Tasty Morsels of Critical Care

Dive into the complexities of managing pulmonary embolism, focusing on high-risk cases. Explore the critical interventions like thrombolysis and anticoagulation strategies, as well as the nuances of using inotropes and fluids. Learn about the role of CPR, the risks of intubation, and the controversial nature of catheter therapies. Discover the potential of VA ECMO as rescue support and the challenges of surgical embolectomy. Insightful discussions highlight the importance of swift decision-making in critical care!

Welcome back to the tasty morsels of critical care podcast. I haven’t managed to cover PE on the podcast yet. I have been involved in lots of small PE projects over the years and have developed something of an interest in it. I got invited to give a talk to the national EM conference this year and these podcasts are sort of the cliff notes version of that lecture. The full talk is linked to on the emergencymedicineireland.com website for those interested. I would emphasise that beyond the mention of the ESC guidelines this is an evidence lite podcast and more than usual represents opinions rather than hard science. The original talk was about PE in the resus room but I definitely think PE in the ICU in an established ICU patient is quite a different beast and I will try to highlight that as we go through it. PE is so ubiquitous that I’m skipping a lot of the core pathophys and work up and instead want to split it into 2 parts, the first today on risk stratifying PE and the second on nuances of management in critical care. PE is common in critical care. Either as a referral from ED with a patient with a nasty PE and bad physiology as the sole problem (less common) or as a finding in an ICU patient with other clinical issues, eg trauma or a surgical patient in whom you have now found a PE (a much more common scenario). From our perspective in ICU the test we need is a CT scan. I think all the other discussion about dimers etc is moot for us and if you need to exclude the diagnosis then CTPA is the way to go. I think for the majority of the ICU population found to have a PE they are relatively innocuous. Yes they have PE but it is frequently quite small and not really contributing to their physiology. Yes they need anticoagulation but rarely anything more. There are a small cohort who need aggressive management of the clot and the physiology but these are much less common. In terms of identifying the sick ones or risk stratifying them you need to be able to cite the ESC 2019 guidelines on PE. This is a substantial piece of work and is well worth a read. In that you will find PE can be split into low risk, intermediate risk, intermediate-high risk and high risk patients. However while a good starting place for risk stratification they remain a little blunt and don’t really tease out the super sick PE patients where the subtleties of management really come out. Most of the ICU cohort will fall in the intermediate risk group who generally do very well as long as you anticoagulate them. It starts getting interesting in the intermediate-high and the high risk group. The intermediate-high group are identified with some form of right heart strain on CT or echo and a bump in a biomarker like troponin and BNP. If you add in low blood pressure then you’re in the high risk group. As noted this risk stratification is, in my opinion, a little too blunt to be of use in the ICU population where there are so many other reasons that the right heart might look funny or the BP low or the troponin raised. How can we be a bit smarter with our risk stratification? Well firstly we need to decide if the low BP is being caused by the PE. Size of clot can be helpful here. If very small then it’s unlikely to be that significant. Especially if we have a much more clinically apparent cause of hypotension like the large empyema also seen on the CT scan. Particularly in the ICU population with multiple reasons for hypotension the pressure is on us to tease out which of the pathologies is causing the hypotension. If they are genuinely hypotensive because of the PE then lysis is probably inidicated – more on that next time. With regards to clot size, however the opposite does not seem to be true: ie the presence of large clot, especially in the ED population does not seem to predict outcomes especially well. Instead of looking in the report for the size of the clot we would better served paying attention to the size of the right heart versus the left and for evidence of contrast reflux into the IVC. These are more useful in predicting right heart dysfunction. An even more useful method is to look at the heart itself with an echo. I’m pretty sure this has little evidence to support it but I find that the echo gives a more accurate description of the impact that the PE is having on the physiology as I think (very much an opinion here) the CT scan often over calls the right heart strain. The obvious confounder here is that the echo is often done after the CT where the right heart has had a little time to recover so I’m very willing to be wrong on that. The useful things to look for on the echo are RV size, TAPSE and septal flattening. While i do love all the other nerdy measures of RV function I remain skeptical of their additive value in making a decision on something as significant as thrombolysis. The other reason I think echo has some advantages over CT on risk stratification is that it’s easy to see the response to therapies on the echo. Does the RV look a bit healthier after an inotrope or lysis etc. ECG can certainly be used to risk stratify and right heart strain on ECG, (think deep inverted T waves anteriorly and inferiorly) seems to predict CT and echo changes quite well. However I know my ECG skills are lacking and even when I do see the changes I see the ECG as a reason to order another test (ie CT/echo) rather than make the definitive diagnosis or thrombolyse. While trop and BNP get a lot of attention in the ESC guidelines for risk stratification I find them to be less than helpful in the critically ill as all of our patients already have a raised trop and BNP even before they get a PE. I do pay attention to our universal badness-metre the lactate. A rapidly rising lactate in a PE patient with a bad RV is certainly worrisome. Next time we’ll look at management options For further reading it is probably best to visit the original lecture post where they are all listed with a little smattering of critical appraisal thrown in for good measure.

Dive into the intriguing world of hypertriglyceridemia-induced pancreatitis, where strikingly lipemic blood samples can be a diagnostic clue. Learn when to suspect this rare cause and how triglyceride levels directly correlate with the severity of pancreatitis. The discussion covers the toxic mechanisms of fatty acids and dives into acute management strategies, including nutrition adjustments and insulin use. Plus, explore plasmapheresis as a rapid triglyceride-lowering option, even as guidelines caution against its routine use in acute scenarios.

Dive into the critical world of acute liver failure, where understanding the distinction from acute-on-chronic liver failure is crucial for diagnosis and management. Discover the main presentations like coagulopathy and encephalopathy, and explore various causes, including toxins and viral infections. The conversation also navigates through complications, such as intracranial hypertension, and highlights cutting-edge treatments like high-dose CRRT and urgent transplant referrals. It's a whirlwind through life-saving critical care insights!

Dive into the fascinating world of diabetes insipidus, where tasteless urine takes center stage. Learn about its two types: cranial DI, marked by a deficiency of antidiuretic hormone, and nephrogenic DI, involving resistance to this important hormone. Discover the critical role of ADH in regulating urine output and the challenges it presents in ICU settings. This discussion clarifies complexities within endocrinology, making the topic accessible for anyone navigating critical care.

Dive into the complexities of Heparin-Induced Thrombocytopenia (HIT), where two forms pose different risks. Type 1 is benign, but Type 2 involves serious immune responses that lead to clotting despite low platelets. Learn how exposure to heparin triggers this condition and the role of platelet factor 4 in generating an immune reaction. The discussion also highlights the importance of proper assessment techniques and alternative anticoagulation strategies for effective management.

Dive into the complexities of empyema, a condition often linked to pneumonia. Discover the key bacterial culprits and the significance of clinical assessments and imaging techniques. Learn about innovative drainage methods and injectable lysis therapies, bolstered by insightful trials like MIST-2. The podcast highlights the importance of combinatorial antibiotic treatments while critiquing research gaps, particularly in ICU representation. Prepare to rethink your understanding of chest drains and pleural therapies!

Discover the intriguing world of chylothorax, a rare condition marked by mysterious chyle accumulation in the pleural space. Learn how chyle, formed in the small intestine, navigates the lymphatic system through the thoracic duct. The discussion dives into potential causes, particularly following surgery, and offers insights into management strategies like dietary modifications and medical treatments. Plus, enjoy some fascinating anatomy tidbits about the cisterna chyli and the thoracic duct's perilous journey.

Welcome back to the tasty morsels of critical care podcast. We’re going to cover a bit of an environmental/tox topic today and look at carbon monoxide poisoning from Oh’s manual chapter 83 on burns. I have previously covered this on the old tasty morsels of EM series back when i was doing my EM fellowship exams. As you no doubt remember from school chemistry classes, carbon monoxide is a colourless, odourless, tasteless gas produced when combustion occurs with insufficient oxygen. We’re likely to see this in a couple of contexts. 1) the house fire victim, pulled from the fire unconscious and sick 2) the sub acute or chronic poisoning in a patient presenting with headaches and flu symptoms that seem to get better when they leave the problem environment. The classic EM example is the whole family who present with flu symptoms and no fever and even the dog is sick. We’re much less likely to see this cohort in the critical care side of things. How does it make people sick? Haemoglobin is a fickle little protein, while evolved to carry oxygen to needy tissue beds it actually has a distinct preference not for our beloved oxygen but for carbon monoxide. Introduce some carbon monoxide at the alveolus and the haemoglobin molecule will bind to CO with an affinity 240 times that than for oxygen. I take that number of 240 somewhat at face value but I presume someone got a PhD from working that out. In visual form my preferred means of explanation for this would be the distracted boyfriend meme where the haemoglobin boyfriend looks longingly over his shoulder at the carobon monoxide while his oxygen girlfriend looks on in horror. Hopefully you get the idea. So instead of having lots of circulating oxyhaemoglobin we’re instead left with lots of not especially useful carboxyhaemoglobin. Let’s imagine 50% of our Hb is now carboxyHb and 50% is OxyHb we’re left with a sort of severe fucntional anaemia where half of our Hb is out of action. One might be inclined to think that this is the major cause of morbidity and mortality in CO poisoning but in fact this is only a small portion of the problem. CoHb actually has a direct cytotoxic effect on things cytochrome oxidase and myoglobin function. As such it interrupts the whole process of oxidative metabolism and life as we know it. We can measure the level of CO fairly easily, any blood gas machine worth its salt should be able to give you a break down of the types of Hb present in the sample. This is co-oximetry and typically it’ll show you oxy, deoxy, carboxy and met haemoglobins. All these different forms of Hb absorb different wavelengths of light. The lowly pulse oximeter does not have the subtlety to distinguish the different wavelengths as it only functions at wavelengths of 940 and 660nm. Indeed the pulse ox often demonstrates a non diagnostic number somewhere in the 80s rather than a true reflection of the CarboxyHb or OxyHb present. Severe CO poisoning resulting in obtundation is going to have high level of COHb on our cooximeter. >10% is quoted but it’s more often over 30%. Patients are going to be pretty sick often from multiple pathologies but COHb on its own is enough to produce severe neurological injury, shock and even cardiac injury is also quite prevalent. Expect a high lactate given the disruption of oxidative metabolism. Resuscitate and investigate as you would any sick patient. Treatment is nice and simple in that we just give loads of oxygen. Oxygen reduces the half life of CO in the blood quite dramatically, commonly quoted numbers are the haf-life of COHb in an FiO2 of 0.21 is 300 minutes the half-life of COHb in an FiO2 of 1.0 is 60-90 minutes  There is a substantial rationale and literature on the use of hyperbaric oxygen as a means of accelerated clearance of COHb. But the RCTs that have been done don’t seem (to me at least) to give a clear benefit. The Lindell Weaver NEJM RCT in 2002 did suggest a neuro benefit but only 8% of the patients in this trial were intubated. A follow up trial in 2011 by ICU steroid guru Djilalli Annane did not find a benefit . So if anyone should get this it might be the non intubated isolated COHb poisoining. This is not really our cohort. Our cohort is likely to be tubed, shocked, with multiple injuruies and not someone you want to transport cross county to put in a single person hyperbaric chamber for hours at a time. Reading Oh Manual Chapter 83 Weaver, L. K. et al. Hyperbaric oxygen for acute carbon monoxide poisoning. The New England journal of medicine 347, 1057–1067 (2002). Annane, D. et al. Hyperbaric oxygen therapy for acute domestic carbon monoxide poisoning: two randomized controlled trials. Intensive Care Medicine 37, 486–492 (2011).      

Delving into the world of pulmonary hypertension management in critically ill patients, the podcast highlights the importance of continuing PH specific meds, the focus on treating PVR over PA pressures, and the challenges of maintaining right-to-left heart flow. The discussion offers practical insights for navigating these complexities in the ICU setting.