Tasty Morsels of Critical Care

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).

Exploring ventilator cycling in critical care, comparing time cycling vs flow cycling. Understanding how these methods impact mean airway pressure and oxygenation. Delving into the benefits and obstacles of each method, with considerations for factors like tracheostomies.

Explore the significance of ICP monitoring in critical care, criteria for monitor insertion, normal values, and diverse techniques. Compare EVD and Prankimal monitors, highlighting pros and cons. Learn about typical ICP waveform spikes and Lundberg A waves indicating auto-regulation issues.

Exploring hepatopulmonary syndrome, pulmonary hypertension, and infectious challenges post-liver transplant. Emphasizing prophylaxis and immunosuppression strategies for a successful outcome.

An insightful exploration of liver transplantation process and considerations, covering eligibility criteria, post-operative complications, MELD score assessment, and the critical need for post-operative care.

Welcome back to the tasty morsels of critical care podcast. Today we have one of the jewels of critical care exam preparation. Not only does this involve niche clinical contexts, the gamma glutamate cycle but also everyone’s favourite acid base mnemonic CAT MUDPILES. The referral to critical care services will likely go something like this. Usually a phone call from a surgical service about an older frail patient who has been in hospital for several weeks with some kind of soft tissue or joint infection who now has become tachypnoeic with a blood gas that appears to be somewhat incompatible with life despite a patient who is clinically a little rough but otherwise keeping all their organ functions largely together. The really smug amongst you can respond even before you hear the full story with “just how much flucloxacillin and paracetamol have you been giving them?” For those of us mere mortals who would prefer some actual medicine instead of social posturing then this pyroglutamic acidosis is a fairly rare cause of a raised anion gap acidosis. There is a sort of double hit needed to set this off. Firstly you need to get pretty glutathione deplete. Being in hospital and frail with poor nutrition is a good start. Couple that with a brainstem reflex analgesia prescription of QDS paracetamol (which needs a reasonable amount of glutathione to conjugate its toxic metabolite NAPQI), then glutathione stores get deplete pretty quick. The second hit comes from something that causes dysfunction of 5-oxoprolinase (which helps create pyroglutamic acid). This is typically flucloxacillin but can also be the surprisingly unpronounceable viagabatrin. The clinical presentation will be a severe raised anion gap acidosis, typically with numbers that seem disproportionate to the usual house officer differential of “sepsis”. Treatment involves removing the offending precipitants, probably some isotonic bicarb and an infusion of everyone’s favourite glutathione donor – N-acetyl-cystine. CRRT is of course an option to make the numbers look better too. References: DP has, unsurprisingly, a great article on this, one for which the chef’s kiss emoji was probably invented.   

Welcome back to the tasty morsels of critical care podcast. So, from the ultra broad topic of AKI in the last podcast to the super specific question of when we should pursue an open lung biopsy in an ICU patient. The answer is probably – very rarely. But while this podcast is intended to be brief even I feel I owe the listener something more than this. When would you consider such an invasive and complication ridden procedure in the ICU? Typically this would be in a patient with progressive respiratory failure with no cause found despite an extensive work up (eg radiology, bronch, micro, fancy acronym ridden blood tests) The CXR will be usually diffuse bilateral infiltrates. The differential in this scenario is fairly broad and includes infectious (bacteria, viral, fungal) inflammatory (COP, interstitial pneumonias, connective tissue disease) may also find end stage diseases (and a reason to stop life sustaining therapies) eg IPF or malignancy If you’re going to do this then it’s probably best done within 1 week of ventilation. This can be challenging as you often want that week to get all your basic results back and to see if your empiric therapies are having an effect.  Given that you’re going to open this patients chest and cut out a wedge of lung tissue it’s probably worth going through the pluses and minuses of this approach. Advantages diagnosis (though you may not get one) decent accuracy can change treatment you’re taking a large section tissue – more likely to get answer than a simple needle biopsy. can be combined with other procedures eg empyema drainage Disadvantage ~1.5% mortality which comes in as one of the more solid disadvantages in this list. invasive and all the complications that come with it, particularly air leaks. may not get the right sample/section of tissue not clear if it changes mortality Overall this is a rarely pursued strategy that probably does have a niche role. It should probably not be immediately dismissed out of hand unlike other “helpful” suggestions like  “maybe it’s time for the bicarb?” Or the discerning intensivist’s favourite suggestion “hey why we don’t try some gelo?” Ultimately the nihilist in me suspects the most useful role of a biopsy may well be in defining pathology without potential treatment, and using this info as a means to discuss with patient and relatives the concept of futility and limitation of life sustaining therapies. References and rationalisations Deranged Physiology LITFL CCC    

Topics include exploring acute kidney injury complexities, Kedigo classification, sepsis causes, imaging guidelines, obstacles in researching AKI pathophysiology, drawbacks of existing biomarkers, and unique therapies for rare renal conditions.

Welcome back to the tasty morsels of critical care podcast. In a break from the not quite established tradition on this show, I’ve split this into two parts. Number 13 covers the process of putting them in. This one focusses more on some physiology and when to take it out. Some useful points on anatomy  and physiology 18-22 rings cricoid to carina about 11cm compared to normal breathing, tracheostomy removes dead space by ~100mls. Probably no realistic change in dead space from an ET tube. most resistance in breathing is through the nose and the mouth so a tracheostomy theoretically removes that but the size of a tracheostomy (ID of 6-8mm) means that you lose that benefit overall less work of breathing in spont breathing patients with tracheostomy when weaning we often cap the tube to allow the patient to breath around it. A smaller tube makes this easier, as do fenetrations. How well the cuff deflates makes a big difference too several studies suggesting reduced WOB with tracheostomy v ETT Dongles you might find on the the end of a tracheostomy Swedish nose. Effectively an HME with an O2 port on it Passy-Muir. Speaking Valve allowing air in but not out Decannulation This is not a straightforward question but there a few things to consider when thinking about taking it out. is the underlying condition resolved/stable ensure there is no ongoing mechanical ventilation need. Including no need for NIV as you wont be able to use NIV in the immediate decanulation period without making the patient look like a michelin man. is there a good cough, good strength what about the secretion burden (though note presence of trache can itself stimulate secretions) have they passed a trial of cuff down (up to 72 hrs) (though I did read a recent RCT that suggested that decannulating based on suctioning frequency rather than passing a capping trial significantly improved time to and successful decannulation) able to tolerate a 25% increase in WOB that comes with moving orifice from neck to mouth. What do you do if it falls out? this is a recurring perennial cause of airway misadventure frequently resulting in death. The UK National Tracheostomy Safety Project is an excellent resource that is well worth some time. I interviewed Brendan Mcgrath for the RCEM Learning podcast and it is well worth a listen The single take home point might be – if it’s not been in very long then it’s safest to just re-intubate from the top end. References and rationalisations: Epstein SK. Anatomy and physiology of tracheostomy. Respir Care. 2005 Apr;50(4):476-82. PMID: 15807905. ANZICS Statement RCEM Learning Podcast on Tracheostomy National Tracheostomy Safety Project.  Martínez, G. H. et al. High-Flow Oxygen with Capping or Suctioning for Tracheostomy Decannulation. New Engl J Med 383, 1009–1017 (2020).