What is the difference between ecmo and cpb
Additionally, all patients were managed with the same high-dose aprotinin protocol. In the case of cardiopulmonary bypass supported lung transplantation, additional 2 million KIU were added to the prime solution. The Medtronic Carmeda heparin-bonded tubing circuit Medtronic Cardiopulmonary, Anaheim, CA was used for both circulatory support systems.
We used well-established criteria for accepting donor lungs including objective evidence of adequate gas exchange and bronchoscopic evaluation to exclude aspiration or purulent secretions [9]. Standardized organ procurement and recipient implantation techniques were utilized for lung transplantation cold crystalloid preservation solution of low-potassium dextran solution or LPD, Vitrolife, Gottenberg, Sweden was infused via the donor pulmonary artery at low pressure in an antegrade fashion immediately following prostaglandine intrapulmonary artery injection.
During the procurement, the vascular structures were divided in situ and the trachea dissected well proximal to the carina. With the lungs partially inflated, the trachea was divided between staple lines and the organ transported to the center was immersed in LPD.
A pulmonary artery catheter was inserted through the right neck to monitor continuously the right arterial and pulmonary artery pressure and a double-lumen endo-tracheal tube was placed allowing isolated lung ventilation. Double lung transplantation was performed using a sequential single lung implantation technique either through bilateral anterolateral thoracotomies without transverse incision of the sternum.
Rarely, bilateral posterolateral thoracotomies were indicated for sequential single lung transplantation when mediastinal shifting led to difficult exposure of lung hilum structures requiring turning and re-draping the patient one patient. Single lung transplantation was performed through a serratus muscle-sparing posterolateral thoracotomy. Once the donor lung was present in the operating room, the recipient pneumonectomy was completed. The bronchial anastomosis was accomplished first and was generally followed by the vascular pulmonary artery and left atrial cuff anastomoses.
De-airing was done thoroughly through the atrial cuff anastomosis. Monofilament purse string sutures were applied to the anterior wall of the femoral artery and vein. The Seldinger canulation technique was used to introduce minimal-invasive cardiac surgery heparin-bonded venous usually 22 Fr and arterial cannulas 18 Fr. In case of small arterial diameter and complete occlusion of the vessel by the arterial cannula, a separate arterial cannulation 10 Fr of the distal limb was performed.
Categorical data were analyzed by chi-square tests. A logistic multivariate regression model was then used to examine synergistic effects of potential predictors massive blood product trasnsfusions of greater than 8 units of packed red blood cells, ECMO use, CPB use, survival. The statistical analysis was performed using SPSS Significant differences are reported as exact p -values.
There were no differences in the surgical implantation technique and the underlying end-stage lung diseases between the CPB and ECMO supported lung transplantation procedures. There were seven sequential bilateral and one single lung transplantation procedures in the ECMO group and six sequential bilateral and one single lung transplantation operations in the CPB group.
All surgical procedures were performed through limited-access muscle and sternum sparing bilateral anterior-lateral or postero-lateral thoracotomies. Lower extremity perfusion was established through a 10 Fr femoral artery cannula insertion. Weaning from mechanical ventilation and subsequent extubation times were significantly shorter in the CPB-supported patients: 3. Following bronchoscopy, chest-X-ray, and chest computed tomography examinations the patients were taken back to the operating room.
The previously ECMO-supported patient improved following evacuation of large chest cavity hematomas, which compromised transplant lung inflation and expansion.
A thorough inspection did not reveal surgical bleeding sites. The CPB supported patient idiopathic fibrosis, secondary pulmonary hypertension, systolic pulmonary artery pressure 90 mmHg, right heart dysfunction with severe ischemia—reperfusion injury developed graft failure and required immediate ECMO support and massive blood product transfusions.
This patient died on post-operative day 10 due to therapy-resistant coagulopathy, right heart failure, and intracranial bleeding. In this patient several re-explorations and thoracotomies for bleeding were performed; however, an obvious surgical bleeding site was never identified. The requirement for blood product administration packed red blood cell was significantly different between both groups during the operation and over the first 72 h. Their average transfusion requirements were For comparison, the patients undergoing lung transplantation without extracorporeal support required 2.
Three of the ECMO and one additional patient of the CPB-supported group died within 90 days of the lung transplantation procedure due to infectious complications. Table 1 summarizes the important findings. The results of the two different extracorporeal circulatory support techniques used for lung transplantation surgery.
The majority of single and sequential bilateral single lung transplantation surgery is performed without extracorporeal circulatory support CPB or ECMO on a routine basis for a wide variety of end-stage lung disorders with steadily improving 5-year morbidity and mortality rates.
The use of CPB has decreased dramatically since the early days of lung transplantation. Our preference is to avoid CPB, whenever possible, and thus, avoiding the CPB-associated complications of coagulopathy and bleeding, neurological and renal dysfunction. Hemodynamic instability, the inability to sufficiently oxygenate with one lung ventilation, dramatic increases in pulmonary artery pressure with pulmonary artery clamping and deterioration of right ventricular function require the employment of CPB.
We, and others, prefer CPB support in lung transplantation surgery when the indication for lung transplantation is accompanied by severely elevated pulmonary artery pressures associated with right heart dysfunction [3 , 10 , 11].
The majority of these patients present either with primary pulmonary hypertension or idiopathic pulmonary fibrosis with secondary severely increased pulmonary artery pressures. These are the highest-risk patients in lung transplantation surgery. The majority of patients in this study presented with markedly increased pulmonary artery pressures and the lung transplantation surgery required CPB support. The use of CPB can further lead to increased blood product transfusions, increasing the release of cytokines, and activation of the systemic inflammatory response syndrome [6 , 12].
Its sequelae of reperfusion injury and early graft dysfunction in clinical lung transplantation are well described in association with CBP-supported surgery [13]. The administration of aprotinin decreased the incidence of severe ischemia—reperfusion injury in clinical lung transplantation [14] ; however, the administration of blood products could not be avoided.
A comparison of peri-operative blood transfusion requirements between double lung transplantation with and without CPB support by Gammie et al. The CPB-supported lung transplantation group of the present study had required markedly less packed red blood cell units 5.
Interestingly, despite the avoidance of high-dose heparin administration due to the integration of heparin-coated tubing systems in the ECMO circuit of the ECMO-supported lung transplantation procedures, the transfusion of blood was significantly increased mean of 13 units. The results of this study revealed that eight and more red blood cell units transfused within 72 h of lung transplantation in the combination with the use of intra-operative ECMO support, reached near significance for adverse outcomes following lung transplantation surgery.
Transfusion-related lung injury is a thoroughly described phenomenon and clinically similar to the adult respiratory distress syndrome [15]. It has been linked to the transfusion of leukocyte antibodies in blood components. There are several potential mechanisms by which massive transfusion might predispose to direct lung transplant injury and impact on the immune system: cognate antigen—antibody interactions, activation of non-specific immunity through soluble mediators present in transfused blood, an increased risk of infection through transfusion-associated immunomodulation leading to infection and sepsis; and volume overload in the face of increased permeability of the alveolar capillary membrane [16].
These combinations of effects could have contributed to the observed increased rate of early post-transplant viral infection and sepsis, which was the cause of significant morbidity and mortality in three lung transplant patients. One explanation for the increased use of blood transfusions in the ECMO group of this study is the significantly reduced priming volume in a patient population which was already present in a therapeutically induced end-stage lung disease related dehydrated state.
In order to maintain effective and adequate high ECMO flow intravascular volume repletion was required. This was performed with high-molecular weight components and blood products to prevent transcapillary leakage and interstitial edema formation.
This protocol assists in the management of the frequently encountered leaky capillary syndrome of lung transplantation patients, in which the administration of crystalloid or colloid like albumin fluid solutions would immediately accumulate within the interstitial and alveolar spaces leading to aggravation of the ischemia—reperfusion syndrome.
The use of extracorporeal membrane oxygenation became a last resort treatment option for lung transplantation patients after surgery who developed severe ischemia—reperfusion injury and graft failure following surgery [8]. Many lung transplant centers judged the elective employment of ECMO as justified if graft failure is related to the ischemia—reperfusion syndrome, which is associated with hypoxia, endothelial permeability increase, and dense pulmonary infiltrates formation [17].
Only limited reports exist, which describe the intra-operative use of ECMO for lung transplantation surgery. Ko et al. ECMO support was extended into the post-operative period. All lung transplant patients had an uneventful recovery with excellent graft function [18]. Bilateral lung transplantation with intra- and postoperatively prolonged ECMO support was used in 17 patients with primary pulmonary hypertension [4].
Of note, they report only two deaths despite the use of ECMO. Locations Main Campus. Satellite Locations. Emergency Care. Urgent Care. Safe Sleep Practices. Pay Your Bill. Financial Assistance. Medical Records. About Us Who We Are. Patient Stories. Get Involved. Health Alerts: Coronavirus. Health Library. Flu Information. Nutrition Videos. Blood flow and oxygenation are regulated to optimise tissue oxygenation and protection. Venous blood usually enters the circuit by gravity into a venous reservoir placed 40 to 70 cm below the level of the heart.
The amount of drainage is determined by central venous pressure; the height differential; resistance in cannulas, tubing, and connectors; and absence of air within the system. Central venous pressure is determined by intravascular volume and venous compliance, which is influenced by medications, sympathetic tone, and anaesthesia.
Venous cannulas are usually made of flexible plastic, which may be stiffened against kinking by wire reinforcement. Tips are straight or angled and often are constructed of thin, rigid plastic or metal Figure 6. Size is determined by patient size, anticipated flow rate, and an index of catheter flow characteristics and resistance provided by the manufacturer. Bicaval cannulation and caval tourniquets are necessary to prevent bleeding and air entry into the system when the right heart is entered during CPB.
Because of coronary sinus return, caval tourniquets should not be tightened without decompressing the right atrium. Bicaval cannulation without caval tapes is often preferred to facilitate venous return during exposure of the left atrium and mitral valve.
For an average adult with cm negative siphon pressure, a 30F cannula in the superior vena cava SVC and 34F in the inferior vena cava IVC or a single 42F cavo-atrial canula suffices.
Canulae are typically inserted through purse-string guarded incisions in the right atrial appendage, lateral atrial wall, or directly in the SVC Figure 7.
Insertion of canulae in bicaval cannulation and single atrial or Cavotrial cannulation. The term extracorporeal membrane oxygenation ECMO was initially used to describe long-term extracorporeal support that focussed on the function of oxygenation.
Subsequently, in some patients, the emphasis shifted to carbon dioxide removal, and the term extracorporeal carbon dioxide removal was coined. Extracorporeal support was later used for postoperative support in patients following cardiac surgery. Other variations of its capabilities have been tested and used over the last few years, making it an important tool in the armamentarium of life and organ support measures for clinicians. With all of these uses for extracorporeal circuitry, a new term, extracorporeal life support ECLS , has come into vogue to describe this technology.
ECMO is frequently instituted using only cervical cannulation, which can be performed under local anesthesia whereas standard cardiopulmonary bypass is usually instituted by transthoracic cannulation under general anesthesia Figure 8. Unlike standard cardiopulmonary bypass, which is used for short-term support measured in hours, ECMO may be used for longer-term support ranging from days and finally.
The purpose of ECMO is to allow time for intrinsic recovery of the lungs and heart; a standard cardiopulmonary bypass provides support during various types of cardiac surgical procedures.
An oxygenator with low flow resistance and high gas transfer efficiency is connected to cannulae placed in the femoral artery and vein. The circuit flow is driven by the femoral arterial pressure and is designed to operate without the help of a mechanical pump in an arterio-venous configuration Figure Based on this principle, adequate mean arterial blood pressure is mandatory. Oxygenation is limited, due to the inflow of relatively well-oxygenated arterial blood.
The capability for efficient CO 2 removal allows for a reduction in ventilator settings. The simplicity of the circuit and its portability also make it suitable for emergency use and transfer.
It has been used in patients with severe acute lung failure due to ARDS, inhalation injury, severe pneumonia, chest injury, foreign body aspiration, and after thoracic surgical interventions. Its use is relatively contraindicated in patients with haemodynamic instability, cardiac insufficiency or peripheral atherosclerosis. The response involves the recognition, not only of the attack, but of its precise location and the consequent localisation of the body's defensive and reparatory processes at the precise site of the insult.
The inflammatory response is, therefore, essentially appropriate and protective. The peculiar significance of the inflammatory response in the context of cardiac surgery lies in the fact that this localised and protective response becomes systemic and damaging to patients' vital organs.
SIRS refers to the situation where the inflammatory response Figure 11 process ceases to be focussed on a localised site of injury, and instead is disseminated throughout the circulation, affecting potentially all vital organs and contributing if severe enough and of significant duration to patient morbidity and mortality.
The cardiac surgical literature contains extensive reports of disturbances in the function of lungs, brain, kidney, liver, gastrointestinal tract and the heart itself, induced by the initiation of systemic inflammation in cardiac surgical patients. Overview of various pathways to inflammatory response intiated by contact actication of blood proteins.
SIRS appears to be the outcome of a complex interaction leading to activation of cellular and humoral mediators of inflammation plus involvement of fibrinolytic and haemostatic systems. Further discussion of the processes involved in contact activation are necessary. Following the initial phase of protein deposition, coagulation factor XII Hageman factor is activated.
Activated factor XIla induces a series of cascade systems involving coagulation,fibrinolysis, kallikrein and complement activation. The final common pathway of these cascade systems leads to activation of blood cells, platelets and most importantly, white cells neutrophils and monocytes leading to dissemination of an inflammatory response throughout the circulation.
Contact activation of coagulation cascade via intrinstic coagulation pathway, proinflammatory cytokines and bleeding. Central to the development of the inflammatory process is the interaction between activated neutrophils in circulating blood, and activated vascular endothelial cells, lining the luminal wall of blood vessels.
Neutrophils become activated and respond by expressing adhesion molecular families selectins and integrins on their cell surface.
They also produce and secrete soluble inflammatory mediators. The adhesion molecules render the neutrophils more adhesive. Similarly, endothelial cells, activated by similar stimuli, express on the cell luminal surface the adhesion molecule ligands corresponding to those being expressed in the activated neutrophil.
The increased adhesive capability of activated circulating neutrophils flowing over activated vascular endothelial cells results in a step-wise interaction comprising three distinctive steps: neutrophil rolling, neutrophil firm adhesion, and neutrophil transmigration Figure This process is mediated by the Selectin family of adhesion molecules. This firm adhesion, the second phase of the process, is mediated by the Integrin family of adhesion molecules.
The third and final phase of neutrophil — endothelial cell interaction is transmigration, which refers to the movement of firmly adherent neutrophils through the blood vessel wall into the adjacent tissue. Neutrophil transmigration involves movement into vascular compartment into the tissues of vital organs. The receptors were initially identified in studies cloning the thrombin receptor, 12 now renamed as protease activated receptor PAR1.
PAR receptors have now been identified on numerous cells, organs and tissues, including neutrophils and endothelial cells — of obvious interest in relation to inflammation, not least the potential role in leukocyte transmigration across vascular endothelium. Most recently, PAR -1 activation of platelets has been reported in patients acutely after ischaemic stroke. PAR has various locations: platelet; endothelium of gut, brain, lung, skin and skeletal muscle; neutrophil; mast cell; and other locations such as heart, fibroblasts, monocytes, T-Cells, osteoblasts, kidney, liver, pancreas, lymph nodes, etc.
Ideally, any strategy to prevent or modify the harmful effects of SIRS should be preceded by an understanding of its pathophysiology. This is clearly a counsel of perfection, but such targeted therapies are more likely to be successful. Research performed in our department has focussed on two strategies:. In our laboratory the Cantharidin blister model 13 has been investigated as a tool to analyse the inflammatory effect of cardiopulmonary bypass in vivo.
The model can provide a detailed molecular insight into the extravascular leukocyte population during cardiopulmonary bypass. The Cantharidin blister model is non-invasive, has few side effects, is easily reproducible and can be maintained for several days to characterize both the induction and resolution of the innate inflammatory response.
In the late s, we pioneered the use of Aprotinin as a blood conservation agent. Although Aprotinin was withdrawn in following preliminary results from a clinical trial as a blood conservation agent, a recent meta-analysis and a review demonstrated that there was no increase in mortality with Aprotinin as compared to other anti-fibrinolytic agents.
Heparin coating was probably the first to gain a sizeable acceptance by many cardiac surgeons, although the technique is by no means generally applied. Again, although many studies were carried out to demonstrate the anticipated reduction in the severity of the CPB -induced inflammatory response, the results were mixed and somewhat unconvincing. Mechanistically speaking, it could be argued that, although surface modification of the CPB circuit is a credible concept, heparin may not be the optimal substance for the coating.
The laudable aim to reduce CPB related contact activation may also be achieved by reducing the surface area of the CPB circuit.
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