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. Selective hepatic artery angiography will locate the site of bleeding, and determine the extent of liver injury. The choice of treatment of hemobilia depends on the severity of the hemorrhage and the extent of injury. The treatment of massive or persistent hemobilia is surgical drainage of hematoma and ligation of bleeding sites. Non-massive hemobilia may be treated conservatively with liver healing documented by serial selective arteriograms. The nonoperative treatment of a case of nonmassive hemobilia with a good result is presented.
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 following abdominal trauma.6'19'25 Blunt or penetrating trauma to the liver may result in an intrahepatic collection from injury to liver parenchyma and branches of the arterial, venous, and biliary ductal systems. Necrosis 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 hemobilia 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, nonmassive hemobilia may be treated by conservative nonoperative measures including careful observation, transfusions, and serial selective arteriography as demonstrated in the following case. EMOBILIA is an uncommon
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.
335
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 quadrant 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 readmitted 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 Guiaicpositive, 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 spurting 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 without 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
336
LOCKWOOD, SCHORN AND COLN
Ann. SLirg. * March 1977
normal in three weeks. The alkaline phosphatase was normal at 6 weeks. Selective hepatic arteriograms were done at 4 weeks and 8 weeks post-injury. The 4-week arteriogram showed a marked decrease in the size of the filling defect in the right lobe with no communication between the arterial and biliary systems (Fig. 3). There was an increase in size of the pseudoaneurysm. At 8 weeks the arteriogram showed complete healing of the liver and disappearance of the pseudoaneurysm (Fig. 4). The patient remains asymptomatic with normal liver function studies 6 months after
injury.
Discussion The diagnosis of traumatic hemobilia should be considered in all cases of gastrointestinal hemorrhage following blunt or penetrating injury to the liver. Biliary colic, jaundice, and anemia associated with gastrointestinal hemorrhage warrant a clinical diagnosis of hemobilia. Endoscopy may identify the bleeding from the ampulla of Vater as the source of hemorrhage while excluding other causes of upper gastrointestinal bleeding. Selective arterial catheterization of the
FIG. la. The arterial phase of the right hepatic arteriogram performed 10 days post-injury demonstrates a pseudoaneurysm of the posterior-superior division of the superior branch of the right hepatic artery (arrow).
FIG. lb. The capillary phase of the right hepatic arteriogram demonstrates a 5.5 cm intrahepatic rounded filling defect in the posterolateral aspect of the right hepatic lobe consistent with hematoma (arrows). Contrast material is seen entering the biliary tree (open arrows) via an arteriobiliary fistula.
FIG. ic. A late phase of the right hepatic arteriogram demonstrates retention of contrast material in the proximal biliary tree secondary to thrombotic occlusion of more distal biliary ducts (arrow). Numerous radiolucent defects in the biliary system represent thrombi.
Vol. 185 No. 3
NONOPERATIVE MANAGEMENT OF HEMOBILIA
337
IL
ANTE; OR
-
bxacs
tm' taL J]
.a,,{,,,,.
FIG. 2a. Transverse view of liver sonogram demonstrates a 5 x 6
cm 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 arteriography by Hendren and others 13 nonoperative treat-
hepatic artery following endoscopy will usually define the 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 7in confirming the size and location of the intrahepatic S hematoma. _ 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,i00 If this is unsuccessful in controlling hemorrhage or _ ,,flXf if the hepatic inJury iS located centrally, ligation of theIX hepatic artery proximal to the origin of the gastrois often effective in controlling hemorrhage by lowering the hepatic arterial pressure sufficiently for clotting to
_ :
gastroduodenal artery. Because of the higher mortality i_s associated with major hepatic resections in the treat- M ment of traumatic hemobilia, resectional therapy _1C7 should be limited to cases of extensive hepatic injury or to cases in which ligation of the bleeding site or the hepatic artery has been unsuccessful in control-l ling the hemorrhage.9"l7"9'22 The mortality for cases ofl hemobilia treated operatively is 19%o and the rebleeding rate is 23%.'3 l"l The nonoperative treatment of hemobilia is controversial. Many authors have stressed the need for 1 * * * r . early surgical intervention for all cases of^ traumatic
hemobilia once the diagnosis is
confirmed.6"17'22
;
:_
f;;;;> ;;; -s Z
!
Y
_
FIG. 3. Selective hepatic arteriogram obtained 4 weeks postinjury demonstrates progressive healing of the liver injury. Although pseudoaneurysm persists (arrow), the arteriobihiary fistula has ~~~~~~~~~the closed and the hematoma cavity is significantly reduced in size
(white arrows).
338
LOCKWOOD, SCHORN AND COLN
Ann. Stirg. a March 1977
TABLE 1. Review of English Literature: Nonoperative Treatment of Traumatic Hemobilia *
Method of Diagnosis
Author, Date 1. Owen, 184818 2. Siegel, 190918
3. Thorlakson, 192921
Autopsy Clinical and operative findings Autopsy
4. Strauss, 192923
Autopsy
5. Wulsten, 193118
Operative or Arteriographic Findings Liver cavity and GB distended with clot
Surgical Treatment
Result
None
Died
Cholecystectomy
Recovered
None
Died: Case 10
None
Died
None
Died
Exploratory laparotomy x2, gastrojejunostomy
Died
Cholecystectomy
Recovered
6. Hermanson, 193414
Autopsy Autopsy
7. Hawthorne, 194112
Branched clot in
8. Grey, 194725
emesis Clinical and operative findings
Blood in GB andd CD
Choledochostomy
Died
9. Sandblom, 194818
Clinical and operative findings
Blood in GB
Cholecystostomy
Recovered
Operative findings
Blood in GB andd CD
Choledochostomy
Recovered
None
Died
Blood in GB
Cholecystostomy
Recovered
Negative laparottomy
Exploratory laparotomy x2
Recovered
I
10. Hart, 195010 11.
Bigger, 1950W
Negative laparotomy
Autopsy
13. Bailing, 19561
Clinical and operative findings Clinical
14. Sworn, 195920
Autopsy
Blood in GB, nelgative cholangiogram
Cholecystectomy, choledochostomy
Died
15. Hutchinson, 196115
Operative findings
Blood in GB andd CD
Recovered
16. Walt, 196922
Selective arteri-
Cholecystostomy, choledochostomy None
17. Katz, 197016
ography Selective arteriography
Intrahepatic
Selective arteri-
Small intrahepat:tic
ography Selective arteriography Clinical Autopsy Selective arteriography Selective arteriography Endoscopy and selective arteriography
cavity Central cavity arrnd extrahepatic hemat ioma
12. Epstein, 19525
18. Sandblom, 197219 19. Sandblom, 197219 20. Sandblom, 197219 21. Sandblom, 197219 22. Hendren, 197213
23. Hendren, 197213 24. Lockwood, 1976
*
psei udo-
None
aneurysm
None
2.5 cm intrahepaatic cavity with arteriobil iary fistula 3 cm intrahepati ic cavity with arteriovernous fistula 5.5 cm intrahepa Ltic cavity with arteriobil iary fistula
Drainage extrahepatic hematoma None None None
Died: Massive hemobilia, died before reaching OR Died: Death due to associated injuries Recovered: Case 43, appendix Recovered: Case 44 Recovered: Case 41 Died: Case 42 Recovered
None
Recovered
None
Recovered
Includes irrelevant operations.
ment resulted in death in 10 of 19 patients in his historical review and, therefore, he concluded that nonoperative treatment was unacceptable. The high mortality rate attributed to the nonopera-
tive treatment of traumatic hemobilia can be viewed skeptically. Five of the reported deaths occurred prior to 1934 and were diagnosed at autopsy (Table 1). In 1941 Hawthorne was the first to recognize the patho-
Vol. 185 No. 3
NONOPERATIVE MANAGEMENT OF HEMOBILIA
genesis of hemobilia prior to necropsy after noting a branched clot in the emesis of his patient.12 The patient was treated with cholecystectomy and recovered. Since 1941 18 cases of traumatic hemobilia treated by either observation or an irrelevant operation have been reported in the English literature (Table 1). In three of these 18 cases, the accurate diagnosis of traumatic hemobilia was first established at autopsy.2'920 In the remaining 15 patients the diagnosis was based on clinical findings in association with either blood in the extra-hepatic biliary system or a positive arteriogram. Of these 15 patients in which the diagnosis was made clinically, observation or an irrelevant operation resulted in 12 long-term survivors. One of the three deaths was related to associated injuries and not to the hepatic arteriobiliary fistula.'6 This survival rate of 80%o includes all cases of traumatic hemobilia treated conservatively since 1941 including massive as well as non-massive hemorrhage. Non-massive hemorrhage is defined as requiring replacement of less than half the total blood volume within a 24-48 hour period with cessation of hemorrhage. In our patient, only two units of packed red blood cells were required in 48 hours to maintain a stable hematocrit and no further bleeding occurred. Although Hendren recently reported a child with hemobilia treated conservatively who required more than his estimated total blood volume in two days to maintain a stable hematocrit,'3 hemorrhage of this magnitude is life-threatening and likely represents an injury to a major branch of the hepatic artery which is unlikely to heal spontaneously. Restricting nonoperative treatment to cases of non-massive hemobilia involving smaller more peripheral branches of the hepatic artery and using arteriography to document healing should reduce the morbidity and mortality. Selective arterial catheterization provides accurate localization of the bleeding site in traumatic hemobilia.4'7"1"'6 Localization of the hemobiliary fistula, should surgery be required, is important. Massive bleeding can be slowed by injection of small amounts of epinephrine through the selective hepatic artery catheter as recommended by Boijsen while the patient is prepared for emergency surgery.4 Boijsen notes that epinephrine, when administered intra-arterially in small amounts, produces a temporary, profound arterial constriction and reduction in blood flow in the hepatic vascular bed. Serial angiography has been used to follow healing in patients with hepatic hematomas3 and with massive and non-massive hemorrhage secondary to traumatic hemobilia.13 Using serial angiography, Hendren noted complete healing in two children with traumatic hemobilia within 3 to 8 weeks.'3 In the present case involving an adult,
339
FIG. 4. The selective hepatic arteriogram obtained 8 weeks post-injury demonstrates complete healing of the liver injury.
healing was noted at 3 weeks following diagnosis with healing completed by 8 weeks. It seems reasonable to recommend careful observation using serial selective arteriograms in patients with traumatic hemobilia who present with non-massive hemorrhage involving smaller branches of the hepatic artery. If the hemorrhage is massive or persists, surgical treatment is indicated.
References 1. Bailing, E. V.: Liver Injuries: Their Association with Massive Hematemesis 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 Hepatic Rupture, Acta Radiol., 2:363, 1971. 4. Boijsen, B., Judkins, M. P. and Simay, A.: Angiographic Diagnosis 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: The Dilemma of Delay, J. Trauma, 9:546, 1969. 7. Fowler, R. and Hiller, H. G.: Selective Hepatic Arteriography in the Management of Traumatic Hemobilia, J. Pediat. Surg., 2:253, 1967. 8. Graff, R. J.: Considerations in the Treatment of Traumatic Hemobilia, Am. J. Surg., 105:662, 1963. 9. Guillen, J. and Elliott, D. P.: Traumatic Hemobilia: A Case Report, J. Trauma, 11:886, 1971.
340
LOCKWOOD, SCHORN AND COLN
10. Hart, D.: In discussion of Biliary Tract Hemorrhage, Ann. Surg., 131:790, 1950. 11. Hawes, D. R., Franken, E. A., Fitzgerald, J. F., and Battersby, J. S.: Traumatic Hemobilia: Angiographic Diagnosis, Am. J. Dis. Child., 125:130, 1973. 12. Hawthorne, H. R., Oaks, W. W., and Neese, P. H.: Liver Injuries with a Case Report of Repeated Hemorrhages through the Biliary Ducts, Surgery, 9:358, 1941. 13. Hendren, W. H., Warshaw, A. L., Fleischli, D. J., and Bartlett, M. K.: Traumatic Hemobilia: Nonoperative Management with Healing Documented by Serial Angiography, Ann. Surg., 174:991, 1971. 14. Hermanson, L. and Cabitt, H. L.: Hematemesis Due to Trauma of 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 of Traumatic Intrahepatic Pseudoaneurysm and Hemobilia, Radiology, 94:95, 1970.
Ann. SLirg. * March 1977
17. McGehee, R. N., Townsend, C. M., Thompson, J. C., and Fish, J. C.: Traumatic Hemobilia, Ann. Surg., 179:311, 1974. 18. Sandblom, P.: Hemorrhage into the Biliary Tract Following Trauma-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 of the 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.
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 following abdominal trauma.6'19'25 Blunt or penetrating trauma to the liver may result in an intrahepatic collection from injury to liver parenchyma and branches of the arterial, venous, and biliary ductal systems. Necrosis 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 hemobilia 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, nonmassive hemobilia may be treated by conservative nonoperative measures including careful observation, transfusions, and serial selective arteriography as demonstrated in the following case. EMOBILIA is an uncommon
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.
335
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 quadrant 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 readmitted 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 Guiaicpositive, 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 spurting 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 without 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
336
LOCKWOOD, SCHORN AND COLN
Ann. SLirg. * March 1977
normal in three weeks. The alkaline phosphatase was normal at 6 weeks. Selective hepatic arteriograms were done at 4 weeks and 8 weeks post-injury. The 4-week arteriogram showed a marked decrease in the size of the filling defect in the right lobe with no communication between the arterial and biliary systems (Fig. 3). There was an increase in size of the pseudoaneurysm. At 8 weeks the arteriogram showed complete healing of the liver and disappearance of the pseudoaneurysm (Fig. 4). The patient remains asymptomatic with normal liver function studies 6 months after
injury.
Discussion The diagnosis of traumatic hemobilia should be considered in all cases of gastrointestinal hemorrhage following blunt or penetrating injury to the liver. Biliary colic, jaundice, and anemia associated with gastrointestinal hemorrhage warrant a clinical diagnosis of hemobilia. Endoscopy may identify the bleeding from the ampulla of Vater as the source of hemorrhage while excluding other causes of upper gastrointestinal bleeding. Selective arterial catheterization of the
FIG. la. The arterial phase of the right hepatic arteriogram performed 10 days post-injury demonstrates a pseudoaneurysm of the posterior-superior division of the superior branch of the right hepatic artery (arrow).
FIG. lb. The capillary phase of the right hepatic arteriogram demonstrates a 5.5 cm intrahepatic rounded filling defect in the posterolateral aspect of the right hepatic lobe consistent with hematoma (arrows). Contrast material is seen entering the biliary tree (open arrows) via an arteriobiliary fistula.
FIG. ic. A late phase of the right hepatic arteriogram demonstrates retention of contrast material in the proximal biliary tree secondary to thrombotic occlusion of more distal biliary ducts (arrow). Numerous radiolucent defects in the biliary system represent thrombi.
Vol. 185 No. 3
NONOPERATIVE MANAGEMENT OF HEMOBILIA
337
IL
ANTE; OR
-
bxacs
tm' taL J]
.a,,{,,,,.
FIG. 2a. Transverse view of liver sonogram demonstrates a 5 x 6
cm 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 arteriography by Hendren and others 13 nonoperative treat-
hepatic artery following endoscopy will usually define the 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 7in confirming the size and location of the intrahepatic S hematoma. _ 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,i00 If this is unsuccessful in controlling hemorrhage or _ ,,flXf if the hepatic inJury iS located centrally, ligation of theIX hepatic artery proximal to the origin of the gastrois often effective in controlling hemorrhage by lowering the hepatic arterial pressure sufficiently for clotting to
_ :
gastroduodenal artery. Because of the higher mortality i_s associated with major hepatic resections in the treat- M ment of traumatic hemobilia, resectional therapy _1C7 should be limited to cases of extensive hepatic injury or to cases in which ligation of the bleeding site or the hepatic artery has been unsuccessful in control-l ling the hemorrhage.9"l7"9'22 The mortality for cases ofl hemobilia treated operatively is 19%o and the rebleeding rate is 23%.'3 l"l The nonoperative treatment of hemobilia is controversial. Many authors have stressed the need for 1 * * * r . early surgical intervention for all cases of^ traumatic
hemobilia once the diagnosis is
confirmed.6"17'22
;
:_
f;;;;> ;;; -s Z
!
Y
_
FIG. 3. Selective hepatic arteriogram obtained 4 weeks postinjury demonstrates progressive healing of the liver injury. Although pseudoaneurysm persists (arrow), the arteriobihiary fistula has ~~~~~~~~~the closed and the hematoma cavity is significantly reduced in size
(white arrows).
338
LOCKWOOD, SCHORN AND COLN
Ann. Stirg. a March 1977
TABLE 1. Review of English Literature: Nonoperative Treatment of Traumatic Hemobilia *
Method of Diagnosis
Author, Date 1. Owen, 184818 2. Siegel, 190918
3. Thorlakson, 192921
Autopsy Clinical and operative findings Autopsy
4. Strauss, 192923
Autopsy
5. Wulsten, 193118
Operative or Arteriographic Findings Liver cavity and GB distended with clot
Surgical Treatment
Result
None
Died
Cholecystectomy
Recovered
None
Died: Case 10
None
Died
None
Died
Exploratory laparotomy x2, gastrojejunostomy
Died
Cholecystectomy
Recovered
6. Hermanson, 193414
Autopsy Autopsy
7. Hawthorne, 194112
Branched clot in
8. Grey, 194725
emesis Clinical and operative findings
Blood in GB andd CD
Choledochostomy
Died
9. Sandblom, 194818
Clinical and operative findings
Blood in GB
Cholecystostomy
Recovered
Operative findings
Blood in GB andd CD
Choledochostomy
Recovered
None
Died
Blood in GB
Cholecystostomy
Recovered
Negative laparottomy
Exploratory laparotomy x2
Recovered
I
10. Hart, 195010 11.
Bigger, 1950W
Negative laparotomy
Autopsy
13. Bailing, 19561
Clinical and operative findings Clinical
14. Sworn, 195920
Autopsy
Blood in GB, nelgative cholangiogram
Cholecystectomy, choledochostomy
Died
15. Hutchinson, 196115
Operative findings
Blood in GB andd CD
Recovered
16. Walt, 196922
Selective arteri-
Cholecystostomy, choledochostomy None
17. Katz, 197016
ography Selective arteriography
Intrahepatic
Selective arteri-
Small intrahepat:tic
ography Selective arteriography Clinical Autopsy Selective arteriography Selective arteriography Endoscopy and selective arteriography
cavity Central cavity arrnd extrahepatic hemat ioma
12. Epstein, 19525
18. Sandblom, 197219 19. Sandblom, 197219 20. Sandblom, 197219 21. Sandblom, 197219 22. Hendren, 197213
23. Hendren, 197213 24. Lockwood, 1976
*
psei udo-
None
aneurysm
None
2.5 cm intrahepaatic cavity with arteriobil iary fistula 3 cm intrahepati ic cavity with arteriovernous fistula 5.5 cm intrahepa Ltic cavity with arteriobil iary fistula
Drainage extrahepatic hematoma None None None
Died: Massive hemobilia, died before reaching OR Died: Death due to associated injuries Recovered: Case 43, appendix Recovered: Case 44 Recovered: Case 41 Died: Case 42 Recovered
None
Recovered
None
Recovered
Includes irrelevant operations.
ment resulted in death in 10 of 19 patients in his historical review and, therefore, he concluded that nonoperative treatment was unacceptable. The high mortality rate attributed to the nonopera-
tive treatment of traumatic hemobilia can be viewed skeptically. Five of the reported deaths occurred prior to 1934 and were diagnosed at autopsy (Table 1). In 1941 Hawthorne was the first to recognize the patho-
Vol. 185 No. 3
NONOPERATIVE MANAGEMENT OF HEMOBILIA
genesis of hemobilia prior to necropsy after noting a branched clot in the emesis of his patient.12 The patient was treated with cholecystectomy and recovered. Since 1941 18 cases of traumatic hemobilia treated by either observation or an irrelevant operation have been reported in the English literature (Table 1). In three of these 18 cases, the accurate diagnosis of traumatic hemobilia was first established at autopsy.2'920 In the remaining 15 patients the diagnosis was based on clinical findings in association with either blood in the extra-hepatic biliary system or a positive arteriogram. Of these 15 patients in which the diagnosis was made clinically, observation or an irrelevant operation resulted in 12 long-term survivors. One of the three deaths was related to associated injuries and not to the hepatic arteriobiliary fistula.'6 This survival rate of 80%o includes all cases of traumatic hemobilia treated conservatively since 1941 including massive as well as non-massive hemorrhage. Non-massive hemorrhage is defined as requiring replacement of less than half the total blood volume within a 24-48 hour period with cessation of hemorrhage. In our patient, only two units of packed red blood cells were required in 48 hours to maintain a stable hematocrit and no further bleeding occurred. Although Hendren recently reported a child with hemobilia treated conservatively who required more than his estimated total blood volume in two days to maintain a stable hematocrit,'3 hemorrhage of this magnitude is life-threatening and likely represents an injury to a major branch of the hepatic artery which is unlikely to heal spontaneously. Restricting nonoperative treatment to cases of non-massive hemobilia involving smaller more peripheral branches of the hepatic artery and using arteriography to document healing should reduce the morbidity and mortality. Selective arterial catheterization provides accurate localization of the bleeding site in traumatic hemobilia.4'7"1"'6 Localization of the hemobiliary fistula, should surgery be required, is important. Massive bleeding can be slowed by injection of small amounts of epinephrine through the selective hepatic artery catheter as recommended by Boijsen while the patient is prepared for emergency surgery.4 Boijsen notes that epinephrine, when administered intra-arterially in small amounts, produces a temporary, profound arterial constriction and reduction in blood flow in the hepatic vascular bed. Serial angiography has been used to follow healing in patients with hepatic hematomas3 and with massive and non-massive hemorrhage secondary to traumatic hemobilia.13 Using serial angiography, Hendren noted complete healing in two children with traumatic hemobilia within 3 to 8 weeks.'3 In the present case involving an adult,
339
FIG. 4. The selective hepatic arteriogram obtained 8 weeks post-injury demonstrates complete healing of the liver injury.
healing was noted at 3 weeks following diagnosis with healing completed by 8 weeks. It seems reasonable to recommend careful observation using serial selective arteriograms in patients with traumatic hemobilia who present with non-massive hemorrhage involving smaller branches of the hepatic artery. If the hemorrhage is massive or persists, surgical treatment is indicated.
References 1. Bailing, E. V.: Liver Injuries: Their Association with Massive Hematemesis 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 Hepatic Rupture, Acta Radiol., 2:363, 1971. 4. Boijsen, B., Judkins, M. P. and Simay, A.: Angiographic Diagnosis 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: The Dilemma of Delay, J. Trauma, 9:546, 1969. 7. Fowler, R. and Hiller, H. G.: Selective Hepatic Arteriography in the Management of Traumatic Hemobilia, J. Pediat. Surg., 2:253, 1967. 8. Graff, R. J.: Considerations in the Treatment of Traumatic Hemobilia, Am. J. Surg., 105:662, 1963. 9. Guillen, J. and Elliott, D. P.: Traumatic Hemobilia: A Case Report, J. Trauma, 11:886, 1971.
340
LOCKWOOD, SCHORN AND COLN
10. Hart, D.: In discussion of Biliary Tract Hemorrhage, Ann. Surg., 131:790, 1950. 11. Hawes, D. R., Franken, E. A., Fitzgerald, J. F., and Battersby, J. S.: Traumatic Hemobilia: Angiographic Diagnosis, Am. J. Dis. Child., 125:130, 1973. 12. Hawthorne, H. R., Oaks, W. W., and Neese, P. H.: Liver Injuries with a Case Report of Repeated Hemorrhages through the Biliary Ducts, Surgery, 9:358, 1941. 13. Hendren, W. H., Warshaw, A. L., Fleischli, D. J., and Bartlett, M. K.: Traumatic Hemobilia: Nonoperative Management with Healing Documented by Serial Angiography, Ann. Surg., 174:991, 1971. 14. Hermanson, L. and Cabitt, H. L.: Hematemesis Due to Trauma of 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 of Traumatic Intrahepatic Pseudoaneurysm and Hemobilia, Radiology, 94:95, 1970.
Ann. SLirg. * March 1977
17. McGehee, R. N., Townsend, C. M., Thompson, J. C., and Fish, J. C.: Traumatic Hemobilia, Ann. Surg., 179:311, 1974. 18. Sandblom, P.: Hemorrhage into the Biliary Tract Following Trauma-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 of the 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.
