year old woman with no significant medical or
Correspondence: Dr 0. Hennessy. Department of Radiology. Repatriation Hospital. Heidelberg West, Vic. 3081. Australia. Accepted for publication 16 May 1990.
surgical history presented to her local hospital with a I-week history of nausea, vomiting and increasing epigastric pain. Two days prior to presenting she
READ ET AL.
160
had become jaundiced, with dark urine and pale stools. Her liver biochemistry revealed a bilirubin of 124 pmoVL, an alkaline phosphatase of 347pmoV L, alanine aminotransferase of 137 pmol/L and a y glucuronyl of 823 pmoUL. An abdominal ultrasound showed multiple gallstones within the gall-bladder; the common bile duct was 9 mm but no calculi were seen in the duct. Cholecystectomy was planned but on the day prior to surgery the patient passed melaena stools and had a small haematemesis of dark blood. Gastroscopy revealed a small duodenal ulcer. The patient was referred to this hospital for endoscopic retrograde cholangiopancreatography (ERCP), On admission the patient was jaundiced. Her haemoglobin was 9.4. At ERCP the gastric antrum and first part of the duodenum were normal, but the papilla and intramural common bile duct were grossly distended and a clot was seen extruding from the orifice of the papilla. The cholangiogram showed marked dilatation of intra- and extrahepatic bile ducts which contained irregular and ill-defined filling defects. Sphincterotomy was followed by the release of a large amount of clotted blood and then by a gush of fresh blood from within the common bile duct (CBD). Urgent visceral angiography was performed. A selective hepatic study showed an area of extravasation of contrast from the cystic artery filling the
Fig. 1. Selective hepatic angiogram showing a 2cm 'blush' of contrast within the gall-bladder lumen. This is compatible with bleeding from the cystic artery. No aneurysm was identified.
lumen of the gall-bladder (Fig. 1). The hepatic arteries and the superior mesenteric artery were otherwise normal. The patient went to theatre. Through a Kocher's incision a thick-walled gall-bladder containing several calculi and associated with marked fibrosis about the porta hepatis was removed. Operative cholangiography was not performed but the CBD was flushed with saline via the cystic duct. Postoperatively the patient made an uneventful recovery, her liver function tests returning to normal over a period of 2 weeks. Macroscopic examination of the gall-bladder showed it to be thick-walled and containing a I .Ocm cystic haemorrhagic mass within its lumen and immediately above the cystic duct. Microscopy revealed chronic inflammation, the wall of the gall-bladder being much thickened by hypertrophy, fibrosis and intramural abscesses. The most striking feature was an aneurysm arising in a deep channel of the cystic artery and rupturing into the gall-bladder lumen. This corresponded to the cystic mass previously noted macroscopically. Other branches of the cystic artery showed features of endarteritis obliterans. Discussion Haemobilia once considered rare has now been reported with increased frequency as a cause of upper gastrointestinal bleeding. The majority of cases are secondary to trauma, which may occur after surgery or following interventional procedures on the hepatobiliary tree. In these situations the haemobilia is caused by a hepatic artery aneurysm that communicates with the bile ducts. Cystic artery aneurysms are rare, causative factors including cholelithiasis, gall-bladder tumours (adenomas, papillomas, sarcomas), heterotopic gastric mucosa in the gall-bladder or direct ulceration from an adjacent duodenal perforation. Haemorrhage is rare in gall-bladder carcinoma. In gallstone disease, coexisting cholangitis increases the risk of haemorrhage from the hyperaemic mucosa; haemobilia is frequent in these cases.' The diagnosis of haemobilia may be difficult and delayed. The classic features of gastrointestinal haemorrhage, biliary colic and jaundice may not be present in each case. Haemorrhage into the biliary tree can be slow, manifesting as melaena and anaemia or be massive, causing shock. In the evaluation of haemobilia the investigations most likely to be of value are ERCP and selective visceral angiography. At ERCP, blood may be identified coming from the biliary tree, and multiple filling defects as a result of clot formation may occupy the gall-bladder and/or the bile ducts. Ideally, angiography should be carried out when the patient is actively bleeding. Selective hepatic
161
BLEEDING CYSTIC ARTERY ANEURYSM
artery catheterization is required to demonstrate aneurysms arising from the hepatic or cystic arteries. The management of a bleeding cystic artery aneurysm or bleeding from the gall-bladder is surgery. Percutaneous embolization of the cystic artery, even if technically possible, would most likely result in gall-bladder infarction. On the other hand, when the site of haemorrhage is from a hepatic artery, embolization at the time of diagnostic angiography has been shown to be succe~sful.~*~
Aust.
References 1. Smmoul P., Slw;esse~F. & Muwovm V. (1984)
Hepatic haemobilia: Haemorrhage from the intrahepatic biliary tract. World J . Surg. 8,41-50. 2. CZERNIAK C., THOMPSON J. N. & HEMMINOWAY A. P. er. al. (1988) Haemobiilia: A disease in evolution. Arch. Surg. 123,718-21. 3. KULEYC.J.,HEMMMOWAYA.P.,MCP~~~NG.A.. ALuscm D. J. & BWART L. H. (1983) Non-surgical management of pt-cholecystectomy haemobilia. Brir. J . Surg. 70, 502-4.
N.Z.J . Surg. 1991.61, 161-162
ENDOSCOPIC MANAGEMENT OF GALLSTONE PANCREATITIS FRANK
c. C H E N , ’ DAVIDA. HILL,2 THOMASB. HUGH,3 BEI L1: St
AND ALANP. MEAGHER,5
Vincent’s Hospital, Darlinghurst, New South Wales
The use of minimally invasive techniques of removing gallstones, and the gall-bladder, is an attractive option for patients who may be severely ill with pancreatitis. We describe here a patient with gallstone pancreatitis who was managed completely by endoscopic techniques consisting of endoscopic retrograde cholangiopancreatography (ERCP) followed by laparoscopic cholecystectomy. Key words: ERCP, gallstone pnncreatitb, lapamcopic chdecystectomy.
Introduction It is now generally accepted that gallstone pancreatitis is caused by obstruction of the ampulla of Vater by a stone, which has usually migrated from the gall-bladder.’ Most authors advocate that cholecystectomy and any necessary procedures to remove common bile duct (CBD) stones should be performed during the initial hospital admission, in order to minimize the risk of further attacks of pancreatiti~.’.~However, there is disagreement about the exact timing of surgical intervention in this condition. In a prospective randomized trial of early (48 h) open operation in the treatment of gallstone pancreatitis, morbidity and mortality were significantly greater in the group of patients subjected to early ~peration.~ Early intervention in the form of endoscopic retrograde cholangiopancreatography (ERCP), sphincterotomy and extraction of stones from the
’
MB, BS; Surgical Registrar. zFRCS. FRCS (Ed.). FRACS; Senior Lecturer in Surgely. ’FRCS. FRACS; Visiting Surgeon. 4MD:Surgical Fellow. ’FRACS; Surgical Registrar. Correspondence:Dr Thomas B. Hugh, Suite 1006, St Vincent’s Clinic, 438 Victoria Street. Darlinghurst. NSW 2010, Australia. Accepted for publication 20 September 1990.
CBD have been suggested as methods of reducing the severity and duration of an attack of gallstone pancreatiti~.~ Unfortunately, this form of management leaves the patient exposed to the risk of further pancreatitis should another stone enter the CBD. The early use of minimally invasive techniques of removing all gallstones, as well as the gallbladder, is therefore an attractive option for patients who may be severely ill with pancreatitis. We describe here a patient with gallstone pancreatitis who was managed completely by endoscopic techniques consisting of ERCP followed by laparoscopic cholecystectomy .
case report A 44 year old man was admitted to hospital as an emergency on 24 July 1990with severe generalized abdominal pain, which radiated to the back and was accompanied by nausea. Apart from occasional ‘indigestion’, for which he took antacids, and a history of left renal colic, he had otherwise been previously well. He drank alcohol rarely and in small quantities. Examination on admission showed him to be distressed and tachycardic. There was generalized
FALSE CAROTID ANEURYSM
affords cerebral protection in the event of the subsequent development of contralateral occlusive extracranial cerebrovascular disease.
Acknowledgement
The authors thank Dr Raymond Garrick FRACP, neurologist, for his assistance in the preparation of the manuscript. References I. LORD R. S. A. (1986) Surgery of Occlusive Cerebrovascular Disease. C. V. Mosby. Missouri. 2. WELLING R. E., TAHAA., GOELT. er 01. (1983) Extracranial carotid artery aneurysms. Surgery 93, 319-23. H., WHEELER W. G . . NOONG.P. & D E 3. MCCOLLUMC. BAKEYM. E. (1979) Aneurysms of the extracranial carotid artery. Twenty-one years experience. Amer. J. Surg. 137, 196-200. 4. RHODE~ E. L., STANLEY J. C., HOFFMAN G. L., CRONENWAIT J. L. & FRYW. J. (1976) Aneurysms of the extracranial carotid mries. Arch. Surg. 111. 339-43. W. K. & HAYS R. J. (1972) False 5 . EHRENFELD
Ausr. N.Z. J. Surg. 1991.61.
6.
7. 8. 9. 10.
11.
12. 13. 14.
aneurysms afkr carotid endarterectomy. Arch. Sure. 104,288-91. SMITHR. B. 111, PERDUE G. D. JR, COLLIERR. H.er al. (1970) Post-operative false aneurysms of the carotid artery. Amer. Surg. 36, 335-41. L.C.. MOOREW. S. & HALLA. D. (1%9) BUSCAGLIA False aneurysm after carotid endarterectomy. JAMA 209. 1529. ANDERSON W. A. D. & S c m T. M. (1972) Synopsis of Parhology. 8th edn. C. V. Mosby, St Louis. PEYMAN G. A. (1980) Principles and Practice of Ophthalmology, Vol. 2. W. B. Saunders, Philadelphia. PLUMF. & POSNER J. B. (1980) The Diagnosis of Srupor and Coma. 3rd edn. F. A. Davis, USA. W. K., Lusev R. J.. F ~ L L.L D., EHRENFELD STOREYR. J. & WYUEE. J. (1982) Carotid plaque haemorrhage: its role in production of cerebral ischaemia. Arch. Surg. 117, 1479. DAVIS1.. Fmm R. S. & GAMELLIR. L. (1987) Clinical Surgery. C . V. Mosby, Missouri. SALMELA K. & AHONEN J. (1981) The effect of methylpdnisolone and vitamin A on healing tissue (I). Acra Chir. Scud. 147, 307. COOPER A. (1836) Account of the first successful operation performed on the common carotid artery for aneurysm in the year of 1808 with postmortem examination in the year 1821. Guys Hosp. Rep. 1,53.
159-161
BLEEDING CYSTIC ARTERY ANEURYSM: RARE CAUSE OF HAEMOBlLlA A. READ.*M. LANNAN,~ S. T. CHOU*AND 0. HENNESSY~ Departments of *Surgery, ?Radiology and $Pathology.Repatriation General Hospital, Heidelberg West, Victoria A case of a bleeding cystic artery aneurysm which presented with recurrent episodes of haemobilia is presented. The diagnosis was established at emergency visceral angiography and cholecystectomy was curative.
Key words: aneurysm, cystic artery, haemobilia.
Introduction
The majority of cases of upper gastrointestinal haemonhage are caused by peptic ulcer disease, bleeding varices and malignancy. Haemohage secondary to haemobilia is uncommon, but in recent years has been diagnosed and reported with increased frequency. Cystic artery aneurysms are
rare. When present, the diagnosis has usually been established at surgery or at post-mortem. These aneurysms may present with massive haemorrhage or be more obscure with episodes of haematemesis and or melaena. Case history A 7 1 year old woman with no significant medical or
Correspondence: Dr 0. Hennessy. Department of Radiology. Repatriation Hospital. Heidelberg West, Vic. 3081. Australia. Accepted for publication 16 May 1990.
surgical history presented to her local hospital with a I-week history of nausea, vomiting and increasing epigastric pain. Two days prior to presenting she
READ ET AL.
160
had become jaundiced, with dark urine and pale stools. Her liver biochemistry revealed a bilirubin of 124 pmoVL, an alkaline phosphatase of 347pmoV L, alanine aminotransferase of 137 pmol/L and a y glucuronyl of 823 pmoUL. An abdominal ultrasound showed multiple gallstones within the gall-bladder; the common bile duct was 9 mm but no calculi were seen in the duct. Cholecystectomy was planned but on the day prior to surgery the patient passed melaena stools and had a small haematemesis of dark blood. Gastroscopy revealed a small duodenal ulcer. The patient was referred to this hospital for endoscopic retrograde cholangiopancreatography (ERCP), On admission the patient was jaundiced. Her haemoglobin was 9.4. At ERCP the gastric antrum and first part of the duodenum were normal, but the papilla and intramural common bile duct were grossly distended and a clot was seen extruding from the orifice of the papilla. The cholangiogram showed marked dilatation of intra- and extrahepatic bile ducts which contained irregular and ill-defined filling defects. Sphincterotomy was followed by the release of a large amount of clotted blood and then by a gush of fresh blood from within the common bile duct (CBD). Urgent visceral angiography was performed. A selective hepatic study showed an area of extravasation of contrast from the cystic artery filling the
Fig. 1. Selective hepatic angiogram showing a 2cm 'blush' of contrast within the gall-bladder lumen. This is compatible with bleeding from the cystic artery. No aneurysm was identified.
lumen of the gall-bladder (Fig. 1). The hepatic arteries and the superior mesenteric artery were otherwise normal. The patient went to theatre. Through a Kocher's incision a thick-walled gall-bladder containing several calculi and associated with marked fibrosis about the porta hepatis was removed. Operative cholangiography was not performed but the CBD was flushed with saline via the cystic duct. Postoperatively the patient made an uneventful recovery, her liver function tests returning to normal over a period of 2 weeks. Macroscopic examination of the gall-bladder showed it to be thick-walled and containing a I .Ocm cystic haemorrhagic mass within its lumen and immediately above the cystic duct. Microscopy revealed chronic inflammation, the wall of the gall-bladder being much thickened by hypertrophy, fibrosis and intramural abscesses. The most striking feature was an aneurysm arising in a deep channel of the cystic artery and rupturing into the gall-bladder lumen. This corresponded to the cystic mass previously noted macroscopically. Other branches of the cystic artery showed features of endarteritis obliterans. Discussion Haemobilia once considered rare has now been reported with increased frequency as a cause of upper gastrointestinal bleeding. The majority of cases are secondary to trauma, which may occur after surgery or following interventional procedures on the hepatobiliary tree. In these situations the haemobilia is caused by a hepatic artery aneurysm that communicates with the bile ducts. Cystic artery aneurysms are rare, causative factors including cholelithiasis, gall-bladder tumours (adenomas, papillomas, sarcomas), heterotopic gastric mucosa in the gall-bladder or direct ulceration from an adjacent duodenal perforation. Haemorrhage is rare in gall-bladder carcinoma. In gallstone disease, coexisting cholangitis increases the risk of haemorrhage from the hyperaemic mucosa; haemobilia is frequent in these cases.' The diagnosis of haemobilia may be difficult and delayed. The classic features of gastrointestinal haemorrhage, biliary colic and jaundice may not be present in each case. Haemorrhage into the biliary tree can be slow, manifesting as melaena and anaemia or be massive, causing shock. In the evaluation of haemobilia the investigations most likely to be of value are ERCP and selective visceral angiography. At ERCP, blood may be identified coming from the biliary tree, and multiple filling defects as a result of clot formation may occupy the gall-bladder and/or the bile ducts. Ideally, angiography should be carried out when the patient is actively bleeding. Selective hepatic
161
BLEEDING CYSTIC ARTERY ANEURYSM
artery catheterization is required to demonstrate aneurysms arising from the hepatic or cystic arteries. The management of a bleeding cystic artery aneurysm or bleeding from the gall-bladder is surgery. Percutaneous embolization of the cystic artery, even if technically possible, would most likely result in gall-bladder infarction. On the other hand, when the site of haemorrhage is from a hepatic artery, embolization at the time of diagnostic angiography has been shown to be succe~sful.~*~
Aust.
References 1. Smmoul P., Slw;esse~F. & Muwovm V. (1984)
Hepatic haemobilia: Haemorrhage from the intrahepatic biliary tract. World J . Surg. 8,41-50. 2. CZERNIAK C., THOMPSON J. N. & HEMMINOWAY A. P. er. al. (1988) Haemobiilia: A disease in evolution. Arch. Surg. 123,718-21. 3. KULEYC.J.,HEMMMOWAYA.P.,MCP~~~NG.A.. ALuscm D. J. & BWART L. H. (1983) Non-surgical management of pt-cholecystectomy haemobilia. Brir. J . Surg. 70, 502-4.
N.Z.J . Surg. 1991.61, 161-162
ENDOSCOPIC MANAGEMENT OF GALLSTONE PANCREATITIS FRANK
c. C H E N , ’ DAVIDA. HILL,2 THOMASB. HUGH,3 BEI L1: St
AND ALANP. MEAGHER,5
Vincent’s Hospital, Darlinghurst, New South Wales
The use of minimally invasive techniques of removing gallstones, and the gall-bladder, is an attractive option for patients who may be severely ill with pancreatitis. We describe here a patient with gallstone pancreatitis who was managed completely by endoscopic techniques consisting of endoscopic retrograde cholangiopancreatography (ERCP) followed by laparoscopic cholecystectomy. Key words: ERCP, gallstone pnncreatitb, lapamcopic chdecystectomy.
Introduction It is now generally accepted that gallstone pancreatitis is caused by obstruction of the ampulla of Vater by a stone, which has usually migrated from the gall-bladder.’ Most authors advocate that cholecystectomy and any necessary procedures to remove common bile duct (CBD) stones should be performed during the initial hospital admission, in order to minimize the risk of further attacks of pancreatiti~.’.~However, there is disagreement about the exact timing of surgical intervention in this condition. In a prospective randomized trial of early (48 h) open operation in the treatment of gallstone pancreatitis, morbidity and mortality were significantly greater in the group of patients subjected to early ~peration.~ Early intervention in the form of endoscopic retrograde cholangiopancreatography (ERCP), sphincterotomy and extraction of stones from the
’
MB, BS; Surgical Registrar. zFRCS. FRCS (Ed.). FRACS; Senior Lecturer in Surgely. ’FRCS. FRACS; Visiting Surgeon. 4MD:Surgical Fellow. ’FRACS; Surgical Registrar. Correspondence:Dr Thomas B. Hugh, Suite 1006, St Vincent’s Clinic, 438 Victoria Street. Darlinghurst. NSW 2010, Australia. Accepted for publication 20 September 1990.
CBD have been suggested as methods of reducing the severity and duration of an attack of gallstone pancreatiti~.~ Unfortunately, this form of management leaves the patient exposed to the risk of further pancreatitis should another stone enter the CBD. The early use of minimally invasive techniques of removing all gallstones, as well as the gallbladder, is therefore an attractive option for patients who may be severely ill with pancreatitis. We describe here a patient with gallstone pancreatitis who was managed completely by endoscopic techniques consisting of ERCP followed by laparoscopic cholecystectomy .
case report A 44 year old man was admitted to hospital as an emergency on 24 July 1990with severe generalized abdominal pain, which radiated to the back and was accompanied by nausea. Apart from occasional ‘indigestion’, for which he took antacids, and a history of left renal colic, he had otherwise been previously well. He drank alcohol rarely and in small quantities. Examination on admission showed him to be distressed and tachycardic. There was generalized
