NIH CLINICAL CENTER GRAND ROUNDS
Episode 2009-017
Time: 1:04:44
Recorded May 13, 2009

CONTEMPORARY CLINICAL MEDICINE: GREAT TEACHERS
Mysterious Cases
Jeffrey G. Wiese, MD
Associate Dean for Graduate Medical Education
Tulane University Health Sciences Center

ANNOUNCER: Discussing Outstanding Science of the Past, Present and Future – this is NIH Clinical Center Grand Rounds.

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ANNOUNCER: Greetings and welcome to NIH Clinical Center Grand Rounds, recorded May 13, 2009. Today's podcast is part of the NIH's Contemporary Clinical Medicine: Great Teachers series. On this edition, we'll hear from Dr. Jeffrey Weise, Associate Dean for Graduate Medical Education at Tulane University Health Sciences Center, who will discuss "Mysterious Cases." We take you to the Lipsett Ampitheater in the NIH Clinical Center in Bethesda, Maryland, where Dr. Paul Plotz, chief of the Arthritis and Rheumatism Branch at the National Institute of Arthritis and Musculoskelatal and Skin Diseases at the NIH, will introduce today's speaker.

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PLOTZ:  Welcome and thank you for attending. Today I want to introduce Dr. Jeffrey Weise from Tulane University. He received his chief resident and fellow and medical education at the University of California San Francisco. And in 2000 he was named the professor of the year award at San Francisco. Thereafter, he moved to Tulane University in New Orleans and he currently is on the faculty of Tulane where he serves as the associate dean of medical education, vice chairman of medicine, the chief of the charity medical service and the director of the Tulane internal medicine program. He devotes his time to teaching and educational research. He is the recipient of numerous teaching awards, and actually with the attending of the year in 2001, 2002, 2003, 2005 and it just goes on and on. He received a number of teaching awards during his 9 years at Tulane and these include the recipient at the Society of Hospital Medicine Educational Award, the Parker Courage to Teach Award, the Robert Glazer Distinguished Teacher Award and American College of Physicians Walter McDonald Award as well as the President's Award of Excellence in Teaching. On a more personal note, he has been a leader among the faculty and the residents there and in the wake of Hurricane Katrina, he traveled over 50,000 miles visiting its displaced residents during this very difficult time. In fact, his residents only lost just a few weeks of the curriculum time and all of them succeeded in finding fellowships after this very difficult traumatic period. He is the author of 4 books including a book entitled, values in conflict the Lincoln Douglas debate. He is going to be trying to help us with differential diagnosis of mysterious cases and I noticed that he has no difficulty dealing with challenges or no difficulty of dealing with fear. And that is what I think epitomized by the fact that he was really a very important member of the Tulane University medical school rugby team. So I think without further adieu, we will welcome Dr. Wiese and present some cases. >>

WEISE:  Fantastic. Thank you. It's a pleasure to be here. And I believe that we have 3 cases to discuss. I’m going to begin by saying I have no financial conflicts of interest to disclose and in fact given the market, I really have no financial interests at all. But let me talk a little bit about what I see as the objectives for these. I’ll tell you, I do many of these. Many for the Tulane residents but also at different institutions and I may go about this a little bit different than some of the speakers you had. I like to focus on the methods, that is to say what I see is the intellectual scalpel than an internist holds, the ability to weed through what is important and what is not. And to have some method of approaching problems. So I’m going to devote a lot of my comments to that, specifically with respect to the thought process. And also methods. Without further adieu, let's see what the first case is.

PLOTZ:  Our first case is presented by Dr. Nan Quo and he will be reading the slides and after each slide we'll either ask you to move on to the next slide when you're ready.

QUO:  Okay. The first case, chief complaint, legs are numb and getting ugly. 60-year-old woman with 40-year history of rheumatoid arthritis, comes clinic for her routine follow-up. Patient first noticed numbness in her right ankle 3 months ago. Episodic with no known aggravating or relieving factors. Denied any weakens or tingling sensation. Denied any trauma to the area and eventually spread to the opposite foot as well.

WEISE:  I’m going ask you a couple of questions and then we can move through and guide me as we go through. For the numbness, was this associated with any motor deficits in the way of the weakness of the extremities.

QUO:  Not at this time.

WEISE:  And secondly, rheumatoid arthritis, and I’m saying this for the benefit of the crowd, how much involvement of the ankles did she have with respect to rheumatoid arthritis, knowing it's not a common joint for RA.

QUO:  Her rheumatoid arthritis mostly involving the small joints of the hands in her wrists but mostly other RA patients like them, the cells have some osteoarthritic features.

WEISE:  So where we are now, and it's the right foot and then spreading to involve the left foot, correct? So this would be my approach and again I’m going to focus on methods and then back into the diagnosis pas we go. We are talking about a neuropathy. It's okay to say that it's not necessarily out of sequence in the way of having two of the longest nerves involved. My approach on to periphery neuropathy is to think about the infusion to the peripheral nerves and the fat cells that insulate the peripheral nerves and to think about things that are going to affect the two. And then there are some primary nerve disorders to address as well. But if there is somebody in the 1 crowd that really loves pneumonics, I’ll give you a therapist who is a pneumonic, diabetes being the first and we'll get to that. But remember diabetes is the glycosaline of proteins that plug up and induce the peripheral nerve damage. Alcohol because of the character, depositing in the cells, nutritional disorders, such as predominantly B vitamin disorders. We can get to that in a little bit after I ask more questions. The therapist is (…) and it's good you already addressed the trauma but it's the reason I ask about the joint erosions involving the ankle. H is hereditary, which believe it or not we see in our Cajun population with some regularity. E is environmental, particularly the lypophilic solvents as well as petroleum products because of the deposition in the swan cells. R is going to be very unsatisfying. That's the remote affects of cancer which is paraneoplastics, primarily from the adenocarcinomas. And then the ISD is the inflammatory immune diseases. But thinking about those things, then we target the history going forward. I won't get into because of the interest of time, asking questions about awful them but perhaps maybe to get more history in the next slide.

QUO:  So a rash developed thereafter. The rash and numbness progressed and now associated with pain. The pain interfered with emulation, sleep and daily activities. Also fever, chills and weight loss. PMD prescribed Seflex in 400 milligrams without any improvement.

WEISE:  So if there is anybody in the audience that is wondering, I wonder if he knows what is this is? No. I have no idea. But I’m going ask a few questions. This rash, what was the distribution of the rash? Was it complete over the body or –

QUO:  In the lower ankle area.

WEISE:  Okay. And I guess we are still on the history. I’ll wait. Remind me to ask about blanching of that rash. For the purposes of the educational discussion, I want to get at this, is an infectious complication, obviously with rheumatoid arthritis it has a baseline immunodeficiency going in, or is this a secondary vasculitis? The distinguishing feature will be appearance and how it blanches. So the fever, chills and weight loss, tell me more about that before I move forward. The fevers are episodic, constant? How long and characterize the weight loss for me.

QUO:  The fever is subjective. She never took the temperature herself. It's episodic but I don't remember how she characterized it. The chills are associated with the fever and the weight loss may be if I remember correctly, 10 pounds over two months, maybe.

WEISE:  Okay. And night sweats associated with this?

QUO: Not particularly. I asked her that and she said sometimes, yes.

WEISE:  She saw a primary physician who obviously looking at the rash, feels this is a strep, staph infection and has been prescribing an (…) to try to address this and she doesn't get better. Which helps us as to whether it is infection or not.

QUO:  No joint pain, no morning stiffness or chest pain or other rashes. And there is no new medicine prior to the onset of rash.

WEISE:  Okay. And we have good confidence that the zero positive rheumatoid arthritis has been well established as a diagnosis?

QUO:  Yes. 40-year history.

WEISE:  Okay.

QUO:  So her past medical history is rheumatoid arthritis, social history, she's a part-time home health aid. Immigrated here in 1988. Her last visit to Sri Lanka is 2006. No tobacco or alcohol use. Her family history is significant, her mom died of coronary artery disease. Her medications include:

WEISE:  Well okay. And she's been on this combination for a while?

QUO:  For a long time.

WEISE:  Good to hear. Let me just say a few words about the drugs, of course. For all cases, if you're following a general approach to diagnose medical mysteries, for me it's the approach looking at the categories of disease but it always begins with the hypergenic. Hydroxy chloroform can have its own complications both dermatologic and also in a neurologic way. Methotrexate in the way of both immunocompromise, which is what it's designed to do but then the complications as well the remainder of these for the most part, I don't see tying in closely to the symptoms we have seen thus far.

QUO:  Her physical exam, she is in no acute distress. Blood pressure is 92 over 57, heart rate 82 and her weight is 50.7 and…

WEISE:  Is there additional physical exams?

QUO:  There is neurological. Neurological exam shows:

WEISE:  Okay. And nodules on the examination?

QUO:  No. No nodules.

WEISE:  Okay. Good. Let me talk about the physical exam a little bit. And I’m going to take you back to the first component. First, the blood pressure of 92 over 57 tells you it's recently tight. Pulse pressure, I don't know that I’d make anything of that at the moment. There doesn't appear to be any embolic phenomenon which for any vasiculated rash, which is what I’m going to get into in the next slide. That's the non-blanching component. The first step to make sure it's an embolic or distal before you move on to the primary s since we are going to get into talking about vascularities, it's nice to know the one has not been perturbed and she is a long time owner of the rheumatoid arthritis which brings into play the fell tee syndrome but nothing in the way of the yearly examination. How it would play in this, I’m not sure than the leukopenia would put you at greater risk for secondary infections. Don't think that's it. Just worth talking about. All the joint examination consistent with the diagnosis, rheumatoid arthritis appears but it's not an active flair with respect to the rheumatoid arthritis and not surprising that you had some of the degenerative joint disease you see here given the history. Okay, so on the neurologic, what I take from neurologic is that we are dealing with a peripheral nerve disorder and this is not a central nerve, the reflexes felt great. It is spell given the distribution of the left ankle and then in the history, you said right side as well. What we're driving towards is this multiplex. Though, again, it would be fine to say that a symmetric distribution of both lower extremities being the longest nerve, that it wouldn't have to be. But I’m going with this now. Then the question s what is causing the multiplex? And you get into the skin. A few comments. The nonblanchable component speaks to more of a vasculitis. And here is the way I teach to the students if a vessel is dilated under a histamine driven disease, as squeeze on it from the left to the right and the color goes away, it's the blood in the vessel that gives the rash. For a rash that has broken the vessel allowing blood to get into the tissue, pushing on that is not taking that clot and pushing it back into the vessels, so it tells you there has been some vessel damage. One other thing to note is the over lying patches of shiny and scaly. And when I think of that, I think of nodules that have been resolved. And it's worth considering not only because of the rheumatoid arthritis. They are rare and a complication. But hydroxychloricate and methotrexate is on that list. We are talking about something that is affecting nerves. A neuropathy is probably affects those nerves and affecting the skin. Which is going to be one of the small vessels, small to medium vessel vasculitides. It brings into play the vasculitis. The others we'll get to here with respect to the labs. And then the final vasculitis of course as we go through this examination, is going to be the polymanusitis.

QUO:  So this is a picture of her face with the rash on the forehead and the next slide will be the picture of the lower extremities with the dry, scaly rash.

WEISE:  Okay. I’m going to just step back and I’m not sure that this would be the diagnosis but to step back and talk about DMPM. Remember there are 6 types but one of the types that is an overlap type, that is to say associated with other diseases such as rheumatoid arthritis. The 6 of the 6 types I think is inclusion, it has the opposite distribution of others, men greater than women and it also has distal weakness more than proximal, which is a distinction feature from the others. I want to step back here. This is just normal for her? Or is this a new rash?

QUO:  No, that's not a new rash.

WEISE:  It's not new? That's her normal pigmentation over the eyelids?

QUO:  Yes.

WEISE:  Okay.

QUO:  Okay, other data ... Laboratory data:

WEISE:  Okay. And to the level of sensitivity for the assay of TSH. Is this or are these two values within the normal range?

QUO:  Yes.

WEISE:  Okay. All right. So not a lot to say about the labs except what you don't see. You see normal creatine, no involvement of the kidneys and no involvement of the liver, which is great but it limits the differential platelets is consistent. Remember its own inflammatory marker consistent with the 78. I’m not sure that changes anything in our diagnosis as we are talking about vasculitis going forward. And nor does the white blood cell count other than to say it's not felties. Diagnostic procedure was performed. That's the end of yours, right?

QUO:  Pretty much. In terms of presentation, yes.

WEISE:  Okay. All right. So in the interest of time, I want to make sure we get to a few cases. Let me just talk to you about what procedure I would then next do. The, again the combination of the multiplex, if you want to call that a definitively pilfer neuropathy, plus skin lesions on the distal extremities but then also face, brings into play the vasculitides, and which one will you put your nickel down on. Medosa would be fine for this, especially given the nerve involvement. It's not -- it is classic to have the skin as opposed to what I call the small vessel vasculidities. But it's okay. The shiny patch of nodules speaks to the hemadose. It's one of the most common post therapies drugs but then you get into other things. It's an unfortunate because the nodules are rarely a feature of polyritis medosa. It's more of a multiplex than the skin nodules itself. So you go to where the money is and for the diagnostic procedure, and I’ll tell what you I’m coming down to. This doesn't feel to me to be nutritional. As there are no other laboratory and or historical or examination features to support it. It feels like vasculitis and it would come down to the dermitis verses medosa and the only way to do that is to get a biopsy. You can go skin lesion, I suppose. You is can go for the DMPM. But in this case, in my mind, going more towards pam than I would do a nerve biopsy as the diagnostic procedure. So tell me how wrong I am.

QUO:  We consulted a dermatology and a skin biopsy was done. Upon differential psoriasis and diabetic 1. And the skin biopsy shows inflammation in the dermis and the bottom shows inflammation -- 100 antibody staining is positive for inflammation around the nerve. And is there a rare staining on the stain.

WEISE:  Look at that. Okay.

QUO:  So the diagnosis is –

WEISE:  See, in rugby we don't wear pads. I should have brought my protective gear.

QUO:  She was treated with 600 milligrams of rifampin daily and her follow-up, the rash continued to worsen and the results in lacerations. Steroid treatment, intensive wound care was started that includes creams, liquids, ointments, gel, lotion, acid and: leprosy. Microbacteria grew best at 27 to the 33 celsius which correlated with the elections for affecting cooler areas of the body in humans that includes…

WEISE:  Okay. Good. Word about the microbacterial disease, TB really doesn't like the periphery and that's the rule when you get into soft tissue such as the muscles and nerves. If you see that first, it's probably not TB for this very reason, it tolerates higher oxygen tensions, leprosy that is, better than TB. I will point out that Louisiana is still the proud home of the leprosy facilities, if you will, and of course credit to a physician there that was one of the initial developers of anti-leprosy antibiotics. Okay. And I owe you one my friend.

PLOTZ:  Our next presenter will be Dr. Adriennea and she will present this case of difficulty diagnosing (…).

ADRIENNEA:  Our patient is a 74-year-old gentleman who complained of new onset of shortness of breath when swimming. He was physically fit and regularly walked up to 3 miles without difficulty. There was no cough, fever night sweats, chest pain or leg pain.

WEISE:  And I’m going to go quickly. No shortness of breath when we exercised outside of swimming.

ADRIENNEA:  Not in the beginning. Patient has well-controlled hypertension, type 2 diabetes and dyslipidemia. His medications include:

WEISE:  So past medical history only significant for diabetes and hypertension. >>

ADRIENNEA:  Yes and it was late onset.

WEISE:  Okay. Let me just say a few words about my method and approach to dyspnea and that's the way I like to approach it. If you ask a resident, they are going to draw a pyramid for you and on the base of the pyramid are the 8 causes of pulmonary causes and then the second up level will be 4 causes of cardiac causes of dyspnea. And then acid base disorders, that is to say true respiratory alkalosis, which is the symptom or the presenting find of the dyspnea. And then blood disorders which have nothing to do with anything hypoxia. But it can under exercise, create the symptoms. And the nice thing about the pyramid if you look at it is there are 3 tests that you need to make the first stab in the way of excluding the causes and that being the EKG, x-ray and APG. Going forward with dyspnea, expect I’m going to look for that information. I’m saying that in my point of view only because in case, it may be not that challenging, but for patients being admitted to the hospital, especially in the middle of the night, even though seen in clinic, it's really easy to shoot from the hip and jump the gun with a premature closure on the diagnosis and of course anything dyspnea means you're driving that respiratory component which is life-threatening. I’m throwing that out as a method and now I’ll talk about this gentleman. Because there is no sensation of shortness of breath when she exercising and standing up or walking around. Just when she she swimming. When type of swim stroke does he do?

ADRIENNEA:  They asked me when we had this last week. I asked the patient and he said tell them, frog style swimming. It's a breast stroke.

WEISE:  Okay, all right. And I’m saying this just in the way of a mechanical feature of the stroke can change the chest dynamics and okay. We can and back to that. And the final thing I will ask, he doesn't have platypnea or the orthodeoxia. When he's lying flat, is he short of breath in bed or –

ADRIENNEA:  Not at this time.

WEISE:  Okay. And what I’m driving at is you think about somebody exercising, what's the difference between running and swimming? Will it's vertical and horizontal and then the second piece is the mechanics of the stroke itself.

ADRIENNEA:  So on physical examination, he appeared healthy. Actually younger than stated age as opposed to the first patient and he was in no acute distress. His blood pressure was 122 over 70. Pulse 76, regulatory rate was normal 12 and temperature was 36.5. He was only mildly overweight with BMI of 26.5. And basically his exam was normal. Heart was regular. Extremities no edema or tenderness. Skin unremarkable and I see now that I don't have abdomen but it was normal.

WEISE:  Okay. And the pulses and blood pressures were equal in both arms?

ADRIENNEA:  Yes.

WEISE:  And the lungs cleared from the patient. No consolidation?

ADRIENNEA:  No. And nothing. >>

WEISE:  And let me ask you about the s1 and s2. When I say normal sound, I know that

ADRIENNEA:  He was 74.

WEISE:  So for a 74-year-old gentleman, give me some commentary on the loudness of s1, for example.

ADRIENNEA:  I did not listen to him. I listened to his history but didn't do exam. I cannot tell you.

WEISE:  Maybe this is a point. I like listening carefully for s1. The problem you is do have to realize what is the normal in different age group. It gives you some commentary on the contractile force of the left ventricle because it's the left ventricle that is closing the valve giving the s1. The s2 is very important here too because of course stenosis or sclerosis would be a fine diagnosis for somebody at 79 years of age and it can come initially with just being locked in an open position and depending upon the infarction, you may not hear the turbulence initially but you should still hear a good closure. Okay. So and on head and neck examination, normal color, no skin rashes or anything?

ADRIENNEA:  No.

WEISE:  I’m just driving the at the hematologic components of this.

ADRIENNEA:  So, his insulin is laboratory assessment which reveals hematically 41% normal white count and differential platelets were normal. Chemistry was normal except slightly elevated glucose and:

WEISE:  Okay. And let me just ask a couple of questions here. The chest x-ray truly normal in the way the lung print came out but also the aortic shadow?

ADRIENNEA:  It was interpreted as normal by radiology. So, his internist performed office pathology and here his numbers before and after bronchodilators. And based on the significant improvement of this after the bronchodilators, diagnosis of asthma was made and he was started on inhaled bronchodilators. However, no improvement after two months of treatment.

WEISE:  Okay. Let me step back and first I’m going make the disclosure that this is exercised induced asthma. And when you say a little bit about joust get it out there in the way we talked about exercise induced asthma. That is at all the diagnosis. First I’m going to qualify this by saying I come from New Orleans and the whole concept of exercise is very foreign to us. This is not a problem that I would see in my patient population at all. But okay. Fair enough. Here is what I know about exercise induced asthma. And maybe it plays in. Because we have a difference between just running and being in the pool is the temperature. And exercise induced asthma has everything to do with the delta going from hot to cold or cold to hot. And it's the reason that you will find, for example, college athletes or high school athletes that are doing 9 indoor track during the winter and they are fine and then you open the doors to start the spring season upon and they go out and get the cool air, that either they get at the beginning of the exercise because of the warm to cold sudden transfer or any exercise, the cool-down period where you get hot and then you cool it down. Okay. That said, I don't know the temperature of the water that he is swimming. I assume this is some controlled environment pool.

ADRIENNEA:  It was a heated community pool.

WEISE:  All right. So they are making a diagnosis of asthma. Which I think is going to be de novo diagnosis out there. I think it's the wrong diagnosis as 79 years of age. So it brings into play cardiac asthma, the exercise induced asthma would be a supposed find but still out there giving his age. And then way out there the exercise induced (…) that may mask as asthma. That last one really should be presented earlier but also really should present with normal exercise, not just swimming. The final thing that is different about swimming verses regular exercise, of course is the period of time that you hold the breath. Because it's not regular ins and outs. It's to hold the breath, swim for a while and then exhale. That's part of why I’m asking which kind of stroke.

ADRIENNEA:  He said it was above the water.

WEISE:  He is breathing with each stroke?

ADRIENNEA:  Yes. So his internist referred him to the pulmonary lab at University Hospital where he did a different kind of testing which was (…) testing with methacholine. This time he was normal and had normal bronchial responsiveness so diagnosis of asthma was abandoned. He suspected his symptoms might be side effects of his medication. So, he talked to his doctor and they discontinued his medication but his symptoms persisted. Metformin was replaced with lipisides and hydrochlorisat was replaced with –

WEISE:  Does that make a difference to switch?

ADRIENNEA:  It did not.

WEISE:  Just a word beg your pardon ace inhibitors. They are so common. Remember that the whole ace inhibitors derived from pit vipir bites. The venom, which works in two ways, one by disrupting the conversion of angio1 and angio2 but also the degradation of (…), which is if you have smaller amount of enzymes to begin with inhibited by the degradation will give you the angiodema associated with ace inhibitor use. While we are playing with the idea of some kind of asthma here, that is dyspnea associated with the exercise that is not due to inherent, we know by the methacholine, not due to inherent bronchial smooth muscle reactiveness, is there something else that is causing low clot swelling during these times of exercise either from the outside or directly from an inflammation and the ace inhibitor would have been a fine thing to do the trial. I probably would have done that. And of course it's not messing with the enzyme at all, just the receptor really should take the (…) and ace induced angiodema out of the equation.

ADRIENNEA:  6 months into his illness, exertion developed. Patient also noticed 10 pound weight loss which he thought was caused by flu-like respiratory illness from which he recovered.

WEISE:  Okay. So now we have progression from the dyspnea during swimming to dyspnea all the time?

ADRIENNEA:  He basically said I can't take deep breaths in bed.

WEISE:  it tells you one or two things when you have the orthopnea. It tells you either there sell a lung disease and sitting up provides more profusion to the lower lungs and people breathe better, probably not it. Or it tells you that this is somebody that can no longer tolerate increases in preload back to the right ventricle and now he starts to bring into play primary cardiac disease and we can work through that now again, s1 and s2 and my pretest assessment, it will be hard to get away from this case without seeing the function of the valves.

ADRIENNEA:  So he underwent exercise testing again at the University Hospital and his nuclear exercise stress test was normal. It showed low likelihood of exercise induced myocardioischemia. He also had cardiopulmonary exercise tests that was also normal. And:

WEISE:  Okay. It looks remarkably normal. Due to the fact we are treating a patient not a elaborate. And was he dyspneic at all during the exercise test?

ADRIENNEA:  I don't know. I didn't ask. He probably was not. Because he used to walk up to 3 miles. and I guess this wasn't -- he was quite fit. So additional symptoms developed and one year after the onset of his symptoms, he noticed during one of his regular walking regimens, that he had right leg discomfort, which he described as if something was pulling at my leg. He had to stop walking. He had a strange sensation that he never experienced before. He was referred to orthopedic surgeon who diagnosed a (…) recommended a block. The patient did not undergo procedure. He said I will think about it. He didn't believe it was sciatica. and at the same time he complained of dysphagia and throat irritations.

WEISE:  Anybody over the age of who develops brand new sudden back pain should think about the big red tube in way of dissecting aneurysm. I’m going to ask, has there any image of the chest other than the chest x-ray, the stress test?

ADRIENNEA:  Not that I’m aware of. But it was not really a pain. It was a strange sensation, some kind of a discomfort. Not really a pain. He underwent gastroenterology work up. He had upper endoscope that showed hiatal hernia and it was added to his medication regimen .

WEISE:  And any evidence of peripheral neuropathy to go with this? >>

ADRIENNEA:  Not that I’m aware of.

WEISE:  Okay. And just to make this point, we are talking about for the gastric study, a couple of things that will go to it and one is whether you have the nerve neuropathy. while this is not a rule, but I will make a point there is say physiologic process, a diabetic neuropathy should make some sense. The longest nerves are the ones that take the greatest hit and the longest nerves being the sake recall and to the hands. So not to say he can't have neuropathy without this and the diabetic patient. It just makes it better. Second component is of course, two other components from the gastric emptying. There is a hormonal component and then this also the muscle itself, which boils down to sometime a deficiency in amyloid disease or lymphoma, infiltrating the stomach wall. How did all that will fit in thus far? I don't know. I’ll tell if you it's amyloid then we start looking at restrictive cardiomyopathy. It will be working and having that echocardiogram going forward. so for this point now, this the dyspnea is still present and now we have the esophyet wisa strange sensation pulling at his lower leg. I am going to assume he is up-to-date on his colonoscopy et cetera.

ADRIENNEA:  I’m not 100% but I believe so.

WEISE:  Okay. So esophagus and stomach of course diabetic neuropathy is fine. scleroderma, okay. I mean it's a lot to add all this in, but worth keeping in mind as we go forward.

ADRIENNEA:  So he develops additional symptoms, almost a year and a half into his illness. Patient complained of loss of strength in his muscles, right leg weakness. muscle waisting and twitching. 20 pounds weight loss. fatigue and dysphagia.

WEISE:  Okay. So the wasting and twitching tells you there is denervation of the muscles and especially the wasting twitching at this age. It's ALS and the especially when you bring in the hoarsness, dysphagia, the upper and lower combo of nerves. And that the age. Sadly it is Lou Gehrig's disease. and I hate to say well, just give somebody that diagnosis, but that's it.

ADRIENNEA:  You're right. yes. Of course neurologic disorder was suspected with all this symptoms and signs and brain MRI was normal for age. Neurology consult was obtained and diagnosis was made. And then his respiratory function was reassessed but it was a little different. So he sat up right vital capacity that was fairly preserved, 71%, which fell significantly to 36% in the supine position.

WEISE:  And just to make the point, when you're up upright, have you gravity on your side. When you're horizontal. that was the difference.

ADRIENNEA:  So arthrosclerosis or Lou Gehrig's disease, that is based upon clinical criteria including upper and lower signs and symptoms such as: this made it very difficult because we don't think of this when we see this. 80% present with asymmetric limb weakness and 20% with dysphagia.

WEISE:  let me make -- great presentation, thank you. Especially since I got it right. [laughter] I appreciate that. [applause] Let me pack a point about this because Jeff and I were talking before. The CPCS are fantastic for medical education. We should do more of this and more about the method and how we think not just what to think. One thing about this case -- here is my one reservation about CPS, I think it sends is the reality that a diagnosis can't be made in a short amount of time. and the reality is that most diseases, the tough ones take persistence on the part of the internist and a teamwork and that transition of care and if you don't have that, this guy 1gets lost up to the point that either the diagnosis is not made or he suffered so much even though this is a non-curable disease and it could have been avoided. so if there are students in the crowd, for all of us, we have to recognize the importance that we play as internists this longitudinal care. We have 7 minutes. Can we do a presentation? I’m going to save my comments to the end. This will be the rubber match.

UNIDENTIFIED: Acute illness case. a 62-year-old man was taken to the emergency room by his wife with major abdominal pain which had been increasing in severity over the previous day. The pain was accompanied by chest pressure. Similar episodes of pain over several years were thought to be thought to be due to related to his insulin-requiring diabetes and now the pain was more severe and penetrated through to the middle of his back and to his shoulders. The pain was considered moderately severe, that's why the ER staff in the ER and was accompanied by nausea without vomiting. no history of diary a the patient was alert, oriented, cooperative and complained of pain radiating to the back and 1of gastric pain. Neither exacerbated nor relieved by anything. Interrupt me if you want to.

WEISE:  Just one question. I want to make sure we get through all of it. But the blood pressure was the same in both arms?

UNIDENTIFIED: It was.

WEISE: Okay. And I’m just for the crowd going to point out the dramatic pulse pressure differential here. And I’m going to come back to some commentary on that. Too often we get folks with the absolute numbers and in a systolic diastolic can give you great insight into what the potential disease is. Let's keep going.

UNIDENTIFIED:  CO2 was a little high.

WEISE:   Anything retro peritoneal in the way of back pain and (…) straight back. Okay. Let's keep going.

UNIDENTIFIED:  They were concerned about not entirely sure what they were concerned about and they did spiral CT with contrast. And nothing in the adrenal. He was sick and he was a puzzle.

WEISE:  Aand that's the leading diagnosis. All right. I’m just going to remember that radiation that he had years ago as we go forward. Okay I think he actually virtually insisted on leaving. Feeling somewhat better. [laughter] but by no means well. The diagnose was a GI motility disturbance secondary to diabetes or possibly gastrointeritis. At home the pain did not abate.

UNIDENTIFIED:  Okay. On the day after discharge the patient's wife notice aid rash over the last scapula and suspected a diagnosis.

WEISE:  Just so I can be two in one. Okay. And those are vesicles I assume? Okay. Okay. Just so you know herpes is to crawl. And it has nothing to do with the herpes virus. But it crawls along and hence the name, herpes for both. It is to remind you of the dermatomes both inside as well as outside and for many patients, especially the elderly, you will see the pain that will precede long before the vesicles appear and here is the method in which we didn't have time to go through it. If you ask any Tulane resident, sit him down, only because I drill them on it, they'll tell you, it is managing a bullet air oh, whatever, going from front to back all the way through the chest. And to think about each tissue as you go through. That is to say you start with the skin and you think of herpes and you just to consider it, and then it's to the bones and then to the muscles and then the pleura and then the lungs and then the pericardium and then the heart and then the aorta and then the esophagus and then the spine. But the method keeps you honest in the way of thinking of each level of tissue gauze through it's very, very important not so much because if you missed therapies it's not a whole lot. We could have done the acyclovir which would have made his life better than the 6 physical exams. Where it does play as an aside, and we kill somebody once a year on this. Somebody that comes win a classic chest pain who is having a dissection and somebody goes straight to the protocol of anticoagulating him and boom, that's it. And this method at least makes you think about it. The fumble is not looking at the x-ray for the dissection as an example before you rush to protocol-based behavior. Let's finish with this and then –

UNIDENTIFIED:  You really said it. The pain precedes the rash by days but he -- even as much as a week. It's due to the replication of the virus and the ganglia and the period before the rash at the time requires the virus to continue replication in the ganglia, spread down the nerve skin and replicates in the skin to induce sufficient necrosis and inflammation to cause the rash. And he was actually -- he called his internist who over the telephone put him on the basis of the description of the rash, put him on acyclovir and it took a while.

WEISE:  Fantastic case. I want to say thank you for your attention during this session. Thank you.

[applause]

ANNOUNCER:  You’ve been listening to discussion on the topic, "Mysterious Cases" -- part of the Contemporary Clinical Medicine: Great Teachers series. Our speaker was Dr. Jeffrey Weise, Associate Dean for Graduate Medical Education at Tulane University Health Sciences Center. You can see a closed-captioned videocast of this lecture by logging onto http://videocast.nih.gov -- click the "Past Events" link. The NIH CLINICAL CENTER GRAND ROUNDS podcast is a presentation of the NIH Clinical Center, Office of Communications, Patient Recruitment and Public Liaison. For more information about clinical research going on every day at the NIH Clinical Center, log on to http://clinicalcenter.nih.gov. From America’s Clinical Research Hospital, this has been NIH CLINICAL CENTER GRAND ROUNDS. In Bethesda, Maryland, I’m Bill Schmalfeldt at the National Institutes of Health, an agency of the United States Department of Health and Human Services.

QUO: We consulted a dermatology and a skin biopsy was done. Upon differential psoriasis and diabetic 1. And the skin biopsy shows inflammation in the dermis and the bottom shows inflammation -- 100 antibody staining is positive for inflammation around the nerve. And is there a rare staining on the stain.

WEISE: Look at that. Okay.

QUO: So the diagnosis is –

WEISE: See, in rugby we don't wear pads. I should have brought my protective gear.

QUO: She was treated with 600 milligrams of rifampin daily and her follow-up, the rash continued to worsen and the results in lacerations. Steroid treatment, intensive wound care was started that includes creams, liquids, ointments, gel, lotion, acid and: leprosy. Microbacteria grew best at 27 to the 33 celsius which correlated with the elections for affecting cooler areas of the body in humans that includes…

WEISE: Okay. Good. Word about the microbacterial disease, TB really doesn't like the periphery and that's the rule when you get into soft tissue such as the muscles and nerves. If you see that first, it's probably not TB for this very reason, it tolerates higher oxygen tensions, leprosy that is, better than TB. I will point out that Louisiana is still the proud home of the leprosy facilities, if you will, and of course credit to a physician there that was one of the initial developers of anti-leprosy antibiotics. Okay. And I owe you one my friend.

PLOTZ: Our next presenter will be Dr. Adriennea and she will present this case of difficulty diagnosing (…).

ADRIENNEA: Our patient is a 74-year-old gentleman who complained of new onset of shortness of breath when swimming. He was physically fit and regularly walked up to 3 miles without difficulty. There was no cough, fever night sweats, chest pain or leg pain.

WEISE: And I’m going to go quickly. No shortness of breath when we exercised outside of swimming.

ADRIENNEA: Not in the beginning. Patient has well-controlled hypertension, type 2 diabetes and dyslipidemia. His medications include:

WEISE: So past medical history only significant for diabetes and hypertension. >>

ADRIENNEA: Yes and it was late onset.

WEISE: Okay. Let me just say a few words about my method and approach to dyspnea and that's the way I like to approach it. If you ask a resident, they are going to draw a pyramid for you and on the base of the pyramid are the 8 causes of pulmonary causes and then the second up level will be 4 causes of cardiac causes of dyspnea. And then acid base disorders, that is to say true respiratory alkalosis, which is the symptom or the presenting find of the dyspnea. And then blood disorders which have nothing to do with anything hypoxia. But it can under exercise, create the symptoms. And the nice thing about the pyramid if you look at it is there are 3 tests that you need to make the first stab in the way of excluding the causes and that being the EKG, x-ray and APG. Going forward with dyspnea, expect I’m going to look for that information. I’m saying that in my point of view only because in case, it may be not that challenging, but for patients being admitted to the hospital, especially in the middle of the night, even though seen in clinic, it's really easy to shoot from the hip and jump the gun with a premature closure on the diagnosis and of course anything dyspnea means you're driving that respiratory component which is life-threatening. I’m throwing that out as a method and now I’ll talk about this gentleman. Because there is no sensation of shortness of breath when she exercising and standing up or walking around. Just when she she swimming. When type of swim stroke does he do?

ADRIENNEA: They asked me when we had this last week. I asked the patient and he said tell them, frog style swimming. It's a breast stroke.

WEISE: Okay, all right. And I’m saying this just in the way of a mechanical feature of the stroke can change the chest dynamics and okay. We can and back to that. And the final thing I will ask, he doesn't have platypnea or the orthodeoxia. When he's lying flat, is he short of breath in bed or –

ADRIENNEA: Not at this time.

WEISE: Okay. And what I’m driving at is you think about somebody exercising, what's the difference between running and swimming? Will it's vertical and horizontal and then the second piece is the mechanics of the stroke itself.

ADRIENNEA: So on physical examination, he appeared healthy. Actually younger than stated age as opposed to the first patient and he was in no acute distress. His blood pressure was 122 over 70. Pulse 76, regulatory rate was normal 12 and temperature was 36.5. He was only mildly overweight with BMI of 26.5. And basically his exam was normal. Heart was regular. Extremities no edema or tenderness. Skin unremarkable and I see now that I don't have abdomen but it was normal.

WEISE: Okay. And the pulses and blood pressures were equal in both arms?

ADRIENNEA: Yes.

WEISE: And the lungs cleared from the patient. No consolidation?

ADRIENNEA: No. And nothing. >>

WEISE: And let me ask you about the s1 and s2. When I say normal sound, I know that

ADRIENNEA: He was 74.

WEISE: So for a 74-year-old gentleman, give me some commentary on the loudness of s1, for example.

ADRIENNEA: I did not listen to him. I listened to his history but didn't do exam. I cannot tell you.

WEISE: Maybe this is a point. I like listening carefully for s1. The problem you is do have to realize what is the normal in different age group. It gives you some commentary on the contractile force of the left ventricle because it's the left ventricle that is closing the valve giving the s1. The s2 is very important here too because of course stenosis or sclerosis would be a fine diagnosis for somebody at 79 years of age and it can come initially with just being locked in an open position and depending upon the infarction, you may not hear the turbulence initially but you should still hear a good closure. Okay. So and on head and neck examination, normal color, no skin rashes or anything?

ADRIENNEA: No.

WEISE: I’m just driving the at the hematologic components of this.

ADRIENNEA: So, his insulin is laboratory assessment which reveals hematically 41% normal white count and differential platelets were normal. Chemistry was normal except slightly elevated glucose and:

WEISE: Okay. And let me just ask a couple of questions here. The chest x-ray truly normal in the way the lung print came out but also the aortic shadow?

ADRIENNEA: It was interpreted as normal by radiology. So, his internist performed office pathology and here his numbers before and after bronchodilators. And based on the significant improvement of this after the bronchodilators, diagnosis of asthma was made and he was started on inhaled bronchodilators. However, no improvement after two months of treatment.

WEISE: Okay. Let me step back and first I’m going make the disclosure that this is exercised induced asthma. And when you say a little bit about joust get it out there in the way we talked about exercise induced asthma. That is at all the diagnosis. First I’m going to qualify this by saying I come from New Orleans and the whole concept of exercise is very foreign to us. This is not a problem that I would see in my patient population at all. But okay. Fair enough. Here is what I know about exercise induced asthma. And maybe it plays in. Because we have a difference between just running and being in the pool is the temperature. And exercise induced asthma has everything to do with the delta going from hot to cold or cold to hot. And it's the reason that you will find, for example, college athletes or high school athletes that are doing 9 indoor track during the winter and they are fine and then you open the doors to start the spring season upon and they go out and get the cool air, that either they get at the beginning of the exercise because of the warm to cold sudden transfer or any exercise, the cool-down period where you get hot and then you cool it down. Okay. That said, I don't know the temperature of the water that he is swimming. I assume this is some controlled environment pool.

ADRIENNEA: It was a heated community pool.

WEISE: All right. So they are making a diagnosis of asthma. Which I think is going to be de novo diagnosis out there. I think it's the wrong diagnosis as 79 years of age. So it brings into play cardiac asthma, the exercise induced asthma would be a supposed find but still out there giving his age. And then way out there the exercise induced (…) that may mask as asthma. That last one really should be presented earlier but also really should present with normal exercise, not just swimming. The final thing that is different about swimming verses regular exercise, of course is the period of time that you hold the breath. Because it's not regular ins and outs. It's to hold the breath, swim for a while and then exhale. That's part of why I’m asking which kind of stroke.

ADRIENNEA: He said it was above the water.

WEISE: He is breathing with each stroke?

ADRIENNEA: Yes. So his internist referred him to the pulmonary lab at University Hospital where he did a different kind of testing which was (…) testing with methacholine. This time he was normal and had normal bronchial responsiveness so diagnosis of asthma was abandoned. He suspected his symptoms might be side effects of his medication. So, he talked to his doctor and they discontinued his medication but his symptoms persisted. Metformin was replaced with lipisides and hydrochlorisat was replaced with –

WEISE: Does that make a difference to switch?

ADRIENNEA: It did not.

WEISE: Just a word beg your pardon ace inhibitors. They are so common. Remember that the whole ace inhibitors derived from pit vipir bites. The venom, which works in two ways, one by disrupting the conversion of angio1 and angio2 but also the degradation of (…), which is if you have smaller amount of enzymes to begin with inhibited by the degradation will give you the angiodema associated with ace inhibitor use. While we are playing with the idea of some kind of asthma here, that is dyspnea associated with the exercise that is not due to inherent, we know by the methacholine, not due to inherent bronchial smooth muscle reactiveness, is there something else that is causing low clot swelling during these times of exercise either from the outside or directly from an inflammation and the ace inhibitor would have been a fine thing to do the trial. I probably would have done that. And of course it's not messing with the enzyme at all, just the receptor really should take the (…) and ace induced angiodema out of the equation.

ADRIENNEA: 6 months into his illness, exertion developed. Patient also noticed 10 pound weight loss which he thought was caused by flu-like respiratory illness from which he recovered.

WEISE: Okay. So now we have progression from the dyspnea during swimming to dyspnea all the time?

ADRIENNEA: He basically said I can't take deep breaths in bed.

WEISE: it tells you one or two things when you have the orthopnea. It tells you either there sell a lung disease and sitting up provides more profusion to the lower lungs and people breathe better, probably not it. Or it tells you that this is somebody that can no longer tolerate increases in preload back to the right ventricle and now he starts to bring into play primary cardiac disease and we can work through that now again, s1 and s2 and my pretest assessment, it will be hard to get away from this case without seeing the function of the valves.

ADRIENNEA: So he underwent exercise testing again at the University Hospital and his nuclear exercise stress test was normal. It showed low likelihood of exercise induced myocardioischemia. He also had cardiopulmonary exercise tests that was also normal. And:

WEISE: Okay. It looks remarkably normal. Due to the fact we are treating a patient not a elaborate. And was he dyspneic at all during the exercise test?

ADRIENNEA: I don't know. I didn't ask. He probably was not. Because he used to walk up to 3 miles. and I guess this wasn't -- he was quite fit. So additional symptoms developed and one year after the onset of his symptoms, he noticed during one of his regular walking regimens, that he had right leg discomfort, which he described as if something was pulling at my leg. He had to stop walking. He had a strange sensation that he never experienced before. He was referred to orthopedic surgeon who diagnosed a (…) recommended a block. The patient did not undergo procedure. He said I will think about it. He didn't believe it was sciatica. and at the same time he complained of dysphagia and throat irritations.

WEISE: Anybody over the age of who develops brand new sudden back pain should think about the big red tube in way of dissecting aneurysm. I’m going to ask, has there any image of the chest other than the chest x-ray, the stress test?

ADRIENNEA: Not that I’m aware of. But it was not really a pain. It was a strange sensation, some kind of a discomfort. Not really a pain. He underwent gastroenterology work up. He had upper endoscope that showed hiatal hernia and it was added to his medication regimen .

WEISE: And any evidence of peripheral neuropathy to go with this? >>

ADRIENNEA: Not that I’m aware of.

WEISE: Okay. And just to make this point, we are talking about for the gastric study, a couple of things that will go to it and one is whether you have the nerve neuropathy. while this is not a rule, but I will make a point there is say physiologic process, a diabetic neuropathy should make some sense. The longest nerves are the ones that take the greatest hit and the longest nerves being the sake recall and to the hands. So not to say he can't have neuropathy without this and the diabetic patient. It just makes it better. Second component is of course, two other components from the gastric emptying. There is a hormonal component and then this also the muscle itself, which boils down to sometime a deficiency in amyloid disease or lymphoma, infiltrating the stomach wall. How did all that will fit in thus far? I don't know. I’ll tell if you it's amyloid then we start looking at restrictive cardiomyopathy. It will be working and having that echocardiogram going forward. so for this point now, this the dyspnea is still present and now we have the esophyet wisa strange sensation pulling at his lower leg. I am going to assume he is up-to-date on his colonoscopy et cetera.

ADRIENNEA: I’m not 100% but I believe so.

WEISE: Okay. So esophagus and stomach of course diabetic neuropathy is fine. scleroderma, okay. I mean it's a lot to add all this in, but worth keeping in mind as we go forward.

ADRIENNEA: So he develops additional symptoms, almost a year and a half into his illness. Patient complained of loss of strength in his muscles, right leg weakness. muscle waisting and twitching. 20 pounds weight loss. fatigue and dysphagia.

WEISE: Okay. So the wasting and twitching tells you there is denervation of the muscles and especially the wasting twitching at this age. It's ALS and the especially when you bring in the hoarsness, dysphagia, the upper and lower combo of nerves. And that the age. Sadly it is Lou Gehrig's disease. and I hate to say well, just give somebody that diagnosis, but that's it.

ADRIENNEA: You're right. yes. Of course neurologic disorder was suspected with all this symptoms and signs and brain MRI was normal for age. Neurology consult was obtained and diagnosis was made. And then his respiratory function was reassessed but it was a little different. So he sat up right vital capacity that was fairly preserved, 71%, which fell significantly to 36% in the supine position.

WEISE: And just to make the point, when you're up upright, have you gravity on your side. When you're horizontal. that was the difference.

ADRIENNEA: So arthrosclerosis or Lou Gehrig's disease, that is based upon clinical criteria including upper and lower signs and symptoms such as: this made it very difficult because we don't think of this when we see this. 80% present with asymmetric limb weakness and 20% with dysphagia.

WEISE: let me make -- great presentation, thank you. Especially since I got it right. [laughter] I appreciate that. [applause] Let me pack a point about this because Jeff and I were talking before. The CPCS are fantastic for medical education. We should do more of this and more about the method and how we think not just what to think. One thing about this case -- here is my one reservation about CPS, I think it sends is the reality that a diagnosis can't be made in a short amount of time. and the reality is that most diseases, the tough ones take persistence on the part of the internist and a teamwork and that transition of care and if you don't have that, this guy 1gets lost up to the point that either the diagnosis is not made or he suffered so much even though this is a non-curable disease and it could have been avoided. so if there are students in the crowd, for all of us, we have to recognize the importance that we play as internists this longitudinal care. We have 7 minutes. Can we do a presentation? I’m going to save my comments to the end. This will be the rubber match.

UNIDENTIFIED: Acute illness case. a 62-year-old man was taken to the emergency room by his wife with major abdominal pain which had been increasing in severity over the previous day. The pain was accompanied by chest pressure. Similar episodes of pain over several years were thought to be thought to be due to related to his insulin-requiring diabetes and now the pain was more severe and penetrated through to the middle of his back and to his shoulders. The pain was considered moderately severe, that's why the ER staff in the ER and was accompanied by nausea without vomiting. no history of diary a the patient was alert, oriented, cooperative and complained of pain radiating to the back and 1of gastric pain. Neither exacerbated nor relieved by anything. Interrupt me if you want to.

WEISE: Just one question. I want to make sure we get through all of it. But the blood pressure was the same in both arms?

UNIDENTIFIED: It was.

WEISE: Okay. And I’m just for the crowd going to point out the dramatic pulse pressure differential here. And I’m going to come back to some commentary on that. Too often we get folks with the absolute numbers and in a systolic diastolic can give you great insight into what the potential disease is. Let's keep going.

UNIDENTIFIED: CO2 was a little high.

WEISE:  Anything retro peritoneal in the way of back pain and (…) straight back. Okay. Let's keep going.

UNIDENTIFIED: They were concerned about not entirely sure what they were concerned about and they did spiral CT with contrast. And nothing in the adrenal. He was sick and he was a puzzle.

WEISE: Aand that's the leading diagnosis. All right. I’m just going to remember that radiation that he had years ago as we go forward. Okay I think he actually virtually insisted on leaving. Feeling somewhat better. [laughter] but by no means well. The diagnose was a GI motility disturbance secondary to diabetes or possibly gastrointeritis. At home the pain did not abate.

UNIDENTIFIED: Okay. On the day after discharge the patient's wife notice aid rash over the last scapula and suspected a diagnosis.

WEISE: Just so I can be two in one. Okay. And those are vesicles I assume? Okay. Okay. Just so you know herpes is to crawl. And it has nothing to do with the herpes virus. But it crawls along and hence the name, herpes for both. It is to remind you of the dermatomes both inside as well as outside and for many patients, especially the elderly, you will see the pain that will precede long before the vesicles appear and here is the method in which we didn't have time to go through it. If you ask any Tulane resident, sit him down, only because I drill them on it, they'll tell you, it is managing a bullet air oh, whatever, going from front to back all the way through the chest. And to think about each tissue as you go through. That is to say you start with the skin and you think of herpes and you just to consider it, and then it's to the bones and then to the muscles and then the pleura and then the lungs and then the pericardium and then the heart and then the aorta and then the esophagus and then the spine. But the method keeps you honest in the way of thinking of each level of tissue gauze through it's very, very important not so much because if you missed therapies it's not a whole lot. We could have done the acyclovir which would have made his life better than the 6 physical exams. Where it does play as an aside, and we kill somebody once a year on this. Somebody that comes win a classic chest pain who is having a dissection and somebody goes straight to the protocol of anticoagulating him and boom, that's it. And this method at least makes you think about it. The fumble is not looking at the x-ray for the dissection as an example before you rush to protocol-based behavior. Let's finish with this and then –

UNIDENTIFIED: You really said it. The pain precedes the rash by days but he -- even as much as a week. It's due to the replication of the virus and the ganglia and the period before the rash at the time requires the virus to continue replication in the ganglia, spread down the nerve skin and replicates in the skin to induce sufficient necrosis and inflammation to cause the rash. And he was actually -- he called his internist who over the telephone put him on the basis of the description of the rash, put him on acyclovir and it took a while.

WEISE: Fantastic case. I want to say thank you for your attention during this session. Thank you.

[applause]

ANNOUNCER: You’ve been listening to discussion on the topic, "Mysterious Cases" -- part of the Contemporary Clinical Medicine: Great Teachers series. Our speaker was Dr. Jeffrey Weise, Associate Dean for Graduate Medical Education at Tulane University Health Sciences Center. You can see a closed-captioned videocast of this lecture by logging onto http://videocast.nih.gov -- click the "Past Events" link. The NIH CLINICAL CENTER GRAND ROUNDS podcast is a presentation of the NIH Clinical Center, Office of Communications, Patient Recruitment and Public Liaison. For more information about clinical research going on every day at the NIH Clinical Center, log on to http://clinicalcenter.nih.gov. From America’s Clinical Research Hospital, this has been NIH CLINICAL CENTER GRAND ROUNDS. In Bethesda, Maryland, I’m Bill Schmalfeldt at the National Institutes of Health, an agency of the United States Department of Health and Human Services.