Book 5, Case 7-OLT

Question 1

What is the MELD score?

Who is it NOT used for?

Answer 1

Stratifies severity of ESLD. The MELD score, which ranges from 6-40, is
calculated using the patient’s serum creatinine, bilirubin, and international normalized ratio
(INR).

Not used for: The MELD score is not utilized for patients with fulminant
hepatic failure and/or a life expectancy of less than 7 days, as these individuals are
designated as “Status 1” and given the highest priority.

Question 2

Dyspnea in a pt with ESLD? What are you thinking, and what are the criteria?

Answer 2

KIM that it could be these: Given this patient’s history of smoking, alcohol abuse, and liver disease, his
dyspnea could be secondary to smoking (COPD), alcoholic cardiomyopathy, cirrhotic
cardiomyopathy, ascites (a tense, distended abdomen with a demonstrable fluid wave
suggests significant ascites ), pleural effusions, hepatopulmonary syndrome, or a combination
of these.

But, hepatopulmonary syndrome:
Hepatopulmonary syndrome is defined by the triad of liver disease, decreased oxygenation
(an alveolar-arterial gradient >20 mmHg and/or a Pa02 < 70 mmHg on room air), and
intrapulmonary vascular dilation, which is diagnosed using contrast-enhanced
echocardiography, perfusion lung scanning, or pulmonary arteriography. Unless completely
unresponsive to supplemental oxygen (indicating an unacceptable perioperative risk of graft
hypoxia and failure), hepatopulmonary syndrome is an indication for liver transplantation.

Question 3

Pathophys of ascites in ESLD

What things does this put them at risk for?

Answer 3

The cause of ascites in cirrhosis is probably
portal hypertension and renal retention of sodium and water resulting in the transudation of fluid into the peritoneal cavity.
The accumulation of ascitic fluid in the peritoneum may exert pressure on the diaphragm and
stomach that result in compromised pulmonary gas exchange and an increased risk of
aspiration, respectively.

Question 4

What are benefits of performing paracentesis? And also-if you do it, what do you need to ensure? What are some bad things that could happen if you do?

Answer 4

increased cardiac output (relieves compression of inferior vena cava by ascitic fluid),
improved pulmonary gas exchange (increased pulmonary compliance and reduced V /Q
mismatch with the reduction of ascitic fluid pressure on the diaphragm and/or pleural
effusions), and decreased risk of gastric aspiration (due to decreased ascitic fluid
compression of the stomach).
I
would ensure adequate volume expansion with colloid solutions to prevent circulatory
collapse with the progressive reaccumulation of ascitic fluid in the peritoneal space.

Bad: possible hypotension

Question 5

Causes of renal failure in ESLD pts that are NOT HRS: (other causes of renal failure)

Answer 5

pre-renal azotemia, acute tubular necrosis, and drug toxicity,

Question 6

How can you figure out if a pt has HRS? (ESLD)

Answer 6

You can give a fluid bolus (being careful with other co-morbidities) to rule out pre-renal azotemia (damage to the kidneys)

The major criteria are as follows: 1) the presence of advanced liver
disease and portal hypertension; 2) a low GFR (serum creatinine > 1.5 mg/dL or creatinine
clearance< 40 mL/min); 3) the absence of shock, infection, fluid losses, or treatment with
nephrotoxic agents; 4) no sustained improvement in renal function in response to a 1.5 L
fluid challenge; 5) the absence of proteinuria ( < 500 mg/day), urinary obstruction, or
parenchymal renal disease (the latter two determined by ultrasonography). The minor
criteria include: 1) oliguria (< 500 mL/24 hours); 2) a low urinary sodium concentration(<
10 mEq/L); 3) a urine osmolality that exceeds plasma osmolality by at least 100 mOsm; 4)
spontaneous dilutional hyponatremia (serum sodium< 130 mEq/L); and 5) the absence of red
blood cells in the urine.

Question 7

Pathophysiology of HRS?

Answer 7

Endothelial (prostacycline and nitric oxide) and
nonendothelial (glucagon) vasodilators lead to splanchnic
arterial vasodilation.
This leads to a reduction in “effective’
blood volume sensed by the juxtaglomerular apparatus, which then leads to a compensatory
activation of the renin-angiotensin-aldosterone system and sympathetic nervous system.
While activation of these systems leads to systemic and renal vasoconstriction, the effects are
insufficient to counteract the vasodilation in the splanchnic circulation. Persistent dilation of
the splanchnic circulation and reduced perfusion of the kidneys results in profound intrarenal
arterial vasoconstriction and, eventually, HRS.

Question 8

Type 1 vs 2 HRS:

Answer 8

Type 1: rapidly progressive renal failure

Type 2: Slower onset

Question 9

So theyve got a liver, but pt’s coagulopathy is not corrected-wyd?

KIM what about this coag status?

Answer 9

Given the urgency of the procedure, I would not attempt to normalize his
coagulation status as long as his platelets were greater than 50,000-60,000 cells/μL, his INR
was< 1.5, and there were no signs of active bleeding.

KIM that when placing invasive lines or monitors, coag status should be taken into account!!!

Plts should be 50 prior to major surgery, and 100 if the surgery involves the brain or eyes.

Question 10

Liver makes all coag factors except:

Answer 10

Factor 8 and vWF

Question 11

ESLD has quantitative and qualitative platelet defects ( T/F)

Answer 11

TRUE

Question 12

Tell me the normal PAP pressures and the ranges for moderate and severe-at what point are people at risk for periop death or RHF?

What’s the problem with PAP and OLT? OLT contraindicated in PAP above what?

What if you have to place a line in a cirrhotic pt-what are you going to do/give/

Answer 12

Mild: 35-50
Mod: 50-70
Severe: >70

PA pressures > 35 mmHg and
pulmonary vascular resistance (PVR) > 250 dyne/sec/cm-5 are at increased risk of
perioperative death from right heart failure or hepatic failure.
liver
transplantation is contraindicated in patients with PA pressures > 50 mmHg, I would
consider right heart catheterization for direct pressure measurement and confirmation of this
estimated PA pressure
If direct measurement indicated moderate pulmonary
hypertension (mean PAP of35-45 mmHg), I would consider placing a pulmonary artery
catheter prior to incision, recognizing that this may prove difficult in a patient with
encephalopathy (patient is taking lactulose and neomycin). Given this patient’s coagulation
status, I would consider administering fresh frozen plasma and using ultrasound guidance to
reduce the risk of significant bleeding during line placement (while platelet administration
could also be considered, there is some evidence that suggests platelet transfusion may prove
detrimental to graft and patient survival).

Question 13

What is Portopulmonary HTN?

Answer 13

Defined as a mean PAP >25 or PVR >120 in presence of normal pumonary capillary wedge pressure.

Question 14

Would you place TEE in a cirrhotic pt with hx of varices?

Answer 14

Only if absolutely necessary

Question 15

Why does hepatic encephalopathy happen?

Answer 15

impaired liver function leads to the
accumulation of circulating neurotoxins, such as ammonia,There are
also several conditions that are associated with the precipitation of hepatic encephalopathy,
such as increased dietary protein, gastrointestinal bleeding, infection, hypovolemia, anemia,
azotemia, paracentesis, recent creation of a portal-systemic shunt (TIPS procedure), diarrhea
and vomiting, or diuretic therapy.

Question 16

If your cirrhotic pt seems confused, what are you going to do?

Evaluate for ICP? when is that more likely?

What happens with ESLD and hypokalemia?

pH and liver failure?

Be cautious with what?

Answer 16

If after considering other potential causes of mild confusion (i.e. chronic subdural hematoma,
psychoactive drugs, and Wemicke’s encephalopathy in this alcoholic patient) I believed this
was hepatic encephalopathy, I would attempt to identify and treat any potential inciting
factors, giving special consideration to esophageal bleeding in this patient with a history of
esophageal varices. In addition, I would evaluate the patient for signs of increased
intracranial pressure, although increased ICP and cerebral edema are more likely in acute
liver failure; avoid hypokalemia, which can increase the renal production of ammonia;
maintain a normal arterial pH, since alkalemia may lead to increased diffusion of ammonia
across the blood brain barrier; correct any hypovolemia or anemia to optimize liver
metabolism of circulating toxins; and use benzodiazepines and other psychoactive drugs
cautiously, recognizing that further suppression of the central nervous system may exacerbate
his condition.

Question 17

What is your memorized answer for why you ARE placing a PAC:

Answer 17

To better monitor intra-operative pulmonary artery pressures, andfacilitate both intra-operative and post-operative hemodynamic and
fluid management (the PAC is especially useful in patients with HRS and/or PPH)

Question 18

Don’t forget to say large bore IV’s in ADDITION to central lines with big cases

Answer 18

freebie

Question 19

What is VVBP?

Answer 19

Veno-venous bypass is a technique whereby the femoral (or distal inferior
vena cava) and portal veins are cannulated to reroute blood flow from below the diaphragm
to the suprahepatic vena cava (via the axillary, subclavian, or jugular vein) following the
interruption of caval flow during the anhepatic phase.

Question 20

Advantages of VVBP:

Answer 20

improved hemodynamic stability, better organ perfusion during the anhepatic phase,
improved cardiac filling, decreased blood and fluid requirements

The bad stuff: Disadvantages include an increased risk of air embolism,
thromboembolism, arm lymphedema, hematoma, vascular injury, and nerve injury.

Question 21

Epidural in cirrhotic pts?

Answer 21

Issa no for me dawg. Even if pts labs are currently okay-no because pt might have prolonged and significant perioperative coagulopathy

AND DON’T FORGET THAT LIVER PTS ARE ALWAYS FULL STOMACH-AND DON’T FORGET TO APPLY CRICOID PRESSURE

Question 22

Succinylcholine for RSI in ESLD patients?

Answer 22

You can still give it, but recognize that it may have a prolonged effect due to reduced production of pseduocholinesterase associated with ESLD

Question 23

Briefly describe the three stages of liver transplantation:

Answer 23

Dissection (PRE-ANHEPATIC) phase: Liver is dissected and mobilized until it is attached ONLY to: IVC, portal vein, hepatic artery and common bile duct

ANHEPATIC: begins with clamping of hepatic artery and proceeds through removal of native liver and implantaion of donor liver

REPERFUSION:
COMPLETION OF ANASTAMOSIS AND ensuring adequate homeostasis

Question 24

At beginning of anhepatic phase, surgeon clamps IVC-BP drops to 78/44-wyd?

Answer 24

FIRST-ask the surgeon to release the clamp since timing suggests it is most likely due to clamping.
Then switch to 100% O2, confirm measurement. Verify proper ETT placement auscultate lungs,, dmin fluids and vasopressors as indicated and talk to surgeon about VVBP. if that couldn’t happen, then volume load

Question 25

Hyperkalemia in both anhepatic and reperfusion phase?

What are you going to do about it?

Answer 25

Yup anhepatic: due to interrupted hepatic uptake of K+and reperfusion: washout of potassium containing preservative soln into systemic circulation following reperfusion.

Administer calcium chloride or gluconate to depress excitability
Ensure immediate access to defibrillator and prepare to treat dysrhythmias and insatbility
correct acidosis
can give insulin and glucose or beta adrenergic drugs or even sodium bicarb

Question 26

Citrate toxicity on EKG? What will you do?

Answer 26

hypocalcemia -can see hypotension
narrow pulse pressure 
prolonged QT 
flat t waves. 
can administer 10-20 mL of 10% calcium gluconate

Question 27

at the beginning of the reperfusion phase the
patient’s blood pressure drops from 112178 mmHg to 64/37 mmHg. What do you think
is going on?

Answer 27

The occurrence ofhypotension at the beginning of the reperfusion phase, is
often due to the removal of the vascular clamps (especially the portal vein), with subsequent
development of post-perfusion syndrome, a condition associated with systemic hypotension,
bradycardia, cardiac arrhythmias, and elevated pulmonary artery pressures. However, other
considerations would include hemorrhage (i.e. bleeding esophageal varices, surgical
bleeding, and severe coagulopathy), tension pneumothorax (i.e. central line placement,
smoker), congestive heart failure (i.e. HPS, complicated fluid management), and
hyperkalemia (patient was already hyperkalemic prior to reperfusion of the graft which may
have added an additional potassium load).

Question 28

What is reperfusion syndrome and what causes it?

Answer 28

of post-perfusion syndrome, a condition associated with systemic hypotension,
bradycardia, cardiac arrhythmias, and elevated pulmonary artery pressures.

NO exact cause, but likely due to release of vasoactive subsatances, excessive potassium load

Question 29

What potential post-operative complications should be anticipated following liver
transplantation?

Answer 29

Potential post-operative complications that I would be anticipating in this
patient would include: 1) bleeding esophageal varices, 2) vascular anastomotic leakage or
failure, 3) coagulopathy (i.e. DIC, hyperfibrinolysis, residual heparin, dilutional
coagulopathy, uremia, and inadequate clotting factor synthesis due poor graft function), 4)
renal dysfunction (i.e. HRS, drug toxicity, pre-renal azotemia, and ATN), 5) congestive heart
failure (PPH, fluid overload), 6) TRALI (massive blood transfusion), 7) pulmonary edema
(congestive heart failure, fluid overload, TRALI), 8) biliary complications (i.e. bile leaks), 9)
hepatic or portal vessel thrombosis, 10) encephalopathy, 11) peripheral nerve injury
(increased risk due to length of case), 12) diaphragmatic or phrenic nerve injury, 13)
systemic infection, 14) acute graft failure or rejection, and 15) metabolic abnormalities
(especially metabolic alkalosis and hypokalemia)