Tasty Morsels of Critical Care

Welcome back to the tasty morsels of critical care podcast. A meandering monologue through critical care fellowship exam preparation. Today we’re looking at Oh Chapter 64 covering some of the absolute basics of pre eclampsia. ICU level pre eclampsia is rare. In Ireland most of it is managed in separate obstetric hospitals by the obstetricians and the anaesthetists. And given that the definitive treatment is removing the baby from the mother, it turns out that this will typically have been done before we even get involved. Unfortunately its rarity does not get us out of having to know it very well as it is an exam favourite. Firstly some definitions. To have pre eclampsia you’ll need to have new onset of hypertension with proterinuria OR new onset of hypertension with end organ damage (inc foetal growth issues) Hypertension here defined as BP >140/90 and proteinuria as >300mg/24hrs or protein +ve on a dipstick. To have eclampsia you simply need to have seizures in addition to the above. To summarise the cause and pathogenesis, the short answer is we don’t know. The longer answer is – we still don’t know but we have lots of science to show it and the medium length, exam appropriate answer answer that I might be able to reproduce is a straight quote from deranged physiology: [pre eclampsia is] a systemic response to placental hypoperfusion, with increased activation of the potent vasoconstrictor endothelin-1, as well as an increased sensitivity to vasoconstrictors in general, and a down-regulation of vasodilatory mechanisms such as nitric oxide synthase. The clinical presentation of pre-eclampsia from a critical care perspective is best split into organ systems Cardiovascular: hypertension is the main player here. You’ll see increased SVR also Neurological: early signs can be headache and visual symptoms. You will see hyperreflexia if you look for it and you probably should. But with progression you’ll start seeing seizures, cerebral oedema and even ICH Renal: protein loss is obvious but the fancy term to pull out is renal endotheliosis which is a form of thrombotic microangiopathy or TMA. A topic that deserves its own post. Haematologic: low platelets but also impaired function. This might come as part of HELLP syndrome Hepatic: HELLP syndrome is part of this but the most dramatic complication can be hepatic rupture which as you can imagine is somewhat bleedy While rare you can even get pre eclampsia in the post partum patient and I always liked the quip from Mel Herbert of EMRAP fame, that the usual definitive treatment of pre eclampsia is of course to deliver the baby but if it’s post partum what are we meant to do? put it back in again? We are unlikely to be given the job of ridding the woman of the placenta so we can instead usefully occupy ourselves with supporting the various failing organ systems. The priorities here will be seizure prevention and treatment. BP control maintaining placental perfusion Seizure control here should lead to a brainstem level reflex of magnesium prescription. The indication is described as eclampsia or imminent risk of eclampsia and BP is often in the 160/110 range by this stage. Recommendations are 4g magnesium over 5 mins followed by 1g/hr as an infusion. Any further seizures can be treated with another 2g of magnesium. The NICE guidance on this has a carefully worded phrase that says “Do not use diazepam, phenytoin or other anticonvulsants as an alternative to magnesium sulfate in women with eclampsia” In terms of a level of magnesium, you’re looking for somewhere in the 2-3.5 range which is obviously much higher than we’re used to. I was once told to just keep giving the magnesium till they’re completely areflexic and then pull back. This may well get you into trouble as the lack of reflexes will be shortly followed by some respiratory insufficiency and you might find yourself having to reach for your calcium as a reversal agent to the magnesium. Magnesium is a well supported critical care intervention with the colossal MAGPIE trial from 2002  which was a 10000 person RCT showing definitive benefit and halving the risk of eclampsia. The recommendations for BP control from NICE are as follows labetalol (oral or IV) nifedipine PO IV hydralazine References Oh Chapter 64 Deranged Physiology Altman D, Carroli G, Duley L, Farrell B, Moodley J, Neilson J, Smith D; Magpie Trial Collaboration Group. Do women with pre-eclampsia, and their babies, benefit from magnesium sulphate? The Magpie Trial: a randomised placebo-controlled trial. Lancet. 2002 Jun 1;359(9321):1877-90. doi: 10.1016/s0140-6736(02)08778-0. PMID: 12057549.  

Welcome back to the tasty morsels of critical care podcast. A meandering monologue through critical care fellowship exam preparation. Today’s podcast is mostly taken from Oh’s manual Chapter 96 covering critical care nutrition. Something we all know and love deeply for exams and then immediately outsource to our dieticians the moment we get the chance. Perhaps the first take home figure is 25kCal/kg/day. This has been around as a recommended energy intake since the late 90s. And like most nutritional things it’s not exactly stellar in its support from the literature. There has been a recent tread in trials towards hypocaloric feeding that have hinted towards benefit at feeding to a lower target with purported mechanisms including that higher targets suppress autophagy which is an important part of killing nasty organisms. The lower target has not panned out as yet but it is worth pointing out that we rarely actually achieve the 25kCal/kg/day that we aim for, so we are probably inadvertently underfeeding people at baseline. On the other side of this it’s clear that if we have prolonged periods of not meeting targets then patients clearly do worse. We could, of course, measure the energy requirements the patient needs instead of a blanket recommendation for all. And there are a variety of methods for doing this. Oh describes indirect calorimetry as “a rather burdensome gold standard” and it seems all the units I have worked in have taken this on board and simply not bothered with getting the metabolic cart needed for doing it. This device, when connected to the vent allows measurement of O2 consumption and CO2 production, and can calculate energy expenditure. The other options for estimating energy expenditure include a bunch of equations of which the Penn-State one is recommended as the best of a bad bunch and finally you can calculate using the reverse Fick method which needs a PA catheter to measure O2 consumption. I mention these only as useful options for a candidate to scribble down in answer to a question rather than perform them in real life. As the good book says, man shall not live by kCal alone so we need to consider what else the patient needs nutritionally. First off – protein. For normal people walking around their everyday business not attached to pressors or a ventilator the daily protein intake is around 0.8g/kg/day. In the critically ill this has been bumped up to at least 1.2g/kg/day or even has high 2g/kg/day in some of the super catabolic patients such as major burns. For bonus points remember that patients require all the micronutrients such as vitamins, thiamine and elements that come as part of a healthy diet. Most enteral formulations will contain these and it’s really in those on parenteral nutrition that you need to stress a little more about it. When calculating the energy intake we need to consider all the sources of intake. Energy is not just glucose but will include the protein that we give and also some of the infusions we use for example the fats in the propofol infusion (which comes in at ~1kCal/ml) and the glucose in the 5% dextrose we’re giving to correct the hypernatraemia. References Oh’s Manual Chapter 96 Deranged Physiology – there is a lovely section on the theoretical maximum and minimum amounts of each class needed including some lovely stuff on inuits and zero carb diets

In this podcast, they discuss treatment options like steroids, IVIG, and plasma exchange for Guillain-Barre Syndrome. They also cover managing GBS in the ICU, including intubation principles, vital capacity monitoring, and patient prognosis.

Explore the clinical significance of Guillain-Barre Syndrome, treatment options like IVIG and plasma exchange, common triggers including infections like Campylobacter-Jjunae, flu, HIV, and mycoplasma. Delve into the intricacies of GBS subtypes like AIDP, MFE, AMAN, and AMSN, highlighting clinical diagnosis and treatment strategies with a focus on challenges in early diagnosis and the role of diagnostic tools like lumbar puncture.

Welcome back to the tasty morsels of critical care podcast. A meandering monologue through critical care fellowship exam preparation. We see C. Diff in the ICU in a couple of contexts. Firstly the poor unfortunate soul who starts with a benign illness and gets some antibiotics and develops a fulminant colitis and shock needing colectomy and an ICU admission. Secondly we have the frequent dilemma of the prolonged ICU patient who is collecting complications like they’re merit badges. They’ve developed new shock and there’s some diarrhoea and you’re worried about c. diff. First off some risk factors. Firstly is antibiotic exposure and topping the list would be beta-lactams and clindamycin, closely followed by the quinolones, aztreonam, and the carbapenems. A truncated list of patient specific risk factors might go as follows: age >65y previous GI surgery or IBD renal impairment prolonged hospitalisation esp with a C. diff contact gastric acid suppression (though PEPTIC trial would suggest against this is unlikely, or at least not more likely than H2RA. However I still think it’s a fair answer in an exam) immunocompromised and chemotherapy patients There are a few useful principles of prevention: Hand washing – remember that spores survive alcohol and on surfaces, need soap and water Isolation Testing of symptomatic individuals avoidance/minimising antibiotics Limit PPI use and get NG tubes out ASAP In terms of diagnosis we’re typically thinking of this in patients with diarrhoea. We send a stool sample and wait patiently by the computer for a result. But what are we actually testing? This will of course depend somewhat on your local lab but there are a few important principles. Most of the time we’re testing for a toxin produced by the bacterium. This can be toxin A or B or both. If both are +ve then cool cool cool you’ve probably got your diagnosis. If you’ve got one +ve and one -ve then IDSA recommends using nucleic acid amplification (or PCR if you like) as a tie breaker. The PCR is very very sensitive. And the issue is that the presence of c diff DNA in your poo doesn’t necessarily imply disease whereas the combination of symptoms a +ve toxin immunoassay and a PCR is much more compelling. An important component of the diagnosis involves some form of mucosal assessment – especially in more severe cases. This can be some form of flexible boweloscopy device or a CT scan looking for colitis or mega colon. Once you’ve made your diagnosis you’re ready to start some treatment. This can be very confusing as treatment is not only determined by severity grade but the recommendations have changed relatively recently (in 2018) so the stuff you learnt for your membership examinations may no longer be relevant. The split here is into non severe, severe and fulminant so keep that in mind. The split between non severe and severe, is defined by a WCC<15 and a normalish creatinine. This distinction would seem an important thing to memorise, however as far as I can work out, IDSA suggests identical treatment for both non severe and severe. Namely Vance 125mg PO QDS OR fidoxamicin note that metronidazole PO is no longer recommended the way it was in the mid noughties when I started. Fulminant disease is primarily determined by shock and the presence of megacolon. This probably is something worth remembering as treatment here is significantly different. Here you give vanc 500mg PO QDS plus metro IV (which after being given IV is secreted unchanged into the GI tract via the biliary tract). For those with nasty distal disease vanc enemas can also be used which will certainly make you super popular with the nursing staff. While rarely done, it’s really important in both clinical practice and certainly in an exam to consider taking out the whole colon. The surgeons will of course make the final decision on this but some may need a little nudge in the right direction. Potential nudges might include Hypotension requiring vasopressor therapy Clinical signs of sepsis and organ dysfunction WCC in excess of 50 Lactate in excess of 5mmol/L Failure to improve on medical therapy after 5 days If you’ve managed to get all this across in your SAQ then you’re flying but if you want to go for gold then you could throw in a few comments like faecal transplant – niche and not really considered until 3rd recurrence IVIG as a toxin binding agent in fulminant (no substantial support) there is a monoclonal antibody to bind toxin but this is really sketchy at this point References and rationalisations Deranged Physiology LITFL IDSA 2018    

Welcome back to the tasty morsels of critical care podcast. A meandering monologue through critical care fellowship exam preparation. HIV in the ICU is becoming a bit of a rare beast as the ID docs seem to have it so well controlled that it becomes a chronic co-morbidity rather than the cause of their presence in the ICU. There are of course exceptions – typically in the poor soul in difficult circumstances, trapped in poverty and with no means to maintain stability in their lives. These patients often have fulminant and uncontrolled disease. Primary HIV will not typically land you in the ICU but it is an important syndrome with a clinical appearance a bit similar to infectious mononucleosis. The key is to consider it and be liberal with testing. In particular patients are often most viraemic at this stage and can spread HIV significantly when they are very much unaware of their status. The CD4 receptor is the primary binding site for HIV and over time these CD4+ T cells become very deplete and indeed this is one of the means of immunosuppresion in HIV. CD4 counts are rarely available out of hours but we do have the lymphocyte count as a reasonably well established surrogate. (Do you remember back in early COVID times the low lymph counts were considered somewhat predictive of SARS CoV2?) CD4 levels <200 are generally considered to put people at risk of opportunistic infections. Though the risks and weirdness of the infections gets greater as the CD4 falls. In general at the higher levels (say 100-200) expect respiratory illnesses, at the super low (<100) expect to see funky things like crypto and toxo more commonly. In terms of diagnosis, as far as I can work out (and I’m no virologist…), most tests to diagnose HIV are some form of antigen/antibody testing. The viral load that we see is used primarily to measure response to treatment. These patients will often be on a lot of unpronounceable medications. The general rule is to continue them all if possible. Breaks in treatment can lead to resistance. However there are often problems with keeping this stuff going. For example: no parenteral preparations currently available and of course, working in the ICU we find it hard to believe that drugs given by a non IV route actually do anything. worse than this many are not crushable so even with an NG we mightn’t be able to deliver them. absorption likely impaired by critical illness with poor cardiac output ileus is common and further reduces absorption feeds need stopped for administration – impairs nutrition clearance may be altered by either hepatic (reduced flow, cirrhosis, acute liver injury) or renal injuries (reducing renal clearance) interactions with other meds used in ICU changing effect of meds All ART are hepatotoxic the NRTI are famous for causing lactic acidosis (at least in exam stems…) Finally it’s worth being aware of an entity called IRIS (Immune Reconstitution Inflammatory Syndrome). This occurs in patients who have relatively advanced HIV at presentation with very depressed CD4 counts. These patients have immune systems that have been culled of their senior and competent staff, somewhat like the hospital at 3am on the Sunday after Christmas. Lots of opportunistic infections have sneaked in and are not causing much of a fuss and are entirely unnoticed. Along comes effective antiretroviral therapy and all of a sudden there are legions of CD4s marching the corridors and uncovering CMV and crypto in every crevice. The newly reconstituted immune system gets excited and does what it does best and causes inflammation somewhat to the detriment of the body overall. All that is to say that occasionally in the critically ill, newly diagnosed HIV patient, you may find your ID team making strong recommendations not to commence ART. References: Oh’s manual Chapter 69

Learn about the process of plasma exchange in critical care and its distinctions from CRRT. Discover how plasmapheresis can reset the immune system by removing harmful components from the blood and its applications in immunoproliferative diseases and autoimmune conditions.

Welcome back to the tasty morsels of critical care podcast. SBS is not a common thing to find in the ICU and the most likely context here is going to be receiving someone from the operating theatre who has had rather more bowel removed than one would like. There are some poor souls who as a result of SBS are dependant on long term TPN who may also appear in ICU from time to time and a working knowledge would be useful. Neither LITFL not Deranged Physiology have an entry for this (which is more reflective of its non importance rather than a reflection on the comprehensiveness of the two resources.) Surgical causes of this are typically going to be surgery for things like Crohn’s disease or ischaemic bowel. The decision to resect enough bowel to put someone at risk of long term TPN is a huge intraop decision and not taken lightly. However it is frequently not one that can be made until the abdomen is entered (especially in the emergency mesenteric ischaemia situation). A useful definition of the syndrome would be  insufficient gut to maintain homeostasis and nutrition. Lengths are not particularly useful in predicting outcomes but having <180cm puts you at risk and <100 cm means you’re almost undoubtedly in trouble. Having some colon left is protective. The part of the small bowel removed will have a different impact depending on which bit. As revision Jejunum function (proximal 2/5 of small bowel) lots of nutrient absorption lots of fluid resorption (the gut secretes about 9L/day of fluids so it’s important to take most of it back) Ileal function (distal 3/5 small bowel) vit B12 absorption bile acid absorption (loss of bile acids impairs fat soluble vitamin absorption) In some bizarre hostage like situation where someone asked you which bit of your small bowel you had to remove it would be best to say jejenum as the ileum seems to be more adaptable overall and gives you a better chance of sufficient intestinal function. in the post op period we’ll be faced with the “acute phase” of SBS where there is generally significant fluid losses and metabolic derangements from whatever kind of “ostomy” is left behind. Management options at this stage include: Acid suppression (eg PPI or H2RA) – gastric secretions are a major contributor to fluid losses here and typically there are more secretions than normal that cause fluid loss and also impair pancreatic enzyme function. Fluids to replace losses – and the answer is probably hartmans as always PN with trial of EN (the EN is the best stimulant of intestinal adaptation needed to establish a functioning intestinal tract) loperamide can be used (though often not in the ICU period) Octreotide (typically when >3L IV fluid a day are required) ICU favourite clonidine can also reduce stool output apparently. References: UTD Article Pironi L, Corcos O, Forbes A, Holst M, Joly F, Jonkers C, Klek S, Lal S, Blaser AR, Rollins KE, Sasdelli AS, Shaffer J, Van Gossum A, Wanten G, Zanfi C, Lobo DN; ESPEN Acute and Chronic Intestinal Failure Special Interest Groups. Intestinal failure in adults: Recommendations from the ESPEN expert groups. Clin Nutr. 2018 Dec;37(6 Pt A):1798-1809. doi: 10.1016/j.clnu.2018.07.036. Epub 2018 Aug 18. PMID: 30172658.

Dive into the world of adrenocortical insufficiency and discover its critical role in the ICU. Learn how cortisol functions and why standard serum levels can be misleading. Explore the different types of adrenal insufficiency, including Addison's, and what signs to look for during an adrenal crisis. Find out the best practices for immediate management, like the importance of hydrocortisone, and how long-term steroid use can lead to secondary adrenal insufficiency. Essential insights for anyone in critical care!

Welcome back to the tasty morsels of critical care podcast. A meandering monologue through critical care exam preparation. The aminoglycosides see themselves as a bit special. Not content with producing deafness and killing kidneys they’ve also demanded awkward dosing schedules, a need for regular levels and even their own section on most drug kardexes that I’ve seen. They are the divas of the antibiotic world. That being said they’re a real work horse in the ICU and it’s hard to say you’ve done due diligence on a septic crashing patient without the ubiquitous “shot of gent” that has wormed its way into the medical nomenclature. In the ED and ICU the only aminoglycosides in town are gentamicin and its lesser used but much respected, big brother, amikacin. In terms of mechanism, these drugs work by inhibiting bacterial protein synthesis by binding to the 30S sub-unit of the ribosome. The preceding is one of those statements that sounds somewhat impressive when delivered in a viva but is quickly followed by a blank look of panic if anyone asks a follow up question.  These drugs are a good example of concentration dependant killing. In brief, this means that we need a nice high peak concentration of the drug, well above the MIC of the bug in question. This is in distinction to the beta-lactams which are classed as time dependant killing, where the time above the MIC is more correlated with efficacy. Aminoglycosides also come with an excellent post antibiotic effect where growth of the bug is inhibited even when the levels of the drug are below the MIC. The idea seems to be that the aminoglycosides bind irreversibly to ribosomes so even when you can’t measure any aminoglycoside in the blood it’s still working away in stopping microbial growth. Their most common use in critical care is as an adjunctive antibiotic for aerobic gram negative bacilli. Perhaps the commonest context will be in the context of septic shock with the belly as public enemy number 1. The other common use is in sepsis of urinary origin, (the dreaded urosepsis, as opposed to that pesky south east asian sepsis… H/T Mike Park…) where the aminoglycosides come in particularly handy as they are excreted unchanged by the kidneys so that concentrations within the urinary tract can be incredibly high. They are usually used in combination with other antibiotics but interestingly gentamicin remains first line therapy for plague which is worth keeping in mind when the inevitable apocalypse comes and the following societal collapse and return to the middle ages. The aminoglycosides penetrate poorly in the acidic environments of the the bronchial secretions and the lung and are thought to be poorly effective here. They also have poor penetration to the CSF and biliary tree. I’ve never been entirely clear when to reach for amikacin over its much more commonly used brethren gentamicin. This is of course the reason we have timely and excellent input from our micro and ID colleagues but what I’ve gleaned suggests that amikacin has a role particularly in those patients carrying the alphabet soup labels of ESBL, KPC etc… Our main concern with these drugs is their toxicity, namely to the kidneys and ears. With regards to the kidneys the ubiquitous presence of the green machine (CRRT) has allowed us to prioritise killing bugs before preserving renal function. I know we’d like to have both but given that we can replace the kidneys then we tend to sacrifice them on the alter of microbial killing.  As a result we have a somewhat laissez faire attitude to nephrotoxicity which is probably not the best. The ototoxicty is somewhat more opaque to us in the ICU as patients are rarely well enough to express their vestibular or cochlear disturbance to us and this is something much more likely to be picked up on the ward following the ICU stay. Our best tool to avoid these toxicities is careful dosing, regular levels and stopping them whenever we have identified the right bug and the right antibiotics for them. Thankfully aminoglycosides are one of the few drugs that you will be asked to review every day and hopefully stop. Finally there is the rarely reported phenomenon of neuromuscular block following aminoglycoside administration. However its rarity outside those with myasthenia gravis makes it gentamicin unlikely to be a serious competitor in the roc v sux debate. References Deranged Physiology – The post antibiotic effect UpToDate has a lovely summary article on the aminoglycosides which forms the bulk reference for this podcast