"I need to reduce recovery time,
complications, and resources....
"I need to avoid fluid overload
during resuscitation...
"I need to see cardiac
filling and function...
"I need to know if it's tamponade
or desaturation...
"I need to get my critical
patients off vent faster...
so I use hemodynamic ultrasound."

Chapter 3: Ultrasound in Trauma, Resuscitation, and Critical Care

Presenter D. Benjamin Christie, III, MD, FACS has many titles, among them: Program Director of Surgery and Associate Director of Trauma for The Medical Center (Navicent Health).

That sounds like more than a full-time job to me, but Dr. Christie is also an Assistant Professor of Surgery at Mercer University School of Medicine.

So you can imagine what a coup it was for him to speak to an eager EAST (Eastern Association for the Surgery of Trauma) audience. Better still, we have the recording and transcript for your pleasure and education.

Dr. Christie: I’ve put together a brief outline to provide a brief overview of where we want to go. I’ve got a few slides just to discuss kind of what hTEE is and where it’s come from and within our practice here, how we use it, and I’ve selected four cases that I consider… it’s pretty routine for us. I’m sure it’s routine for you, as well.

I’ve got a brief sort of section on methods of interpretation and then future directions. I’m hoping to hustle so we can have some good questions discussion time.

Hemodynamic management and fluid balances in the resuscitation case is a constant challenge. It’s never been easy. The holy grail for end points resuscitation continues to elude medical and surgical researchers. We’re well aware that under-resuscitation has deleterious effects as it relates to survival statistics. Over-resuscitation has its unwanted outcomes, in terms of morbidity and mortality statistics, of its own. Finding that sweet spot in resuscitation is really our goal and challenge on a day-to-day basis.

Transesophageal echocardiography has been around for many decades. It’s been in the hands of cardiologists and maybe some cardiac anesthesiologist, primarily. It’s excellent. It’s been increasingly utilized in the field of critical care over the last decade and a half at this point. It’s accurate. It’s reproducible. It’s a fine assessment tool for cardiac anatomy and functional performance.

But large multi-plane TEEs get several drawbacks. It requires a full-scale monitoring module. The probes are bulky, bigger, and less flexible than endoscopes. They require the probe to be inserted and reinserted it for each and every exam. These things statistically limit the clinicians’ ability to accurately follow changes over time and makes it a little impractical in the ICU.

But with the newly developed hTEE probes and monitors this is changing. So, you can see on the left-hand side of your screen there’s an older gentleman, who’s one of my mentors, his name is John Hudson. He’s a cardiologist and intensivist. He’s my mentor for echocardiography. He’s standing with a relatively contemporary multi-plane hTEE monitor and probe. The other picture is representative of what the full-scale hTEE probe looks like. Behind me is our monitor, as well.

So, with the advent of hTEE there are several advantages that multi-plane and full-scale TEE didn’t allow. It allows for continuous anatomical assessment of the heart rate vessels. This device and this technology allows for cardiac evaluations to be performed real time in the critically-ill or injured patients. Because it can be left indwelling for up to 72 hours, it allows you the opportunity to continuously reassess how your patients performing after each and every therapeutic maneuver you may perform.

If you haven’t seen the probe, this is another full-scale image the probe is about 17 French in diameters about the size of a good NG tube, it’s semi-flexible at the tip. It has a handle or a wand that allows for an inflection and retroflexion, and then torque being provided by the operator to allow for satisfactory image capture.

During the exam, the idea is that because your access to cardiac performances is continuously available, from the visualization perspective, you can assess your hypertensive patient, your hemorrhagic shot patient, you can obtain your three views, you can decide where their needs may be, and then make a therapeutic maneuver, whether it be add volume, the add pressors, or changed pressors, deescalate therapy, with the ultimate goals of improving end-organ perfusion and preventing organ failure and survival, improving outcomes.

The three examinations you obtained by hTEE or the transgastric view, which is a short axis view, that allows for a visualization of both cardiac ventricles and permits measuring of the left ventricular size, calculation of the left ventricular fractionary contraction, and examination septal size, shape, and wall motion abnormalities that may or may not exist.

The four-chamber views, mid-esophageal view, it’s a long access of view provides visualization of the four cardiac chambers. It gives you the opportunity to measure or estimate left ventricular and right ventricular end-diastolic and end-systolic size, calculate a LV ejection fraction. And then the superior vena cava views, along access view, set the level of SVC in the right atrium, and this examination point, the SVC diameter, during the respiratory cycle and this variation can be assessed and determined. I’ve got real-time videos of these coming out.

I told myself I wasn’t gonna to cite everything in the literature that has to do with hTEE but I did want to bring up, and I have some at the end, as well, relatively recent paper in intensive care medicine journal, the probe is inserted in 94 patients and was left indwelling for 72 hours. Most of those examinations were performed and the hemodynamic assessment with the hTEE allowed for direct therapeutic impact of 66 percent of patients they studied.

This is what we found in our practice, as well, the probe is incredibly impactful and despite what clinical markers we made and assumptions we may have coming into a clinical case, the probe has often been a tool that has sort of spotlighted the patient’s real needs that we may have underestimated or even overestimated.

One of the first cases I wanted to get to, is a trauma case that would eventually develop an ARDS picture. This was a gunshot wound to the chest. This patient was shot in the right chest. He came in with large right-sided hemothorax. A chest tube was placed. He had a tremendous amount of blood loss from his chest tube. MTP was activated. He went to the operating room. He wound up getting about four, if I’m not mistaken, four rounds of MTP. The blood loss overall was on the order of biblical.

But he recovered and went to the ICU and wound up developing a trolley that progressed into an ARVS type picture. He was requiring APRV to oxygenate. He puffed out his non-contused, non-hemorrhaged lung to a point where too much fluid would potentially put us in an uncomfortable respiratory position, even more so. But as pressure was, somewhat, soft and his heart rate had been in the low teens, so we really weren’t sure what to expect.

We put a probe down and initially the team was thinking he may be dry. We want to protect that lung. So, when we put the probe down, you can see his left ventricle, in the transgastric view, is hyperdynamic and beating wall-to-wall and filling very poorly and his superior vena cava is varies significant with respirations. The superior vena cava view and in the middle of the screen you can see it varies significantly with respirations. Then in the four-chamber view you can see the trabeculation of the back wall in the right ventricle swinging in as it’s very under-filled.

So instead of a diuretic, we actually gave this patient more blood. This was after one unit had been infused and another was on the way. You can see his vena cava is a lot plumper, the first image on your left-hand side. His four-chamber view demonstrates better filling and a more robust right ventricle and then his left ventricle actually has a smoother and even wall motion and fills much more appropriately.

While a young man who had multiple rounds of MTP, one would think, at least I would have estimated that his volume was overloaded, but in fact he was not. The probe helped us understand the physiologic needs a little bit better.

The next case also a little bit of a surprise. This is where I feel like hTEE really made a big difference in guiding a resuscitation strategy in a pretty complicated, everyday patient. This patient, one of my partners did an uneventful, very successful, laparoscopic appendectomy on a 72-year-old male.

The patient went to the recovery room but in recovery room they had some monitor changes implying ST segment elevation. They got a 12-lead EKG in the recovery room. They were real. But he was hemodynamically stable. He was asymptomatic. They chose to monitor him in one of our cardiac observation step-down floors.

But on post-op day number two, his enzymes had risen a little bit and his troponin was involved. It wasn’t astronomical, but it definitely was a noteworthy lab. He developed respiratory distress. He got short of breath had an oliguria trend in his urine output. His creatinine was rising. They intubated him on the floor and sent them to the ICU.

Here in the story and checking the complaint film, the initial assessment on our end was he’s probably volume overloaded and we need to be prepared to maybe be a little restrictive with the fluid balance and also maybe even Diuresin.

But we used hTEE to help us understand him, in fact, it was the opposite. He was volume depleted his left ventricle filled very poorly with hyperdynamic wall motion. The superior vena cava was very collapsible. His right ventricle and four-chamber view was also very volume depleted.

He actually got aggressively resuscitated. We rechecked at four hours and he had smoother left ventricular wall motion. He had better filling. He had a more plump and robust vena cava. His RV filled better. And he had much more even cardiac wall motion after resuscitation.

This was just after four hours. He went on to do fine. He began making adequate urine per hour. He never had any further rise in his cardiac enzymes. I really feel that being able to see him respond and understand what he needed with direct visualizations was one of the reasons.

He went on to do fine… I really feel that being able to see him respond and understand what he needed with direct visualizations was one of the reasons.

This is a routine trauma case, case number three. Those that are and careful attention in the audience could probably qualify this as an M&M and I’ve already taken this beating. But this was a 58-year-old male who came in as a two-car head-on MVC. He was awake, alert, and oriented. He was tachycardic in the 120s. He had pain. He had sources for pain. But otherwise his vital signs were stable. He sounded fine. He had left hip pain and an obvious right ankle deformity.

He had got some CT scans after his primary secondary survey. He had a very small spleen lag. He had a relatively complex left hip fracture but had a small pelvic hematoma. And then a left tib/fib fracture with the distraction at the level the right ankle.

For whatever reason the orthopedist and the operating room were just ready to go. He’d gotten two liters of crystalloid in the trauma bay and was getting some more. They had, in a rather expeditious fashion, just wanted to take the patient on up and we allowed it.

He got an ORIF tib/fib and stabilization of his tab, but intraoperatively his heart rate had stayed in the 120s and his blood pressure seemed to sag in the mid-90s. They checked interruptive lactate. It was 3.5. Hemoglobin was stable, intraoperatively from you know admission values. But the anesthesia reported giving him two units of blood, five liters of crystalloid, two amps of bicarb, an amp of calcium gluconate. The orthopedist only reported 125 ccs of blood loss with all that.

He came to the ICU and he was unstable. He had what I would feel was a relatively reasonable volume of resuscitation in the operating room, but he remained tachycardic and hypotensive. So, we placed a probe to better understand him. He was a very volume depleted.

You can see his vena cava is almost riven like. His left ventricle functions very poorly and fills very poorly. We began resuscitating him with more crystalloid. This is just a demonstration of the vena cava, the superior vena cava as pre-bolus and post-bolus. This is around the four-hour mark. He had very ribbon-like vena cava baseline and then after fluid resuscitation he responded very nicely and you can see the vena cava was a lot more plump.

Here’s the same sort of comparison view with the transgastric view. The left ventricle feels poorly and functions poorly on the pre-bolus image and then post-bolus, it’s a little smoother and is a little bit better at filling volumes. This is the four-chamber view. Basically, he had an obliterated right ventricle with no volume and still under-resuscitated, but a better right ventricle after his therapeutic interventions with crystalloid infusions.

The final case we’re kind of run through is an MVC. He was ejected from the back of the truck. He had multiple injuries, including a multi-level c-spine fracture that gave him a component of spinal shock. He had resuscitated in the trauma bay, had an operation the night of his arrival, and was in that kind of complex position where he’s had a tremendous amount of volume, yet, he’s got a component of spinal shock. When we were rounding on him, he’d somehow found a way to have pressors titrated all the way up to the 20s.

So, we checked with our probe. We’d been following him. We started recording where he was. On the last trans-gastric view, this is him on 22 Allevafed. He looks like he’s got a little hyperdynamic-wall motion that needs volume. The vena cava supports this. It’s very collapsible and implies he would respond to volume. We gave him volume and we weaned his pressors.

He’s a little more you euvolemic, now, at about 3.5 hours. His Levo down to 12. His SVC is less collapsible. It’s got a little more structure to it. 16 hours later, we’re still weaning pressors, in fact, they’re off. He’s got very smooth left ventricular wall function. He feels very well. His vena cava is a very satisfactory in size and implies it would not necessarily be responsible to volume therapy. The left ventricle at 24 hours looks normal. Mid-esophageal view 24 hours, his left and right ventricle both look normal.

So, once you get the images, you practice getting the images, “What do you make of them?” That’s a question I’ve heard before. I just showed you the pictures. But there’s a lot of ways to calculate and measure what you’re seeing and translate that into what it means as it relates to a patient needs.

With the superior vena cava there are indices where, if one would expect the patient to be volume responsive or volume unresponsive – about 36% is the number around which the collapsibility implies volume responsiveness or unresponsiveness – you can calculate fractional area change, left-ventricular and right-ventricular size ratios, left-ventricular end-diastolic area, target ranges.

These are all well-supported and they’re exercised and not just in the hTEE world, but in the cardiology world, as well. There is the visual estimation method. With enough practice and sometimes when we’re standing over extremes in performance, just understanding where a patient is and where they’re going and what you’ve changed and how they’re performing clinically is more than satisfactory.

These indices and measurements, as you work with the probe and the device and practice or gather your measurements, there’s software driven computations provided by the device that are embedded in its operating system. This allows for your exam findings, such as, ventricular chamber size and diastole or systole to be entered and then the physiologic data for cardiac output can be generated. This can then be used as you carry your clinical management further.

So, future directions, what I feel we’ve been doing with hTEE is we’ve been standing over extremes and now we’re starting to tailor our therapy better. We’re being a little bit more refined, a little bit more precise and accurate.

I think that there’s been some excellent work specifically in the ECMO world and even the cardiac surgery world. And real recently, there was a paper that demonstrated the document the RV dysfunction is a new data point. I think RV dysfunction should be a new data point.

I think RV dysfunction should be a new data point.

If you consider what cardiology has been doing in the years past, which sort of dis-associated the two sides of the heart, the left and the right side, as we’ve understand more and more about pre-existing diastolic dysfunction, how is that going to impact you know resuscitation strategy in a patient with a previous and cardiac issue.

If left side is basically the filling and then, secondarily, our systemic pressure, the right side is our flow. And without good function of your right side, you won’t have good flow. Without good flow, you won’t have good filling. Without good filling, you won’t have a good blood pressure. So, I think as we respect the RV more, I think we’ll see that it’s become a new data point.

I think as we respect the RV more, I think we’ll see that it’s become a new data point.

I think as it relates to management of trauma patients or acutely injured patients, the concept of avoiding hospital-associated events, is certainly a big deal in my facility. And in using hTEE to avoid AKI driving to CRT is something that I feel there’s a real role for. A lot of people are working with hTEE and how they can better manage fluid to be more renal protective.

Also, management strategies, such as, massive transfusion protocol, when have we had enough? A small study was done that did demonstrate the massive transfusion protocol responsivity. I think hTEE would be a great tool to work with to use MTP a little bit better from a resource utilization standpoint. Then organ procurement, another study that was presented at a big transplant meeting that demonstrated an uptick in the usability – eight percent of organs that were managed after brain death and the life link had taken over the patient care – there was uptake, eight percent of utility after hTEE had been used to manage their hemodynamic status.

As a final thing would be de-escalation of therapy, with ICU metrics and outcome measures kind of benchmarking towards the federal mandates as it relates to link to stay and ventilator stay days. De-escalating therapy may very well be a good tool to allow us to whether it be to wean, or fluid restrict, wean the ventilator, understand someone physiologic reserve as these maneuvers are being done, so we can make more conscientious and accurate decisions.

I think de-escalation of therapy is definitely a place that hTEE is going to help us in the future.

Educational resources for hTEE… obviously, the point here that echo is Charity alluded to, the colleges have got courses, the East has got some courses. Decided Critical Care Medicine has got courses, but, hTEE, there’s not one out there. The ImaCor website’s got some very satisfying, very robust references. And, and some lectures and some visual aids and quizzes. And, if you start using it, and within your region, your colleague collaboration is something that we’ve found, we have people come to our institution. We’ve had meetings, we swap videos, and share media across different, hospitals and answer each other’s questions. But, hopefully, maybe one day we could see an expansion of some of these governing bodies of education to allow for a little bit more exposure to hTEE in the education setting.

Matt Martin: Benjie, when I did my fellowship, we did a month of TEE and I forgot how great those images are… you can get looking at the heart and the cardiac function. Most of your cases, it seemed like it was helping you out with volume status.

Have you have found it to be helpful for other things, like you’re having a question of a PE, and it gives you your diagnosis of PE? Or you have the patient who’s you know decompensating from a myocardial infarction and their cardiac output is rapidly changing? Have you found it to be helpful those scenarios, also?

Dr. Christie: Yeah. We’ve had some of those. We’ve had a couple of PE finds, where right side is profoundly dilated, whereas, a day and a half or two days earlier in their care, maybe, it wasn’t. Then, eventually, the PE was diagnosed.

And, we’ve had a couple cardiac decompensation cases where you can see like a change in wall motion from something that’s maybe smoother and even to no more hypokinesis or akinesis. And, those images are you know definitely noticeable and fun to compare. But, yeah, we catch those from time to time.

David Morris: So, Benjie, I have a quick question for you. How long, when you have a patient you want to put the probe in… How long from decision to acquiring images? Does it take a long time to boot up and place the probe? Or what’s that timeframe look like?

Dr. Christie: Oh, it’s quick. We turn the machine on and once it’s ready, you have a probe. Usually, we just have to walk down to central supply and bring it right back. Once you put the probe down, put the patient information into the hard drive and then take your handle, assemble it to your probe and you’re in business. The image is pretty immediate, venous capture.

Charity: Benjie, how much did it cost to get this started? For example, how much was the machine to read it and the probes? You have an idea?

Dr. Christie: Probes are about a thousand dollars. What the cost to get this started was, I don’t know. Here we’ve been doing it since I want to say 2010, maybe, and so we’re pretty very early adopters. I can’t remember hearing anything about cost. Sorry for that.

David Morris: I want to ask you both, and maybe Charity first, and then Benjie, how much are you using ultrasound in the code setting? You know, patient not doing well or ICU, they code or whatever. While everything else is going on, are you guys finding a way to sort of get a probe in and get into the action? And, how does that affect the way that you run a code? Maybe Charity first.

Dr. Charity Evans: We do use the ultrasound. We don’t currently have the ImaCor available to us. However, the ultrasound machine… there is a machine in every ICU and obviously in the trauma base. So, when a person comes in extremis, into the trauma bay, it is definitely used as a part of the workup. And, then I would say, obviously, not immediately in a code on the floor. Because we’re, obviously, doing a lot of other things. But, once things settle in, we get a return of circulation, then, we will go ahead and use the ultrasound to get an idea of what the heart is doing.

Dr. Christie: The code situation is a little tough with the hectic array of care that’s being provided. Usually once there’s been some restoration of vital signs, that’s where we would put a probe down. Within the code itself, usually a probe… we would have to wait till some survivability there.

John Cole: The goal for standard fluid responsiveness is an increase in systolic stroke volume with fluid administration. I’m not aware of any studies that describe the sensitivity or specificity of the hTEE probe in suggesting fluid responsiveness. How does the hTEE probe compare to cheaper modalities such as IJ measurements and velocity time interval (VTI)? Maybe, Benjie, you want to take that one?

Dr. Christie: There are some studies that sort of compare the fluid responsiveness of the vena cava. It’s a SVC view and even the IVC view obtained through transabdominal approaches to more traditional methods. I don’t have the reference off top of my head, as it relates to what CDP has done in the past. But I can’t give you a direct reference right now. But, as it relates to cheaper modalities, we’ve used cheaper modalities, in the past, and I feel, just anecdotally, that this is more accurate.

I’ve walked into a room where cheaper modalities have also been used, whether it be someone said situated with CVP, for example, and we put a probe down and, not that CVP is misleading, but, we’ve been surprised with how much more we learned about needs because of hTEE.

David Morris: Are hTEE probe measurements affected by things like high positive end-expiratory pressure (PEEP) or high inspiratory pressures like your CVP or other wedge pressures?

Benjie: Certainly. In your superior vena cava view, if you are on [?], elevated PEEP, the SVC would be a little bit plumper, but you’d consider that in your interpretation. That’s about it.

Victor Koba: How much time is needed for an operator to be trained to be able to use hTEE?

Dr. Christie: I don’t personally think it’s that hard, to be honest with you. I know ImaCor has clinical specialists that make it very easy. We train residents and fellows. They pick it up quite quickly and once you practice capturing images, the next step is just conceptual interpretation. I don’t find it to be difficult. It’s something that takes a little bit of runtime and I think it’s a great tool. I think anyone who would have an interest really should give it a try.

Rich Lesperance: The benefit of using cardiac view of FAST during initial evaluation of a pulseless patient: Do you factor that in deciding whether to terminate or continue resuscitation?

Dr. Evans: We absolutely do. So in a patient who comes in with CPR in progress, one of the first things we do is a part of the ATLS (advanced trauma life support) primary survey and look at the heart. If there is not cardiac activity, their chances of survival are very slim and so, depending on the circumstances – how old, how young, what the reserve – it will sway us one way or the other. If there is no cardiac activity, let’s say, in the 90 year-old who fell, then yes, we would decide to terminate the resuscitation at that point.

Scott Rock: Do you rely on volume responsiveness alone or is LV filling and RV function important in resuscitation?

Dr. Christie: LV and RV filling are very important. In fact, responsiveness alone may not necessarily tell you what our flow is gonna be. With the idea of right-sided dysfunction or function, you have to respect the right ventricle because in just 15 seconds you can overdistend in the right ventricle, have very poor right ventricular cardiac wall motion, have very poor function and then, secondarily, have very poor filling so I would say that, yes, RV dysfunction is pretty key as well as LV function. Those functions dictate responsiveness.