Complex Hepatic Injuries Tanya L. Zakrison Ryder Trauma Center Dec. 8th , 2009 Complex Hepatic Injuries

Outline – management options Hemodynamically stable Blunt Penetrating Hemodynamically unstable Specific injuries: Parenchymal injuries Grade V juxtahepatic venous injuries Portal triad Complications

Anatomy – Couinaud’s Segments There are 4 sources of bleeding in the liver

Anatomy – Hepatic Suspensory Ligaments Falciform ligament Ligamentum teres Coronary ligaments Triangular ligaments Hematomas may be contained within suspensory ligaments

Liver Injury May injure: Management options: Blood vessels: Retrohepatic IVC Hepatic veins Portal veins Hepatic arteries Biliary radicles Parenchyma Perihepatic structures Management options: Packing Direct suture Finger fracture Omental packing Penetrating tract Open it (tractotomy) Pack it (multiple adjuncts) Hemostatic agents Liver bag Vascular isolation Atriocaval shunting Resection & tranplantation Veno-veno bypass Bleeding & Air embolism

AAST Organ Injury Scale

Blunt Hepatic Injury - Stable 85% of pts. with blunt liver injury are stable 89% of these are managed non-operatively Majority venous blood supply to liver (low pressure) Non-operative management (NOM) leads to: Less transfusions of blood products Decreased length of stay Decreased infectious complications Few contraindications to NOM Must be hemodynamically stable Failure in 14% grade IV injuries, 23% grade V

Penetrating Hepatic Injury - Stable Role for non-operative management Renz et al. (1994): NOM in 13 pts. with TA GSWs Follow with serial PE’s, contrast-enhanced CT scans Demetriades et al. (1999): NOM in 16 pts. with TA GSWs Failure of NOM 33% Omoshoro-Jones et al. (2005): NOM in 31/33, including pts. with grade V liver injuries Most complications also treated non-operatively Ultimately only 30% of penetrating hepatic trauma will be eligible for NOM Pt. selection important: HD stability no peritonitis GCS = 15 no active bleed on CT AAST grade does not determine eligibility for NOM

Multimodality Approach in Hepatic Injuries – Angioembolization Angioembolization (AE): Pseudoaneurysm, blush, active extravasation May be used in NOM, pre-op. or post-op. Asensio et al. (2003 & 2007) Early hepatic AE in all pts. with grades IV, V injuries Improved survival with Immediate surgery Early hepatic packing Direct pt. transport from OR to angio suite

Unstable Hepatic Injuries: Penetrating or Blunt Classic teaching is operative management Operative principles: Hemostasis Adequate exposure Debridement Drainage Results poor with severe, high grade injuries (V) Traditional operative approach being revised Multidisciplinary approach also advocated by some in unstable patients

Basic Operative Approach Diagnostic & therapeutic maneuvres Pack – what is bleeding? Pringle maneuver (1908) Hepatic arterial bleeding Portal venous bleeding May use safely for up to 75 minutes

Basic Operative Approach If ongoing venous bleeding with pringle maneuvre Retrohepatic IVC Major hepatic veins Direct visualization of bleeding vessels to suture ligate Even if need to divide uninjured parenchyma Tractotomy Finger fracture

Basic Operative Approach In severe injuries, vascular exclusion / isolation techniques may be used Aortocaval shunt Complete vascular inflow occlusion Pringle Aorta Infrahepatic IVC Suprahepatic IVC

When Thing Are Really Bad… May resort to veno-veno bypass Allows for direct repair of injuries juxtahepatic venous injuries

Who, When & How to Pack? Onset of triad of death Extensive bilobar injuries Large, expanding or ruptured hematomas Failure of other maneuvers Pts. who require transfer to a level I trauma center Juxtahepatic venous injuries Watch IVC with packing Remove < 72 hrs

“Much has been written on the topic of hepatic venous injuries and there are possibly more authors on the subject than survivors of the procedures described” A. Walt, 1978

Management of Juxtahepatic Venous Injuries (V)

Anatomy – Juxtahepatic Veins Retrohepatic IVC 7 cms in length Phrenic & right adrenal vein Completely circumscribed by hepatic suspensory ligaments Major hepatic veins Right, middle, left Supernumerary veins Typically 7, additional smaller veins Drain right and caudate lobes RIVC & MHVs are resistant to collapse or compression

Juxtahepatic Venous Injuries – Buchman R Juxtahepatic Venous Injuries – Buchman R. et al, Juxtahepatic Venous Injuries: A Critical Review of reported Management Strategies, J Trauma, 48 (5), 2000 Most deadly form of liver trauma Non-compressible, do not collapse Surgically inaccessible Injury causes Life-threatening exsanguination Fatal air embolism Poor outcomes may be due to Lack of familiarity with anatomy Limited surgical experience Current management strategies are flawed

Juxtahepatic Venous Injuries – Buchman R Juxtahepatic Venous Injuries – Buchman R. et al, Juxtahepatic Venous Injuries: A Critical Review of reported Management Strategies, J Trauma, 48 (5), 2000 Elements of injury include: Direct injury to vein Intraparenchymal Extraparenchymal Injury to surrounding tamponading tissues Parenchyma & capsule (intraparenchymal) Areolar tissue, diaphragm, hepatic suspensory ligaments Free bleeding occurs IFF there is a breach in the containing tissues in association with a venous injury These breaches may occur with surgical decompression which can lead to massive, uncontrollable free bleeding

Juxtahepatic Venous Injuries – Patterns of Injury: Type A Hepatic venous injury is intraparenchymal Associated disrupted liver parenchyma and capsule Injuries bleed directly through disrupted liver parenchyma May have associated injury to portal veins or hepatic arteries

Juxtahepatic Venous Injuries – Patterns of Injury: Type B Venous wound is extraparenchymal Associated disruption of suspensory ligaments, diaphragm or both Bleeding mainly Around the liver Into chest Much less common than type A

Determinants of Hemorrhage & Treatment Strategies Amount of free bleeding depends on: Extent of venous laceration Severity of injury of associated structures Operative strategies: Direct suture repair +/- vascular isolation Lobar resection for bleeding control Tamponade / containment of venous bleeding

Operative Strategy – Direct Suture Repair +/- Adjuncts Direct repair done in accordance with historic beliefs, approach taken elsewhere in body Ochsner (1961) & Starzl (1962) pioneers for repair of IVC injuries Infrahepatic IVC injuries, none were retrohepatic Technical difficulties lead to vascular exclusion / isolation techniques as adjuncts Atriocaval shunt (Schrock – 1968) First successful suture of JHVI Bricker, 1971 Complete vascular exclusion (Waltuck – 1970, Yellin – 1971) Clamps applied to the suprahepatic and infrahepatic IVC, portal vein, aorta Prohibitively high rate of cardiac arrest if done while pt. severely hypovolemic Need for venous suturing has never been questioned

Operative Strategy – Anatomic Resection McClelland & Shires (1965) 80% survival in 25 pts. undergoing lobectomy for severe hepatic trauma Unclear prevalence of JHVI Other series demonstrate high mortality when done for bleeding or precise anatomic resection Main success is with debridement for devitalized tissues Not widely applied for treatment of acute hemorrhage from hepatic venous injury Complete resection = hepatic transplantation Few successes in case reports

Operative Strategy – Tamponade & Containment Deep parenchymal suturing to control venous bleeding ‘standard of care’ Stone & Lamb (1975) Omental inclusion with deep sutures Near complete success in 37 pts. Fabian & Stone (1980) 104 pts. with blunt hepatic injury & venous bleeding Hemostasis in 95%, 8% died Repeat study in 1991 with JHVI Survival 80% Mortality 3x lower vs. direct venous repair +/- isolation Ideal for type A injuries

Operative Strategy – Tamponade & Containment Beal (1990) Perihepatic gauze packing in 35 pts. including JHVI Mortality 14% vs. 70% with AC shunts & DVR Balloon tamponade used in bilobar GSWs Very few with actual hepatic venous injury

Conclusion Wide hepatic mobilization & direct venous ligation should be abandoned for JHVIs Omental and gauze packing provide alternatives with lower mortality Recurrence of bleeding or thrombosis are not major sources of mortality when veins are not repaired Based on injury pattern, restoration of containment structures around disrupted veins may be a preferred approach

Conclusion: What is New? Can we improve how we pack? Hemostatic agents prepacking? Packing material itself? New multimodality approaches Endovascular stenting of IVC Intraoperative percutaneous deployment of venous balloons Right femoral vein to infrahepatic IVC Right internal jugular to retrohepatic IVC Proceed with suture repair of venous injuries

Options to Improve Packing? FloSeal may be applied to actively bleeding vessels. Made of bovine gelatin & thrombin, hemostasis occurs in wet fields up to arterial pressure FloSeal effectively stopped hemorrhage in arterial & venous injuries (IV, V) in coagulopathic swine. Leixnering M., et al., J Trauma, 64 (2), 2008

Options to Improve Packing? Modified chitosan (N-acetyl glucosamine) used in an animal model of liver injury Grade V major hepatic venous involvement Animals also coagulopathic & hypothermic MC group: Higher MAP Less total blood loss All MC animals survived 50% controls died Bochicchio G. et al, Use of a modified chitosan dressing in a hypothermic, coagulopathic grade V liver injury model, American Journal of Surgery (2009) 198, 617–622

Injury to the Portal Triad Portal vein Mainly seen with penetrating injuries May ligate portal vein Fluid requirements massive Second look laparotomy for small bowel viability Elevate & wrap extremities with compression stockings Splenectomy? Proper hepatic artery May ligate with impunity Holds true for normotensive pts., pts. in shock may experience hepatic necrosis Common bile duct High rate of failure & stenosis with primary end-to-end anastomosis Roux-en-Y hepaticojejunostomy preferred Drain & refer to specialized hepatobiliary surgeon

Post-Operative Complications 35M, POD# 14 blunt, grade IV hepatic injury, NOM. Increasing bilirubin over last 4 days. You are called urgently to assess him in the TICU as c/o RUQ pain, has hematemesis. What is going on? How do you treat? 35M, POD #14 blunt, grade IV hepatic injury, NOM. Significantly increasing bilirubin over last 2 days, normal LFT’s.

Post-Operative Complications 35M, POD# 6, penetrating TA injury, grade IV hepatic injury, NOM, minimal injury to liver on CT, HD stable. Small pleural effusion R side over past 4 days. Called to assess re: sudden SOB and desaturation. What is going on? How do you treat this?

Post-Operative Complications: Fistulas Hemobilia: blood (arterial) into bile Quincke (1871): RUQ pain, jaundice, UGIB Treat with ERCP, angioembolization or OR if fails Bilhemia: bile into blood (venous) Presence of hyperbilirubinemia, normal LFT’s Treat with ERCP Thoracobiliary fistula: bile into pleura May progress to bronchobiliary fistula Treat with chest tube & ERCP

Post-Operative Complications Abscesses Bilomas Necrosis Pseudoaneurysms

In Summary Grade V hepatic injury? Watch for complications Consider injury pattern Consider a different approach Consider new adjuncts FloSeal (gelatin bovine & thrombin) Modified chitosan packs Angioembolization Watch for complications

Thank you!