Extracorporeal membrane oxygenation
(ECMO) is used in critical
care to manage patients with severe respiratory and cardiac failure.
ECMO brings blood from a critically ill patient into contact with
a non-endothelialized circuit which can cause clotting and bleeding
simultaneously in this population. Continuous systemic anticoagulation
is needed during ECMO. The membrane oxygenator, which is a critical
component of the extracorporeal circuit, is prone to significant thrombus
formation due to its large surface area and areas of low, turbulent,
and stagnant flow. Various surface coatings, including but not limited
to heparin, albumin, poly(ethylene glycol), phosphorylcholine, and
poly(2-methoxyethyl acrylate), have been developed to reduce thrombus
formation during ECMO. The present work provides an up-to-date overview
of anti-thrombogenic surface coatings for ECMO, including both commercial
coatings and those under development. The focus is placed on the coatings
being developed for oxygenators. Overall, zwitterionic polymer coatings,
nitric oxide (NO)-releasing coatings, and lubricant-infused coatings
have attracted more attention than other coatings and showed some
improvement in in vitro and in vivo anti-thrombogenic effects. However, most studies lacked standard
hemocompatibility assessment and comparison studies with current clinically
used coatings, either heparin coatings or nonheparin coatings. Moreover,
this review identifies that further investigation on the thrombo-resistance,
stability and durability of coatings under rated flow conditions and
the effects of coatings on the function of oxygenators (pressure drop
and gas transfer) are needed. Therefore, extensive further development
is required before these new coatings can be used in the clinic.
All human cells are coated by a surface layer of proteoglycans, glycosaminoglycans (GAGs) and plasma proteins, called the glycocalyx. The glycocalyx transmits shear stress to the cytoskeleton of endothelial cells, maintains a selective permeability barrier, and modulates adhesion of blood leukocytes and platelets. Major components of the glycocalyx, including syndecans, heparan sulfate, and hyaluronan, are shed from the endothelial surface layer during conditions including ischaemia and hypoxia, sepsis, atherosclerosis, diabetes, renal disease, and some viral infections. Studying mechanisms of glycocalyx damage in vivo can be challenging due to the complexity of immuno-inflammatory responses which are inextricably involved. Previously, both static as well as perfused in vitro models have studied the glycocalyx, and have reported either imaging data, assessment of barrier function, or interactions of blood components with the endothelial monolayer. To date, no model has simultaneously incorporated all these features at once, however such a model would arguably enhance the study of vasculopathic processes. This review compiles a series of current in vitro models described in the literature that have targeted the glycocalyx layer, their limitations, and potential opportunities for further developments in this field.
Retroperitoneal haemorrhage is a rare but potentially life-threatening event. It may occur either spontaneously or secondary to percutaneous vascular access procedures, trauma, or ruptured aortic, iliac, or mesenteric aneurysms. As a result, the clinical presentation is variable. Computed tomography and/or angiography are vital for diagnosis. Management may range from conservative treatment for stable patients to emergency laparotomy or embolization for catastrophic haemorrhage. Direct percutaneous puncture of a deep intra-abdominal pseudoaneurysm is an accepted but infrequently performed technique due to a number of diagnostic and technical challenges. We describe the successful percutaneous transabdominal angioembolization of a superior mesenteric artery rupture in a 77-year-old woman with a large retroperitoneal haematoma. This was performed after a conventional femoral transarterial approach was unsuccessful.
Limb ischemia is a major complication associated with peripheral venoarterial extracorporeal membrane oxygenation (VA‐ECMO). The high velocity jet from arterial cannulae can cause “sandblasting” injuries to the arterial endothelium, with the potential risk of distal embolization and end organ damage. The aim of this study was to identify, for a range of clinically relevant VA‐ECMO cannulae and flow rates, any regions of peak flow velocity on the aortic wall which may predispose to vascular injury, and any regions of low‐velocity flow which may predispose to thrombus formation. A silicone model of the aortic and iliac vessels was sourced and the right external iliac artery was cannulated. Cannulae ranged from 15 to 21 Fr in size. Simulated steady state ECMO flow rates were instituted using a magnetically levitated pump (CentriMag pump). Adaptive particle image velocimetry was performed for each cannula at 3, 3.5, 4, and 4.5 L/min. For all cannulae, in both horizontal and vertical side hole orientations, the peak velocity on the aortic wall ranged from 0.3 to 0.45 m/s, and the regions of lowest velocity flow were 0.05 m/s. The magnitude of peak velocity flow on the aortic wall was not different between a single pair versus multiple pairs of side holes. Maximum velocity flow on the aortic wall occurred earlier at a lower pump flow rate in the vertical orientation of distal side holes compared to a horizontal position. The presence of multiple paired side holes was associated with fewer low‐velocity flow regions, and some retrograde flow, in the distal abdominal aorta compared to cannulae with a single pair of side holes. From this in vitro visualization study, the selection of a cannula design with multiple versus single pairs of side holes did not change the magnitude of peak velocity flow delivered to the vessel wall. Cannulae with multiple side holes were associated with fewer regions of low‐velocity flow in the distal abdominal aorta. Further in vivo studies, and ideally clinical data would be required to assess any correlation of peak velocity flows with incidence of vascular injury, and any low‐velocity flow regions with incidence of thrombosis.
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