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THE WVESTERN Journal of Medicine Refer to: Burt TB, Nelson JA: Extrahepatic biliary duct trauma- A spectrum of injuries. West J Med 134:283-289, Apr 1981 Extrahepatic Biliary Duct Trauma A Spectrum of Injuries TODD B. BURT, MD, and JAMES A. NELSON, MD, Salt Lake City Blunt traumatic injury of the extrahepatic bile ducts (EBD) is uncommon. Familiarity with the wide spectrum of possible EBD injuries is essential, how- ever, because of the increasing number of nonpenetrating abdominal injuries seen in modern society. These injuries include contusion with edema, hema- toma and varying degrees of laceration. Edema and hematoma can result in transient bile duct obstruction that clears spontaneously or cicatrizing inflam- matory reaction resulting in stricture and obstruction. Common bile duct stricture following blunt trauma is extremely rare, but is an unfortunate late complication requiring biliary decompression to relieve progressive jaundice. Laceration (partial or complete) can occur at any location in the EBD and can be life-threatening if the diagnosis is overlooked. Hemobilia is an unusual complication of laceration of the EBD. Failure to recognize the clinical mani- festations of these uncommon injuries results in delayed and often incorrect diagnoses. Percutaneous transhepatic cholangiography is a safe and accurate procedure that is an important step in the workup of jaundice following blunt trauma. EXTRAHEPATIC BILE DUCT (EBD) injury from blunt abdominal trauma (such as motor vehicle accidents or acts of violence) is uncommon. Se- vere injuries, such as laceration or transection require immediate surgical intervention to assure patient survival. Injuries that are less obvious clinically, including contusion with edema, hema- toma from intramural and retroperitoneal hemor- rhage and low-volume hemobilia, may be easily overlooked particularly in patients suffering from multiple trauma. From the Department of Radiology, University of Utah College of Medicine, Salt Lake City. Submitted July 25, 1980. Reprint requests to: Todd B. Burt, MD, Department of Radi- ology, University of Utah Medical Center, 50 North Medical Drive, Salt Lake City, UT 84132. Posttraumatic obstructive jaundice is an un- fortunate sequela to EBD injuries. We report two cases of jaundice resulting from obstruction of the common bile duct following blunt trauma. In one case obstruction was caused by duodenal hematoma and edema which eventually cleared spontaneously. In the other case retroperitoneal and paraduodenal hematoma was followed by fibrosis resulting in stricture that required surgical bypass. Although upper gastrointestinal (GI) ba- rium studies suggested the diagnosis and ultra- sound testing showed bile duct dilatation, the site and gross nature of the obstruction was best demonstrated by thin-needle percutaneous trans- hepatic cholangiography (PTC). Our experience THE WESTERN JOURNAL OF MEDICINE 283

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  • THE WVESTERNJournal of Medicine

    Refer to: Burt TB, Nelson JA: Extrahepatic biliary duct trauma-A spectrum of injuries. West J Med 134:283-289, Apr1981

    Extrahepatic Biliary Duct TraumaA Spectrum of InjuriesTODD B. BURT, MD, and JAMES A. NELSON, MD, Salt Lake City

    Blunt traumatic injury of the extrahepatic bile ducts (EBD) is uncommon.Familiarity with the wide spectrum of possible EBD injuries is essential, how-ever, because of the increasing number of nonpenetrating abdominal injuriesseen in modern society. These injuries include contusion with edema, hema-toma and varying degrees of laceration. Edema and hematoma can result intransient bile duct obstruction that clears spontaneously or cicatrizing inflam-matory reaction resulting in stricture and obstruction. Common bile ductstricture following blunt trauma is extremely rare, but is an unfortunate latecomplication requiring biliary decompression to relieve progressive jaundice.Laceration (partial or complete) can occur at any location in the EBD andcan be life-threatening if the diagnosis is overlooked. Hemobilia is an unusualcomplication of laceration of the EBD. Failure to recognize the clinical mani-festations of these uncommon injuries results in delayed and often incorrectdiagnoses. Percutaneous transhepatic cholangiography is a safe and accurateprocedure that is an important step in the workup of jaundice following blunttrauma.

    EXTRAHEPATIC BILE DUCT (EBD) injury fromblunt abdominal trauma (such as motor vehicleaccidents or acts of violence) is uncommon. Se-vere injuries, such as laceration or transectionrequire immediate surgical intervention to assurepatient survival. Injuries that are less obviousclinically, including contusion with edema, hema-toma from intramural and retroperitoneal hemor-rhage and low-volume hemobilia, may be easilyoverlooked particularly in patients suffering frommultiple trauma.From the Department of Radiology, University of Utah College

    of Medicine, Salt Lake City.Submitted July 25, 1980.Reprint requests to: Todd B. Burt, MD, Department of Radi-

    ology, University of Utah Medical Center, 50 North MedicalDrive, Salt Lake City, UT 84132.

    Posttraumatic obstructive jaundice is an un-fortunate sequela to EBD injuries. We report twocases of jaundice resulting from obstruction ofthe common bile duct following blunt trauma. Inone case obstruction was caused by duodenalhematoma and edema which eventually clearedspontaneously. In the other case retroperitonealand paraduodenal hematoma was followed byfibrosis resulting in stricture that required surgicalbypass. Although upper gastrointestinal (GI) ba-rium studies suggested the diagnosis and ultra-sound testing showed bile duct dilatation, the siteand gross nature of the obstruction was bestdemonstrated by thin-needle percutaneous trans-hepatic cholangiography (PTC). Our experience

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    with these two unusual cases prompted this reportand a review of the literature.

    Reports of CasesCASE 1. A healthy 20-year-old woman sustained

    blunt trauma to her right upper abdomen fromthe steering wheel in a head-on auto accident.Although the patient had considerable right upperabdomen pain, there was no evidence of acuteabdomen or blood loss. Liver function test find-ings and amylase determinations were normalexcept for mildly elevated levels of lactate dehy-drogenase (LD). After a three-day stay in hos-pital the patient was discharged with only a com-plaint of mild pain of the right upper quadrant.Two and one half weeks later, the patient re-turned, complaining of persistent right upper ab-domen pain, nausea and the recent onset ofbrownish-colored urine. She stated that she hadnot been exposed to hepatitis, blood transfusion,alcohol or intravenously given drugs. On physicalexamination, yellowish discoloration of skin andstriking scleral icterus were noted. Findings of anabdominal examination were normal except for

    s. Figure 1.-Uppergastrointestinal bariumstudy showing narrow-

    ing and irregularity inthe second portion ofthe duodenum (arrow)that suggests hema-

    toma or edema.

    mild right upper quadrant tenderness. Significantlaboratory findings included the following: totalbilirubin 12.2 and direct bilirubin 9.6 mg per dl,alkaline phosphatase 228 units, LD 222 units andSGOT (serum aspartate aminotransferase; formerlyserum glutamic oxaloacetic transaminase) 131units. Amylase, a complete blood count, pro-thrombin time and partial thromboplastin timewere within normal limits.

    The patient was admitted to hospital and aliver-spleen scan using technetium 99m sul-phur colloid showed a liver and spleen without-defect. An upper GI study suggested an intraduo-denal hematoma in the second portion of theC-loop (Figure 1). An ultrasound test showedmildly enlarged gallbladder and extrahepatic bileducts. PTC was done with a 23-gauge Chiba needleon the third hospital day. This demonstrated anormal intrahepatic biliary tree with obstructionof the distal common bile duct by a persistent,smooth-mass effect with failure to empty into theduodenum. Follow-up films at one hour showedpersistent contrast in the biliary tree (Figure 2).

    Figure 2.-One hour follow-up film after thin-needlepercutaneous transhepatic cholangiography. Tapereddistal common duct with meniscal obstruction (smallarrow) and no passage of contrast into duodenum.Excretory urograms from contrast entering vascularsystem from obstructed biliary system.

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    ABBREVIATIONS USED IN TEXTEBD=extrahepatic bile ductsGI= gastrointestinalLD =lactate dehydrogenasePTC= percutaneous transhepatic cholangiography

  • EXTRAHEPATIC BILIARY DUCT TRAUMA

    Because of symptomatic improvement it waselected to only observe the patient. Over the nextseveral months the patient's jaundice graduallysubsided without surgical intervention and allsymptoms resolved. Two years following the ac-cident, the patient was asymptomatic with normalfindings on liver function tests.

    CASE 2. A 22-year-old man sustained a crushinjury to the upper abdomen in a drilling accident.An exploratory laparotomy was done immediatelybecause of grossly bloody peritoneal tap. Duringthe operation hematomas involving the secondand third portions of the duodenum, the retro-peritoneal space and the posterior aspect of thepancreas were found. The gallbladder was intactand there was no evidence of bile duct lacerationor transection. The hematomas were drained andthe patient was later discharged with abdominalwounds healing well and normal findings on liverfunction tests except for mildly elevated LD levels.

    The patient was readmitted approximately three

    weeks later for persistent nausea, vomiting, a 25-pound weight loss, and increasing malaise andweakness. An upper GI study was done, whichshowed compression of the duodenum by hema-toma or fibrosis (Figure 3). Abdominal ultra-sound testing demonstrated a normal pancreas,and no dilated biliary ducts were seen. Duringthis hospital stay the patient was noted to havescleral icterus. Laboratory results included totalbilirubin 5.2 mg per dl, alkaline phosphatase 504units and SGOT 141 units. PTC was done with a23-gauge Chiba needle, which showed dilatedhepatic and common bile ducts with completedistal obstruction (Figure 4). No intraluminalfilling defects were present in the ducts or gall-bladder. An operation was carried out immedi-ately following the PTC and massive adhesions inthe area of the duodenum, gallbladder and liverbed were discovered. Pronounced fibrosis andthickening were present in the periampullaryregion, but no residual hematomas were found.

    Figure 3.-Two views from upper gastrointestinal study showing irregularity and narrowing involving the secondand third portion of duodenum, which proved secondary to massive adhesions.

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    Surgical decompression with T-tube drainage wascarried out and the patient's liver function gradu-ally improved and symptoms slowly resolved.However, because of persistent obstruction notedon the follow-up T-tube cholangiograms, Roux-en-Y cholecystojejunostomy was done. The patienttolerated this procedure well, and his post-

    Figure 4.-PTC with injection into gall bladder showsdilated extrahepatic biliary ducts and abrupt obstruc-tion of the distal common bile duct. The obstructionwas secondary to pronounced fibrosis in the paraduo-denal and retroperitoneal region (PTC = percutaneoustranshepatic cholangiography).

    TABLE 1.-Causes of Jaundice FollowingBlunt Abdominal Trauma

    Trauma-relatedLiver lacerationLiver hematomaLiver abscessHepatic vascular accident

    Budd-ChiariHemobilia

    Acute pancreatitisPosttraumatic hepatic dysfunction syndromeIntrahepatic and extrahepatic duct damagePosttraumatic cholecystitis

    Surgery-relatedlatrogenicOperative stress on preexisting liver diseaseGeneral anesthesiaPostoperative cholecystitis

    MiscellaneousHemolysis (transfusions, resolving hematoma)Viral hepatitisDrug toxicity

    operative course was uncomplicated. During fol-low-up, findings of liver function tests returnedto normal and all symptoms resolved.

    DiscussionJaundice Following Trauma

    Jaundice is often a perplexing complication thatdevelops following major abdominal traunma. His-torical, clinical and laboratory data will often dis-tinguish hemolytic, obstructive or hepatocellularcauses of jaundice. Following traumatic injuries,however, many patients receive multiple bloodtransfusions, may have preexisting liver disease,and often undergo operations requiring generalanesthesia. In these cases, the differential diagnosismay be difficult and easy differentiation becomesimpossible. Some important causes of jaundicefollowing blunt abdominal trauma are listed inTable 1.

    Liver lacerations, hematomas, abscesses andvascular injuries may all result from blunt ab-dominal trauma and lead to jaundice.1 Rarely, asillustrated in these two case reports, hematoma,edema, or both, and fibrosis can compress thedistal common bile duct and result in temporaryor permanent obstruction. Recently, the posttrau-matic hepatic dysfunction syndrome has beendescribed as a distinct clinicopathologic entity.2This syndrome is considered to result from hepaticischemia caused by either hypoxia or hypotensionfollowing resuscitation from major trauma.

    In a traumatized patient who has undergone anoperation, mild hyperbilirubinemia in the first fewpostoperative days may be viewed with interestbut without serious concern because many of thesepatients are suspected of having hemolysis fromblood transfusions or from resorption of hema-toma. If jaundice is persistent or progressive, how-ever, iatrogenic surgical trauma to the biliary tree,anesthetic toxicity and operative stress on preexist-ing liver disease should be considered as potentialcauses.1 3'4 Acute acalculous cholecystitis mustalso be considered because of its known occur-rence in both traumatized and surgical patients.5'6When obstructive jaundice is suspected, ab-

    dominal ultrasound testing and PTC are essentialto arrive at the correct diagnosis. Ultrasonographyis very helpful in demonstrating dilated biliaryducts, gallbladder and common bile duct stones,as well as abdominal hematomas, abscesses andcysts. However, ultrasound testing alone cannotdiagnose an EBD laceration or indicate the site of

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    TABLE 2.-EBD Rupture Due toBlunt Abdominal TraumaType No. of Cases NVo. of Deaths

    Transected common duct .... 25 7Lacerated common duct ..... 31 10Transected hepatic duct ..... 2 0Lacerated hepatic duct ...... 27 10Lacerated cystic duct .....1.. 0Unknown site ............. 5 1

    TOTAL .................. 91 28EBD=extrahepatic bile duct

    an obstruction.7 As illustrated in our case reports,PTC is a fast, accurate and safe method for dif-ferentiating obstructive from nonobstructive jaun-dice and for defining the level of obstruction whenpresent. PTC may also show extravasation secon-dary to either a liver or biliary tree laceration,intraluminal filling defects secondary to eitherblood clots or stones, or deviation of the biliaryducts from abscess or hematoma.

    Pathophysiology of EBD InjuriesThe exact nature of the force necessary to cause

    injury to the EBD iS unknown, although the fol-lowing have been postulated: (1) impingementand compression of the ductal system on the ver-tebral column,8 (2) external compression of thegallbladder with transmitted rise in intraductalpressures resulting in "blowout of the duct"9 and(3) laceration of the ductal system at the junc-tion of its fixed and mobile portions.10"'1 The firsttheory seems to explain best the duct injuries thatresult in hematoma and edema, especially in theperiampullary and retroperitoneal region. Injuriesto the vessels supplying the EBD in this regionresult from the crushing abdominal blow and re-sult in hematoma and ischemia which may healwith fibrosis. The last postulate best explains ductlaceration and is clinically supported in that rup-ture of the EBD is most frequently encounteredwhere the mobile common bile duct becomes fixedas it enters the superior edge of the pancreas.'2The blowout theory has not been confirmed inanimal models or in clinical situations.'3 Althoughthe exact pathophysiology still remains unclear,it is likely that a combination of the mechanismsproposed above is responsible for EBD injuries.The rarity of injury to the portal vein and

    hepatic artery has intrigued many writers. Dor-ton'4 suggested that the tortuous and elastic hepa-tic artery has no points of fixation near the area

    of trauma, making it less susceptible to injury.He also suggested that because the portal veinhas no valves, intraluminal pressure from a directblow is decompressed into the splenic reservoir,dissipating the energy.Extrahepatic Biliary Duct Injuries

    Complete and partial laceration occurring inall portions of the EBD have been previously de-scribed. A careful review of the literature from1890 to 1970 by Rydell uncovered 91 cases ofEBD lacerations.'2 Table 2 tabulates the locationand degree of these ruptures. Since that time,avulsion of the ampulla of Vater," "I as well asseveral other reports of EBD ruptures,"-725 havebeen added to the literature. The most commonlocation for duct disruption is the suprapancreaticretroduodenal portion (superior border of thepancreas."' 7'22 Laceration may be limited to asingle portion of the biliary tree'5 18,20,22,2" or maybe found in combination with other EBD injuries.2'EBD injuries may also be isolated or may be foundin any combination with other abdominal visceralinjuries with the liver, duodenum, pancreas, andspleen being the most common sites.2 When distalcommon bile duct injuries occur, pancreatic andduodenal injuries are commonly associated.'6

    In severely injured patients, indications forexploratory laparotomy are often clearly evidentand unsuspected biliary tract trauma may befound during the operation. When the abdominalinjury is less severe or confined to the biliary tree,however, indications for laparotomy may not bepresent and a significant occult injury of the EBDmay remain undiagnosed. Walt and Grifka28 re-ported on 307 consecutive cases of blunt ab-dominal trauma and found that injuries to thecommon bile duct were the least frequent injuryto result in exploratory laparotomy. To add tothe difficulty in differential diagnosis, a historyof trauma may not be given because the patientmay either feel that it was insignificant or failto recall it.The clinical course of EBD lacerations has a

    characteristic pattern20'22 as follows: (1) The ini-tial injury may be followed by shock of varyingdegree that usually lasts for only a few hours;(2) this is often followed by a symptom-freequiescent period of several days; (3) finally, pro-gressive abdominal pain, nausea, vomiting, jaun-dice and, in some cases, abdominal distentionfrom bile ascites ensue. Acholic stools, fever,rapid wasting of abdominal muscles and scleral

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    icterus often develop as well. Although this se-quence usually occurs over three to ten days,symptoms may not become intense enough tocause the patient to seek medical advice for weeksto months. Abdominal paracentesis may yield bile,at which time the diagnosis should be clear.27

    Biliary duct obstruction resulting from edemaor hematoma in the duodenal, periampullary or.retroperitoneal region is uncommon. During thepast 30 years more than 170 cases of intramuraland paraduodenal hematomas from blunt ab-dominal trauma have been reported. 2930 In onlyfour of these previously cited cases did the hema-toma result in obstruction of the distal commonbile duct.733 To these, we add an additionalcase, bringing the total to five. Of these cases,three patients did not recall abdominal trauma,one considered the traumatic episode minor andone had significant blunt trauma to the abdomen.This attests to the fact that a history of trauma isnot always obtained even when a serious duodenaland retroperitoneal hematoma is present. In thepreviously reported and currently presented casesof biliary obstruction, one required decompres-sion by cholecystojejunostomy,33 two resolvedafter evacuation of the blood clot14,35 and the othertwo resolved spontaneously (patients in reference7 and in case 1). Jaundice developed as early asthree days,34 and as late as three weeks (case 1)following the traumatic episode. Davis33 has sug-gested that the characteristic delay between injuryand jaundice is secondary to gradual increase inthe size of the hematoma. He postulates that as

    Blunt Abdominal Trauma

    / +~~~~~ACUTE Contusion and

    edema

    7Compression

    EBD

    SUBACUTE Spontaneous

  • EXTRAHEPATIC BILIARY DUCT TRAUMA

    and hemobilia, only four originated from EBDinjuries.38(P)6 Hemobilia often develops followingtrauma, with the classic triad of biliary colic,jaundice and gastrointestinal bleeding. The pain,produced by the distention of the bile ducts withblood, precedes external evidence of bleeding, sothat a patient with recurrent episodes of bleedingmay be able to predict the onset of melana orhematemesis. Arteriography is diagnostic whenhemorrhaging is actually occurring; intermittencyof bleeding, however, is characteristic of hemo-bilia. A related complication of theoretic interestis the formation of gall stones from intraluminalclots, which has been demonstrated by Sand-blom.39 The incidence of this condition is un-known but is undoubtedly rare.

    Surprisingly, no reports of posttraumatic EBDfistulae or cysts were encountered in the litera-ture. Bronchobiliary and pleurobiliary fistulae,however, have been reported from intrahepaticducts to the chest after severe thoracic and ab-dominal trauma.40

    ConclusionExtrahepatic bile duct trauma may clearly result

    in a wide spectrum of injuries as summarized inFigure 5. Although these injuries are uncommon,clinicians as well as radiologists must be thor-oughly aware of their existence in order to provideadequate care for these traumatized patients. Ab-dominal ultrasound and GI studies will often sug-gest an EBD injury, which can be safely and di-rectly demonstrated by PTC. Treatment of EBDlaceration and transection is clearly surgical.22When trauma results in edema or hematoma,however, therapy must be based on the conditionof the individual patient and consideration of otherabdominal injuries.29

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    Textbook of Surgery, 11th Ed. Philadelphia, Saunders, 1977, pp429-430

    2. Champion HR, Jones RT, Trump BF, et al: Post-traumatichepatic dysfunction as a major etiology in post-traumatic jaundice.J 'rrauma 16:650-657, 1976

    3. Seror J, Schmitt JC, Pateras C, et al: Operative injuries tothe bile ducts. Int Surg 63:108-113, 1978

    4. Hillis TM, Westbrook KC, Caldwell FT, et al: Surgical in-jury of the common bile duct. Am J Surg 134:712-716, 19775. Howard RJ, Velany JP: Postoperative cholecystitis. Am J

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    9. Mason LB, Sidnury JB, Guiang S: Rupture of the extra-hepatic ducts from non-penetrating trauma. Ann Surg 140:234-241, 1954

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    18. Janss G, Freimark L: Isolated transection of the commonduct. JACEP 8:161-163, 1979

    19. Sinclair MC, Moore TC, Asch MJ, et al: Injury to hollowabdominal viscera from blunt trauma in children and adolescents.Am J Surg 128:693-698, 1974

    20. Shorthouse AJ, Singh MP, Treasure T, et al: Isolated com-plete transection of the common bile duct by blunt abdominaltrauma. Br J Surg 65:543-545, 1978

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    22. Turney WH, Lee JP, Raju S: Complete transection of thecommon bile duct -due to blunt trauma. Ann Surg 179:440.444,1974

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    24. Caro AM, Losa JMO: Complete avulsion of the commonbile duct as a result of blunt abdominal trauma. J Pediatr Surg5:60-62, 1970

    25. Haynes CD, Given KS, Stone HH, et al: Nonsurgicaltrauma to the extrahepatic ducts. South Med J 62:1323-1326, 1969

    26. Moffat RC, Lucas RJ: Transection of the common bile ductas an isolated injury following blunt trauma. Can J Surg 12:334-335, 1969

    27. Longmire WP, McArthur MS: Occult injuries of the liver,bile duct, and pancreas after blunt abdominal trauma. Am J Surg125:661-666, 1973

    28. Walt AJ, Grifka TJ: Blunt abdominal injury, In GurdjianES, Lange WA, Patrick LM, et al (Eds): Impact Injury andCrash Protection. Springfield, IL, Charles C Thomas, 1970, pp101-123

    29. Fullen WD, Selle JG, Whitely DH, et al: Intramural duo-denal hematoma. Ann Surg 179:549-555, 1974

    30. Maull KI, Fallahzudeh H, Mays ET: Selective managementof posttraumatic obstructing intramural hematoma of the duo-denum. Surg Gynecol Obstet 146:221-224, 1978

    31. Izant RF, Drucker WR: Duodenal obstruction due to in-tramural hematoma in children. J Trauma 4:797-813, 1963

    32. Resnicoff SA, Morton JH: Changing concepts concerningintramural duodenal hematomas. J Trauma 9:561-576, 1969

    33. Davis DR, Thomas CY: Intramural hematoma of the duo-denum and jejunum. Ann Surg 153:394-398, 1961

    34. Parrish RA, Edmondson HT, Moretz WH: Duodenal andbiliary obstruction secondary to intramural hematoma. Am J Surg108:428-430, 1964

    35. Ferguson IA, Goade WJ: Intramural hematoma of the duo-denum. N Engl J Med 260:1176-1177, 1954

    36. Felson B, Levin ET: Intramural hematoma of the duo-denum: A diagnostic sign. Radiology 63:823-831, 1954

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    39. Sandblom P, Mirkovitch U, Saegesser F: Formation andfate of fibrin clots in the biliary tree. Ann Surg 185:356-366, 1977

    40. Operal SS, Mandal AK: Traumatic thoracobiliary fistulae:Clinical and review study. J Trauma 18:539-544, 1978

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