Tasty Morsels of Critical Care

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

c-spine injuries

facial fractures

complex base of skull

severe TBIs

hanging

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.

Reading

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.

Reading:

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

Turgeon, A. F. et al. Liberal or Restrictive Transfusion Strategy in Patients with Traumatic Brain Injury. N. Engl. J. Med. (2024) doi:10.1056/nejmoa2404360.

English, S. W. et al. Liberal or Restrictive Transfusion Strategy in Aneurysmal Subarachnoid Hemorrhage. N. Engl. J. Med. 392, 1079–1088 (2025).

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

changes in inflation

redistribution of ventilation

redistribution of perfusion

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.



Reading

Tobin Chapter 49

Deranged Physiology 

Prone Position and Mechanical Ventilation

Guerin, C. et al. Prone Positioning in Severe Acute Respiratory Distress Syndrome. New England Journal of Medicine 368, 2159–2168 (2013).

Guérin, C. et al. Prone position in ARDS patients: why, when, how and for whom. Intens Care Med 46, 2385–2396 (2020).

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.