Background The use of veno–arterial extracorporeal membrane oxygenation (VA‐ECMO) decannulation with different percutaneous closure devices has been increasing. At our center, ProGlide devices have been used since November 2018, and Manta devices became an alternative since March 2020. This study aimed to compare the success and complication rates and the clinical outcomes of ProGlide and Manta devices for VA‐ECMO decannulation after arteriotomy wound closure. Methods We retrospectively reviewed the results of bedside VA‐ECMO decannulation between November 2018 and June 2021. Patients with VA‐ECMO who could be bridged to recovery were recruited and divided into the ProGlide or Manta group based on the closure device used. Procedure time, amount of blood loss, amount of blood products transfused, and use of vasoactive medications during the procedure were documented. Clinical examination and Doppler ultrasound were performed to detect any complications. Results After the closure technique, ProGlide was used in 44 patients and Manta was used in 13. There was no significant difference in the success rate between the ProGlide and Manta groups (86.4% vs. 100%). Amount of blood loss was greater in the ProGlide group than in the Manta group (290 [100–400] ml vs. 50 [50–100] ml), and more patients in the ProGlide group required an increased dose of inotropes during the procedure (59.1% vs. 15.4%), but the transfusion requirement was similar between the two groups. Conclusions The success rate of hemostasis using arteriotomy wound closure during VA‐ECMO decannulation was similar between the two devices.

Critical Care 2017, 21(Suppl 1):P349 Introduction Imbalance in cellular energetics has been suggested to be an important mechanism for organ failure in sepsis and septic shock. We hypothesized that such energy imbalance would either be caused by metabolic changes leading to decreased energy production or by increased energy consumption. Thus, we set out to investigate if mitochondrial dysfunction or decreased energy consumption alters cellular metabolism in muscle tissue in experimental sepsis. Methods We submitted anesthetized piglets to sepsis (n = 12) or placebo (n = 4) and monitored them for 3 hours. Plasma lactate and markers of organ failure were measured hourly, as was muscle metabolism by microdialysis. Energy consumption was intervened locally by infusing ouabain through one microdialysis catheter to block major energy expenditure of the cells, by inhibiting the major energy consuming enzyme, N+/K + -ATPase. Similarly, energy production was blocked infusing sodium cyanide (NaCN), in a different region, to block the cytochrome oxidase in muscle tissue mitochondria. Results All animals submitted to sepsis fulfilled sepsis criteria as defined in Sepsis-3, whereas no animals in the placebo group did. Muscle glucose decreased during sepsis independently of N+/K + -ATPase or cytochrome oxidase blockade. Muscle lactate did not increase during sepsis in naïve metabolism. However, during cytochrome oxidase blockade, there was an increase in muscle lactate that was further accentuated during sepsis. Muscle pyruvate did not decrease during sepsis in naïve metabolism. During cytochrome oxidase blockade, there was a decrease in muscle pyruvate, independently of sepsis. Lactate to pyruvate ratio increased during sepsis and was further accentuated during cytochrome oxidase blockade. Muscle glycerol increased during sepsis and decreased slightly without sepsis regardless of N+/K + -ATPase or cytochrome oxidase blocking. There were no significant changes in muscle glutamate or urea during sepsis in absence/presence of N+/K + -ATPase or cytochrome oxidase blockade. ConclusionsThese results indicate increased metabolism of energy substrates in muscle tissue in experimental sepsis. Our results do not indicate presence of energy depletion or mitochondrial dysfunction in muscle and should similar physiologic situation be present in other tissues, other mechanisms of organ failure must be considered. , and long-term follow up has shown increased fracture risk [2]. It is unclear if these changes are a consequence of acute critical illness, or reduced activity afterwards. Bone health assessment during critical illness is challenging, and direct bone strength measurement is not possible. We used a rodent sepsis model to test the hypothesis that critical illness causes early reduction in bone strength and changes in bone architecture. Methods 20 Sprague-Dawley rats (350 ± 15.8g) were anesthetised and randomised to receive cecal ligation and puncture (CLP) (50% cecum length, 18G needle single pass through anterior and posterior wa...

Background: When veno-arterial extracorporeal membrane oxygenation (VA-ECMO) support can be terminated, open repair of arteriotomy wounds in operating theaters is the standard of practice. Comparable outcomes by percutaneous decannulation using different closure devices have been reported. However, transport of the critically- ill, man-power and timeslots of operating theaters could be saved if decannulation was performed at bedside. Method: Bedside percutaneous arteriotomy wound closure became our default method of decannulation since November 2018. We reviewed our 1-year data to evaluate if such practice could be safely adopted in a local high-ECMO-volume center. Results: Between November 2018 and October 2019, 25 patients had their VA-ECMO terminated at the bedside. Twenty-one patients (84%) had successful decannulation. For those who failed, emergency open repair resulted in no additional complications. Two ProGlide devices were used in 15 (71.4%) patients and three were used in 6 (28.6%) patients. The procedure time was 27 (15–45) min. The median blood loss was 300 mL (250–400). Minor complications were found in 4 (19.1%) patients, including two arterial clot formation, one pseudoaneurysm and one wound infection. There were no other major complications. Conclusion: Our 1-year experience showed that percutaneous bedside VA-ECMO decannulation was feasible to commence in a local large-ECMO-volume center.

Percutaneous closure of arteriotomy wound during peripheral venoarterial extracorporeal membrane oxygenation decannulation was shown to be safe and allow earlier mobilization. The new MantaTM vascular closure device (Essential Medical), designed for the closure of arterotomy wound created by large-bore vascular sheaths up to 25Fr during endovascular catheterization procedures, was reported to be applicable in venoarterial extracorporeal membrane oxygenation decannulation. In this article, we would like to share our experience of using real-time ultrasound guidance to ensure the safe application of Manta during bedside venoarterial extracorporeal membrane oxygenation decannulation.

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