Transplants II Flashcards

1
Q

What variables are used to calculate the MELD score?

What is it used for?

What else is used for transplant selection?

A
  • MELD variables:
    • creatinine
    • bilirubin
    • INR
    • sodium
  • MELD score determines where pt is on “the list”
  • Acute liver failure pts given priority, next is the highest MELD score, then compatible blood group
  • Pts are screened for infectious diseases
    • HIM
    • CMV
    • epstein-Barr
    • malignancy
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2
Q

ESLD pre-op:

Renal function

CV

A
  • Renal dysfunction very common with ESLD
    • creatinine not reflective of severity (slight increase will mean serious dysfunction d/t lack of muscle mass)
  • Hepatorenal syndrome
    • increased renal vasocontriction
    • reduced GFR
    • subsequent increase in creatinine
    • impaired Na and H2O excretion
  • CV- 30 day mortality often associated with CV causes
    • CAD common- need extensive work-up
      • Stress test
      • cardiac cath- might need angioplasty pre-op
      • ECHO
    • Low SVR, high Cardiac index, and increased mixed venous sat
    • Cirrhotic cardiomyopathy- will have blunted response to beta agonists
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3
Q

ESLD pre-op:

pulmonary

labs

A
  • Pulmonary:
    • evaluate presence of portopulmonary hypertension
      • PA pressure > 25 mmHg (>50 is absolute contraindication)
      • PVR >240 Dyne
      • PAOP 12 mmHg or lower
    • Evaluate PFTs and presence of hepatopulmonary syndrome
      • marked A-a gradient
      • intrapulmonary shunting
      • pleural effusions
  • Labs
    • coags do not accurately predict bleeding in this population
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4
Q

ESLD pre-op:

meds

A
  • Recent treatment for Hep C with Telaprevir inhibits CYP3A, prolonging effects of versed
    • usually avoid versed in general
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5
Q

What are the changes that impair homeostasis and promote homeostasis in the ESLD pt?

(table)

A
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6
Q

Liver transplant anesthesia “set-up”

Anesthetic technique?

A
  • RSI- d/t gastroparesis and ascites and often these cases are emergencies
  • Art line (maybe 2)- radial and fem
    • central pressure is higher because vasodilation causes lower read in periphery
  • PA catheters to follow PVR +/-
  • TEE- caution with varices
  • TEG- evaluate coagulation
  • ability to monitor labs frequently (I-STAT)
  • Rapid infustion catheters (14 g) and CVL
  • Rapid infusion system primed and ready
  • Colloids in the room
  • active warming mechanisms
  • Foley/NGT
  • Use balanced technique: narcotic, inh agent, NMB
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7
Q

Phases of liver transplant:

Pre-anhepatic

A
  • Native liver is dissected and removed
  • major vessels are compressed or occluded
  • If there is a large drainage of ascites (>5L) at incision, replace with albumin to prevent renal decompensation
    • give 6-8 g/L of ascites drained
  • Phase ends with clamping of inferior vena cava, portal vein and hepatic artery and removal of liver
  • major anesthetic goals:
    • correct coagulopathies
    • maintain IV volume for renal protection
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8
Q

How should you handle the significant blood loss during the Pre-anhepatic phase?

A
  • Follow TEG
  • FFP used to maintain an INR of 1.5 or less
    • may need Ca++ d/t inability to metabolize citrate
  • Keep fibrinogen above 150 mg/dL with cryoprecipitate
  • plt > 50K, but plt transfustions lead to poorer outcomes (may not need them with cryo/ffp)
  • Call-save if not a transplant b/c of cancer
  • activated factor VII: rescue for refractory critical bleeding unresponsive to more standard management
  • TXA or aminocaproic acid
    • EACA 5 g load and 1 g/hr infusion
    • ensure adequate volume replacement- colloids preferred
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9
Q

What happens during the anhepatic phase?

A
  • Portal vein and IVC are crossclamped- may decrease CO up to 50%
    • fluid volume load prior to clamping
  • Some surgeons use a “piggyback” technique where the inferior vena cava is only patially occluded
    • less derangement
  • Alternative option is to use a temporary portocaval shunt or venovenous bypass
    • V-V bypass has fallen out of favor
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10
Q

What happens during the transition from anhepatic phase to neohepatic phase?

A
  • New liver is anastomosed into place and re-perfused
    • vena cava unclamped–adequate venous return to the heart restored
      • BP and CO improve transiently
    • Portal vein is then opened–cold, acidotic, hyperkalemic blood from below clamp goes directly into right heart
      • significant drop in BP, bradycardia, other arrhythmiac, occasionally cardiac arrest: reperfusion syndrome
      • Surgeon must communicate they will unclamp
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11
Q

What can be done to reduce the effects of the reperfusion syndrome?

A
  • Perfect timing of calcium chloride and bicarbonate
  • Have available for immediate use:
    • epi
    • vasopressin
    • lidocaine
    • atropine
    • methylene blue (vasoplegia of reperfusion- not responding to pressors)
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12
Q

What is the warm ischemia time?

A
  • the time taken to sew the new graft in place
    • can be very damaging to the graft, limiting warm ischemia time is critical to graft success
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13
Q

What is the neohepatic phase?

A
  • Hepatic artery and bile duct anastomoses- usually with a cholecystectomy
  • looking for signs that the new liver is starting to function
    • improvement in acidosis
    • clearing of lactic acid
    • improved homeostasis
    • production of bile
  • Renal function hopefully improves after reperfusion
  • Assess bleeding on field and need for antifibrinolytics
  • sources of bleeding are corrected
  • drains placed and abdomen is closed
  • Consider extubation based on surgical course and fluid status
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14
Q

Lung transplant:

options

What has better survival?

A
  • Single lung trasplant
  • en bloc double (both at same time)
  • sequential double (put one side in first then the other)
  • heart-lung transplant
  • Long term survival better for bilateral than single lung
  • **double lung required for pathological process if remaining lung would jeopardize new lung
    • CF
    • severe emphysema
    • PHTN
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15
Q

What are the indications for lung transplants?

A
  • Poor pulmonary function despite maximal medical therapy
  • COPD
    • O2 requirement
    • FEV1 <25% of predicted value after bronchodilators and/or PaCO2 =55 mmHg and/or PHTN (esp with cor pulmonale)
  • Idiopathic pulmonary fibrosis
    • vital capacity <60-65% of predicted
    • resting hypoxemia
    • progression of disease despite therapy
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16
Q

Lung transplant:

plan

access

post-op pain control

A
  • Often emergency cases, may have full stomach. RSI
  • Pre-op sedation: use caution, have minimal reserve
  • GETA +/- thoracic epidural
  • Access:
    • CVL, PAC, A-line
    • Fiberoptic bronch
    • DL ETT
  • Post op pain control
    • thoracic epidural
    • paravertebral blocks
    • intercostal nerve blocks
    • multi-modal analgesia
  • ** chronically intravascularly volume depleted
  • **pulmonary HTN common
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17
Q

Lung transplant:

How is the surgery usually done?

Where is it anastomosed?

A
  • Lateral thoracotomy
    • usually lung with poorer function is replaced
  • Bronchial anastomosis more common that tracheal anastamosis
18
Q

Lung transplant:

Issue with induction?

maintenance technique?

A
  • Prone to hypotension with induction d/t intravascular volume depletion
    • give reduced doses
  • Maintenance
    • balanced anesthetic- VA + narcotic w/NMB
    • avoid N2O- may exacerbate bullous emphysematous disease, PHTN, or intra-op hypoxemia
    • Fluid restriction is optimal- use small volumes of colloids and pressors (CVP <7)
19
Q

Lung transplant:

ventilation

When is CPB indicated?

A
  • Use lung protective ventilation
    • TV 6 ml/kg
    • PEEP
    • lowest FiO2 settings
    • PCV
  • Hypoxemia during single lung ventilation
    • PEEP to the dependent lung
    • CPAP to the nondependnet lung
    • PA clamping of the non-ventilated lung by surgeon
  • CPB indications
    • inability to oxygenate despite above efforts
    • inability to provide adequate ventilation
    • RV failure: TEE is very helpful to evaluate RV and need for CPB
20
Q

Lung transplant:

What happens after re-anastomosis?

A
  • following re-anastomosis of atrial/pulmonary vein patch, bronchus, and PA, the lung is unclamped and perfused
    • hypotension can be seen, but not usually as severe as w/liver
  • Hemostasis is checked
    • may use FOB to remove secretions and blood from freshly anastmosed lung
  • Ventilation is attempted with new lung
  • After closing, attempt to exchange DLT for single lumen ETT
    • indication to wait for exchange: significan oropharyngeal edema, high PEEP, or need for differential lung ventilation
21
Q

Lung transplant:

How are double lung transplants done?

A
  • Supine position, clamshell incision vs midline sternotomy
    • deflate lungs before sternotomy
  • En bloc double lung tx requires CPB, can use standard ETT
  • Bilateral sequential tx requires lung isolation (DLT)
  • expect severe post-op pain, thoracic epidural advisable
22
Q

Lung transplant:

complications?

A
  • Acute transplanted lung failure
    • acute graft rejection
    • inadequate pulmonary venous drainage
    • primary graft dysfunction
      • allograft dysfunction w/in 72 hours of ransplant
      • factors:
        • prolonged ischemic time w/ reperfusion injury
        • advanced donor age
        • recipient PHTN
        • use of CPB or ECMO
      • iNO therapy may be used to decrease PVR and improve oxygenation
        • methemoglobinemia risk
23
Q

Heart Transplan:

Plan

A
  • Cold ischemia is ~6 hours or less
    • Ischemic time starts with aortic cross clamping during the harvest and ends with removal of cross-clamp from recipient aorta
  • Emergent case with fast, efficient evaluation
    • review recent CXR and labs
    • evaluate pulm, hepatic, and renal compromise associated with CHF
  • get blood products ready (FFP, cryo, plt, PRBCs)
  • determine if previously exposed to aprotinin–can have anaphylaxis with re-exposure
  • Aprotinin- bovine trypsin inhibitor used to reduce bleeding during surgery
24
Q

Heart transplant:

Access

pressors

A
  • Evaluate:
    • current inotropic infusions
    • chronic meds for heart failure
      • if on ACEI, may want to start vasopressin
    • presence of LVAD, pacemaker or defibrillator
      • antiarrhythmic devices need to be interrogated and reprogrammed
  • Access
    • A-line pre-induction
    • large bore IV for resuscitation prior to induction
  • Inotropes and pressors on hand
    • dobutamine or milrinone
    • epi, NE, dopamine
    • vasopressine
    • phenylephrine
  • Hve ultrasound ready for CVL and PAC placement
25
Q

Heart transplant:

anesthetic technique

A
  • Surgery is done by median sternotomy with CPB
    • many different techniques, may leave behind SA node causing extra P-wave
  • High dose narcotic for induction and maintenance
    • alternative is balanced technique with lower narcs and IA
  • NMB
  • Hypotension may not be responsive to ephedrine or phenylephrine
  • TEE should be done after induction and after weaning from CPB
    • risk of intracardiac thrombus is increased in the recipient heart
26
Q

Heart transplant:

Heparin dosing

cannulation

PAC

CPB

A
  • Heparin dosing is similar as for other CPB procedures
  • Cannulation is done so that the surgical field is bloodless
  • PAC should be withdrawn from the surgical field prior to resection of the native heart
    • can be readvanced after removal of the superior cava cannula
  • Maintenance of CPB and weaning from CPB are associated with the same issues as for other cardiac surgical procedures ???
27
Q

Heart transplant:

What should be done prior to weaning from CPB?

What is the significance of deneravation?

Why is acute R heart failure a complication?

A
  • Prior to CPB:
    • air should be evacuated
    • heart is reevaluated with TEE
  • Donor heart is denervaed so feedback for inotropy and chronotropy are lost
    • isoproterenol is used for its direct effects on cardiac B receptors to increase graft heart rate
    • temporary pacing may be needed
  • Acute right heart failure is a complication b/c donor heart is not used to high PVR
28
Q

Heart transplant:

What is resting HR for transplanted heart? Why?

How does this affect CO?

Which drugs can be used to increase HR?

A
  • Transplanted heart has no autonomic influence so HR is determined by SA node. HR 100-120
  • CO is HR x stroke volume; if HR is fixed, SV becomes dependent on preload–these pts are sensitive to hypovolemia
  • Drugs to stimulate HR:
    • those that directly stimulate SA node:
      • epi
      • isoproterenol
      • glucagon
  • Drugs that DONT stimulate HR in a transplanted pt:
    • Those that indirectly stimulate SA node
      • atropine
      • glyco
      • ephedrine
29
Q

Heart transplant:

How does a pt with a heart transplant respond differently to cholinesterase inhibitors?

A
  • They will not cause decrease in HR, but will cause all other sypmtoms of PNS stimulation
  • must still treat with glyco
30
Q

Denervation effects on pharmacology

(table)

A
31
Q

Pearls of transplant anesthesia

A
  • Pre-op: focus on determining the degree of immunosuppression and transplanted organ function, evaluating for any co-existing infection and review co-morbidities
  • Minimum labs:
    • CBC
    • CMP
    • LFTs
    • viral panels/viral loads
    • CXR
    • EKG
  • strict aseptic technique for all invasive procedurese
  • elective and non emergent cases should be postponed if pt is in active rejection or has an infection
  • Regional anesthesia is controversial post-transplant
  • avoid nasal intubation d/t immunocompromise
32
Q

Post-transplant anesthesia:

A
  • Signs of infection are masked in post-tx pts
  • evaluate fxn of grafted organ
  • evaluate liver/kidney function
  • immunosuppression can significantly effect renal elimination
  • Post-renal tx: give adequate fluid for renal perfustion
  • Maintain administration schedule of: abx, antiviral, antifungal, and immune suppression drugs
  • Avoid NSAIDS in general
33
Q

Post-tx anesthesia:

What is unique about pt with tracheal anastomosis lung tx?

General guidelines for lung tx?

A
  • Lung tx with tracheal anastomosis have no cough reflex below suture line d/t denervation
    • increased risk of retained secretions and PNA and have increased airway hyperreactivity and bronchospasm
  • General guidelines post lung tx
    • evaluate:
      • PFT
      • ABG
      • CXR
    • prefer regional when feasible
34
Q

Post heart transplant:

How does rejection present?

What will the heart respond to?

What wont it respond to?

A
  • Rejection presents like CHF
  • ECG and TEE before surgery
  • cannot respond to:
    • indirect agents (ephedrine, dopamine)
    • peripheral attempts to induce hemodynamic changes
      • carotid massage
      • valsalva
      • laryngoscopy
  • B-receptor effects of epi and NE are exaggerated over alpha effects
  • Isoproterenol is the mainstay of chronotropic terapy and should be in OR
35
Q

Infection risk after transplant timeline of causes

A
  • within 1 month: likely caused by allograft
  • 2-6 months: opportunistic infections or reactivation of disease syndromes (TB)
    • Trimethoprim-sulfamethoxazole prophylaxis for pneumocystis pneumonia for at least 6 months
    • inflammatory response blunted; sometimes diff to identify source of infection
  • >6 months: many do well and infection risk decreases
    • some have chronic progressive viral infections
      • hep B, C
      • CMB
      • EBV
      • herpes zoster
36
Q

Chronic immunosuppression:

side effects

overimmunosuppression

A
  • General side effects:
    • lower sz threshold
    • diabetes
    • CV disease
    • increased infection risk
    • increased malignancy risk
    • pancytopenia
    • decreased GFR
    • hyperkalemia
    • hypomagnesemia
  • Overimmunosuppression leads to renal toxicity
  • Protocols vary with transplant team
  • be sterile!
  • maintain abx, antifungal, and antiviral regimens
37
Q

What are the different anti-rejection regimens?

A
  • Calcinereurin inhibitors (cyclosporin)
  • Purine antagonists: Mycophenolic acids, azathioprine
  • corticosteroids
  • monoclonals (ATG, OKT3, IL-2 receptor antagonists)
38
Q

Calcineurin inhibitor:

name

MOA

SE

A
  • Cyclosporin and tacrolimus
  • MOA
    • inhibits T-lymphocyte activation, differentiation, and cytokine production
  • SE
    • HTN
    • hyperlipidemia
    • ischemic vascular disease
    • DM
    • nephrotoxicity
  • Tacrolimus metabolized by CYP450 3A4 and causes upregulation
39
Q

Purine antagonists:

names

MOA

SE

A
  • Mycophenolic Acids, Azathioprine
  • MOA- antiproliferative drugs
  • SE-
    • bone marrow suppression can cause pancytopenia
    • Cardiac arrest and severe upper airway edema
40
Q

Corticosteroids

MOA

SE

A
  • MOA- disrupt expression of many cytokines in T cells, antigen-presenting cells, and macrophages
  • SE
    • HTN
    • DM
    • hyperlipidemia
    • weight gain
    • GI ulceration
41
Q

Monoclonals:

name

MOA

SE

What is ATG?

A
  • ATG, OKT3, IL-2 receptor antagonists
  • MOA- depletion of T cells
  • SE (rare)
    • acute serum sickness (sx: jaw pain)
      • stop the drug, plasmapheresis, corticosteroids
  • Antithymoglobulin (ATG)- purified rabbit immunoglobulin G taken from animals immunized with human thymocytes