Tasty Morsels of Critical Care

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

Explore the indications and scenarios for cardiac pacing in critical care, including second or third-degree block, sinus node dysfunction, and ventricular tachycardia. Delve into the intricacies of pacing systems, wire placement, functions, and potential complications. Uncover a secret code for describing the type of pacing used in the cardiac intensive care unit.

Welcome back to the tasty morsels of critical care podcast. Continuing along a theme of words with with too many i’s in them, (see TM 007 for more) today we look at necrotising fasciitis or “nec fasc” to its friends. What clinical signs might help us find this? necrotic skin bullous changes dishwater coloured drainage from the bullae/tissue everyone’s favourite: POOP or pain out of proportion crepitus people with DM, immunosuppression, lines in situ or water exposure the other thing I’ve found useful over the years is that whenever you see a cellulitis with hypotension or a cellulitis going to ICU then you should be strongly considering nec fasc that you just haven’t found yet. Many of you will have heard of the LRINEC score but, like many of these scores for uncommon critically illnesses, it’s not that useful for making decisions but does highlight some of the features that should prompt you to think about it. You can diagnose it clinically with plain film, ultrasound, with CT or god help us all… MRI. (it’s not that MRI isn’t good, but any time you combine “time dependant surgical diagnosis” with MRI you’re in for diffs…) First amongst the lesser known facts about nec fasc comes the various types it is split into. Type 1: polymicrobial infection affecting the trunk perineum, typically in poorly controlled diabetics. Type 2: monomicrobrial infection (usually a beta haemolytic strep), mainly affecting the limbs of usually fairly normal patients Type 3: Clostridial infections or gram -ve, possibly even vibro. Can affect limbs, trunk, perineum and be associated with trauma or water exposure Type 4: candida, typically in the immunosuppressed as you might expect Obviously types 1 and 2 are what we see most of. There are some identifiable risk factors for nec fasc but type 2 infections, being mainly group A strep often have no risk factors so this list is more for the other types. Diabetes Alcohol misuse PVD Renal failure Recent surgery or trauma Malignancy/immunosuppression Injection drug use VZV is an unusual but well described risk factor in kids If you weren’t already aware then a key take home point is that surgical debridement is of the essence here. Surgery involves removing everything where the fascia pulls away when it’s not meant to. Generally a second look at 24-48 hrs to see if there’s been any progression is good idea. Medical treatment lies more in our domain as intensivists. Antibiotics are the mainstay and recommendations will vary by country and hospital. For example my current hospital’s empiric recommendations are ben pen and flucloxacillin ciprofloxacin gentamicin clindamycin MRSA is relatively uncommon so simple penicillins are often fine. Clindamycin is used as it inhibits protein (ie toxin) synthesis, though it is worth adding there are no high level data supporting this. I’ve heard similar physiological reasoning for linezolid against the staph PVL toxin in this regard. IVIG is frequently given (again with little data supporting). IDSA makes no recommendation on IVIG, the World Federation Emergency Surgeons give very weak recommendation to consider its use. Hyperbaric oxygen is much more complicated to deliver in a crashing critically ill patient. It is not recommended by IDSA. References and rationalisations Tasty Morsels of EM 012 Oh Chapter 72 Stevens, D. L. et al. Practice guidelines for the diagnosis and management of skin and soft tissue infections: 2014 update by the infectious diseases society of america. Clinical infectious diseases : an official publication of the Infectious Diseases Society of America 59, e10-52 (2014). Sartelli, M. et al. World Society of Emergency Surgery (WSES) guidelines for management of skin and soft tissue infections. World Journal of Emergency Surgery 9, 403–18 (2014).