Novel Surfaces in Extracorporeal Membrane Oxygenation Circuits

Abstract

The balance between systemic anticoagulation and clotting is challenging. In normal hemostasis, the endothelium regulates the balance between anticoagulant and prothrombotic systems. It becomes particularly more challenging to maintain this physiologic hemostasis when we are faced with extracorporeal life support therapies, where blood is continuously in contact with a foreign extracorporeal circuit surface predisposing a prothrombotic state. The blood-surface interaction during extracorporeal life support therapies requires the use of systemic anticoagulation to decrease the risk of clotting. Unfractionated heparin is the most common anticoagulant agent widely used in this setting. New trends include the use of direct thrombin inhibitor agents for systemic anticoagulation; and surface modifications that aim to overcome the blood-biomaterial surface interaction by modifying the hydrophilicity or hydrophobicity of the polymer surface; and coating the circuit with substances that will mimic the endothelium or anti-thrombotic agents. To improve hemocompatibility in an extracorporeal circuit, replication of the anti-thrombotic and anti-inflammatory properties of the endothelium is ideal. Surface modifications can be classified into three major groups: biomimetic surfaces (heparin, nitric oxide, and direct thrombin inhibitors); biopassive surfaces [phosphorylcholine, albumin, and poly- 2-methoxyethylacrylate]; and endothelialization of blood contacting surface. The focus of this paper will be to review both present and future novel surface modifications that can obviate the need for systemic anticoagulation during extracorporeal life support therapies.

Platelets and extra-corporeal membrane oxygenation in adult patients: a systematic review and meta-analysis

“…However, their results might be affected by the patient illness, the lower baseline platelet count, and the development of hepatic or renal failure. After the initial activation of the inflammatory response, the endothelization process that occurs after few days on ECMO surfaces, especially in the oxygenator, could protect from a steady thrombocytopenia and platelet dysfunction [50,51]; the new generated platelets after 8-9 days (platelet lifespan) might be not affected anymore by the inflammatory and coagulative cascade triggered by ECMO [52].…”

Hematologic concerns in extracorporeal membrane oxygenation

“…Exposing large volumes of blood to circuit surfaces during ECMO is unavoidable. This exposure results in inflammation, platelet dysfunction, and disruption of the hematologic system 32 . Blood exposure to artificial surfaces results in fibrinogen, albumin, and other hematologic proteins coating the artificial surface, platelet activation, and inflammation 33‐36 .…”

“…Current ECMO tubing is made from polyvinyl chloride, though connectors and hubs may be made of other materials. Attempts to change circuit membrane characteristics to dampen or eliminate the blood‐membrane response can be broken into 3 broad categories: biomimetic surfaces, biopassive surfaces, and endothelialization 32 . The most common variants of each and their properties are summarized in Table 2.…”

“…It is currently not technically feasible due to the large surface area of an ECMO circuit requiring coverage, nor to produce this in an urgent or emergent fashion. Long‐term stability, risk of infection, and cost also remain obstacles 32 . In vivo endothelialization is an alternative approach in which EPCs derived from bone marrow are circulated at low concentration to generate a functioning endothelium in hardware 59 .…”

Anticoagulation in Pediatric Extracorporeal Membrane Oxygenation

“…Nitric oxide (NO) is an endogenous substance released by the endothelial cells. NO temporarily inactivates platelets resulting in decreased function and aggregation [50,51]. However, the effect of NO only temporarily inhibits platelets and after rapid degradation of NO by hemoproteins, platelets will regain normal function [52].…”