The following program was recorded during the 1972 seminar on surgical and orthopedic aspects of trauma as presented by Brooke General Hospital. In cooperation with the University of texas Medical school at SAn Antonio Brooke Army Medical Center presents the United States Army Medical Department continuing education program, post traumatic pulmonary insufficiency. A current review with richard W. Virgilio, Lieutenant commander, Medical corps U.S Naval Hospital san Diego California. Thank you. Doctor Colonel George as dr Baxter very vividly demonstrated us on the first day of this meeting with our present aggressive attitude towards the treatment of the traumatic patient. When he arrives in the emergency room, we are able to successfully initially resuscitate most of these patients that arrive in the emergency room after an episode of low flow state were shocked as a result of this, we're seeing an increasing number of patients who develop progressive pulmonary insufficiency following an episode of low flow state or shock. In our institution alone. Approximately 50% of the adult deaths in the surgical intensive care unit following an episode of trauma being by a transgenic or otherwise go on and develop progressive pulmonary insufficiency. The pulmonary insufficiency that we see after blunt chest trauma can readily be explained on the basis of lung contusion and our ad Alexis. It's usually well treated successfully treated with a respirator and respiratory support until the contusion clears the pulmonary insult that develops after non thoracic trauma, however, has essentially the same path a physiologic picture as that scene after chest trauma. However, the ideology is very obscure the treatment much less precise and the outcome very dismal. Let's take now a closer look at this syndrome that's plaguing those of us who have to take care of the traumatic patient uh all over this country. We have the house lights out, please. Okay. The hypoxia can occur obviously, together with hypercar bia or with hipAA car bia. It's not the syndrome that we see in the chronic longer who has hypercar beyond hypoxia or the postoperative patient who we can't get to wake up because he's been to market ties or hasn't fully recovered from his an STD yet. These patients have hypoxia but they also have elevated PCO two. They obviously need to be ventilated. This group of patients that I'm particularly talking about today have hipAA car B. A. In other words, they're ventilating to the fullest their PC. O two's. These are the average PC O two's on about 20 patients who have post traumatic pulmonary insufficiency during the 1st 48 hours and as you can see, the mean is somewhat less than 30. Obviously, they're ventilating at the same time. They're very hypoxic. Their P. O. Two's are averaging around 50. This is on room air. So we have to say that they are ventilating, however, they're not able to oxygen name. There's only one circumstance or set of circumstances in the lung that can cause this particular syndrome and that's demonstrated by this slide here. This is a open available here. This is one that's collapsed. The venus blood comes into this one goes through, gets oxygenated and leaves almost fully oxygenated. However, if we now perf use this lower Avila's that's collapsed, it's not gonna be able to oxygenate and in turn it's gonna leave with the same venus P. 02 as it had when it arrived there. Thus we're gonna get venus admixture over on this end over here and this is essentially the set of circumstances that we see in the lung of patients who have present with hypoxia and with a low PCO two. There is some sort of intra pulmonary shunting going on. And as I go on with the talk we'll talk more about shunning. And this is essentially what we're talking about. When we talk about villa arterial oxygen gradients, we're talking about the gradient between the oxygen and the surveillance and the arterial blood that we're able to measure the syndrome of post traumatic pulmonary insufficiency can really be broken down into four phases. As I said before, Phase One is associated with the initial trauma episode patient whether it's a perforated ulcer or leading officer or ruptured aneurysm or an automobile accident. The initial injury is usually followed uh today with rather aggressive resuscitation and the patient seems to do rather well when the patient arrives uh he's usually not hypoxic one room air. However he is hyperventilating going off of C. 02 and has a modern amount of alcohol. Oh sis initially upon his arrival. He might have been a psychotic. But once his low flow state is corrected and he is again refusing his periphery he sort of washes out his lactic acidosis. And this is followed uh by a mild alkali Asus at this point the majority of it being respiratory al kalo sis as I said is predominantly respond to it. But you got to remember in these patients they usually all have an N. G. Tube. They've usually all been had multiple transfusions. And between these three things between the hyperventilation the metabolism of the citrate by the liver to bicarbonate and also the withdrawal of gastric juice. These three things are usually the things that uh are they responsible for the patients al colossus following the resuscitation of the patient. He's back in the recovery room in the intensive care unit. There are several things that would lead us to believe that this patient was going to go on to do. Well. Obviously if he's able to maintain his secretary homeostasis if he's able to return to his urinary output and the C. V. P. Uh he's able to maintain in other words he's got cardiovascular stabilization and if he has normal P. 02 on room air this is rather significant. And I think the cynic winona this syndrome is hypoxia on room air in the face of hipaa. Car bia and at this point if he's able to maintain an arterial PCO two of 80 or above on room air, it's rather good outlook. Mhm. Unfortunately uh a lot of these patients, a very large percentage of them continue to be hypoxic on room air. And this is something we miss because when we bring the patient back to the recovery room, we sometimes and usually do have them supplemented with some oxygen and we don't realize what this patient can do in his room air. And usually they are hypoxic and again in the face of hyperventilation. In other words, the PCO two is down, patient will then slip into phase two and this is characterized by secretary stabilization. As I said, they have usually early respiratory problems. Um And this is diagnosed again, they're very subtle changes. The patient's hyperventilating PCO two is 20 and his P. O. To maybe a little hypoxic. This is very suggestive that the patient is gonna go on to develop further trouble at this point. He does have early physiologic showing if we measured it, uh We would find that approximately 10 to 15, maybe 20% of his cardiac output was being shunted around collapsed. Avila's just like I showed on that previous slot. Uh He's got a gradient. Uh villa terra oxygen gradients somewhere around 200 to 300. And he has definite evidence that something is going on in his lungs although at this time he might appear fairly stable. He goes on to Phase three which is really advancing pulmonary insufficiency at this time. His inter pulmonary showing is increasing his review. Our oxygen gradients are increasing his compliance is decreasing. He's obviously a pulmonary problem at this point at this point. If he hadn't been intubated before, he usually is intubated and he's got. Now for the first time, we're seeing increasing acidosis. Originally when he came in, he was a tad as idiotic but this was successfully reversed. At this point, however, the low flow state begins to come back. He begins to have the lactic acidosis. In addition to that, he begins to be difficult to mentally for the first time we're beginning to see increasing shunt and also some hypercar bia. If we take the patient off the respirator, he no longer has hypoxia associated with hipAA carbon. He now has hypoxia associated with hypercar via. Some people feel that when the hypercar bia presents us a picture that the damage in the lung is irreversible at that point. If the patient does not go through phase three and begin to reverse the pathological changes that are occurring, He entered stage four, which is really terminal hypoxia, we are no longer able to ventilate this patient even with 100% oxygen. Uh his P. 02 is 100% as you'll see in a few minutes, sometimes 40 and 50. He's shunning about 50 to 60% of his cardiac output through his lungs without having the benefit of being oxygenated. He's hypercar vic in spite of our newest and best respirators were no longer unable to finally him and then he dies in terminal hypoxia. Uh They system, let's now take a look at a typical course of a patient. And again, we're looking at the patient's uh pulmonary shunt fraction down here. We're looking at his ph PCO two and eight A gradients up here. And as you can see during phase one, he's got a fairly normal response to 100% oxygen having a P. 025 or 600. Again down here, he's hipaa car vic. And down here has shown fractions fairly normal. And as you can see as we progress from stage one to phase four things start to happen. His response to 100% oxygen, which is probably the single best test. If you don't have a cell sophisticated means of monitoring patients and calculating shunts, just turn them up to 100% oxygen as a days ago, woman. And you can see as he progresses through to phase four his response lessons again, initially he is al Kalanick over here and as we go on, he becomes acid attic Initially as Hipaa Karmic and eventually were unable to ventilate him down here. His pulmonary showing which is initially well less than 20% gradually comes down over here to over 60%. Can we have the house lights off these X rays. I think they'll probably project better. Please let's just go through a couple quick clinical cases to show you the depth and the rapidity uh with which this syndrome can hit this patient was a 56 year old gentleman who arrived in the emergency room following which he had a cardiac arrest. He was successfully resuscitated. The ideology of the arrest appeared to be an electrolyte imbalance to doing an appropriate A. D. H. Response needless to say he was brought up the intensive care unit. And at this point this was his initial chest X ray and fairly normal for a man of his age. And really it was no problem ventilating. He was on a ventilator because of his arrest, but he was triggering the ventilator. He was at eight a gradient that was somewhere less than 200 his intra pulmonary showing was not significant. We were able to maintain him on room air with the ventilation here he is 12 hours later and again, nothing startling on the chest X ray. However, at this point we began to have to increase his F. I. 02. And within 48 hours here's the chest X ray not dissimilar to the previous X ray. You saw the patient drown in the old days. I guess this would have been called pneumonia. However, now we know pathologically that their pneumonia is not a very uh strong part of this particular syndrome. At this point we're up against it were no longer able to ventilate him. This happened rather quickly in this gentleman, People would say we drowned the patient. However, if you look at this patient's fluid balance, you'll see that at this point he was kept extremely dry and had a negative fluid balance of about 5000 CCS. Within two days, we were able to get the fluid that they resuscitated him with well off. If you look at the patient's clinical course, you can see that over here with an F. I. 02 or 40% his arterial P. 02 was fine, his eight A gradient was not exceptionally high within 48 hours. With a F. I. 02 80 we were unable to get his P. O. To above 50 and with 100 he didn't respond much better than that. And as you can see his eight A gradient. Let me focus that. As you can see here. His eight A gradient is almost off the scale at this point. And he dies. A Sadat hypercar vic hypoxia. Uh his heart uh unable to tolerate this. If you look just at his Q. S. Q. T. S. And his pulmonary shunting as you can see at this point, he's well over 50%. Some people feel that any intra pulmonary shunt greater than 50% has to be considered a lethal shot again. The patient's response to 100% oxygen as you can see initially very good response down here. He couldn't even get an arterial PCO 200 while getting 100% oxygen. This man was a young 20 year old man who was in an automobile accident, he had a fractured arm and a ruptured spleen. He was successfully resuscitated. He had a splenectomy and he had his arms set. Three weeks later he was sent home on leave. However he returned within 48 hours with high fevers, low blood pressure and chills. It was felt that he had also an epic gastric mass. It was felt that he probably had a uh Sub National abscess. He was successfully resuscitated with fluid steroids. All the things we used to resuscitate person in septic shock And he was taken to surgery. A small sub national abscess was uh drained and the patient did well for approximately 24 hours after that. Here's his X ray. However, really on the night after operation and already you're beginning to see a bilateral fluffy type of infiltrate beginning to manifest itself. However at this point he was not difficult to ventilate and we could maintain a fairly good arterial P. 02 with just 30% F. I. 02. Here he is one full day post operative chest bilateral wipe out the white lung syndrome. The wet lung syndrome. The shock long whatever you wanna call it. But at this point the patient in extreme trouble have to increase our F. I. O. Two's. All the little tricks that we know how to reverse this and two days later again no improvement in his chest X ray. And at that point we were again unable to ventilate him became hyper carbon candace idiotic. If you look at this this patient's course, as you can see over here with an F. I. 02 of 40% he was had a fairly adequate P. 02. However, over here on 100% oxygen. Again, very hypoxic, demonstrating a very large inter pulmonary shunt. And as you can, As you can see here at the time of the patient's death is shut was over 60%. I put this in just to prove to everyone that we're not drowning these patients. This is a patient's fluid balance over his hospital course this is his intake, this is his output. And at the end of this, at the time of his death he had a negative fluid violence of almost 10 liters of fluid. His urinals, moralities were 12 and 1300. He was about as dry systemically as we could get him. This is a young 26 year old man who had a gunshot wound through his upper abdomen, rupturing his spleen, pancreas and the right lobe of his liver. Again, he was successfully resuscitated, taken to the operating room, partial hepatic lumpectomy, partial pancreatic to me and splenectomy and really bounce right back and on the second postoperative day looked like he was home free here he is. However, his chest X ray again, beginning to show a bilateral fluffy type of infiltrate and as you can see going on to the same type of pictures we've seen before and in spite of all ways that we knew how to improve his oxygenation. He follows essentially the same course as a previous man. And as you can see Over here, 100% oxygen. Again, unable to oxygenate his blood at the same time, he has a really large Baylor to arterial oxygen gradient. Again, here's the patient shunt fraction. As I say, he went over 50% and I have not seen a post traumatic patient have shut one over 50% live others have not seen this either. And this is one of the reasons that a shunt over 50. Some people use 60% is called a lethal shot. This is a young girl with a similar injury however, due to a blunt trauma and she had a laceration on the left lobe of her liver which was successfully resected. And as you can see from the following X rays Within 48 hours, she again has a similar picture. Uh at this point uh there was no chance of salvaging this patient because we just could not oxygenate her cardiac output. Everything increased. Try to make up for the fact that she was hypoxic. However, she arrested assad attic and hypercar pick again. Here's her clinical picture and 100% oxygen down here, unable to oxygenate her blood. This was a man who had no external trauma. Uh he just had unfortunate to have an acute episode of pancreatitis. Uh he wasn't even an alcoholic and he just had an idiopathic pancreatitis, followed by pancreatic abscess, which had to be drained, followed three days later by a progression of this X ray to this point. And as you can see from this point, there is no way that we could actually ventilate this patient and again, the same type of thing. Early on, a fairly good response to 100%. Uh we felt he had a little too much food, he was given out movement and diuretics and had a little response. It was only a transient response. And by the time we got over here, he's Unsalvageable. Here's his shunt it got the 60% of the day, the day he died. These are all pretty bad cases, all cases of post traumatic pulmonary insufficiency, obviously don't die. These next two patients are a group that we feel a little more comfortable handling because we feel that we know what the ideology is. These are patients with long bone fractures. We feel that the ideology most likely is fat embolism. And again, we feel that a little more comfortable with this patient than we do with the previous patients because their previous patients, we just don't know what's causing it. So we don't really know how to treat it. This was a young 21 year old boy, uh who sustained this fracture while sliding into second base really at a baseball game. So he did not have extra contusion being thrown off a motorcycle. This is his initial chest X ray except for his hand over his left chest was felt to be fairly normal within 2036 hours. The patient had this chest X ray which really didn't look at me. And however his arterial PCO two was 33 he had all of the same stigmata as the previous patients. He had large arterial oxygen granny and he had a 43% pulmonary shunt and he was severely hypoxic and hipaa karmic on roomier. He also had the other things that we find in patients with fat embolism. He had fever, he had kidney, he had petechiae Liberia and elevated serum. My pace is not that we find this in every patient with fat embolism with this particular patient did have that. As you can see, the patient was treated with a tube in place on the volume ventilator, given steroids and by the fourth day or fifth day post treatment, his jet X ray was uh fairly normal. Again, when you look at this man, of course you can see that over here 100%. He didn't even get up to a P. 02 is 60 was severely hypoxic, very severe shock at that time, although it didn't get 50% was 43%. And as you can see by the time over here, on room air. His P. 02 is almost 100 on spontaneous ventilation. His villa Otero oxygen gradients gradually fell down over the period of time. You look at his course at this point because we had been reading the literature and everybody said steroids were the thing to use on fat embolism and support. We certainly did. In addition to the steroids, however, he was intubated and placed on a respirator and as you can see uh rather prompt response, rather gratifying type of patient to take care of when you used when you have three or four of the ones that I presented previously. There's another man with a fractured femur and had essentially the same course. Uh here he is 48 hours. Actually. This patient did well for 48 hours was taken down to surgery in order to manipulate his fracture to get better alignment following which uh he spiked a fever 104 that night uh had two kidney a and all the other stigmata of cannibalism including Batista and his ex illa. And this was his chest x ray just before he was intubated and put on a ventilator here. He is about 24 hours after that. As you can see two days later, he's beginning to clear bilaterally. And here's the patients follow up chest X ray completely clear. Uh We look at this patient's room Air roomier P. O. Two's. And you can see that on his admission as P. 02 was almost 90 on Premier. And by 48 hours it was down just above 30. But gradually with support really. This patient only got ventilatory support because we just wanted to under pretty controlled conditions determine exactly what effect do steroids have in this. Uh And this is presently under study at our institution. Uh This is just one particular case. As you can see. His shunt got up to about 35% and gradually came down. Again. Here's his uh gradient and again came down. This patient's course was just identical to the previous patient. However, uh no steroids were given. All was done was he was intubated and placed on a volume ventilator and supported for several days. And he got better in the same time span as the previous patient with steroids. As I say presently this uh this is understudied our institution to see really what effect if any steroids does play. What about the pathology and these lungs? I've said before that pneumonia is a small aspect of it. There certainly is not a lot of confluence pneumonia. We see a lot of interstitial edema, interstitial fibrosis, focal hemorrhaging or cell hypertrophy. And actually highland membrane deposition and really fibrosis after just a few days. Okay. Grossly. Uh The lungs are heavy two or three times normal weight. They almost look like liver uh they don't collapse when the chest is open here. You can see very nicely the amount of interstitial edema and the little lobular septus. Also some fibrosis and also some uh fibrosis and thickening of the available here. You can see the hypertrophy of the avail ourselves. You can see the beginning of the fiberglass proliferation and within the air spaces themselves. These uh they're almost organizing now into the progression in the highland membrane. And as you can see, this certainly is the setup for a profusion of non ventilated segments because the blood flow still goes through here. However, obviously there's no ventilation. This almost looks like the lungs of a newborn baby who dies with the membrane disease. This this is only three days after a patient died. A post traumatic pulmonary insufficiency I think quite strikingly, you could see the island membrane deposition here and they're really the lack of ad Alexis uh per se and the lack of pneumonic infiltration. Again here, look at the hypertrophy of these cells in the miller septa just three or four times normal and uh really stain. I think that because most of these people are initially treated with nasal tracheal innovation. However, if if they're gonna be prolonged ventilatory support their trick uh we originally used to see an awful lot of tricky ideas erosion, all the other complications that most people see uh with having a tracheostomy tube. We have Since gone to the use of the preset straight tubes like most people have and as you can see the bagging this of this trick to your left as compared to the tightness of this when they're both filled up. This is very baggy actually. They're both filled with the same amount of inclusive pressure, 10 cm of air. The actual pressure within this bag is 300 of mercury. The pressure in this bag when you're left is only 30 of mercury. There's quite a reduction. And even though the cortex company has brought out these new pre stretched tubes, if you measure the pressure, it's still about seven or eight times what it is. If you then pre stretch those tubes. This is a trick tube of a patient who had this trick asked me in for five months and subsequently died. Uh And I think you can see here rather nice looking mucosa without any erosions. When you start talking about the ideology of this syndrome, you really get up against it. Uh because nobody really knows. There's so many. Here's a list of the things that list of a few of the things that are involved in the resuscitation of most patients after trauma. As you can see there's infusion of blood salt solution, anesthetic agents, narcotics, the surgery itself, there are many, many things in the background of all these things that could lead one to speculate that this was the ideology or the reason that the patient developed a problem. If we sort of take most of the things that are listed in the literature now and we talk about fluid overload near drowning by the doctor. I don't think that there's no question that you can take a previously healthy young man and give him enough fluid that cause them to go into pulmonary demon. However, this pulmonary oedema is similar to the one you see in drowning. There's frothy sputum, there's hypercar via, there's hypoxia, certainly is not the pulmonary insufficiency that we see with Hipaa Carvey and hypoxia. And uh these patients usually respond to diuretics, digitalis, ventilation etcetera very dramatically when they're treated in such a matter. However, the patients that I've just presented to you don't respond so nicely, Let me just go ahead one and show you the fluid figures. Uh dr Procter went out to danang to try to prove once and for all that we were drowning too many people and uh he set up the unit was there and he decided to treat these patients so that they just got the minimum amount of fluid necessary for resuscitation. And I'm sure a lot of people in this audience who have been to Vietnam realizes that sometimes that's an extremely large amount of fluid here was this flu in the 1st 24 hours, as you can see, the patient got uh five liters of salt solution a liter and a half of water and 11,000 CCs of blood. However, only none of his patients went into phase three or phase four, they all showed a little bit of evidence of pulmonary edema earlier one. Uh but after diaries has responded very nicely. I don't think at the present time we can say that fluid overload per se physiological factor in any post traumatic pulmonary insufficiency syndrome. However, I do think indiscriminate use of fluid during the resuscitation certainly can compound a lung and add insult to injury, so to speak. And a lung that's already had the insults of the low blue state, whatever that may be multiple blood transfusions. You heard that spoken up monday. There's no question that the long acting as a filter and as we give blood under pressure and in a hurry, uh white cell aggregates. Platelet aggregates are accumulated in the lung. They release vezo active means like serotonin, which cause congestion and all the other problems. But the truth of the matter is that most patients receiving multiple blood transfusions do not go on and develop post traumatic pulmonary insufficiency In the Army series out of Vietnam. Less than 1% of patients receiving multiple, 15 units of blood or more really developed a full blown syndrome. Some of them had transient hypoxia. But uh they never went on. And I think all we have to say here again is that in any particular instance it certainly might be a contributing factor. But it's certainly not the whole answer to the problem about sepsis. Well, I think in the background of each of these patients somewhere. you can pull out that the patients didn't have sepsis. Some sort of sepsis. Usually a gram negative sepsis is pretty well shown recently that uh, compounds been isolated from the plasma of a septic animal that has molecular between one and 10,000 felt to be a greater kind in or one of the fiber peptides that can go ahead and produce the exact same lung lesion in a dog whose non septic, I think probably eventually we're gonna find out that uh something associated with a septic process is responsible for setting up the lung for this syndrome, disseminated intravascular coagulation. Let me just go ahead here second. There's a greater cutting in the fiber peptides associated with sepsis. Uh there's a whole group of people who feel that that's focused, who feel that the ideology of all this problem stems from disseminated intravascular coagulation. Whether we're able to diagnose it or not, they feel that clean cut coagulation studies are almost impossible in the acute patient and that this is the reason that we're missing it. And I think dr Baxter alluded to this earlier on monday. But as you can see each of these things here, uh, sepsis, low flow states, fat, everything lead to micro embolism, which then lead to pulmonary thrombosis embolism. And then you can go either way with the obstruction, the release of the means and the whole picture of the highland membrane deposition, the congestion, the heaviness of the lungs. Again, I'm sure that in unique situations and I have personally taken care of to patients who I felt that there was no doubt about it. The D. I. C. Was diagnosed at the same time, the lung picture development. The patient was given Hepburn, following which there was clearing. However, these are very unique situations and certainly is not the answer to the majority of patients who develop pulmonary insufficiency, oxygen toxicity. As I said, there's no question that oxygen is probably as toxic as anything we know to the lungs. And indeed, if you keep somebody on a respirator with 100% oxygen for 24 hours or closer to 48 hours, there's little chance that you're gonna be able to get him off that respirator. And this has been shown in an animal studies very well, here's a typical clinical picture of somebody that was mistreated with oxygen. As you can see at this point, because his arterial PCO two was only 60. They jumped him up to 100% oxygen with a rather marked increase in his arterial oxygen up to 200. But as we all know, nobody needs an arterial P. 02 200. And as time went on a gradual fall uh in the patients arterial P. 02. And I think we have to realize that oxygen is toxic. On the other hand, uh the brain gets softer, a lot faster than the lung gets harder and I think we have to realize that oxygen is good, but it has to be used very discretely and certainly we know we have to stay away from increasing F. I. 02 is just to get a bare minimum increase in the arterial PCO two of these patients. And when we get to the stage that we need 100% oxygen, we're usually at the last stage and can't go any further because the patients got irreversible damage At that point, fat embolism, as I said, it's one of the syndromes that we feel a little more comfortable with because we sort of know what's going. At least we feel we know what the ideology is. We're not quite sure all the ramifications of how the patient to be treated, but we have found that we are developing or identifying three groups of patients, really. The two patients that I demonstrated to you earlier who had a full blown syndrome were federal toxic, obviously clinically sick. Another group of patients who have a long bone fractures who retained fairly normal. And in this particular group of patients here where you see that the patient's room Air P. 02 was a little bit hypoxic. One admission fell down into the 40 range uh within the 1st 24 hours. However, the patient was lying in bed and no distress whatsoever and gradually spontaneous remission without any therapy whatsoever if you look at this patient's pulmonary artery pressures. There's no doubt about it that he has pulmonary hypertension. His chest x rays are perfectly normal. Something is symbolized into his lung, causing his pulmonary artery pressure to go up because it doesn't come down even when you put the patient on 100% oxygen, uh, whether this is the neutral fats and they haven't been hydrolyzed to free fatty acids that are so toxic to the lungs, we just don't know. But there certainly is a definite group of patients who Go through this type of clinical course. As you can see his intra pulmonary shunning almost approached 30% but gradually with no treatment at all came back to normal. Hopefully, in another year or so, we have enough of these patients that will be able to better define this particular type of syndrome. How about the treatment? Well, with such a varying ideology, obviously there's going to be a varied amount of recommendations for treatment. I think the resuscitation, all I can say about fluid is that use them indiscriminately and not indiscriminately because although I do not think that fluid in itself causes the lung lesion, there's no doubt that indiscriminate use of it can compound the the long problem. I feel that we all know that the response to trauma in the body is to hold onto water and hold on the sodium. And I think following resuscitation to these patients early use of diuretics to sort of beat their own diuretic phase by 24 or 48 hours, help eliminate some of the fluid the excess fluid that they have from the resuscitation at a time when it can be most detrimental to their loans. Mechanical ventilation early. I think probably all post traumatic patients if the facilities exist, probably ought to be left all traumatic patients. I'm sorry I ought to be left intubated and supported for a day or two to see if they're gonna develop any pulmonary problems. Uh The use of the volume ventilator and as mentioned earlier, constant positive pressure, breathing has become are quite frequent occurrence in most intensive care units treating this type of patient because it allows us to decrease the amount of inspired story oxygen while increasing the arterial P. O. To the word of caution. However, if the patient is hypovolemic, uh this will decrease venus returns decreased cardiac output and cause the patient to get hypotensive. So as long as the patient is normal bulimic uh you're really not in that danger. There is a danger. However, these patients lungs are very stiff. You're talking about taking maybe 50 or 60 centimeters of water to ventilate him anyway and then you throw 10 centimeters of positive pressure breathing on top of that and it's not unusual to wind up with this type of thing in the middle of the night, attention in the thorax, which carries a rather high mortality rate unless somebody is right on top of the scene at the time to put a chest tube in. I have gotten myself now that if I have a patient is requiring that much pressure and then I go to constant positive pressure. I usually put prophylactic chest tube, I have not been sorry for this. I think the complication here's another, they get more media steinem uh they got they dissect up into their neck and they get acutely ill immediately and certainly can die just some attention. And with over accidents it's recognized. Yeah, there's another one, as you can see the amount of tension in this patient right here. I think the complications of prophylactic chest tubes are probably less than the complication of uh incurring a tension pneumothorax like this in the middle of the night. And this is not uncommon if you I guarantee you, if you have to take 60 summaries of pressure ventilator patient, you throw CPP be on top of that given time the lungs will blow out. It's pretty nice to have chest tubes in there and suddenly see the air come out in the patient. Not in any distress steroids. Oops, I think there's no doubt that steroids have been used in post traumatic pulmonary insufficiency, especially when fat embolism. I'm not so sure that they add anything in the fat embolism. They obviously may add something in the septic patient. All I can say is that the people who preach using steroids feel that they have a stabilizing influences on the capillary membranes. And as was stated earlier, they do decrease the inflammatory reaction. Uh and I just don't know what to tell you as far as whether they do. I don't think anybody has proved that they alone are responsible for decreasing the intra pulmonary shunting and improvement in the chest X ray Hepburn. I think definitely when there's documented disseminated intravascular coagulation. However, uh that those cases are so infrequent that I don't think we can recommend some clinical doses of heparin. Every trauma patient who gets hypoxic. The last thing is, I think is gonna be our only salvation in the future to save these patients who go into phase four. Uh and that is some type of extracorporeal support uh for the oxygenation short of us having to use 100% oxygen. We have to get these people on an extracorporeal system early before we have to insult their lungs with 100% oxygen at this phase. This is strictly experimental. It's been doing, it's being done around the country. However, there are very few survivors and certainly hasn't been perfected yet, but it's something that we have to strive for in the future. In summary. Then I think that post traumatic pulmonary insufficiency is a life threatening derangement obviously in pulmonary function uh resulting in increasing pulmonary shunning decreased compliance uh rumor hypoxia, a very severely ill patient. The ideology of this syndrome is obviously obscure as I've stated, uh but prominent in the background of all these cases has sort of been an episode of sepsis in a low flow state. Those two combinations are bad combinations that appears to be in these types of patients. I think in selective cases you can implement the oxygen toxicity fluid, overload, disseminated intravascular coagulation, fat embolism, extensive transfusions. But again, these are only in selected cases. I don't think we can say across the board that these are implicated. I think rather than any one of those factors is going to be a combination of an additive or synergistic effect of some of those factors that eventually is going to lead us to the real ideology of this syndrome. Thank you. Mhm. The preceding program was recorded during the 1972 seminar on surgical and orthopedic aspects of trauma as presented by Brooke General Hospital, in cooperation with the University of Texas Medical School at SAn Antonio post traumatic pulmonary insufficiency. A current review with Richard W. Virgilio. Lieutenant Commander, Medical Corps U. S. Naval Hospital. San Diego California has been produced by the television division Brooke Army Medical Center, Fort Sam Houston texas