9
EARLY RESULTS FOLLOWING THERAPEUTIC LIGATION OF THE HEPATIC ARTERY PRELIMINARY REPORT OF CASES* ARTHUR I. CHENOWETH, M.D. BIRMNGHAM, ALA. THAT MEDICAL MANAGEMENT of cirrhosis of the liver is currently the treatment of choice is undisputed. However, in spite of the best efforts of the physician, supported by complete cooperation on the part of the patient, such treatment is all too often inef- fectual, and the patient succumbs to pro- gressive liver failure, inanition with wasting ascites, or exsanguination after one or re- peated bouts of hemorrhage from esopha- geal varices. The last two manifestations of cirrhosis of the liver, ascites and esophageal varices, have for many years commanded the atten- tion of surgeons, who have sought, by oper- ative measures, to correct the existing com- plication. In many cases the result has been gratifying, and the patient restored to a life of activity. In many other cases disappoint- ing failure has been experienced. As a measure of the lack of uniform suc- cess attending surgical treatment, we might cite the number and variety of procedures utilized by surgeons. Among these are omentopexy, splenectomy, injection of scle- rosing substances into esophageal varices, total gastric resection, resection of eso- phagogastric junction, excision of peri-eso- phageal veins, and portocaval shunts. Most, if not all, of these surgical proce- dures have been concerned with a direct attack upon some portion of the portal venous system of the liver. An exception to this statement is the procedure of splenic artery ligation. Since first reported by Blain5 in 1918, this procedure has not been widely employed. During the past few years, however, the procedure has received some emphasis by such reports as those of Everson and Cole,9 Blain and Blain,6 and Moore, Shingleton and Pickett.16 All of these authors, as well as others, have found it a useful palliative procedure in patients with intractable ascites whose condition was too poor to expect them to endure a very exten- sive procedure. Recently a different approach to the problem has been suggested, namely the alteration of the hepatic arterial circulation by ligation of the hepatic artery. DISCUSSION The concept that there is an interde- pendent pressure relationship between the hepatic artery and the portal vein is not new. Betz,4 working in Ludwig's laboratory in 1863, sought to answer the following ques- tion: Does the amount of blood entering the liver through the portal vein and the hepatic artery depend upon their relative pressures? He demonstrated as a result of his studies the influence of the portal pressure in de- creasing the arterial flow. Gad,11 in 1873, concluded as a result of experimental work, that the arterial circula- tion in the liver performed a double func- tion in that it brought oxygen and mechan- ically controlled the portal flow. 756 * Read before the Southern Surgical Associa- tion, Hot Springs, Virginia, December 5, 1951.

of the liver, ascites and esophageal varices, omentopexy

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EARLY RESULTS FOLLOWING THERAPEUTIC LIGATION OFTHE HEPATIC ARTERY

PRELIMINARY REPORT OF CASES*ARTHUR I. CHENOWETH, M.D.

BIRMNGHAM, ALA.

THAT MEDICAL MANAGEMENT of cirrhosisof the liver is currently the treatment ofchoice is undisputed. However, in spite ofthe best efforts of the physician, supportedby complete cooperation on the part of thepatient, such treatment is all too often inef-fectual, and the patient succumbs to pro-gressive liver failure, inanition with wastingascites, or exsanguination after one or re-peated bouts of hemorrhage from esopha-geal varices.The last two manifestations of cirrhosis

of the liver, ascites and esophageal varices,have for many years commanded the atten-tion of surgeons, who have sought, by oper-ative measures, to correct the existing com-plication. In many cases the result has beengratifying, and the patient restored to a lifeof activity. In many other cases disappoint-ing failure has been experienced.As a measure of the lack of uniform suc-

cess attending surgical treatment, we mightcite the number and variety of proceduresutilized by surgeons. Among these areomentopexy, splenectomy, injection of scle-rosing substances into esophageal varices,total gastric resection, resection of eso-phagogastric junction, excision of peri-eso-phageal veins, and portocaval shunts.

Most, if not all, of these surgical proce-dures have been concerned with a directattack upon some portion of the portalvenous system of the liver. An exception to

this statement is the procedure of splenicartery ligation. Since first reported byBlain5 in 1918, this procedure has not beenwidely employed. During the past fewyears, however, the procedure has receivedsome emphasis by such reports as those ofEverson and Cole,9 Blain and Blain,6 andMoore, Shingleton and Pickett.16 All of theseauthors, as well as others, have found it auseful palliative procedure in patients withintractable ascites whose condition was toopoor to expect them to endure a very exten-sive procedure.

Recently a different approach to theproblem has been suggested, namely thealteration of the hepatic arterial circulationby ligation of the hepatic artery.

DISCUSSION

The concept that there is an interde-pendent pressure relationship between thehepatic artery and the portal vein is notnew.

Betz,4 working in Ludwig's laboratory in1863, sought to answer the following ques-tion: Does the amount of blood entering theliver through the portal vein and the hepaticartery depend upon their relative pressures?He demonstrated as a result of his studiesthe influence of the portal pressure in de-creasing the arterial flow.

Gad,11 in 1873, concluded as a result ofexperimental work, that the arterial circula-tion in the liver performed a double func-tion in that it brought oxygen and mechan-ically controlled the portal flow.

756

* Read before the Southern Surgical Associa-tion, Hot Springs, Virginia, December 5, 1951.

THERAPEUTIC LIGATION OF THE HEPATIC ARTERY

It remained, however, for Herrick,13 in1907, to carry out carefully controlledstudies on liver blood flow which undoubt-edly provide the rationale upon which theoperation of hepatic artery ligation is based.Herrick's studies were based upon the as-

sumption that the liver represented a freelyexpansible tissue framework housing twoseparate afferent circulations, the hepaticarterial and the portal venous, both ofwhich were drained by a single efferent sys-tem, the hepatic vein. He recognized thatbranches of'both the hepatic artery and theportal vein flowed into the sinusoids, andthat there were also direct arteriovenouscommunicati'ons between the branches ofthe artery and the vein proximal to thesinusoids. The validity of this anatomicalarrangement has been verified by manyinvestigators throughout the years." 19 Heconcluded that the factors contributing toportal hypertension in cirrhosis were: (1)the direct communication of the arterialpressure to the portal vessels through di-lated capillaries, and (2) the larger volume-flow of the hepatic artery in proportion tothe portal flow in cirrhosis as compared tothat in the normal liver.Numerous other studies have since been

conducted to determine the relativeamounts of blood carried by the hepaticarterial and the portal venous systems. Bur-ton-Opitz7 stated that the hepatic arteryunder normal conditions carried approxi-mately 25 per cent of the total volume ofblood reaching the liver, the rest being car-

ried by the portal vein. Markowitz, Rappa-port and Scott15 in 1949, measured thehepatic flow in dogs and found that theartery contributed 20 per cent of the totalflow. Other investigators have made esti-mates of arterial flow ranging from 12 percent to 39 per cent of the total.The pressure in the portal vein under

normal conditions is between 8 and 12 mm.Hg. That, in the hepatic artery, is normallybetween 120 and 130 mm. Hg. There is ap-

parently a wide variation in these pressures

from time to time in the same individual,and the two pressures are interdependent,as has been shown by studies later to bequoted. In general, it has been shown thatthe arterial circulation is represented by a

high-pressure, small volume system and theportal circulation by a low-pressure, largevolume system. In cirrhosis these conditionsare more or less directly reversed.

Nearly half a century after Herrick's ob-servations were reported, Dock8 carried outa similar study, which for the most part con-

firmed the results reported by the formerauthor. Using kerosene as a perfusion fluidto avoid edema, Dock carried out doubleperfusion experiments in normal and incirrhotic livers. Cannulas of suitable sizewere tied in the portal vein and the hepaticartery, and each was connected to a mano-

meter. The pressure in each system couldthus be varied at will and the flow undervarying conditions of pressure measured.The total portal and hepatic flow was

found to average 2420 cc. per minute in nor-

mal livers, 2270 cc. in cirrhotic livers fromalcoholics, 1880 cc. in non-alcoholic cir-rhotics, and 900 cc. in one large fatty liverfrom an alcoholic. These figures were ob-tained with a'portal pressure of 20 mm. Hg.

and an arterial pressure of 100 mm. Hg.Measurements were made with portal pres-

sure at 0 and arterial pressure at 100; withportal at 20 and arterial at 0; and with por-

tal at 20 and arterial at 100.' There was in-variably a decrease in portal flow when thearterial inflow was opened, the decreasebeing as follows: in normal livers 30 per

cent, in non-alcoholic cirrhotics 21 per'cent,and in alcoholic cirrhosis 78 per cent. In hisconclusions Dock suggests that "in healedalcoholic cirrhosis, with ascites or danger offatal hemorrhage, procedures to reducehepatic arterial inflow may be worth con-

siderationIt is thought that in the production of

portal hypertension in cirrhosis at least two

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ARTHUR I. CHENOWETH

factors operate: (1) decrease in the avail-able portal bed, and (2) increase in thearterial bed, probably with associated ab-normally large arteriovenous communica-tions within the liver substance.

In their excellent paper dealing with this

subject, Berman, Koenig, and Muller2 sum-

marize the results of experimental work on

were the first to point out the importanceof the role of bacteria in death followingligation of the artery. At the same timethey demonstrated that the pre- and post-operative administration of antibiotics pre-vented death in most of the animals. Theseobservations have since been confirmed byother investigators.

TABLE I.

Mr. A. P. W. M. 38Date Ceph.-Floc. Prothrombin Proteins A/G B. S. P. N. P. N.

March 24 34%April 3 0 1+ 43% 4.9 3.3/1.6 20April 24 43% 4.9 2.6/2.3May 23 0 0 71.4% 6.4 3.5/2.9 70% 15%July 9 6.96 3.9/3.0 80% 20% 34.1November 23 0 1 + 72.3% 7.20 1.7/1. 55% 15%

portal hypertension carried out over a

period of several years. A few of their ob-servations may be cited, as follows:

1. Ligation of the hepatic artery at theceliac axis caused a fall in portal pressureof 10-20 mm. of water.

2. Ligation of splenic artery after liga-tion of hepatic artery caused an additionalfall of 40-50 mm. of water.

3. Ligation of the splenic artery firstcaused a slight fall of 5-10 mm. of water;after the hepatic artery was ligated therewas an additional fall of 40-60 mm. ofwater.

4. Ligation of the hepatic artery and thenof the splenic artery one month later pro-duced an additional fall in portal pressure.

5. If the splenic artery was tied first, thenthe hepatic artery 30 days later, there was a

precipitous fall in portal pressure.

The authors conclude that experimentson dogs seem to indicate that ligation of thehepatic and splenic arteries will produce a

sustained fall in portal pressure and may beapplicable in the treatment of portal hyper-tension.That ligation of the hepatic artery is com-

patible with survival is now well recog-nized. Markowitz, Rappaport, and Scott15

Recently, however, Fraser, Rappaport,Vuylstere, and Colwell10 have shown a mor-

tality rate of 35 per cent in dogs subjectedto ligation of the hepatic artery, in spite ofantibiotic therapy. They demonstrated thatin addition to the role played by infection,a significant factor in the deaths followingligation was ischemic necrosis of the liver.They further demonstrated that even inthose dogs that survived there was evidenceof some degree of liver impairment, mani-fested by abnormal liver function tests dur-ing life, or by pathologic examination of theliver after the surviving dogs had beensacrificed.

It is thus evident that, in spite of the use

of antibiotics, ligation of the hepatic arteryis not an entirely innocuous procedure.

CLNICAL EXPERIENCE

The first case reports dealing with liga-tion of the hepatic artery for control ofascites or hemorrhage were those of Rien-hoff,17 published in April, 1951. He reportedtwo cases in detail and cited four others,treated in the interval 1947 to 1950. In twocases the procedure was performed for mas-sive hemorrhage from varices, and in the

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Annals of SurgeryJune, 1952

THERAPEUTIC LIGATION OF THE HEPATIC ARTERY

other four for ascites. All six patients pre-

sented good results for the follow-up periodat hand.Berman, Muller, Fisch, and Martz3 have

recently reported ligation of the hepaticand splenic arteries close to the celiac axisin an elderly man with cirrhosis of the livercomplicated by ascites and varices. The pa-

tient has improved remarkably in strength,appetite and general condition. There hasbeen no further bleeding from the gastro-in-testinal tract, and there has been no recur-

control of massive hemorrhage from eso-

phageal varices in two desperately illpatients.

Case 1.-Mr. A. P.: A 38-year-old service sta-tion operator was admitted to Jefferson-HillmanHospital at 4:00 A.M., March 24, 1951, with a his-tory of having vomited a large amount of brightred blood 6 hours previously. Significant findingsin the past history were as follows: the patient hadhad frequent bouts of epigastric discomfort forseveral years and had been told by his physicianthat he had an "ulcer," although gastro-intestinalroentgenograms were not taken. For the previous

TABLE II.

Mrs. L. B. W. F. 43Date Ceph.-Floc. Prothrombin Proteins A/G B. S. P. N. P. N.

April 15 1+ 2+ 100% 4.8 2.6/2.2April 19 6% 6%April 28 2 + 3 + 100% 6.4 3.6/2.8September 18 1+ 2+ 89% 7.8 3.1/4.7 40% 10% 23.7November 24 4+ 4+ 70% 7.0 30% 25%

rence of ascites with the patient on a low-salt diet. On the other hand, various liverfunction studies have not been significantlyaltered. These authors state that five otherpatients have been subjected to the ligationprocedure and are to be reported later.During the past year or more this proce-

dure has been carried out in a number ofother cases in this country, though the re-

ports have not appeared in the literatureat the time of this writing. It is known thatamong these as yet unreported cases therehave been some deaths. Whether death inthese cases has been due to failure of theprocedure to arrest the progress of the dis-ease, or whether the procedure itself con-

tributed to the ensuing mortality, is notknown.Some additional investigative work in

connection with the ligation procedure isnow in process in more than one institution,and it is to be hoped that in the near futurefurther light will be shed upon the mech-anism involved.A short time after Rienhoff's report be-

came available, there arose the problem of

ten years he had consumed alcohol with regularity,"about 5 or 6 drinks a day." In November, 1950,he had been hospitalized at another institution be-cause of jaundice and ascites. A diagnosis of cir-rhosis of the liver had been made, a paracentesisperformed and the patient placed on a regimen ofhigh carbohydrate, high protein diet, with vitaminsupplements. After 3 weeks in the hospital he was

discharged and remained fairly well but did notadhere to the prescribed regimen, and took occa-

sional drinks of whiskey. The abdomen again be-came moderately enlarged, but did not requiretapping. He had anorexia and a general lack ofenergy, but had no vomiting and no melena priorto the episode requiring admission.

Six hours before admission he vomited a smallamount of black fluid, had three tarry stools, thenvomited a large amount of bright blood. At thetime of admission, temperature was 97.8, pulse 90,and blood pressure 110/70. The patient was paleand looked chronically and acutely ill but was notin shock. Physical findings of interest were limitedto the abdomen, which was moderately distended,with dullness at the flanks and a palpable fluidwave. The liver could be felt four fingersbreadthbelow the costal margin on the right and in themid-line. The edge was irregular and the surfaceuneven. There was no tenderness. The spleen was

barely palpable. There was no edema of the lowerextremities.

Laboratory. Urinalysis: Negative. Blood count:Hemoglobin 10.5 Gm., R.B.C. 3,400,000, W.B.C.

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ARTHUR I. CHENOWETH

14,250. Differential: Normal. Blood Kahn: Nega-tive. Prothrombin time: 34 per cent of normal.Cephalin flocculation: Negative at 24 hours, oneplus at 48 hours. Additional laboratory studieswere carried out at intervals, as shown in Table I.

Course. The patient did not appear to bebleeding actively at the time of admission. Hewas placed on a regimen of nothing by mouth,given morphine at regular intervals for sedation,and was given glucose and supplementary vitaminsintravenously. About 6 hours after admission hevomited approximately 300 cc. bright red blood.

sis. The spleen was not enlarged. There was noevidence of duodenal ulcer. The gastrohepaticligament was divided betwen clamps and thestomach retracted downward and to the left. Whenthe hand was introduced into the lesser peritonealsac a vigorous machinery-like thrill was palpablealong the course of the hepatic artery. This arterywas identified by touch, lying just beneath theupper margin of the pancreas. With moderatedifficulty a heavy silk ligature was passed aroundthe artery near its point of emergence from theceliac axis. The portal venous pressure was then

Mfr. A. P. W. K. 38 Admltted March X4, 1951

haXh 2 S26 P. 7 M 29M30 1 I P, a 4 5 6 7 a 2 lo n 12 1.3

14 a I I

10 _XXX_____

14

_ ._

7.

4 _ _ A. L__... - H__|___

3

FIG. 1.-Alternate loss of blood by hemorrhage, and restoration by transfusion.On each of the following 2 days he was given atransfusion of 500 cc. His course thereafter wasone of alternate loss of blood by hemorrhage, andrestoration by transfusion. This is graphically rep-resented in Figure 1. Melena was a prominentmanifestation of the bleeding. This feature, sup-plementing the patient's statement that he had hadan ulcer, prompted us to depart from our custom-ary policy and secure an upper gastro-intestinalseries. This study revealed definite esophagealvarices and evidence of-esophagitis; it also revealeda deformity of the first portion of the duodenumconsistent with an ulcer, and dilatation of the sec-ond and third portions of the duodenum. After aperiod of 12 days of intermittent bleeding it wasapparent that the patient was losing ground andthat a fatal outcome was imminent.

Therefore, on April 6, the patient was taken tothe operating room and the abdomen was openedthrough an upper right rectus incision. There wereapproximatelly 3 liters of ascitic fluid present. Theliver was markedly enlarged and nodular, havingthe characteristic appearance of advanced cirrho-

measured in a vein on the greater curvature ofthe stomach. It was found to be 370 mm. water.The artery was then ligated in continuity and theportal pressure, measured in the same vein, wasfound to be 330 mm. water. The machinery-likethrill had completely disappeared. A biopsy of theliver was taken and the abdomen closed.

The patient's postoperative course was un-eventful and he had no further evidence of bleed-ing. He was placed on penicillin and aureomycinfor 6 days after operation and was given largedoses of vitamin B and C. He was also givendaily doses of vitamin K, intramuscularly, in spiteof the fact that the prothrombin time did notrespond to this. Ascites developed and becamemore marked than that existing before operation.Paracentesis of 8 liters and 7 liters were performedon the tenth and seventeenth days after operation.He gradually regained strength and was dis-charged from the hospital the eighteenth day afteroperation-to be maintained on a regimen of high-carbohydrate, high protein diet, large doses of

760

Anials of SursyJune. 1952

Volume 135 THERAPEUTIC LIGATIONNumber 6

vitamins B and C, and to be given crude liverextract intramuscularly 3 times a week.

Since his discharge from the hospital the pa-tient has been followed at regular intervals. Forthe first 2 months his appetite was poor, he lackedenergy and strength and felt bad generally. Dur-ing this time there was pronounced ascites, whichon one occasion was almost sufficient to justifyparacentesis. There was also at this time a 2+pitting edema of the ankles. At the end of the2-month period, without any change in manage-ment, he began to make progressive improvement;appetite and energy increased and he returned tohis occupation. The ascites diminished and ankleedema disappeared. When seen 3 months afteroperation there was no ascites; the liver edge wasbarely palpable; the spleen not palpable; andthere was no bruit audible in the epigastrium. Hehas continued well to date. Various blood chem-ical and liver function studies are recorded inTable I.

Case 2.-Mrs. L. B., a 43-year-old housewife,was admitted to Jefferson-Hillman Hospital, April14, 1951, because of massive hematemesis. A sum-mary of the history revealed that approximately1 month previously she had had several bouts ofmassive hematemesis, requiring a total of 28 pintsof blood. In another city a laparotomy had beencarried out with the findings of an enlarged spleenand a "cirrhotic liver." The surgeon at the timeelected to carry out no therapeutic procedure. Fol-lowing operation there was no further bleeding for26 days. Then 4 days before admission she againhad several bouts of hematemesis. Her local sur-geon inserted a nasal tube with a balloon and shewas transported by ambulance to Jefferson-HillmanHospital. On admission, temperature was 99.6°,pulse 100, and blood pressure 130/100. Examina-tion disclosed a middle-aged white woman whowas rather lethargic and looked both acutely andchronically ill, but was not in shock. Interest cen-tered on the abdomen: there was dullness in bothflanks. An enormous spleen extended well belowthe left iliac crest. The liver was not palpablyenlarged. A finding of particular interest was aloud machinery-like bruit audible just below thexyphoid.

Laboratory. Urinalysis negative. Blood: Hemo-globin: 6.8 Gm., R.B.C. 2,200,000, W.B.C. 6150.Differential normal. Hematocrit 22. Cephalin floc-culation 1+ in 24 hours, and 2+ in 48 hours.Total protein 4.8 mg., albumin 2.6 mg., globulin2.2 mg. Prothrombin time 100 per cent.

Course. The patient was placed on nothing bymouth, given parenteral fluids, including blood

OF THE HEPATIC ARTERY

transfusions, while preparations were made tocarry out a laparotomy. Figure 2 represents thispatient's hospital course. The morning after ad-mission the patient vomited a small amount ofblood around the nasal tube and the tube was re-moved. There was no evidence of further bleedingduring the first 48 hours after admission and oper-ation was planned for the morning of the thirdhospital day. However, the evening before, thepatient vomited an estimated 1500 cc. of brightred blood, went into shock and lapsed into coma.There were no localizing neurologic signs, and itwas thought that the coma was due to cerebralanoxia. Esophageal tamponage was accomplishedby means of a Levin tube with a large balloon at-tached. During the next 3 days the patient's con-dition remained about the same, but the fourthday she showed remarkable improvement and wasmentally clear. Therefore, on that afternoon, theseventh day after admission, the patient was takento the operating room. Under ether anesthesia aleft thoraco-abdominal incision was made. Therewas a small amount of ascitic fluid present. Theliver was surprisingly smooth and was not en-larged; the omentum was adherent to the undersurface of the right lobe. The spleen was of enor-mous size, and there were extremely large, dilatedveins in the omentum. (The findings strongly sug-gested portal hypertension on the basis of extra-hepatic portal vein obstruction. A biopsy of theliver was taken. The lesser peritoneal cavity wasentered by division of the gastrohepatic ligament.Palpation revealed a vigorous machinery-like thrillalong the course of the hepatic artery. The arterywas isolated near the celiac axis and a heavy silkligature passed around it. The portal pressure,measured in a vein on the greater curvature ofthe stomach, was 440 mm. water. After the ligaturearound the common hepatic artery had been tied,the portal pressure was 370 mm. water, and thethrill had disappeared. The splenic artery was thenligated near the hilum of the spleen. The finalportal pressure was 310 mm. water. The chest andabdomen were then closed. Immediately after oper-ation the esophageal tampon was removed. Shewas placed on large doses of penicillin and aureo-mycin. The postoperative course was smooth, andthere was no further hematemesis. On the eveningof the third postoperative day, however, the pa-tient passed several liquid tarry stools. At thetime, this was thought to represent simply thepassage of residual blood already in the bowel.In view of the fact that a blood count the follow-ing day revealed a slight drop in hemoglobin, onemust conclude that this represented an episode ofactive bleeding (see Figure 2). The course after

761

ARTHUR I. CHENOWETH

this was entirely uneventful, although the patientcomplained for several days before discharge of a

pain in the left flank. There was no ascites. Thepatient was discharged 14 days after operation.

Inasmuch as this patient lives in a distant city,it has not been possible to examine her at frequentintervals; however, she has remained under thecare of her local surgeon, and has reported to us

on 2 occasions for follow-up studies. She was ex-amined for the first time September 17, ten weeksafter discharge from the hospital. At that time she

Efforts to establish the cause of the chills andfever have been unsuccessful to date. They arealmost certainly not a result of hepatic artery liga-tion. Whether or not they bear a causal relation-ship to the portal hypertension is of course notyet established. Numerous studies, includingcatheterization of the hepatic vein, are beingplanned for this patient, and it is hoped that thecomplex picture will be clarified as time goes on.Results of laboratory studies to date are revealedin Table II.

FIG. 2.-Blood count showing drop in hemoglobin, indicative of an episode of active bleeding.

related that 2 weeks after leaving the hospital, shehad a chill, with temperature elevated to 105° F.;the fever lasted only 2 hours. Since then she hashad repeated episodes at intervals of 2 or 3 days,characterized by nausea, chills, and fever, lasting2 or 3 hours. In the intervals between thesebouts she feels very well. For the first timeshe then disclosed that she has been subject tosimilar attacks for 15 years. Her appetite has beengood and she has had no hematemesis or melena.

The patient was again seen November 23, 1951,during the course of a chill followed by fever of1040. Examination of the abdomen at that timerevealed no ascites. The liver, which had not beenpalpable prior to operation, had been distinctlypalpable just below the costal margin when exam-

ined in September, and at the time of this lastexamination was markedly enlarged to 3 finger-breadths below the costal margin. The bruit, whichhad disappeared following surgery, was againaudible, both in the epigastrium and over the rightlobe of the liver.

COMMENT

A few comments regarding the manage-ment of these two cases are in order.The use of the makeshift balloon tampon

in case 2 may have been a life-saving pro-

cedure. If there had been available the ex-

cellent balloon tampon described and usedby Sengstaken, it would have been of greatvalue not only in case 2 but in case 1 as

well. Certainly the use of this type of tam-ponage is indicated in dealing with suchpatients, regardless of the definitive treat-ment to be adopted later. Judged by theexperiences of Sengstaken and Blakemore,17it provides the means of successfully con-

trolling hemorrhage while the condition ofthe patient is fortified by transfusions, vita-mins and general care.

762

Annals of SurgeryJune, 1952

Ni.. L. B. W. F. 43 Adttted Ka 14, 1951NW 16 17 18 19 2 2 2 2 2 26 WY n2 3 3 1 2 3 4

13 * U s_ II____1 L_L2 ,- L -L-_ -_10 O JI

1 _-- __5

4 ! '4- _ ___--4~~~~~~~~~~~'

3 U U Ur U

__ -f - _-

THERAPEUTIC LIGATION OF THE HEPATIC ARTERY

The site of ligation of the hepatic arteryin these cases differed from that describedby Rienhoff. He ligated the common hepaticartery distal to the gastroduodenal branch.Our decision to ligate near the celiac arterywas based upon the presence in both pa-tients of the vigorous, machinery-like thrillalong the entire course of the hepatic artery.We are not sure, even now, of the signifi-cance of this thrill, but have thought that itmight possibly be due to the presence of ab-normal arteriovenous communications out-side the liver. In this event it seemed desir-able to eliminate this condition, if possible.

Support for the selection of this site isalso derived from a paper by RoscoeGraham.'2 In reporting a case of accidentalligation of the hepatic artery, he reviewedthe literature on the subject and concludedthat, because of potential collateral circula-tion, the prospect of liver necrosis increasessteadily as the point of ligature of the

hepatic artery moves toward the periphery.This much can be stated with certainty:

the procedure as carried out in either ofthese patients was not technically easy. Ac-cess to and exposure of the main trunk ofthe common hepatic artery was difficultthrough the abdominal incision and onlyslightly less so through the thoraco-abdom-inal approach. If, therefore, ligation of thevessel in the region of the common ductprovides the same end result, certainly thatis the desirable site, for it is much more

accessible.It is to be noted that the splenic artery

was not ligated in the first case. The deci-sion not to ligate this vessel was arbitrarilymade, based upon the fact that the spleenwas not enlarged. The wisdom of this deci-sion remains in doubt, as it depends in partupon the rationale of the ligation procedure.Although chief emphasis in the discussion

of hepatic artery ligation has thus far beenplaced upon the mechanical factor of portalhypertension, it seems quite likely that an

altered physiology is likewise brought about

by the ligation procedure. If this is so, itmay be accomplished by the increased por-

tal flow attendant upon the diminished ar-

terial flow. For example, Mann and Ma-gath14 found that in dogs, liver regenerationwas retarded by diversion of the portal flowthrough an Eck fistula. Whether restorationof portal flow in patients with cirrhosis maybe followed by regeneration of functionalliver tissue is, at this point, purely conjec-tural.Based upon experimental observations

herein cited, and the very limited clinicalexperience thus far available, it is my opin-ion that the procedure of hepatic arteryligation may prove to have merit. However,much additional information, both experi-mental and clinical, is needed to clarify thecomplex physiologic process involved.Until such information is available, it is mybelief that the procedure should be utilizedonly in carefully selected cases on whom in-tensive follow-up studies can be made.

SUMMARY

Experimental observations which providea rationale for the procedure of therapeuticligation of the hepatic artery in cirrhosis ofthe liver are cited. An account is given ofthe few clinical cases thus far reported, andtwo additional cases are reported in detailin which the procedure has been utilizedfor the control of massive hemorrhage fromesophageal varices. A few comments re-

garding the technical aspects of the proce-

dure are offered. Attention is called to a

vigorous machinery-like thrill along thecourse of the hepatic artery in two patients,manifested also by an audible bruit in theepigastrium of the second patient. Thisbruit may be of significance in portal hyper-tension.

Acknowledgment. The second patient reportedwas referred to me through the courtesy of Dr.Charles M. Donald, who participated with me inthe surgical procedure.

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ARTHUR I. CHENOWETH

BIBLIOGRAPHYAndrews, W. H. H., G. G. Maegraith and C. E.

M. Weayon: Studies on Liver Circulation;Micro-anatomy of Hepatic Circulation. Ann.Trop. Med., 43: 229, 1949.

2 Berman, J. K., H. Koenig and J. P. Muller: Li-gation of Hepatic and Splenic Arteries inTreatment of Portal Hypertension. Arch.Surg., 63: 379, 1951.

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4 Betz, cited by Herrick.'35 Blain, A. W.: Ligation of the Splenic Artery for

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11 Gad, cited by Herrick.'312 Graham, R. R., and D. Cannell: Accidental

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13 Herrick, F. C.: Experimental Study into Causeof Increased Portal Pressure in Portal Cirrho-sis. J. Exper. Med., 9: 93, 1907.

14 Mann, F. C., and T. C. Magath: Production ofChronic Liver Insufficiency. Am. J. Physiol.,59: 485, 1922.

15 Markowitz, J., A. Rappaport and A. C. Scott:Prevention of Liver Necrosis Following Liga-tion of Hepatic Artery. Proc. Soc. Exper.Biol. & Med., 70: 305, 1949.

16 Moore, R. M., A. 0. Singleton and W. H.Pickett: Splenic Artery Ligation in Palliationof Ascites. Ann. Surg., 131: 774, 1950.

17 Rienhoff, W. F., Jr.: Ligation of the Hepaticand Splenic Arteries in the Treatment ofPortal Hypertension with a Report of SixCases. Bull. Johns Hopkins Hosp., 88: 368,1951.

18 Sengstaken, R. W., and A. H. Blakemore: Bal-loon Tamponage for the Control of Hemor-rhage from Esophageal Varices. Ann. Surg.,131: 781, 1950.

19 Wakim, K. G., and F. C. Mann: IntrahepaticCirculation of Blood. Anat. Rec., 82: 233,1942.

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