Bedside Ultrasound Quiz Part 2: A 50 yr old man with dyspnea, acidosis, hepatitis and leg edema. #FOAMed, #FOAMer, #FOAMus

So I was glad to see some great answers on twitter about this case, so let me fill you guys in on the management and the details.

So my diagnosis was of a (likely viral) myocarditis as a subacute process over the last weeks, with a superimposed pneumonia causing the acute deterioration and presentation to ED.  I didn’t think that his elevated lactate represented shock, but rather a reflection of adrenergic activation and reduced hepatic clearance due to congestive hepatitis.  He also had congestive renal failure. Of course, the LV had a 4 x 2 cm apical thrombus, which is likely secondary to the dilated cardiomyopathy.

So the management was diuretics, antibiotics, and anticoagulation, which resulted in a gradual improvement of the respiratory status and renal/hepatic dysfunction. He had a coronary angiogram the day following admission which showed two 50% stenoses deemed to be innocent bystanders.

Bottom Line:

I think the learning point in this case is that, without POCUS, this could easily have been treated as severe sepsis with multiple organ failure (potentially rationalizing away the BP of 140 as a “relatively low” BP due to untreated hypertension), and as such, may have received fluids… Especially south of the border where they are mandated to give 30 cc/kg to anything deemed “septic.”  This would have been the polar opposite of the necessary treatment.

The scarier thought is that he may have then progressed to “ARDS,” been intubated and then the debate between keeping him dry and giving fluids for the kidneys may have ensued.  Though a formal echo likely would have been done, it may not have happened in the first 24-48 hours… If MSOF progressed and he succumbed, the rational may have been that he was “so sick,” and died despite “best care…”

The reality is that he is not yet out of the woods today, with an EF of 15% and afib, but he is off O2 and sitting up in a chair. Fingers crossed he falls in the group of those with myocarditis who improve…

Love to hear anyone’s thoughts!

 

Cheers

Philippe

Bedside Ultrasound Clip Quiz! A 72 year old man with fever, weight loss and tachycardia. #FOAMed, #FOAMcc, #FOAMer

So a 72 year old man is brought to the ER after collapsing at home. His family had noted weight loss in the last months, and recently some fever and general weakness.  His HR is 108, T 38.8, BP 80/40, GCS 14 – somnolent – he is in lactic acidosis (4.5) and renal failure (cr 180 – baseline 120), with some vague abdominal pain, a clear chest and warm extremities.

POCUS shows a normal IVC, normal RV/LV, A profile lungs, no ascites, and this on the left flank:

 

What is the main diagnosis?

Scroll below for the answer:

 

 

 

 

 

 

 

 

 

So the clip shows fairly severe hydronephrosis, the “bear paw” with very dilated calyces.  The patient was suffering from obstructed pyelonephritis due to massive retroperitoneal adenopathy later found to be lymphoma.  A couple of hours later he got a nephrostomy tube to take care of the septic source (double J could not pass) and his sepsis resolved within a few days, and he headed off to chemo for the NHL.

The advantage of POCUS here is. once again, the speed of diagnosis. He went straight from CT to the readied urologists and source control happened within a couple of hours. His relatively benign abdomen may not have prompted a rapid CT otherwise.

See here for more POCUS!

cheers!

 

 

Philippe

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:

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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).

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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.

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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.

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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%!

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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.

N=1 Principle in ARDS and esophageal pressure directed mechanical ventilation. #FOAMed, #FOAMcc

So i recently came across a review on esophageal pressure-guided ventilation in ARDS, which is in fact a technology I’ve had in my shop since 2008, but rarely use.

The truth is that I haven’t seen much “ARDS” in the last years, and I believe quite strongly that this reflects simply our hospital’s increased awareness of the nocive effects of over-zealous fluid resuscitation. Although in the ICU we still admit patients who, in our opinion, have received a bit more fluid than they should have, we have become more aggressive with diuresis “despite” the presence of shock, and usually see “ARDS” resolve. This is a direct consequence of actually “looking” at our patients’ volume status using ultrasound (for more see, well…most other posts on this blog!).

However, what seems like genuine ARDS does come around once in a while, and we recently had severe respiratory failure develop in a morbidly obese patient, and all of a sudden, in the presence of an FiO2 of 100%, a PEEP of 14, intra-abdominal pressures between 20 and 25, and on Flo-Lan, it seemed it might be a good idea to tailor ventilation.

Current Practice:

The most common practice currently is the ARDSnet type low volume (5-7ml/kg) lung protective ventilation, using a PEEP/FiO2 scale and aiming for plateau pressures (Pplat) below 30. Generally speaking a good idea, but one has to understand that this is, once again, a one-size-fits-all (except for the per kg) approach, which isn’t ideal if you try to follow  the N=1 Principle.

Why is this?  Because, due to physical characteristics (obesity, chest wall stiffness, etc,) and pathology (increased abdominal pressure, etc), the airway pressure reflects the respiratory system pressure (Prs) rather than the transpulmonary pressure (Ptp), which is the variable most related to volutrauma (which has eclipsed barotrauma as the mechanism for most ventilator-induced lung injury (VILI).  Ptp essentially relates to overdistension, which is what results in pneumothoraces. In terms of parenchymal micro-injury, it seems to be most related to atelectrauma, in essence the opening and closing of alveoli, with the resultant shear forces disrupting surfactant and cell surface. This type of injury relates best to finding optimal PEEP to both recruit and prevent de recruitment – in effect minimizing the amount of lung tissue collapsing and reopening.

 

Esophageal pressure (Pes)-guided Practice:

So Pes is used as a measure of pleural pleural pressure, and:

Ptp = Paw – Pes

That equation is the central tenet to this, and basically, you have to reset your goals to:

a. Ptp (exp) around zero – optimal PEEP – (meaning no over distension and no de-recruitment)

b. Ptp (insp) below 25 – though this is not really individualized as a hard data point, but has been shown to be a reasonable cutoff for volutrauma.

 

How do you do this?

By slipping in a special oro/naso-gastric tube with a balloon connected to the ventilator, one is able to simultaneously measure airway pressure (as is standardly done) and esophageal pressure. This is what it looks like:

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Here we can see that this patient has a PEEP of 20 (top), a Pes of about the same, and thus a Ptp (bottom) near zero.

We’ll discuss this case hopefully tomorrow, but just to show the mechanics/technique of it.

 

Bottom Line:

So this involves tossing out the ARDSnet charts and trying to individualize and optimize Ptp (insp and exp) instead of plateau pressures and PEEP.  How may it be useful clinically? Well, you may be able to detect unsuspected states of de-recruitment/ateletasis due to excessive chest wall or abdominal pressure, and allow you to increase PEEP “safely.”

When should I use this?

I’m not sure what everyone else is doing, but we are in the process of setting up a protocol where esophageal balloons will be inserted for any patient whose ventilator settings are approaching or exceeding FiO2 70%/PEEP 15, indicative of sufficiently severe respiratory failure warranting this additional level of fine-tuning.

I tend to use it when ventilating two groups: those with (a) elevated intraabdominal pressure, and (b) the obese patients, as they often have elevated Pes (usually due to diaphragmatic displacement. Interestingly, the correlation between obesity and Pes is not very good, so one should not “blindly” feel they can crank up the PEEP to 25 and ignore plateau pressures, as some obese patients have normal Pes (likely due to compliant abdominal walls.

Would love to hear what others do.

 

Here are the relevant articles/references:

talmor-nejm-2008

ajrccm-2014-review

 

Cheers!

 

Philippe

 

POCUS Course: Quebec city 2017!

Here’s a chance to learn with one of the masters in the field, my friend Andre Denault, internist-anaesthetist-intensivist extraordinaire, and a true mentor to me.

Designed for acute care docs, this is an approach to respiratory failure, shock and renal failure. I recommend it to anyone in the field!

 

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I’ll likely be an instructor there is I can free up my schedule, so see you there!

 

cheers

 

Philippe

Bedside ultrasound case: Fibroids, Syncope and Dyspnea. #FOAMed, #FOAMus, #FOAMcc

So today, a 33F presented following syncope. She was mildly tachypneic wiyh a HR of 135 and BP of 130/80. I’m inserting the clip of my bedside ultrasound evaluation, as this takes place essentially simultaneously with my history-taking:

So this clip runs thru a few views, starting with an IVC long axis, showing a relatively plethoric IVC with minimal variation. This is not normal. Tells me to expect something abnormal downstream, unless someone has flooded the patient with IV fluids. The next view is the parasternal long, then short axis, showing an increased RV to LV ratio, and a small, hypercontractile LV, with septal flattening consistent with RV pressure overload, the “D” sign.  The apical 4 chamber follows with little else to add (difficult to measure TAPSE well in that segment).

So this is sure looking like pulmonary embolism, and I’m already toying with a half dose TPA, MOPETT-style, until the reveals that the cause of her starting oral contraceptives two months ago was to control heavy menses associated with large uterine fibroids… So I figure I’ll buy myself some decision time anyhow by ordering the CT angio – unless in pre-arrest, I don’t thrombolyse without formal confirmation – but I did start IV heparin on the echo findings. Here is the CT:

So this indeed confirms submissive embolism, particularly to the left PA.

Next?  I work in a community hospital, and although I’m totally comfortable thrombolysing PE, in this case, I was concerned about bleeding related to the fibroids, and I haven’t yet figured out a way to embolize bleeding vessels at the bedside, so I felt that the safest thing was to transfer her to a tertiary care center with a solid interventional radiology program. So off she went. I’ll update if anything funky was done like a catheter suction and I can get some clips.

So in terms of POCUS, I think this illustrates how speedily a diagnosis can be made, and although in this case the pre-test probability and index of suspicion was pretty high, it isn’t always!

cheers!

 

Philippe

 

For more POCUS tips, see here!

Bedside Ultrasound Case: Control the source. #POCUS #FOAMed, #FOAMcc, #FOAMus

So this morning a 65yr old man with shock and respiratory failure was admitted to the ICU, hypotensive on levophed and vasopressin, with a lactate over 10.

So, as usual, my first reflex was to reach for the probe to assess hemodynamics. He had been well resuscitated by a colleague, and the IVC was essentially normal, somewhere around 15 mm and still with some respiratory variation. However, scanning thru the liver, my colleague had noted a large hepatic lesion, which on CT scan (non-infused since patient had acute renal failure) the two radiologists argued whether it was solid, vascular or fluid filled.

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Having the advantage of dynamic ultrasound, you can tell that there is some fluid motion within the structure, very suggestive of an abcess, especially in the context of severe septic shock:

So the next step was source control:

 

Pretty nasty. Pardon my french!

We got over 1.5 L of exceedingly foul pus.

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Within a couple of hours the lactate dropped to 3 and the levophed was down by more than half.

I think this case illustrates once again, the power of POCUS in the hands of clinicians.  While I am certain that the diagnosis would have been made without POCUS, it probably would have taken additional time as the radiologists themselves were debating its nature, and without POCUS, bedside drainage in the ICU would have been out of the question. That liter might still be in there tonight…

For those interested in how to integrate POCUS in their daily rounds, I think I put together a fair bit of clinical know-how and tips in this little handbook.

 

Cheers!

 

Philippe