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Nonoperative management of blunt extrahepatic biliary duct transection in the pediatric patient: Case report and review of the literature
Nonoperative Management of Blunt Extrahepatic Biliary Duct Transection in the Pediatric Patient: Case Report and Review of the Literature By Richard P. Sharpe, Michael L. Nance, and Perry W. Stafford Philadelphia, Pennsylvania
An 11-year-old boy sustained a grade IV liver injury and complete disruption of the left hepatic duct (LHD) secondary to a sledding accident. Although he became hemodynamically stable after initial resuscitation in the emergency department and the intensive care unit (ICU), serial paracentesis procedures were necessary to manage abdominal compartment syndrome (ACS). The fluid initially was serosanguinous but subsequently became bile stained. A bile leak was confirmed by a technetium 99m dimethyliminodiacetic acid (HIDA) scan and an endoscopic retrograde cholangiogram (ERCP). The LHD transection was treated with percutaneous drainage of the subhepatic space and a transampullary biliary stent. The leak sealed within 8 days,
and follow-up ERCP as an outpatient showed no extravasation but could not visualize the LHD. Repeat computed tomography (CT) scan 31⁄2 months after injury showed the liver laceration to be healed with atrophy of the left lobe and no ductal dilatation. The patient has had a complete recovery, resumed all activities, and currently is 20 months after his injury with no sequelae. J Pediatr Surg 37:1612-1616. Copyright 2002, Elsevier Science (USA). All rights reserved.
CASE REPORT
partial thromboplastin time (PTT) of 17.5 seconds and 39.2 seconds, respectively. CT scan of the head was normal and an abdominal CT scan with intravenous and oral contrast showed a grade IV laceration of the liver and a large amount of intraperitoneal blood (Fig 1). He was admitted to the intensive care unit (ICU), received 2 units of packed red blood cells (PRBC’s) and 2 units of fresh frozen plasma (FFP). After resuscitation, he remained hemodynamically stable with a Hgb level of 11 to 12 g/dL. His total blood product requirement was 25 mL/Kg PRBCs and 20 mL/kg FFP, all during the first 24 hours after injury. Over the next 48 hours, he awoke from his sedation and was extubated. By hospital day (HD) 5, his abdomen had slowly become tense and distended with worsening discomfort, tachypnea with shallow breaths, low urinary output (UO), decreased BP to 90/60 mm Hg, and increased HR to 130 beats per minute. His Hgb level remained unchanged; the TBili was 1.1 mg/dL, AST 2223 U/L, and ALT 3487 U/L. Because he was hemodynamically stable, a paracentesis was performed to relieve his abdominal compartment syndrome (ACS) and yielded 3,500 mL of thin, bloody fluid with immediate improvement in respiration, HR, BP, and UO. His transaminase levels slowly decreased, but a return of his ACS prompted a second paracentesis on HD 10, which yielded 2,100 mL of thin, bloody fluid. His condition improved initially, but he required a third paracentesis on HD 16 in which the fluid returned was darker in color and tested positive for bilirubin. At this time, the transaminase levels were continuing to decrease, but the serum TBili had risen to 3.3 mg/dL. A technetium 99m dimethyliminodiacetic acid (HIDA) isotopic scintiscan was positive for extravasation, and an ERCP showed complete disruption of the left hepatic duct (Fig 2). An endoscopic sphincterotomy was performed to facilitate placement of a 9.0-cm 10Fr endobiliary stent. Advancement of the stent into the left hepatic duct was unsuccessful; therefore, it was left in the common hepatic duct proximally with extension down the common bile duct and through the ampulla. Additionally, under ultrasound guidance, an 8.5Fr locking-loop pigtail catheter was placed into the subhepatic space with initial output of 900 mL bilious fluid. The patient continued to improve with gradual decrease in output from the abdominal drain. A return of bowel function prompted oral feeding, which he tolerated well, and total parenteral nutrition (TPN) was
The patient is an 11-year-old, 40-kg boy who suffered blunt injury to the right upper quadrant of his abdomen when the sled he was riding struck a tree stump. He was reported to have had a brief loss of conciousness at the scene but was awake and alert when the ambulance arrived and transported him to a local emergency room. On arrival, he had a Glascow coma score (GCS) of 15, heart rate (HR) 150 beats per minute, blood pressure (BP) 80/50 mm Hg, respiratory rate (RR) 30 breaths per minute, and arterial oxygen saturation (SaO2) 100%. His vital signs normalized with infusion of 20 mL/kg crystalloid and 2 units of packed red blood cells (PRBCs). A computed tomography (CT) scan of the abdomen without intravenous (IV) contrast showed what was interpreted as a grade II laceration of the liver and a small amount of free intraperitoneal blood. The initial hemoglobin (Hgb) was 12 g/dL, and he was transported to our facility. During transport, he was administered 12.5 mg of Phenergan and 4 mg of morphine sulfate for “combativeness.” On arrival at our institution 21⁄2 hours after injury, he had a Glasgow Coma Scan (GCS) of 12, HR 144 beats per minute, BP 81/56 mm Hg, and RR 30 breaths per minute. He was intubated electively for airway protection and responded well to a 20 mL/kg crystalloid infusion. Laboratory values showed a Hgb level of 12.9 g/dL, total bilirubin (TBili) 0.4 mg/dL, aspartate aminotransferase (AST) 916 U/L, alanine aminotransferase (ALT) 853 U/L, and prothrombin time (PT) and
From the Department of Pediatric General and Thoracic Surgery, The Children’s Hospital of Philadelphia, and the Division of Traumatology and Surgical Critical Care, Department of Surgery, Hospital of the University of Pennsylvania, Philadelphia, PA. Address reprint requests to Michael L. Nance, MD, Department of Pediatric Surgery, Children’s Hospital of Philadelphia, 34th St and Civic Center Blvd, Philadelphia, PA 19104. Copyright 2002, Elsevier Science (USA). All rights reserved. 0022-3468/02/3711-0019$35.00/0 doi:10.1053/jpsu.2002.36194 1612
INDEX WORDS: Blunt hepatic injury, extrahepatic bile duct, nonoperative management.
Journal of Pediatric Surgery, Vol 37, No 11 (November), 2002: pp 1612-1616
BLUNT BILE DUCT INJURY
1613
Fig 1. CT scan of the abdomen obtained on admission shows grade IV liver laceration and hemoperitoneum.
discontinued. A repeat HIDA scan on HD 24, 8 days after ERCP, showed no leak; the abdominal drain had minimal serosanguinous output and was removed. He was discharged on HD 28. All hepatic enzymes had returned to normal. An ERCP was performed 6 weeks after stent placement which showed no biliary leak but was unable to visualize the LHD (Fig 3). The stent was removed. A CT scan of the abdomen 31⁄2 months after injury showed complete healing of the hepatic laceration with atrophy of the left lobe and no ductal dilatation (Fig 4). The patient had a complete recovery, resumed all activities, and currently is 4 months after his injury with no sequelae.
DISCUSSION
Nonoperative management of hemodynamically stable pediatric patients with blunt hepatic trauma is well recognized. Although the overall success and minimal mor-
Fig 2.
ERCP shows transection of the left hepatic duct.
Fig 3. ERCP 6 weeks after stent placement with inability to visualize the left hepatic duct and no leak.
bidity of this approach in selected patients is established,1-4 presence of a biloma or biliary fistula has been reported in patients with and without operative management.5-8 The incidence, diagnosis, and management of a bile leak from extrahepatic sources after blunt liver injury remain to be elucidated. Extrahepatic bile duct injury from blunt trauma is uncommon.9,10 In our review of the literature, no large series were found. A review by Ahmed11 found a total of 33 pediatric patients who sustained blunt injury to the extrahepatic biliary ducts dating back to the year 1893. We found an additional 14 cases from 1953 to 199912-24 plus our patient for a total of 48 cases. Injuries to the gallbladder or cystic duct were not included in this
Fig 4. CT scan of the abdomen 31⁄2 months after injury shows a healed liver laceration and an atrophic left hepatic lobe.
1614
SHARPE, NANCE, AND STAFFORD
Table 1. Summary of 48 Pediatric Patients With Blunt Trauma to the Extrahepatic Biliary Tree Study
Ahmed11 Reported 3 cases
Review of 17 articles (total 33 patients)
Patient Age (yr)
21⁄2, 6, 5
“Childhood”
Gross12 Nikishin13 Sewell14 Shorthouse et al15 Kernohan and Humphreys16
4 3 14 8 8
Rohatgi and Gupta17 Bourque et al18 Kim et al19 Moulton et al20 Drabble et al21 Poli et al22 Arkovitz et al23
10 3 17 2 5 14 12 7
Yahib et al24 Current study
3 11
Mechanism of Injury
Vehicle, 24 Heavy object falling over abdomen, 4
Child abuse, 2 Child abuse, 2 Kick, 1 Fall, 1 Unknown, 1 Blow to abdomen by board Run over by auto Auto accident Iron bar fell over abdomen Run over by van
Fell onto handlebar Sledding accident Fall onto handlebar Soil compacting machine Struck by car Motor vehicle accident Horse kick Ambulance backed into patient Run over by van Sledding accident
Location of Ductal Injury
Associated Intrabdominal Injuries
CBD, 19 CHD, 7
Liver, 10 Lesser omentum, 2
LHD, 4 LHD, 4 Unknown, 3
Pancreas, 1 Spleen, 1 Jejunum, 1
CHD RHD LHD CBD CBD
CBD CBD CBD CBD LHD CBD CHD LHD & RHD
None None Liver None Liver Lesser omentum Right hepatic, splenic, and cystic arteries None None None Liver Liver L1 fracture Liver Liver
LHD & RHD LHD
Small bowel injury Liver
Abbreviations: CBD, common bile duct; CHD, common hepatic duct; LHD, left hepatic duct; RHD, right hepatic duct.
review. A summary of these cases including mechanism, location of ductal injury, and associated intrabdominal injuries is supplied in Table 1. The diagnosis of a bile duct injury often is difficult in the multiply injured patient and demands a high index of suspicion. Worsening abdominal discomfort, distention, nausea, vomiting, persistent ileus, hyperbilirubinemia, and low grade fever commonly are associated with bile duct injury but are nonspecific. The first diagnostic test should be an abdominal ultrasound or CT scan to confirm free fluid, but a concomitant liver injury with hemoperitoneum often is present. HIDA scanning in the pediatric trauma patient further defines hepatic parenchymal abnormalities and may localize an injury to the intra- or extrahepatic biliary tree.25,26 A paracentesis with testing for bilirubin is sensitive but not specific; ERCP defines the area of injury more precisely. The diagnostic modalities to be used and the order of testing depends greatly on the stability of the patient, risk, or suspicion of associated injuries, and other indications that may necessitate operative exploration. The treatment options for an extrahepatic biliary leak have broadened. Until recently, such injuries usually
mandated surgical repair utilizing debridement and closure with or without T-tube; patch closure using gallbladder, cystic duct, vein, serosa or jejunum; biliary enteric ananstamosis using duodenum or jejunum; or ligation and drainage with plans for subsequent enteric diversion.9,22,27 When the only relative indication for surgery is the bile leak, nonoperative management consisting of percutaneous drainage of the subhepatic space and ERCP for stent placement and sphincterotomy has been reported. This was first described in an adult patient with a left hepatic duct tear28 and has been used subsequently in 2 pediatric patients with tears of the left hepatic duct and common hepatic duct.20,22 Follow-up range was 18 to 24 months with no evidence of stricture. Several points should be made regarding our patient. First, he became hemodynamically stable soon after admission to the ICU and had a stable Hgb level of 11 to 12 g/dL. If his bleeding continued, angiography for embolization or surgical exploration would have been necessary. Second, his slowly increasing abdominal distension was felt to be secondary to ascites and accumulated blood. When ACS developed this required decompression, and he responded immediately to paracentesis.
BLUNT BILE DUCT INJURY
1615
Measuring urinary bladder pressures, although not done in this case, is adjunctive information and can be helpful in certain patients.29 Third, it was not until the third paracentesis that a color change prompted testing for bilirubin. Although a delayed leak from duct ischemia is possible, a delay in the diagnosis of an existing leak cannot be ruled out. In this setting, we strongly recommend testing the fluid for TBili regardless of the color and, if it is greater than serum levels, evaluating for a duct leak with HIDA or ERCP. Finally, nonoperative management by percutaneous drainage of the subhepatic space and stent placement by ERCP has been described only in 2 pediatric patients.20,22 These were partial duct injuries with excellent results at 18 to 24 months follow-up. The percutaneous drain is utilized until the leak seals. Sphincterotomy and stent placement have a theoretical role in promoting leak closure. Placement of a biliary endoprosthesis across the ampulla decreases ductal pressures.30,31 Also, the stent appears to be better than sphincterotomy alone.30,31 When possible, the stent should be placed across the injury but often cannot when the leak involves the more proximal, smaller hepatic ducts.20,22,32 A nasobiliary tube provides easy
access for cholangiography and ease of catheter removal, but is more uncomfortable for the patient if prolonged use is necessary. We chose the 9.0-cm stent for a planned 6-week drainage period with repeat ERCP and removal as an outpatient. On repeat ERCP, no leak was detected, but the left hepatic duct is likely not patent. Duct ligation has been shown to cause the affected liver parenchyma to atrophy, but it is unclear if it will eventually result in crosshepatic drainage.33 Sewell14 in his case report ligated the LHD and documented normalization of alkaline phosphatase and bilirubin and atrophy of the obstructed lobe. His patient, like ours, remained asymptomatic during this process. We present a case of a grade IV liver injury with complete disruption of the LHD and successful nonoperative management utilizing percutaneous drainage and stent placement by ERCP. An extensive literature review was conducted and, to our knowledge, this is the first report of a complete extrahepatic ductal injury treated in this manner. Our patient has returned to full activity, has normal serum hepatic enzyme levels and no sequelae from his injury.
REFERENCES 1. Giacomantonio M, Filler RM, Rich RH: Blunt hepatic trauma in children: Experience with operative and nonoperative management. J Pediatr Surg 19:519-522, 1984 2. Oldham KT, Guice KS, Ryckman F, et al: Blunt liver injury in children: Evolution of therapy and current perspective. Surgery 100: 542-549, 1986 3. Miller K, Kou D, Sivit C, et al: Pediatric hepatic trauma: Does clinical course support intensive care unit stay? J Pediatr Surg 33:14591462, 1998 4. Siplovich L, Kawar B: Changes in the management of pediatric blunt splenic and hepatic injuries. J Pediatr Surg 32:1464-1465, 1997 5. Arkovitz MS, Liang H, Pachter HL, et al: Complete biliary avulsion from blunt compression injury. J Pediatr Surg 34:1559-1562, 1999 6. Howdieshell TR, Purvis J, Bates WB, et al: Biloma and biliary fistula following hepatorrhaphy for liver trauma: Incidence, natural history, and management. Am Surg 61:165-168, 1995 7. Moulton SL, Downey EC, Anderson DS, et al: Blunt bile duct injuries in children. J Pediatr Surg 28:795-797, 1993 8. Scorpio RJ, Leventer R, Taylor R: Biloma and resulting biliary fistula complicating the non-operative care of a child with blunt liver trauma. Pediatr Surg Int 9:281-283, 1994 9. Ivatury RR, Rohman M, Nallathambi M, et al: The morbidity of injuries of the extra-hepatic biliary system. J Trauma 25:967-973, 1985 10. Krishna A, Kaul PB, Murali MV: Isolated extrahepatic bile duct injury: Diagnosis and surgical management. Pediatr Surg Int 7:143145, 1992 11. Ahmed S: Bile duct injuries from non-penetrating abdominal trauma in childhood. Aust N Z J Surg 46:209-212, 1976 12. Gross RE: The Surgery of Infancy and Childhood. Philadelphia, PA, 1953 13. Nikishin IF: Rupture of the extrahepatic ducts following a nonpenetrating injury to the abdomen. J Int Coll Surg 36:573-580, 1961
14. Sewell JH: Avulsion of the left hepatic duct. Ann Surg 165:628631, 1967 15. Shorthouse AJ, Singh MP, Treasure T, et al: Isolated complete transection of the common bile duct by blunt abdominal trauma. Br J Surg 65:543-545, 1978 16. Kernohan RM, Humphreys WG: Closed abdominal trauma in a child causing avulsion of the common bile duct and gastric stasis. Injury 16:235-237, 1985 17. Rohatgi M, Gupta DK: Isolated complete transection of common bile duct following blunt bicycle handlebar injury. J Pediatr Surg 22:1029-1030, 1987 18. Bourque MD, Spigland N, Bensoussan AL, et al: Isolated complete transection of the common bile duct due to trauma in a chile, and review of the literature. J Pediatr Surg 24:1068-1070, 1989 19. Kim PCW, Gilas T, Brule MFM: Unusual isolated common bile duct injury after blunt trauma. Can J Surg 36:533-536, 1993 20. Moulton SL, Downey EC, Anderson DS, et al: Blunt bile duct injuries in children. J Pediatr Surg 28:795-797, 1993 21. Drabble EH, Gani JS, Davidson P, et al: Partial laceration of the distal bile duct and wedge fracture of L1 caused by blunt trauma: A new perspective on treatment. Br J Surg 81:120, 1994 22. Poli ML, Lefebvre F, Ludot H, et al: Nonoperative management of biliary tract fistulas after blunt abdominal trauma in a child. J Pediatr Surg 30:1719-1721, 1995 23. Arkovitz MS, Liang H, Pachter HL: Complete biliary avulsion from blunt compression injury. J Pediatr Surg 34:1559-1562, 1999 24. Yahib SB, Rabeeah AA, Sammarrai AA: An unusual bile duct injury in a child after blunt abdominal trauma. J Pediatr Surg 34:11611163, 1999 25. Nadel HR: Hepatobiliary scintigraphy in children. Semin Nuc Med 1:25-42, 1996
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26. Feliciano DV: Biliary injuries as a result of blunt and penetrating trauma. Surg Clin North Am 74:897-907, 1994 27. Bade PG, Thomson SR: Surgical options in traumatic injury to the extrahepatic biliary tract. Br J Surg 76:256-258, 1989 28. Eid A, Almongy G, Pikarsky AJ: Conservative treatment of a traumatic tear of the left hepatic duct: Case report. J Trauma 41:912-913, 1996 29. DeCou JM, Abrams RS, Miller RS, et al: Abdominal compartment syndrome in children: Experience with three cases. J Pediatr Surg 35:840-842, 2000 30. Marks JM, Ponsky JL, Shillingstad RB, et al: Biliary stenting is
SHARPE, NANCE, AND STAFFORD
more effective than sphincterotomy in the resolution of biliary leaks. Surg Endosc 12:327-330, 1998 31. Youngelman DF, Marks JM, Ponsky T, et al: Comparison of bile duct pressures following sphicterotomy and endobiliary stenting in a canine model. Surg Endosc 11:126-128, 1997 32. Griffin M, Ochoa J, Boulanger BR: A minimally invasive approach to bile peritonitis after blunt liver injury. Am Surg 66:309312, 2000 33. Jurkovich GJ, Hoyt DB, Moore FA, et al: Portal triad injuries. J Trauma 39:426-434, 1995
An 11-year-old boy sustained a grade IV liver injury and complete disruption of the left hepatic duct (LHD) secondary to a sledding accident. Although he became hemodynamically stable after initial resuscitation in the emergency department and the intensive care unit (ICU), serial paracentesis procedures were necessary to manage abdominal compartment syndrome (ACS). The fluid initially was serosanguinous but subsequently became bile stained. A bile leak was confirmed by a technetium 99m dimethyliminodiacetic acid (HIDA) scan and an endoscopic retrograde cholangiogram (ERCP). The LHD transection was treated with percutaneous drainage of the subhepatic space and a transampullary biliary stent. The leak sealed within 8 days,
and follow-up ERCP as an outpatient showed no extravasation but could not visualize the LHD. Repeat computed tomography (CT) scan 31⁄2 months after injury showed the liver laceration to be healed with atrophy of the left lobe and no ductal dilatation. The patient has had a complete recovery, resumed all activities, and currently is 20 months after his injury with no sequelae. J Pediatr Surg 37:1612-1616. Copyright 2002, Elsevier Science (USA). All rights reserved.
CASE REPORT
partial thromboplastin time (PTT) of 17.5 seconds and 39.2 seconds, respectively. CT scan of the head was normal and an abdominal CT scan with intravenous and oral contrast showed a grade IV laceration of the liver and a large amount of intraperitoneal blood (Fig 1). He was admitted to the intensive care unit (ICU), received 2 units of packed red blood cells (PRBC’s) and 2 units of fresh frozen plasma (FFP). After resuscitation, he remained hemodynamically stable with a Hgb level of 11 to 12 g/dL. His total blood product requirement was 25 mL/Kg PRBCs and 20 mL/kg FFP, all during the first 24 hours after injury. Over the next 48 hours, he awoke from his sedation and was extubated. By hospital day (HD) 5, his abdomen had slowly become tense and distended with worsening discomfort, tachypnea with shallow breaths, low urinary output (UO), decreased BP to 90/60 mm Hg, and increased HR to 130 beats per minute. His Hgb level remained unchanged; the TBili was 1.1 mg/dL, AST 2223 U/L, and ALT 3487 U/L. Because he was hemodynamically stable, a paracentesis was performed to relieve his abdominal compartment syndrome (ACS) and yielded 3,500 mL of thin, bloody fluid with immediate improvement in respiration, HR, BP, and UO. His transaminase levels slowly decreased, but a return of his ACS prompted a second paracentesis on HD 10, which yielded 2,100 mL of thin, bloody fluid. His condition improved initially, but he required a third paracentesis on HD 16 in which the fluid returned was darker in color and tested positive for bilirubin. At this time, the transaminase levels were continuing to decrease, but the serum TBili had risen to 3.3 mg/dL. A technetium 99m dimethyliminodiacetic acid (HIDA) isotopic scintiscan was positive for extravasation, and an ERCP showed complete disruption of the left hepatic duct (Fig 2). An endoscopic sphincterotomy was performed to facilitate placement of a 9.0-cm 10Fr endobiliary stent. Advancement of the stent into the left hepatic duct was unsuccessful; therefore, it was left in the common hepatic duct proximally with extension down the common bile duct and through the ampulla. Additionally, under ultrasound guidance, an 8.5Fr locking-loop pigtail catheter was placed into the subhepatic space with initial output of 900 mL bilious fluid. The patient continued to improve with gradual decrease in output from the abdominal drain. A return of bowel function prompted oral feeding, which he tolerated well, and total parenteral nutrition (TPN) was
The patient is an 11-year-old, 40-kg boy who suffered blunt injury to the right upper quadrant of his abdomen when the sled he was riding struck a tree stump. He was reported to have had a brief loss of conciousness at the scene but was awake and alert when the ambulance arrived and transported him to a local emergency room. On arrival, he had a Glascow coma score (GCS) of 15, heart rate (HR) 150 beats per minute, blood pressure (BP) 80/50 mm Hg, respiratory rate (RR) 30 breaths per minute, and arterial oxygen saturation (SaO2) 100%. His vital signs normalized with infusion of 20 mL/kg crystalloid and 2 units of packed red blood cells (PRBCs). A computed tomography (CT) scan of the abdomen without intravenous (IV) contrast showed what was interpreted as a grade II laceration of the liver and a small amount of free intraperitoneal blood. The initial hemoglobin (Hgb) was 12 g/dL, and he was transported to our facility. During transport, he was administered 12.5 mg of Phenergan and 4 mg of morphine sulfate for “combativeness.” On arrival at our institution 21⁄2 hours after injury, he had a Glasgow Coma Scan (GCS) of 12, HR 144 beats per minute, BP 81/56 mm Hg, and RR 30 breaths per minute. He was intubated electively for airway protection and responded well to a 20 mL/kg crystalloid infusion. Laboratory values showed a Hgb level of 12.9 g/dL, total bilirubin (TBili) 0.4 mg/dL, aspartate aminotransferase (AST) 916 U/L, alanine aminotransferase (ALT) 853 U/L, and prothrombin time (PT) and
From the Department of Pediatric General and Thoracic Surgery, The Children’s Hospital of Philadelphia, and the Division of Traumatology and Surgical Critical Care, Department of Surgery, Hospital of the University of Pennsylvania, Philadelphia, PA. Address reprint requests to Michael L. Nance, MD, Department of Pediatric Surgery, Children’s Hospital of Philadelphia, 34th St and Civic Center Blvd, Philadelphia, PA 19104. Copyright 2002, Elsevier Science (USA). All rights reserved. 0022-3468/02/3711-0019$35.00/0 doi:10.1053/jpsu.2002.36194 1612
INDEX WORDS: Blunt hepatic injury, extrahepatic bile duct, nonoperative management.
Journal of Pediatric Surgery, Vol 37, No 11 (November), 2002: pp 1612-1616
BLUNT BILE DUCT INJURY
1613
Fig 1. CT scan of the abdomen obtained on admission shows grade IV liver laceration and hemoperitoneum.
discontinued. A repeat HIDA scan on HD 24, 8 days after ERCP, showed no leak; the abdominal drain had minimal serosanguinous output and was removed. He was discharged on HD 28. All hepatic enzymes had returned to normal. An ERCP was performed 6 weeks after stent placement which showed no biliary leak but was unable to visualize the LHD (Fig 3). The stent was removed. A CT scan of the abdomen 31⁄2 months after injury showed complete healing of the hepatic laceration with atrophy of the left lobe and no ductal dilatation (Fig 4). The patient had a complete recovery, resumed all activities, and currently is 4 months after his injury with no sequelae.
DISCUSSION
Nonoperative management of hemodynamically stable pediatric patients with blunt hepatic trauma is well recognized. Although the overall success and minimal mor-
Fig 2.
ERCP shows transection of the left hepatic duct.
Fig 3. ERCP 6 weeks after stent placement with inability to visualize the left hepatic duct and no leak.
bidity of this approach in selected patients is established,1-4 presence of a biloma or biliary fistula has been reported in patients with and without operative management.5-8 The incidence, diagnosis, and management of a bile leak from extrahepatic sources after blunt liver injury remain to be elucidated. Extrahepatic bile duct injury from blunt trauma is uncommon.9,10 In our review of the literature, no large series were found. A review by Ahmed11 found a total of 33 pediatric patients who sustained blunt injury to the extrahepatic biliary ducts dating back to the year 1893. We found an additional 14 cases from 1953 to 199912-24 plus our patient for a total of 48 cases. Injuries to the gallbladder or cystic duct were not included in this
Fig 4. CT scan of the abdomen 31⁄2 months after injury shows a healed liver laceration and an atrophic left hepatic lobe.
1614
SHARPE, NANCE, AND STAFFORD
Table 1. Summary of 48 Pediatric Patients With Blunt Trauma to the Extrahepatic Biliary Tree Study
Ahmed11 Reported 3 cases
Review of 17 articles (total 33 patients)
Patient Age (yr)
21⁄2, 6, 5
“Childhood”
Gross12 Nikishin13 Sewell14 Shorthouse et al15 Kernohan and Humphreys16
4 3 14 8 8
Rohatgi and Gupta17 Bourque et al18 Kim et al19 Moulton et al20 Drabble et al21 Poli et al22 Arkovitz et al23
10 3 17 2 5 14 12 7
Yahib et al24 Current study
3 11
Mechanism of Injury
Vehicle, 24 Heavy object falling over abdomen, 4
Child abuse, 2 Child abuse, 2 Kick, 1 Fall, 1 Unknown, 1 Blow to abdomen by board Run over by auto Auto accident Iron bar fell over abdomen Run over by van
Fell onto handlebar Sledding accident Fall onto handlebar Soil compacting machine Struck by car Motor vehicle accident Horse kick Ambulance backed into patient Run over by van Sledding accident
Location of Ductal Injury
Associated Intrabdominal Injuries
CBD, 19 CHD, 7
Liver, 10 Lesser omentum, 2
LHD, 4 LHD, 4 Unknown, 3
Pancreas, 1 Spleen, 1 Jejunum, 1
CHD RHD LHD CBD CBD
CBD CBD CBD CBD LHD CBD CHD LHD & RHD
None None Liver None Liver Lesser omentum Right hepatic, splenic, and cystic arteries None None None Liver Liver L1 fracture Liver Liver
LHD & RHD LHD
Small bowel injury Liver
Abbreviations: CBD, common bile duct; CHD, common hepatic duct; LHD, left hepatic duct; RHD, right hepatic duct.
review. A summary of these cases including mechanism, location of ductal injury, and associated intrabdominal injuries is supplied in Table 1. The diagnosis of a bile duct injury often is difficult in the multiply injured patient and demands a high index of suspicion. Worsening abdominal discomfort, distention, nausea, vomiting, persistent ileus, hyperbilirubinemia, and low grade fever commonly are associated with bile duct injury but are nonspecific. The first diagnostic test should be an abdominal ultrasound or CT scan to confirm free fluid, but a concomitant liver injury with hemoperitoneum often is present. HIDA scanning in the pediatric trauma patient further defines hepatic parenchymal abnormalities and may localize an injury to the intra- or extrahepatic biliary tree.25,26 A paracentesis with testing for bilirubin is sensitive but not specific; ERCP defines the area of injury more precisely. The diagnostic modalities to be used and the order of testing depends greatly on the stability of the patient, risk, or suspicion of associated injuries, and other indications that may necessitate operative exploration. The treatment options for an extrahepatic biliary leak have broadened. Until recently, such injuries usually
mandated surgical repair utilizing debridement and closure with or without T-tube; patch closure using gallbladder, cystic duct, vein, serosa or jejunum; biliary enteric ananstamosis using duodenum or jejunum; or ligation and drainage with plans for subsequent enteric diversion.9,22,27 When the only relative indication for surgery is the bile leak, nonoperative management consisting of percutaneous drainage of the subhepatic space and ERCP for stent placement and sphincterotomy has been reported. This was first described in an adult patient with a left hepatic duct tear28 and has been used subsequently in 2 pediatric patients with tears of the left hepatic duct and common hepatic duct.20,22 Follow-up range was 18 to 24 months with no evidence of stricture. Several points should be made regarding our patient. First, he became hemodynamically stable soon after admission to the ICU and had a stable Hgb level of 11 to 12 g/dL. If his bleeding continued, angiography for embolization or surgical exploration would have been necessary. Second, his slowly increasing abdominal distension was felt to be secondary to ascites and accumulated blood. When ACS developed this required decompression, and he responded immediately to paracentesis.
BLUNT BILE DUCT INJURY
1615
Measuring urinary bladder pressures, although not done in this case, is adjunctive information and can be helpful in certain patients.29 Third, it was not until the third paracentesis that a color change prompted testing for bilirubin. Although a delayed leak from duct ischemia is possible, a delay in the diagnosis of an existing leak cannot be ruled out. In this setting, we strongly recommend testing the fluid for TBili regardless of the color and, if it is greater than serum levels, evaluating for a duct leak with HIDA or ERCP. Finally, nonoperative management by percutaneous drainage of the subhepatic space and stent placement by ERCP has been described only in 2 pediatric patients.20,22 These were partial duct injuries with excellent results at 18 to 24 months follow-up. The percutaneous drain is utilized until the leak seals. Sphincterotomy and stent placement have a theoretical role in promoting leak closure. Placement of a biliary endoprosthesis across the ampulla decreases ductal pressures.30,31 Also, the stent appears to be better than sphincterotomy alone.30,31 When possible, the stent should be placed across the injury but often cannot when the leak involves the more proximal, smaller hepatic ducts.20,22,32 A nasobiliary tube provides easy
access for cholangiography and ease of catheter removal, but is more uncomfortable for the patient if prolonged use is necessary. We chose the 9.0-cm stent for a planned 6-week drainage period with repeat ERCP and removal as an outpatient. On repeat ERCP, no leak was detected, but the left hepatic duct is likely not patent. Duct ligation has been shown to cause the affected liver parenchyma to atrophy, but it is unclear if it will eventually result in crosshepatic drainage.33 Sewell14 in his case report ligated the LHD and documented normalization of alkaline phosphatase and bilirubin and atrophy of the obstructed lobe. His patient, like ours, remained asymptomatic during this process. We present a case of a grade IV liver injury with complete disruption of the LHD and successful nonoperative management utilizing percutaneous drainage and stent placement by ERCP. An extensive literature review was conducted and, to our knowledge, this is the first report of a complete extrahepatic ductal injury treated in this manner. Our patient has returned to full activity, has normal serum hepatic enzyme levels and no sequelae from his injury.
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