Jeff Green Revelation Focuses Attention on Aortic Aneurysm

Posted on June 16, 2012 by cazzie

With the revelation this past week by the Boston Celtics that their forward, Jeff Green, will be operated on soon for repair of an aortic aneurysm, attention has been focused on this potentially catastrophic condition.

WHAT IS AN AORTIC ANEURYSM?

Simply put, an aneurysm is an area of a blood vessel where the vessel wall has become weakened. This weakening may occur from age-related degeneration of the tissues that make up the vessel wall, or as a result of inherited or congenital conditions at birth. Under the pressure of blood flow, the weakened area may cause abnormal stretching and thinning of the vessel wall, and consequent enlargement of the vessel diameter. This stretching and thinning process may ultimately lead to rupture of the vessel. When the vessel involved is a major artery, such as the aorta, rupture can have catastrophic effects. The difficulty with aortic aneurysms is that they very often cause no symptoms whatsoever (are asymptomatic) until the fateful day when they rupture. In a young man such as Jeff Green, the problem is almost certainly something he has had the potential to develop from birth. One of the more common genetically inherited causes of aortic aneurysm is a condition known as Marfan’s Syndrome. This syndrome is termed a disorder of “connective tissue”. Normal connective tissues are critical to the strength and integrity of many of the structures in the human body, including blood vessels, ligaments, tendons and the connective framework of fibers in muscles, capsules, cartilage, bone, adipose (fatty) tissue, and lymphatic tissue. In Marfan’s Syndrome, the connective tissues are not healthy at the cellular level, and have a tendency to degenerate at an abnormally accelerated rate. One of the characteristics of Marfan’s Syndrome is the tendency for those affected to be unusually tall, so, it is tempting to wonder if Jeff Green may be affected by the condition (his height is reported as 6′ 9″).

THE ANATOMY AND FUNCTION OF THE AORTA

The aorta is the “big Kahuna” of arteries in the human body, responsible for the distribution of freshly oxygenated blood to EVERY organ and living tissue, including the heart itself via the coronary arteries. Take a look at the following 3D medical animation of aortic anatomy and function to get a more graphic idea of how the aorta works.

ANATOMY AND FUNCTION OF THE AORTA

As is apparent from the above animated review, a rupture of the aorta anywhere along it’s length will result in a profound loss of blood flow to tissues and organs distal to (beyond) the rupture. The higher up (or more proximal) the rupture, the greater the adverse effect on blood flow (perfusion). Taking this concept to its logical conclusion, if the aneurysm is located at the root of the aorta at its origin in the heart, a rupture would result in a sudden cut-off of blood flow to the entire body. Following is a 3D medical animation of a rupture involving an abdominal aortic aneurysm.

RUPTURE OF ABDOMINAL AORTIC ANEURYSM

Pretty scary, isn’t it?

RUPTURE OF THE THORACIC AORTA AND CARDIAC TAMPONADE

As if interruption of blood flow to every organ in the body weren’t enough, there is another potentially life-threatening complication of aortic aneurysm rupture. The heart is enclosed by a membranous envelope called the “pericardial sac” or “pericardium”. This membrane serves to isolate the heart and coronary arteries from surrounding structures in the chest cavity (thorax), primarily the lungs. The pericardial attachment to the diaphragm also helps to stabilize and anchor the heart within the chest. Please take a look at the following 3D medical animation demonstrating the relationship of the heart, aota, and pericardium to get a better idea how this all works. Note especially that the first couple of inches of the aorta and its root are also enclosed by the pericardium.

ANATOMY OF THE PERICARDIAL SAC (PERICARDIUM) AND CARDIAC CHAMBERS

While the pericardium is rather elastic in nature, permitting expansion and contraction of the cardiac chambers (ventricles and atria), it clings relatively tightly to all surfaces of the heart, neither permitting fluid to exit, or enter, the sac. It follows, then, that an aortic aneurysm of the aortic root (or close to the root) will also be enclosed by the pericardium, and if the aneurysm were to rupture, the very brisk flow of bleeding (hemorrhage) from the point of rupture will be contained within the pericardial sac (hemopericardium). Although the pericardial sac is capable of considerable expansion over days or weeks if there is a slow accumulation of fluid within its margins, the rapid introduction of blood into the sac, such as occurs with a sudden rupture of an aortic aneurysm, very quickly exhausts the ability of the pericardium to expand. This results in an extremely sudden (paroxysmal) increase in the pressure within the sac, which is exerted on the cardiac chambers. If not relieved on an emergent basis, the increasing pressure on the ventricles and atria causes cessation of the heart’s ability to pump blood, with chamber action coming to a complete standstill (cardiac arrest or asystole). This dangerous phenomenon is known as “acute cardiac tamponade”. Following is a 3D medical animation that demonstrates how rapidly a rupture in the aortic root (such as may result from an untreated aortic aneurysm) leads to asystole. I produced this animation for a criminal case in which a rupture occurred from a knife blow, but the situation is virtually identical to what can happen with sudden rupture of an aortic aneurysm.

RUPTURE OF THE AORTA WITH ACUTE CARDIAC TAMPONADE

TREATMENT OF AORTIC ANEURYSM – ENDOVASCULAR GRAFT PLACEMENT

From the preceeding, it can be seen that early diagnosis and treatment of aortic aneurysm is essential (prior to rupture!). There are 2 approaches to treatment, both surgical. Aortic aneurysms that are located distal to (away from) the heart, particularly those located in the abdomen, may be treated with a low-invasive procedure known as an “endovascular graft”. In this procedure, the aorta is accessed through small incisions in the femoral arteries, through which a variety of instruments, including a collapsable graft, may be introduced. After positioning across the area of the aortic aneurysm, the graft is expanded to shore up the weakened area. As the old scholar said, “a picture is worth a thousand words”. I have extrapolated this maxim to animation – “an animation is worth a thousand words”. So please take a look at the following 3D medical animation that demonstrates how an endovascular graft works far better than any verbal description.

PLACEMENT OF ENDOVASCULAR GRAFT FOR ABDOMINAL AORTIC ANEURYSM

TREATMENT OF AORTIC ANEURYSM – OPEN SURGERY

Unfortunately, not all aortic aneurysms lend themselves to the relatively low-risk placement of an endovascular graft. Particularly aortic aneurysms that are located in the upper chest, close to the heart, or involving the aortic root, must be treated with an open procedure, where the chest cavity is opened. Moreover, many such cases also require that the heart be stopped during the procedure, and the patient place on a heart-lung machine (cardiopulmonary bypass). When working on, or in close proximity, to the heart, temporary cessation of the heartbeat provides a far easier environment for the operating surgeon. While the heart is stopped, the cardiopulmonary bypass machinery draws oxygen-poor blood from the patient’s venous system, adds oxygen back in, then returns the reoxygenated blood back to to the arterial system. Following is a 3D medical animation showing how cardiopulmonary bypass works.

CARDIOPULMONARY BYPASS

Typically, patient’s undergoing open surgery will have the area of aortic aneurysm removed either partially or completely, and a synthetic graft sewn into place. As is clear, treatment of aortic aneurysm via the open surgery method is far riskier than endovascular graft placement, but relative to the often fatal prospect of an aortic aneurysm rupture, with death occurring either from hemorrhagic shock or acute cardiac tamponade, open aortic aneurysm surgery is yet another example of modern Medicine’s amazing life-saving and cutting edge capabilities.

JEFF GREEN’S AORTIC ANEURYSM

The news reports of Jeff Green’s particularly situation have been somewhat vague as to the precise nature of his aortic aneurysm. The Celtics are apparently doing a great job so far of protecting his confidentiality (and so they should). All credit goes to the medical personnel who diagnosed the condition. As mentioned earlier, aortic aneurysms are usually silent until they rupture. They are difficult, if not impossible, to detect on routine physical examination, even if thorough. Plain film xrays may or may not show the widened area of the aorta, whereas they are much more readily detected by ultrasound imaging. However Mr. Green’s aortic aneurysm was picked up, his diagnosis is a testament to the thoroughness with which the Celtic’s medical staff care for the players. Despite the lack of specificity of medical reports to the press, the term “open heart surgery” seems to keep cropping up in many of the dispatches. This inclines me to believe that Jeff’s aortic aneurysm likely involves, or is very close, to the root of the aorta where it emerges from his heart. We can only hope (and chances are good) that Jeff’s surgery goes without incident, and that he can return to his role with the Celtics unimpaired, and so ultimately fulfill the athletic promise of his young career. Best of luck with it Jeff…

From Walt Disney to 3D Medical Animation…

Posted on June 16, 2012 by cazzie

Recently I had a client express uncertainty regarding the term “3D medical animation” on my company website. Did the 3D animation I produced have to be viewed with special “3D” glasses? I assured him that wasn’t the case. “Well then”, he asked, “how does the “3D” part of it work?” And therein lies a confusing aspect of the term “3D Medical Animation, or “3D animation” in general, for the term refers to animation created with the use of virtual 3D objects, and not a “3D viewing experience”, as we have recently become accustomed to seeing at the movies. I’m hoping that today’s post will shed a little light on the difference.

A LITTLE ANIMATION HISTORY

In understanding what modern 3D animation is, it’s helpful to look at a bit of the history of animation. Historians have traced man’s desire to graphically depict motion as far back as cave paintings from the paleolithic era, where, for example, horses were pictured with multiple sets of legs in different positons to impart the idea of motion. There are many similar examples over the millenia since, but one of the earliest devices to successfully give the illusion of motion was the Zoetrope. The first known instance of this device was in China in 180 AD, but the “modern” appearance dates to 1834. The Zoetrope consisted of a wheel, lined on its inner surface with a series of drawings, each drawing portraying an animal or characters, with slight differences in the positon of the subjects from one drawing to the next. The wheel had a series of vertical slits. Each slit permitted the viewer to see just one of the images. When the wheel was rotated, the images, as viewed in sequence through the slits, gave the illusion of motion. The number of drawings that could be placed in the Zoetrope was limited to a dozen or so, so while the effect was mesmerizing to the viewers of the time, there was limited opportunity to tell any kind of a story with the animation, and it remained just a novelty.

The Zoetrope

ANIMATION GOES TO THE MOVIES

At the beginning of the Twentieth Century, animation made a huge leap forward when drawings could be photographed onto motion picture film, one drawing per frame of film, and then played back at 24 frames per second. Suddenly, there was no limit to how long an animation could be, and the creative possibilities for story telling were endless. The first known example of an animated motion picture was produced by J. Stuart Blackton in 1906. Titled “Humorous Phases of Funny Faces”, it depicted what appeared to be a cartoonist drawing faces on a chalkboard, with the faces coming to life with movement.

Humorous Phases of Funny Faces – J. Blackton 1906

From that point forward, animated motion pictures evolved rapidly. Favorite characters were born - Krazy Kat, Betty Boop, and Mickey Mouse. Sound was added; Argentinian Quirino Cristiani‘s 1931 production of “Peludopolis“ was the first to use synchronized sound. Color was added; Walt Disney won an Academy Award for ”Flowers and Trees” (1932), the first animation to use full, three-color Technicolor. Cartoons a few minutes in length gave way to feature-length animated motion pictures. Disney’s “Snow White” is easily the best known, and most successful, of the early features, but there were at least 8 feature-length animated pictures produced internationally prior to “Snow White” (none of these early features survive today). “Snow White” was also the first animated feature to use “cel animation”. In the cel technique, pictures are drawn using colored ink onto individual sheets of transparent celluloid (hence the term “cel”). The cel technique provided several major advantages; backgrounds and non moving objects in the foreground of a scene could be drawn on separate cels, as could the moving objects or characters in a scene. In this way the same background cell could be used repeatedly from one frame to the next. This saved an enormous amount of time in producing the animation, and eliminated the “jittery” characteristic of earlier animations, in which the entire scene, backgrounds, characters and all, had to be completely redrawn in each frame.

As well, the quality of artists creating animations saw steady improvement as the years went by. Again, Walt Disney was one of the first to pioneer the hiring of top-notch artists for his studio, providing them with ongoing training in the latest animation techniques. Eventually, Walt formed the California Institute of the Arts (CalArts), in Valencia, as an institution for the training of animation artists.

“MOVING PERSPECTIVE” AND THE MULTIPLANE CAMERA

The net result of all of these innovations was a steady improvement in the look and feel of animated productions (whether they be features or shorts). But prior to the computer age, there was an essential limitation in animation that no amount of artistic talent could overcome, and that was the fact that animation was a two-dimensional medium. It was very difficult, if not impossible, to convey a feeling of moving perspective in an animation. An example of moving perspective can be seen as you drive your car along a highway, surrounded by forests in the foreground, and hills and mountains in the background. As you view the scene from your moving car, the trees closest to you have an appearance of moving much more rapidly than trees in the background; at the same time, the hills move by at a quicker pace than the mountains behind them.

2D moving perspective – objects all move at the same speed irrespective of distance from the viewer

3D Moving Perspective – note how the apparent speed of the 3D objects varies with their distance from the viewer

This type of relative movement is extremely complex when trying to draw all of these elements one frame at a time, even with the cel technique. Walt Disney understood this limitation, and, in an attempt to overcome it, ever the innovator, he invented the “multiplane camera”. The multiplane camera consisted of a device that resembled a bookshelf (see figure 1), capable of housing 4 cel paintings inserted like shelves into the housing. The motion picture camera was attached at the top of the housing, and aimed downward through the paintings. Typically, foreground elements or characters were painted onto the top shelf or shelves, while deeper background elements occupied the lower shelves, with the deepest elements of all on the bottom shelf. As the animation was filmed, the camera could be moved (or “panned”) from side to side at the top of the housing. This would provide an illusion of moving perspective – elements on each painting would appear to be moving across the scene at different speeds. Foreground elements on upper paintings would appear to move more rapidly than background elements on the bottom. Walt first used this technique on “Snow White”, and for years afterward, the multiplane camera set the standard for “3 dimensionality” in animated films.

But the 3D effect created with the multiplane camera was just that – an effect. It permitted variable movement on 4 different planes within the animated scene. It did not capture the true experience of moving perspective, in which we see an almost infinite variation in movement of objects as we pass by a scene. Let’s go back to our drive by the forest and mountains. As we cruise along, the mountains in the background appear to move at a slower speed that the trees in the foreground, but each tree is also at a different distance from us. Therefore, our perception is that each tree moves at a slightly different speed as well. Even the individual branches on a particular tree are at varying distances, so that branches closer to us appear to be moving more rapidly than those further away. The needles on an individual branch are subject to the same phenomenon, and on and on. Thus, the infinite complexity of moving perspective.

THE COMPUTER AGE AND TRUE 3D

With the advent of the computer, it became possible to create “3D” objects in the virtual space of the computer screen. Unlike traditional 2D animation drawings, which can have height and width but not depth, these objects truly have three dimensions, and once created, can be manipulated on the screen just like an apple can be manipulated in your hand; the 3D object can be rotated, flipped top to bottom, and any side of it viewed from any angle. The manipulation of 3D objects in virtual space provides tremendous advantages over 2D when it comes to conveying information about an object to the viewer This comes in especially handy in technical or scientific animation, such as the 3D medical animation I have specialized in for the past decade. Take a look at 3D Medical Animation #1. This is an animation depicting the male pelvic anatomy. Each anatomical object was “built” as a 3D object, hence we can view these objects from any angle, and as the camera chnages perspective, the relationships of the structures are readily revealed. In this segment, the anatomical structures are viewed, first, from the front, then from the side, and finally, from above.

3D Medical Animation 1 – Male Pelvic Anatomy

3D Medical Animation #2 is another example; in this case, a newborn baby with a “nuchal” umbilical cord. Note how readily the relationship of the umbilical cord to the baby can be discerned as a result of the ability to view the baby from all sides.

3D Medical Animation 2 – Nuchal Umbilical Cord

A scene built in 3D space can be populated with a whole group of 3D objects, all placed at different distances from the viewer, and all moving at different speeds with respect to each other as well as the viewer. Hence, a true experience of “moving perspective” can be achieved. The complex mathematical calculations involved in generating such a “3D” scene are taken care of by the big brain of the computer.

NOT ANIMATION IN 3D, BUT 3D ANIMATION…

So when animators use the term “3D animation”, we are generally not referring to a “3D viewing experience”, such as “Toy Story 3 in 3D”, where one feels as though the objects on the screen are jumping out at us.. We are, instead, referring to the manner in which the animation has been created, using virtual 3D objects and manipulating them in a virtual 3D universe, rather than drawing 2D images on paper or celluloid. In other words, it is not necessary to wear special glasses to view 3D Animation, but it is necessary to don them in order to have a 3D viewing experience at the movies (or increasingly, at home on the big screen).

It may well be that in the not too distant future, all animated productions, whether for pleasure or for knowledge, will be presented as a “3D viewing experience”. I’m certain the time will come when we will be able to throw away the 3D glasses altogether, and enjoy a true 3D holographic production. For the time being, anyway, the “3D viewing experience” will be confined to the movie houses and home entertainment rooms, and my clients (and jurors) will not be required to wear special glasses to view 3D medical animation at trial. Stay tuned…

cjs

click here to read more about 3D medical animation and use at trial…

Man Runs Marathon with a Pulmonary Embolism…

Posted on June 16, 2012 by cazzie

The title of this post sounds kind of cheesy, doesn’t it? It reminds me of when I was a kid, and we use to marvel at the headlines in the “National Enquirer” down at the local candy store, with stories like “Man lives for 2 years without head…” But that’s the amazing thing about the practice of medicine – you run into patients time and again that lend credence to that old saw about truth being stranger than fiction. And the title of this post is true, or at least, it could be. I guess I had better explain…

PULMONARY EMBOLISM DUE TO DEEP VENOUS THROMBOSIS

PULMONARY EMBOLISM

WHAT IS A PULMONARY EMBOLISM?

For the uninitiated, simply put, a pulmonary embolism is an abnormal clot of blood present in the arterial side of the blood circulation in the lung(s). I use the term “abnormal” because not all blood clots in the pulmonary circulation are problematic. In fact, small clots are constantly being formed throughout our bloodstreams 24/7. As soon as these clots are formed, naturally generated “clot-busting” chemicals rush to the affected spot and dissolve the clots, so that any interruption in blood flow through the affected artery is kept to a minimum. This clotting and de-clotting process is just another of the numerous examples of a balanced system within our physiology. In the case of a pulmonary embolism, however, the clot, or clots, are large enough, or numerous enough, that the natural clot-busters can’t keep up with the demand to dissolve. This results in a prolonged interruption of blood flow through the affected artery or arteries. In the lungs, this interferes with the transfer of oxygen from the airways (bronchial system) to the bloodstream. The greater the total amount of abnormal clot present (“clot burden”), the greater the interference with the oxygenation process. Healthy children and adults have a fairly large respiratory capacity – at any given moment, we are using only a fraction of our bodies capacity to absorb oxygen. As a result, most of us can tolerate the presence of smaller amounts of abnormal clot in the pulmonary arterial system with minimal or sometimes even no obvious symptoms. As the amount appear of clot increases, signs of lowered blood oxygen levels (hypoxia) appear – primarily shortness of breath very often associated with chest pain. The onset and severity of the symptoms is also a function of the level of fitness and physical activity of the affected individual - given the same clot burden, and all other things being equal, a couch potato is less likely to notice symptoms than a marathon runner. (For more information on pulmonary embolism, please see my pulmonary embolism review article.)

THE MARATHON RUNNER

Which brings me to the subject of today’s post – the marathon runner. In addition to running my medical legal graphics business Monday to Friday, I still see patients at a local Urgent Care center on weekends. Some months ago, a 25 year-old man presented to our clinic with a complaint of shortness of breath and chest pain. Let’s call him “Fred”. Fred had noted the shortness of breath for about a week prior, but had just developed the chest pain 24 hours before coming to see me. He was a long-time runner, logging about 40 miles per week, and had just completed the Portland marathon 3 weeks prior to his clinic visit. He had been scheduled to run a half-marathon right around the time his shortness of breath developed, and found that he could complete less than a mile, and then had to stop because he felt so short of breath. He had been under a lot of pressure at work recently, and thought perhaps his shortness of breath was stress-related. But when he developed fairly sharp, persistent pain in the center of his chest 24 hours prior to his visit, he decided to get it checked out.

THE HISTORY

Fred had no history of previous serious medical problems. Specifically, he had no history of clotting disorders, nor of abnormal clots anywhere in his body, was on no medications, and had never been a smoker. Nor did his family members have any such history. He denied any pain or swelling in his legs (a common source of pulmonary embolism is clots that form in the deep veins of the legs – these are called deep venous thromboses or DVT – see my article on pulmonary embolism for more information). The only point of interest in his history was that he had come to his regular doctor about a month prior (1 week before running the marathon) with a complaint of mild central chest discomfort on exertion that had been present for several days. This was not interfering with his marathon training, but with just 1 week to go before his marathon run, he was being extra cautious about any bodily changes, and wanted to nip any possible problem in the bud, lest it stop his run (I’ve been there - I ran my one and only marathon in the 80′s, and as the run approached, I was sure every little ache and pain was about to become something big!) On examination that day, his doctor was able to demonstrate some tenderness in Fred’s anterior chest wall, but the exam was otherwise normal. A chest x-ray and EKG looked perfectly normal as well. His doctor concluded it was some mild irritation in the chest wall, and prescribed some anti-inflammatory medication, which Fred stated seemed to do the trick. By the day of the marathon, the chest discomfort was resolved.

THE PHYSICAL EXAMINATION

On examination, he was a lean, fit appearing young man – he looked like someone capable of running 26.2 miles. He was clearly anxious about his current symptoms, and was close to tears when discussing the stress he had been under at work. I think he felt like a fraud, and that his symptoms were being generated by his anxiety. Fred’s physical examination was completely normal. his vital signs – blood pressure, pulse, and temperature were all normal, as was the oxygen saturation (pulse ox) in his blood – 99% on room air – anything at 96% or higher is considered normal). His lungs were clear when I listened with my stethoscope, as were his heart sounds and pulse rhythm. His lower limbs showed no sign of unusual swelling or tenderness – the kinds of findings we would see with deep venous thrombosis (DVT). In fact, the most interesting aspect of his physical examination was what wasn’t present - try though I might, I could not elicit tenderness when I pressed on Fred’s chest wall. This was the opposite of his examination a month prior, when his own Doc had demonstrated tenderness, and it left me with a fairly large problem: what was causing Fred’s chest pain?.

THE DIFFERENTIAL DIAGNOSIS

So here was a seemingly very healthy 25 year-old man, who nevertheless had a 1 week history of shortness of breath – severe enough to prevent him from running, and a 24 hour history of sharp chest pain, for which my physical exam had yielded no clues as to its origin. Based on all of this, I had fairly rapidly formulated a list of possible diagnoses for Fred – a so-called “differential diagnosis”. That’s a term doctors use when they’re not absolutely certain what the diagnosis is – this happens a good percentage of the time – (Medicine is, as yet, still an inexact science). The “differential” gives us a list of possible diagnoses. We then take further steps to attempt to eliminate the diagnoses on our list, until we are (hopefully) left with the one, true, diagnosis. Of course, it doesn’t always work that simply, but you get the idea. Once we have created a differential diagnosis, the steps we take generally involve some type of testing, be it blood tests, imaging studies, etc. Sometimes, we discuss the case with someone smarter than us (we call these smarter people “specialists”) to help guide us along the way.

But I digress! My differential diagnosis for Fred that day came down to three possibilities:

1) myocardial infarction (heart attack) – not impossible, but extremely unlikely in a fit 25 year old – I’ve never seen an MI in one so young in 30 years of practice

2) pulmonary embolism – again, very unlikely in a fit specimen like Fred, with no risk factors, no personal history of similar problems, and no family tendency to such problems.

3) anxiety – really? Can anxiety cause sharp chest pain? Absolutely! I’ve seen this dozens of times. What about shortness of breath? Well, yes, I’ve definitely seen shortness of breath in anxious folks, but typically, this occurs during a special kind of very acute anxiety called a “panic attack”. Prolonged shortness of breath, persistent over several days is a bit unusual for anxiety.

THE DIAGNOSIS

So – 3 possible diagnoses to sort through – what steps to take to nail down the one, true diagnosis? When anxiety is on the differential list, the only way to make the diagnosis is to rule out all of the other diagnoses on the list first. If they all turn up negative, then you’re left with anxiety. This is known as a “diagnosis of exclusion”. Exclude all the other diagnoses, and you’re left with the diagnosis that hasn’t been excluded. Sounds a bit unscientific, but, unfortunately, there’s no blood or imaging test one can perform that will positively show that a physical symptom is related to anxiety.

Ruling out a myocardial infarction (heart attack) is relatively easy – get an EKG (electrocardiogram - I’ve never been sure where the “K” came from!) and test Fred’s blood for cardiac enzymes – these are enzymes that are released when fibers of the heart muscle (myocardium) are damaged or die, as in a heart attack – see my article on MI for further info).

PULMONARY EMBOLISM AND THE D-DIMER TEST: THE DOUBLE-EDGED SWORD

Ruling out a pulmonary embolism is a bit trickier proposition. These days, if we suspect pulmonary embolism, we do a blood test for “D-Dimer”. D-Dimer is a protein fragment that occurs as a product of the activity of natural clot-busters on clots. The larger the clot, the greater the level of D-dimer detectable in the bloodstream. The difficulty with D-dimer is that it lacks a high degree of specificity – that is, there are processes in the human body that can give rise to an elevated level other than the abnormal clots we see in pulmonary embolism. This may give rise to falsely positive (ie elevated) D-dimer levels. On the other hand, the sensitivity of the test is very high. High sensitivity means that there is a very low rate of falsely negative results with D-dimer. That is, if the levels are not elevated, you can bet your bottom dollar that there is not an abnormal clot process occurring anywhere in the body (including the lungs), because the D-dimer test is very sensitive to the presence of abnormal amounts of clot.

So if the D-dimer is normal, hallelujah, we’ve ruled out a pulmonary embolism. The problem arises if the test is elevated, even slightly elevated. Not only have we not ruled out a pulmonary embolism – now we have to take a further step to test for it. Currently, that further step is a CT (Computed Tomography) scan of the lungs. The CT can show us definitive proof of the presence or absence of pulmonary embolism. Why not just do the CT in the first place, you ask? For one thing, to get the best imaging results, CTs are generally done after an injection of contrast into the patient intravenously. A small percentage of patients may have a significant allergy reaction or intolerance ot the contrast. Secondly, and of greatest significance for all who undergo a CT, is the high amount of radiation exposure the CT involves. A CT of the chest is delivers the radiation equivalent of 200 plain film chest x-rays! That’s a significant amount of radiation, particularly in individuals who, for one reason or another, have to have repeated CTs over the course of their lives. And where there is more radiation, there is more cancer. It is now estimated that up to 2% of all cancers in the United Sates annually are related to imaging study radiation exposure.

So when a physician orders a D-dimer, knowing that the test carries with it a significant probability of a falsely positive result, she is acknowledging, up front, that the patient involved may end up having a CT scan, and therefore, be exposed to high levels of radiation. For this reason, we try to limit D-dimer testing to patients in whom there are symptoms, and/or risk factors, that increase the pre-testing chance that they may have a pulmonary embolism. And because each radiation exposure adds to the previous exposures over a lifetime, we are particularly reluctant to use the CT scan in younger patients without a really good reason for doing it. (For further info on D-dimer and pulmonary embolism testing, please see my article).

FRED SAYS “ENOUGH TALK! PLEASE DIAGNOSE ME ALREADY!”

Ok Fred – what am I going to do with you? You’re 25 years old, you’ve had shortness of breath for a week, and chest pain for a day, and you have no risk factors for pulmonary embolism. Not only are you low risk for pulmonary embolism you’re an athlete – you’re not sitting around all day waiting for the blood in your veins to clot, you’re out pushing that blood around your system, decreasing the chance of abnormal clotting. You have a completely normal physical exam, and you’re oxygenating at 99% of your bloodstream’s capacity (not a finding you would typically correlate with pulmonary embolism). And you’ve been under a lot of stress lately, and we know that stress can cause just about any physical symptom in the book. All of these considerations are racing through my mind after I’ve spoken to and then examined, Fred. How would I decide whether or not to risk exposing this very young man to a potentially needless dose of CT radiation?

Well, in the end, I did order the D-dimer test, and I did it for 3 reasons: First, even taking into account his recent anxiety, Fred’s shortness of breath seemed inappropriately severe and persistent to be blamed on on a case of nerves. Second, I had no good explanation for his chest pain. The previous diagnosis of chest wall pain a month prior just didn’t apply based on his current exam. And even before I saw his EKG, I knew that a myocardial infarction (heart attack) was extremely rare in a fit young individual. And third, something in my gut told me that there was more to Fred’s current physical problems than anxiety. Call it intuition if you will, but after 30 years of practice, there are just times when you feel that something significant is going on in a patient, even though you can’t put your finger on exactly what it is, or why you feel that way. And that’s how I felt about Fred that day in clinic.

THE PAYOFF

Fred’s chest xray and EKG were normal, as were all of his blood tests, with the exception of the D-dimer. The D-dimer level was 3300 (normal at our lab is 500 or less). So off to CT we bundled him for a lung scan, and lo and behold, his pulmonary artery system was full of clots on both the left and right side. He was promptly transferred to the Emergency Department, and subsequently admitted to hospital for anit-coagulation therapy. My gut feeling paid off – this time…

TIMELINE

In considering Fred’s very unusual case after the fact, I found myself dwelling on one question: how long had Fred been walking (or running) around with his pulmonary embolism (or emboli as it turned out)? I’m 100% certain that he’d had the lung clots for at least the week prior to his visit with me – the period of time when he had noted the marked shortness of breath on exertion. But wait, he’d visited his own physician a month before with complaints of chest pain. Might he have had some degree of pulmonary embolism then? And if so, how is it possible that he could have completed a marathon run just 1 week later. One would presume that, with any degree of blood flow compromise in his lungs due to embolism, he’d have perceived some kind of problem with his endurance.

RECANALIZATION

Actually, it is possible that Fred could have had chest pain due to a pulmonary embolism, and then run a marathon 1 week later. Earlier in the post, I touched on the ongoing balance between small clots forming in the body, and naturally occurring clot-busting chemicals that dissolve the clots to keep us out of harms way. When an abnormal clot, such as a pulmonary embolism, initially occurs, the clot-busters in our body go to work, just as they would on a smaller clot, and in the early stages of the embolism, the clot-busters may actually succeed in re-opening blocked arteries. This process is known as recanalization, and it can permit an individual with pulmonary embolism to have initial symptoms, followed by periods of apparently normality (see an animated depiction of recanalization below). Unfortunately, particularly where there is a process feeding the pulmonary embolism, such as clots in the legs (DVT) that repeatedly break off and travel via the venous system to lodge in the pulmonary arteries, eventually, the total amount of abnormal clot (clot burden) simply becomes more than the clot-busters can cope with, and the affected individual inevitably experiences significant symptoms, or even death.

PULMONARY EMBOLISM WITH RECANALIZATION

PULMONARY EMBOLISM

This process of recanalization may well have been the factor that allowed Fred to run a marathon after an initial pulmonary embolism. I’ll never know for sure whether he had the embolism that week prior to the marathon. It could have simply been a coincidence – some minor chest wall inflammation a week prior to the marathon, then onset of pulmonary embolism sometime after. But coincidences in medicine have always made me uncomfortable. My experience has been that events in a patient’s medical condition that appear coincidental, more often than not, turn out to be related.

DENOUEMENT

Fred’s doing well now. Six weeks after diagnosis, he is still on anti-clot medication, but is back training for another marathon. Even after a very extensive workup, we never did figure out what caused his pulmonary embolism. This inability to pin down the underlying cause of embolism is unusual but not rare. My guess is that he’ll be returning to the clinic very promptly should he ever develop any kind of chest pain or shortness of breath in the future…

cjs

Living the Dual life…medical art and the art of medicine

Posted on June 16, 2012 by cazzie

I spend Monday to Friday each week immersed in the production of 3D medical animation and medical illustrations for legal cases, but most weekends, you’ll find me seeing patients at a local Urgent Care clinic attached to a major area hospital. As much as I love the hours spent at my workstation translating a physiological process or a surgical procedure into images, the actual practice of medicine still holds a unique fascination for me after more than 30 years at it. It seems that this fascination derives from 2 aspects of clinical practice; the first is simply the intellectual challenge in considering the patient’s history and physical examination, and attempting to arrive at the correct diagnosis and treatment. Well, very often, not so simple as it turns out, but of course, therein lies the challenge. Just like fingerprints and snowflakes, no two humans are the same, and no disease process manifests itself quite the same way in two different people. To give a relatively straightforward example, acute appendicitis usually presents with short-term abdominal pain, but beyond that, there can be incredible variability in the presentation. Some folks start with pain around the umbilicus, which lasts for several hours to a day or two before localizing to McBurney’s point in the right lower quadrant; some develop rapid onset of pain that starts at McBurney’s from the get go; some have an elevated white count of 15,000, and others have no elevation at all; some are doubled-over from the pain, while others complaining of three days of pain appear completely unphased. The process of sorting through these nuances is not something that can be learned from a book. It can only be engendered by repeated encounters with the disease over a period of years – in other words, through experience.

EFFECTIVE COMMUNICATION

But there is a second aspect to medical practice that keeps me coming back to clinic year after year. Simply put, it is the opportunity to communicate effectively with patients. “Communicate effectively” sounds a bit dry, doesn’t it? But for me, it’s the essence of the ”Art of Medicine”. And effective communication can be particularly difiicult in the Urgent Care setting. Unlike regular clinical practice in Primary Care, where you have a chance over the course of months or years to really get to know, and form a relationship with a patient, in Urgent Care, seeing patients who are complete strangers is the norm. In a very brief period of time (usually 10-20 minutes), the Urgent Care clinician must gain the trust of a person they’ve never met; in most cases, a person who is not feeling or functioning anywhere near their best; make that person feel that they are really being listened to while eliciting the critical details of the history and performing an appropriate physical examination, and then arrive at a diagnosis and treatment plan, and explain all of this to the patient in a way that is comprehensible. To carry all of this out properly requires a finely honed skill – a skill well beyond the basic ability to correctly diagnose and treat. It tests one’s powers of concentration – to be able to shift your focus exclusively to the patient in front of you (while in the middle of juggling the workups of half a dozen other patients); to appear calm and unhurried when you may be anything but; to maintain eye contact and body language that says “I care about you”; and to be empathetic, kind and gentle, when your reserves of these quantities may be perilously low.

THE PAYOFF

The culmination of the visit, the “payoff” if you will, that, for me, yields the greatest enjoyment, is the “explanation”. It represents the summing up of all that has gone before, and it can make or break the visit from the patient satisfaction point of view. It requires taking all you’ve learned in that few minutes you’ve spent speaking with and examining the patient, integrating that with your accumulated fund of medical knowledge and experience, and finally, synthesizing all of that into a concise, cogent, non-medicalese description that the patient can understand and accept. It’s not always easy to do, in fact, seldom, but when you get it right, you can feel the positive energy flowing to you from a patient who not only understands and trusts in what you are saying, but who also appreciates the fact that you’ve put your best effort forth in caring for and about them. I liken the good feeling I derive from such encounters to the way a comedian must feel when a joke hits the mark with an audience, or when a musician elicits a roar from the crowd with a particular song. This love of “good vibrations” may sound a bit narcissistic, but we all want positive feedback from our fellow beings, and if that provides the inspiration to work towards constructive goals in our lives, or others lives, I fail to see the downside.

COMMON THREADS

Indeed, the crafting of the “explanation” is the common thread that runs through both my clinical work as a physician, and my work as an animator/illustrator. Just as it is critical that I effectively communicate the explanation to a clinic patient, I must also take the important points of a medical-legal case and convert them into a visual form which simplifies the concepts as much as possible without stripping them of their essence. The positive return in a legal case is not as direct or immediate as when working with a clinic patient, but it feels good when one learns that your contributions have aided in returning a favorable verdict.

Ah, the symbiosis of the dual life…

cjs