Tasty Morsels of Critical Care

Welcome back to the tasty morsels of critical care podcast. DKA is bread and butter for critical care providers. In fact the combination of bread and butter in the absence of insulin is a core part of the pathophysiology of the disease. An exam worthy summary of the pathophys might go as follows. lack of insulin stimulates lipase which leads to the production of free fatty acids from lipid stores peripherally FFAs are converted to ketone bodies in the liver in the presence of excess glucagon ketones dissociate significantly at physiological pH, this sucks up the supply of base buffer in the body and eventually overwhelms it with unbuffered acid and acidaemia developing. Beta hydroxybutarate is a name of a ketone that you might want to mention if pressed to name one.  both the high sugar and high ketones lead to osmotic diuresis which results in water, sodium and other electrolyte loss.  It’s probably worth contrasting this with the pathophysiology of Hyperglycaemic Hyperosmolar State which used to rejoice in the onomatopoeic glory of HONK. In fact comparing and contrasting DKA and HHS seems to be a favourite exam question. HHS is characterised physiologically by  just enough insulin to prevent ketone generation but not enough to allow peripheral uptake slower onset and hyperosmolarity as a key feature HHS has impaired thirst mechanisms in context of hyperosmolarity hyperglycaemia itself is proinflammatory (and the higher degree of it in HHS suggests the higher rise in VTE) What criteria might we use to diagnose DKA. Ketone>3 GLucose>11 HCO3<15 +/- pH<7.3 The one niche novelty version of DKA is the much discussed and not particularly frequently seen euglycaemic DKA. This seems to be a feature of the SGLT2 inhibitors which is secondary in difficult pronounciation only to their actual generic names of the glifozins. These meds are going to become a much more common med given that the EMPEROROR and DAPA-HF trials have declared these drugs mortality reducers in heart failure even in those with out diabetes. Management here is pretty much as expected if you’ve been doctor for longer than 2 years. I would refer you to your hospital’s or a national guideline for the details. Some points for style include. given some insulin (though not too much) give some fluid (though the evil abnormal saline can cause its own issues) ketones are probably a better treatment target than the glucose level. look for some precipitants (even though the answer is always non compliance and even in those with pumps it’s non compliance as the tubing kinked somewhere and no one noticed) be careful with the K as this is probably the best way to kill them. a pH of 7.1 with a K of 3 is a real danger zone as both insulin and correction of acidosis will cause the K to drop fairly precipitously. finally on a logistic point it’s fairly common for these guys in Ireland to end up getting an art line for the frequent sampling but as one of my very grey and wise ICU bosses pointed out – a CVC would be infinitely more use than an art line in this scenario given that it gives access for bloods, multiple lumens for infusions and allows concentrated potassium correction. References: Tasty Morsels of EM 122 Oh’s Manual Chapter 59

Welcome back to the tasty morsels of critical care podcast. In the main we get excited about systolic dysfunction. We obsess over the ejection fraction with numbers like EF of 12% being reproduced recurrently in handover sheets. But this is to neglect what constitutes the vast majority of the time of cardiac cycle in those with sensible heart rates. It has become clear that a lot of cardiac dysfunction occurs during this phase of relaxing and we neglect it at our peril. In terms of terminology heart failure with preserved ejection fraction is the preferred term. This gets abbreviated to the wonderful HFpEF which always makes me think of Hufflepuff from Harry Potter. This is in contrast to HFrEF – heart failure with reduced ejection fraction. From a physiological perspective diastole goes from AV closure to MV closure. It consists of the following phases following AV closure IVRT – Iso Volumic Relaxation Time. Where the muscle is relaxing but the volume as yet remains unchanged Early diastolic filing – when the MV pops open and the suction effect of the relaxing LV pulls blood from the LA into the LV.  Diastasis – where the nothing really happens and they all pop out for a quick smoke Atrial contraction – the atria gives its puny little ‘kick’ as an attempt to justify its musculature MV closure While we talk about diastole as cardiac relaxation it is actually an active and passive process. Active relaxation begins towards the end of systole continues until end of early filling. Late filling (from end of e wave to end of a wave) is largely passive. From our point of view we’re looking for it in patients who look like they’ve got heart failure but maybe don’t have an obvious history of it or the cardiac PoCUS looks fairly normal. We should think of it more in Hypertensives Older patients Those with certain echo signs such as raised right sided pressures, big left atria and things like abnormal E/e’ (which sadly have nothing to do with optimus prime)(of note I misspoke on the audio here and talked about a high e’ being the problem – soz…) Typically the diagnosis is made with echo and there is a comprehensive guideline document endorsed by the American and European echo societies with lead author Nagueh from 2016 but increasingly it seems that many of the numbers and criteria in that document may not transfer well to the critical care population. This has relevance to the ICU population in 2 major ares Sepsis. EF does not correlate with particularly well with mortality in sepsis though diastolic dysfunction does It may be  due to under filling and the reduced diastolic filling due to the ubiquitous tachycardia in sepsis. This raises the tantalising possibility of beta blocking the patient on 40mcg/min of norad which as yet can only be described as physiologically interesting but unsupported fluid resus here is very tricky as too little bad and too much is bad with no room for error Weaning failure cardiac is a common cause of failure at extubation. You pull the tube, lose afterload reducing effect of the PEEP and your patient gets reintubated with pulmonary oedema.  it seems that B lines and filling pressure estimations with echo are more predictive of failure than systolic dysfunction or diaphragmatic dysfunction on ultrasound This is all very interesting but we are left with the typical conundrum that advancing the understanding of a particular disease process often brings about – we have no proven treatments. Beta blockers and BP control remain important in the OP population but it is difficult to know how they apply to the ventilated septic ICU patient. From physiological reasoning it may be wise to maintain sinus rhythm maintain a normal preload a low afterload and a slowish rate References and justifications: Deranged Physiology McClean et al, Advanced Critical Care Echo Sanfilippo F, Scolletta S, Morelli A, Vieillard-Baron A. Practical approach to diastolic dysfunction in light of the new guidelines and clinical applications in the operating room and in the intensive care. Ann Intensive Care. 2018 Oct 29;8(1):100. doi: 10.1186/s13613-018-0447-x. Erratum in: Ann Intensive Care. 2018 Nov 6;8(1):106. PMID: 30374644; PMCID: PMC6206316. Karrowni W, Chatterjee K. Diastolic heart failure: the current understanding and approach for management with focus on intensive care unit patients. J Intensive Care Med. 2014 May-Jun;29(3):119-27. doi: 10.1177/0885066612453131. Epub 2012 Jul 10. PMID: 22786981.  

Welcome back to the tasty morsels of critical care podcast. TTP is a lovely ICU diagnosis. Not so much for the patient but it’s one of those ones that is niche enough to not have been picked up via the usual filters of ED, medical team to the ward. There is a definitely a chance to shine and make the diagnosis. This is  form of MAHA (microangiopathic haemolytic anaemia). Best to avoid detail on what these are for now but suffice to say some of them are very ICU relevant and the ket feature will be something called schistocytes which are found on the blood film that you haven’t ordered yet but definitely will next time you see something like this. The pathophysiology involves something in an autoimmune sense getting all excited and reduces the levels of your favourite ADAMSTS13. ADAMSTS13 is a mouthful of an acronym that you would hope was named after Dr Adams with a few letters added on but is in actual fact a mouthful of an acronym abbreviating an even more ugly sentence worthy protease called “a disintegrin and metalloproteinase with a thrombospondin type 1 motif, member 13”. The trigger for your body attacking the unfortunately named protease is useful some kind of stressful event like surgery, trauma or some nasty infection. In normal circumstances ADAMSTS13 is there to stop your platelets and your vWF getting two cosy in these things called multimers. When the ADAMSTS13 disappears then all your platelets disappear and you start clogging up small vessels with these big multimer thingies. TTP is therfore a form of TMA (or thrombotic microangiopathic anaemia). This “TTP for dummies” level explanation is enough to suggest the clinical features… Which are: some funny neuro things inc seizures a rashy petechial thing an AKI a profound, “no joking around” thromboyctopaenia fever is common There is a “PLASMIC” score that can be used as a diagnostic tool where you score points for certain features and we all know that points mean plasmapheresis in this game. I have never used the score but it is a thing. Ultimately you will need your ADAMSTS13 to seal the diagnosis which will be nice when it comes back 4 days after you’ve already started treatment. And this is key. Treatment should be started based on suspicion. Low platelets and a MAHA with maybe an AKI may well be all you need to start treating this. If you don’t then mortality is in the 90% range. Treatment consists of: PLEX – actual proper PLEX with plasma replacement as opposed to just washing out all the good stuff and giving albumin as replacement. The plasma replacement replaces factors and reduces the bleeding risk (which is already high) but also acts as a source of ADAMSTS13. This is believe it or not an intervention actually supported by an RCT back in 1991 of just over 100 patients.  Some kind of immune suppression to stop the production of autoantibodies that are wiping out the ADAMSTS13 steroids commonly used rituximab can be used Giving platelets is poor form generally with people objecting on the basis of “fanning the flame” type arguments which sounds very reasonable. Theoretically giving them FFP while waiting on PLEX seems like it might be sensible but in reality probably does nothing when the autoantibodies are still around. UPDATE: Caplacizumab is a new drug with now 2 RCTs supporting its use and is finding an increasing role, early in the role of TTP, even immediately after PLEX is started. Some suggestion it might even replace PLEX. References: Rock GA, Shumak KH, Buskard NA, Blanchette VS, Kelton JG, Nair RC, Spasoff RA. Comparison of plasma exchange with plasma infusion in the treatment of thrombotic thrombocytopenic purpura. Canadian Apheresis Study Group. N Engl J Med. 1991 Aug 8;325(6):393-7. doi: 10.1056/NEJM199108083250604. PMID: 2062330. Deranged Physiology Tasty Morsels of EM 070 https://emergencymedicineireland.com/tasty-morsels-em-070-ttp/

At this stage (Oct 2020), PGY17 and still in training I have done a fair number of exams and I feel that now, pushing 40 and vowing never to do another exam, I may have finally perfected my examination technique. But that’s for another post. I have accumulated a large number of summarised and truncated notes across two specialties (three if you include the echo stuff…) and they exists as a useful compilation of information that I felt tricky enough and important enough to create a note for. Like many people on t’internet, I feel it’s somewhat of a shame to keep these hidden behind my somewhat poorly secured google account and have tried to translate them to this here forum for public appreciation/scorn. In addition the transposition of said notes from brief notary form to the longer, and better hyperlinked form is an exercise in curation and improvement itself. Ultimately I am engaged in an ongoing project to turn these notes into spoken word in the style of the great Mark Crislip’s “Gobbet of pus” to which this podcast is a humble and greatly inferior derivative of. The Goal The aim here is brief, <5min episodes that address a topic in hopefully just enough detail to stick in the mind in a manner that might be retrievable in a situation of extreme stress – namely a fellowship examination. The knowledge contained will hopefully be sufficient to allow you to not look completely clueless on the ICU round when the topic of PR3+ve ANCA vasculitis comes up. They are not designed to be comprehensive coverage of a topic and the concepts included are deliberately simplified to maximise retention. As such this hopefully will occupy the niche of “exam prep/board review” in the already somewhat crowded critical care podcast scene. While tagged and categorised on the site to some degree, I have decided to mix and match the EM with the ICM in the hopes of upholding the shared knowledge base and skill set that the two specialties enjoy. If the ortho turns off the intensivists and the antifungals turns off the emergentologists then apologies in advance and I strongly encourage the healthy use of the “skip” button on your podcatcher/player/thingamadoodle. While not exactly a podcast of me reading aloud the LITFL or Deranged Physiology entry, it’s hard to overemphasise the importance and primacy of these resources in this publication and any suggestions that some of the material is derivative is entirely valid. You can find all the details on the podcast on the dedicated page