The Subtleties of the SHOC-ED Trial: Don’t Just Read The Abstract! #FOAMed

So this was my comment to my friend Jon’s awesome discussion on the SHOC-ED Trial, which is certainly interesting.

Jon, great post as always! I do agree with most of it, but would have to caution readers about reading it with the filtered glasses that make people too often take home the message that they want to – usually the path of least resistance (or change). I think your main point and most critical one is that there is no protocol or recipe that should ever be applied to resuscitation, especially single-variable-based resuscitation (eg old school orders like CVP>12 lasix and <12 bolus), and substituting the IVC for CVP won’t help. And from a standpoint of volume-responsiveness, I totally agree, with the understanding that as the IVC gets more plethoric, the percentage of responsive patients will decrease, inevitably, but one cannot predict with certainty whether that one patient will or will not. However, the parallel change is that, as the IVC gets more plethoric, the volume tolerance is likely decreasing as well, so that your benefit to risk ratio is dropping. And of course you can’t recipe that just based on IVC, but should be looking at the site of pathology (eg lung, brain abcess, pancreatitis with ACS, etc…), physical exam, to determine your patient’s volume tolerance. Because we all know that most of that miraculous fluid will end up clogging the interstitium, with consequences ranging from cosmetic to fatal (though usually blamed on the patient being “so sick” in the first place, absolving the clinician from any wrongdoing). So comments like the one previous to mine, stating “give volume and see if the response occurs” are, in my mind, a poor approach. We know from studies that you cannot simply remove the fluid you gave and go back to the start with lasix (glycocalyx damage, etc), and we also know that much of the effect of said fluid administration dissipates in minutes to hours (I’m sure Jon can quote these studies off the top of his head!).

As we have discussed in the past, I think POCUS is much underused as a fluid stop point – most of its use is on the ‘let’s find a cool reason to give.’  I would argue that you should hardly ever give fluid to a full IVC (especially if markers of pathological congestion are present – portal vein pulsatility and all), unless you are dealing with temporarily improving tamponade or tension pneumo, because even if you are volume responsive, you are likely not volume tolerant. This also goes to the point that a single, initial POCUS exam will potentially not have the same impact as a whole POCUS-based management which will use it to reassess congestion status, cardiac function, etc.

Having said all this, the most important part of the SHOC-ED article is, in my mind, their discussion, which is full of all the important reasons why the final conclusion is not `we don’t need to do POCUS in shock,’ which is what I see happening (similarly to the TTM reaction), as they outline the cognitive fallacy of putting on trial a diagnostic tool whilst the therapeutics are not yet clearly established. Those only reading the abstract or conclusion will actually miss the important points of this study which the authors clearly explain.

In particular, the ‘rare’ instances of tamponade or aortic aneurysm or PE in their series would be diluted out by the sepsis, but for those patients, it would matter. As the authors state:

‘one might argue that even a single unanticipated emergency procedure would justify the use of POCUS in critically ill patients.

I would have to wholeheartedly agree.

cheers

 

Philippe

H&R2019! Final Programme. Register Now! Montreal, May 22-24, 2019! #HR2019

 

Click here to register!

Registration is open and we have said goodbye to the snail mail process. Fortunately, we are a lot more cutting edge in medicine than in non-medical technology.

We are really excited about this programme, and a lot of it comes from the energy and passion coming from the faculty, who are all really passionate about every topic we have come up with.

The hidden gem in this conference is the 4 x 40 minutes of meet the faculty time that is open to all. Personally I’ve always felt that I learn so much from the 5 minute discussions with these really awesome thinkers and innovators, so wanted to make it a priority that every participant should get to come up to someone and say ‘hey, I had this case, what would you have done?’   Don’t miss it!

Scientific Programme

Wednesday May 22 – PreCongress courses

NOTE DUE TO LIMITED SPACE AND UNTIL JANUARY 1ST REGISTRATION FOR THESE IS RESERVED FOR H&R2019 ATTENDEES, FOLLOWING WHICH REMAINING SPOTS WILL BE OPENED TO ALL-COMERS. H&R2019 REGISTRANTS SHOULD RECIEVE A CODE ENABLING REGISTRATION. FOR ANY QUESTIONS CONTACT HOSPRESUSCONFERENCE@GMAIL.COM.

Full day Resuscitative TEE Course THIS COURSE IS CURRENTLY FULL. DUE TO DEMAND WE MAY ADD A SECOND TEE DAY. EMAIL US (above) TO BE PUT ON THE WAITING LIST.

Full day Keynotable

Half day Hospitalist POCUS (PM)

Half day Critical Care Procedures (AM)

Half day Brazilian Jiu-Jitsu for MDs (AM)

(for more details on these pre-conference courses please see here)

 

Thursday May 23 – Day 1

0800-0820 – Respiratory failure on the wards – MALLEMAT

0820-0840 – Phenotyping Cardiac Arrest – SPIEGEL

0840-0900 – Help! my patient is bleeding! AJJAMADA

0900-0920 – Perioperative basics. KAUD

0920-0940 – Advanced POCUS-based management of CHF – ROLA

0940-1020 – MEET THE FACULTY OPEN DISCUSSION

1020-1040 – Pharmacology Pearls – VINCENT

1040-1100 – Green Medicine: Can We Help Save the Planet? ZIGBY

1120-1140 – A Free Upgrade to your WBC: The NLR! FARKAS

Critical Care track

1240-1300 – pH-guided fluid resuscitation – FARKAS

1300-1320 – the Great EPI debate – SPIEGEL

1320-1340 – Revisiting CPR physiology: What do we know? – TERAN

1340-1400 – Cardiogenic Shock 2019 – OLUSANYA

1400-1420 – Late Breaker TBA – MALLEMAT

1420-1440 –  Intra-Arrest Hemodynamics: One Size Doesn’t Fit All – TERAN

Hospitalist track

1240-1310 EKG Pearls – MULLIE

1310-1330 Nutrition in the Hospitalized Patient – RUBINO

1330-1400 The Best Neuro Exam Ever! – TBA

1400-1420 Dermatology 101 – SKINNER

1420-1500 MEET THE FACULTY OPEN DISCUSSION

Workshops (1500-1700) 

Workshops will have an open format where you can attend as many or as few as you would like, and spend as much time as you choose. This will enable you to focus on the areas you want to gain the most from:

Basic Hospitalist POCUS (IVC, lungs, heart, renovascular and GI, US-guided venous access),

Pharmacology Cases 

EKG Cases 

Nuts & Bolts: Troubleshooting Thoracic Drainage

Mid-Line Catheter Insertion  

KENNY’s Cardio-Pulmonary Physiology Workshop 

SPIEGEL’s The Art of the Bougie – Airway Workshop 

 

Meet the Faculty cocktail! 1900 – Location TBA

 

Friday May 24 – Day 2

0800-0820 Metabolic Resuscitation: is is for real? FARKAS

0820-0840 Acid-Base in 3 Parts – SPIEGEL

0840-0900 Late-Breaker TBA

0900-0920 Gut POCUS – BAKER

0920-0940 Diastology for Intensivists – CHEN

0940-1020 MEET THE FACULTY OPEN DISCUSSION

1020-1040 The Art of the Bougie – SPIEGEL

1040-1100 Renal Doppler in Acute Care. HAYCOCK

1100-1120  The IVC don’t Lie: Ask the Right Question! KENNY

1120-1140 Blood Pressure: a Closer Look. MAGDER

Trauma track

1240-1300 Permissive Hypotension: Permissive Death?  NEMETH

1300-1320 Thoracic Trauma – HAYCOCK

1320-1340 Massive transfusion – MALLEMAT

1340-1400 To REBOA or Not To REBOA – HAYCOCK

1400-1440 Traumatic Cardiac Arrest: How To Avoid Killing the Dead! NEMETH

Critical Care Track

1240-1300 Inhalation Therapy for acute RV Failure – DENAULT

1300-1320 Advanced Doppler for the Intensivist – KENNY

1320-1340 Pmsa: Is There a Clinical Use? OLUSANYA

1340-1400 Got ROSC! Now What? TERAN

1400-1420 – Insights on Delirium Using POCUS – DENAULT

1420-1500 – MEET THE FACULTY OPEN DISCUSSION

Workshops (1500-1700)

Advanced POCUS (venous, shock, advanced CHF, GI, neuroPOCUS)

TERAN’s Intro to Resus TEE

HAYCOCK’s Intro to REBOA

Intro to ECMO

POCUS-SIM

KENNY’s Advanced Physiology Workshop

 

Register here!

contact us at hospresusconference@gmail.com with any questions!

Shock Macro and Micro-circulation: Piecing things together. (Part 1) #FOAMed, #FOAMcc

 

So I have really, really enjoyed the discussions I had with these bright people on shock circulation:

Segun Olusanya (@iceman_ex) Resus Track 2

Rory Spiegel (@EMnerd) Resus Track 3

Korbin Haycock (tell him to get on twitter) Resus Track 4

Jon Emile (@heart-lung)  Resus Track 5

 

Some take home points so far:

I think that more questions than answers truthfully came out of this, and that is really the best part. But lets see what the common agreed upon thoughts were:

a. the relationship between the MAP and tissue perfusion it quite complex, and definitely not linear. So scrap that idea that more MAP is more perfusion. Could be more, same, or less…

b. you can definitely over-vasoconstrict with vasopressors such that a increasing MAP, at some point, can decrease tissue perfusion. Clinically, we have all seen this.

c. no matter what you are doing theorizing about physiology and resuscitation, THE MOST IMPORTANT IS TO CONTROL THE SOURCE!

 

Some of the interesting possibilities:

a. Korbin sometimes sees decreasing renal resistive indices with resuscitation, particularly with the addition of vasopressin.

b. the Pmsa – can this be used to assess our stressed volume and affect our fluid/vasopressor balance?

c. trending the end-diastolic velocity as a surrogate for the Pcc and trending the effect of hemodynamic interventions on tissue perfusion.

This stuff is fascinating, as we have essentially no bedside ability to track and measure perfusion at the tissue level. This is definitely a space to watch, and we’ll be digging further into this topic.

 

Jon-Emile added a really good clinical breakdown:

I think one way to think of it is by an example. Imagine 3 patient’s MAPs are 55 mmHg. You start or increase the norepi dose. You could have three different responses as you interrogate the renal artery with quantitative Doppler:

patient 1: MAP increases to 65 mmHg, and renal artery end-diastolic velocity drops from 30 cm/s to 15 cm/s
patient 2: MAP increases to 65 mmHg and renal artery end-diastolic velocity remains unchanged.
patient 3: MAP increases to 65 mmHg and renal artery EDV rises from 10 cm/s to 25 cm/s

in the first situation, you are probably raising the critical closing pressure [i know i kept saying collapse in the recording] relative to the MAP. the pressure gradient falls and therefore velocity falls at end diastole. one would also expect flow to fall in this case, if you did VTI and calculated area of renal artery. in this situation you are raising arteriolar pressure, but primarily by constriction of downstream vessels and perfusion may be impaired. ***the effects on GFR are complicated and would depend on relative afferent versus efferent constriction***

in the second situation, you have raised MAP, and probably not changed the closing pressure because the velocity at the end of diastole is the same. if you look at figure 2 in the paper linked to above, you can see that increasing *flow* to the arterioles will increase MAP relative to the Pcc [closing pressure]. the increase in flow raises the volume of the arteriole which [as a function of arteriolar compliance] increases the pressure without changing the downstream resistance. increasing flow could be from beta-effects on the heart, or increased venous return from NE effects on the venous side activating the starling mechanism. another mechanism to increase flow and therefore arteriolar pressure relative to the closing pressure is the provision of IV fluids.

in the third situation, MAP rises, and EDV rises which suggests that the closing pressure has also fallen – thus the gradient from MAP to closing pressure rises throughout the cycle. how might this happen? its possible that raising the MAP decreases stimulus for renin release in afferent arteriole, less renin leads to less angiotensin and less efferent constriction. thus, paradoxically, the closing pressure falls with NE! another possibility is opening shunts between afferent and efferent arterioles [per Bellomo]. as above ***the effects on GFR are complicated and would depend on relative afferent versus efferent resistance changes***

 

This is really, really interesting stuff. So in theory, the MAP-Pcc gradient would be proportional to flow, so if we can estimate the direction of this gradient in response to our interventions, we may be able to decrease iatrogenism. I’ll have to discuss with Jon and Korbin which arterial level we should be ideally interrogating…

More to come, and next up will be Josh Farkas (@Pulmcrit), and I’m sure anyone following this discussion is looking forward to what he has to say. I know I am.

cheers!

 

Philippe

H&R2018: Final Program! Only a few spots left!

Do you take care of sick patients?  If so, you’ll be liking these two days.

Jon-Emile Kenny, Rory Spiegel, Josh Farkas and Andre Denault in the same, small auditorium. It’s a treat.

So here is the schedule for both days, including the workshops, which at this point are almost filled. We’re quite excited as it has really come along well, and all the speakers are amped to teach and learn, which is the point of this whole thing.

 

Due to fire code, space is limited so register now! And honestly, the workshops are almost full, but if there is sufficient demand, we might add one or two, so don’t be shy. Someone even asked for a Neuro-POCUS workshop. A couple more inquiries and we’ll do it!

Download the brochure and registration form here: H&R2018 – Brochure-Participants

 

Thanks and see you in Montreal in April!

 

The Scientific & Organizing Committee

The Hospitalist & The Resuscitationist. Montreal, April 18th & 19th, 2018. #Hres2018

NOTE: THIS WAS THE H&R2018 PAGE, SO IF YOU ARE LOOKING FOR H&R2019, CLICK HERE!

So for this winter, we’ve put together a little gem of a conference which will be a mix of hospitalist and critical care medicine, both with a dash of POCUS for good measure. Our focus here will be short, to the point, highly relevant and highly physiological talks on key topics, in short, 15 minute talks.

What are we going to talk about?

Day 1: The Hospitalist

 

Day 2: The Resuscitationist

 

 

You can figure there will also be late-breakers, “ask the crowd” talks and more.

Workshops? Sure:

Yup. You can ask for a workshop. Enough similar requests will probably make it happen. A few have already asked for Neuro-POCUS, so that is a likely addition.

 

So, who will be talking?  The lineup already includes Andre Denault, Josh Farkas (@Pulmcrit), Jon-Emile Kenny (@heart_lung), Rory Spiegel (@EMnerd), Hussein Fadlallah, Peter Barriga, Daniel Kaud, Davide Maggio, Michael Palumbo, William Beaubien-Souligny, and a few more to confirm. And who knows who might do an impromptu drop-in…

 

The short answer is yes. Of course, it does depend on what you do. If you are a hospitalist, involved in critical care or acute care of any kinds, you will find something here for you. Totally awesome for IM residents/FM residents planning on doing some hospital medicine or ICU coverage. Who will get the most bang for his or her buck here? Real docs training or working in the trenches. This isn’t a cutting edge research conference, but a cutting edge clinical application conference.

 

Oh yes, and the CME, of course:

 

This will be a small, fun conference. Space is purposely limited, for an intimate feel and to encourage discussion between peers. No need for these exclusive “meet-the-professor lunch” or anything like that: that’s what the whole event is like!

 

Registration is open! Print, fill, write a cheque and send the form below:

RegistrationV2

If you’re crazy busy, or have any questions, feel free to email hospresusconference@gmail.com or tweet (@ThinkingCC) to reserve a spot! 

Download the brochure here:

H&R2018 Brochure – Participants

 

cheers!

 

The H&R 2018 Scientific & Organizing Committee:

Dr. Philippe St-Arnaud – ER and Critical Care doc, POCUS instructor and constantly pushing the clinical envelope.

Dr. Carola Zambrana – our Hospitalist on the panel, constantly seeking excellence in care and working on bringing POCUS to the wards.

Dr. Mario Rizzi – our friendly neighborhood respirologist and educator.

Dr. Philippe Rola – Critical Care doc, long time POCUS aficionado and instructor, working at bringing POCUS into the everyday physical exam.

 

A Discussion on Fluid Management Protocols with Rory Spiegel. #FOAMed, #FOAMcc, #POCUS

 

So Rory (@EMnerd) is in the process of working on a fluid resus protocol for Shock-Trauma, and asked me if we could have a chat about it, which I feel very honored for – and had a brief impostor syndrome crisis – but it’s always great to chat with people who are really bright, really physiological and after the same goal, to make patients better. Always a pleasure to chat with Rory, so here it is.

I really can’t wait to see their protocol, because I think this is a huge and complex endeavor, but has to be done.  I will try to put pen to paper (probably really pixels to a screen but that doesn’t sound as good) and put what I try to do for fluid resus on a diagram of sorts.

Love to hear comments and questions.

PS please skip the first 30 seconds which are a technical blank… Ièm not tech saavy so can’t trim it!

cheers!

Philippe

 

A great comment by Dr. Korbin Haycock

One issue to consider is the degree of pulmonary vascular leakage. If, as in the case of sepsis, the pulmonary vasculature is more prone to the development of lung interstitial edema, lower LVEDP’s possibly will still result in as much lung wetness as higher LVEDP’s. Therefore, reliance of E/e’ ratios may not be the best measure of a fluid resuscitative endpoint in sepsis (and aren’t we really talking about sepsis resuscitation here?). I believe that it’s relatively clear that EVLW will adversely affect outcomes, but pushing for every bit of increased stroke volume/fluid responsiveness is less clear to be beneficial, even if it makes sense from a DO2/VO2 perspective (which may not be the real issue in sepsis anyway, as mitochondrial utilization of the DO2 provided may be the real problem, rather than DO2/VO2 balance). If the assumption is that the kidneys and lungs are the most delicate organs and most at risk to over aggressive fluid administration, and will impact mortality/LOS in the ICU, perhaps a combined strategy of attention to E/e’ ratios, development of B-lines, or the renal resistive index increasing would be a signal for a different strategy rather than fluids to increase venous return (i.e. switching from crystalloids to norepinephrine or vasopressin if the CO is elevated and will tolerate a minor ding from the increase in SVR). If any of those three variables indicate a problem, stop the fluids, switch to a vasopressor. If the issue is the CO rather than the SVR, use an inotrope instead. Of course RV/LV interactions as mentioned in the comments above must be considered. No point in giving fluids to an empty LV if the RV is failing–you’ll just congest the kidneys.

Wicked Clinical Case: POCUS & Prone save the day! #FOAMed, #FOAMcc, #FOAMer

So I get a call from a colleague in the ED at about 2am, telling me about a 39 yr old woman post-arrest. So I start putting on my boots and warming up the car (it’s January in Montreal folks).  Apparently she had presented earlier in severe acidosis, the diagnosis is unclear, but she apparently got 2 units for an Hb of 49, then went into respiratory failure and got intubated. She arrested about 30 minutes later, cause unknown.

I tell the ICU to prepare a bed but I want to see her in the ED first. Twenty minutes later I put probe to patient and see a full IVC with spontaneous echo contrast. On that I tell the nurse to hold the fluids – there was a bag and tubing and a pump with 100ml/hr on it – and turn into a subxiphoid view to see a normal RV and a hypokinetic LV with some WMAs. She has marked consolidations  in both posterior lung fields and B lines laterally, with small effusions and dynamic air bronchograms (indicating patent airways). At this point she has a HR of about 120, but there is neither perceptible BP (by NIBP) nor saturation. She’s on levophed at 20mcg. She’s about an hour post arrest which was witnessed and brief (<10min to ROSC).

The theories about the arrest are possible hyperkalemia: she was intubated with succinylcholine before the K of 6.1 was back from the lab, and her pre-intubation pH was 7.0, and post-intubation she was only ventilated at 400 x 18, possibly precipitating a drop in pH and a rise in K. Her EKG had some nonspecific signs at this point, but also a poor anterior R wave.

So we head to the ICU, as instrumentation was needed. Cerebral saturation (SctO2) is 42% and ETCO2 is 20mmhg, which reassures me that the BP is probably in the measurable range (normal SctO2 is >60% and varies, but 47% is certainly viable)…  A jugular CVC with continuous ScVo2 and a femoral arterial line goes in:

screen-shot-2017-01-05-at-10-44-50-pm

So with a BP of 59/44 (ignore the 100/46, not sure whose arm that was on!) I start epinephrine, as the POCUS is similar, as I want some added beta-agonism. ScVO2 matches SctO2 in the 40’s. We get the BP up the the 90-1oo range, the ETCO2 goes to 30, the SctO2 and ScVo2 go up into the high 40’s, which is very reassuring, because with this I know that my epi drip is improving perfusion and NOT over-vasoconstricting. Without looking at a real-time tissue perfusion index of some sort or other, it is nearly impossible to know rapidly whether your therapy is helping or harming (will discuss tissue saturation & resuscitation monitoring in more detail in another post sometime soon).

screen-shot-2017-01-05-at-10-46-31-pm

So now the sat finally starts to record in the low 60’s. We have a PEEP of 5, so start bringing it up. We hit 16 before the BP starts to drop, and that only gets us to the mid 70’s sat%. She actually squeezes my hand to command.

screen-shot-2017-01-05-at-10-45-21-pm

At this point I take a few seconds to recap in my mind. I’d spoken to the husband briefly and she had had recurrent episodes of feeling unwell with headache, nausea and diaphoresis, and that had been out for dinner earlier and she felt fine until later in the evening when this came on and eventually brought her to hospital. There was also a notion of hypertension at an ER visit a couple of weeks ago. Her history was otherwise not significant. Nonsmoker.

Pheo? Maybe, but shock?  I repeat the EKG, and now, in I and AVL, there is perhaps a 1mm ST elevation. She’s 39 and essentially dying. Lactate comes back >15, pH 6.9.  I give her a few more amps of NaHCO3. You can see the BP respond to each amp. I decide we need to go to the cath lab and get the cardiologist on call to get on the horn with the interventional team at a nearby hospital with a cath lab and ECMO, which is what I think she needs. Hb comes back at 116, making that initial 49 that prompted 2 PRBCs probably a technical or lab error…very unfortunate. There are no visible signs of significant bleeding.

But back to the patient, because this isn’t really a transferrable case.

Recap: a 39yr old woman in cardiogenic shock AND in severe congestive heart failure exacerbated by fluids and packed red cells, with a PO2 in the 40’s and sat in the 70’s.

So I decide to prone her.

screen-shot-2017-01-05-at-10-47-44-pm

Along with draining tamponades, this had to be one of the most rapid and rewarding maneuvers I’ve done. There was a scry drop of sat to the 40’s for a few seconds (may have been a technical thing), but then within a few minutes: BP to the 130’s, SctO2 to 59% and sat 100%!

screen-shot-2017-01-05-at-10-46-46-pmscreen-shot-2017-01-05-at-10-47-31-pm

screen-shot-2017-01-06-at-12-08-05-am

 

We dropped the vasopressors, the FiO2, and all breathed a collective sigh of relief. Now for the novices out there, prone ventilation improves VQ mismatch by moving perfusion from diseased, posterior lung fields to now-dependant, relatively healthy, anterior lung fields.

So transfer at this point was in the works. I planned to leave her prone until the last minute. The miraculous effect started to slowly wane within about 30 minutes, with sat and BP creeping down. At the time of transfer, we were back up to 80% FiO2.

So why is this?  Simple enough, this being simple pulmonary edema – rather than consolidated pneumonia – it migrated to dependent areas  relatively quickly. This was confirmed by a quick POCUS check:screen-shot-2017-01-05-at-10-48-06-pmscreen-shot-2017-01-05-at-10-48-26-pm

So in the still shots, you see a pristine “A” profile (normal, no edema) from the patient’s back, and a severe consolidation or “C” profile with ultrasound bronchograms in the antero-lateral (now dependant) chest. Impressive. (for those wanting some POCUS pearls see other posts and here). This is the reverse of her initial POCUS exam.

So we flipped her back and transported her – lights & sirens – the the cath lab, where they were waiting with ECMO cannulae. As an aside, it was quite refreshing to speak to the ICU fellow who spoke POCUS as well as french and english – it’s not usually the case, but I’m glad to see the change. I do believe it to be a direct effect of the influence of my friend and mentor, Dr. Andre Denault, one of the POCUS deities.

So she turned out to have a normal cath and a large adrenal mass. She did well on ECMO, being weaned off it today, and is now alpha-blocked and waiting for surgery, neurologically intact for all intents and purposes. A big thanks to the interventionists and the ICU team at the Montreal Heart Institute. Puts a smile on my face.

 

Take Home Points:

  1. don’t resuscitate without POCUS. I wouldn’t want anyone guessing with my life on the line, would you?
  2. keep pheo in mind as a cause of “acute MI” and shock
  3. if you’re not using some form of realtime monitor of perfusion (continuous CO, SctO2, ETCO2, ScvO2) then all you’ve got is looking at the skin and mentation, so you are essentially flying blind. Lactate and urine output are not realtime in real life.
  4. get ECMO in the house, it’ll come in handy. I’m working on it.

 

Love to hear some comments!

cheers

 

Philippe

 

ps I’ll try to add more ultrasound clips from this case in the next few days.