Tasty Morsels of Critical Care

Welcome back to the tasty morsels of critical care podcast.

Today we’re going to have a quick overview of the oesophageal balloon. If you’re directed to a patient in your long case who has an oesophageal balloon in, then you’re probably having a bad day. It would seem very unfair to have too many questions on this but an awareness of their existence and some cliff notes on their basic use might come in handy especially if you’re doing well and you’re in the medal type territory of the exam. Exams aside they’re a useful gateway drug into some important respiratory mechanics that are relevant to all of us.

At their most basic these are fancy NG tubes with an inflatable balloon that should end up in the lower third of the oesophagus. Inflating the balloon with a small amount of air allows you to transduce the pressure at the area the balloon lies. While that sounds straightforward there are large sections of review papers dedicated to troubleshooting placement and means of assuring the number you generate is actually accurate. I refer you to the below references for further reading.

The pressure measured is called the oesophageal pressure, often abbreviated to Pes because it seems the Americans won the spelling war on that one. Oesophageal pressure is a reasonable surrogate (with assumptions of course) for pressure within the pleural space. Once we have an estimate of pleural pressure we can subtract that from the plateau pressure displayed on the vent and we end up with a fancy number called the transpulmonary pressure. The transpulmonary pressure or Ptp is the distending pressure applied to the lung either from the muscles of spontaneous ventilation or from positive pressure ventilation from the ventilator.

Whoopdy do says the examiner – you now have another number you don’t really know what to do with. What should we use this data for, the examiner is asking? Well a short list of useful aspects you can look at with the oesophageal balloon include

compensating for the effect of the chest wall on respiratory mechanics

appropriate titration of PEEP

assessing the contribution of respiratory muscle use to potential lung injury

assessing triggering and synchrony issues

At this stage you’d be hoping the examiner is satiated and you can move on to something else but in the unlikely and terrifying event that they ask for more detail you might want to mention some of the following.

Our typical approach to safe ventilation in the passively ventilated patient is to look at driving pressures and tidal volumes. But this takes no account for the contribution of the chest wall. In the very obese patient there is a lot of flesh pressing down on the chest wall, this leads to an increasingly positive pleural pressure. It would make sense that we would need more pressure to distend the lungs in this scenario. The balloon in this scenario will allow you to set your PEEP appropriately. The Ptp at end expiration needs to sit somewhere in the 0-10cmH20 range to avoid derecruitment and in end inspiration it needs to be less than 25cmH20. This may need a lot more PEEP or less driving pressure than you’re used to giving and the balloon can help you feel safe about doing that.

In the patient weaning from the ventilator in a spontaneous mode the oesohpageal balloon can be used to make an estimate of the contribution of the patients muscular effort to the transpulmonary pressure. Your patient may be on 10/5 on a pressure support mode and you may well be lulled into a false sense of security that because the pressure numbers on the vent are modest then the pressures being exerted across the lung are also modest. What we are not measuring in this scenario is the distending pressure being applied to the lungs by the respiratory muscles, the Pmus. The balloon in this scenario can give an estimate of this as it reflects the negative pleural pressure generated by the patients inspiratory efforts allowing us to come up with a Ptp number that takes Pmus into consideration. Sometimes this might encourage you to increase the support from the vent, sometimes this might encourage you to increase the sedation depending on the context.

So given all the wonderful things the balloon can do for us why are we not doing it on everyone? A list of reasons not to use oesophagaeal balloons might include

cost – these fancy NG tubes are pricier than you would think

compatible software on the ventilators. These frequently don’t come as standard

appropriate placement. These are tricky to get right and knowing that the number generated is valid is not entirely straightforward. Lots of assumptions are made

the Pes number reflects pleural pressure only at a single location and does not take account of heterogeneity.

the evidence base is unclear if this adds anything over doing something like simply following the high PEEP table from ARDSnet.

Interestingly several research groups (thinking the folk from Toronto or Luigi Camporata in london)  have used balloons to identify surrogate ways of measuring recruitment or estimating Pmus that we can easily measure on a standard ventilator set up. This may well be a way of bringing the important concepts of transpulmonary pressure to the bedside.

Reading:

The Toronto Mechanical Vent Course was an excellent intro for resp mechanics for me. They offer a virtual version

Mauri, T. et al. Esophageal and transpulmonary pressure in the clinical setting: meaning, usefulness and perspectives. Intens Care Med 42, 1360–1373 (2016).

Yoshida, T., Grieco, D. L. & Brochard, L. Guiding ventilation with transpulmonary pressure. Intensive Care Med 45, 535–538 (2019).

Mireles-Cabodevila, E., Fischer, M., Wiles, S. & Chatburn, R. L. Esophageal Pressure Measurement: A Primer. Respir. Care respcare.11157 (2023) doi:10.4187/respcare.11157.

Jonkman, A. H., Telias, I., Spinelli, E., Akoumianaki, E. & Piquilloud, L. The oesophageal balloon for respiratory monitoring in ventilated patients: updated clinical review and practical aspects. Eur. Respir. Rev. 32, 220186 (2023).

Deragned Physiology

LITFL

Welcome back to the tasty morsels of critical care podcast.

This is the second of 2 parts on PE in critical care. The first focused on risk stratification and this one will focus on management. There is a link to a transcript of a more comprehensive talk with references on emergencymedicineireland.com for those keen enough to dive a little deeper. As noted in the last podcast this one leans very heavily on “in the my experience” level of the evidence pyramid and should be weighted as such.

For this discussion I’m going to assume your patient is in the ESC High risk category, ie hypotensive with a PE on imaging and you’re satisfied that the PE is causing the hypotension. I do believe there is a tiny cohort of the PE population who warrant aggressive reperfusion even with a normal appearing BP but at this stage I cannot say I have any evidence or guidance to really identify who they are and back that up.

For the original talk I gave on this to an EM audience, I split the interventions into helpful , distractions, and not helpful. It was probably a little bit of a provocative division if I’m honest. The slide is on the site for reference and viewing it will likely make what follows more edifying.

For the resus room patient in the first 30-60 mins I feel comfortable to standby my assertion that a short list of “helpful interventions” should includes lysis, anticoagulation, noradrenaline, oxygen and some CPR. In the ICU however we’re often present both at the first 30-60 mins but over next hours and many of the items on the “distraction” list become a little more relevant with time.

Number 1 on my list of helpful interventions is thrombolysis. As mentioned, if you have found PE and you have satisfied yourself that the sickness and hypotension you’re seeing is caused by that PE then you need to have a good reason not give thrombolysis. The evidence base is not high level RCTs but it is a class 1 recommendation on the ESC guidelines and the list of class 1 interventions is really quite short. In the 25 year old in resus with a massive PE day 3 after an arthroscopy the decision here seems pretty straightforward. However in the post trauma patient in the ICU with massive PE with a small traumatic SAH and an improving SDH and a recent laparotomy then the decision is orders of magnitude more complex and you may well find a very good reason why lysis is not an option.

There is not a straightforward answer to lysis because it will vary from patient to patient but I would emphasis that it is a question worth dedicating a decent chunk of your cognitive bandwidth to.

Dosing in an unstable patient is often 10mg of alteplase followed by 90mg over 2 hrs. Dosing in a cardiac arrest situation is typically a 50mg bolus.

Anticoagulation is one of the other class 1 recommendations on the ESC list. Opinions vary on agent of choice. With my ICU hat on I will almost always advocate for UFH as I feel confident that if i stop it, the heparin effect will be gone in a couple of hours when the inevitable bleeding starts. Opinions vary and I know smart people who advocate for LMWH in this scenario with one of the arguments being you probably get more reliable and quicker anti Xa effect.

Both the guidelines and your esteemed narrator recommend against volume resuscitation. Dumping a litre of crystalloid into the venous circulation will shift the IVS further towards the left impairing cardiac filling and doing the opposite of what you intended.

A much better resuscitation fluid would be noradrenaline. This is remarkably effective in improving BP and perfusion and I have often used it when I am 90% sure the patient has a PE but haven’t quite got the CT scan to prove it. The noradrenaline can also buy you a little time to make a better decision about the lysis and reperfusion, converting what would have been an immediate decision into something that you maybe have more like 30 mins to make. Certainly if the noradrenaline dosage is rising and the right heart is struggling then adrenaline would be my add on inotrope of choice.

Of course we know in the ICU we have a plethora of other agents available to us with lots of theoretical advantage on pulmonary vascular resistance etc. They would rarely be my first line, certainly not in the ED population but I would often reach for them a little further down the line once i have a better handle on the physiology and what they might tolerate. Enough to say that staring someone on 0.5mcg/kg/min milrinone as a single agent with a starting BP of 60/40 is not likely to end well in this context

Oxygenation is strongly endorsed given its proclivity for reduction in PVR, however intubating someone in this context to facilitate oxygenation is likely to result in a catastrophic haemodynamic collapse. The adage “resuscitate before you intubate” or even “reperfuse before you intubate” has some relevance here.

I find CPR to be helpful in the context of massive PE, not simply for the usual reasons of preserving some degree of forward flow but I suspect there is a mechanical effect of breaking up or moving clot more distally. I have frequently seen stuttering intermittent ROSC in this context. I would suggest caution with the mechanical CPR devices as the presence of a liver lac in the context of tPA is unlikely to be well tolerated.

While not available or that relevant to the emergency medicine population I do think the addition of nitric in the ventilated ICU patient who develops nasty PE seems like a low risk intervention with potentially massive gains. There is a small RCT of nitric in the spontaneous breathing PE population that did not however show benefit.

I put mechanical devices in the “distraction” category in my original talk as I don’t think they have much relevance in the early stage of resuscitation. However if you have kept them alive long enough or if you have a true contraindication to lysis or a failed lysis then they may well have a role. I have found the evidence base so far here decidedly underwhelming and for catheter directed lysis in particular i struggle to see how a mg/hr tpa via a pulmonary catheter is any different than a mg/hr of tpa via a peripheral IV line given that the entire venous return ends up in the pulmonary circulation either way.

The thrombectomy devices are certainly more compelling from a physiological perspective and the obvious and dramatic changes in physiology on removal of clot are quite compelling. But they are a tremendous faff requiring a catheter akin to an ECMO catheter to be threaded into the pulmonary circulation. The recent PEERLESS trial gave an average 90 min procedure time emphasizing the need to keep the patient alive long enough to receive the intervention.

I do feel this has a role in our management quiver I am just unsure what that role is, but more evidence in the coming years will likely clarify

VA ECMO is undoubtedly a fantastic physiological support for a dying PE patient but bear in mind it is almost definitely not available to you in the vast majority of hospitals in the Ireland and the UK.

PERT teams are groups of relevant physicians willing to weigh in on difficult PE cases to advise on management. I put PERT teams in the distraction category. And I feel bad about that because they’re usually filled with knowledgeable and enthusiastic people . But there are 2 errors I’ve seen on this that we should be aware of.

One is on us as primary clinicians where we outsource the decision to lyse in someone who has a clear indication. This is not necessarily the fault of the PERT team but there is risk to the patient in delaying as it is a tremendous faff trying to get hold of the relevant people and then get them to agree.

The second distraction that can happen is the recommendation for interventions in a patient that they have not seen and are not present to. A couple of times I have had to talk people out of IR interventions that frankly were not needed because the patient was getting better with conventional treatment. Do not underestimate the importance of being at the bedside and seeing the patient and evaluating response to treatment.

Surgery, in terms of pulmonary embolectomy is the third and final class 1 recommendation in the ESC guidelines for high risk PE. All be it with a very low evidence rating. It gets talked about in papers and guidelines but you’re talking about taking someone who is already mostly dead into theatre, lined, anaesthetised, chest opened and onto bypass. There probably is a role for it somewhere and in certain institutions and it’s often raised in the context of contraindications to lysis but those same contraindications to lysis usually apply to the 30000 units of heparin you need to get them on bypass. It seems to suffer from the old goldilocks flaw of “not sick enough” for theatre or “too sick” for theatre

I have clearly done way beyond my usual brevity in this scenario but honestly didn’t think anyone could tolerate a 3rd part on PE. Full refunds are available on request

For further reading it is probably best to visit the original lecture post where the relevant papers are all listed with a little smattering of critical appraisal thrown in for good measure.

Welcome back to the tasty morsels of critical care podcast.

I haven’t managed to cover PE on the podcast yet. I have been involved in lots of small PE projects over the years and have developed something of an interest in it. I got invited to give a talk to the national EM conference this year and these podcasts are sort of the cliff notes version of that lecture. The full talk is linked to on the emergencymedicineireland.com website for those interested. I would emphasise that beyond the mention of the ESC guidelines this is an evidence lite podcast and more than usual represents opinions rather than hard science. The original talk was about PE in the resus room but I definitely think PE in the ICU in an established ICU patient is quite a different beast and I will try to highlight that as we go through it.

PE is so ubiquitous that I’m skipping a lot of the core pathophys and work up and instead want to split it into 2 parts, the first today on risk stratifying PE and the second on nuances of management in critical care.

PE is common in critical care. Either as a referral from ED with a patient with a nasty PE and bad physiology as the sole problem (less common) or as a finding in an ICU patient with other clinical issues, eg trauma or a surgical patient in whom you have now found a PE (a much more common scenario). From our perspective in ICU the test we need is a CT scan. I think all the other discussion about dimers etc is moot for us and if you need to exclude the diagnosis then CTPA is the way to go.

I think for the majority of the ICU population found to have a PE they are relatively innocuous. Yes they have PE but it is frequently quite small and not really contributing to their physiology. Yes they need anticoagulation but rarely anything more. There are a small cohort who need aggressive management of the clot and the physiology but these are much less common.

In terms of identifying the sick ones or risk stratifying them you need to be able to cite the ESC 2019 guidelines on PE. This is a substantial piece of work and is well worth a read. In that you will find PE can be split into low risk, intermediate risk, intermediate-high risk and high risk patients. However while a good starting place for risk stratification they remain a little blunt and don’t really tease out the super sick PE patients where the subtleties of management really come out.

Most of the ICU cohort will fall in the intermediate risk group who generally do very well as long as you anticoagulate them. It starts getting interesting in the intermediate-high and the high risk group. The intermediate-high group are identified with some form of right heart strain on CT or echo and a bump in a biomarker like troponin and BNP. If you add in low blood pressure then you’re in the high risk group. As noted this risk stratification is, in my opinion, a little too blunt to be of use in the ICU population where there are so many other reasons that the right heart might look funny or the BP low or the troponin raised.

How can we be a bit smarter with our risk stratification? Well firstly we need to decide if the low BP is being caused by the PE. Size of clot can be helpful here. If very small then it’s unlikely to be that significant. Especially if we have a much more clinically apparent cause of hypotension like the large empyema also seen on the CT scan. Particularly in the ICU population with multiple reasons for hypotension the pressure is on us to tease out which of the pathologies is causing the hypotension. If they are genuinely hypotensive because of the PE then lysis is probably inidicated – more on that next time.

With regards to clot size, however the opposite does not seem to be true: ie the presence of large clot, especially in the ED population does not seem to predict outcomes especially well. Instead of looking in the report for the size of the clot we would better served paying attention to the size of the right heart versus the left and for evidence of contrast reflux into the IVC. These are more useful in predicting right heart dysfunction.

An even more useful method is to look at the heart itself with an echo. I’m pretty sure this has little evidence to support it but I find that the echo gives a more accurate description of the impact that the PE is having on the physiology as I think (very much an opinion here) the CT scan often over calls the right heart strain. The obvious confounder here is that the echo is often done after the CT where the right heart has had a little time to recover so I’m very willing to be wrong on that. The useful things to look for on the echo are RV size, TAPSE and septal flattening. While i do love all the other nerdy measures of RV function I remain skeptical of their additive value in making a decision on something as significant as thrombolysis. The other reason I think echo has some advantages over CT on risk stratification is that it’s easy to see the response to therapies on the echo. Does the RV look a bit healthier after an inotrope or lysis etc.

ECG can certainly be used to risk stratify and right heart strain on ECG, (think deep inverted T waves anteriorly and inferiorly) seems to predict CT and echo changes quite well. However I know my ECG skills are lacking and even when I do see the changes I see the ECG as a reason to order another test (ie CT/echo) rather than make the definitive diagnosis or thrombolyse.

While trop and BNP get a lot of attention in the ESC guidelines for risk stratification I find them to be less than helpful in the critically ill as all of our patients already have a raised trop and BNP even before they get a PE. I do pay attention to our universal badness-metre the lactate. A rapidly rising lactate in a PE patient with a bad RV is certainly worrisome.

Next time we’ll look at management options

For further reading it is probably best to visit the original lecture post where they are all listed with a little smattering of critical appraisal thrown in for good measure.

Welcome back to the tasty morsels of critical care podcast.

Hypertriglyceridaemua induced pancreatitis came up at a recent trainee presentation and I thought despite it being pretty niche and rare, it’s still common enough that it might be fair game for an SAQ or perhaps a side bar in a viva discussion.

Pancreatitis is of course a common presentation to the ICU and can range from the straightforward to the never ending complication fest that carries a not insubstantial mortality rate. This is not the post that will cover the full gammut of pancreatitis.

So what is the deal with the cumbersomely named “hypertriglycerdiaemia induced pancreatitis”. UTD has the helpful statement that this is the causative factor in “1-35%” of cases of pancreatitis. This tells me nothing except that we don’t know how common it is. In terms of cases coming to your unit you should probably consider it if you can’t find gallstones and they don’t ingest alcohol. It should probably come higher on your differential than scorpion bites for example.

I’ve seen a few of these and the main trigger for the diagnosis was the lab ringing and saying that the blood is so lipaemic that they can’t process it. There are some lovely images online of the bizzare appearance of the blood. It’s one of the few diagnoses you can make by simply looking at the blood as it fills the bottle (the other being methaemogobinaemia)

The higher the trigs, the worse the pancreatitis generally. It may be a familial thing to do with generation and metabolism of trigs or it may be secondary hypertriglyceridaemia due to something common like diabetes or even pregnancy.

How does the fatty stuff cause the pancreatitis? At this stage in the viva expectations will be low – no one expects detail though a complete silence is likely not going to be well received. A statement along the lines of “well now, it’s not the trigs themselves that are toxic but instead the fatty acids produced by lipases that are the precipitating agent”. This is likely to pacify any potential predatory examiner and you can move onto something more relevant like how it might change your management.

Your management will be the same as for almost all pancreatitis with organ support, and some fluids etc…. The subtleties of management of pancreatitis associated with hypertriglyceridaemia are somewhat predictable. You should restrict fats in your nutrition till things are under control. If they’re severe enough to be in ICU they’re often hyperglycaemic and on some insulin already but as we know insulin can help reduce fatty acid release, therefore being aggressive with insulin (maybe in the 5-10 unit/hr range) , and supporting with dextrose if needed, would seem prudent.

The more eye catching therapy that you should be aware of is plasmapheresis. As one can imagine removing all of the plasma from the person will result in removal of the triglycerides from the blood. Indeed a 50-80% reduction is quoted in the available observational studies used to support the practice. There are no RCTs to support its use in this scenario though if you’ve been around for long enough you’ll of course note that most of what we do is not supported by RCT level evidence. Neither the 2013 APA guidance or the 2019 WSES guidance mentions plasmapheresis

Somewhat surprisingly, the classic outpatient lipid drugs like the statins, the fibrates and ezetimibes etc do not seem to play a prominent role in the acute management but are naturally important in prevention of recurrence in the longer term.

Reading

heavy dependence on the doctor’s little helper here (otherwise known as UTD)

Oh Chapter 43 covers pancreatitis generally and I am sure we will return here in due course

Welcome back to the tasty morsels of critical care podcast.

Today we’re going to try and cover the not insubstantial topic of acute liver failure from Oh’s Manual chapter 44. As you can imagine this will be a superficial skim of the topic so set your expectations appropriately.

First point is differentiating acute from acute on chronic liver failure. This has a massive impact on presentation, diagnosis and management and I must confess for many years as a trainee my understanding of the distinction between the two was a little cloudy and it was only really in fellowship that it became clear to me.

Oh describes it as a massive parenchymal liver injury with multi system impact and organ failure. Coagulopathy and encephalopathy with various degrees of hypotension and renal failure are the main presentations. Encephalopathy and coagulopathy are needed to make the diagnosis. This happens in the context of a previously normal liver.

Acute on chronic liver failure occurs when someone with pre-existing liver disease eg cirrhosis has a decompensation. This may be a consequence of portal hypertension like bleeding or encephalopathy or sometimes it’s infection. Encephalopathy may or may not be a part of it. Portal hypertension is a substantial feature whereas it is typically absent in acute liver failure.

So what we’re expecting to see to make a diagnosis of acute liver failure in the critical care environment is a patient with what is thought to be a previously normal liver present with a rapid progression of symptoms and jaundice leading to encephalopathy. Now “acute” can be within 6 weeks from jaundice to encephalopathy but they’re not typically the type of patients that come to us.

The rapid outpatient to ICU trajectory is typically within days and a differential arranged by prevalence in the western world should include

paracetamol

the commonest and is not always obvious and can be large single overdose or a staggered intentional overdose or even a therapeutic misadventure on the ward in someone with a low BMI

idiopathic

while a common end point of the work up it is not a helpful diagnostic category

drugs

idiosyncratic reactions to any number of medications including things as simple co amoxiclav or an NSAID

viral

these are the alphabet soup of hepatitides. This is no doubt commonest world wide but is much less likely in our part of the world. The tests should definitely be sent but don’t expect much

autoimmune

vascular

the commonest liver injury we see is usually ischaemic as part of sometihng like OOHCA. But usually it’s not the liver on its own that causes the mortality as the brain injury usually kills them first

portal vein thromboses and budd chiari (blockage of venous outflow) do happen and why the imaging is important

Heat related

we’ve had a couple of these in the past few years related to exertional heat injury. The context is obvious and the care largely supportive

pregnancy

HELLP syndrome and acute fatty liver of pregnancy fall under this banner

mushrooms

i have never looked after an amanita poisoning but they do exist in Ireland. You are orders of magnitude more likely to get in trouble with paracetamol than mushrooms but you should still keep mushrooms on your list.

When investigating this there is a long list of labs that should be sent but beyond the routine labs you get on anyone you should check for the hepatitis viruses, have a look at eosinophil count if you’re thinking about drug reactions and if you really are unsure then they all end up getting urinary copper and ceruloplasmin to look for Wilson’s. Imaging with either US or more likely US and CT is important. Liver biopsy is often indicated but it is disappointing in it’s yield and comes with bleeding complications

Encephalopathy is assessed with a specific 4 level grading system known either as the West Haven or Parson’s Smith scale. Grades 3-4 is where we’re likely to get involved. There are multiple reasons for the encephalopathy – ammonia is obviously part of it but there are other factors involved. Ammonia is taken up by astrocytes and deamination to glutamine  which in turn draws in water leading to astrocyte swelling. In addition there is likely loss of autoregulation and integrity of the blood brain barrier as part of inflammatory response to acute liver injury. Ultimately this means that these patients are at risk of an ICP crisis (unlike acute on chronic liver failure where the brain has been able to compensate). The ICP crisis can be a real source of morbidity and mortality and all of our usual arsenal of ICP management strategies have been employed in supporting these patients.

The coagulopathy is often profound in terms of the numbers measured. Thombocytopaenia is typically consumptive. The INR is prognostic and correcting it routinely does not seem of much benefit. Indeed we should remember that levels of both pro and anticoagulant factors are depressed though we only measure the procoagulant ones typically. As a result the coagulopathy may have a degree of balance to it that we simply don’t measure. Surgical procedures probably need attempted correction of coagulopathy but simple things like CVC insertion are probably safe.

NAC is a truly life saving and effective drug in paracetamol overdose and should be used liberally. It is unclear how helpful it is in other forms of liver failure but given its benign side effect profile it is used early and liberally and a decision to give some should not be something to spend too much time on.

Kidney injury is common but we should probably be filtering earlier than we might conventionally do so. The idea is that CRRT can wash the blood of some of the foul humors that the liver isn’t dealing with. The dose of CRRT here is typically a lot higher at 45ml/kg or higher rather than our usual 25. This has a limited evidence base but it is published on and frequently used.

On a similar vein (pun intended) of removing evil humors, plasma exchange has been used and a small open label RCT exists.

An SAQ or viva may raise the existence of MARS – Molecular Absorbent Recirculating System. This was thought of as “liver dialysis” but does not seem to have panned out and does not seem to be in regular use

Finally it is critical to consider liver transplant as an option for these patients. Unlike in heart or lung transplant where you need a stable patient with limited organ failures to be a candidate, in acute liver failure you can be in the throes of severe multiorgan failure and still be a candidate for liver transplant. Hopefully your liver physicians will have made the referral for you but if not you should be making the phone call.

Reading

Oh chapter 40

Larsen, F. S. et al. High-volume plasma exchange in patients with acute liver failure: An open randomised controlled trial. J Hepatol 64, 69–78 (2016).