Liver Transplant (FINAL EXAM) Flashcards
Neurologic changes with liver disease
Hepatic Encephalopathy
- Behavioural changes to coma
- Impaired ammonia metabolism
- Lactulose, Rifaximin
Cerebral Edema
- Acute liver failure
- Pathophysiology unclear
Cardiac sytem changes
- Low SVR
- High cardiac output
- Elevated resting heart rate
- Vasodilation
- Activation RAAS, SNS
- Sodium & fluid retention
- Cirrhotic cardiomyopathy
Pulmonary system changes
- Reduced FRC
Hepatic hydrothorax (10%)
- Ascites in the right chest
Hepatopulmonary syndr (10%)
- Hypoxia, intrapulmonary shunts
Portopulmonary hypert’n (6%)
- Elevated PVR with cirrhosis
Hepatorenal Syndrome
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
Hematologic system changes
- Coagulopathy
- Thrombocytopenia
GI system
- Esophageal varices
- Spont bacterial peritonitis
preop eval
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
CAD screening
- Prevalence: 2.5% - 38%
- Leading cause of non-graft-related mortality
CAD risk factors
- Age >50
- DM
- h/o CV dz
- tobacco
- HTN
- dyslipidemia
CAD next steps
non-invasive stress test –> coronary cath
optimal screening with %s
Hepatopulmonary syndrome - prevalence and defination
- Prevalence: 4-19%
Defined as: - Chronic liver disease
- [A-a]O2 gradient ≥15mmHg (≥20 for >65yrs old) * Intrapulmonary shunting (TTE or 99mTc-MAA)
Hepatopulmonary syndrome classifications
- Mild – PaO2 >= 80mmHg
- Moderate – 60-79 mmHg
- Severe – 50-69mmHg
- Very Severe <50mmHg
Hepatopulmonary syndrome - symptoms, prognosis, and treatment
- 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
HPS screening and management
Portopulmonary Hypertension
- 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)
Portopulmonary HTN
Classification:
* Mild – mPAP 25-35mmHg
* Moderate – mPAP 35-45mmHg
* Severe - ≥ 45mmHg
portopulmonary HTN
- Increased RV myocardial oxygen demand
- RCA perfusion limited to diastole
- Reduced LV preload
OLT and PoPH mortality
PoPH Screening & Management
Nictric oxide pathway
PoPH Treatment & Response
Sildenafil
Tadalafil
Bostentan
Ambrisentan
Epoprostenol
Iloprost
Treprostinil
Response to treatment:
PAP <35mmHg;
PVR<400dynscm-5
- List for liver transplant
- MELD exception points
Hepatorenal Syndrome
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
Hepatorenal syndrome types and treatment
- 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
Acute liver failure
- 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%
Encephalopathy - grades
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
Subcategories acute liver failure
acute liver failure (anesthesia goals)
- Severe coagulopathy, renal dysfunction, metabolic disarray
- Management of cerebral perfusion - Maintain CPP >60mmHg
- Decrease ICP
- Head of bed >30°
- Hypertonic saline
- Mannitol
- Hyperventilation
monitoring
Standard ASA
Arterial line
CVP / PA
TEE
Practice guidelines for using intra-op TEE
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)
What is the speed you can run through different IV access lines?
- 9Fr 10cm - **1200cc/min **
- 8.5Fr 6cm - 1400cc/min
- 14G 2.25” - 750cc/min
- 16G 2.25” - 350cc/min
- 18G 1.75” - 250cc/min
Factors associated with increased transfusion include
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
Strategies to minimize transfusion
- Surgical technique
- Intraoperative cell salvage
- Low CVP
- Dedicated anesthesia team
- Antifibrinolytics
- Transfusion protocols
- TEG/TEM
How is coagulopathy monitoring intra-op?
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
Liver transplant antimicrobial coverage
-Ampicilin-Sulbactam
-Piperacillin-Tazobactam
+/- Fluconazole
Anesthetic agent requirement for pts with liver failure
In general, patients w. ESLD will require LESS
Judicious premedication in encephalopathic
Titrate anesthetic to awareness monitor
Titrate NMB to twitches
Reduced opioid requirement
Induction for liver transplant
Rapid Sequence Induction
Significant ascites
Recent history of GI bleeding
Full stomach
Low SVR, High cardiac output state
PEARLs of Pre-Anhepatic Phase
Incision to portal venous clamping
Hypotension/Hemorrhage
PEARLs of Anhepatic Phase
Portal venous clamp to reperfusion
Metabolic derangement
PEARLs of Neohepatic Phase
Reperfusion to end of case
Coagulopathy/Hepatic Perfusion
Surgical steps of Pre-anhepatic phase
- Drainage of ascites
- Lysis of adhesions
- Dissection vessels, biliary
- Mobilization of liver
+/- Veno-venous bypass
Pre-Anhepatic Phase - Anesthetic
- Ascites drainage = replace with albumin
- hemorrhage = transfuse based on labs
coagulopathy, thrombocytopenia
elevated venous pressures
collaterals
adhesions - Compressed vena cava = inform team, volume & pressors
Key takeaways for Venovenous bypass method
- Stable BP
- Decompress
- increased Time/Cost
Key takeaways for piggyback method
Stable BP
Decreased time
Decreased cost
Key takeaways for transplant without bypass or piggyback
Hypotension
Decreased renal perfsion/risk for injury
What are the metabolic derangements that occur in the anhepatic phase and why?
- Hypocalcemia: Citrate binds ioCa++
- Metabolic acidosis: Lactic acid not metabolized
- Hypoglycemia: Absent liver
How do we manage the metabolic derangements in the anhepatic phase?
ABG, Lytes, Glucose
ioCa++ <1.0: bolus CaCl2
Significant acidosis: consider NaHCO3
Treat hypoglycemia
What is the blood flow and O2 delivery of the portal vein?
60-70% of blood flow to liver from portal vein
50% of oxygen delivery from the portal vein
What are the surgical details during graft reperfusion?
- Graft flushed to remove preservative solution
- Caval and portal anastomoses completed
- Portal flow re-established
Reperfusion is associated with abrupt ______
Increase in potassium
Decrease in pH
Increase in EtCO2
Increase in preload
Decrease in SVR
Decrease in MAP
Decrease in core temperature
What should you do prior to graft reperfusion?
- FiO2 1.0 in anticipation of hypoxemia
- Respiratory alkalosis via increased minute ventilation to offset metabolic acidosis
- Administer CaCl2 to offset hypocalcemia and cardiac effects
- Administer NaHCO3 to offset acidemia
- Pretreat with vasopressor
What if we get hyperkalemia on reperfusion?
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
What does post reperfusion syndrome look this? What are predictors of it?
- Decrease in MAP > 30%
- ≤ 5min reperfusion time
- > 1min
Predictors: Donor age, Donor risk index, Recipient CVP
What are the surgical details of the neohepatic phase?
Hepatic arterial reconstruction
Biliary reconstruction
Closure
What are signs of graft function?
a. improvement of ioCa2
b. improvement in acidosis
c. biliary output from graft
What are the anesthetic goals in the neohepatic phase?
- Low CVP (Keep CVP <10mmHg)
- Manage coagulopathy
- Emergence and extubation
What is the blood flow and O2 delivery of the hepatic artery?
blood flow: 30-40%
O2 delivery: 50%
What is the driving pressure inside the hepatic artery?
LARGE
MAP-CVP
What is the driving pressure inside the portal vein?
SMALL
PVP-CVP
Normal coagulation is a balance between ___
the bleeding and thrombosis
Thrombosis is brought about through ____.
- The actions of the coagulation cascade which promotes fibrin formation
- Platelet aggregation to form the hemostatic plug
Control of thrombosis is brought about through ___.
- Inhibitors of the coagulation cascade
- Fibrinolysis
Coagulopathy in the neohepatic phase is a result of derangements in _____.
Both bleeding and thrombosis.
- Decreased level of coagulation factors during anhepatic phase- notably Factors VIII and V
- “Heparin-like” effect
- 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
Coagulopathy in the neohepatic phase may be exacerbated by ____
hypothermia, delayed graft function, acidosis and hypocalcemia
How do we manage the coagulopathy in the neohepatic phase?
- Monitor
- Treat for
a. INR > 2
b. Plt < 50,000
c. Fibrinogen < 100 - Antifibrinolytics / PCC (prothrombin complex concentrate) / Factor VIIa
