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This is part 2 of infective endocarditis, this time covering the highlights of endocarditis management from the ICU perspective.

Once the diagnosis is made and checked that the diagnosis is solid (remember there are published criteria about how to reach the diagnosis) then you should be reaching for some antibiotics. The guidelines have multiple, tedious tables describing antibiotic combos for native and prosthetic valves all guided by knowing what bug you are dealing with. If you are at the stage where you know what bug it is you will almost have a specialist in infection giving advice so I think this is somewhat beyond the scope of the ICU exam setting. Having a broad overview that of what bugs are gram +ve and gram -ve I think is key and will allow you to put together an appropriate reigime in any septic scenario, not just IE. As such i’m not going to go into detail.

I suspect the more relevant scenario for us will be the crashing patient with an eaten out valve lesion at 2am and we’re the first person to be considering the diagnosis and have no micro to guide us. If you find yourself in such a situation then ceftriaxone and amoxcillin and some vancomycin will cover all the bases included prosthetics for the first 12 hours till help is available. This will cover all the commonest bugs of staph, strep, e faecalis and prosthetics. If you want to cover the weird culture -ve bugs then I have one, somewhat predictable word for you – doxycycline.

If they’re in crit care they’ll almost undoubtedly be septic and any of your arsenal of sepsis interventions is probably appropriate and again beyond the scope of this post.

The major modifiable part of your sepsis resus here will be determined by the echo. Are you dealing with severe, torrential AR then keeping the BP a little lower and diastolic period a little shorter with a tachycardia might be in your benefit. Have you got torrential MR from a perf or flail – then a balloon may be helpful. Again, the physiological management of a bad valve pending surgery is great fun but also beyond the scope of this post.

So perhaps time would be better spent thinking about surgical indications in IE. The guidelines again have fairly clear indications here but many patients fall foul of the usual problem of having surgical disease when they are not surgical candidates.

You can split surgical indications into 3 categories

Be aware that the guidelines use the words “urgent” and “emergency” differently from what we might expect with “emergency” not meaning “right now” but “within 24 hrs”. There are often multiple good reasons for deferring theatre when there is the opportunity to optimise someone for a challenging bypass run. Intracranial emboli with bleeds also pose a big challenge when you’re proposing giving someone 30000 units of heparin. Lots of painful but necessary MDT discussion needed.

Finally a common question appears regarding whether or not you anticoagulate to prevent the emboli causing strokes. . We do it when we find clot in the heart so why not veg (which inevitably have clot and infection in them). The guidelines give a reasonably clear answer with anticoagulation not recommended as a prophylaxis strategy.  To give a direct quote from the ESC guidance “To date, no data support initiation of either antithrombotics nor anticoagulants for treatment or prevention of stroke in IE.” In distinction  continuing anticoagulation in someone on it for pre existing reasons (eg a fib) does not seem especially high risk.

– Fowler, V. G. et al. The 2023 Duke-International Society for Cardiovascular Infectious Diseases Criteria for Infective Endocarditis: Updating the Modified Duke Criteria. Clin. Infect. Dis. 77, 518–526 (2023).

– Delgado, V. et al. 2023 ESC Guidelines for the management of endocarditis. Eur. Hear. J. 44, 3948–4042 (2023).

Welcome back to the tasty morsels of critical care podcast.

For the next couple of posts we’re going to focus on infective endocarditis. We have had something of a run of these over the past few months with every other cardiac surgery seemingly being done for IE. Not all of this will be relevant to every intensive care unit but as I work in an ICU with lots of cardiac surgery we will be covering the relevant aspects. This episode we’ll look at the diagnostic process and next time we’ll look at management.

IE is a common consideration in patients with infection being admitted to the hospital. But we’re going to very much focus on what the ICU presentation might look like. Often they’ll be coming in with the diagnosis already made but a lot of the time you’ll be looking after a generically sick patient and only over time does the the diagnosis of IE raise its head.

3 main types of presentations of undiagnosed IE may present themselves to the critical care doctor (and there are of course others)

How do we formally make the diagnosis of IE? Well, especially as this is exam focussed we need to be able to drag out Duke’s criteria. There have been some recent updates in 2023 and while it would seem unfair to expect a trainee to regurgitate all the details it would be helpful to have an overview.

You will probably have in your memory something about major and minor criteria. Major criteria can be split into

The minor criteria include many less specific features that I’m not going to go through here. A bit like failing your driving test you can get IE by having 2 major criteria , or 1 major and 3 minors or even 5 minors on their own can make the diagnosis.

There are pathological criteria which are considered the gold standard and that involves isolating the bug from tissue, typically a valve removed at surgery but typically that’s a diagnostic standard that most patients will not reach

I think it is helpful to have an idea of the common bugs involved. From European wide data it seems we could give the following prevalence of bugs

Of note bacteraemia is constant (you do not need cultures just at time of fever) and most cultures should be +ve when IE is the cause.

Most culture -ve IE is due to the patient already being on antibiotics. You can expect blood culture -ve IE in ~10% but the vast majority of this are just standard bacteria in patients that someone had already started on antibiotics and now you can’t grow it. For the true “culture -ve” crowd  the following bugs should be on your list (and this is not a complete list

When it comes to imaging TOE remains the test of choice as it just gives you much better pictures. Even if you can see a vegetation on TTE then the guidelines recommend that most patients should still have TOE to properly assess valve complications and other valve involvement not obvious on TTE. The exception to this might be a TV endo with good images. Vegetation size has some prognostic implications and should be measured in its longest plane.

But we should also be thinking about other tests. CT in particular has a role in looking at aortic root abscesses, especially in prosthetics. PET scan is also becoming a more important test but i find getting this for an ICU patient somewhat impractical.

In terms of what bacteraemias should trigger an echo, the guidance would suggest staph aureus, e faecalis and classic streps as an indication. But not every bug in the blood needs an echo which I think is a message worth communicating.

– Fowler, V. G. et al. The 2023 Duke-International Society for Cardiovascular Infectious Diseases Criteria for Infective Endocarditis: Updating the Modified Duke Criteria. Clin. Infect. Dis. 77, 518–526 (2023).

– Delgado, V. et al. 2023 ESC Guidelines for the management of endocarditis. Eur. Hear. J. 44, 3948–4042 (2023).

Welcome back to the tasty morsels of critical care podcast.

Today we look at blunt cerebrovascular injury or BCVI. I added this to my list to cover for unclear reasons as when i looked back at my notes i had about 8 bullet points and a couple of referenced articles. So this will be shorter than usual I suspect.

Effectively this refers to injuries to the carotids and vertebral arteries in the context of trauma. The pathology here is typically a pinch, twist or stretch of the vessel leading to an intimal tear in the vessel. The exposed endothelium then is a nidus for thrombus formation. The main downstream consequence is stroke and it’s a real shame to have a successful haemostatic and surgical resus of a major trauma patient only to have them suffer a life changing stroke 3 days into their hospital stay.

They’re also pretty tricksy injuries as there are rarely obvious clinical signs to indicate their presence until they you find the dense hemiplegia, so this is one of those things were the term “index of suspicion” comes into play. It is especially important seeing as we have now effectively outsourced all diagnosis to the radiologists and these injuries are not picked up on the typical trauma pan scan that we so love.

Given that I described the pathology of the injury as pinching, twisting and stretching we can probably get a sense of the mechanism of injury associated with these injuries. Top of the list here are c-spine injuries – if the neck has moved enough to break it you should think about the delicate blood vessels beside the c-spine. This is particularly pertinent to the vertebrals whose course, evolution in her wisdom, placed inside the tiny little vertebral foramen transversarium of the c spine itself. To make life more difficult for the poor little vertebrals they have to navigate a few 90 degree turns to get between C1 and the skull to get into the foramen magnum. This is reflected in the higher incidence of BCVI in high spine injuries.

Obvious other associations are with severity of TBI and complex facial fractures (remember the carotid has to navigate its way past these).

You might get some pointers to diagnosis from your clinical exam. Horner’s syndrome would be a classic (disruption to sympathetic neurons in the carotid) but if you’re diagnosing a Horner’s syndrome in your primary survey then you’re either over achieving or doing it wrong or possibly both. They may have stroke features on arrival which would be an obvious trigger for imaging. A bruit is also listed as a sign of injury but I think that’s a sign for better clinicians than you or I.

Most of the time you will have an injured patient without specific symptoms of BCVI. Who do we pursue further imaging on given that I’ve already noted the initial trauma pan scan will often not pick up this?

Enter stage left the geographically titled criteria each named after the academic centre that developed it. Denver, Memphis and Boston have all contributed a published criteria. The Denver criteria appear to be the most commonly used and referenced. I think listing the individual components is probably beyond the scope of the post but I’d emphasise the main headlines

Once you’ve decided the patient needs imaging then you should be reaching for our trusty friend the CT scanner. in this case a well done CT angiogram of the neck vessels extending into the intracranial vessels. It is not (unsurprisingly) a perfect test but it is a very good test and certainly where you should start. If you do find a BCVI you may even have the joy of seeing it classified I to V according to the wonderfully named Biffl classification system. It covers things like intimal tears and degrees of narrowing and occlusion.

once you’ve found a BCVI it’s unclear who your go to specialist might be and I have seen vascular, neurosurgery and stroke all give opinions on treatment. Overall risk of stroke in BCVI is ~8% but changes significantly depending on grade with higher grades having higher stroke risk.

For the vast majority of patients your treatment options come down to heparin vs aspirin. There does not appear to be a clear proven superiority of one strategy over the other. Some form of antithrombotic does, in observational data, seem to reduce stroke rate and is probably worth doing. Aspirin is generally easier delivered and seems to be the most common choice in our region. Many of the injuries would actually be amenable to surgical repair but the vast majority are surgically inaccessible hence the antithrombotic treatment as next best thing.

The decision to give something that makes clotting more difficult in a patient who is either still bleeding or at risk of major bleeding is not an easy one. Hence there is typically a day or two of hand wringing amongst several specialties till we are all comfortable giving it. Observational work suggests that we’re likely a little overcautious on this in a similar way to our reluctance to commence VTE prophylaxis in TBI.

Doctor’s Little Helper

Radiopaedia

Welcome back to the tasty morsels of critical care podcast.

Today we’re going to look at the red stuff – blood, and when to give it. This will cover some of Oh’s Manual chapter 97 covering blood transfusion. But we’ll have a focus on transfusion targets. There’s a nice narrative of evidence here over the past 20 years that has given us a relatively robust evidence base for practice in this area, something quite novel in critical care.

Blood is expensive and unlike fossil fuels currently remains a renewable resource in the healthy population, it is obviously quite limited and nations frequently experience shortage of various blood groups and products that can have significant impacts on health care delivery. The red cells we give undergo a number of changes in the donation process with “storage lesions” becoming more prevalent over the duration of storage. A list of potential problems with stored red cells might run as follows:

red cells change in shape biconvave to spherocytes (echinocytes) losing flexibility

change in red cell membrane leading to sticking to the endothelium (esp in activated states like sepsis)

2,3 DPG depletion (which means Hb holds onto Oxy)

reduced NO

progressive increase in K+

acidosis

The ABO reactions of transfusion should be dealt with by good governance of your transfusion service but fevers and other reactions are still an issue. The wonderfully named TRALI and TACO are also well described and space precludes a detailed discussion of these in this post.

Now that we know giving red cells is not an entirely benign intervention we are left with the question that all competitive limbo dancers are faced with on a daily basis – how low can you go. What would be an appropriate Hb target for a critically ill patient.

So let me tell you a little story… back in the late 90s when i was binging on OK Computer some Canadians led by Paul Hebert produced a large observational cohort of ICU patients called the TRICC trial suggesting that those with lower Hb did poorly and those who got more transfusions did better. But they were good empiricists and acknowledged that this could all be confounded by unmeasured factors. The only way to deal with that is randomisation and so 2 years later, Paul Hebert was at it again producing the TRICC 2 trial. This time an 800 pt multicentre randomised trial looking at Hb of 7 v 10. The headline result here was that the restrictive group did at least as well and probably better than the liberal transfusion group. This was a major trial and I’m pretty sure triggered a major change in practice. The caveats to this were as expected – those with ischaemic heart disease should probably have a higher target.

Things went quiet for a few years but in 2010 we saw the TRACS trial from Brazil looking at one of the sacred cows of transfusion targets – cardiac surgery. Can we lower the Hb target in those with dodgy coronaries? They looked at Hb 9 vs 10.5 and found no difference.

Villaneueva in 2013 took on upper GI bleeds. They smartly excluded the unstable active bleeders but in 500 patients randomised to 7 v 9, the lower target won out.

The trials started to come thick and fast now with TRISS trial in 2014 taking on sepsis. The problem in sepsis is oxygen delivery so surely more Hb is good. But yet again, in 1000 pts with sepsis there was no benefit in targeting 9 vs 7

2015 brought the TRIGGER trial (hopefully you’re starting to see the unofficial naming convention here…) looking again at UGIB and again finding no benefit to the higher target

2017 brought the TRICS 3 trial, looking at 5000 patients undergoing cardiac surgery. Again randomised, this time 7.5 v 9.5, again no advantage to the higher target

in 2021 they took on ACS patients in the REALITY trial, the most obviously ischaemic group and randomised 8 v 11 and no benefit to the higher target

Most recently in 2025 the TOP RCT looked at vasculopaths having vascular surgery and in 3000 pts there was no benefit to the higher target.

Phew… that’s a lot of trials but I think you’re starting to get the point that in general the answer to the question “what is your Hb target” is going to be 7-8

There are of course caveats to throw in at this stage.

Firstly, it’s important to note that none of these trials looked at the exsanguinating patient where you should be targeting physiology like HR and BP and perfusion rather than Hb. Restrictive Hb targets are in general questions for the daily ward round rather than the massive transfusion protocol.

Finally, in the past couple of years we’ve seen 2 RCTs looking at critically ill patients with sick brains. One looking at TBI and the other looking at SAH. Both suggest that if you have a sick brain you probably should be targeting a higher Hb of 9 or so. When you look at their outcomes the differences do not reach statistical difference in either trial but the trends are clearly to my eye towards more blood leading to better outcomes.

LITFL has a lovely written summary of all the major trials

I have included the two neuro trials here as they’re not noted in the LITFL summary

Welcome back to the tasty morsels of critical care podcast.

Today we look at something we do fairly frequently in ICU, especially in the post COVID era: prone positioning or to use its preferred technical term: adult tummy time. This has been around for a long time but was uncommonly done in the pre COVID days and was always a talking point when it did happen. But then 2020 came and you’d spend significant portions of the day proning and supinating patients in the unit. Fair to say it’s something we should have a keen understanding of.

Firstly we’ll talk about the physiology and potential mechanism of benefit behind proning. This comes from the proning chapter in Tobin’s mechanical ventilation textbook. Written by none other than the late, great Gattanoni. He argues that there are 3 mechanisms by which proning affects ventilation and oxygenation

A lot of this comes from Gattanoni’s early work where they managed to do a whole bunch of CT scans on critically people with ARDS in both the supine and the prone position. Yes you heard that right they did the CT scan prone. The typical CT scan for many ARDS patients is a basal dorsal distribution of disease. One would think that flipping the patient might redistribute this atelectasis to the ventral surface. But what seems to happen is more of a homogenisation of the lung with an overall improved inflation of the lung tissue. No longer are you just hyperinflating the baby lung and doing nothing for the atelectatic lung. This should lead to better recruitment, better perfusion/ventilation matching, better oxygenation and in turn better clinical outcomes. There are some suggestions it may also aid secretion clearance which in a paralysed supine patient is obviously a problem.

Proning (as we shall we see) does seem to improve outcomes but the precise mechanism is unclear. Improved oxygenation seems plausible but it may also be a reduction in VILI by having a more homogenous lung that is less prone to injury of the baby lung.

Guerin (lead PROSEVA author) wrote a nice review article in 2020 highlighting that proning can make chest wall compliance worse. The anterior ventral wall is normally more mobile than the dorsal chest wall. When prone the ventral bit is now wedged and immobile against the bed hence the fall in chest wall compliance. However lung compliance is probably improved and now that the chest wall is moving less it’s probably increased diaphragmatic movement that recruits the bases. Overall compliance should improve.

We turn now to the evidence base for proning our patients. This, like many critical care interventions, this  has a little bit of a narrative to it with some early trials lacking benefit followed by the paradigmatic trial that shapes practice. What follows is a brief summary of some of the important studies and is neither intended nor considered to be comprehensive.

Back in the early noughties there were a flurry of RCTs looking at prone positioning in ARDS. The late and great Gattanoi was of course involved in some. The “dose” of proning was variable with sometimes only short periods like 6 hours being used. Results were variable and a 2011 meta analysis of 7 RCTs did not show a definitive mortality benefit but did suggest that those with the sicker lungs had a benefit

Enter PROSEVA. A name, that if you’re going into an ICU viva, is probably something that you should keep in your head. This was 26 centres in France who were already experienced with proning. They took people with severe ARDS and randomised them to 16 hrs a day of proning vs no proning. They used mortality at 28 days as a primary outcome and they were looking for a 15% absolute reduction in mortality (which is pretty huge). It was, for obvious reasons, an open label trial. They enrolled 450 patients and found a 32% vs a 16% mortality favoring proning. It’s possible this trial found a benefit due to the dose – they proned for much longer than many of the other trials.

It’s worth having some problems related to proning in your back pocket to pull out. The list of potential contraindications was initially quite long pre-COVID but it turns out that when your back is up against the wall we all became a little bolder with our proning. While you can prone the vast majority of patients it’s not going to be possible in those with unstable spinal injuries. One would think that abdominal surgery or advanced pregnancy might be a problem but you can usually work round this with some discussion with your surgeons.

The main downsides (beyond the hassle factor) are related to safety. The facial oedema and skin injuries are not insignificant and no matter how careful you are some people just aren’t a great shape for proning. There is a chance that the ET tube can kink or dislodge either on the proning or on the head turns so you need to have a good plan in your head how to confirm this and get someone flipped back if they need it.

Tobin Chapter 49

Deranged Physiology 

Prone Position and Mechanical Ventilation

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

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

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:

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.

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.

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

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.

Oh chapter 40