Renee Dversdal @DRsonosRD
Renee Dversdal is an Associate Professor in the Division of Hospital Medicine at Oregon Health & Science University (OHSU), Director of OHSU Point-of-Care Ultrasound, and General Medicine Ultrasound Fellowship Director.
Competitors for the Volume Assessment Region
The Volume Assessment Region includes a veritable what’s what of volume assessment techniques from historic to cutting-edge, complete with excellent and current literature. I’m not going to try to top that. But “We’re not in the dialysis unit anymore, Toto,” and I am going to convince you that the inferior vena cava (IVC) has a place along with other contemporary volume assessments using point-of-care ultrasound, making “New School” come out on top, both in and out of the HD unit.
In the summary post, IVC ultrasound was listed with “Old School” which makes sense if it was only being used to appreciate right atrial pressure, and thus estimate volume status. However, given the more modern nature of the technology and implementation at the bedside, and the fact that you can quickly assess for extravascular/interstitial volume with the same tool at the same time, I’m going to lump all point-of-care ultrasound (POCUS) into “New School” for this post.
First, we’re going to imagine working in the overnight acute care space, where there’s not a nephrologist to be found other than the poor fellow starting that MICU patient on CVVH or, in rural areas, perhaps hours away. In this space, I need to make immediate clinical decisions about my patient’s extracellular volume status, effective circulatory volume, and perfusion.
So, it is Sunday morning at 2 AM, and you’re paged by the Emergency Department (ED) to admit a 69-year-old man with sepsis due to an infected great toe metatarsophalangeal joint ulceration with possible osteomyelitis, and surrounding cellulitis. He has a history of end-stage kidney disease (ESKD) due to poorly controlled type 2 diabetes mellitus, on hemodialysis. He attends dialysis “religiously” and his last treatment was Friday afternoon. On arrival to the ED he was febrile to 39 degrees Celsius, tachycardic into the 120s, blood pressures were soft in the 90s/40s, O2 saturations were normal on room air, and weight was 3 kg above “dry weight.” He was started on intravenous vancomycin, piperacillin/tazobactam, and received 500 cc of normal saline. The ED provider noted chronic pitting edema, and a large neck/beard obscuring JVP. BNP was not sent, lactate was elevated.
Here is a key IVC point: It’s about volume tolerance, not volume responsiveness. As outlined in the summary, central venous pressure (CVP) (regardless of how it is measured) is not a good predictor of blood volume or response to fluid challenge. There are, however, fancier new school ways to try to detect volume responsiveness with passive leg raise such as corrected carotid flow time, left ventricular outflow tract velocity time integral, or mitral valve velocity time integral. The problem is that these are more technically challenging studies, and I don’t believe in letting perfection be the enemy of good. So we’re going to talk about common sense, easy-to-perform scans that anyone from an 8th grade student to an Emeritus Professor can learn.
Let’s start with our intravascular volume assessment. It has been two days since the patient’s last dialysis session, and his weight is up, so we believe he is total body volume overloaded. But what is happening in this portion of Figure 1 circled in purple?
To figure this out, we take a look at the IVC. If the “Old School” IVC is really only useful for estimating CVP at the high or low extremes, how can we use an IVC that looks plethoric like in the next clip?
If I see that on my screen, I am thinking “the highway is backed up” and the CVP is elevated, arguing for both intravascular in addition to total body volume overload. To be fair, there are conditions where the IVC is dilated, right atrial pressure (RAP) is elevated, and the left atrial pressure (LAP) is low. These include pericardial tamponade, pulmonary embolism, severe sleep apnea, pulmonary hypertension, or right ventricular infarct. However, in this case we do not suspect any of these conditions; thus, if we saw it, we would truly believe our dilated, non-collapsing IVC is indicative of volume overload.
However, our patient’s IVC looks flat like the following clip:
In this case, despite the fact that we believe he is total volume overloaded, given his infection and inflammatory response it appears his CVP is low, and he can likely tolerate a fluid challenge as we try to improve his effective circulatory volume.
Let’s say we give him another 500cc of fluid, and his vital signs have not changed, but his IVC is now in that “less helpful middle range”: Not >2cm without collapse, and also not flat. We are now left with an estimated CVP in the moderate range, and are not certain if additional fluid will improve his heart rate and blood pressure. Maybe this really is pure vasodilatory septic shock and more fluid is needed for perfusion, but perhaps more fluid will simply contribute to worsening interstitial volume overload and complications like pulmonary edema and hypoxemia.
We used a flat IVC to support a safer volume challenge initially, but with no clinical improvement. Can we now use POCUS to get additional information to guide our care? Since the alluring suit in the next graphic is no longer an accepted approach to improve intravascular blood volume without administering further fluid, we have to move on and try to get a sense of what is going on in the interstitial piece of the puzzle.
Speaking of puzzles, I like to tell my learners that POCUS is not a magical test that lets us ignore all our other clinical information like the history, physical exam, and laboratory and other diagnostic tests. It is one piece of a puzzle, and it is ALWAYS easier to interpret the puzzle subject when you have additional pieces in place. We do not make volume assessments on IVC only, or cardiac function assessments on one view only. We use a variety of views and information to help us piece together the overall clinical status of the patient in front of us.
Thankfully, the lungs add easily obtained and interpreted ultrasonographic data points. Unlike ultrasounding the kidney, where even a novice can see the kidney looks kind of like a bean or Peanut M&M®, lung ultrasound is all about artifact. Think of the normal, aerated lung like a balloon. 99.9% of ultrasound beams will be reflected back once they stop traveling through the skin/soft tissue/muscle and hit the air under the pleura. This will cause horizontal, equidistant lines from skin to pleura, and downward, called A lines, seen here:
Just think A for air. However, as hydrostatic pressure increases or oncotic pressure drops as happens with hypervolemia, there is more extravasation of fluid into the interstitium of the lungs. As this process occurs, we start to see vertical lines, originating from the pleura, and radiating through the far field (bottom of the screen). These are called B-lines, and pictured in the next clip:
Sure, B-lines can be caused by other reasons for increased lung density, like pulmonary fibrosis, focal non-cardiogenic pulmonary edema from a pneumonia deep to the pleura, acute respiratory distress syndrome, and more. Again, it is all about clinical context and the other pieces of your puzzle.
Finally, time to summarize and round out our case! Our patient with sepsis due to cellulitis with possible osteomyelitis appeared intravascularly volume depleted upon our initial exam, despite being two days post-dialysis and above his dry weight. On admission from the ED (after 500cc intravenous fluids there), he was ultrasounded and a flat IVC and A-line lung pattern were seen. After 500cc of additional fluid he no longer had ultrasonographic signs of low CVP with a moderate change in IVC through respiration and lungs with diffuse B-lines. These findings were interpreted as consistent with extravascular lung water, and an increased interstitial compartment volume. A plan was made to transfer him to the intensive care unit for pressors instead of more IV fluids with any further clinical decompensation. He remained stable through the early morning with normalizing heart rate and improving blood pressures around 12 hours after antibiotic initiation.
All of that without recurrent needle sticks for labs, premature central line placement for CVP measurement, and/or vasoconstricting meds.
Speaking of #POCUS / #IMpocus…huge thanks to Dr. Noelle Northcutt @NsquaredPOCUS for the useful edits and comments to this post. I hope those of you who made it this far down the page found it educational and you’ve been inspired to try your hand at ultrasound!
– Guest Post written by Renee Dversdal @DRsonosRD
As with all content on the AJKD Blog, the opinions expressed are those of the author of each post, and are not necessarily shared or endorsed by the AJKD Blog, AJKD, the National Kidney Foundation, Elsevier, or any other entity unless explicitly stated.