The Resuscitation Tracks 1: Portal Vein POCUS with Dr. Andre Denault. #FOAMed, #FOAMcc, #FOAMus

So this is one of the key discussions I wanted to have in my process of synthesizing my resuscitation algorithm. Dr. Denault is the one guy I’d call a mentor, and I think one of the rare and true clinician-scholar, who is just as comfortable being the anaesthetist/intensivist at the bedside of the crashing patient as he is being the keynote speaker in major conferences, or writing the textbooks that lead the field in acute care/perioperative TEE and critical care POCUS.

So to put some perspective to this discussion, back in 2014 I organized a resuscitation afternoon for internists with Andre and another awesome guy you probably all know, Haney Mallemat (@criticalcarenow). In a quick 15 minute discussion between talks, he shared with me the most recent of his discoveries, portal vein POCUS as a marker of right-sided failure/volume overload in his post-op cardiac patients, and how aggressively managing these resulted in much improved post-operative courses in terms of weaning, vasopressors and even delirium.

Interesting stuff.

So here you are:

So I’ll let you all ponder that and I would really like to hear comments and ideas. Sometime in the next few weeks I’ll be finalizing my resus algorithm – which will not be a recipe approach, as you might suspect if you have been following this blog, and will rely heavily on POCUS and the clinical exam.

cheers and thanks for reading and listening!

Philippe

 

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.

Twittercase: Fouled urine and #POCUS discussion. #FOAMed, #FOAMcc, #FOAMer

So I admitted a patient to the ICU yesterday from the ED.  He’s an 80-something gentleman from a nursing home with an indwelling catheter, and presented with stupor, hypotension, fever, leukocytosis and clearly infected urine.  His labwork showed a lactate of 5.3, a double-normal creatinine and, after 3 liters or so of crystalloid, he was started on norpeinephrine and hence came to the ICU. His extremities were fairly warm, and his cerebral saturation was 62%.

Before seeing the POCUS info, however, consider a clearly septic patient with AKI and elevated lactate. He did get 3 liters of fluids, but i’ve seen these patients get more fluids, whether for hemodynamics, lactate, AKI or any combination of the aforementioned.

Below is the clip, a quick POCUS sequence going from IVC (with hepatic vein flows), subxiphoid cardiac views, both lung views.

So here, we see a plethoric and fixed IVC (sorry I didn’t include the short axis but it was round and full, so in this case the LAX is reliable) with biphasic hepatic flow. Cardiac views show normal ratios and a poor LV function. Chest views show bilateral effusions and consolidations.

So what did I do?

  1. stopped fluids (I do not believe in routine maintenance fluids any more than in maintenance antibiotics or vasopressors).
  2. gave lasix (given that he is on the flat part of FS curve, I was unconcerned with some diuresis decreasing his preload, vasopressors and lactate notwithstanding, and with the goal to decongest his kidneys, likely suffering from congestive insult on top of the septic one).
  3. did not try to chase his lactate with increasing cardiac output (lactate being a great alarm bell and prognosticator, but little else, and because he was worm and with a decent cerebral saturation, I did not feel that there was a major cardiogenic component to his shock).

So what happened?

This morning, after a negative balance of 1,500 cc in 24 hours, his levophed dose has dropped by half, his lactate is normal and his creatinine is decreasing. A decade ago, I would have chased down the last ounce of volume responsiveness with fluids, aggressively trying to drive down the lactate and creatinine, and maybe, 24 hours later, he would have developed “ARDS” because he was “so sick.”  😉

cheers

 

Philippe

 

Bedside Ultrasound Quiz Part 1: a 50 yr old man with dyspnea, acidosis, hepatitis and leg edema. #FOAMed, #FOAMer, #FOAMus

So last night, an interesting call from the ED about a 50 year old man who presented with a 3 week history of increasing dyspnea, leg edema, temp of 39,  a lactate of 3.9, an INR of 1.7, elevated LFTs and a WBC of 18, but a BP of 130/75.

Fortunately, I was dealing with a saavy ER doc with some POCUS capabilities, so he also told me he saw a pretty big IVC and he was a bit leery about giving fluids, though this looked like pretty severe sepsis with 3 or 4 affected organ systems…

So I asked him to hold fluids until I got there. Here is what POCUS found:

He revealed a past history of untreated hypertention, and a flu-like illness 3-4weeks ago.

What’s the diagnosis (-es) and management?

Answers & Clinical evolution in part 2 tomorrow!

 

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.

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