Tasty Morsels of Critical Care

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)

sepsis. this is of course bread and butter to us in ICU but IE needs to remain in the differential for septic patient in the ICU, rather than just pinning it on the first minor infiltrate we see on the CXR

the embolic presentation. The most common would be an intracranial event, either stroke or intracranial bleeding from a mycotic aneurysm or embolus. Certainly anything suggesting embolic stroke (like bilateral strokes for example) should you make you consider IE (along with of course, the much more common LAA thrombus in A fib). Outside the brain the main emboli that might show up for us will be obvious on CT scans with splenic and renal infarcts in left sided disease or cavitating pulmonary lesions in right sided valve disease. You will also get the occasional dramatic bleeder where some intrabdominal vessel has a mycotic lesion that bleeds dramatically needing an IR intervention

heart failure. this is usually because the vegetation has eroded through something important like a valve leaflet and now there is torrential insufficiency of this valve. these tend to be fairly dramatic presentations with wet lungs and cardiogenic shock in the left sided lesions.

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

imaging major criteria – with a vegetation on echo still being the main sign and TOE preferred over TTE. But CT has some important findings that can fit in here too

micro major criteria – growing certain common IE bugs in the blood would be the commonest here though it does allow for some serologies of the weird culture -ve bugs in this category

surgical major criteria – if, at operation the surgeon sees vegetation or abscess or perforation consistent with IE then that counts as a major criteria

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

Staph Aureus (30%)

oral streps (17%)

coag -ve Staph (11%)

e faecalis ( remember 95% faecalis, 5% faecium)

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

coxiella burnetti [Q fever]

bartonella,

brucella

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.

Reading:

– 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

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