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

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

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

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

8. 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

9. AAST Organ Injury Scale

10. 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

11. 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

12. 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

13. 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

14. 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

15. 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

16. 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

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

18. 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

19. “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

20. Management of Juxtahepatic Venous Injuries (V)

21. 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

22. 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

23. 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

24. 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

25. 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

26. 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

27. 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

28. 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

29. 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

30. 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

31. 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

32. 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

33. 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

34. 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

35. 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

36. 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.

37. 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?

38. 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

39. Post-Operative Complications
Abscesses
Bilomas
Necrosis
Pseudoaneurysms

40. 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

41. Thank you!