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Orthotopic Liver Transplantation

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Hyperkalemia ( liver is primary site of insulin action, even in ESLD) ... Insulin with glucose ( 10 U with 50 ml of 50% glucose) B agonist ( 10-20 mg nebulized ... – PowerPoint PPT presentation

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Title: Orthotopic Liver Transplantation


1
Orthotopic Liver Transplantation
2
Orthotopic liver transplantation
  • Approximately 2500 liver transplants per year in
    the United States
  • 1 yr survival approx 76
  • Majority are orthotopic ( native hepatectomy with
    donor implantation in RUQ )
  • Typically reserved for non-malignant ESLD that
    will not recur in hepatic graft

3
Indications
  • Post necrotic cirrhosis 35
  • Post hepatitis
  • Alcoholic (Laennecs cirrhosis)
  • Cryptogenic
  • Auto-immune
  • Primary biliary cirrhosis
    12
  • Malignancy (isolated) 12
  • Biliary Atresia 10
  • Acute fulminant failure 8
  • Sclerosing choangitis 6

4
Contraindications
  • Have evolved over the last several years
  • Now generally include
  • Widespread malignancy
  • Uncontrolled infection
  • Severe cardiac / neurologic disease
  • Inability to maintain appropriate
    immunosuppression

5
Pre-Anesthetic considerations
  • Vast array of physiologic derrangements
  • Many are not correctable until after
    transplantation
  • Identify most important areas of physiologic
    compromise and treat only those that threaten the
    safe induction of anesthesia ( ie. Pleural
    effusions, coagulopathy )

6
Pathophysiology
  • GI portal HTN, Esophageal Varices, Ascites
  • Renal Oliguria (pre-renal v. hepatorenal v.
    other )
  • CV Hyperdynamic circulation ( low SVR, high CO
    )
  • Pulmonary ( Intrapulmonary shunting, pleural
    effusions, decreased FRC, atelectasis, decreased
    compliance, pulmonary HTN )
  • CNS Encephalopathy /- increased ICP
  • Heme Coagulopathy (thrombocytopenia, synthetic
    dysfunction, fibrinolysis, DIC )

7
Monitoring
  • Standard ASA /- institutional variations
  • Fundamental goals are the same
  • Sufficient IV access to administer rapid
    infusions, drips, other products
  • Arterial line(s)
  • Central Line ( /- PAC)

8
Anesthetic management
  • Induction RSI vs. awake
  • Maintenance Isoflurane opioids muscle
    relaxants (Nitrous Oxide?)
  • Also
  • Renal dose Dopamine
  • CaCl infusion

9
OLT terminology
  • Pre-anhepatic Stage Dissection of the porta
    hepatis and mobilization of the native liver
  • Anhepatic Stage Begins after clamping of native
    livers blood supply
  • Neo-hepatic Stage Reperfusion of the allograft,
    biliary reconstruction

10
Preanhepatic (dissection) stage
  • Pre-anhepatic Stage Dissection of the porta
    hepatis and mobilization of the native liver

11
Pre-anhepatic Stage
  • HD instability -secondary to acute loss of
    ascites, hemorrhage from abdominal venous
    collaterals, excessive retraction, pericardial
    effusions
  • Electrolytes citrate toxicity, rapid
    transfusion/ hemolysis
  • Coagulopathy- factor deficiencies,
    thrombocytopenia, hemodilution, fibrinolysis,
    hypothermia
  • Metabolic Acidosis
  • Hypothermia
  • Oliguria
  • Air embolism

12
Pre-anhepatic Stage
  • Increased risk in patients with
  • preop coagulopathy (significant)
  • previous abdominal surgery (ie. Kasai
    procedure in pediatric pt.s)

13
Anhepatic Stage
  • Anhepatic Stage Begins when native liver is
    removed after clamping of its blood supply

14
Anhepatic Stage
  • Clamping hepatic artery, portal vein,
    infrahepatic vena cava, suprahepatic vena cava
  • Typically lasts 60 90 minutes
  • Typically requires venovenous bypass

15
Anhepatic Stage
  • Clamping and Veno-venous bypass related
    complications
  • Air embolism
  • Thromboembolism
  • Hypotension
  • Hypothermia
  • Vericeal Hemorrhage (Sengstaken-Blakemore tube)
  • Hyperkalemia ( liver is primary site of insulin
    action, even in ESLD)
  • Hypocalcemia (total lack of citrate metabolism)
  • Continued problems associated with all stages of
    OLT (hypothermia, coagulopathy, acidosis and
    other metabolic derrangements, atelectasis, HD
    instability, hemorrhage)

16
Venovenous Bypass
  • Blood from femoral and portal vein bypasses liver
    via extracorporeal circulation and returns to
    heart via axillary / subclavian vein.
  • Helps maintain HD stability
  • Improves renal perfusion
  • Reduce portal venous pressures
  • In pt.s gt 15 kgs
  • No heparinization needed
  • Bypass flow should be gt25 CO (gt 1 L/Min)

17
Neohepatic (post-anhepatic) stage
  • Neo-hepatic Stage Reperfusion of the allograft,
    biliary reconstruction
  • Allograft is flushed of air, debris, and
    preservative solution
  • Subsequent unclamping can release significant
    load of Potassium and Metabolic Acids into
    circulation

18
Neohepatic Stage
  • Continued pre-anhepatic, anhepatic problems
  • Hemodynamic changes hypotension, bradycardia,
    supraventricular and ventricular arrythmias,
    cardiac arrest.
  • Hemorrhage
  • Continued risk of air or thromboembolism

19
Postreperfusion Syndrome
  • Aggarwal et al. defined as decreased MAP of at
    least 30 from baseline for at least one minute
    within five minutes of reperfusion
  • Labile SVR, and CO
  • Incidence as high as 30
  • Lower incidence in non VVB cases (attributed to
    increased intravascular volume before
    reperfusion)

20
Mechanism(s) of PRS
  • Isolated RV dysfunction (as detected by echo
    paradoxical motion of IVS, etc.)
  • Impaired LV function
  • Endotoxemia , Cytokine release (TNF, IL-1,
    IL-6 , and other vasoactive substances following
    decompression of the portal circulation
  • Most likely multifactorial in nature

21
Other factors affecting post reperfusion
hemodynamics
  • Hyperkalemia
  • Hyocalcemia
  • Continued blood loss
  • Air embolism
  • If graft function is adequate, hemodynamic
    stability generally occurs within 15 min
    following reperfusion

22
Treatment of Post -Reperfusion instability
  • Inotropic support
  • Calcium
  • Sodium Bicarbonate
  • 100 Oxygen
  • Aggressive electrolyte management pre-reperfusion
  • ACLS

23
Hyperkalemia
  • ECG changes generally seen at gt 6.0 meq/L
  • Immediate tx with Calcium salt
  • Then
  • Insulin with glucose ( 10 U with 50 ml of 50
    glucose)
  • B agonist ( 10-20 mg nebulized albuterol )
  • Sodium Bicarbonate
  • K removal (Loop diuretic, Kayexelate,
    Dialysis)

24
UW or Belzers Solution
  • K lactobionate 100 mmol
  • Dihydrogen Phosphate 25 mmol
  • Adenosine
    5 mmol
  • MgSO4 5 mmol
  • Glutathione 3 mmol
  • Raffinose 30 mmol
  • Allopurinol 1 mmol
  • Insulin 100 U
  • Penicillin 40 U
  • Dexamethasone
    8 mg
  • Hydroxyethyl starch
    50 g
  • Osmolality
    320-330 mOsm
  • pH 7.4

25
UW Solution
  • Cell impermeant agents Lactobionic Acid,
    Raffinose, Hydroxyethyl starch
  • Glutathione Antioxidant
  • Adenosine Cellular metabolism

26
Autologous Flush
  • Prior to reperfusion
  • All vascular anastamoses completed except for
    infrahepatic IVC
  • Graft perfused via unclamping Portal Vein, and
    Hepatic Artery
  • 500 cc of blood allowed to flow out of partially
    anastamosed infrahepatic IVC, then into cell
    saver
  • Blood supply then reclamped, and infrahepatic IVC
    anastamosis completed
  • Associated increase in HD stability, decreased
    serum K levels, improved early graft function,
    increased patient and graft survival ( Fukazawa
    et al., 1994)

27
Reperfusion Hyperglycemia
  • Massive release of glucose from donor liver
  • Gradually resolves with return of hepatic
    function
  • Persistent hyperglycemia is indicator of impaired
    glucose utilization
  • May be prognostic factor for liver viability

28
Reperfusion Coagulopathy
  • Related to release of heparin from the donor
    liver
  • Reversible with protamine
  • Accompanied by diminished platelet count, factor
    V, and VIII.
  • 80 of patients experience primary fibrinolysis
    from release of TPA from liver
  • 20 require specific treatment with
    cryoprecipitate and platelets
  • Continued refractory coagulopathy indicates high
    likelihood of graft failure

29
Thromboelastography
  • Monitors entire coagulation process
  • This includes clot formation and lysis
  • Valuable in directing blood product replacement
    and pharmacologic intervention

30
Thromboelastography 101
  • R (reaction time) denotes time to onset of the
    start of coagulation ( 6-8 min )
  • Prolonged R time represents factor deficiency, tx
    with FFP
  • Coagulation time (r k ) is time from start of
    TEG to the generation of an amplitude of 20 mm,
    and measures speed of clot formation
  • Alpha angle (clot formation rate) Normally
    greater than 50 degrees. Abnormalities represent
    plt dysfunction, fibrinogen, IP. Tx with
    Cryoprecipitate
  • MA (max amplitude) Most indicative of plt
    function (normally 50-70 mm) Treat with
    platelets
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