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Anesthesia MM/TL > Liver Transplant > Flashcards

Liver Transplant Flashcards

1
Q

What are the complications in the pre-anhepatic stages?

A

Obvious and insidious blood loss from adhesions and dissection
Potential compression of native vessels
Worsening of pre-existing coagulopathy

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2
Q

What is contained in the University of Wisconsin solution?

A

Potassium (120 mmol/l)
Lactobionate and raffinose (to prevent cell swelling)
Hydroxylethyl starch (to increase oncotic pressure)
Allopurinol
Glutathione
Adenosine
Dextrose

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3
Q

What does the MELD score look at?

A

Creatinine
Bilirubin
INR
Albumin

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4
Q

How does the simple venous cross clamping technique work?

A

The liver is removed with retro hepatic IVC after cross clamping the supra hepatic and infra hepatic IVC, hepatic artery and portal vein

Re-anastomosis the supra and infra IVC then flush the liver with 1LR thru a cannula in the portal vein

Then reperfuse

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5
Q

How does veno-venous bypass work?

A

A cannula is out in the femoral vein and iliac vein or axillary vein for bypass.

Bypass –> hepatectomy –> reperfusion –> decannulate

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6
Q

What is the piggyback technique?

A
  1. Diseased liver is removed WITHOUT the retro hepatic IVC (so venous return is preserved)
  2. Anastomosis done with left and middle hepatic v. To supra hepatic IVC or graft for hepatic drainage
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7
Q

What are the issues in the anhepatic stage?

A

Decrease in venous return due to cross clamping
Progressive coagulopathy
Progressive metabolic acidosis
Hypocalcemia

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8
Q

What are the goals in the first stage of OLT?

A 
Keep euvolemic (keeping up with blood loss)
Correct coagulopathy 
Octreotide for splanchnic vasoconstriction to control bleeding
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9
Q

What are the goals of the anhepatic stage?

A 
Maintain hemodynamic stability
Correct coagulopathy 
Give solumedrol
Turn off octreotide
Tank up for reperfusion
Treat hyperkalemia with goals if K of 4
Treat glucose
Treat hypocalcemia 
Treat metabolic acidosis
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10
Q

What happens in reperfusion?

A 
Hypothermia
Cytokine load
Hyperkalemia
Emboli
--> pulmonary HTN, increased ICP, hypotension, arrhythmias, worsened coagulopathy
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11
Q

Why is the heart hyper dynamic in ESLD?

A

Because there are lots of vasodilators (NO made from gut flora) that cause a decrease in SVR, so you increase CO to maintain your MAP

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12
Q

What are your sources of preload loss in the first stage?

A

Ascites, surgical bleeding, vascular compression

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13
Q

What are the issues with MTP?

A

Hypothermia
Hypocalcemia
Hypomagnesemia
Hyperkalemia

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14
Q

What are the hemodynamic changes due to in the anhepatic phase?

A

Decreased preload from cross clamping of the IVC and portal vein

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15
Q

What happens in the anhepatic stage?

A

Ischemia
Blood sequestering in kidneys, GI and pelvic organs leads to renal venous congestion with associate acidosis, intestinal swelling, hematuria

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16
Q

What is the transient hypovolemia and hypotension after unclamping of the infra hepatic IVC and portal vein due to?

A

Acute sequestration of the blood in the engrafted liver

17
Q

What does unclamping of the supra hepatic IVC result in?

A

Increased preload from mobilization of blood from lower extremities and splanchnic circulation

18
Q

What is postreperfusion syndrome

A

A decrease in MAP greater than 30% of baseline for 1 minute in the first 5 minutes of reperfusion

19
Q

What are the associated hemodynamic changes with postreperfusion syndrome?

A 
Bradycardia
High CVP
High PCWP
Low SVR (from vasodilators released from the allograft and congested viscera) 
Arrhythmias 
Myocardial depression 
RV strain (from acute increase in preload)
Hypothermia
Embolism 
Hyperkalemia
Acidosis
20
Q

What is the MOA of octreotide?

A

Increases splanchnic tone and SVR by affecting VIP

21
Q

What happens to minute ventilation in OLT.

A

Decreases to match reduced oxygen consumption

Increased during neohepatic stage due to increased oxygen consumption and high ETCO2

22
Q

Why is there an increase in tPA level in neohepatic stage?

A

Because the new live has not begun clearing tPA yet and plasminogen activator inhibitor is overwhelmed

23
Q

How long does it take from fibrinolysis to resolve?

A

2 hours after reperfusion

24
Q

What is EACA.

A

An anti-fibrinolytic used for severe fibrinolysis to minimize the loss of factors I, V, VIII.

25
Q

What is aprotinin?

A

A nonspecific inhibitor of plasminogen and serine professes

26
Q

How can desmopressin be used

A

To increase endothelial release of VIII, vWF, and plasminogen

27
Q

What is THAM used for?

A

Correction of acidosis without affecting sodium concentration

28
Q

How much THAM is equal to an amp of bicarbonate?

A

150 ml of 0.3 molar THAM

29
Q

What does dichloroacetate do?

A

Reduces lactate production by stimulating pyruvate oxidation

30
Q

What are the two independent risk factors for postreperfusion syndrome?

A

Diastolic dysfunction

Long cold ischemia time

31
Q

What are the effects of methylene blue?

A
  1. Inhibition of nitric oxide synthase

2. Inhibition of guanylate cyclase

32
Q

What can vasopressin help to reverse in OLT?

A

Vasoplegia precipitating LVOT obstruction and MVR

33
Q

What has terlipressin been shown to be good for?

A

Improved postop renal function with no adverse effects on hepatosplanchnic function

34
Q

What matters age of donor matters in a patient with a moderate MELD score?

A

Greater than 46 with greater than 9 hour cold ischemic time

35
Q

What matters with a patient with a high MELD score?

A

Cold ischemic time over 9 hours regardless of age of donor

36
Q

How long should cold ischemia time be limited to?

A

6-8 hours

37
Q

What are the factors associated with a high risk graft?

A 
Age over 70
Procurement after cardiac arrest 
Degree of steatosis 
Type of sharing (split graft)
Donor's length of stay in hospital before procurement
BMI > 30
Map lower than 60 for longer than 20 minutes after withdrawal of life support 
Cold ischemia time longer than 6 hours 
Hep B positive antibody 
Hep C
Malignancy

Anesthesia MM/TL (36 decks)

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