6
Nonoperative Management of Hemobilia TED E. LOCKWOOD, M.D., LARRY SCHORN, M.D., DALE COLN, M.D. Traumatic hemobilia is an uncommon complication of blunt or penetrating liver injury and is characterized by jaundice, biliary colic, gastrointestinal hemorrhage, and a recent history of abdominal trauma. The clinical diagnosis of hemobilia is confirmed by endoscopy and selective arteriography. Selec- tive hepatic artery angiography will locate the site of bleeding, and determine the extent of liver injury. The choice of treat- ment of hemobilia depends on the severity of the hemorrhage and the extent of injury. The treatment of massive or persis- tent hemobilia is surgical drainage of hematoma and ligation of bleeding sites. Non-massive hemobilia may be treated con- servatively with liver healing documented by serial selective arteriograms. The nonoperative treatment of a case of non- massive hemobilia with a good result is presented. EMOBILIA is an uncommon complication of major hepatic injury. In a recent review of the English literature McGehee,17 gathered 69 cases of traumatic hemobilia, while Sandblom,19 found 137 cases in the world's literature. Hemorrhage into the gastrointestinal tract through the biliary tract as a result of liver injury was termed "traumatic hemobilia" by Sandblom in 1948.18 This syndrome is characterized by jaundice, biliary colic, gastrointestinal hemorrhage, and a recent history of trauma. Although the onset is variable, hemobilia frequently appears one to four weeks follow- ing abdominal trauma.6'19'25 Blunt or penetrating trauma to the liver may result in an intrahepatic collec- tion from injury to liver parenchyma and branches of the arterial, venous, and biliary ductal systems. Necro- sis of the damaged liver can result in an intrahepatic cavity which may be associated with a fistula between the arterial and biliary systems. The resultant hemo- bilia is often massive and may be life-threatening.19'22 Massive or persistent hemobilia should be treated by appropriate surgical therapy.17'19 In contrast, non- massive hemobilia may be treated by conservative non- operative measures including careful observation, transfusions, and serial selective arteriography as demonstrated in the following case. From the Department of Surgery, The University of Texas Southwestern School of Medicine and the Trauma Surgical Service, Parkland Memorial Hospital, Dallas, Texas Case Report R.M., a 22-year-old previously healthy man, presented to the Parkland Memorial Emergency Room with a small caliber gunshot entering his back at the level of the tenth thoracic vertebra in the midscapular line with the missile palpable in subcutaneous tissue in the right anterior axillary line at the same level. Vital signs were stable. His abdomen was tender in the right upper quad- rant and his bowel sounds were absent. The chest x-ray was normal. At laparotomy a bleeding stellate laceration of the lateral aspect of the right lobe of the liver was noted. Hemostasis was obtained by the placement of a single 0-chromic mattress suture and the liver injury was drained through a separate stab wound in the right flank. The postoperative course was uneventful and the patient was discharged on the fifth postoperative day. He was read- mitted three days later with colicky right upper quadrant abdominal pain, jaundice and a hemoglobin of 9.7 gm. The serum amylase and liver enzymes were elevated. Nasogastric aspirate yielded Guiaic- positive, coffee ground appearing material. The patient was treated with nasogastric suction, antacids, intravenous fluids, and bed rest. Two units of packed red blood cells were required over the next 48 hours to keep the hemoglobin stable. A diagnosis of hemobilia was made the following day at endoscopy when blood was seen spurt- ing from the ampulla of Vater. The remainder of the endoscopic exam was normal. Emergency celiac arteriography demonstrated a 5.5 cm, rounded filling defect in the posterolateral aspect of the right hepatic lobe consistent with a post-traumatic hematoma (Fig. 1). A pseudoaneurysm with an arteriobiliary fistula was noted at the edge of the filling defect in the posterior-superior division of the superior branch of the right hepatic artery (Figs. la and b). Blood clots could be visualized in the biliary tree of the right lobe (Fig. ic). Active bleeding was not demonstrated on the anteriogram. A defect in the right hepatic lobe consistent with hematoma was confirmed by sonography (Figs. 2a and b). Because the patient was not bleeding and the location of the pseudoaneurysm was in a peripheral hepatic branch where it might heal, it was elected to treat the patient with bed rest and observation for signs of recurrent hemorrhage or sepsis. No further bleeding occurred. Four units of packed red blood cells were transfused to raise the hemoglobin to 13 gm%. The patient remaine, asymptomatic and afebrile with- out signs of sepsis during a three-week hospitalization. The white blood cell count rose to 17,000 but returned to normal in a week. Serum amylase was normal within three days of admission. All liver function studies except the alkaline phosphatase were 335 Submitted for publication June 29, 1976. Reprint requests: Dale Coln, M.D., Department of Surgery, University of Texas Health Science Center, 5323 Harry Hines Boulevard, Dallas, Texas 75235.

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Nonoperative Management of Hemobilia

TED E. LOCKWOOD, M.D., LARRY SCHORN, M.D., DALE COLN, M.D.

Traumatic hemobilia is an uncommon complication of bluntor penetrating liver injury and is characterized by jaundice,biliary colic, gastrointestinal hemorrhage, and a recent historyof abdominal trauma. The clinical diagnosis of hemobilia isconfirmed by endoscopy and selective arteriography. Selec-tive hepatic artery angiography will locate the site of bleeding,and determine the extent of liver injury. The choice of treat-ment of hemobilia depends on the severity of the hemorrhageand the extent of injury. The treatment of massive or persis-tent hemobilia is surgical drainage of hematoma and ligationof bleeding sites. Non-massive hemobilia may be treated con-servatively with liver healing documented by serial selectivearteriograms. The nonoperative treatment of a case of non-massive hemobilia with a good result is presented.

EMOBILIA is an uncommon complication of majorhepatic injury. In a recent review of the English

literature McGehee,17 gathered 69 cases of traumatichemobilia, while Sandblom,19 found 137 cases in theworld's literature. Hemorrhage into the gastrointestinaltract through the biliary tract as a result of liver injurywas termed "traumatic hemobilia" by Sandblom in1948.18 This syndrome is characterized by jaundice,biliary colic, gastrointestinal hemorrhage, and a recenthistory of trauma. Although the onset is variable,hemobilia frequently appears one to four weeks follow-ing abdominal trauma.6'19'25 Blunt or penetratingtrauma to the liver may result in an intrahepatic collec-tion from injury to liver parenchyma and branches ofthe arterial, venous, and biliary ductal systems. Necro-sis of the damaged liver can result in an intrahepaticcavity which may be associated with a fistula betweenthe arterial and biliary systems. The resultant hemo-bilia is often massive and may be life-threatening.19'22Massive or persistent hemobilia should be treated byappropriate surgical therapy.17'19 In contrast, non-massive hemobilia may be treated by conservative non-operative measures including careful observation,transfusions, and serial selective arteriography asdemonstrated in the following case.

From the Department of Surgery, The University of TexasSouthwestern School of Medicine and the

Trauma Surgical Service, Parkland MemorialHospital, Dallas, Texas

Case Report

R.M., a 22-year-old previously healthy man, presented to theParkland Memorial Emergency Room with a small caliber gunshotentering his back at the level of the tenth thoracic vertebra in themidscapular line with the missile palpable in subcutaneoustissue in the right anterior axillary line at the same level. Vitalsigns were stable. His abdomen was tender in the right upper quad-rant and his bowel sounds were absent. The chest x-ray wasnormal. At laparotomy a bleeding stellate laceration of the lateralaspect of the right lobe of the liver was noted. Hemostasis wasobtained by the placement of a single 0-chromic mattress sutureand the liver injury was drained through a separate stab wound inthe right flank. The postoperative course was uneventful and thepatient was discharged on the fifth postoperative day. He was read-mitted three days later with colicky right upper quadrant abdominalpain, jaundice and a hemoglobin of 9.7 gm. The serum amylase andliver enzymes were elevated. Nasogastric aspirate yielded Guiaic-positive, coffee ground appearing material. The patient was treatedwith nasogastric suction, antacids, intravenous fluids, and bed rest.Two units of packed red blood cells were required over the next 48hours to keep the hemoglobin stable. A diagnosis of hemobilia wasmade the following day at endoscopy when blood was seen spurt-ing from the ampulla of Vater. The remainder of the endoscopicexam was normal. Emergency celiac arteriography demonstrated a5.5 cm, rounded filling defect in the posterolateral aspect of theright hepatic lobe consistent with a post-traumatic hematoma(Fig. 1). A pseudoaneurysm with an arteriobiliary fistula was notedat the edge of the filling defect in the posterior-superior divisionof the superior branch of the right hepatic artery (Figs. la and b).Blood clots could be visualized in the biliary tree of the right lobe(Fig. ic). Active bleeding was not demonstrated on the anteriogram.A defect in the right hepatic lobe consistent with hematoma wasconfirmed by sonography (Figs. 2a and b). Because the patient wasnot bleeding and the location of the pseudoaneurysm was in aperipheral hepatic branch where it might heal, it was elected totreat the patient with bed rest and observation for signs of recurrenthemorrhage or sepsis. No further bleeding occurred. Four unitsof packed red blood cells were transfused to raise the hemoglobinto 13 gm%. The patient remaine, asymptomatic and afebrile with-out signs of sepsis during a three-week hospitalization. The whiteblood cell count rose to 17,000 but returned to normal in a week.Serum amylase was normal within three days of admission.All liver function studies except the alkaline phosphatase were

335

Submitted for publication June 29, 1976.Reprint requests: Dale Coln, M.D., Department of Surgery,

University of Texas Health Science Center, 5323 Harry HinesBoulevard, Dallas, Texas 75235.

336 LOCKWOOD, SCHORN AND COLN

normal in three weeks. The alkaline phosphatase was normal at6 weeks. Selective hepatic arteriograms were done at 4 weeks and8 weeks post-injury. The 4-week arteriogram showed a markeddecrease in the size of the filling defect in the right lobe with nocommunication between the arterial and biliary systems (Fig. 3).There was an increase in size of the pseudoaneurysm. At 8 weeksthe arteriogram showed complete healing of the liver and dis-appearance of the pseudoaneurysm (Fig. 4). The patient remainsasymptomatic with normal liver function studies 6 months afterinjury.

Discussion

The diagnosis of traumatic hemobilia should be con-sidered in all cases of gastrointestinal hemorrhagefollowing blunt or penetrating injury to the liver. Biliarycolic, jaundice, and anemia associated with gastro-intestinal hemorrhage warrant a clinical diagnosis ofhemobilia. Endoscopy may identify the bleeding fromthe ampulla of Vater as the source of hemorrhagewhile excluding other causes of upper gastrointestinalbleeding. Selective arterial catheterization of the

FIG. la. The arterial phase of the right hepatic arteriogram per-formed 10 days post-injury demonstrates a pseudoaneurysm of theposterior-superior division of the superior branch of the righthepatic artery (arrow).

FIG. lb. The capillary phase of the right hepatic arteriogramdemonstrates a 5.5 cm intrahepatic rounded filling defect in theposterolateral aspect of the right hepatic lobe consistent withhematoma (arrows). Contrast material is seen entering the biliarytree (open arrows) via an arteriobiliary fistula.

FIG. ic. A late phase of the right hepatic arteriogram demon-strates retention of contrast material in the proximal biliary treesecondary to thrombotic occlusion of more distal biliary ducts(arrow). Numerous radiolucent defects in the biliary system repre-sent thrombi.

Ann. SLirg. * March 1977

Vol. 185 No. 3 NONOPERATIVE MANAGEMENT OF HEMOBILIA 337

IL

ANTE; OR ...t... i......0

- bxacs W FIG. 2b. Right oblique view of liver sonogram shows the sametm' taLJ]< eNtflUllC W. .,>.a,,{,,,,. onolucent defect in the right lobe (arrow).

FIG. 2a. Transverse view of liver sonogram demonstrates a 5 x 6cm sonolucent area in the posterolateral aspect of the right hepatic McGehee'7 acknowledged that while healing of arterio-lobe consistent with hematoma (arrow). biliary fistulae had been documented by serial arterio-

graphy by Hendren and others 13 nonoperative treat-hepatic artery following endoscopy will usually definethe site of the bleeding and extent of liver injury ^and help to plan the surgical approach should opera-+tion be indicated.4'7'8'11'16 Sonography may be useful 7- ; :_in confirming the size and location of the intrahepatic Shematoma. _The treatment of massive or persistent hemobilia is jy i

laparotomy with thorough debridement and drainage of }the liver cavity and suture ligation of bleeding sites.17"19 _4,i00If this is unsuccessful in controlling hemorrhage or _ ,,flXf f;;;;> ;;;if the hepatic inJury iS located centrally, ligation of theIXhepatic artery proximal to the origin of the gastro- -s

is often effective in controlling hemorrhage bylowering _ Z ! Ythe hepatic arterial pressure sufficiently for clotting to :

gastroduodenal artery. Because of the higher mortality i_sassociated with major hepatic resections in the treat- Mment of traumatic hemobilia, resectional therapy _1C7should be limited to cases of extensive hepatic injury _or to cases in which ligation of the bleeding site orthe hepatic artery has been unsuccessful in control-lling the hemorrhage.9"l7"9'22 The mortality for cases oflhemobilia treated operatively is 19%o and the re-bleeding rate is 23%.'3 l"lThe nonoperative treatment of hemobilia is contro- FIG. 3. Selective hepatic arteriogram obtained 4 weeks post-

versial. Many authors have stressed the need for injury demonstrates progressive healing of the liver injury. Although1 * * * r ^ . ~~~~~~~~~thepseudoaneurysm persists (arrow), the arteriobihiary fistula hasearly surgical intervention for all cases of traumatic closed and the hematoma cavity is significantly reduced in sizehemobilia once the diagnosis is confirmed.6"17'22 (white arrows).

LOCKWOOD, SCHORN AND COLN

TABLE 1. Review of English Literature: Nonoperative Treatment of Traumatic Hemobilia *

Operative orMethod of Arteriographic SurgicalDiagnosis Findings Treatment

Autopsy

Clinical and op-erative findings

Autopsy

Autopsy

Autopsy

Autopsy

Liver cavity and GB dis-tended with clot

Negative laparotomy

7. Hawthorne, 194112 Branched clot inemesis

8. Grey, 194725 Clinical and op- Blood in GB anderative findings

9. Sandblom, 194818 Clinical and op- Blood in GBerative findings

10. Hart, 195010 Operative find- Blood in GB andings

11. Bigger, 1950W Autopsy

12. Epstein, 19525 Clinical and op- Blood in GBerative findings

13. Bailing, 19561 Clinical Negative laparot

14. Sworn, 195920 Autopsy Blood in GB, nelcholangiogram

15. Hutchinson, 196115 Operative find- Blood in GB andings

16. Walt, 196922 Selective arteri-ography

17. Katz, 197016 Selective arteri- Intrahepatic pseiography aneurysm

18. Sandblom, 197219 Selective arteri- Small intrahepat:ography cavity

19. Sandblom, 197219 Selective arteri- Central cavity ar

ography hepatic hemat

20. Sandblom, 197219 Clinical

21. Sandblom, 197219 Autopsy

22. Hendren, 197213 Selective arteri- 2.5 cm intrahepaography with arteriobil

23. Hendren, 197213 Selective arteri- 3 cm intrahepatiography with arteriover

24. Lockwood, 1976 Endoscopy and 5.5 cm intrahepaselective ar- with arteriobilteriography

* Includes irrelevant operations.

ment resulted in death in 10 of 19 patients in hishistorical review and, therefore, he concluded thatnonoperative treatment was unacceptable.The high mortality rate attributed to the nonopera-

d CD

d CD

tomy

gative

d CD

udo-

tic

rnd extra-ioma

atic cavityiary fistula

ic cavitynous fistula

Ltic cavityiary fistula

None

Cholecystectomy

None

None

None

Exploratory laparo-tomy x2, gastro-jejunostomy

Cholecystectomy

Choledochostomy

Cholecystostomy

Choledochostomy

None

Cholecystostomy

Exploratory lapa-rotomy x2

Cholecystectomy,choledochostomy

Cholecystostomy,choledochostomy

None

None

None

Drainage extrahepatichematoma

None

None

None

None

None

Ann. Stirg. a March 1977

Result

Died

Recovered

Died: Case 10

Died

Died

Died

Recovered

Died

Recovered

Recovered

Died

Recovered

Recovered

Died

Recovered

Died: Massive hemobilia,died before reaching OR

Died: Death due to asso-ciated injuries

Recovered: Case 43,appendix

Recovered: Case 44

Recovered: Case 41

Died: Case 42

Recovered

Recovered

Recovered

tive treatment of traumatic hemobilia can be viewedskeptically. Five of the reported deaths occurred priorto 1934 and were diagnosed at autopsy (Table 1). In1941 Hawthorne was the first to recognize the patho-

338

Author, Date

1. Owen, 184818

2. Siegel, 190918

3. Thorlakson, 192921

4. Strauss, 192923

5. Wulsten, 193118

6. Hermanson, 193414I

Vol. 185 No. 3 NONOPERATIVE MANAGEMENT OF HEMOBILIA 339

genesis of hemobilia prior to necropsy after noting abranched clot in the emesis of his patient.12 Thepatient was treated with cholecystectomy and re-covered. Since 1941 18 cases of traumatic hemobiliatreated by either observation or an irrelevant opera-tion have been reported in the English literature(Table 1). In three of these 18 cases, the accuratediagnosis of traumatic hemobilia was first establishedat autopsy.2'920 In the remaining 15 patients the di-agnosis was based on clinical findings in associationwith either blood in the extra-hepatic biliary system ora positive arteriogram. Of these 15 patients in whichthe diagnosis was made clinically, observation oran irrelevant operation resulted in 12 long-term sur-vivors. One of the three deaths was related to asso-ciated injuries and not to the hepatic arteriobiliaryfistula.'6 This survival rate of 80%o includes all casesof traumatic hemobilia treated conservatively since1941 including massive as well as non-massive hemor-rhage. Non-massive hemorrhage is defined as requiringreplacement of less than half the total blood volumewithin a 24-48 hour period with cessation of hemor-rhage. In our patient, only two units of packed redblood cells were required in 48 hours to maintain astable hematocrit and no further bleeding occurred.Although Hendren recently reported a child withhemobilia treated conservatively who required morethan his estimated total blood volume in two days tomaintain a stable hematocrit,'3 hemorrhage of thismagnitude is life-threatening and likely represents aninjury to a major branch of the hepatic artery whichis unlikely to heal spontaneously. Restricting non-operative treatment to cases of non-massive hemobiliainvolving smaller more peripheral branches of thehepatic artery and using arteriography to documenthealing should reduce the morbidity and mortality.

Selective arterial catheterization provides accuratelocalization of the bleeding site in traumatic hemo-bilia.4'7"1"'6 Localization of the hemobiliary fistula,should surgery be required, is important. Massivebleeding can be slowed by injection of small amountsof epinephrine through the selective hepatic arterycatheter as recommended by Boijsen while the patientis prepared for emergency surgery.4 Boijsen notes thatepinephrine, when administered intra-arterially insmall amounts, produces a temporary, profoundarterial constriction and reduction in blood flow inthe hepatic vascular bed. Serial angiography has beenused to follow healing in patients with hepatichematomas3 and with massive and non-massive hem-orrhage secondary to traumatic hemobilia.13 Usingserial angiography, Hendren noted complete healing intwo children with traumatic hemobilia within 3 to8 weeks.'3 In the present case involving an adult,

FIG. 4. The selective hepatic arteriogram obtained 8 weekspost-injury demonstrates complete healing of the liver injury.

healing was noted at 3 weeks following diagnosiswith healing completed by 8 weeks. It seems reason-able to recommend careful observation using serialselective arteriograms in patients with traumatic hemo-bilia who present with non-massive hemorrhage in-volving smaller branches of the hepatic artery. If thehemorrhage is massive or persists, surgical treatmentis indicated.

References

1. Bailing, E. V.: Liver Injuries: Their Association with MassiveHematemesis and Melena, Aust. N.Z.J. Surg., 26:70, 1956.

2. Bigger, I. A.: In discussion of Biliary Tract Hemorrhage, Ann.Surg., 131:790, 1950.

3. Boijsen, E., Kaude, J. and Tylen, U.: Angiography in HepaticRupture, Acta Radiol., 2:363, 1971.

4. Boijsen, B., Judkins, M. P. and Simay, A.: AngiographicDiagnosis of Hepatic Rupture, Radiology, 86:66, 1966.

5. Epstein, H. J. and Lipshutz, B.: Hemobilia, Cholecystitis,and gastrointestinal bleeding with rupture of the liver,"'JAMA, 149:1132, 1952.

6. Fish, J. C. and Nippert, R. H.: Traumatic Hemobilia: TheDilemma of Delay, J. Trauma, 9:546, 1969.

7. Fowler, R. and Hiller, H. G.: Selective Hepatic Arteriographyin the Management of Traumatic Hemobilia, J. Pediat.Surg., 2:253, 1967.

8. Graff, R. J.: Considerations in the Treatment of TraumaticHemobilia, Am. J. Surg., 105:662, 1963.

9. Guillen, J. and Elliott, D. P.: Traumatic Hemobilia: A CaseReport, J. Trauma, 11:886, 1971.

340 LOCKWOOD, SCHORN AND COLN Ann. SLirg. * March 1977

10. Hart, D.: In discussion of Biliary Tract Hemorrhage, Ann.Surg., 131:790, 1950.

11. Hawes, D. R., Franken, E. A., Fitzgerald, J. F., andBattersby, J. S.: Traumatic Hemobilia: Angiographic Diag-nosis, Am. J. Dis. Child., 125:130, 1973.

12. Hawthorne, H. R., Oaks, W. W., and Neese, P. H.: LiverInjuries with a Case Report of Repeated Hemorrhages throughthe Biliary Ducts, Surgery, 9:358, 1941.

13. Hendren, W. H., Warshaw, A. L., Fleischli, D. J., andBartlett, M. K.: Traumatic Hemobilia: Nonoperative Manage-ment with Healing Documented by Serial Angiography,Ann. Surg., 174:991, 1971.

14. Hermanson, L. and Cabitt, H. L.: Hematemesis Due to Traumaof the Liver, Am. J. Surg., 26:568, 1934.

15. Hutchinson, W. B.: In discussion of Hemobilia, Arch. Surg.,83:80, 1961.

16. Katz, M. C. and Meng, C. H.: Angiographic Evaluation ofTraumatic Intrahepatic Pseudoaneurysm and Hemobilia,Radiology, 94:95, 1970.

17. McGehee, R. N., Townsend, C. M., Thompson, J. C., andFish, J. C.: Traumatic Hemobilia, Ann. Surg., 179:311, 1974.

18. Sandblom, P.: Hemorrhage into the Biliary Tract FollowingTrauma-Traumatic Hemobilia, Surgery, 24:571, 1948.

19. Sandblom, P.: Hemobilia, Springfield, Charles C Thomas, 1972.20. Sworn, B. R.: Traumatic Hemobilia with Severe Hematemesis

and Melena, Br. J. Surg., 47:254, 1959-60.21. Thorlaksen, P. H. T., Hay, A. W. S.: Rupture of the Liver,

Can. Med. Assoc. J., 20:593, 1929.22. Walt, A. J.: The Surgical Management of Hepatic Trauma and

its Complications, Ann. R. Coll. Surg. Eng., 45:319, 1969.23. Whelan, T. J. and Gillespie, J. T.: Treatment of Traumatic

Hemobilia, Ann. Surg., 162:920, 1965.24. Wilkinson, G. M., Mikkelsen, W. P. and Berne, C. J.:

The Treatment of Post-traumatic Hemobilia by Ligation ofthe Common Hepatic Artery, Surg. Clin. North Am., 58:1337, 1968.

25. Wright, P. W. and Orloff, M. J.: Traumatic Hemobilia, Ann.Surg., 160:42, 1964.