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Liver malfunction after liver transplantation

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Predict the severity of early graft dysfunction ... Confirmed T-tube cholangiogram, or a hepato-iminodiacetic acid (HIDA) scan. ... – PowerPoint PPT presentation

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Title: Liver malfunction after liver transplantation


1
Liver malfunction after liver
transplantation
  • by Intern ???

2
Overview
3
Predict the severity of early graft dysfunction
  • Criteria obtained within the 72 postoperative
    hours

4
  • Patients with a total score (1) good outcome up
    to 6(2) poor graft function a score of 7-9

5
Donor related factors
  • Steatosis gt 50
  • Age gt 60
  • High plasma Na
  • Nutritional status
  • Use of vasopressor drugs and hemodynamic
    instability
  • Hypotension during harvesting

6
Cold preservation injury
  • Graft stored in the preservation solution (UW)
    more than 12 hours is accompanied with injury of
    the vascular system with detachment of sinusoidal
    endothelial cells via specific angiogenic
    mediators

7
Re-warming injury
  • Interval between removal of organ from cold
    storage and resumption of perfusion of organ with
    recipient blood, which correspond to the time to
    perform vascular anastomoses
  • Long (gt 120 min) period of rewarming ischemia is
    a risk factor for primary non function/ initial
    poor function due to hepatocellular damage

8
Reperfusing injury
  • Reperfusion injury, begins at the time of
    reoxygenation, namely, the end of vascular
    sutures and unclamping of afferent vessels to the
    transplanted organ

9
Operative complexities
  • 1. Operative bleeding
  • 2. Thrombosis of the portal vein
  • 3. Hepatic arterial reconstruction
  • 4. Hyper acute rejection on ABO incompatible
    grafts

10
Post-transplant management
  • Common complications
  • Immunologic consenquences
  • Recurrent of disease

11
lt1gt Common complications
  • 1. Primary nonfunction
  • 2. Intra-abdominal bleeding
  • 3. Vascular thrombosis
  • 4. Biliary leak
  • 5. Infections

12
1. Primary non-function
  • 2 to 5 of liver grafts
  • May relate to donor variables, inadequate
    preservation, prolonged cold ischemia, or the
    humoral immune response.
  • surgical emergency that can be successfully
    treated by early re-transplantation. (within 7
    days)
  • Delayed nonfunction failure of all liver
    functions? persistent coagulopathy, progressive
    hyperbilirubinemia. ? vital organs fail or get
    infections

13
2. Intra-abdominal bleeding
  • High risks for postoperative bleeding(1)
    persistence of coagulopathy, fibrinolysis, (2)
    multiple vascular anastomoses
  • Coagulopathy spontaneously corrects itself.
  • A persistent drop in Hb and the need for
    transfusion of more than 6 units of PRBC are
    usually indications for reexploration and
    evacuation of the hematoma.

14
3. Vascular thrombosis
  • More common in the pediatric population
  • Directly related to the small size of the vessels
    used for reconstruction.
  • The most frequent hepatic artery thrombosis.
  • Early recognition and successful thrombectomy may
    salvage the graft.
  • Deteriorating liver function and bile duct
    necrosis indicate the need for immediate
    retransplantation.

15
4. Biliary leak
  • Reconstructionduct-to-duct anastomosis or
    choledochojejunostomy
  • secondary to technical error or ischemia of the
    donor duct.
  • Early diagnosed? bile in the drains
  • Confirmed? T-tube cholangiogram, or a
    hepato-iminodiacetic acid (HIDA) scan.
  • Surgical exploration and revision of the
    anastomosis
  • Ischemic bile duct injury secondary to early
    hepatic artery thrombosis is an indication for
    retransplantation.

16
5.Infections
  • Direct correlation (1) preoperative status of
    the recipient, patients who await a
    transplant in ICU. (2) the incidence of
    bacterial and fungal infections.
    high-dose immunosuppression after TX
  • Resistant G() bacteria gt G(-).
  • Broad-spectrum antibiotics in the
    immunosuppressed patient contributes in part to
    the development of systemic fungal infection (
    Candida, Aspergillus).
  • Begin antibiotics for common bacteria as soon as
    clinical status suggests the presence of
    infection. ? modified if cultures and
    sensitivities available.

17
lt2gt Immunologic consequences
  • Good long-term outcome may due to (1) low
    immunogenicity(2) regeneration ability(3) ABO
    compatible (HLA matching may not to be
    necessary)
  • Long-term immunosuppression is necessary.
  • Acute rejection ? high dose steroids
  • Chronic rejection? retransplantation

18
lt3gt Recurrent of disease
  • Recurrence of viral hepatitis is likely within a
    short time after transplantation in infected
    recipients.
  • Control of active HBV infection is possible using
    lamivudine.
  • In contrast, interferon alfa or ribavirin are
    ineffective in HCV infection.
  • Reinfection of the liver graft may be mild and,
    in many cases, will not result in liver failure.

19
Long-term results
20
Higher mortality
  • Poor preoperative status
  • Immediate function of the liver allograft
  • Older age
  • Ventilator dependency
  • The need for dialysis
  • Re-transplantation

21
Back to the patient
  • Pathology report liver biopsymarked
    centrilobular congestion with atrophy of
    hepatocyte and cholestasis. Focally, necrosis of
    centrilobular hepatocytes is seen.No evidence of
    cellular rejection is seen.
  • Bedside echo no evidence of vascular
    thrombosis is seen.

22
  • Pathology centrilobular congestion ?
    vein problem
  • EchoNo evidence of hepatic vein problem.
  • What happened?smaller vein? ? VOD
    (venous-occlusive disease)

23
VOD
  • 1. Diagnosis histologically fibrous
    obliteration of hepatic veins and
    centrilobular hemorrhagic necrosis on liver
    biopsy.
  • 2. Clinical diagnosis hyperbilirubinemia (bil
    gt 2mg/dl) hepatomegaly weight gain gt2-5
    of admission weight

24
  • Cause (1) chemotherapeutic agents
    (2) irradiation.
  • (3) azathioprine
  • Incidence of VOD after liver Tx 1.9
  • Occurred from 5-133 days after TX.
  • Outcome was poor 63 of the patients died.
  • 89 of the patients with VOD had an episode of
    acute rejection before or at the time of VOD.
    Transplantation. 72(7)1237-1240, October
    15, 2001.

25
Case report life threatening VOD after LRLT
  • 48 y/o male, s/p liver transplantation secondary
    to Carolis disease related cirrhosis.
  • Left lobe graft from his elder sister.
  • Immunosuppressive FK-506, steroids
  • POD12, ALT and AST increased, so did Bilirubin.
  • POD20, liver biopsy? acute rejection
  • POD26, Bil 25.6mg/dl, coagulopathy, ascites
  • POD45, ascites- Pseudomonas sputum-
    MRSA
  • POD57, sepsis
  • POD63, died of multiple organ failure.

  • Transplantation. 75(5)727-730, March 15, 2003.

26
  • VOD with fatal outcome occurred in a LRLT
    recipient who had never been exposed to any
    agents that have the potential to induce VOD.
  • Histologically most small hepatic veins less
    than 300 ?m in diameter were affected, exhibiting
    concentric intimal thickening with sparse
    inflammatory cells.? accompanied by severe
    congestion and centrilobular necrosis.

27
  • Despite intensified immunosuppression, the
    observed fibrous obliterative changes were
    irreversible. ? immunohistochemical studies for
    collagens I highlighted a proliferation of mature
    collagen in the subintimal zone of the hepatic
    veins.
  • Although the cause of VOD in this patient is
    tentative, the damage to the endothelium,
    associated with acute rejection, is likely to be
    attributable.
  • VOD deserves recognition as one of the causes for
    liver dysfunction and persistent ascites after
    liver transplantation.

28
Defibrotide for the treatment of VOD
after liver transplantation
  • The use of antithrombotic and thrombolytic agents
    is limited by their toxicity (fatal hemorrhage).
  • Defibrotide is a polydeoxyribonucleotide with
    thrombolytic and antithrombotic properties and no
    systemic anticoagulant effect.
  • Transplantation. 72(7)1237-1240, October
    15, 2001.

29
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30
  • Resolution of VOD42, 55 in stem-cell
    transplant patient
  • Defibrotide is a promising drug for the treatment
    of VOD after liver transplantation.
  • Needs to be evaluated in large, prospective
    studies.

31
Thank you for attention!
32
Defibrotide
  • Machanism(1) Increase levels of prostacyclin,
    PGE2 and thrombomodulin.
  • (2) Up-regulates tissue-factor pathway
    inhibitor and t-PA.
  • (3) Decreases thrombin generation and
    levels of circulating plasminogen activator
    inhibitor
  • (4) Inhibits fibrin deposition and modulate
    fibropectin release .
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