Complex Hepatic Injuries

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Transcript Complex Hepatic Injuries

Tanya L. Zakrison
Ryder Trauma Center
University of Miami Miller School of Medicine
Sept. 20th, 2014

18 male helmeted patient, high speed
motorcycle collision
 Thrown off motorcycle hits barrier

EMS arrives

Patient is unresponsive, significant blunt
trauma to right torso, blood pressure 80/50
mmHg

Pre-hospital care
 most important is prompt transportation to a trauma
center
▪ SCOOP AND RUN
 A - Intubate (possibly)
 B - Needle decompression for any concern about a
tension pneumothorax
 Circulation – IV access, hypotensive resuscitation?
 D – TBI with spinal cord injury – probable
 Exposure


ATLS protocol in the trauma bay
Work as a team, excellent communication
 Repeat the ABCDEs
 Verify ETT placement
 Help the surgeons place a tube thoracostomy on
decompressed side
▪ Contralateral side too if still hypotensive
 Verify that the IV sites are in place, 20 cc/kg crystalloid
▪ Blood (massive transfusion protocol)
 ED thoracotomy?
 FAST & CXR
 Do we need to operate or not?

Diasylate fluid is infused intraperitoneally to
increase intra-abdominal pressure to reduce
bleeding in the pre-hospital phase
 Compared to previous models of abdominal
hypertension using CO2 insufflation
Animal model demonstrated efficacy in animal
models of liver injury
 Abdominal pressure of 15 mmHg achieved
 Mean arterial pressure, hematocrit and glucose
concentration higher in dialysate group

 Adjunct to increase survival in the pre-hospital phase

Hemodynamically stable
 Blunt
 Penetrating
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Hemodynamically unstable
 Blunt
 Penetrating
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Specific injuries:
 Parenchymal injuries
 Grade V juxtahepatic venous injuries
 Portal triad

Complications
There are 4 sources of bleeding in the liver

Falciform ligament
 Ligamentum teres

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Coronary ligaments
Triangular ligaments

Hematomas may be
contained within
suspensory ligaments

May injure:
 Blood vessels:
▪
▪
▪
▪
Retrohepatic IVC
Hepatic veins
Portal veins
Hepatic arteries

Management options:
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
Bleeding &
Air embolism 

 Biliary radicles
 Parenchyma
 Perihepatic structures
Packing
Direct suture
Finger fracture
Omental packing
Penetrating tract
▪ Open it (tractotomy)
▪ Pack it (multiple adjuncts)

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Hemostatic agents
Liver bag
Vascular isolation
Atriocaval shunting
Resection & tranplantation
Veno-veno bypass

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

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
 GCS = 15

no peritonitis
no active bleed on CT
AAST grade does not determine eligibility for NOM

Angioembolization (AE):
 Pseudoaneurysm, blush, active extravasation
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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
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
Classic teaching is operative management
Operative principles:
 Hemostasis
 Debridement
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
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Adequate exposure
Drainage
Results poor with severe, high grade injuries (V)
Traditional operative approach being revised
Multidisciplinary approach also advocated by
some in unstable patients
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Diagnostic &
therapeutic maneuvres
 Pack – what is bleeding?
 Pringle maneuver (1908)
▪ Hepatic arterial bleeding
▪ Portal venous bleeding
▪ May use safely for up to 75
minutes

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

In severe injuries,
vascular exclusion /
isolation techniques
may be used
 Atriocaval shunt
 Complete vascular
inflow occlusion
▪
▪
▪
▪
Pringle
Aorta
Infrahepatic IVC
Suprahepatic IVC

May resort to venoveno bypass

Allows for direct repair
of injuries
 juxtahepatic venous
injuries
Onset of triad of death
Extensive bilobar injuries
Large, expanding or
ruptured hematomas
4. Failure of other
maneuvers
5. Pts. who require transfer
to a level I trauma center
6. Juxtahepatic venous
injuries
 Watch IVC with packing
 Remove < 72 hrs
1.
2.
3.

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
 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

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
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

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

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
Direct repair done in accordance with historic beliefs,
approach taken elsewhere in body
 Ochsner (1961) & Starzl (1962) pioneers for repair of IVC
injuries
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 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
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Need for venous suturing has never been questioned

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
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Deep parenchymal suturing to control venous bleeding
‘standard of care’
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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%
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Mortality 3x lower vs. direct venous repair +/- isolation
Ideal for type A injuries

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
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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

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
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

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

Portal vein
 Mainly seen with penetrating injuries
 May ligate portal vein
▪ Fluid requirements massive
▪ Second look laparotomy for small bowel viability
▪ 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
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Abscesses
Bilomas
Necrosis
Pseudoaneurysms
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Hemobilia: blood (arterial) into bile
 Quincke (1871): RUQ pain, jaundice, UGIB
 Treat with ERCP, angioembolization or OR if fails
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Bilhemia: bile into blood (venous)
 Presence of hyperbilirubinemia, normal LFT’s
 Treat with ERCP
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Thoracobiliary fistula: bile into pleura
 May progress to bronchobiliary fistula
 Treat with chest tube & ERCP
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Grade V hepatic injury?
 Consider injury pattern
 Consider a different approach
 Consider new adjuncts
▪ FloSeal (gelatin bovine & thrombin)
▪ Modified chitosan packs
▪ Angioembolization

Watch for complications
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¡Muito obrigado!