hepatic artery lesions v

Hepatic Artery Lesions V

R. W. POSTLETHWAIT, M.D., R. R. HERNANDEZ, M.D., M. L. DILLON, M.D.

From the Duke University Medical Center and the Veterans Administration Hospital,Durham, North Carolina

OPERATIONS requiring repair, replace-ment, temporary occlusion or ligation of thehepatic artery or a major branch have beenreported with increasing frequency. Thelesions and the operations include aneu-rysm, arteriovenous fistula, accidental in-jury or ligation and intentional ligation(Table 1). The newest operation involvingthe hepatic artery, as well as other majorstructures, is transplantation of the liver.Reported studies have described in de-

tail the collateral circulation and both theintrahepatic and extrahepatic distributionof the arteries and veins of the liver. Inaddition, the effects of alterations of thecirculation on liver function have been in-vestigated and the limits of tolerance atleast partially established. It is beyond thescope of this paper to review all of thereports on these subjects and only an out-line will be given.

Haberer,30 in 1905, reported that experi-mental ligation of the hepatic artery proxi-mal to the gastroduodenal branch was tol-erated by animals whereas ligation of thehepatic distal to the gastroduodenal wasfatal. Some later investigators have foundthe distal ligation to be almost invariablyfatal; 16, 27, 44-46 others have not.7' 35 Thevariation in results appears to be dependenton differences in technic and on the col-lateral arterial supply remaining. The distal(or peripheral) ligation would seem to befrequently but not always fatal in dogs.

* Presented before the Southern Surgical Asso-ciation, Hot Springs, Virginia, December 10-12,1963.

Extensive necrosis of liver cells does in-variably occur.

In 1909, Wolbach and Saiki73 found in21 of 23 healthy dogs an anerobic spore-forming bacillus in the liver which causedgas formation and to which they attributedthe so-called aseptic liver autolysis of dogs.Later, Ellis and Dragstedt20 showed con-clusively that this bacillus caused liver au-tolysis and death of dogs after hepaticartery ligation. Markowitz and his asso-ciates 44 then demonstrated the protectivevalue of penicillin in the prevention of thisinfection after the arterial ligation. They

TABLE 1. Lesions of the Hepatic Artery

Lesion Operation

Aneuiysm Ligation, excisionArteriosclerotic replacementTraumaticOther

Arteriovenous fistula Repair, ligationCongenital excisionAcquired

Accidental injury & ligation Repair, ligationTraumaticOperativeT-tube, stones

Occlusion Replacemnt, bypassArteriosclerosisTumorInflammationOther

Deliberate Ligation of Hepatic Artery

Portal hypertensionTumor (stomach, liver)Laceration of liverHemobilia, traumaticOther

895

896 POSTLETHWAIT, HERNANDEZ AND DILLON

suggested the importance of the hepaticartery blood in maintaining normal oxygentension which prevernted proliferation ofthe anerobes. Later studies by the sameworkers confirmed the fall in oxygen ten-sion after hepatic artery ligation and alsodemonstrated the protective action of anarteriovenous fistula into the portal vein.Orloff, Peskin and Allis 51 found portalblood from patients to be sterile as wereessentially all reported cultures of thehuman liver. This led them to suggest thatthe results of animal experiments concern-ing the bacterial factor in hepatic ischemiawere not applicable to man.Popper and his associates 53' 54 have

shown the lethal effect of simultaneous he-patic artery and portal vein interruption,which is not affected by antibiotics. Dra-panas and his co-workers 70 performed aportacaval shunt in dogs and then inter-rupted hepatic artery flow. Death followedocclusion for 90 minutes or longer and, ifarterial flow was restored, shock developedand death occurred even earlier. Ibrahimand Ageeb 33 temporarily occluded the por-tal vein and hepatic artery of experimentalanimals and noted a similar period of shockafter restoration of the circulation whichwas directly related to the duration of theocclusion. Release of a histamine-like sub-stance was considered at least partly re-sponsible. The critical period of occlusionof 20 to 30 minutes could be extended to 50minutes or more by hypothermia.

Tygstrup, Winkler, Mellemgaard and An-dreassen 71 in eight patients undergoingsurgery determined the effect of occludingthe hepatic artery proper, for periods aver-aging 24 minutes, on hepatic blood flowand oxygen consumption. The arterial flowaveraged 35 per cent of the hepatic venousflow; oxygen consumption was unchangedduring clamping but the portal hepatic ve-nous oxygen difference increased. Theyconcluded that under these conditions oxy-gen in the portal blood is sufficient to main-tain liver function, but if oxygen require-

Annals of SurgeryJune 1964

ments increase or if portal venous oxygensaturation falls, the hepatic arterial bloodsupply may be necessary for normal func-tion.

Collateral Arterial Routes

The studies and detailed descriptions byMichels 50 of the distribution of the arteriesto the upper abdominal organs form thebasis for the following brief review. Only55 per cent of the population have thetypical pattern of the hepatic artery arisingfrom the celiac and dividing into threemajor hepatic branches. A branch of thehepatic, the gastroduodenal, in this situa-tion provides the major collateral pathwayby way of its pancreatic branch communi-cating with the superior mesenteric arterywhen the hepatic is ligated.

Michels 50 describes 26 collateral routes,dividing these into three groups. The re-placed hepatic arteries are those arisingfrom a source other than the celiac axis;the accessory hepatic arteries are additivevessels from sources other than celiac. Thefollowing is an outline of these collateralroutes.

A. Hepatic arteries from sources other thanthe celiac-common hepatic trunk:1. Replaced left hepatic from left gastric

(10% in Michel's 50 dissections)2. Replaced right hepatic from superior

mesenteric (11%)3. Replaced right and left hepatics (1%)4. Replaced common hepatic from supe-

rior mesenteric, aorta or left gastric5. Accessory left hepatic from left gastric

(18%)6. Accessory right hepatic from superior

mesenteric (7% )7. Both accessory right and left hepatics

(1%)8. One replaced and one accessory hepatic

(2%)9. Accessory right hepatic of variable or-

igin other than superior mesenteric10. Cystic artery arising from gastroduode-

nal or retroduodenalB. Pathways outside hepatic arteries, capable

of connecting with severed hepatic or itsbranches:

HEPATIC ARTERY LESIONS

1. Infragastric epiploic (omental) path-way

2. Supragastric omental pathway3. Infracolic retro-omental route4. Paraesophageal hepatogastric omental

route5. Transpancreatic route6. Retroesophageal route

C. Pathways outside of celiac blood supply:1. Anterior and posterior pancreaticodu-

odenal arcades2. Transverse and dorsal pancreatic ves-

sels3. Inferior phrenics4. Superior phrenics5. Vessels in falciform ligament and liga-

mentum teres6. Vessels in coronary, right and left tri-

angular ligaments7. Intercostal arteries8. Posterior abdominal wall vessels9. Arterioles in hepatic veins, portal veins

and inferior vena cava

10. Filamentous arterioles along common,

cystic and hepatic ducts

Aneurysm

Approximately 135 cases of hepatic ar-

tery aneurysm have been reported. Accord-ing to McCorriston, Allin and Crowell,47over half were located in the hepatic arteryproper, a third in the right hepatic branch,a tenth in the left hepatic, and the remain-ing in an accessory artery or in various

combinations. Dwight and Ratcliffe 19 notedthat three-fourths of these lesions were

extrahepatic and the remainder intrahe-patic except for three patients who hadboth. Arteriosclerosis has been the mostcommon cause; others reported are trauma,syphilis, cholelithiasis, medial degenera-tion,74 and periarteritis nodosa.93 The le-

sions are usually small if a true aneurysm,larger if false in type. At least one instanceof concomitant aortic aneurysm has beenreported.The sex incidence is about equal in some

series; in others men predominate. McCor-riston, Allin and Crowell 47 found the aver-

age age of reported patients to be 38.4years. The diagnosis has been made infre-quently before operation or autopsy. Mas-

sive hemorrhage is often the cause of thefirst symptoms. According to Dwight andRatcliffe,19 rupture of the aneurysm in 70reported cases was intraperitoneal in 30,into the gallbladder or bile ducts in 29,into the stomach or duodenum in five, intothe portal vein in one, and into the peri-toneum and another site in five.The triad of abdominal pain, gastro-

intestinal hemorrhage and jaundice shouldsuggest the diagnosis. Other symptoms in-clude anorexia, nausea, vomiting, fever, andabdominal distension. An abdominal mass

may be present, which may be pulsating.A bruit may be heard over the abdomenor the mass. Ascites may be found. Kirklinand his associates,37 in 1955, first employedaortography in the diagnosis of hepaticartery aneurysm and Steinberg and his co-

workers 67, 68 have emphasized the value ofthis study. More recently, celiac and supe-

rior mesenteric arteriography has beeneven more helpful in demonstrating theseand similar vessel lesions.6As far as can be determined 27 patients

have been operated upon successfully: tenby excision of the aneurysm, six by liga-tion of the common hepatic artery, four byendoaneurysmorrhaphy, three by wrap-ping and one each by wiring, suture of theliver, suture of the hepatic artery, and ex-

cision with replacement by anastomosis ofthe splenic artery to the hepatic. The vari-ous authors repeatedly emphasize the neces-

sity for preservation of the gastroduodenalbranch when the aneurysm of the commonhepatic can be excised. Careful closure ofthe hepatic near the gastroduodenal branchis described by Hansborough and Lipin 31

and by McCorriston, Allin and Crowell.47The latter authors reported an extremelyinteresting method of insuring adequatecirculation after excision of an aneurysmof the common hepatic artery. They were

able to mobilize an eight centimeter seg-ment of the splenic artery; the proximalfree end of this vessel was then anastomosedend-to-end to the hepatic.

Volume 159Number 6 897


Case 1. A 49-year-old woman had gallbladderdisease for five years. Eight months before admis-sion in 1947, the gallbladder containing manystones was removed. She recovered uneventfullybut about a month after closure, the drain woundreopened. Bile stained material drained, but sixweeks before admission massive bleeding occurredfrom the site. Right upper quadrant pain and sev-eral episodes of minor bleeding followed. Theliver was palpable; the wound was dry at the timeof admission. The hemoglobin was 9.0 Gm. andthe bilirubin 1.1 mg.%. Operation was performed.Dense adhesions surrounded the sinus tract. Afalse aneurysm was eventually identified involvingthe right hepatic artery and extending into theliver substance. The laminated clots were re-moved but the arterial opening could not be foundas it apparently was within the liver. Bleedingwas controlled with a muscle pack. The woundhealed but she left the hospital against advice,refusing a second procedure. She died of massivehemorrhage five days after returning home.

Case 2. A 45-year-old man was admitted be-cause of severe abdominal pain a week earlier.He had been hospitalized by his physician andthe pain had decreased but extensive studies hadfailed to disclose the cause. His hemoglobin fellfrom 14.0 to 10.0 Gm. and made his physiciansuspect bleeding from a ruptured abdominal aor-tic aneurysm. Family history showed his motherhad died of a stroke, a brother died at 46 yearsof an abdominal aneurysm, a nephew died at 28years of a ruptured abdominal aneurysm, and aniece died at 21 years of a cerebral aneurysm.

Physical examination showed nothing remark-able. The hematocrit was 28 per cent, hemoglobin9.5 Gm. and bilirubin 1.25 mg.%,. Roentgen studiesshowed a faint area of calcification just below theleft sacroiliac joint and a retrograde arteriogramdemonstrated a left common iliac aneurysm. Atoperation, this was resected and replaced by agraft. Also a 7 cm. mass with a palpable thrill wasfound in the region of the hepatic artery. Theceliac, left gastric and splenic arteries were iso-lated; then the hepatic proper and the gastro-duodenal on the distal aspect of an aneurysm.The aneurysm was exposed. After dissection, itwas found that the gastroduodenal branch couldnot be preserved. A Teflon graft insertion wasattempted but the hepatic artery was too smalland friable to accomplish the anastomosis. Afteroperation, bilirubin increased to 6.3 mg.%. On thefifth day, massive hemorrhage developed and atreoperation, multiple superficial gastric ulcers werefound and sutured. Bleeding recurred and the pa-tient expired on the seventh postoperative day.Autopsy showed multiple areas of necrosis through-


out the liver, pulmonary emboli, multiple stressgastric ulcers, splenic artery thrombosis, severehemorrhagic pancreatitis and a small aneuirysm ofthe right common iliac artery.

Arteriorvenous Fistula

Nine patients have been reported withhepatoportal arteriovenous fistula. One wasdue to a gunshot wound and the otherswere thought to be congenital. Foster andSandblom 21 point out the unusual physio-logic implications of this lesion: the venoussinusoidal system lies between the fistulaand the right side of the heart, no reportedpatients had cardiac decompensation, nomention is made of the pulse slowing onclosure of the fistula, and all reported pa-tients except one have had portal hyper-tension. The latter had hemorrhage fromvarices in the esophagus, stomach or duo-denum. Ascites was present in two patients.Foster and Sandblom 21 emphasize the diffi-culty in diagnosis of this lesion, as the com-plications of the portal hypertension willmask the underlying cause. The color of theblood and the nature of the flow notedwhile measuring portal pressure are spe-cifically mentioned as a clue to the correctdiagnosis.

Five of the nine reported patients sur-vived. The patient of Wheeler and War-ren 72 had an emergency procedure withoversewing of bleeding varices in the sub-mucosa of the duodenum. Subsequently, asplenorenal shunt was performed to befollowed the next day by the appearance ofan epigastric bruit and later a thrill. Aorto-gram demonstrated an hepatic artery aneu-rysm emptying apparently into dilated por-tal veins. At operation, a large vein wasentered and a slit into the artery closed.The aneurysm was wired and the patientrecovered. Grant and his associates 26 re-ported the patient with a gunshot woundwhich resulted in an hepatoportal and alsoan aortocaval fistula. These were success-fully closed. DuBourg18 resected an aneu-rysm with an hepatoportal fistula and the

Volume 159 HEPATIC ARNumber 6

patient was well a year later. Foster andSandblom's patient had an aneurysm of theright hepatic artery extending into theliver, with the fistula within the liver. Theright branch of the portal vein was ligatedbut the ligatures removed at a second oper-ation when the hepatic artery was ligatedjust proximal to the aneurysm. The aneu-rysm then became soft; the patient was welltwo and one half years later. Shumackerand Waldhauser 62 found the fistula in theirpatient to be within the left lobe of theliver and achieved success by removalof the lobe. The frequent description ofanomalous blood vessel distribution inthese patients is of some importance.

Accidental Hepatic Artery Injuryand Ligation

The classic description entitled "Acci-dental Ligation of the Hepatic Artery" waspublished by Graham and Cannell,25 in1933, and few instances have been reportedsubsequently. The natural reticence of sur-geons to describe operative trauma requir-ing hepatic artery ligation is understand-able. It should be noted, however, that ina number of the cases reviewed by theseauthors, the ligation was deliberate andconsidered necessary in the treatment ofthe lesion observed.Graham and Cannell 25 found 27 patients

previously reported and described one oftheir own. The common hepatic artery wasligated in four with three deaths, the he-patic artery proper in seven with fourdeaths, the right hepatic artery in eightwith four deaths and the left hepatic ar-tery in seven with five deaths. In two pa-tients the site of ligation was not specifiedand both recovered. Thus, 16 of the 28patients died. The authors note the diffi-culty of determining the exact role of livernecrosis in death; they attribute liver insuf-ficiency as the cause of death in at leastseven of these patients.As might be expected, accidental injury

or ligation occurred most often during op-

'TERY LESIONS 899

erations on the gallbladder and commonduct or during difficult gastric resectionsfor carcinoma or ulcer. The importance ofduct and vessel anomalies in this regionhas been emphasized so often in discus-sions of biliary tract surgery that no repe-tition is necessary here. The potentiallydangerous situation described by Friesen,22however, has not received adequate empha-sis. His patient died a day after palliativeresection of a carcinoma of the esophagus.Infarction of the left lobe of the liver hadresulted from ligation of a replaced lefthepatic artery originating from the ligatedleft gastric artery.Andreassen and his associates 4 reported

two patients of interest. One had hemate-mesis after uneventful recovery from chole-cystectomy and choledochotomy. At a lateroperation, another choledochotomy showedthe bleeding to be coming from the hepaticduct. The hepatic artery was ligated distalto the pancreaticoduodenal branch, fol-lowed by recovery. Another patient hadexploration for common duct injury andafter dissection was complete, only the por-tal vein was intact and no arterial branchescould be seen in the porta hepatis. He re-covered after a Roux anastomosis of je-junum into the right hepatic duct.

Jesseph and May38 resected a portion ofthe common duct for a papillary cyst ade-noma of the pancreas which enveloped andprotruded into the common duct. End-to-end duct anastomosis was possible. She didwell for five months, then bled massivelyand at operation, a false aneurysm wasfound with the opening at the site of theanastomosis. The vessel, thought to be theright branch of the hepatic but possiblythe hepatic proper, was ligated, the ductagain anastomosed and the patient recov-ered uneventfully.Grove 28 reported two patients of interest.

The first had a cholecystectomy duringwhich, according to the surgeon, difficultywith bleeding occurred and hemostasis hadto be secured with a suture ligature. After


several episodes of pain, bleeding and jaun-dice, operation showed a fistula from theright hepatic artery into the adjacent com-mon duct. The openings were closed, withrecovery. He believed the suture ligatureused at the first operation acted as a ne-crosing suture between the involved struc-tures. Grove's 28 second patient had chole-cystectomy and T-tube drainage of thecommon duct for cholelithiasis and chronicpancreatitis. Five months later, a pseudo-cyst of the pancreas was drained internally.Postoperatively, hematemesis and bleedingfrom the T-tube occurred. The latter wasaccidentally removed and episodes ofbleeding continued. Operation showed anopening between the right hepatic arteryand the common duct. The artery wasrepaired, and the duct anastomosed to aRoux jejunal segment. She had then donewell except for pancreatic pain. Erosion bythe T-tube was considered the most likelycause of the arterial injury.

Rabinovitch and Rabinovitch 56 reporteda patient who bled massively through aT-tube; the bleeding stopped promptly afterremoval of the tube. A second patient hada similar course but the bleeding did notstop after removal of the tube. Reoperationand choledochotomy showed only a super-ficial erosion of the mucosa of the commonduct which, they state, could have been thesite of bleeding. She recovered withoutfurther bleeding. Manfredi 43 reported apatient who, a year after cholecystectomy,had common duct stones removed after ob-structive jaundice developed. The T-tubewas left in place. He returned two monthsafter operation because of bleeding fromthe T-tube. He expired two days later andautopsy showed that the T-tube had erodedinto the hepatic artery and caused exsan-guination.

Occlusion of the Hepatic ArteryIt seems reasonable to assume that oc-

clusion of the hepatic artery or a majorbranch might occur fairly often due to an


intraluminal process such as arteriosclero-sis or to extraluminal pressure as from atumor or scar. In incomplete studies, Prich-ard has noted the infrequency of arterio-sclerotic involvement of the hepatic artery.A cursory search produced a single com-parative study, that of Brooks in 1906. In400 autopsies serious arteriosclerosis of thevisceral vessels occurred as follows: aorta333; coronary 270; brain 132; renal 81;pancreatic 74; hepatic 43; splenic 35; celiac19; and pulmonary 11. A single case reportwas found to illustrate this lesion.'4

This was a 77-year-old woman who hada right hemiplegia and was admitted be-cause of hematuria. She eventually expiredin uremia. At the time of admission, shewas slightly jaundiced and the bilirubinwas 3.2 mg.%o. Autopsy showed the leftlobe of the liver to be almost completelyatrophic. The hepatic artery was severelyatherosclerotic and the left branch was oc-cluded by old thrombotic and atheroscler-otic material.

Case 3. A 65-year-old man was admitted in1958 because of a chondrosarcoma of the left hip,constrictive pericarditis and congestive heart fail-ure. The tumor was treated by irradiation followedby hemipelvectomy. He returned on several occa-sions because of congestive failure. In 1961, twoareas of infiltration were found in the left lungand cytoxan was given. His last admission was inAugust 1963 when he showed evidence of con-tinued congestive heart failure, although he feltfairly well. The liver was palpable and asciteswas present. Bromsulphalein retention was 19 percent, alkaline phosphatase 23 K.A. units and otherliver function tests normal. The lung densitieshad enlarged slightly and a new one was seen.Pericardial calcification was present. The hilarareas were prominent and barium swallow showedmultiple pressure defects along the esophagus. Arose-bengal liver scan showed several large areasindicative of metastases. Celiac arteriogram showedthe obstruction and collateral circulation noted inFigure 1 and 2. He improved with no specifictherapy other than that for his heart failure.

The abnormal finding in the celiac arteri-ogram has been considered due to a massof lymph nodes involved by metastatictumor. The anomaly could be congenital

HEPATIC ARTERY LESIONS 901

FIG. 1. Case 3. Celiac arteriogram shows abrupt termination of hepatic artery distal to celiac.

and a definite answer may be obtainedlater.

Case 4. A 48-year-old man was admitted in1955. He had a five-year history of peptic ulcerwith several bleeding episodes. He developed se-

vere abdominal pain and fever for which afterfive days he was hospitalized. He was believed to

have had a perforation which had walled off and,after no improvement on intensive therapy, an

abscess was thought to have formed. Operationshowed a cavity inferior to the liver containingabout 300 ml. of bile stained fluid. The duodenumwas diffusely inflamed. Exploration was limited,as the preoperative diagnosis appeared to be sub-stantiated. The gallbladder was also inflamed anda cholecystostomy with catheter drainage was

performed. The cavity was drained also. He hadconsiderable fever and, after some improvement,was transferred to our hospital on the eighth post-operative day.

The catheter was in place and drained bile;drains protruded through another stab woundfrom which a mucoid, bile-stained material ap-

peared. The only evidence of liver damage was

a thymol flocculation test of three plus and brom-sulphalein retention of 10 per cent. Injection of

contrast material into the catheter outlined a

patent common duct and also the abscess cavitywhich measured about 15 cm. in diameter. Biledrainage from the catheter ceased and this was

removed. Drainage persisted from the stab woundand weight loss became serious, so operation was

performed. The gallbladder was necrotic and laycompletely free in a cavity which occupied an

estimated two-thirds of the right lobe of the liver.Numerous huge pieces of necrotic liver were re-

moved with the hand, no attachments being ob-served. Practically no bleeding occurred and no

pockets of purulent material could be found.Drainage persisted for nearly four months but re-

covery was otherwise uneventful.He has subsequently returned on several occa-

sions because of cardiac decompensation. Liverfunction tests were normal. A celiac arteriogramwas made recently and is shown in Figure 3.

Case 5. A 38-year-old man had an 11-year his-tory of duodenal ulcer; pyloric obstruction finallyrequired operation at his local hospital. A largeposterior penetrating ulcer was found. Accordingto the surgeon, during the dissection in the indu-rated tissues, the gastroduodenal artery was sev-

ered. This was controlled promptly and the hepatic

Volume 159Number 6

POSTLETHWAIT, HERNANDEZ AND DILLON Annals of SurgeryJune 1964

FIG. 2. Case 3. Superior mesenteric arteriogram demonstrates excellent collateral circulation throughthe pancreatic vessels and pancreaticoduodenal into what appears to be the hepatic proper.

FIG. 3. Case 4. Celiac arteriogram shows no major branches of the hepatic to the liver.

902

HEPATIC ARTERY LESIONS

artery carefully inspected and found to be intact.A subtotal gastric resection was performed. Hesubsequently developed profuse biliary and pan-creatic drainage.

The drainage decreased but persisted and asecond operation was performed six weeks afterthe first. The fistulous tract was traced down tothe portal triad. The liver was slightly enlarged,soft, and red. The duodenal stump closure was

intact. The gallbladder had sloughed completelyand was lifted out without dissection. Small ne-crotic segments of the common duct were identi-fied and removed. The common duct was absentfrom the superior border of the pancreas to theliver. The right and left ducts were identified andcatheters placed in them. The hepatic artery, theportal vein and both branches of each were ex-

posed. No pulsations were felt in the artery andno blood could be aspirated from it but no liga-ture or point of constriction could be found. Inci-sion into the artery showed obliteration of thelumen. No other arteries could be found in theportal triad area. Drains were placed, and theseand the catheters brought out.

A carefully-planned postoperative regimen re-

sulted in gradual improvement. About five months

after the first operation, he was transferred toanother hospital where the two major hepatic ductswere anastomosed to a jejunal loop. Although heimproved considerably, drainage persisted and hewas admitted here four months after the lastoperation. Bile stained material drained from themid portion of a subcostal wound. The liverwas down three cm. and the spleen five cm.

Bilirubin was 0.95 mg.%, bromsulphalein re-

tention 10 per cent, alkaline phosphatase 39.8K.A. units, thymol turbidity 20.6 and prothrombin88 per cent. Sump drainage resulted in closure ofthe fistula. The radiologic findings are shown inFigure 4. He has retumed on two occasions inthe past nine months and, other than slightlygreater enlargement of the spleen, has remainedunchanged. He has had several minor episodes offever thought to be due to cholangitis and now

takes an antibiotic daily. Further complicationsmay require operation.

In both of these patients, the hepaticartery occlusion appears to be secondaryto severe inflammatory reaction. In Case 4,no opportunity existed for injury to the

Fic. 4. Case 5. Celiac arteriogram shows apparent absence of right hepatic with no major branches toright lobe an absence of gastroduodenal.

Volume 159Number 6 903


vessels, as only drainage was instituted.Such an opportunity did develop in Case 5,but the surgeon was immediately aware ofthe possibility of hepatic artery injury andassured himself that the vessel was intact.

Deliberate Ligation of Hepatic Artery

In the preceding discussion, ligation ofthe hepatic artery has been described inthe treatment of several lesions. Althoughthere is some duplication (see hemobilia),separate consideration of the followingcategories appears justified.

Portal Hypertension

Based on the possibility that intrahepaticarteriovenous shunts in cirrhosis contributeto the portal hypertension, Rienhoff,57 in1951, suggested hepatic artery ligation. Thiswas performed distal to the gastroduodenalbranch to decrease collateral circulation.The splenic artery was also ligated to di-minish total portal blood flow. Two yearslater, Rienhoff and Woods 58 reported 23patients with six postoperative deaths andone late death. In a re-appraisal in 1958,59no additional patients had had the ligationbecause no real decrease in portal pressureoccurred and several patients continued tohave recurrent hemorrhage. Berman andhis associates,8-" in a series of papers from1951 to 1954, also reported 23 patients withseven postoperative and nine late deaths.Both of these groups noted improvementof ascites.The experience of others 1, 34, 41, 60, 63 was

not favorable on the whole. The postopera-tive mortality rate was high although theincidence of liver necrosis was not exces-sive. As far as we can determine, in theentire group of 76 patients, only four of the20 reported postoperative deaths were dueto liver failure. The persistence of varicesand recurrent bleeding from these, how-ever, has decreased enthusiasm for thisprocedure.


TumorAppleby,5 in 1953, noted again that an

intact gastroduodenal artery is usually thecritical point in the collateral blood supplyto the liver after ligation of the hepaticartery proximal to this branch. In order toobtain a more thorough lymph node dissec-tion, in 13 patients with carcinoma of thestomach, he removed the stomach contain-ing the malignancy, the spleen, and theleft two-thirds of the pancreas. The celiacartery was ligated and the gastrohepaticomentum removed along with the hepaticartery over to the gastroduodenal branch.He had no postoperative deaths.

Clarke,15 two years later, reported two pa-tients who had the same operation but diedon the eighth and twenty-fourth postopera-tive days. Both had focal infarction in theliver but not extensive enough to cause liverfailure. In the first case, the remaining an-trum was necrotic; in the second patient,the first part of the duodenum showed ne-crosis and perforations. Andreassen, Lind-enberg and Winkler,4 in 1962, performeda similar operation on one patient, al-though the gastroduodenal and two hepaticbranches were ligated separately. He hada moderate rise in bilirubin and transami-nase postoperatively. Five months later, anepisode of jaundice developed and liverfunction tests showed evidence of paren-chymatous drainage.These experiences suggest that, when an

extensive resection is planned for carcinomaof the stomach, celiac and superior mesen-teric arteriography might be performedpreoperatively in order to delineate the ar-terial supply to the liver. Demonstrationof adequate collateral vessels would per-mit rapid completion of the procedure. Inaddition, this radiographic technic mightdisclose unsuspected metastases.

Massive resections of the liver for malig-nancy, both primary and metastatic, arebeing reported with increasing frequency.23'38, 47, 51 These obviously require ligation of

Volume 159 HEPATIC ARNumber 6

major hepatic vessels but as the tissue sup-

plied is removed, these patients are not

within the category under discussion. An-

dreassen, Lindenberg and Winkler, how-ever, report an eight-month-old infant whoat operation had a tumor thought to bean hemangioma occupying an estimatedfour-fifths of the liver substance. Resectionwas impossible. The liver continued to en-

large, and as the patient was deterioratingrapidly, hepatic artery ligation was per-

formed in the hope of decreasing the sizeof the liver. Bilirubin increased slightly andshe recovered, but she was admitted threemonths later and expired. Autopsy showedthe liver half the size noted at operation.The tumor was a liver cell carcinoma; theremaining liver was normal.

Laceration of the Liver

Although both primary and secondaryhemorrhage are frequent causes of deathafter serious injury to the liver, ligationof the major hepatic arteries is not men-

tioned for control of bleeding in two recentreports of large series.'7 65 Breton and hisassociates 12 did employ right hepatic ar-

tery ligation as an emergency procedure tocontrol bleeding from a laceration of theliver due to a crushing injury. After a

ITERY LESIONS 905

complicated course, the patient recovered.When resection of a traumatized lobe of theliver is necessary, ligation is part of theprocedure. Ligation is mentioned most fre-quently, however, in the care of patientswith traumatic hemobilia.

Traumatic Hemobilia

Amerson and Ferguson 2 recently foundthat 28 cases of traumatic hemobilia hadbeen reported. Blunt trauma was the cause

in 23, gunshot wounds in two, and three

followed cholecystectomy and choledo-chotomy. Bleeding occurred as early as 16hours and as late as four months after thetrauma. Bleeding was usually from a cavitywithin the liver substance, filled with bloodand necrotic material and communicatingwith the biliary ducts. Diagnosis is sug-

gested by: 1) a history of abdominaltrauma with liver injury; 2) periodic boutsof colicky right upper quadrant pain; 3)gastro-intestinal hemorrhage, frequentlywith temporary relief of the pain; and 4)jaundice of the obstructive type.

Various types of therapy have been em-

ployed including T-tube decompressionand opening of the cavity with ligature ofbleeding points and packing. Hepatic ar-

tery ligation has been performed in five

TABLE 2. Hepatic Artery Ligation for Traumatic Hemobilia

Senior Probable Prior Operations Artery SubsequentAuthor Cause For Bleeding Ligated Course

Schatzki Auto None Lt. hepatic Lt. lobectomyaccident necessary later,

with recovery

Gwynn Cholecys- Choledochotomy Lt. hepatic Expired PO 12tectomy

Spector Auto 1. cavity drained Rt. hepatic Recoveryaccident 2. cavity packed,

cholecystostomy3. cavity packed

Mackay Cholecys- 1. gastrectomy Rt. hepatic Recoverytectomy 2. (luodenotomy,

choledochotomv

Andreassen Cholecys- 1. repair hiatal Hepatic Recoverytectomy hernia proper

906 POSTLETHWAIT, HERNANDEZ AND DILLON Annals of Surgery

patients, as summarized in Table 2. One ex-pired after operation, one subsequently re-quired removal of the left lobe of the liver,and three recovered uneventfully. Thesingle case of traumatic hemobilia at thismedical center has previously been re-ported by Hart.32

SummaryLesions of the hepatic artery and those

injuries and diseases which may requirehepatic artery ligation have been reviewed.A survey of experimental studies of the

effects of hepatic artery ligation showssome disagreement, in part due to differ-ences in technic. In adult dogs, death com-monly occurs after ligation due to the toxiceffects of the growth of gas-forming, aner-obic bacillus which is a normal inhabitantof the adult dog liver. Collateral circulationcarrying adequately oxygenated blood willprevent this growth, as will antibiotics.Anatomic studies of the arterial supply

of the liver in humans show considerablevariation. The most dependable collateralpathway after hepatic artery ligation is viathe gastroduodenal branch through thepancreatic vessels and the superior mesen-teric artery. Michels 50 describes 26 possibleroutes for blood to reach the liver afterhepatic artery ligation.Aneurysms are usually arteriosclerotic in

cause, and located in the common or righthepatic. Pain, hemorrhage and jaundice aremost often present; a pulsating mass maybe felt. Approximately 135 cases have beenreported and 27 successfully operated upon,most often by excision.An hepatoportal arteriovenous fistula is

usually congenital and is manifested byportal hypertension and its complications.Five of the nine reported patients havebeen treated by a surgical procedure, eitherby ligation or closure, with recovery.

Accidental injury and ligation of the he-patic artery appears to be uncommon, butdoes occasionally occur. Occlusion by ar-teriosclerosis or tumor is also seldom re-

ported; increased utilization of aortographyand arteriography may well show this tobe a common development. Severe inflam-matory reaction is suggested as the causeof hepatic artery occlusion in two personalcases.

Deliberate ligation of the hepatic arteryfor portal hypertension is now infrequentlyemployed. Such ligation to extend the re-section for carcinoma of the stomach maybe justified. Ligation may be necessary asan emergency procedure to control hemor-rhage from a traumatic laceration of theliver. Deliberate ligation has been success-fully employed in three cases of traumatichemobilia.

Although only brief reference has beenmade to arteriography, this technic shouldbe of great value in the assessment of pa-tients with lesions of the hepatic artery orwith an injury or lesion which may requireligation of this vessel.

References1. Altemeier, W. A., W. T. McElhinney and

B. G. MacMillan: Treatment of Portal Hyper-tension with Hepatic Artery Ligation. Arch.Surg., 71:571, 1955.

2. Amerson, J. R. and I. A. Ferguson, Jr.: Trau-matic Hemobilia. Surgery, 54:729, 1963.

3. Andreassen, M. and J. Lindenberg: Late Post-operative "Hemobilia" Treated with Periph-eral Ligation of the Hepatic Artery. Surgery,46:870, 1959.

4. Andreassen, M., J. Lindenberg and K. Wink-ler: Peripheral Ligation of the Hepatic Ar-tery During Surgery in Noncirrhotic Pa-tients. Gut, 3:167, 1962.

5. Appleby, L. H.: The Coceliac Axis in the Ex-pansion of the Operation for Gastric Carci-noma. Cancer, 6:704, 1953.

6. Baum, S., M. Nusbaum and W. S. Blakemore:Celiac and Superior Mesenteric Arteriog-raphy. Exhibit, Clinical Congress, AmericanCollege of Surgeons, San Francisco, 1963.

7. Behrend, M., H. E. Radasch and A. G. Kersh-ner: Comparative Results of the Ligation ofthe Hepatic Artery in Animals, Its Applica-tion to Man. Arch. Surg., 4:661, 1922.

8. Bermlan, J. K., L. P. Mtiller, C. Fiseli an(d W.Martz: Ligation of the Hepatic and SplenicArteries in a Patient with Atrophic Cirrhosisof the Liver. Arch. Surg., 63:623, 1951.

Volume 159 HEPATIC ARTERY LESIONS 907Number 6909. Berman, J. K. and J. E. Hull: Hepatic, Splenic,

and Lymphogastric Arterial Ligations in Ad-vanced Portal Cirrhosis. Arch. Surg., 65:37,1952.

10. Berman, J. K. and J. E. Hull: Circulation inthe Normal and Cirrhotic Liver. Ann. Surg.,137:424, 1953.

11. Berman, J. K. and D. C. Fields: AdvancedAtrophic Cirrhosis. Arch. Surg., 58:432,1954.

12. Breton, G. J., D. F. P. Gordon, T. S. Cooksonand D. P. Nicholson: Liver Injury InvolvingRight Hepatic Artery Ligation Complicatedby Survival. Canadian M. A. J., 81:836,1959.

13. Brooks, H.: A Preliminary Study of VisceralArteriosclerosis. Am. J. Med. Sc., 131:778,1906.

14. Case Reports of the Massachusetts GeneralHospital, Case 5-1963. New Engl. J. Med.,268:153, 1963.

15. Clarke, J. S.: Hepatic Necrosis FollowingCeliac Artery Ligation During Gastric Resec-tion in Man. Arch. Surg., 71:171, 1955.

16. Cob, L. M., K. A. McKay, J. Archibald andJ. Markowitz: Clostridial Infection of theLiver in the Canine After Ligation of theHepatic Artery. Canadian J. Surg., 5:450,1962.

17. Crosthwaith, R. W., J. E. Allen, F. Murga,A. C. Beal, Jr. and M. E. De Bakey: TheSurgical Management of 640 ConsecutiveLiver Injuries in Civilian Practice. Surg.,Gynec. & Obst., 114:650, 1962.

18. DuBourg, G., P. Broustet, H. Bricaud and F.Fountan: Anivrisme Arterio-veinous Hepati-co-portal. Mem. acad. Chir., 84:770, 1958.(Cited by Foster, J. H. and P. Sandblom,1961.)

19. Dwight, R. W. and J. W. Ratcliffe: Aneurysmof the Hepatic Artery. Report of a CaseTreated by Wiring. Surgery, 31:915, 1952.

20. Ellis, J. C. and L. R. Dragstedt: Liver Au-tolysis in vivo. Arch. Surg., 20:8, 1930.

21. Foster, J. H. and P. Sandblom: Portal Hyper-tension Secondary to an Hepato-portal Ar-teriovenous Fistula. Ann. Surg., 154:300,1961.

22. Friesen, S. R.: The Significance of the Anom-alous Origin of the Left Hepatic Arteryfrom the Left Gastric Artery in OperationsUpon the Stomach and Esophagus. Am. Sur-geon, 23:1103, 1957.

23. Glassman, E. and P. V. Skerrett: Rupture ofan Intrahepatic Aneurysm Duie to Polyarter-itis Nodosa. Am. J. Med., 28:143, 1960.

24. Goldsmith, N. A. and R, T. Woodburne: Sur-

gical Anatomy Pertaining to Liver Resection.Surg., Gynec. & Obst., 105:310, 1957.

25. Graham, R. R. and D. Cannell: AccidentalLigation of the Hepatic Artery. Report ofOne Case with a Review of the Cases inthe Literature. Brit. J. Surg., 20:566, 1933.

26. Grant, R. N., M. L. Griedman and R. A. De-terling, Jr.: Co-existing Traumatic Arterio-venous Fistulae Between the Aorta and VenaCava, and the Hepatic Artery and PortalVein, Complicated by a "Goldblatt" Kidney.Ann. Surg.., 148:286, 1958.

27. Grindlay, J. H., S. C. Mann and J. L. Bollman:Effect of Occlusion of the Arterial BloodSupply to the Normal Liver. An Experimen-tal Study. Arch. Surg., 62:806, 1951.

28. Grove, W. J.: Biliary Tract Hemorrhage as aCause of Hematemesis. Arch. Surg., 83:67,1961.

29. Guynn, D. L. and J. T. Reynolds: SurgicalManagement of Hemobilia. SpontaneousHemobilia in Intrahepatic Origin. Arch.Surg., 83:73, 1961.

30. Haberer, H.: Experimentelle Unterbindungder Leberarterie. Arch. klin. Chir., 78:557,1905.

31. Hansbrough, E. T. and R. J. Lipin: HepaticArtery Aneurysm with Excision of CeliacAxis. Ann. Surg., 149:273, 1959.

32. Hart, D. H., quoted in Sparkman, R. S.: Mas-sive Hemobilia Following Traumatic Rup-ture of the Liver. Report of a Case and Re-view of the Literature. Ann. Surg., 138:899,1953.

33. Ibrahim, H. and M. Ageeb: Effects of Tem-porary Occlusion of Portal Vein and HepaticArtery in Normothermic and HypothermicAnimals. Bull. Soc. Internat. Chir., 22:76,1963.

34. Jahnke, E. J., Jr., S. F. Seeley and E. D.Palmer: Evaluation of Hepatic and SplenicArtery Ligation for Portal Hypertension witha Case Report. Ann. Surg., 137:98, 1953.

35. Jefferson, N. C., M. M. Proffitt and H. Neche-les: Collateral Arterial Circulation to theLiver of the Dog. Surgery, 31:724, 1952.

36. Jesseph, J. E. and K. J. May, Jr.: False Aneu-rsym of the Hepatic Artery with MassiveHemobilia and Jaundice. A Case Report.Arch. Surg., 81:646, 1960.

37. Kirklin, J. W., E. Shocket, M. W. Comfortand K. A. Huizenga: Treatment of Aneu-rysm of the Hepatic Artery by Excision. Re-port of a Case. Ann. Stnrg., 42:110, 1955.

38. Laufman, H., A. Ross, D. H. Bernhard, R. V.Bourdeau, W. E. Furr and T. C. Douglass:Graded Hepatic Arterial Ligations in Ex-

908 POSTLETHWAIT, HERNANDEZ AND DILLON Annals of Surgeryperimental Ascites. Surg., Gynee. & Obst.,96:409, 1953.

39. Longmire, W. P., Jr. and S. A. Marable:Clinical Experiences with Major HepaticResections of Direct Vision Annuloplasty.Ann. Surg., 154:460, 1961.

40. Mackay, A. G. and H. G. Page: HematemesisAssociated with Hemobilia. Report of a CaseDue to an Intrahepatic Artery Aneurysmwith Survival. New Engl. J. Med., 260:468,1959.

41. Madden, J. L.: Ligation of the Hepatic andSplenic Arteries in the Treatment of Cir-rhosis of the Liver. Surg., Gynec. & Obst.,96:594, 1953.

42. Madding, G. F., W. L. Smith and L. R.Hershberger: Hepatoportal ArteriovenousFistula. J.A.M.A., 156:593, 1954.

43. Manfredi, D. H.: Gastrointestinal HemorrhageOriginating in the Biliary Tract. New YorkState J. Med., 58:2397, 1958.

44. Markowitz, J., A. Rappaport and A. C. Scott:The Function of the Hepatic Artery in theDog. Am. J. Digestive Dis., 16:344, 1949.

45. Markowitz, J., A. Rappaport and A. C. Scott:Prevention of Liver Necrosis Following Li-gation of Hepatic Artery. Proe. Soc. Exper.Biol. & Med., 70:305, 1949.

46. Markowitz, J. and A. M. Rappaport: The He-patic Artery. Physiol. Reviews, 31:188, 1951.

47. McCorriston, J. R., G. E. Allin and D. E.Crowell: Splenohepatic Arterial Anastomosisfor Aneurysm of Hepatic Artery. Surgery,47:636, 1960.

48. McDermott, W. V., Jr., N. V. Greenberger,K. J. Isselbacher and A. L. Weber: MajorHepatic Resection. Diagnostic Techniquesand Metabolic Problems. Surgery, 54:56,1963.

49. Michels, N. A.: The Hepatic Cystic and Retro-duodenal Arteries and Their Relations to theBiliary Ducts. Ann. Surg., 133:503, 1951.

50. Michels, N. A.: Collateral Arterial Pathwaysto the Liver after Ligation of the HepaticArtery and Removal of the Celiac Axis. Can-cer, 6:708, 1953.

51. Orloff, M. J., G. W. Peskin and H. L. Ellis:A Bacteriologic Study of Human PortalBlood. Implications Regarding Hepatic Is-chemia in Man. Ann. Surg., 148:738, 1958.

52. Pack, G. T. and D. W. Molander: MetabolismBefore and After Hepatic Lobectomy forCancer. Studies in 23 Patients. Arch. Sturg.,80:685, 1960.

53. Popper, H. L., N. C. Jefferson and H. Meclhe-les: Liver Necrosis Following Complete In-terruption of Hepatic Artery and Partial Li-

gation of Portal Vein. Am. J. Surg., 86:309,1953.

54. Popper, H. L., N. C. Jefferson and H. Nechels:Survival of Dogs After Partial or Total De-vascularization of the Liver. Ann. Surg., 140:93, 1954.

55. Prichard, R. W.: Personal communication.56. Rabinovitch, J. and P. Rabinovitch: Massive

Bleeding from Common Bile Duct Causedby Indwelling T-tube. Arch. Surg., 69:849,1954.

57. Rienhoff, W. F., Jr.: Ligation of the Hepaticand Splenic Arteries in the Treatment ofPortal Hypertension with a Report of SixCases. Preliminary Report. Bull. Johns Hop-kins Hospital, 88:368, 1951.

58. Rienhoff, W. F., Jr. and A. C. Woods, Jr.:Ligations of Hepatic and Splenic Arteriesin Treatment of Cirrhosis with Ascites.J.A.M.A., 152:687, 1953.

59. Rienhoff, W. F., Jr. and A. C. Woods, Jr.:Re-evaluation of Ligation of the HepaticArtery for the Treatment of ComplicationsFollowing Intrahepatic Disease. Surgery, 43:863, 1958.

60. Rosenbaum, D. and H. L. Egbert: Liver Ne-crosis and Death Following Hepatic ArteryLigation. J.A.M.A., 149:1210, 1952.

61. Schatzki, S. C.: Hemobilia. Radiology, 77:717,1961.

62. Shumacker, H. B., Jr. and J. A. Waldhausen:Intrahepatic Arteriovenous Fistula of He-patic Artery and Portal Vein. Surg., Gynec.& Obst., 112:497, 1961.

63. Smith, J. C., R. W. McNealy and E. A. Zaus:Effect of Hepatic Artery Ligation on AscitesDue to Laennec's Cirrhosis. Report of TwoCases. Arch. Surg., 66:344, 1953.

64. Sparkman, R. S.: Massive Hemobilia Follow-ing Traumatic Rupture of the Liver. Reportof a Case and Review of the Literature.Ann. Surg., 138:899, 1953.

65. Sparkman, R. S. and M. J. Fogelman: Woundsof the Liver. Review of 100 Cases. Ann.Surg., 139:690, 1954.

66. Spector, N.: Ligation of the Right HepaticArtery and Hemobilia. Report of a Casewith Recovery. Ann. Surg., 145:244, 1957.

67. Steinberg, I.: Diagnosis of Aneurysms of theHepatic and Splenic Arteries by IntravenousAbdominal Aortography. New Engl. J. Med.,263:341, 1960.

68. Steinberg, I., N. Finby and J. A. Evans: In-travenou.s Abdominal Aortography in theDiagnosis and Differential Diagnosis ofAneurysms of the Splenic, Hepatic andRenal Arteries. Am. J. Roentgen., 86:1108,1961.

Volume 159 HEPATIC ARTERY LESIONS 909

69. Strickler, J. A. H., N. Lufkin and C. 0. Rice:Hepatic Portal Arteriovenous Fisttula. A CaseReport. Surgery, 31:583, 1952.

70. Drapanas, T., D. R. Becker, G. S. Alfano,W. H. Potter and J. D. Stewart: Some Ef-fects of Interrupting Hepatic Blood Flow.Ann. Surg., 142:831, 1955.

71. Tygstrup, N., K. Winkler, K. Mellemgaard andM. Andreassen: Determination of the He-patic Arterial Blood Flow and Oxygen Sup-ply in Man by Clamping the Hepatic ArteryDuring Surgery. J. Clin. Invest., 41:447,1962.

72. Wheeler, H. B. and R. Warren: DuodenalVarices Due to Portal Hypertension fromArteriovenous Aneurysm. Report of a Case.Ann. Surg., 146:229, 1957.

73. Wolbach, S. B. and T. Saiki: A New AnerobicSpore-Forming Bacteria Commonly Presentin the Livers of Healthy Dogs, and Believedto be Responsible for Many Changes At-tributed to Aseptic Autolysis of Liver Tissue.J. Med. Research, 21:267, 1909.

74. Zeppa, R. and N. A. Womack: Medial De-generation and Aneurysm of the Hepatic Ar-tery. Arch. Surg., 86:252, 1963.

DISCUSSION

DR. KENNETH W. WARREN (Boston): Dr.Postlethwait permitted me to read his manuscriptfor a very unique reason. I had operated on thefifth patient of those reported. The patient hadbeen operated on previously on two occasions, thefirst for the removal of a duodenal ulcer. Subse-quently, a biliary and pancreatic fistula developed.When this patient came to me, he had a largefistula involving both pancreatic and biliary ducts.It was possible, however, to dissect the hilar struc-tures of the liver for a distance of 3.8 cm. withinthe substance of the liver and to identify the rightand left hepatic ducts separately. These hepaticducts were anastomosed separately to the jejunum.Convalescence was hectic and prolonged but thepatient recovered and is doing well at the presenttime.

I would like to confine my remarks, therefore,to traumatic injuries to the hepatic artery at thetime of surgery. Obviously, the best treatment isto prevent these injuries. If you see an anomalyin this complicated anatomic area you assume thatother anomalies may be present. Dr. Postlethwait'sadvocacy of aortography is extremely well takenin such a situation in the evaluation of the subse-quent events and in planning an operation whichshould offer an optimal result.

When massive hemorrhage occurs in the regionof the hepatic artery or the portal vein, the bleed-ing is best controlled initially by digital compres-sion at the stite of the hemorrhage. Then theoperative field should be cleared by careful suc-tion. The point of bleeding can almost always beidentified. It is much safer and more satisfactoryto secure the point of bleeding by using fine ar-terial silk sutures than by applying hemostats in-discriminately. When multiple hemostats are ap-plied in a fit of panic, vital structures cannot beidentified and protected.

During the course of resecting the head of thepancreas, surgeons at the Lahey Clinic have di-vided the hepatic artery in three cases. We have

been able to anastomose the divided artery inevery instance and all of these patients survived.If such an injury is recognized immediately andif the artery is not destroyed by the indiscriminateapplication of hemostats, an adequate repair ofthe vessel can be achieved.

The same considerations apply with respect tosome of the anomalies which Dr. Postlethwait dis-cussed. We abandoned pancreatic resection in oneinstance because the main hepatic artery arosefrom the superior mesenteric artery and traversedthe head of the pancreas.

In approaching some of these problems thatinvolve the hepatic artery distal to the pancreato-duodenal artery, it is best to isolate all of themajor vascular structures first, isolate the hepaticartery near its origin, secure the gastroduodenalartery near its junction with the hepatic artery, andif possible, dissect the hilus of the liver where allof these structures can be identified and isolatedseparately. This applies particularly to aneurysmsin this area. This discussion by Dr. Postlethwaitdeserves careful consideration.

DR. CHARLES A. HUFNAGEL (Washington,D. C.): I would like to tell you about one patientwith an aneurysm of the hepatic artery which pre-sented in an unusual way, which may be usefulinformation in the future. This patient presentedwith a large pulsating abdominal mass and gastro-intestinal bleeding which was chronic, and gastro-intestinal studies demonstrated that he had hemo-bilia. He was explored and the mass was identi-fied as an aneurysm and the abdomen was closed.

We then asked to see this patient and aortog-raphy demonstrated that this was a large aneurysmof the hepatic artery. It was approximately 25cm. in length. The origin from the aorta was inthe usual position. The aneurysm went first tothe extreme left of the abdomen, turned back tothe right in a sausage shape then extended to theright flank and then finally came back and enteredthe hilum of the liver.

Just at its origin, in the first centimeter, the

hepatic artery lesions v

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