62 episodes

Bite size chunks of critical care medicine targeted at fellowship exam preparation

Tasty Morsels of Critical Care Andy Neill

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Bite size chunks of critical care medicine targeted at fellowship exam preparation

    Tasty Morsels of Critical Care 061 | Asthma

    Tasty Morsels of Critical Care 061 | Asthma

    Welcome back to the tasty morsels of critical care podcast.

    Today we’re looking at asthma. In reality I find this is much more commonly discussed than seen in real life. No doubt this is due in part, to an improvement in asthma care chronically which is of course a good thing. I think it gets discussed and comes up on exam papers so much partly because it is such a nice illustration of physiology and ventilation.

    I am guilty of over teaching this myself having delivered not one, but 2 talks on the subject, and even a prior tasty morsel of EM on the subject.

    Oh’s manual devotes a whole chapter, number 35 to the subject.

    We definitely see much less of this than we used to. I suspect that’s largely due to better access and provision of primary care but there remains a cohort of fairly brittle folk out there who will occasional crop up in resus or the ICU.

    To begin with, let’s cover some aetiology and pathophysiology, asthma has well described allergic and atopic associations as we all learn in medical school but also some important environmental triggers such as the infamous “thunderstorm asthma” that occurred in Australia some years back with 1000s of patients affected.

    There are several major consequences of severe asthma that Oh describes:

    * increased work of breathing – dynamic hyperinflation a big part of this

    * V/Q mismatch and shunting

    * CV instability from intrathoracic pressure

    Status asthmaticus is a term commonly found in textbooks but I don’t think it has anywhere near the utility of it’s Latin equivalent status epilepticus. Oh applies the term to those not responding to nebulised bronchodilators which could be fairly broad.

    For management of asthma like this, the mainstay of treatment is inhaled beta agonists with a chaser of ipratropium and some steroid. There is plenty of evidence suggesting simple inhaled beta agonist with an MDI can be as effective as neublisation but for ICU level asthma (which this post is aimed at) you will be reaching for an oxygen driven nebuliser aiming to get particle sizes somewhere in the 1-3um range. however it is well known that 10% of the drug gets delivered to target and it is likely that in the most severe asthmatics where very little gas is moving that the drug delivery is even worse. Hence the existence of the IV therapies.

    All of these are controversial on some level and I am not here to advocate for one or the other but more to provide a pithy line or two on each that one could reasonably throw into an SAQ or a viva answer and look somewhat smart.

    IV salbutamol is commonly used in the UK and Ireland but like pretty much all of these therapies could not be said to have a robust evidence base. Concerns have been expressed that it adds a significant metabolic load to the work of breathing with the inevitable rise in lactate and fall in BE leading to an increased minute volume and an increase burden of respiration.

    IV magnesium is likely more benign and given out extremely commonly in these cases but once again the evidence base is hardly stellar.

    IV adrenaline is a common go to and has some physiolgoic rationale beyond flogging the already overstimulated beta agonists. It’s alpha agonist effect may have beneficial effects on secretion burden and plugging.

    Aminophylline continues to be used though anecdotally I’ve not seen it to be that helpful

    Heliox often crops up in the text books as it allows for the goldilocks phenomenon of laminar flow.

    • 8 min
    Tasty Morsels of Critical Care 060 | The post cardiac surgery patient

    Tasty Morsels of Critical Care 060 | The post cardiac surgery patient

    Welcome back to the tasty morsels of critical care podcast.

    Oh chapter 26 devotes a whole chapter to this and for those of us in cardiac units the arrival of several post cardiac surgery patients a day in your unit is a routine part of the day. At least it was pre-pandemic anyhow. As such it presents a fairly predictable work load and patient cohort for your ICU. Given the bewildering number of conditions that can present to a mixed ICU on a given day, knowing that you have a couple of hearts moving along the production line provides a degree of predictability to the workflow.

    The scheduled, usually elective nature of cardiac surgery lends itself to large scale outcome prediction and indeed, cardiac surgery has found its outcomes examined very closely over the past few decades. Outcomes are often examined in great detail and are more likely than most patient cohorts to be reflected onto the hospital and even individual surgeons.

    Today we’ll focus mainly on the routine cardiac surgery patient and some of the common significant issues you’ll see.

    Before we look at any specific cardiac surgeries, it is worth addressing the hand over. There is frankly a lot of information to assimilate and sift through. You will often be receiving handover from the anaesthesia team but also trying to tease out information from the surgeons almost simultaneously. Key points of information to glean are:

    * pre surgical state, including what the heart looked like on TOE pre bypass – eg. is the ventricle good or bad at baseline

    * what was done and how the plumbing stands as of now

    * bypass time, cross clamp time

    * how did separation from bypass go – are they on 2 pressors and 2 inotropes and some nitric? or have they arrived on some propofol and a tincture of noradrenaline and a big sticky label saying “extubate me”

    * heart rhythm and presence and need for pacing (indeed if not being used is it at least on backup?)

    * what did the heart look like on TOE following the surgery – is the valvular lesion fixed? are they, dare i use the terrible phrase, “underfilled”

    * products given and current state of reversal and need for protamine

    * where the drains are and what they’re doing (are they just mediastinal or are they pleural too? Was that 400mls of red stuff there when you left theatre or has it just appeared)

    Contra to most ICU patients, cardiac surgery patients often benefit from a bit of the salty water stuff. Likely driven by rewarming induced vasodilation and hypothermia induced diuresis they can be hypovolaemic. It doesn’t take them long to transition to the more conventional ICU patient where fluid does nothing but increase the oedema but in the first 6-12 hours fluid resuscitation often has a role.

    Episodes of hypotension are common and the major concerning causes are going to be surgical bleeding or tamponade. The drains that you checked at handover are both diagnostic and therapeutic. A big gush of blood from the drain and hypotension usually points to the problem while at the same time relieving any potential tamponade. Significant bleeding might be >200ml/hr in the first hour or two and >100ml/hr after that.

    Unfortunately blood can clot focally around the heart causing a focal tamponade. This can be a bit trickier to diagnose as one might imagine, and indeed some form of imaging is often needed to make the diagnosis. Oh is very down on the utility of TTE in cardiac surgery patients and while of course you aren’t going to get all the windows, a good sonographer can usually answer many of the key questions. That being said if the patient is crashing you often need a TOE to look at the tricky spots like behind the LA where clots have tendency to form obstructing LA inflow.

    • 7 min
    Tasty Morsels of Critical Care 059 | Dead space

    Tasty Morsels of Critical Care 059 | Dead space

    Welcome back to the tasty morsels of critical care podcast.

    Today we’re talking about dead space. While it may sound like something from The Expanse, we’re actually talking about the physiological concept of dead space here. This is pretty core physiology that crops up in clinical practice all the time so I think it’s worth thinking about.

    As usual this represents a sort of idiot’s guide to the topic with just enough information to scrape by in an exam and in clinical practice but likely with large gaps, simplifications and occasional frank errors in description.

    Definition is “the fraction of tidal volume which does not participate in gas exchange.” But let’s be clear the word participation here refers more to an inability rather than a surly choice by the dead space fraction not to participate as it didn’t get picked for football till last. The dead space fraction never has the option of participating in gas exchange as it never reaches any functional gas exchange surface.

    At its most basic (and that’s the only form I’m interested in) it can be split into:

    * Apparatus dead space – the amount of gas in the circuit and associated dongles like ETT, an NIV face mask or an HME.

    * Physiological dead space – this is split further into:

    * anatomic- gas in the conducting airways and

    * alveolar – gas in non perfused alveoli

    Phsyiological dead space usually takes up ~20-30% of the Vt. As mentioned above it splits into two components, anatomic and alveolar. As you can imagine the anatomic is pretty fixed but the alveolar dead space can vary markedly depending on V/Q matching.

    Anatomic dead space is ~2ml/kg (about 150mls) but this includes the oropharynx that will be bypassed with the placement of an ETT or even better a tracheostomy with both of these interventions reducing anatomic dead space. I think the most important clinical take away about anatomical dead space is that it is fairly fixed. Assuming a 2ml/kg anatomic dead space, if you’re ventilating someone at 8ml/kg PBW and want to reduce to 6ml/kg PBW the fraction of anatomic dead space in each breath goes from 20% to 33%. In other words, while you’ve only reduced the Vt by 20% you’ve reduced the portion of gas participating in gas exchange by a third. There is of course good empiric evidence that a lower Vt is better but in terms of clearing CO2 dropping the Vt disproportionately reduces the fraction of gas available at the alveolus and may cause big issues with your CO2. Indeed at some point a rate reduction rather than Vt reduction may be the more favorable factor to reduce overall mechanical power delivered to the lung. That all seees very persuasive and logical but is countered by the simple fact that it doesn’t seem to be true when tested.

    It seems that at very low Vt gas exchange continues to be more effective than one might expect likely due to 2 mechanisms beyond simple mass gas movement.

    * laminar flow occurs allowing a central column of gas to move in and out

    * there is expiratory gas mixing – basically diffusive gas mixing that ensures the right molecules are in the right place at the right time

    Moving onto alveolar dead space, there are a number of things that might increase it:

    * reduced cardiac output: eventually lung units stop receiving perfusion

    * parenchymal disease: air space cavities no longer with effective perfusion due to thickening of interstitium

    * high airway pressures: ensures aerated alveoli but may limit blood inflow to the lung unit

    * pulmonary vascular occlusion: eg PE (one of probably several mechanisms of hypoxia)

    • 6 min
    Tasty Morsels of Critical Care 058 | Haematological malignancy

    Tasty Morsels of Critical Care 058 | Haematological malignancy

    Welcome back to the tasty morsels of critical care podcast.

    Of the many things I poorly understand, I suspect that haematology holds a special place. Knowing the intricacies of the haematological malignancies was not exactly core knowledge for emergency medicine and to be fair an exhaustive knowledge is hardly key to ICM either. However in ICM there is a need to have a broad understanding of what some of the haematological acronyms might mean given that a fair number of these patients end up in the ICU. Most of this post will be navigating the basics of the diseases rather than super specific ICU management.

    Oh dedicates a whole chapter, number 101 to the haematoloigical malignancies implying that it is certainly worth our attention. As a broad definition haematological malignancies involve the bone marrow or the lymphoid tissue, they occupy a different niche in the oncology world with the haematologists running the show rather than the general oncologists. They are also distinct in histology and outcomes from the solid organ malignancies.

    We’ll start with the leukaemias and these can be split neatly into myeloid and lymphoid leukaemia. The cells gone bad in AML are the myeloid precursor cells, the cells gone bad in ALL are the lymphoid precursor cells. This type of statement is however only useful if you have any concept of how a myeloid precursor cell is different from any other type of cell in the bone marrow.

    The attached image on the show notes, comes from the leading source of all medical knowledge, wikipedia. It’s a nice overview of the different types of cells stemming (see what i did there…) from myeloid and lymphoid precursors. It clearly works really well as an educational aid in audio form…

    Myeloid cells differentiate into, well, most of blood cells that appear on your FBC, things like red cells, platelets, neutrophils, basophils. On the other hand, lymphoid cells have a much smaller and narrower family tree differentiating into different types of lymphocytes and plasma cells.

    For AML there are a variety of causes from various genetically triggered issues, to transformation from a myelodysplastic syndrome or related to prior chemo or radiotherapy. It also includes the very ICU relevant disease of acute promyelocytic leukaemia. As a result, expect to see more AML in the older adult population. ALL is much more common in younger people with a much heavier CNS component, hence the prevalence of intra thecal treatment.

    Each of the acute leukaemias has it’s own chronic version. With CLL being a form low grade lymphoma. CML begins as a chronic, somewhat indolent process that accelerates towards a blast crisis towards the end of the disease and for most people is more of a comorbidity than a malignancy.

    Lymphomas, understandably come from lymphoid cells, these could be b cells or t cells for example. Classically lymphomas get lumped into two big categories of hodgkins and non-hodgkins with the former generally having the better outcomes.

    Finally on the list of common haematological malignancies is multiple myeloma. This is a cancer of plasma cells which are the grown up and left home versions of B lymphocytes. In general plasma cells have developed to produce large amounts of proteinaceous antibodies and are triggered as part of an immune response. In myeloma they are inappropriately making large amounts of their specific protein or globulin reflected in the high total protein count and hyponatraemia associated with this disease.

    So that’s a very broad, sub medical student overview of the different malignancies but why would they end up in your ICU?

    Sepsis is probably number 1 on the list.

    • 6 min
    Tasty Morsels of Critical Care 057 | Myasthenia Gravis

    Tasty Morsels of Critical Care 057 | Myasthenia Gravis

    Welcome back to the tasty morsels of critical care podcast.

    Today we’re looking at a small section of Oh Chapter 58 covering myasthenia gravis. I don’t think I’ve ever looked after a true myasthenic crisis in the ICU. Likely because they’re well managed by their neurologists on an OPD basis or well managed from an anaesthetic perspetive when they need an operation done. I have made the diagnosis twice de novo in the ED (or at least admitted them with that as the leadning diagosis) so it is out there.

    It does make excellent exam level material as there is some interesting physiology and compare and contrast type tables to be made comapring with other neuromuscular diseases.

    To give a flavour of what might you see in the ED (and these patients will rarely need ICU) it’s typically some kind of cranial nerve issue, typically ptosis and diplopia complaints, sometimes with some speech and swallowing issues. The cardinal features of the neuro dysfunction is flucutating weakness. Typically this is described as fatigueability. For example the ptosis isn’t too bad in the morning but by afternoon it’s much worse.

    Involvement of bulbar muscles (BTW, bulbar being an archaic name for the medulla and the cranial nerves that stem off it) should be recongised as a bit of a concern given that swallowing and airway protection fall under the remit of cranial nerves 9-12.

    The edrophonium test that you may have heard about in medical school can be safely forgotten about as it is no longer recommended. On the other hand the ice test can be used as a cool demonstration of the physiology. In its essence, the ptosis that improves after having some ice on the eyelids would suggest myasthenia.

    The pathophysiology of the illness is likely one of the more testable aspects here. Myasthenia is an auto immune disease where antibodies are made against acetylcholine receptors in the post synaptic neuromuscular junction. As a result Ach cannot bind to these receptors and therefore cannot complete the transmission of neurologic impulse to the muscle. The ice test works because NM transmission is apparently more efficient at lower temperatures.

    Once the diagnosis is made you can look super smart by thinking about their thymus as thymomas are found in ~15% of people with antibody +ve myasthenia. Many more are found to have some kind of abnormality in the normally negleted and unloved thymus.

    As an outpatient these people will typically be established on pyridostigmine, a nifty medication that potentiates the remaining ACh at the NM junction. They are usually immunosupopressed on some kind of steroid or maybe some azathioprine. Some may have had their unsuspecting thymus removed in the interim.

    In the ICU we’re likely to see someone in myasthenic crisis. This is commonly seen when tapering immunosuppressives or when faced with some sort of actue stress like spending time under anaesthesia while a surgeon ectomises some part of your body. There are also a large list of drugs that we can misprescribe that can mess people up.

    The fundamental feature of a myasthenic crisis will be respiratory insufficiency, this is defined as need for NIV or intubation. Remember it is unusual for myasthenia to affect respiratory muscles so if it is you’re looking at big trouble. Expect this to be a quiet, undramatic sort of respiratory failure. FVC and cough will quietly disappear without any of the usual increased work of breathing we usually use to quantify respiratory failure. Hence they look fine until they’re really not.

    There are a variety of vital capacity cut offs described as reasons to intubate. But as discussed in the GBS post these are somewhat arbitary.

    • 7 min
    Tasty Morsels of Critical Care 056 | Aspergillosis

    Tasty Morsels of Critical Care 056 | Aspergillosis

    Welcome back to the tasty morsels of critical care podcast.

    Today we look at everyone’s favorite mould – aspergillus. We see a number of fungal infections in the ICU, most commonly it’ll be the yeasts – forms of candida. Yeasts are single celled organisms. The moulds, of which aspergillus is a member are multicellular organisms. To continue into a brief foray of wikipedia inspired irrelevance the name aspergillus comes from the liturgical implement known as the aspergillum, more commonly known as the thing your priest man shakes to sprinkle the holy water. Apparently it was named aspergillus by the Italian priest who discovered it under his microscope and named it for the resemblance.

    The biggest issue comes for us in the ICU in differentiating colonisation from active infection. Proper invasive pulmonary aspergillosis is characterised histologically by invasion across tissue planes, particularly into vessels. As you can imagine getting a lung biopsy to prove such on ICU patients can be a tad challenging so we’re stuck with the usual conundrum of trying to work it out based on probabilities and surrogate tests.

    the LITFL entry has 4 types of aspergillosis described that we should be aware of:

    1) allergic bronchopulm aspergillosis. This is generally an OPD condition that is rarely the cause of why the patient is in the ICU

    2) the aspergilloma – the dirty great fungus ball hanging out in one of the lobes of the lung causing all kinds of bother. Surprisingly this can also often be an out patient problem

    3) chronic necrotising pneumonia (described as semi-invasive in the post)

    4) invasive pulmonary aspergillosis – the type we’re likely to see and most worried about.

    The IBCC covers aspergillosis very well, and if this podcast does no more than refer you to the IBCC then my work is done. Josh makes an excellent point of pointing out that there is probably a different clinical pattern in the neutropaenic vs the non neutropaenic patient.

    For any kind of fellowship exam you would be expected to reproduce a somewhat cogent list of risk factors for such an illness. Of note we are all exposed to aspergillus and exposure to aspergillus is a simple fact of being alive. But generally it doesn’t cause us a trouble unless something else is going on. A reasonable (but by no means complete) list of risk factors might include

    * most famously stem cell and lung transplants or anyone with prolonged neutropaenia, typically >10 days (remember that haematological malignancy are the main groups to reach this level of prolonged neutropaenia)

    * can also occur in much less immune suppresses people who are just really sick in ICU, or even COPD with recurrent steroids (typically at least 20mg/day of pred)

    * cirrhotics

    * patients post severe influenza seem to be a risk (looks like severe superinfection 3-5 days into course)

    * most other solid organ transplants seem to be fairly low risk.

    * COVID-19 as a risk factor is almost certainly a risk factor. However many of the studies have assumed that growth on a sputum implies invasive disease which is probably a bit of a stretch. That being said if you find that the whole airway is covered in plaques on bronch then you’ve probably established a diagnosis.

    So a common clinical context might be a haematological cancer patient in the ICU as part of a neutropaenic sepsis process. They might be in a week or two with profound neutropaenia and develop recurrent fevers and a respiratory deterioation. A sequence of micro growth and adjunctive tests established a diagnosis of aspergillosis.

    More recently we’ve seen it in the unfortunate chronically co morbid patient who gets a bad dose of the auld COVID and 2 weeks into their vent course they deteriorate and the bronch ...

    • 7 min

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