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Concepts 3 > Liver Transplant (FINAL EXAM) > Flashcards

Liver Transplant (FINAL EXAM) Flashcards

1
Q

Neurologic changes with liver disease

A

Hepatic Encephalopathy
- Behavioural changes to coma
- Impaired ammonia metabolism
- Lactulose, Rifaximin

Cerebral Edema
- Acute liver failure
- Pathophysiology unclear

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2
Q

Cardiac sytem changes

A
  • Low SVR
  • High cardiac output
  • Elevated resting heart rate
  • Vasodilation
  • Activation RAAS, SNS
  • Sodium & fluid retention
  • Cirrhotic cardiomyopathy
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3
Q

Pulmonary system changes

A
  • Reduced FRC

Hepatic hydrothorax (10%)
- Ascites in the right chest

Hepatopulmonary syndr (10%)
- Hypoxia, intrapulmonary shunts

Portopulmonary hypert’n (6%)
- Elevated PVR with cirrhosis

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4
Q

Hepatorenal Syndrome

A

Hepatorenal syndrome (18-40%)
- Cr >1.5mg/dL; no other cause
- Reduced renal perfusion
- SBP, GI bleed, paracentesis
- Type 1: rapid, severe
- Type 2: slow, less severe
- Midodrine+octreotide+albumin

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5
Q

Hematologic system changes

A
  • Coagulopathy
  • Thrombocytopenia
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6
Q

GI system

A
  • Esophageal varices
  • Spont bacterial peritonitis
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7
Q

preop eval

A

History, Physical Exam, Laboratory Studies
* CBC, ‘Lytes, Chemistries, LFTs
* Coagulation studies
* Blood group and antibody screening Other Studies
* EKG, CXR, TTE/DSE, PFT Screening for
* CAD, PoPH, HPS, HRS

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8
Q

CAD screening

A
  • Prevalence: 2.5% - 38%
  • Leading cause of non-graft-related mortality
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9
Q

CAD risk factors

A
  • Age >50
  • DM
  • h/o CV dz
  • tobacco
  • HTN
  • dyslipidemia
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10
Q

CAD next steps

A

non-invasive stress test –> coronary cath

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11
Q

optimal screening with %s

A
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12
Q

Hepatopulmonary syndrome - prevalence and defination

A
  • Prevalence: 4-19%
    Defined as:
  • Chronic liver disease
  • [A-a]O2 gradient ≥15mmHg (≥20 for >65yrs old) * Intrapulmonary shunting (TTE or 99mTc-MAA)
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13
Q

Hepatopulmonary syndrome classifications

A
  • Mild – PaO2 >= 80mmHg
  • Moderate – 60-79 mmHg
  • Severe – 50-69mmHg
  • Very Severe <50mmHg
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14
Q

Hepatopulmonary syndrome - symptoms, prognosis, and treatment

A
  • Dyspnea, Platypnea, Orthodeoxia
  • Prognosis: increased mortality; lower quality of life
    Treatment: Liver transplantation
  • Cured/improved in >85% at 6-12mos post-op
  • MELD exception for HPS w. PaO2<60mmHg
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15
Q

HPS screening and management

A
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16
Q

Portopulmonary Hypertension

A
  • Prevalence of 5-8.5%
  • Defined as:
  • Portal hypertension
  • mPAP>25mmHg with mPAOP<15mmHg
  • Transpulm gradient (mPAP-mPAOP >10mmHg)
  • PVR >240dyn.s.cm-5 (>3 Woods units)
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17
Q

Portopulmonary HTN

A

Classification:
* Mild – mPAP 25-35mmHg
* Moderate – mPAP 35-45mmHg
* Severe - ≥ 45mmHg

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18
Q

portopulmonary HTN

A
  • Increased RV myocardial oxygen demand
  • RCA perfusion limited to diastole
  • Reduced LV preload
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19
Q

OLT and PoPH mortality

A
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20
Q

PoPH Screening & Management

A
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21
Q

Nictric oxide pathway

A
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22
Q

PoPH Treatment & Response

A

Sildenafil
Tadalafil
Bostentan
Ambrisentan
Epoprostenol
Iloprost
Treprostinil

Response to treatment:

PAP <35mmHg;
PVR<400dynscm-5
- List for liver transplant
- MELD exception points

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23
Q

Hepatorenal Syndrome

A

Patients with ascites
* 18% at 1yr
* 40% at 5yrs

Precipitating factor in 1⁄2 the cases:
* SBP
* GI bleed
* Therapeutic paracentesis

Dx: exclusion
* Chronic liver disease
* Cr >1.5mg/dL in absence of other causes

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24
Q

Hepatorenal syndrome types and treatment

A
  • Type 1: Rapidly progressive
  • Cr doubles in 2wks (usu. up to 2.5mg/dL) * Median survival ~2wks
  • Occurs in 1/3 of patients with SBP

Type 2: slowly progressive
* Cr usually up to 1.5mg/dL
* Median survival ~4-6months

Treatment: terlipressin + albumin
* (midodrine+octreotide+albumin)
* HD bridge to LTx

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25
Q

Acute liver failure

A
  • Acute elevation in transaminases (2-3x nl)
  • Coagulopathy (INR ≥1.5)
  • Encephalopathy (any degree of alteration)
  • No pre-existing liver disease*
  • acute presentation of AIH, Wilson disease, Budd- Chiari if <26wks

2,000 cases/yr in US
Mortality: ~50%

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26
Q

Encephalopathy - grades

A

Grade I
Mild unawareness, euphoria or anxiety; short attention span; impairment of calculation; lethargy

Grade II
Disorientation to time; inappropriate behavior

Grade III
Somnolence to stupor; confusion; responsiveness to stimuli; gross disorientation; bizarre behavior

Grade IV
Coma

  • In subacute liver failure, even low-grade encephalopathy indicates poor prognosis
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27
Q

Subcategories acute liver failure

A
28
Q

acute liver failure (anesthesia goals)

A
  • Severe coagulopathy, renal dysfunction, metabolic disarray
  • Management of cerebral perfusion - Maintain CPP >60mmHg
  • Decrease ICP
  • Head of bed >30°
  • Hypertonic saline
  • Mannitol
  • Hyperventilation
29
Q

monitoring

A

Standard ASA
Arterial line
CVP / PA
TEE

30
Q

Practice guidelines for using intra-op TEE

A

TEE may be used for patients with oral, esophageal, or gastric disease, if the expected benefit outweighs the potential risk, provided the appropriate precautions are applied. (American Society of Anesthesiologists)

31
Q

What is the speed you can run through different IV access lines?

A
  • 9Fr 10cm - **1200cc/min **
  • 8.5Fr 6cm - 1400cc/min
  • 14G 2.25” - 750cc/min
  • 16G 2.25” - 350cc/min
  • 18G 1.75” - 250cc/min
32
Q

Factors associated with increased transfusion include

A

Severity of liver disease
Etiology of liver disease
Age of patient
Prior surgeries
Preoperative INR, Plt, BUN, Hgb
Preoperative MELD (or component of: i.e. Bili, INR, Cr)
Cold Ischemic Time
Duration of anhepatic phase
Operative time

33
Q

Strategies to minimize transfusion

A
  • Surgical technique
  • Intraoperative cell salvage
  • Low CVP
  • Dedicated anesthesia team
  • Antifibrinolytics
  • Transfusion protocols
  • TEG/TEM
34
Q

How is coagulopathy monitoring intra-op?

A

Standard labs, TEG and TEM
* TEG and TEM provide the continuous measurement and display of the viscoelastic properties of a whole blood sample from the initial phase of fibrin formation to clot retraction and fibrinolysis
* Clotting is accelerated by incorporating contact activators
* TEG incorporates kaolin
* ROTEM incorporates tissue factor in EXTEM cuvettes; contact activator in INTEM cuvettes (intrinsic pathway)
Heparinase-coated cuvettes allow monitoring of a heparinized patient by removing effects of heparin on tracing
Advantages of TEG/TEM: faster turnaround; whole blood used-interactions of plasma + blood components; reduction in non-evidence-based transfusion

35
Q

Liver transplant antimicrobial coverage

A

-Ampicilin-Sulbactam
-Piperacillin-Tazobactam
+/- Fluconazole

36
Q

Anesthetic agent requirement for pts with liver failure

A

In general, patients w. ESLD will require LESS
Judicious premedication in encephalopathic
Titrate anesthetic to awareness monitor
Titrate NMB to twitches
Reduced opioid requirement

37
Q

Induction for liver transplant

A

Rapid Sequence Induction
Significant ascites
Recent history of GI bleeding
Full stomach
Low SVR, High cardiac output state

38
Q

PEARLs of Pre-Anhepatic Phase

A

Incision to portal venous clamping
Hypotension/Hemorrhage

39
Q

PEARLs of Anhepatic Phase

A

Portal venous clamp to reperfusion
Metabolic derangement

40
Q

PEARLs of Neohepatic Phase

A

Reperfusion to end of case
Coagulopathy/Hepatic Perfusion

41
Q

Surgical steps of Pre-anhepatic phase

A
  • Drainage of ascites
  • Lysis of adhesions
  • Dissection vessels, biliary
  • Mobilization of liver
    +/- Veno-venous bypass
42
Q

Pre-Anhepatic Phase - Anesthetic

A
  • Ascites drainage = replace with albumin
  • hemorrhage = transfuse based on labs
    coagulopathy, thrombocytopenia
    elevated venous pressures
    collaterals
    adhesions
  • Compressed vena cava = inform team, volume & pressors
43
Q

Key takeaways for Venovenous bypass method

A
  • Stable BP
  • Decompress
  • increased Time/Cost
44
Q

Key takeaways for piggyback method

A

Stable BP
Decreased time
Decreased cost

45
Q

Key takeaways for transplant without bypass or piggyback

A

Hypotension
Decreased renal perfsion/risk for injury

46
Q

What are the metabolic derangements that occur in the anhepatic phase and why?

A
  1. Hypocalcemia: Citrate binds ioCa++
  2. Metabolic acidosis: Lactic acid not metabolized
  3. Hypoglycemia: Absent liver
47
Q

How do we manage the metabolic derangements in the anhepatic phase?

A

ABG, Lytes, Glucose
ioCa++ <1.0: bolus CaCl2
Significant acidosis: consider NaHCO3
Treat hypoglycemia

48
Q

What is the blood flow and O2 delivery of the portal vein?

A

60-70% of blood flow to liver from portal vein
50% of oxygen delivery from the portal vein

49
Q

What are the surgical details during graft reperfusion?

A
  1. Graft flushed to remove preservative solution
  2. Caval and portal anastomoses completed
  3. Portal flow re-established
50
Q

Reperfusion is associated with abrupt ______

A

Increase in potassium
Decrease in pH
Increase in EtCO2
Increase in preload
Decrease in SVR
Decrease in MAP
Decrease in core temperature

51
Q

What should you do prior to graft reperfusion?

A
  1. FiO2 1.0 in anticipation of hypoxemia
  2. Respiratory alkalosis via increased minute ventilation to offset metabolic acidosis
  3. Administer CaCl2 to offset hypocalcemia and cardiac effects
  4. Administer NaHCO3 to offset acidemia
  5. Pretreat with vasopressor
52
Q

What if we get hyperkalemia on reperfusion?

A

EKG features: peaked T waves earliest then increased PR interval, flattening of P waves, widening QRS, sinusoidal pattern
Treatment:
CaCl2: 100mg at a time titrate to EKG effect.
Onset immediate, duration of action short
Insulin:
10U insulin IV with 25g dextrose (1 amp D50)
Onset of hypokalemic action: within 15min
Duration: at least 60min
Reduction in K = 0.65-1.0 mmol/L
Albuterol
Onset about 30min
0.3-0.85mmol/L reduction in K
HCO3
Small reduction
Within 30-60min

53
Q

What does post reperfusion syndrome look this? What are predictors of it?

A
  1. Decrease in MAP > 30%
  2. ≤ 5min reperfusion time
  3. > 1min

Predictors: Donor age, Donor risk index, Recipient CVP

54
Q

What are the surgical details of the neohepatic phase?

A

Hepatic arterial reconstruction

Biliary reconstruction

Closure

55
Q

What are signs of graft function?

A

a. improvement of ioCa2
b. improvement in acidosis
c. biliary output from graft

56
Q

What are the anesthetic goals in the neohepatic phase?

A
  1. Low CVP (Keep CVP <10mmHg)
  2. Manage coagulopathy
  3. Emergence and extubation
57
Q

What is the blood flow and O2 delivery of the hepatic artery?

A

blood flow: 30-40%
O2 delivery: 50%

58
Q

What is the driving pressure inside the hepatic artery?

A

LARGE
MAP-CVP

59
Q

What is the driving pressure inside the portal vein?

A

SMALL
PVP-CVP

60
Q

Normal coagulation is a balance between ___

A

the bleeding and thrombosis

61
Q

Thrombosis is brought about through ____.

A
  1. The actions of the coagulation cascade which promotes fibrin formation
  2. Platelet aggregation to form the hemostatic plug
62
Q

Control of thrombosis is brought about through ___.

A
  1. Inhibitors of the coagulation cascade
  2. Fibrinolysis
63
Q

Coagulopathy in the neohepatic phase is a result of derangements in _____.

A

Both bleeding and thrombosis.

  1. Decreased level of coagulation factors during anhepatic phase- notably Factors VIII and V
  2. “Heparin-like” effect
  3. Platelet entrapment in donor liver sinusoids

**Increased **fibrinolysis brought about by
* Accelerated release of t-PA

Decreased levels of
* Plasminogen activator inhibitor – 1
* Alpha anti-plasmin

64
Q

Coagulopathy in the neohepatic phase may be exacerbated by ____

A

hypothermia, delayed graft function, acidosis and hypocalcemia

65
Q

How do we manage the coagulopathy in the neohepatic phase?

A
  1. Monitor
  2. Treat for
    a. INR > 2
    b. Plt < 50,000
    c. Fibrinogen < 100
  3. Antifibrinolytics / PCC (prothrombin complex concentrate) / Factor VIIa

Concepts 3 (12 decks)

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