BackgroundDonation after circulatory death (DCD) can increase the pool of available organs for transplantation. This pilot study evaluates the implementation of a controlled DCD (cDCD) protocol using normothermic regional perfusion in Norway.MethodsPatients aged 16 to 60 years that are in coma with documented devastating brain injury in need of mechanical ventilation, who would most likely attain cardiac arrest within 60 minutes after extubation, were eligible. With the acceptance from the next of kin and their wish for organ donation, life support was withdrawn and cardiac arrest observed. After a 5-minute no-touch period, extracorporeal membrane oxygenation for post mortem regional normothermic regional perfusion was established. Cerebral and cardiac reperfusion was prevented by an aortic occlusion catheter. Measured glomerular filtration rates 1 year postengraftment were compared between cDCD grafts and age-matched grafts donated after brain death (DBD).ResultsEight cDCD were performed from 2014 to 2015. Circulation ceased median 12 (range, 6-24) minutes after withdrawal of life-sustaining treatment. Fourteen kidneys and 2 livers were retrieved and subsequently transplanted. Functional warm ischemic time was 26 (20-51) minutes. Regional perfusion was applied for 97 minutes (54-106 minutes). Measured glomerular filtration rate 1 year postengraftment was not significantly different between cDCD and donation after brain death organs, 75 (65-76) vs 60 (37-112) mL/min per 1.73 m2 (P = 0.23). No complications have been observed in the 2 cDCD livers.ConclusionA protocol for cDCD is successfully established in Norway. Excellent transplant outcomes have encouraged us to continue this work addressing the shortage of organs for transplantation.

Background: In order to meet the increasing demand for donor organs the concept of donation after circulatory death (DCD) was reintroduced in Norway. First a pilot study, followed by the use of DCD as an institutional practice. We here report the current Norwegian experience with liver transplantation following DCD. Methods: After acceptance from next of kin, life support was withdrawn and cardiac arrest observed. After a five minute "no-touch" period, extracorporeal membrane oxygenation for post mortem normothermic perfusion (NRP) by ECMO circuit was established. Data from all liver transplant recipients receiving cDCD livers in Oslo were analyzed. Results: From 2015 to 2017, 8 patients underwent liver transplantation with cDCD and NRP livergrafts in Norway. Median MELD was 26, (range 6-40). There were no cases of delayed graft function or graft loss. Seven patients have reached 1 year of follow-up, 1 patient has reached 6 months. Two patients have recurrence of primary disease (PSC and steatohepatitis). All patients had normalized liver function at last follow-up. Two patients underwent procedures for the biliary complications: One with leakage from the cystic duct which was successfully handled endoscopically by stenting. In the other patient, a suspected stricture on MRI led to an ERCP procedure which did not confirm signs of biliary stenosis. There was one instance of hepatic artery stenosis, which was managed with endovascular technique. Conclusion:

Circulating compounds such as drugs and nutritional components might adhere to the oxygenator fibers and tubing during ECMO support. This study evaluated the amount of nutritional supplements adsorbed to the ECMO circuit under controlled ex vivo conditions. Six identical ECMO circuits were primed with fresh human whole blood and maintained under physiological conditions at 36 °C for 24 h. A dose of nutritional supplement calculated for a 70 kg patient was added. 150 mL volume was drawn from the priming bag for control samples and kept under similar conditions. Blood samples were obtained at predetermined time points and analyzed for concentrations of vitamins, minerals, lipids, and proteins. Data were analyzed using mixed models with robust standard errors. No significant differences were found between the ECMO circuits and the controls for any of the measured variables: cobalamin, folate, vitamin A, glucose, minerals, HDL cholesterol, LDL cholesterol, total cholesterol, triglycerides or total proteins. There was an initial decrease and then an increase in the concentration of cobalamin and folate. Vitamin A concentrations decreased in both groups over time. There was a decrease in concentration of glucose and an increased concentration of lactate dehydrogenase over time in both groups. There were no significant alterations in the concentrations of nutritional supplements in an ex vivo ECMO circuit compared to control samples. The time span of this study was limited, thus, clinical studies over a longer period of time are needed.

The total results suggest a positive net effect of ACT in patients with NVAF and TIAs. Without comparable data, no definite conclusions concerning the effect of ACT on patients with SIP can be drawn. The rate of bleeding complications was similar to that in other studied materials and is not negligible. In patients with SIP and TIAs, ACT beyond 6 months should probably only be continued if aspirin is not tolerated or has proven ineffective in the particular patient.

Charcoal haemoperfusion was performed for 5-12 h in three patients with maximal plasma phenobarbital concentrations of 600, 946 and 1044 mumol/l (138, 217 and 240 micrograms/ml). During haemoperfusion with constant blood flow phenobarbital elimination followed first order kinetics with half-lives of 11.1, 10.0 and 7.2 h, respectively. After termination of the haemoperfusion there was no rebound effect in plasma phenobarbital concentration and the elimination was first order with half-lives of 51, 82 and 48 h, respectively. Thus, the plasma phenobarbital half-life was reduced by 78-88% during haemoperfusion. In the same period 76-86% of the total body clearance of phenobarbital was due to the haemoperfusion column at a calculated volume of distribution of phenobarbital of 1.1-1.21/kg. This is clear evidence for recommending haemoperfusion in cases of serious poisoning with phenobarbital.