Journal
BMC ANESTHESIOLOGY
Volume 15, Issue -, Pages -Publisher
BMC
DOI: 10.1186/s12871-015-0080-2
Keywords
Liver transplantation; Cardiac function; Postreperfusion syndrome
Categories
Funding
- Swiss National Science Foundation, Berne, Switzerland
- Ministry of Health (Gesundheitsdirektion) of the Canton of Zurich
- Switzerland for Highly Specialized Medicine
- Swiss Society of Anesthesiology and Reanimation (SGAR), Berne, Switzerland
- Swiss Foundation for Anesthesia Research, Zurich, Switzerland
- Bundesprogramm Chancengleichheit, Berne, Switzerland
- CSL Behring, Berne, Switzerland
- Vifor SA, Villars-sur-Glane, Switzerland
- Novo Nordisk Health Care AG, Zurich, Switzerland
- CSL Behring GmbH, Marburg, Germany
- LFB Biomedicaments, Courtaboeuf Cedex, France
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Background: Postreperfusion syndrome and haemodynamic instability are predictors for poor outcome after liver transplantation. Cytokine release has been claimed to be responsible for postreperfusion syndrome. However, the underlying pathophysiologic mechanism is not clarified. The aim of this prospective observational study was to correlate cardiac performance (measured by transoesophageal echocardiography (TEE), Doppler and Tissue Doppler Imaging (TDI)) to plasmatic cytokines: IL-6, IL-8, CXCL1, TGF-beta and CD40L at 5 different time points during liver transplantation. Methods: Seventeen consecutive patients scheduled for orthotopic liver transplantation, age 18 to 75 years without contraindication for transoesophageal echocardiography were included. Patients were monitored with TEE and TDI. Systolic and diastolic cardiac function, MAP, MPAP, CVP, PCWP, CO and blood samples for cytokine assays were recorded or collected after induction, 15 min after vena cava inferior clamping, 2 to 5 min after reperfusion, 60 min after reperfusion and at the end of surgery. Results: Mean arterial pressure and catecholamine requirements remained unchanged, MPAP, CVP and CO increased, SVR decreased after unclamping. Postreperfusion syndrome did not develop. The haemodynamic parameters and the variations of TEE parameters were consistent with the volume load changes during clamping and declamping and did not reveal systolic or diastolic cardiac dysfunction. All cytokines, except TGF-beta, increased. Conclusion: These findings suggest, that significant cytokine release during liver transplantation is not necessarily coincident with haemodynamic instability and impaired cardiac function.
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