welcome to the world shared practice forum.i'm dr. jeff burns, chief of critical care at boston children's hospital and harvardmedical school. we're very pleased to have with us today dr. jacques lacroix. dr. lacroixis professor of pediatrics at the university of montreal and he is also on the facultyfor pediatric critical care medicine at the hospital st. justine in montreal, canada.jacques, welcome to the world shared practice forum. and on behalf of my colleagues aroundthe world, we acknowledge the wonderful research that you've done for decades now on transfusionmedicine. and we also know that you've developed a research interest in multiple organ dysfunctionsyndrome. what is multiple organ dysfunction syndrome?
well the concept of multiple organ dysfunction,or mod, if you want, appeared 40 years ago in 1975. and the idea was just because dr.baue and colleagues found in their surgical patients that some patients developed moreand more organ dysfunctions, and that something was happening that was not only an additionof organ dysfunction, but something was going on. over the years, by the way, many nameshave been used use for to describe multiple organ dysfunction syndrome, like multipleorgan failure or even hypermetabolism failure complex and other names. but presently, ithink there is a consensus to keep and use the name multiple organ dysfunction syndrome. so what it is, the definition presently ofmods is quite simple. there is a mods in critically
ill patients if we observe at the same timedysfunction of two organs, and up to seven organs are considered. there are a few listsof diagnostic criteria, we'll talk about that in a minute. but we are looking at respiratory,cardiovascular, neurological, hematological, renal, hepatic, and, in one case, gastrointestinal.i think the most important job was done first by dr. wilkinson in 1986, because they werethe people who suggest some criteria for pediatric multiple organ dysfunction syndrome. but tensyears later we felt that we must a little bit adapt that, so my colleague, francoisproulx, suggests a new list. and in 2005, dr. goldstein, in symposium onsepsis and mods brought up a new list of diagnostic criteria. so presently we have many listsof diagnostic criteria, and we'll discuss
a bit later about the problem that can happenwith those different lists. so i said to you mods is not the only addition of organ systemdysfunction, and it is characterized in typical mods, well-blown mods, you will find highblood levels of both pro- and anti-inflammatory agents. which is strange, because usuallyin normal inflammation first you have a release of pro-inflammatory for a while. the anti-inflammatorycomes in, stops the release of pro, and the inflammation stops this way. but in mods, something happens that is wrong,and you will see at the same time very high levels of pro- and anti-inflammatory mediators.there are many other characteristics also that we can see in those patients. i willtalk about physiopathogy a little later on.
so if we look at mods, mods is indeed characterizedby a consistent group of organ system and dysfunction. it is common in the icu, it'sat least 20% of all patients. the mechanism is not clearly delineated, but we know, asi told you, that there is a common denominator which is an uncontrolled inflammatory process.some people talk about an inflammatory storm. many conditions can cause mods. an infectioncan cause mods, and then we call that a sepsis. a trauma, hypoxia, shock, even intoxicationcan cause mods. and by the way, mods is closely associated with mortality. so it fills upvery well the criteria for syndrome. we'd like to stop now and ask our colleaguesaround the world a question. in your answer, could you first please state your city andcountry location? and the question is this--
in your pediatric intensive care unit, whatis the common inciting process that triggers multiple organ dysfunction syndrome? for example,infection, trauma, or unknown causes? we're back now with dr. jacques lacroix. so maybe i can talk a little bit about therelationship between mods and sepsis, because for some people it's different, and i believethat sepsis is just a specific type of mods. it is mods caused by an infection. so beforewe talk about that, we have to talk a little bit about the systemic inflammatory responsesyndromes. by the way, some people believe this is not a syndrome at all, but at leastit brings the idea that some of our patients, at least in the icu have a severe or inflammatoryresponse. and some criteria have been suggested
to diagnose sirs. i will not go through allthese criteria, but one is about temperature, about respiratory rate, about leukocyte count,and heart rate, too. but they are not very specific. the point is that a sepsis is asystemic inflammatory response syndrome with an infection. that's why we have to talk abit about sirs. a severe sepsis is a sepsis with a cardiovasculardysfunction and acute respiratory distress syndrome, or two or more organ dysfunction.in a septic shock it is a sepsis with a shock. that's it. now on that figure there, the firststep in the figure showed the relationship between sirs, systemic inflammatory responsesyndrome, multiple organ dysfunction syndromes, and death. well, with sepsis what happenedis that the sirs is caused by infection, and
we immediately name that a sepsis. if it issevere enough, severe sepsis, and if there is a shock, septic shock. all these conditions--i call that these septic states-- can develop to become a mods. and by the way, septic shockis a mods. but i really want to repeat that a significantproportion of multiple organ dysfunction syndrome are caused by non-infectious insult. and clinically,mods caused by an infection or not caused by an infection are absolutely similar. youcan not make the difference. well, most of the time. you know, if you get a purpura fulminans,it's obvious that there is an infection behind that. or a congenital deficiency of proteinc. but that's it. but in most instances, you cannot, when the patient gets in the icu,you will not be able to make the difference
between a multiple organ dysfunction syndromecaused by an infection or not. maybe this is why in many randomized controlledtrials on sepsis, at the end, they were not able to find an infection in most instances.and probably these randomized controlled trials were more about mods than about sepsis. butthat's a hypothesis that i bring up. to give you an idea of the importance of theproblems, there is not too much data on the epidemiology of sepsis states and mods. andby the way, i hope that there will be more in the forthcoming years. but 20 years agoat st. justine, we followed our patients, all consecutive patients, over one year. andwe report that 23% of those patients got sepsis or have sepsis when they get in. 4% severesepsis, 2% septic shock. and in those years,
18% have mods. and if you look in the literature,presently, the incidence rate of mods in the icu patients range most of the time between11% and 25%. in some papers it goes even higher than that. but the usual range of betweenis between 11% and 25%. so it is frequent and all of us observe that quite frequently. i'd like to stop now and ask our colleaguesaround the world a question. the question is this-- in your pediatric intensive careunit, approximately what percentage of your patients have the diagnosis of multiple organdysfunction syndrome? we're back now with dr. jacques lacroix. welljacques, it's one of those syndromes that i know all the intensives around the worldare thinking i know it when i see it, and
yet it's hard to articulate how to diagnoseit. how does one diagnose it? well, with mods presently, as i told you,the definition of mods, there is mods if you observe at least two organ dysfunctions atthe same time in patients. and we considered a list of up to seven organ dysfunctions.presently the lists that are used to diagnose mods are the list suggested by dr. proulxin 1996 and a list published by dr. goldstein in 2005. and one other problems is that thoselists are not similar. and because they are not similar, it brings out different epidemiologies.among the caveats and pitfalls about those two lists, or those two sets of diagnosticcriteria of mods, is that at least in one set, they just did not take into account age.so immunoglobulin levels change with age.
white blood cells counts are-- the normalrange is not the same in the first days of life than they are in adolescence. same thing for creatinine. and also anotherproblem is that there is a significant difference in the criteria listed in the two differentset of diagnostic criteria. i'm not saying one is better than the other, i'm just sayingthey are different. and that can be a problem. to give you an example, i just compare onthat side the criteria of goldstein for cardiovascular dysfunction and the criteria by proulx andby wilkinson, before that. and you'll see they are quite different. with goldstein itstarts with one question-- did the patient receive a bolus of at least 40 millilitersper kilogram in the last hour? and if so,
then we're looking to different criteria.while with proulx, nobody was looking for a bolus of liquids. so what is better? i don'tknow, but there is a significant difference. so just to see what is this difference, westarted a prospective study in 2009 at st. justine hospital over a year. and we did thatover a year to be sure that there was no seasonal bias. and at the end you can see on that slidethe difference in the prevalence at picu entry of mods. with criteria, the diagnosis, bythe way, were done by an adjudicating committee. and with proulx diagnosed mods at entry inabout 15% of patients, while in goldstein it was about 30%. and we look also at whathappens thereafter, and if we add the mods present at entry and the incident mods withproulx it was at 21% and with goldstein 37%.
so a huge difference in the incidence ratewhen we use those two different lists. so we go further and ask the question didthese two sets of diagnostic criteria diagnose mods in the same patients? because maybe it'snot the case, so we look at that. again, two adjudicators did that without knowing theywere independent, and what did they find? well first if we look at mods at picu entry,the concordance was 81%, which is good. but we also look at the kappa score. the kappascore tells you if the concordance was statistically different than others can bring out. and thekappa score was 0.49, which is moderate. it's not huge. it's not too bad, but it's not sogood. we also look at new mods, the mods that appear after the patients get in the icu.
again, while a greater concordance, it was93%, but the kappa score is still 0.5. so altogether, we have quite good concordance,quite good, a moderate kappa score, but it's far from perfect. so we look at the differentorgan dysfunction in the same study trying to find why this happens. and on this slideyou can see what we found with the different organ dysfunction. and immediately you cansee that most of the discrepancy came from the cardiovascular system, because when welooked just at cardiovascular systems the concordance looks great, 86%. but the kappascore was 0.17, very low. and quite the same thing with the neurological system. quitegood concordance. 67% is not so bad, but the kappa score is 0.34. again, very low.
so again, i'm not saying that one list isbetter than the other, but this shows that these two lists are not looking at the samepatients. so, take home message about mods diagnosis. the two sets of diagnostic criteriathat i was talking about are not interchangeable and can mislead readers on the epidemiologyof mods. to give you an example, if you look on papers that use goldstein's criteria andpapers that look on proulx's criteria, it will tell you that there are more mods inthe last years than the '90s, but probably the difference is just because we use differentdiagnostic criteria. another lesson, i think, is that the diagnostic criteria of mods shouldbe revisited, at least some of the criteria that we are using presently.
and also another lesson is that one cannotchange that diagnostic criteria for diseases or syndromes like mods without changing itsepidemiology and its capacity to describe or to predict outcomes. so in papers frequentlywe read that people use lists of diagnostic criteria, but they are modified lists. wellit means that you cannot compare that modified list with the list we have before becausethey have modified the list. so modifying a list has an impact on the epidemiology andon the capacity to describe outcomes again. i'd like to stop now and ask our colleaguesaround the world a question. in your answer, what criteria do you use to diagnose multipleorgan dysfunction syndrome? we're back now with dr. jacques lacroix. sojacques, i can't help but wonder, in your
practice at the hospital justine in montreal,which criteria do you use? at the bedside. we use the goldstein criteriapresently. but when i'm doing research i use both, because frequently when i want to comparesome data with study that used the criteria of proulx, i want to be able to use the criteriaof proulx. to give you an example, with some of the studies i have done in transfusionmedicine the criteria of goldstein were not available. so if i want to be able to understandthe result of some of my study, i have to use a criteria of proulx. so what i'm suggestingto people-- you can do what you want, but if you do research and compare it to somethingthat uses criteria of proulx, you have to use it again.
same thing-- you know it's true for the prismscore also. if you want to compare a study where they use the old prism score you needto get data for the prism score, too. what is the pathophysiology of multiple organdysfunction syndrome? they're saying that we don't know what startsmods, but once mods is well-organized, in full blown mods, it is quite clear what clearwhat's going on. at least 20 years ago, michael pinsky wrote that severe sepsis and mods,and i quote, "can be thought of as the endocrine expression of cytokine effects because itrequires a systemic response for signals that normally function on and autocrine or paracrinelevel." to give you an example, if you have a small injury on the skin, there will besome tumor necrosis factors that will reproduce
some interleukins, et cetera. but it willremain there. if it is a huge infection, it will expandall over the body and then you can get a multiple organ dysfunction syndrome. another example,another data that we know that is important, if you inject tumor necrosis factors, whichis not infectious at all, it's a cytokine. it's one of the first cytokine in the inflammatorycascade. well if you inject the tnf you will get it in the animal-- because we inject animals--a septic state that will look exactly as a sepsis, but it's not a sepsis. and if youwould inject enough tnf you'll get a mods, a multiple organs dysfunction syndrome. anotherpoint that i want to raise again is that no infection is found even by autopsy in morethan 50% of cases of severe and inflammatory
response syndrome in our patients even ifthe patient's present the clinical hallmark of septic state. so what i'm saying, again, is what differentiatessepsis and mods, or severe sepsis and mods is really that there is an infection in sepsis,but actually how to differentiate that at the bedside is not so obvious. in mods i toldyou that what is chatacteristic of severe mods is there is at the same time a lot ofpro-inflammatory and anti-inflammatory mediators. and by, a lot i mean sometimes the level,the blood level are huge. and another thing that is lost in well blown mods is that thepro- and anti-inflammatory retroaction system is not working well. we observe at the sametime both high and low, pro- and anti-inflammatory
mediators. and if these levels are high enough,at least in kids, we know that it predicts mortality. so there is a link there. what can cause these inflammatory storms?it can be a severe infection or it can be multiple little insults. let's talk aboutthe big insults like purpura fulminans. when we have a big insult, a big hit like thatit, the aggression can be severe enough to prime cells, first like macrophage, endothelialcells, leukocytes. and then if the aggression is really severe, a mods will result. andwe know that, for example, with purpura fulminans, again, in this case, when it is there andthat's enough. but something strange happens in our patients in the icu. sometimes theyget with, for example, just an asthma crisis,
and that's it. there is no organ dysfunctionat all. and then they get something else, a little hint. they get a little nosocomialinfection, something that in normal people will not bring out any problems. but in our patients sometimes it's enoughto trigger a mods. and beyond that is the two hits or multiple hits theory. i told youthat once there is an insult in critically ill patients, our inflammatory cells are primed.it doesn't mean they are activated, they are prime. but if a small or a trivial insultcomes in at the wrong time, it can cause an overreaction of these cells and then you getthe mods. so again, in mods there is a huge amount of inflammatory mediators, and theretro-control system is not working at all.
it's not all. we also observe disturbed apoptosisin patients with mods. and what's the link with the inflammatory process is not so clear. but we know, for example, that tumor necrosisfactors interleukin-1 or -6 retard apoptosis in white blood cells and macrophage. so maybethere is something there also. but again, something that is normal behaves in a waythat is not normal in patients with mods. so to summarize what i have said, at the molecularlevels we observe high blood levels of a lot of inflammatory bioreactive agents. at thecellular levels, i did not talk about mitochondrial dysfunction because i can talk about thatfor a long time, but in full blown mods there is a mitochondrial dysfunction. in severesepsis it's always there, and this translates
with problems with lactic acidosis if theinfection is severe enough, and it results in a cellular energetic crisis. and maybe what we observe in mods starts inthe mitochondria. maybe. that's a hypothesis. at the organ system levels, as i told you,there is a problem in the interaction within systems and between systems. for example,in full blown mods we lose a normal variability in systems like the inflammatory systems,neural controls, the respiratory system, the cardiovascular system, and even the endocrinologicalsystems. and, as i told you, there is simultaneous dysfunction of many organ dysfunctions. jacques, are there unrecognized complicationsof mods that we're not appreciating in the
intensive care unit? there are a few that are not as well-recognizedas i would like. to give you an example, tamof, for thrombocytopenia-associated multiple organfailure has been described by joel carcillo and his team in pittsburgh. tamof is a specifictype of mods. it's a mods with low platelet counts and more than three organ failures.in a small study but well done study, they followed prospectively 37 consecutive picupatients with at least two organ dysfunctions. 28 or, if you want, 76% of those patientshad tamof, and all 7 patients who die had tamof. so tamof maybe is important, at leastin that subgroup of patients. with patients with tamof, we found von willebrandfactors, rich macrovascular thromboses, and
those children with tamof had decreased adamts-13activities. and again, the team in pittsburgh shows that intensive plasma exchange in thosepatients with tamof replenish adamts-13 activity and is associated with organ failure recoveryif we succeed to replenish adamts-13. so maybe in that type of patient there is somethingthere that we can do which is plasma exchange. another example of what is missed frequentlyis capillary leak syndrome. all of us see that our patient with mods has edema everywhere.but sometimes people miss the point that this edema is really caused by a capillary leak. and why is there any capillary leak like that?well, we know that some cytokines like bradykinin, some leukotrienes, platelet-aggregating factors,widen a space between endothelial cells. and
other cytokines like tumor necrosis factor,interleukin-1, and again, platelet-aggregating factors just are able to cause a destructionof the endothelial cells. so this opens the way for big molecules like albumin, it getsout from the blood vessels, and it brings with them water. which explains that we havehyproteinemia, low blood oncotic pressure, and proteinuria. and there are problems that are caused bycapillary syndrome. it can cause lung edema. another example of complication is reactivehemophagocytic syndrome. reactive hemophagocytic syndromes can cause a lot of things. it causeslow platelet counts, leukopenia, thus some immunosupressions, sometimes severe anemia.the diagnosis of hemophagocytic syndrome is
quite straightforward. again, the best wayto get the diagnosis is to do a medullary puncture. and you can see on the figure thatis on the slides an example of that. there is a huge histiocyte, and within the hisitiocyteat the same time as you'll see red cells and a macrophage, which is quite specific. the consequence of that syndrome is that moretransfusion may be required. these patients get a lot of infection and they can developdic and some significant bleeding. but if you see that, don't stop treating these patients.they can cure completely. and they don't need any of those drugs they use on the oncologyunits, by the way. another example that i think people know alittle better, but not as well as i will dream
of, is the critical illness, polyneuropathyand myopathy. in adults, we know what the incidence rate is great. for example, thereare people showing that in adults who stay in the icu more than five days, the incidencerate of neuropathy and/or myopathy is 26%. in kids we have no data, but we know thereare cases. i've seen a lot of those cases. there are some risk markers or risk factorsof this polymyoneuropthy. they are observed in very severe cases. if patients are on vasopressorsduring more than three days they have a good chance to get that. probably, again, becauseof the severity of illness. if there is a bacterium or if you need renal replacements,if you use neuromuscular blockade for a long time, you increase the risk of this. as wellas if you use benzodiazepine or steroids for
a long time you increase the risk to contractneuropathy or neopathy. what are the clinical indicators? well, for the neuropathy it'ssimple. you have no deep tendon reflex or they are sluggish. if you have a myopathy,and remember, you can get just the neuropathy, you can get the myopathy alone, or both. and by the way, in my experience with patients,with cardiac surgery patients, i've seen a lot more myopathy than neuropathy. and thatmyopathy can be seen because they were unable to raise their arm over the bed. and that'sa great sign of proximal muscular weakness. and this is what is typical about that myopathy.it attains the proximal muscles. how can we make the diagnosis? well, for the neuropathy,sometimes just with the reflex, it's enough.
but you can do also an electromyography ora neuromusuclar biopsy. but we do that rarely. if you are talking about myopathy, otherwisein the clinics you can make a biopsy, too. what are the consequences? the most frequentconsequence is a difficult weaning from the ventilator. if the myopathy is there, youlose your accessory respiratory muscles. so you can have problems-- to wean those patientsfrom the respirator. and other problems is severe post-ic weakness. in adults, it canremain for years. in kids, we don't know. i have followed a few patients and it canbe there at least for a few months. and i believe there is something that maybe we cando there. presently the treatment is symptomatic, but some people believe that we can decreasethe severity of those neuropathies or myopathies
by starting physical exercise soon in theicu. so i am aware of a few trials that are coming just looking at that, and we'll seewhat happens. but i believe that we must do some study onthe epidemiology of this critical illness neuropathy and myopathy. so another lessercomplication that is frequently ignored is the endocrinological system. for example,the sick euthyroid syndrome that was not popular but a lot of people talked about it, in the'80s actually is a problem to mods. same thing with the increase with the problem with cortisolsand also with, for example, the pulsatility of growth hormone. all these abnormalitiesare related to what's going on in the epiphysis. another thing that is common is insulin resistance.it's always there if you have some multiple
organ dysfunction syndrome. so jacques, it's a systemic inflammatory responsewith no clear inciting agent. how do we treat this? thank you for that question. my answer will--there will be two parts in my answer. i will speak about what i will name specific treatment,or immunomodulatory approach, or major bullet approach, and nonspecific treatment. by specifici mean single molecule. for example, there is too much tnf or tumor necrosis factors.let's go ahead and give some anti tumor necrosis factors. there is too much interleukin-1,same thing. or, if there is not enough of a bioreactive agent, like activated proteinc, let's give activated protein c. or if in
mods you read a level of antithrombin iiiis very low, let's give antithrombin iii. well at least 40, if not 50, randomized criticaltrials have been done with that approach, that single molecule approach. and billions--not millions-- billions of dollars have been spent on this. and i just put that slide witha list of some of those rcts. and in red are rcts that shows that what we talked will helppatients kill patients. i talked to you about growth hormone, but it was also with tnf alphareceptors. giving that increased the risk of death. same thing with anti-endotoxin,that was a great, great surprise. in black, the results are so and so. we don't know andprobably doesn't work. the only little molecule that merits, i think, to be looked at againis an anti-bactericidal protein inhibitor.
this molecule has been studied. within ourcity that has been published in the lancet, but the trials were too small to get an answer.but it makes sense that this molecule works but this is not a cytokine at all. it's somethingelse. it's not involved in the inflammatory process, so i think that this is why maybeit can work. why magic bullets did not work? i think it is because most inflammatory bioreactiveagents are pleiotropic and redundant. and the definition of pleiotropic is one agentmodulates many effects. so on that slide, mip10 just modulates fever. so it's not pleiotropic,but interleukin-6 and -8 are pleiotropics. the other point is that most of those inflammatoryagents are redundant, which means that one activity is moderated by many agents. andif we had on that picture the list of activities
of tnf alpha in interleukin-1, admittedlyunderstand that if you want to treat only one cytokine like tnf, interleukin-1, wouldjust, i believe it explain at least partly why the one magic bullet approach did notwork, and why probably it will never work. but that's my opinion, i'm not sure aboutthat. that's why i believe that the future is to get better general support. and whati mean by general support is still giving fluids, mechanical ventilation, helping thinkthe patients go through that big illness. nutrition probably also. there are data suggestingthat good nutrition-- not too much, but enough-- can help those patients. what about transfusion? that's my field ofinterest. i'm sure that too much transfusion
is bad for patients. but not enough sometimesis bad, too. and the important question now is to find when we must give a transfusion.you know that i've completed a randomized controlled trial showing that if patientsare stable or stablizied-- hemodynamically stable or stabilized-- they don't need a transfusion.and it's true for cardiac patients, septic patients. for all those patients the resultswere absolutely consistent. if the hemoglobin level is over 7 gram per deciliter, you don'tneed a transfusion. but we don't know about unstable patients at all. for example, incyanotic cardiac patients we don't know also. so there is room there for research. what about plasma exchange? we don't knowunless there is tamof. and even with tamof
we have one small study, so we need more thanthat. what about the immunoglobulins? we don't know. so there is room for nonspecific treatments,there is room for good trials there, i believe and i think. what do we do at st. justine? well yes, weuse ecmo, we use hemofiltration and hemodialysis, but always, for example, to support the kidneyfor extra-renal operations. not to get rid of the cytokines, but this is something maybewe must look at in good trials. we still give a significant-- 30% of our patients stillreceive a transfusion, mostly because they are unstable. but as i told you, i'm not sure it's a goodthing to do. we need to do more research to
know the right answer to that. in summary,how should we treat mods? well, first control the basic disease. if there is an infection,take care of it. if there is a pulmonary emboli, take care of it. if there is a very severesystemic hemolytic syndrome, treat it. also support all the organs. if there is kidneyfailure, obviously, start extra-renal operations. another point that is important is to preventa second hit and avoid all risk factors, for example, of nosocomial infection. so if youcan, don't use paralyzing agents. get rid of invasive mechanical ventilation and assoon as you can. and if you don't need a catheter, whateverthe catheter is, just take out that catheter, because it can cause a second hit. and treataggressively all complication even if it looks
trivial, because it can cause a mods or itcan entertain the mods for a long time. jacques, that's a wonderful overview. whatare the take home messages about multiple organ dysfunction syndrome? well, i have a few. i have many more, butwith respect to that presentation i think one of the first take home messages is thatthe diagnostic criteria of mods can be improved. what we have presently is not useless. ithelps us and we have done great research, but we can improve that. we should look fora better alignment between diagnosis of mods and its pathophysiology. to give you an example,it means that we must understand in a better way what's going on, at least when it starts.when it's there we understand it quite well,
but when it starts we don't know exactly what'sgoing on there. hopefully we'll get better diagnostic criteriathat will help us to have better predictive value. presently, as i tell you with a differentset of diagnostic criteria, the predictive value is very different. another take homemessage is that those new criteria must be validated. another message will be many newtechnologies, and by technology i mean all tests or that maybe we can use, our candidateto describe the severity and to monitor the progression of cases of mods. like, for example,heart and respiratory variability or the progression of some biomarkers or cytokine levels. i believewe need those things in order to follow our patients better than we are presently. butwe have to do research just on that to see
what are the best tests or technologies thatwe can use to follow our patients. also, another take home message-- mods iscommon. it's always over 10%. it can be up to 25% and even 40% in some units. anothermessage-- many kinds of triggering events can cause mods, trauma, extensive surgery,hypoxia, intoxication, like monoxide, carbon intoxication. drowning and obviously infectioncan cause a mods. remember also that the death rate of picu patients with mods is very high,it's between 36% and 54%, so we can do better, i think. and the last take home message isthat treatment is mostly supportive with aggressive prevention. so beware of second hits as wellas you can. well dr. jacques lacroix, thank you for thiswonderful talk about multiple organ dysfunction
syndrome. and, as i said earlier, on behalfof our colleagues around the world, thank you for all of the research that you've doneon transfusion related injuries. thank you.
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