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Tony Fisher Harefield Hospital U.K.

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1 Tony Fisher Harefield Hospital U.K.
EMERGENCY OXYGENATOR CHANGEOUT Predisposing Factors and Resulting Incidence Tony Fisher Harefield Hospital U.K. Good morning. My name is Tony Fisher and I’m from Harefield Hospital which is famous for heart and lung transplants and is situated on the outskirts of London. Today I’m going to talk about the factors that predispose towards an oxygenator no longer adequately functioning and the resulting chance of having to perform an emergency oxygenator changeout. To those of you with experience of changing out oxygenators, and that is probably the majority of experienced perfusionists here, you will know how stressful it is to perform and how potentially dangerous it is to the patient. I am going to look at previously published work on this problem and at the results of the research that I am presently conducting and whilst I will be able to explain some of the problems, I will probably end up asking more questions than I answer. One quick comment; The abstract was written before I had time to fully analyse all the data. Due to the presence of some false positive results, there are a few differences in the figures between those printed in the abstract and those presented here. Let us start by looking at how common a problem it really is

2 There has been eight major surveys over the years looking at a range of perfusion relating problems. From these, I have extracted the problems specifically relating to oxygenator problems.. Before discussing the results I need to add a few words about the reliability of the results. Firstly these are all retrospective surveys and therefore their accuracy will depend upon memory going back up to six years. Secondly, the exact form of the question is rarely published and how it is interpreted by the respondant may add further inaccuracies. If a problem is dealt with simply, is it still considered as a reportable problem. For example, a leak in the outer casing of an oxygenator might be dealt with by filling it with bone wax and a sticky plaster - would this be routinely reported. With these limitations in mind, let us look at the overall results. The two earliest surveys gave an incidence of oxygenator problems of about one in every two thousand cases with no mention of whether these resulted in oxygenator changeouts. The following six surveys gave a huge range of incidence of problems from 1 in every seventy cases in Sweden to one in every one thousand cases here in the U.S.A. This must reflect the previously mentioned differences in methodology. However when we look at the reported incidence of resulting changeout, then there are fewer differences; Kurusz, Svenmarker, Jenkins and Stensved report that there is a changeout about once every thousand cases, whilst Mejak’s and my survey report about one in four thousand. I would like to believe in my survey as it means that in the standard U.K. unit, there would be one changeout every three years. Let us break these numbers down a bit

3 OXYGENATOR PROBLEMS Leaks in; Grossly contaminated circuit
Membranes Housing Heat Exchanger Grossly contaminated circuit Clots in Oxygenator / Reservoir Oxygenator Failure Raised trans - oxygenator pressure The problems reported can be divided into Leaking Oxygenators, Grossly contaminated Oxygenators, Clotted off Oxygenators, what is usually defined as Failed Oxygenators, and the most recently reported problem of a blocked or failed oxygenator as a result of a raised trans oxygenator pressure gradient. Let us look at each of these categories.

4 LEAKING OXYGENATORS INCIDENCE Stoney I in 23,426 cases Kurusz 2,371
Jenkins ,932 Fisher , Housing leaks resulting in EOC Stensved 1,635 Mejak , Water to blood leaks Kurusz, Jenkins and Stensved quoted an incidence of leaking oxygenators of about one in every two thousand cases. I think we can assume that the majority of these were casing leaks that were dealt with at the time. My survey gave an incidence of one in every twenty thousand cases all of which were leaks bad enough to justify an emergency 0xygenator changeout. Mejaks survey reported on one in every forty thousand all of which were heat exchanger leaks and must have resulted in oxygenator changeout. The problem of an oxygenator failing due to plasma leak after extensive use is not included in this section. As you can see, whilst this occurs, it appears to be a very rare event.

INCIDENCE Stoney 1 in 374,819 cases Kurusz ,260 Jenkins ,762 Mejak 23,148 Four surveys reported on Grossly contaminated oxygenators. I am not sure how an oxygenator becomes grossly contaminated except via a water to blood leak due to a leaking heat exchanger. So here is my first question to you, is this purely a problem that occurs during setup and therefore will not result in emergency changeout or can it happen during bypass. Anyway, Stoney only had one reported in his 1979 survey whereas Kurusz, seven years later in 1986 reported on one hundred and seventy six occurrences in a survey covering almost six hundred thousand cases - an incidence of one every three thousand cases. However just to complicate this issue, Mejak reported an incidence of a grossly contaminated oxygenator every two thousand three hundred cases in addition to the previously mentioned water to blood leak which I think really does illustrate one of the problems of the respondants understanding of the questions of a survey. However if Kurusz and Jenkins reflect the real incidence of leaking heat exchangers then this is a real quality control issue that the manufacturers need to address

INCIDENCE Stoney in 787 cases Wheeldon ,667 Kurusz ,479 Svenmarker Jenkins ,005 Mejak ,283 Clots appearing in the circuit is a serious and well known problem for perfusionist. I find these particular figures fascinating as well as particularly horrifying. Apart from Stoneys very early survey and Svenmarkers very small survey, the incidence of clotted of oxygenators has remained amazingly stable from 1981 with an incidence of about one in every three thousand cases. Given that anticoagulation control is now well established and routinely performed throughout the world with the dangers fully understood, one would have expected to see a marked decline in the incidence and yet it has not happened. So here is my next question, why has the incidence of clotted off oxygenators not gone down over the years. I may have part of the answer.

7 CLOTS IN OXYGENATOR 1990 - 92 1994 - 96 n= 68,937 97,313
n= , ,313 Oxy clotted going back on bypass + aprotinin back on bypass Oxy clotted + aprotinin Oxy clotted When I conducted my survey into oxygenator failures in the U.K., in order to get a large and relativelyaccurate database, I divided the survey up into two periods of three years. The first period covered 1990 to 92 and contained reports on sixty nine thousand cases. There were ten reports of clotted oxygenators. Three of these were in patients who had been treated with aprotinin with a further six cases which clots occurred after having to go back on bypass a second time in patients who had also been treated with aprotinin. There was only one instance of an oxygenator clotting during a routine case. The second part of the survey covered the years and contained reports on ninetyseven thousand cases. The pattern of problems has now greatly changed with only one case related to the use of aprotinin, two instances of clotting during routine cases and one when going back on bypass for a second time. The period was a time in the U.K. when aprotinin had only recently been introduced but control of anticoagulation was still poorly understood. By the understanding of the problem was greatly improved along with the commercial production of ACT tests that are relatively unaffected by aprotinin. The lesson these results suggest is that there can be increased risk with new technology until that technology is fully understood.

8 FAILED OXYGENATORS INCIDENCE Stoney 1 in 3,022 cases Wheeldon 2,063
Kurusz ,134 Mejak ,458 Now let us look at failed oxygenators. The reported incidence of failed oxygenators has, like the previously reported problems, stayed relatively constant at about one in every two thousand cases

Clot formation Plasma or blood leak Raised trans-oxygenator pressure gradient (R.T.P.) How can our modern membrane oxygenators fail. Essentially there are three major potential causes. Clots can form in them reducing the surface area available for gas exchange. Over time, plasma will leak through the membrane and coat the inner surface of the membrane. This will effectively block the pores in the membrane and increase the distance that the gas has to diffuse through and hence reduce the ability to oxygenate. A similar but generally more immediate effect will happen if there are broken fibres resulting in a blood to gas leak. And finally there is the relatively recent problem of oxygenators failing due to the development of a specific type of thrombus which is monitored by measuring the trans-oxygenator pressure. I will look at this in more detail in a minute.

Gas supply problems Metabolic requirements State of anaesthesia, Poor oxygenator design Large patients + + + The problem of a failing oxygenator can be amplified by many other factors. Amongst these will be any problem with the gas supply system which in itself will present problems along with the different oxygen requirements of patients. Design problems with oxygenators especially when associated with large patients may result in a reduced ability to oxygenate.

11 Here, for example are some results published by Fried of the ability of two different oxygenators to add oxygen. Although neither oxygenator is available today, the Bard HF5000 can maximally transfer about 450 ml of oxygen per minute whilst the Univox can only transfer about 300. Patients requiring more than 300 ml per minute of oxygen when on bypass with a Univox oxygenator would present as a failing oxygenator

A.C.T. is greater than 480 secs Starts to occur immediately upon going on bypass Pressure drop across oxygenator increases rapidly Reaches a plateau Reduces rapidly back to base line after about 30 minutes or on rewarming Now let us look at the problem of a raised trans-oxygenator pressure gradient in relation to failed oxygenators. This is a problem that was first reported in the early nineties and is now raising some concern amongst perfusionists. The first problem to deal with is that of terminology. This problem has been given different names by different authors but for the rest of this talk I will refer to it as a raised trans-oxygenator pressure or RTP. The second problem is in the definition of the event. The definition I will use and one that has been used by some authors is that there is an event when the pressure gradient is at least double the normally expected one. When we look at the incidence of this event, I am sure that much of the varience in incidence is due to the use of different definitions What are the reported characteristics of this phenomena. Firstly whilst it involves the formation of a thrombus, anticoagulation always appears effective and ACT’s are normal. Immediately upon going on bypass the pressure gradient that can be measured across the heat exchanger oxygenator compartment of the oxygenator rises rapidly. Within minutes it reaches a peak and will then maintain that peak for a variable amount of time. Usually within 30 minutes or on rewarming it starts to rapidly decrease back to normal levels

Effect may be reduced by rewarming Oxygenation may become inadequate If the oxygenator is changed out it does not recur The rate of rise of pressure gradient can be reduced by gently rewarming. However in the extreme cases, the oxygenator might become completely blocked off or its ability to oxygenate severely compromised resulting in an emergency oxygenator changeout becoming necessary. If there is a changeout, the phenomena does not recur.

The blockage is caused by the development of a fibrin - platelet thrombus This appears to start in the heat exchanger but grows into, or breaks away into the oxygenator fibre bundle What causes this blockage. The basic cause is the development of a fibrin platelet thrombus which appears to start on the heat exchanger and then grow . It either grows into, or bits break away into the oxygenator fibre bundle. Whilst this is known, what is not yet known is the initiating factors that start the growth of this white thrombus. Later on in this talk I will look at this in more detail.

INCIDENCE Study Incidence Requiring Size E.O.C. Stensved , in in 954 Blomback , Wahba , Fisher , ,228 So what is the incidence of the problem. There has been 4 studies on this problem. Stensved conducted a retrospective multicentre survey in Sweden and reported an incidence of raised trans oxygenator pressure gradients of one in every 89 cases which resulted in an emergency oxygenator changeout about once in every thousand cases. Blomback did a retrospective look at his own unit in Sweden in 1995 and found 11 patients with a high gradient of which three required an emergency changeout. Wahba also reported on the results from his unit in Germany in 1998 and reported on an overall incidence of a raised pressure gradient of one in every 42 cases which resulted in an emergency changeover once in every 490 cases. Because of this variation in results I have conducted a multicentre prospective survey of eight hospitals in the U.K. All cases done at these hospitals from February to October last year were included and all the hospitals used a standardised measuring and reporting system They have reported on a total of 3684 cases during which there was a total of 16 raised pressure gradients - an incidence of one in every 228 cases. There were 3 emergency oxygenator changeouts - an incidence of one in every twelve hundred cases. The two multicentre surveys gave an incidence of emergency changeovers of about one in a thousand whilst the single centre studies gave a much higher incidence. I will look at the reason for this in a minute.

16 One problem encountered by workers in this field has been a definition of what is an event. An often used one is where the pressure gradient rises to a level twice that normally encountered. However as these pressures are flow dependant this definition becomes difficult to use practically. In order to resolve this, what is needed is a standardised way of defining the problem and in order to do so we have to define firstly the normal situation. Here is the relationship between pressure gradient and flow across a Capiox SX25 oxygenator as published in the company’s instructions of use. It has been measured using bovine blood with a haemoglobin of 12 gram per decilitre at a temperature of 37 oC. As you can see this is a fairly linear relationship

Reasonably linear relationship between Pressure Gradient and Flow Therefore can be based on Poiseuille’s Formula Flow =  x p x r4 8 x  x l Because of this linear relationship we can assume that there is laminar flow through the device for the range of flows that we use and therefore it is approximately obeying Poiseuilles formula where p is the pressure gradient  is the viscosity and r and l are related to the dimensions of the device. As a result, the trans oxygenator pressure gradient was measured in a variety of devices in clinical use in a range of different hospitals for twenty patients with each device. Because of the above relationship instead of using the actual pressure gradient, we can divide it by the flow to get a measurement of pressure gradient per litre flow.

18 Here are the results for the Sorin Monolyth Pro and the Cobe Duo
Here are the results for the Sorin Monolyth Pro and the Cobe Duo. The pressure drop across both devices as measured in mm Hg per litre blood flow stayed relatively constant throughout the 90 minutes bypass. All other devices followed a similar pattern. The only difference between devices was the measured pressure drop. Thus the Monolyth Pro had a pressure drop of about 12 mm Hg per litre flow. A flow on bypass of say 5 litres per minute would therefore result in a pressure drop of 60 mm Hg. If the Duo was used, it had a pressure drop of 32 mm Hg per litre flow and so its gradient at 5 litres per minute would be160 mm Hg. We now have a baseline from which to measure any pathological changes

Variations in measurements due to; Viscosity changes Haematocrit Prime constituents Flow Temperature Site of measurement OVERALL Variation about 10% In the real clinical world, there will be variations in this baseline figures. These will be due to two variables. Firstly viscosity. The major effect on viscosity will be haematocrit which as we all know does vary somewhat. Viscosity will also be affected by the prime constituents and by the fluids given prebypass by the anaesthetist. In addition because blood is a non-neutonian fluid, its viscosity will change a bit with flow.It will also change with temperature. And finally there is a wide range of substances in the blood whose concentration will also affect viscosity. The second major effect is the site of measurement. Because of the design of oxygenators, it is common to measure the pressures a few inches away from the inlet and outlet of the device. The resistance of the tubing will have an effect and this will vary slightly between different hospitals. However my results were taken from eight different hospitals, and the variation in baseline readings between hospitals and patients for any specific device was only around 10% which I think is an acceptable variation for any physiological measurement. By using this method we have a relatively stable baseline against which we can now compare the pathological situation.

20 Let us now look at the pathological situation
Let us now look at the pathological situation. In my prospective study, there were 16 incidents. Let us look at some of the results. Here is an incident with a Terumo SX25. The purple line is the normal baseline. The terumo SX25 has a normal pressure drop of about 17 mm Hg per litre flow. I went on bypass and at 5 minutes the pressure gradient was normal but rose rapidly over the next 10 minutes to a gradient of 35 mm Hg per litre flow. It stayed there for about 30 minutes and then gradually returned to the baseline. Oxygen transfer was compromised but was managed by increasing FiO2. Prebypass platelets were 235. This dropped to 44 at 20 minutes but had returned to 133 by 80 minutes. One big advantage of this method of describing raised pressure gradients is that it can accurately describe and define an event. The eight hospitals involved in this study actually reported on 20 events, but four were shown by using this analysis to not actually have happened. One was a mini event where the gradient rose by only fifty per cent, one was a high flow problem and two were falsely reported but appeared to be cannulation problems.

21 Here is another example using the Cobe Duo
Here is another example using the Cobe Duo. The pattern is repeated, the main difference is that the baseline pressure gradient is about 32 mm Hg per litre flow and the peak pressure gradient reached about 75 mm Hg per litre flow

22 And again another event this time with the Quantum oxygenator
And again another event this time with the Quantum oxygenator. Let us term this Type 1 gradient. Just over half of the events followed this pattern. Because the trans oxygenator gradient starts of normal on going on bypass, it suggests that the initiating factor is something to do with the perfusion circuit or the perfusion technique. Blomback in 1995 suggested that the initiating factor was a temperature unstable form of fibrinogen termed cryofibrinogen. That precipitated onto the heat exchanger whilst cooling immediately upon going on bypass. The pattern shown here would be supportive of this theory or some similar type of initiating factor. Unfortunately there were many cases that arose that did not fit this theory and so workers have been looking at other factors on the assumption that the phenomena of raised trans- oxygenator pressure gradient is a singular event. But let us look at further analysis of the problem.

23 However almost half of the incidents presented with a different pattern. Here is an event with the Sorin Monolyth Pro. The baseline measurement was about 12 mm Hg per litre flow and the peak gradient achieved was 52 mm Hg per litre flow. However the important difference here is that this peak gradient occurred immediately on going on bypass. In other words in this event the thombotic cascade had already started pre bypass whereas in the previous three instances it did not start happening until we had gone on bypass. Let us define this as Type 2 gradient. In other words the initiating factor occurred either during anaesthesia or the surgical preparation before going on bypass but not when going on bypass. There must be a second method for activating platelets and or fibrinogen that also results in white clot formation and this would explain why Blombacks theory does not hold universally

24 Here is another example of Type 2, this time with a Cobe Duo.

25 And finally here is the third type of pattern
And finally here is the third type of pattern. Here, like Type 2, immediately upon going on bypass the pressure gradient was raised. However, as you can see it never really got back to the baseline but remained high during the entire case. Now it is possible that this is just a monitoring problem. However if it is a true recording then this is not showing the development of reversible white clot but the formation of a longer lasting thrombus. I would suggest that this could be due to clots in the oxygenator possibly as a result of suction of unheparinised blood or due to cannulation before heparin has taken effect. The ACT’s were always above 480 seconds. As a sort of substantiation of this theory, this was only incident in my study to show this pattern which gives it an incidence of one in 3,800 cases - an incidence very close to that of clotted of oxygenators as discussed previously

26 Let us look at some of the other factors that we have to take into account.
Here is another incident with a Bard Quantum. The gradient started off relatively normal but rose very rapidly and the perfusionist was forced to make an emergency changeout. I am sure you will appreciate that during this time there were more important things to do than take records - hence the relative paucity of results shown here. What however this does show is that when the new oxygenator is used it acts perfectly normal. This means that either a sequence of events maybe such as the degree of dilution is not occurring or the initiating factor has been cleared from the blood which means that limited amounts of it can only have been present and it has not been remanufactured.

27 INCIDENCE by HOSPITAL Hospital 1 2 3 4 5 6 7 8
No. cases No incidents No. of cases per incidence Another factor to consider. My prospective survey involved eight hospitals. As this slide shows, they all had a different incidence of the event, with the commonest occurrence here in hospital 7 where it happened once in every 44 cases and the rarest here in hospital 3 where it happened once in 982 cases. Although these numbers are relatively small, a Yates corrected Chi squared test showed that there was a probability of less than that there is a difference in incidence between different hospitals.This fact has also been noticed by other workers. In other words there is something that is done differently in different hospitals up to the moment of going on bypass that is involved in the triggering process. This could be patient pre-treatment, anaesthetic technique or perfusion set up technique. What is extremely important about this result is that it cannot be a purely patient related event, otherwise there would be much less, if any, variation between units

Oxygenator No. Used No.Incidents Terumo SX Terumo SX Medos Hilite Affinity Sorin Monolyth Cobe Duo Cobe Optima Dideco Avant Bard Quantum Gish Vision Of these I believe that most perfusionists blame the oxygenator. For example, Wahba found a difference between coated and uncoated oxygenators and Palanzo found a relationship with the selection of the material used in the heat exchanger. Because the event results in the activation of either platelets or fibrinogen, if a device contains a surface to which these will preferentially stick to, then one probably should expect to see a higher incidence in that device. In my study I looked at the incidence per oxygenator but statistical analysis showed that there was no difference between any of the oxygenators except that the Cobe duo was worse than all the others and the Avante was better than the others. This however is not really conclusive as the numbers are quite small and these few differences may be due to pure luck in that these devices just happened to be used in hospitals were the local risk factors were either higher or lower. Other reports have also stated that the event happens in all makes of oxygenator. The Cobe Duo was used by three hospitals in the trial and the Quantum oxygenator was used by a different three centres. There was a highly significant probability that there was a different incidence rate between the hospitals using the same oxygenator. This again suggests that the specific brand of oxygenator may not necessarily be an important factor. It would need a much larger survey than this one to substantiate the involvement of the oxygenator.

29 Raised Trans-Oxygenator Pressure Gradient can only be seen if it is monitored
Greater awareness of the problem results in more monitoring If monitoring is not done then the problem presents as a “Failed Oxygenator” And here is the final factor that needs to be taken into account. In order to know that there is a raised pressure gradient, it is necessary to measure it. This was very rarely done in the early nineties when perfusionists first started realising that something may be going wrong. As information about this problem has increased, more perfusionists are monitoring for it. However if it is not monitored, the only indication that anything has happened is that one gets a failed oxygenator. So let us look again at the incidence of failed oxygenators

30 FAILED OXYGENATORS INCIDENCE YEAR Stoney 1 in 3,022 cases 1979
Wheeldon , Kurusz , Mejak , Here is the chart I showed you earlier but with the addition of the dates when the survey was done. As you can see the reported incidence of failed oxygenators has not changed much since reporting began. But what kind of oxygenator were they reporting on. Stoney and Wheeldon reported purely on bubble oxygenators, Kurusz had a split between bubble and membrane oxygenators and Mejak reported purely on membrane oxygenators. So the reported incidence of a failed bubble oxygenator is about the same as that for a membrane oxygenator. This prompted me to ask a question that does not really appear to have been asked before and that is how could a bubble oxygenator fail. The first answer is that the sparger holes could get blocked off. In reflection an unlikely event but given the simplicity of bubble oxygenators, it appears to be the only one. But here is a suggestion. Towards the end of the bubble oxygenator era, the mechanism of how the devices worked became better understood. One important consideration was that a substantial part of the gas exchange took place in the defoamer. This was used by Bentley who brought out the Bentley 10 plus bubble oxygenator

31 This had a device fitted into the oxygen delivery system whereby gas could be distributed between the sparger and the defoamer and thus separately control oxygen and carbon dioxide exchange. If there was a platelet-fibrin production as we see today, it would have been trapped by the defoamer and reduce its ability to be an oxygenator - hence the device would be seen to fail. Unfortunately there is no way nowadays to test this hypothesis - however if it is true and unless someone in the audience can suggest a third common cause of a bubble oxygenator failing, I would suggest that this indeed happened, then the basic initiating events resulting in raised trans-oxygenator pressure gradients have always been with us. This further suggests that it is not, as has been suggested, a basic problem of low prime membrane oxygenators.

32 SUMMARY Happens immediately upon going on bypass Eventually disappears
Does not recur upon emergency changeout Incidence varies between different units At least two different possibly unrelated initiating factors These factors may always have been present If we are to find the initiating factors then they must fit the pattern of events. A mini summary may help us at this time. READ SLIDE What initiating factors can fit this pattern. At present no one knows, although the fact that there is at least two different and possibly independent factors which has not known until today may help in the search. For example Blomback produced a very compelling argument suggesting cryofibrinogen as the initiating factor. Because it did not fit the pattern in many cases, and this work shows why, workers have looked elsewhere. However it is quite possible that this is the underlying cause in my Type 1 blockages. Further work will be needed to confirm this and also to find the initiating factor for Type 2. So let me finish by summarising the incidence and predisposing factors of oxygenator failure which result in emergency changeout

33 CONCLUSION Oxygenators may need emergency replacing due to mechanical failures A rare event - maybe 1 in 20,000 cases This can only be improved by better quality control by the manufacturers READ SLIDE

34 CONCLUSION Oxygenators may need emergency replacing due to clotting problems Incidence 1 in 3,000 cases This problem needs to be addressed by improving anticoagulation monitoring READ SLIDE + Although the problem of why the incidence of clotted of oxygenators has not decreased needs to be addressed

35 CONCLUSION Oxygenators may need emergency replacing due to a fibrin - platelet thrombus which may be demonstrated by a raised trans-oxygenator pressure gradient. Incidence 1 in 1,000 cases This problem may always have been with us, and needs to be addressed by continuing research into its aetiology.

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