What’s this sign? Bedside Ultrasound Picture Quiz! #FOAMed, #FOAMcc, #FOAMus

Here is a one of the “classic” and physiologically important echocardiographic signs:

 

Screen Shot 2014-05-18 at 11.34.10 PM

 

What do you see in this parasternal short axis view, and what are the physiological implications?

Scroll below for the answer!

 

 

 

 

 

 

 

 

 

 

This is the “D” sign, aptly named for the D-shape taken by the LV (normally circular) when RV overload occurs and there is paradoxical septal motion and flattening, as early diastolic RV pressure exceeds early diastolic LV pressure.  This is NOT a good thing and points to a very strained hemodynamic pattern.

Note the RV is huge in this cut, bigger than the LV (remember that in all views, the RV should be about 60% of the LV size – this is simply due to the semi-lunar shape the RV takes as it “wraps” around the LV – they both have the same stroke volume). Also note the small posterior pericardial effusion.

So what is the diagnosis here?  Well there isn’t enough information to say with just this image.  This happens to be a case of worsening ARDS, but all you can tell is that there is acute right ventricular failure due to pressure overload, so that the diagnosis includes (a) PE, (b) acute pulmonary hypertension due to some kind of pulmonary disease – ARDS, pneumonia, etc…  Obviously, in the absence of significant parenchymal abnormalities on CXR or B lines/effusions/consolidations on lung ultrasound, PE should be strongly considered.

 

Happy scanning!

 

Philippe

Here is an excellent review on RV dysfunction and focused bedside ultrasound assessment:

RV bedside echo

or its link:

Click to access 38TOCCMJ.pdf

Bedside Ultrasound for Internists / L’Échographie Clinique pour l’Interniste – ASMIQ/CCUS, May 23rd, 2014.

Although bedside ultrasound truly started in the emergency room and is slowly spreading to critical care, its usefulness extends to all aspects of medicine, particularily in hospitalist and consultation medicine. The CCUS Institute is proud to be involved in a forward-thinking undertaking by ASMIQ to increase bedside ultrasound use by its members.

For the second year, the Critical Care & UltraSound Institute (CCUS) is hosting ASMIQ (Association des Spécialistes en Médecine Interne du Québec / Quebec Association of Internal Medicine Specialists) members for a day of bedside ultrasound, tailored for internal medicine practice.  This year’s program will review volume status, focused cardiac and lung ultrasound as well as ultrasound-guided bedside procedures. There will be 3.5 hours of workshops in the day.

The didactic presentations will be given in french, and the workshops both in french and english.

Programme: word echo-Programme scientifique et atelier-1 – copie – copie-1

 

For participants:

Welcome to the course!  Here are a few papers which should be read in preparation and as reference, in order to enable you to get the most out of the course:

EGLS fulltext

JASE Focused echo

ICC Lung US

Thank you and looking forward to meeting you on May 23rd!

 

Philippe Rola

Course Director

 

Another wicked ultrasound case! Can you see the culprit? Another reason to do bedside ultrasound… #FOAMed, #FOAMcc, #FOAMus

Reviewing some TEE cases with Max Meineiri of TGH yesterday (Max is an anaesthetist-intensivist-sonographer extraordinaire who has been kind enough to help me brush up my TEE skills recently), here is one that stood out for two reasons. Here is the story: An 84 year old woman is sent from a peripheral hospital to the cath lab for chest pain.  She arrests on the table after they found normal coronaries and the code blue is called. Max arrives on the scene, and due to CPR making TTE difficult (and also because Max walks around with a TEE probe in a hip holster by Dolce & Gabbana), in goes the TEE probe and right away they note a massively dilated and hypokinetic RV, and a small and under filled LV. Yup, sure looks like a PE in these circumstances. Not being satisfied with a presumptive diagnosis, Max gets to a short axis view of the aortic valve and pulls out the probe slightly, following the bifurcation of the main PA.  On the screen, the right PA is on the upper left field, and the left PA disappears towards the upper right (the left main stem bronchus makes it difficult to visualize).

Anything seem a little odd?   Yup, you can see the occlusive culprit a couple of centimetres into the right PA, moving with each beat.  Being in angio already, they threaded a PA cath and administered thrombolysis, but despite some visual fragmentation, she did not survive. So why is this case interesting? 1. the image is pretty cool. 2. More importantly, it highlights the importance of bedside ultrasound.  If a rapid, focused cardiac exam had been done at her presentation at the peripheral hospital, the first-line physicians most likely would have noted the severe RV dysfunction and questioned the diagnosis of coronary syndrome, possibly (hopefully) thrombolysing the patient, and very possibly averting the cardiac arrest. …I know, I know, we don’t have all the info, the ECGs, etc, and maybe this was really an ACS and she happened to have a DVT which embolized during transport, etc…do you buy that?  Ockham and his parsimonious razor don’t, and I would tend to side with them.   love to hear some thoughts!   Philippe

Bedside Ultrasound: Quite a Case! #FOAMed, #FOAMcc

So here is an awesome clip from an ICU colleague of mine, Lorraine Law.  She was managing a post arrest (elderly woman who collapsed at home and was resuscitated but remaining in profound shock) case using bedside ultrasound and came across this pathology:

video courtesy of Lorraine Law & Shirish Shantidatt

what do you think?

scroll below for my thoughts…

 

 

 

 

So the clip starts with a subxiphoid 4 chamber view that clearly shows a massively dilated RV with a hyperdynamic and underfilled LV.

[For the hemodynamic novices, remember that the ventricles are kind of like roommates who share a pericardium. Especially in acute scenarios, if one gets overloaded, the other will have to give way, until the pressure equilibrates. If the process is exceedingly slow, they can do some renovations and stretch the pericardium, but this takes likely weeks. In this case, the elevated PAP overloads the RV and the RVDP > LVDP, resulting in decreased diastolic filling, which in turn drops the stroke volume/cardiac output/MAP.]

We can see that the RV TAPSE (tricuspid valve excursion towards apex) is really minimal, supporting an acute or acute on chronic process.

The clip then shows a long axis view of the IVC with echogenic material, most likely thrombus, with a to and fro motion, going in and out of the RA. Wow. You don’t see this very often.  The only thing preventing further travel is actually the fact that the cardiac output is so low due to massive embolism so that the flow can in fact barely carry the clots forward anymore at this point, similar to the sluggish IVC clip I put up a few months ago (http://wp.me/p1avUV-5t).

The most likely diagnosis is pulmonary embolism, and thrombolysis is indicated. Unfortunately despite my colleague’s timely diagnosis, the clot burden was likely too much, and despite thrombolysis, the patient passed away of intractable shock.  One can imagine that the TPA actually has to make it to the lungs, and with such a degree of obstruction, it is likely that very little actually got to the pulmonary vasculature…

Unfortunate case, but quite impressive images.

A crazy thought, using hindsight and with the luxury of knowing the fatal prognosis: intracardiac (RV) TPA bolus? Small spinal needle?  Anyone bold enough? Food for thought if (when) I see one like this…

 

cheers!

 

Comments:

Marco says:

Really quite impressive images. A couple of weeks ago I admitted a pretty young patient after a successful resuscitation due to massive pulmonary embolism. Immediately after ROSC in emergency department, he was transported to the cath-lab where TPA bolus was administered directly through a PA cathether. In ICU we continued the infusion. In less than 24 hours we obtained a relative hemodynamic stability and discontinued all the vasopressors, but the case remains unfortunate because despite therapeutic hypothermia the post-anoxic damage was so severe that led to cerebral death declaration two days later.

 

Thanks Marco, very interesting.  There is a recent study on catheter directed thrombolysis in PE reviewed at PulmCCM:(http://pulmccm.org/main/2014/randomized-controlled-trials/catheter-directed-thrombolysis-submassive-pe-better-heparin-rct/)

A physiological point about PE resuscitation is the relative inefficiency of CPR, as both venous return and LV filling is severely limited, so systemic perfusion is even worse than the usually poor output during chest compressions…

Thanks for reading!

Marco replies:

Thanks, Philippe!
The point about the possible inefficiency of CPR is crucial in my opinion. The patient I brought as example had a witnessed cardiac arrest (he called EMS when in respiratory distress) and CPR without interruption from the beginning, nevertheless he resulted in brain death declaration.
I remember very clearly a 43-year-old woman that 3 years ago had a massive PE in the OR shortly after a long lumbar vertebral stabilization. We admitted her to ICU after more than 80 minutes of CPR, a bolus of rTPA and with severe hemodynamic instability. RV was extremely dilated. When she eventually regained stability I had little hope about her neurological recovery, but surprisingly she was extubated the following day and last year she returned to our 12-months post-ICU follow-up showing perfect recovery.
I think that systemic and cerebral perfusion during “obstructive” cardiac arrests such as massive PE is very difficult to asses with current technology. A couple of times I was tempted to check it with trans cranial doppler, but usually there’s too much confusion during CPR.
When I was a resident I witnessed to a iatrogenic cardiac arrest in a patient with advanced monitoring that led to an interesting publication: http://www.researchgate.net/publication/10832333_Cerebral_perfusion_pressure_and_cerebral_tissue_oxygen_tension_in_a_patient_during_cardiopulmonary_resuscitation

 

Wow, very interesting cases.  What fortune to have been able to record that data, as obviously getting that in during CPR would be almost impossible.  TCD, at least after ROSC, could be contributory… Another option is using NIRS, which I’ll be working with this summer.

thanks again!

Philippe

Bedside Ultrasound Clip Quiz #8. #FOAMed, #FOAMcc

So a patient presents with worsening peripheral edema and right upper quadrant discomfort. Biochemical data only reveals some mild elevation of the transaminases.

Here is what you see:

These are the right sided chambers.

And this is a hepatic vein.

 

What do you think is going on?  Scroll below for the answer!

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

This patient has severe tricuspid regurgitation. The second clip shows significant retrograde flow in the hepatic vein (red doppler signal). Hepatic congestion was the cause of pain.

Analysis of hepatic vein flow can be useful to establish the presence of right heart dysfunction when cardiac views are difficult.

 

cheers!

 

Philippe

The IVC Assessment by bedside ultrasound: Let’s apply some common sense! #FOAMed, #FOAMcc

So I have a huge issue the IVC and its ultrasound assessment. For the most part, neither the yay-sayers or the nay-sayers are applying much sound physical principles, as far as I’m concerned.

To assess a patient’s volume status, it may be practical to begin with the sub-xiphoid view of the IVC, since the decision to give fluids or not – especially in emergency situations – can then be taken within the first few seconds of examining the patient. The physiological rationale behind assessing the IVC as a marker for volume responsiveness is simple and solid. As the venous compartment fills, the size of the IVC will gradually increase until it reaches a maximal size of about 20-25mm or even 30mm, depending on physical size and chronicity.

Concomitantly, the phasic respiratory variation will decrease as the venous pressure increases and the effect of varying intrathoracic pressure is no longer felt. At this point, the flat part of the Starling curve of the right ventricle is approaching, and there is little response to volume, and little physiological rationale to support giving more.

Currently, many use a variation of about 20% or more to suggest a volume responsive state in ventilated patients or an inspiratory collapse “sniff test” of 50% or more in spontaneously breathing patients.

There remains controversy around using IVC assessment for volume responsiveness, and with good reason! There are a few important reasons why:

a. technique – First of all, there is the manner in which IVC measurement has been taught: the M-mode measurement of the antero-posterior (AP) diameter during breathing (usually of ventilated patients) about 3 cm below the diaphragm. Although highly practical and reproducible, it has many shortcomings. If we look at the physiology, what changes with cycles of respiration is the volume of blood entering the chest/right atrium. Hence the key variable we are trying to assess is the transient variation in IVC size – which is a volume, not a linear dimension (I’m getting painful flashbacks of using pressure  to determine volume!)Hence the use of a single linear measure on one point along the length of the IVC to assess this is inherently flawed. For instance, the figure to the left shows how, if this IVC were to be measured in its AP diameter, the variability may not be that great. In the short axis, however, one can clearly see the significant change in surface area, and hence volume between phases of mechanical ventilation. Also, the IVC is rarely perfectly circular, but often ovoid, and occasionally with the greatest diameter in an anteroposterior axis, making that single AP measurement even less relevant.

b. intrathoracic pressure – Secondly, the variation in intrathoracic or intrapleural pressure (Pip) must be measured, as, for instance, a young and fit patient can generate large changes, which would result in more significant IVC variation, as compared to a frail elderly patient, even if they are on the same point of their Starling curve, invalidating the IVC measurement. All “sniffs” are not created equal.

c. intra-abdominal pressure – Finally, the intra-abdominal pressure (IAP) must also be assessed, since an elevated pressure would decrease the size of the IVC and make that measure no less accurate, but less relevant in terms of representing venous filling.

So what should we do?

Instead, a more global assessment of the IVC volume, measuring short axis area measurements and variation at several points along the IVC would give a much more accurate estimate of IVC volume variation. This is currently being studied by our group.

“Eyeballing the IVC” Attempting to link evidence and physiology, some bedside sonographers’ approach is to take a global look at the IVC in both long and short axis during respiration, while clinically assessing the respiratory effort and the abdominal pressure. This approach is analogous to the “eyeballing” of LV function – versus more formal measurements such as Simpson’s disk method, etc – which has been proven just as accurate with sufficient clinical experience.

The figure below shows an IVC that is about 10-12mm along most of its intrahepatic segment on expiration, and collapses almost completely on inspiration. If this belongs to a patient breathing with little effort and with a soft abdomen to palpation, it is physiologically quite clear that this patient would be fluid responsive. It also shows how impressive the collapse is in the short axis.

IVC insp dual

For instance, let’s say Patient A is in respiratory distress and using accessory muscles and presents to the ER with a respiratory rate of 35 and a systolic BP of 80. His IVC measures approximately 21 mm in diameter at several points along its axis, and has a brief collapse to about 10 mm with strong inspiratory efforts. His abdomen is soft during inspiration but firm during a prolonged expiratory phase.

Patient B is brought to the ER somnolent with a respiratory rate of 10 and a systolic BP of 80. His IVC measures 15 mm with minimal respiratory variation. His respirations are shallow and his abdomen soft. These two patients show how the IVC assessment needs to be taken in clinical context.

Patient A has some 50% inspiratory collapse of a large IVC in the context of large variations in Pip, whereas Patient B has little variation of a mid-sized IVC in the context of very small variations in Pip. In all likelihood, Patient A is not very volume responsive, while Patient B probably is.

Volume Responsiveness vs. Volume Tolerance – it is critically important to distinguish the difference between these two concepts as they are often misused interchangeably: Volume responsiveness refers to an increase in cardiac output (CO) to a fluid challenge. This is a purely hemodynamic concept. Volume Tolerance refers to whether or not a patient can tolerate volume without clinically significant side effects. This is a complex clinical assessment that should include: -the patient’s plasma oncotic pressure (serum albumin) and level of capillary leak, if present, -the patient’s pathology – is there risk of capillary leak in critical tissues such as lung, brain, abdomen? -the type of fluid being considered (isotonic crystalloid vs hypertonics or colloids/blood products). It is important to distinguish that not all patients who are volume responsive are necessarily volume tolerant.

Volume assessment summary – this issue remains a difficult one, even with the use of bedside ultrasound, because the optimal point for any one patient to be on his or her Starling curve at any one time in different clinical conditions remains elusive. Despite considerable study and several proposed management algorithms, there is no means by which to determine exactly how much of any given fluid is enough, without being too much.

In my opinion… – no direct evidence – keeping an IVC below 20mm and probably below 15mm with significant respiratory variation, if hemodynamics allow, is probably ideal. However, bedside ultrasound allows to clearly identify the cases where fluid is clearly needed and those where fluid is unlikely to benefit. Both of these scenarios are easily and routinely missed by traditional examination. Additionally, when the IVC assessment is done in conjunction with lung ultrasound, it becomes possible to detect early development of pulmonary edema and halt aggressive fluid resuscitation (FALLS Protocol, Daniel Lichtenstein).

 

Technical Pearl: the part of the IVC we generally assess being the intrahepatic segment, it is possible to find it almost by scanning through any part of the liver, which happens to provide a great acoustic window. This may be particularly useful when the epigastric area is difficult to access (incision/bandage, drains, in the OR, etc…) or when there is bowel gas in the epigastrium. The figures below show the same IVC, first in a “traditional” epigastric view, then in a view approximately along the plane of the red arrow on the CT scan.

2 views IVC std:liver

CT liver IVC views

 

Bottom line?

When assessing volume status, it is absolutely essential to keep the clinical question in mind. It is a great minority of patients who are volume responsive who actually need volume. Normal, healthy humans are very much fluid responsive and fluid tolerant but certainly not in need of any. Much of the current studies and literature focus on assessing volume responsiveness in the setting of shock, which, although arguably the most important, is not the only type of information that can be obtained from the IVC. For instance, as will be discussed in the chapter on congestive heart failure, knowing that your patient is very “full” should prompt further diuresis. If you are dealing with managing severe anasarca, knowing that a patient’s intravascular volume is low may prompt the use of albumin or hypertonics prior to further diuresis to help resorb some of the interstitial fluid. Another critical question to which there is currently no answer is just how much fluid to give to patients in shock. There are many opinions but no certainty. It is common practice to fill a patient in shock until they are no longer fluid responsive, in an effort to avoid or minimize the use or dose of vasopressor medications. There is no study to date that compares a “moderate fluid/early vasopressors” vs “aggressive fluid/avoid-vasopressors-if-possible” approach.

Hopefully this will be answered soon. In light of the clear evidence linking positive fluid balance and mortality, it would seem wise to fill to a “moderate fullness” where some respiratory variation remains, rather than to the point of no longer being fluid responsive. After all, physiologically, the only time humans are really full (>20mm IVC with little or no variation) is in pathological states of congestive heart failure or obstructive shock. So again, when assessing an IVC, keep in mind what your clinical question is and interpret the sonographic data accordingly.

 

cheers!

 

Comments:

Marco says:

Thanks Philippe, very interesting post.
Using your great categorization, I think that the worst scenario is represented by a patient who is volume responsive but poorly volume tolerant. In that case, it is important to have clear in mind which is our target: cerebral perfusion, oxygenation and lung extravascular fluid, ventilatory weaning, renal function, avoiding vasopressors or mechanical ventilation, etc…
Very often, maintaining a brain dead heart beating donor, every organ would require a different volemic status, and if all of them are suitable for transplantation you have to compromise.
Just a last thought: as well as “all sniffs are not created equal”, also tidal volumes are very variable. Assessing respiratory variations during protective (low TV) ventilation requires a thoughtful interpretation of the results.

 

Absolutely. Interpretation of the findings in each individual case is key. 

Philippe

“Doc, I can breathe!” – Thrombolysis in PE…a case discussion. #FOAMed, #FOAMcc

So I was on call last weekend and got a call from one of the internists on the ward about a potential admission who may need dialysis.   She was a woman in her 60’s, diabetic, hypertensive with minimal baseline renal dysfunction, who had been admitted with a hepatic abscess due to biliary obstruction. This had been stented and a pigtail catheter had been inserted to drain the abscess.  However, over the last few days, her creatinine had risen to about 500 and she was becoming oliguric.  Her O2 requirements had also increased and she was now on 15 liters by nasal prongs. This had been ascribed to pleural effusion and possible pneumonia.

When I saw this lady, she was visibly dyspneic at 30 with a heart rate 115-120 and a systolic BP of about 105-110, saturating 90% on 50% face mask.

So on physical examination, she had a soft abdomen (the first thing I feel just before I put probe to skin), her skin was cool, and the CUSE revealed a large (>20mm) IVC with no respiratory variation (despite the effort).  I unfortunately forgot to hit the record clip button…and the parasternal long axis and apical 4 chamber are here:

Lung views showed “A” profiles except for the right base which had a small effusion and some consolidation/atelectasis and some B lines, but not very extensive.

So further assessment revealed she was not a smoker, previously quite active and easily able to go up and down several flights of stairs.  She had noted dyspnea about 3 days ago, without chest pain. There were no leg symptoms, and she had been on LMWH for dot prophylaxis.  The CXR was not very impressive – in a sense that there was not enough parenchymal disease to explain pulmonary hypertension.

This is PE until proven otherwise, and I would have been comfortable without further confirmation, but with the presence of some lung disease and an intrahepatic catheter, I preferred to have 100% confirmation before initiating thrombolysis.

After CT angiogram confirming bilateral and extensive embolism, I had a thorough discussion with her and her family and they all agreed to go ahead with TPA.  She was quite concerned with cardiorespiratory limitation, given that she was quite active. She was comfortable with a quoted risk of intracerebral bleeding below 2%. I used the MOPETT half-dose of 50mg.

Overnight, her HR slowed to about 100, and sats increased to 93-94%.

When I rounded on her in the morning, she said “Doc, I can breathe!” with a big grin. Her HR was 95-100, she was not on 3 litters by NPs, BP 115-120 systolic, and CUSE showed:

So we can see that even though the RV is still quite impaired, it has decreased in size and the LV is now filling better. This was about 12-13h post thrombolysis. She was able to sit up without dyspnea and mobilize to the chair. Her IVC, although it remained around 18-19 mm, had clear respiratory variation.

So…success? Who really knows. It is concievable that, with heparin alone, she might have improved similarly. It is possible. I’m not putting this up to formally support the concept of thrombolysis in “submassive” PE but more to contribute to the #FOAMed discussion regarding the “grey zone” of thrombolysis, since she was technically not in shock (eg SBP>90, lactate normal), but the degree of impairment of the RV to me and the clinical picture, 3 days post, was concerning enough to warrant thrombolysis, but importantly to stress the following:

Point 1: the importance of bedside ultrasound, especially in acute cases.  Without it, over a weekend, and with a patient in renal failure, how quickly would I have ordered a CT angio?  Not without some hesitation…

I won’t review the MOPETT trial, these guys did a much better job than I could hope to, so definitely listen to this if this topic is of any interest to you (and it should!!!):

http://emcrit.org/wee/mopett-trial/

http://ragepodcast.com/rage-session-two/

Great case debates in the RAGE podcast.

Keep in mind that morbidity, not mortality, is the main thing to focus on in sub-massive embolism and the MOPETT – even though I don’t really like the term, its quite vague – benefit in embolism with shock is quite clear.

Point 2: Equally interesting to me was the fact that the renal failure improved. In fact, overnight following thrombolysis, she had a urine output (without diuretic) over a litre, and over the next few days her creatinine normalized and renal replacement therapy was not needed.  Interesting, since she even got a good blast of toxic dye with the CT.  Some will feel that it is the improvement in CO that improved renal function, and this may be partly true, but in view of the lack of “systemic shock,” I think that venous decompression resolved the congestive renal failure, which I think was the main cause of her ARF. I posted about this topic a few months ago, so for more on this see:

http://thinkingcriticalcare.com/2013/09/25/chf-associated-renal-failure-low-flow-or-not/

so thanks for reading and love to hear anyone’s opinion!

PR

COMMENTS:

QUESTION. IF SOMEONE DOES NOT HAVE A PALPABLE PULSE BUT HAS CARDIAC ACTIVITY ON THE ECHO AND RATE IS 90 AND BP IS 50.  DO YOU CONSIDER THIS PEA AND INITIATE CPR?

SEAN

Great question!  There is a whole grey area in “PEA” and management is unclear. I don’t think there is a single answer to that, but physiologically and without further information about RV/LV, I would say your patient needs vasopressor/inotrope support, so I would probably give a small bolus of epi (maybe 100ug) and start an infusion. If I see little reaction (eg HR/BP doesn’t pick up in 30 seconds, I would probably give a short cycle of CPR to get the epi back to the heart.   Of course, hopefully there is a reversible cause (MI/PE), that can be addressed.

Thanks!

 

Philippe

Central line insertion: US-spotted “Blind” technique Video (HERE IT IS!) #FOAMed, #FOAMcc

My apologies, had technical issues with the video uploading so here it is in two formats:

 

 

 

…please let me know if there is a problem!

 

thanks

 

Philippe

Central line insertion: US-spotted “Blind” technique video. #FOAMed, #FOAMcc

So a few months ago I posted about central line insertion and my concerns about the current standardization of care of ultrasound guidance:

http://thinkingcriticalcare.com/2013/10/21/ultrasound-guided-central-venous-catheter-insertion-standard-of-care-or-preventing-procedural-skills-foamed-foamcc

I promised a video so finally got around to remembering to do it.  This one actually happens to be a dialysis catheter so a bit bigger, but otherwise the technique is the same. In this case I am using my standard ultrasound-spotted procedure with “blind” insertion.

So here, I spot the vein, confirm it is just lateral to the carotid, and that it collapses nicely, without thrombosis:

Now, I insert the line. A few important points to note that are not seen in the frame:

Line Insertion video:

a. my introducer needle/syringe and loaded guide wire (pulled pack and “loaded”)  are ready  and within my vision, and also nearby are the dilator and catheter.

b. note that the off hand (right hand in this line) protects the carotid and stays in place until there is venous flashback, then secures the needle position.

 

Note that in this particular case, I didn’t quite make a large enough incision so the dilator insertion was a little difficult – unnecessary delay, and also unfortunately lost the last few seconds as my iPhone memory was full. 

Next, I confirm position in the internal jugular vein, and verify for lung sliding to rule out and anterior/apical pneumothorax.

In me experience, the key mistake I see inexperienced operators (and sadly, some experienced ones also) make is not to have a proper setup, such that once they do find the vein with the introducer needle, their subsequent steps are not immediately ready, and in the process, the relationship between needle tip and vein is lost, resulting in an inability to thread the guidewire (often blamed on mysterious anatomical abnormalities). It is key to find the vein with the freezing/searcher needle, fix the depth/angle relationship in your mind, withdraw and reach for the introducer needle/syringe using peripheral vision so as not to break the visual fix, and reproduce this while introducing it.

This is what I try to install in students/residents rounding with me, and in fact this approach is useful for any procedure.  Not having to turn your head, reach and fiddle with things that are not ready prevents mistakes.

If you haven’t read my previous post on central line insertion, I’m not advocating agains the use of ultrasound guidance, but for the maintenance of the ability to insert blind lines if necessary.

cheers!

Philippe

Pleural effusion in the sick patient (Part 2 of 3): Physiology & Literature! #FOAMed, #FOAMcc

So once your routine cardiopulmonary bedside ultrasound examination has revealed the presence of a significant pleural effusion, should you drain it?

I guess the first real question is actually what is a significant pleural effusion?  As you can imagine, the N=1 principle pops up again, and there is no single threshold answer (e.g.: >750ml  drained and <749ml  ignored), naturally.  So here are the main factors that impact physiologically:

1. underlying global respiratory function – eg how much reserve you have. With healthy lungs, a young adult can usually tolerate complete atelectasis of one lung or even more, which would take 2-3 liters of effusion at least. However, the more compromised gas exchange is, the less atelectasis can be tolerated.  This also encompasses the level of required ventilatory support, including the level of PEEP. Basically, the worse your lungs are, the more significant the effusion becomes.

2. thoracic compliance – which combines chest wall and abdominal pressure, since the diaphragm is thin and easily displaced.  The greater the compliance, the less atelectasis will occur as the diaphragm and chest wall will shift to accommodate some of the fluid. This is very important especially in surgical patients (or anyone with a tense abdomen).

…so there is no number.  Of course, if you take it to the extremes, I think everyone would agree that if you have 200ml,  it’s probably not worth doing, and if you have 2,000ml, it is. But in the grey zone of, say 500-1,000 ml, you have to make a call given the patient in front of you.

Now what does the literature say?

First of all, there is no large study looking at the impact of effusions in generally ill patients (ED/ICU).  There are some small, specific studies showing worse prognosis in some pathologies (eg Legionella pneumonia) but nothing that can really be extrapolated to general ED/ICU patients.

What about in ARDS? Talmor et al, (Surgery 1998, v 123) showed benefit in survival in a small study of ARDS patients.

I think the best overall study was Vignon et al (CCM 2005, v 33) who demonstrated that bedside ultrasound was much more sensitive in diagnosing pleural effusion (CXRs read as normal had as much as 1,000 ml effusions, as well as diagnoses of effusions which were actually consolidations ), but also that it was quite accurate in quantifying (inter-pleural distance >45-50mm at the base correlates with effusions >800 ml).

Usta et al (Interactive CV and thor surg, 2010 v 10) had similar results in spontaneously breathing post op patients with 45 mm (interpleural distance between diaphragm and base of lung) corresponding to about 700ml, although their range was quite wide, and they were using a somewhat impractical sitting position. They actually came up with a formula (16xdistance in mm) to estimate effusion volume.

Sikora et al (ISRN Emergency Medicine 2012) did a good review on the whole thing as well.

Sikora et al review

My empiric observations: I must have put in at least a thousand pigtails or (back in the day) CVCs in pleural effusions over the last 14 years, and my therapeutic goal has always been to drain effusions at least 750 to 1,000 mls. I have drained 350-500 ml in patients in severe respiratory failure a few times, some with apparent benefit, others without. I don’t recall regretting putting one in, but I do regret a few cases of not draining, only to have recurrent respiratory failure post-extubation. Grossly, I would say 750-1,000 or more in a patient with respiratory failure warrants drainage, but 1,000 mls in a CHF patient on nasal prongs can wait for the outcome of diuretic therapy. Of course we are talking about therapeutic and not diagnostic drainage. Under ultrasound guidance with an experienced operator, pneumothoraces should be exceedingly rare.

Bottom Line: start by examining your patient, physically and by bedside ultrasound. Understand his degree of respiratory failure and estimate the size of the effusion and the compliance of his chest.  Then you have to make the call (that’s why we’re MDs) as to whether this particular amount of pleural effusion in this particular patient is worth draining.

Next week:  how to do it video!

cheers!

Philippe

@shanxonline says:

Great post Phillippe and I fully agree that a global assessment is necessary before draining an effusion. With ultrasound we’ve become really good at identifying effusions, but need to understand physiology and especially chest wall/abdominal compliance to understand the physiological implications of drainage vs conservative management.