46
Perioperative Heart Transplant Management and Complications Aliessa Barnes MD Division of Cardiology Medical Director of Heart Transplantation

Perioperative Heart Transplant Management and Complications by Dr. Aliessa Barnes, Medical Director , Pediatric Cardiac Transplantation, Ward Family Heart Center at Children's Mercy

Embed Size (px)

Citation preview

Perioperative Heart Transplant Management and Complications

Aliessa Barnes MDDivision of CardiologyMedical Director of Heart Transplantation

Comprehensive EvaluationListingDonor selectionTransplantationPost operative careChronic management

Heart Transplant process

Outline

Risk AssessmentSurgical IssuesPost Operative ManagementComplications

Risk Assessment

Primary Graft Failure (PGF) Severe dysfunction of the allograft

without any anatomic or immunologic cause▪ Need for multiple inotropes and/or

mechanical circulatory support in the first 24 hours

Varying rate based on definition▪ 1.4%-20% or more

Can be RV, LV or biventricular failure▪ RV most common

Risk Assessment- PGF

Most common cause of death (40%) in the first 30 days after transplant

18% of mortality in the first 12 months

30 day survival 1992-1997- 43% 1998-2004- 57%

Also decreases 1 year survival

Risk Assessment- PGF

Risk Factors Recipient

▪ High PVR▪ ECMO

Donor▪ Long Ischemic Times▪ Poor organ preservation▪ Reactive Oxygen Species

Risk Assessment

Other hypothesized factors▪ Female donors▪ Size mismatch▪ Marginal or Extended donors

Risk Assessment

Risk Assessment

ISHLT Official Pediatric Heart Transplant Report ( 2007) 25 years

experience Reduce era effect

1995-2005 400 heart

transplants a year 80 centers

Risk Assessment

Risk Assessment

Risk Assessment

Risk Assessment

VAD versus ECMO Review since 2002 Toronto, Canada VAD available since 2004 36 patients (21 ECMO; 12 VAD) Waitlist mortality 38% on ECMO

decreased to 13% with VAD Survival post transplant to hospital

discharge better in VAD 92% versus ECMO 80%

Historical Surgical Appproach

1960 Lower and Shumway

Leaves large atrial cavities

Abnormal geometry lead to increased TR

Sinus node dysfunction from surgical trauma

Scar =AFib/Flutter

Bi-atrial anastomosis

Current Surgical Approach

Bi-caval anastomosis

Current Surgical Approach

Surgical Adaptations

Tunnel of Left SVC to Right atrium

Reconstruction of Hepatic Veins entered left atrium

Surgical Adaptations

Reconstruction of Systemic and Pulmonary veins in situs

inversus

Post Operative Note

Things to note Special surgical adaptations Ischemic time Bypass Time Blood Products required Post op TEE

Physiology – At Harvest

Harvesting site Function CAD Contusion

Procurement Fluid shifts harm RV

Myocardial Preservation Ischemic strategy

Hypothermia Pharmacologic arrest

Physiology –During Ischemia

No Oxygen to the muscle cells Decreased ATP use Can used stored Glycogen to make

ATP ATP too low= irreversible myofiber

contracture Ion homeostasis

Preservation Na-K pump reduced but still a

gradient Na H Ca-Ca lead to myofiber

damage

Physiology

Preservation Fluid Cold K to chemically arrest the heart Mg to protect from Ca Impermeants to stop cellular

swelling Free radical scavengers

HemodynamicsRhythmVentilationBleedingRejection/Immunosuppression Infection Prophylaxis

Post-op Care

Hemodynamics

Goals Inotropic support of the LV and RV Chronotropic support Decrease PVR Decrease SVR

Hemodynamics

Best Drug Isoproterenol

▪ Increases contractility and HR▪ Decrease PVR and SVR▪ Titrate HR

Milrinone▪ Increased contractility▪ Vasodilatory

Hemodynamics

Best Drug RV protection Avoid acidosis Hyperventilate 100% O2 Milrinone iNo Sildenafil Bosentan Prostacyclin if needed ECMO if needed

Function Hypoxic/Ischemic damage

( Troponin/ Lactate) Systolic function recovery rapid Diastolic function may persist for

weeks “Slump”-12 hours back off 2-5 days

Hemodynamics

Tools Exam CVP/RA line Arterial Blood Pressure Pacing wires

Hemodynamics

Elevated CVP (goal 8-12), with decrease CO Right heart failure ( pulmonary HTN,

massive blood transfusion, anatomic issue)

Decreased HCT without increase in the output of the tubes Cardiac tamponade

Troubleshoot

Factors Parasympathetic denervation Surgical trauma Catecholamines

Typical Sinus RBBB (14%-60%)

Possible Sinus node trauma-Bradycardia (2 weeks)-

18%-27% Recovers in 1-3 days CO= SV X HR

Rhythm- Physiology

Target Infant 140-150 bpm Teenager 100-120 bpm

Use Isoproternol or pacing if no response.

Pacing AAI ( preferred) or DDI Check the underline rhythm every

shift if the patient is paced. ECG upon arrival if not paced.

Rhythm

Ventilation

Similar principalsEarly extubationTracheobronchomalaciaPersistent atelectasis

Bleeding

Previous Cardiac SurgeriesCheck coagulation disorder pre-

opSame post bypass principalsBlood products= sensitization

One donor platlets Irradiated, Leukoreduced, Single

donor- PRBC FFP from pool of donors

Types of Rejection

Hyperacute- minutes to hours Cellular “Acute” (T cell)-attacks the

muscle 80% in first year

Humoral/Vascular “Chronic” (B cell)- antibodies attack the blood vessles creating narrowings

Immunologic Mechanisms of Rejection

Allorecognition

Activation of Antigen

Presenting Cell (APC)

APC recognized by T cell

TCR and costimulatory

signals are activated

Copyright ©2004 American Heart Association

Lindenfeld, J . et al. Circulation 2004;110:3734-3740

Immunologic mechanisms leading to graft rejection and sites of action of immunosuppressive drugs

Types of Therapy

Induction Administration of a brief course of

high-dose immunosuppression in the preoperative and perioperative time period

Maintenance Less intense long term treatment

Rejection Additional therapy initiated due to

evidence of rejection

Anti-lymphocyte Polyclonal

ATGAM (horses)▪ Urticaria, serum

sickness, leukopenia, thrombocytopenia

ThymoglobulinO (rabbits)

Antibodies to surface receptors (CD3/CD45) cause apoptosis

Follow CD3 levels (5%-10% baseline/<50/ml)

SE both: fever, chills, rash

CMV!!!!! Need prophylaxis

Copyright ©2004 American Heart Association

Lindenfeld, J . et al. Circulation 2004;110:3734-3740

Immunologic mechanisms leading to graft rejection and sites of action of immunosuppressive drugs

Anti-Cytokine Receptor Antibodies

Bind to IL2 R Basiliximab

( Simulect) SE:

Infection Malignancy

Copyright ©2004 American Heart Association

Lindenfeld, J . et al. Circulation 2004;110:3734-3740

Immunologic mechanisms leading to graft rejection and sites of action of immunosuppressive drugs

Steroids

Diffuse freely across cell membrane and bind to receptors

Affect number, distribution and response of T and B cells

SE: hypertension, emotional lability, cosmetic changes, hyperlipidemia, salt and water retention, diabetes, osteopenia, growth retardation

Corticosteroids Induction/

maintenance and rejection therapy

Transcriptional regulation

80-85% rejection responds to pulse treatment

SE: Cosmetic changes Hypertension Hyperlipidemia Diabetes Osteopenia

Antiproliferative Agents Mycophenolate

(MMF) (Cellcept) Maintenance

Therapy Inhibits DNA

synthesis and Tcell/B cell proliferation

Side Effects:▪ Nausea▪ Vomiting▪ Diarrhea

Calcineurin Inhibitors

Tacrolimus (FK506/Prograf) Maintenance

therapy Block IL-2

transcription Stimulates TGF- b

production Side Effect:

▪ Similar to CSA but hyperglycemia/diabetes, and neurologic toxicity are more common

Immunosuppression3 categories of outcomes Desired immunosuppressive effects

Adverse effects of immunodeficiency▪ Infection ▪ Malignancy

Nonimmune Toxicities▪ Diabetes▪ Hypertension▪ Renal insufficiency

Infection

Invasive lines and drains out ASAP Post-op antibiotic coverage with

First generation cephalosporin Vancomycin if MRSA

Prophylaxis CMV prophylaxis:▪ Ganciclovir

PCP prophylaxis:▪ Bactrim DS

Candida Prophylaxis:▪ Nystatin

Thank you Any Questions?