Tasty Morsels of Critical Care

Discussions on the causes and solutions for recurrent clotting of filters in ICU, including filter usage duration, anticoagulation methods, and catheter placement. Exploring considerations for clotting issues in filter placement, including safe and effective tip positioning, assessing volume status, prothrombotic state, and viscosity.

Welcome back to the tasty morsels of critical care podcast. There’s not a huge amount of notes on procedural stuff that I accumulated for the exams but I did collect some interesting bits on bronchoscopy, particularly because it was so novel to me as an EM trainee who really had no experience with bronchoscopy prior to starting to my critical care fellowship. After 2 years of frequent, if not daily use of the bronch, I find it hard to see how I would manage in an ICU without it. Now, when I say bronch I want to be clear that I’m talking about the flexible, disposable pieces of gear. The respiratory people sometimes come and laugh at us when they arrive with their big stacks and multi-thousand euro pieces of kit. Why might we pull out the bronch in the ICU? Well I’m not sure there is a clear or authoritative list, but the following would be reasonable as an assistance in intubation as a guide in percutaneous tracheostomy as a therapeutic in mucous plugging sudden refractory hypoxia without obvious cause. I often find putting the bronch down quickly answers a lot of questions about tube position and mucous plugging and bleeding a whole lot quicker than waiting for the CXR BAL. We all love to know what we’re treating and especially in the hospital acquired or  immunocompromised, it can be lovely to grow a bug. Though I don’t want to suggest this is particularly data driven. Airway bleeding. Finding the bleeding, clearing it, treating it. In general we will almost always be passing the bronch through some kind of device. I have on occasion post tracheostomy spent some time practicsing getting the bronch through the cords in a sort of a poor man’s fibre optic intubation, and damn if it’s not tricky… Credit should be due to the respiratory guys who do this all the time. All be it with much weller patients and nicer and shiner equipment. What do we look for then once we’ve passed a bronch into the large airways? We should have a good look at the airways themselves. Is there a lot of suction trauma? Is there bronchomalcia, (esp in the slow trache weans), are there hyphae and mushrooms growing in the airways suggestive of aspergilllus? We often forget to simply look at the walls as we chase down into the lobes to get our sample. Once it comes to the process of BAL itself then I realise I’m often a little shy and cautious in my installations of saline. When I went and read up on this it turns out typically recommended volumes for installation of saline are more like 100mls rather than the paltry 20-40mls I was using when I first started. A lot of what I (and I suspect many of you) have been doing is perhaps better classified as bronchial washings rather than true bronch alveolar lavage. Also important, once you stick the saline in, to give it a decent amount of time (30-60 secs) before aspirating. In terms of where we are aiming for, typically aim for the segment that looks worst on imaging. If it’s all awful or nil focal then the RML and the lingula are often recommended. In some of the reading there was discussion on “wedging” the bronch which is not the infantile practice of pulling someone’s underwear up really high when they’re not suspecting it. Bronchoscopic wedging involves getting the tip of the bronch into a segment far enough where there is partial airway collapse (though not complete) on suction. If it doesn’t collapse at all you’re too proximal, If it collapses completely then you’ll likely not get a good aspirate. Once you’ve got your samples then the qunadry you face next is what to test it for. This will likely depend on the situation, but you have a variety of options available to you routine culture cytology, things like eosonophils for daptomycin induced pneumonitis, inclusion bodies for things like CMV/HSV galactomannan on a BAL sample apparently more useful for aspergillus than serum PJP PCR (very sensitive, not specific) and silver staining is a useful test CMV reactivation is another common concern in the critically ill Bronchs are not without their potential complications and can be summarised as follows bleeding barotrauma – this may be related to the sudden and extreme pressure changes from being on +ve pressure one moment and attached to wall suction the next. The vent settings itself will also change things as if you really ask the vent to deliver 400mls while the airways are largely occluded with a plastic bronch then expect airway pressures to be very high References the UTD article was useful on this but you will need access LITFL covers it well as expected there is a nice simulator but it needs flash and it seems flash has not graduated into the pandemic era so it’s hard to run finally there’s a nice and brief anatomy review that is worth reviewing on a regular basis so you actually have some idea where the hell you are in the lungs at any given time.  

Delve into the complications and metabolic issues of Parenteral Nutrition, including misconceptions about sepsis and risks of line-related infections. Explore the challenges of overfeeding and liver complications, along with the delicate balance between carbohydrates and lipids in nutrition bags.

Exploring spinal cord injuries, differentiation between primary and secondary injuries, EASIA score for motor prognosis, A to E grading system, cord syndromes, ICU management emphasizing respiratory complications, hemodynamics, tracheostomy necessity, predictive value of clinical examinations in determining post-injury outcomes

Explore the clinical aspects of Candida in critical care settings, including risk factors, diagnosis, and treatment options. Learn about the importance of eye examinations for Candidiasis and potential risks of Candida endophthalmitis.

Welcome back to the tasty morsels of critical care podcast. Today we look at anaphylaxis. Oh’s Manual 67 forms the basis for most of this. In many ways this is fairly straightforward. You give adrenaline and they get better. However once you get into the pathophys behind it you start to realise why immunologists are much smarter than you are. Oh starts with a few nice descriptions of what it is: an acute multi system disorder with release of multiple mediators from mast cells and basophils. Usually this is a hypersensitivity reaction mediated by IgE to a foreign substance. The term anaphylactoid is reserved for non IgE mediated reactions. (These still involve mast cell degranulation) The current guideline accepted definition goes like this serious, life threatening generalised or systemic hypersensitivity reaction that may or may not be immune (ie IgE) mediated While accurate this doesn’t really help me very much in knowing what it looks like. A better description for what it looks like goes as follows: Anaphylaxis is highly likely in the following scenarios acute onset with skin or mucosal involvement plus at least one of respiratory compromise or reduced BP. Rash and shock or rash and SOB means anaphylaxis the term mucosal involvement can mean the tongue and pharynx but also the rest of the GI tract. Let’s say you eat a peanut get tummy cramps, diarroeah and a BP of 60 systolic. No wheeze, no rash – this is still anaphylaxis. reduced BP after exposure to a known allergen for that patient. The pathophysiology is mostly beyond me but the predominant features are mainly histamine mediated and there is release of serotonin and tryptase in addition. The precipitants can be split up into a number of classes Food peanuts, crustaceans and fish, sometimes persisting into adulthood. Interestingly there is there is food associated, exercise induced anaphylaxis where exercise 2-3 hrs post the allergen causes the reaction  Drugs are incredibly common. penicillins and cephalosoporins are the commonest antibiotics NMBs such as rocuronium are an important bogey man in anaesthesia and may occur without prior exposure. If you only ever use it in the critically ill then it’ll be a while before you pick up a serious case of it appears to me. NSAIDs, Aspirin Radiology contrast Protamine Chlorhexidine is a common and often overlooked cause Rare beasts like mast cell disorders like systemic mastocytosis Tryptase gets a lot of attention (not without reason) in both anaesthesia and EM circles. Peak levels occur ~15-120 mins post event and decline predictably (T1/2 ~2hrs). This influences the timing of sampling as recommended in the UK guidelines with one sample taken as soon as possible and another within 4 hrs and then a 3rd convalescent sample either >24 hrs post resolution or at allergy clinic. It is critical to understand that this is a test useful in follow up to confirm diagnosis and should not be involved in the decision whether or not to give adrenaline acutely. Treatment is adrenaline. The ALS guidance is all about the IM and this should continue to be the case though there is a caveat for IV adrenaline use by “experts” in quotation marks. Oh is quite pro IV infusions and certainly in the ICU and OT this is ubiquitous and generally well done in my experience. Oh mentions vasopressin, glucagon and even methylene blue as rescue treatments but UK ALS only recommends glucagon for those beta blocked and vaso for those refractory to IV adrenaline. Another interesting point from the UK guidance is an emphasis on lying the patient flat, reflecting the rapid and massive vasodilation that might be enough to precipitate LOC in some. They are clear in that medications such as antihistamines and steroids have no real role in the routine management of anaphylaxis despite their almost ubiquitous use. Finally they quote a 95% survival rate for anaphylaxis associated cardiac arrest and while this may be contaminated by an in hospital OT sample it’s still important to know that these patients are much more likely to have a good outcome than your typical cardiac arrest cohort. References Oh’s Manual 67 RCEM Learning Podcast June 2021 UK Anaphylaxis Guidelines Tasty Morsels of EM 105, August 2017

Welcome back to the tasty morsels of critical care podcast. This week we’ll make a fly by at part of Oh Chapter 100 looking at haemostatic failure. The understanding of the haemostatic system seems a little like the universe at times with our knowledge, and the gaps in our knowledge expanding away from us quicker than can we track. As a result this summary will be necessarily superficial, brief and likely inaccurate. The traditional understanding of haemostasis was centred on circulating coagulation factors, the modern understanding holds that coagulation takes place mostly on the surface of activated or damaged cells. However, I think it still holds true that the core of haemostasis involves vascular constriction, platelet plugging with fibrin clot formation to seal the deal.  I was reared with the idea of two pathways towards clotting in the old fashioned clotting cascade – the intrinsic and the extrinsic pathway. These appear to have been renamed in the interim with the intrinsic pathway (always on the left hand side in the diagrams i can visualise from memory) being renamed the contact activation pathway and the extrinsic pathway (being on the right side of the diagram) now renamed the tissue factor pathway. It seems that most coagulation activation occurs via this latter tissue factor pathway where the protein tissue factor is exposed by tissue injury beginning the process. Platelet plugging (or primary haemostasis) results with subsequent fibrin formation by the action of thrombin on fibrinogen, to complete the process. (secondary haemostasis) Though to say the process is now completed is to neglect the presence of native anticoagulant processes which to be fair are rarely measured. This consists of several types of inhibitory proteins such as protein C and S to give a couple of well known examples. These act as a sort of brakes on the system to ensure everything is held in balance. We have various tests we can apply to the haemostatic system but the more you look into this the more you realise you’re not measuring one thing but the test really reflects the activity of potentially multiple factors and an abnormal result cannot simply be used as a surrogate for any given coagulation factor but instead reflects the blended result of upset of multiple different factors. Platelet number is relatively easy to measure but tells us very little about platelet function which can be affected by things like vWF or the aspirin they took 3 days ago. Platelet function is a little bit of a holy grail that we have not quite nailed down yet. Prothrombin time measures the extrinsic or tissue factor pathway and is most obviously prolonged in people on vitamin K antagonists such as warfarin where it is expressed in the INR. In the critically ill it can also reflect vitamin K deficiency or deficiency of any number of factors in that pathway say from liver dysfunction. You can distinguish between vitamin K dependant causes using an Echis time. This fascinating test involves adding snake venom from Echis carinatus multisquamatus, an Asian viper to a sample of blood. If the prolonged INR is vit k dependant it should normalise, whereas if it is factor deficient it will remain prolonged. The APTT is felt to reflect the intrinsic or contact activation pathway. it is most commonly used for measuring heparin activity (which is a post in itself) but if the APTT is raised in in the absence of heparin then it might reflect factor deficiency (eg one of the thrombophilias) where it should correct to normal with a mixing study where normal plasma is added. A long APTT in the absence of heparin may also reflect the presence of some kind of inhibitor with the commonest example being the lupus anticoagulant. Of course we have the viscoelastic assays which are likely a more functional assay of global haemostasis than our traditional tests but they remain fairly niche in their use in critical care (as opposed to anaesthesia) in Ireland so far. They are due their own post in due course. References Oh’s Manual Chapter 100 Data Interpretation in Critical Care Medicine

Tackling the topic of Abdominal Compartment Syndrome, this episode delves into the prevalence and management strategies, including guidelines from the World Society of Abdominal Compartment Syndrome. From evacuating luminal contents to surgical treatments, the discussion offers valuable insights into this common surgical issue.

Welcome back to the tasty morsels of critical care podcast. Oh dedicates an entire chapter, number 88 to CBRN issues. While not commonly seen you can rest assured that critical care will be expected to turn up and manage these patients if an incident does occur so it is something we need to know fairly well. I will cover the content of chapter 88 here but I will borrow from a lecture I gave at the EuSEM conference back in 2019 when we used to actually go to conferences. Ultimately you’re going to get an edited selection of the available nasty agents. These agents can be damaging, incapacitating or lethal and can come in persistent (liquids, particles etc) and non persistent (eg gases or volatile substances) forms. We can be exposed through a whole variety of routes from inhalation to the skin to ingestion. There is a real risk of health care provider exposure and illness so you need to be sure that you are safe in caring for the patient. When it comes to approaching these I found the CBRN chain of survival to be useful. This was published in 2019 by the Paris fire brigade and is an excellent illustration of the response. There is an image of this in the show notes but to run through it verbally, remembering that these are all meant to be performed pre hospital. spot decontamination – Initial decontamination is wiping with paper roll and disrobing. this is likely to remove 80% of decontamination early toxidrome recognition eg if its organophopshates early antidotes extensive decontamination transport to hospital. In terms of agents there is quite the cornucopia to choose from but we’ll begin with the chemical ones, and nerve agents such as sarin are up first. Sarin acts as an organophosphate resulting in overwhelming cholinergic activity due to inhibition of acetylcholinesterase. The toxidrome here is on the wet side with wet lungs, wet pants and salivation and diarroeah with small pupils and a side course of apnoea. The knee jerk response should be bucket loads (literally) of atropine to dry things up and some pralidoxime to get the breathing going by resurrecting the inhibited AChE, hopefully enough to enable muscular contraction working again. When it comes to biological agents we’re just going to look at anthrax for today. Most famously brought to world attention in the days following 9/11 where packets of white powder where mailed to various parts of the US government, some of which actually contained anthrax. Bacillus anthracis is the bug, a gram+ve rod, usually found in grass eating animals (hence the leather industry exposure) but it is also big in the IDU population in recent years. It causes mainly skin disease in humans but also GI and respiratory disease, usually with <48 hrs incubation period. Cutaneous anthrax is usually painless with a red papule developing into an ulcer with septicaemia in 20%. Animal exposure is the obvious risk here. Inhalation anthrax is more what we are worried about which can present as a flu like illness with cyanosis, sub cutaneous oedema and mediastinal widening from lymph nodes which can cause a haemorrhagic mediastinitis. This is unfortunately fairly non specific so you’ll like diagnose this from a culture off the skin lesion. Person to person airborne transmission does not occur so you don’t need a hazmat suit to manage them. Management is good old fashioned antimicrobials inc cipro, penicillin and clindamycin in combination. Ionising radiation no doubt deserves its own post but to give an ultra summary here. We can get exposed in a few ways eg by radioactive waves such as gamma rays which is what happened to Bruce Banner. This type of radiation can usefully be blocked by something like a big concrete wall. Beta particles are a type of high speed electron emitted by radioactive decay. They penetrate tissue but can be blocked by relatively simple things like wood. If anyone saw the TV series Chernobyl – the extensive skin burns that many of the firefighters received were mainly from beta particles. Alpha particles consist of 2 protons and 2 neutrons bound together. Produced as part of alpha decay of a radioactive substance. They can only pass a a few cm through the air and are easily blocked even by skin and are effectively non toxic unless inhaled or ingested. They are at least 20 times more ionising than gamma or beta. The polonium 210 involved in the murder of Alexander Litvinenko involved alpha particles and the Lancet article on his death is a compelling read. If your patient was exposed to something like pure gamma or X-ray radiation then there’s little role for decontamination as the radiation as passed through them and out the other side. They are no longer radioactive and the damage is done. If however there are concerns for beta or alpha particles involved (Chernobyl is a good example again) then the patients are likely to be covered externally with radioactive dust containing these ongoing radioactive particles and they may well have inhaled or ingested more particles meaning that their blood and secretions likely contain ongoing radioactivity. A geiger counter can help in assessing external exposure to these things. Assessing the dose of radiation to the patient is important prognostically. There’s a couple of ways to do this but if you were to actually remember two things then: how quickly the lymphocyte count drops time to first emesis, the earlier you puke the more likely you’re going to die a dose >5 gray puts you in the high risk for death. References Oh’s Manual 88 Criminal Poisoning Lecture form 2019 Tasty Morsels of EM numbers 87 and 88

Welcome back to the tasty morsels of critical care podcast. It is with trepidation that I approach any topic that involves the negative feedback loops of endocrine control as I really struggle to keep it all straight in my head, but today I’m going to try and cover the basics of calcium in the critically ill from Oh Chapter 63. We’ll start from some very basic physiology. 99% of the calcium is held in the bones. Of the calcium not in the bones, most of the rest is in the cells. So as an important starter, the serum level of calcium does not tell us much about overall levels in the body. In the plasma itself, 50% is ionised, 40% is plasma bound and 10% is chelated to various anions. There is a large gradient between the ionised calcium in the plasma and the tiny ionised fraction in the cells. Finally the ionised fraction is the active bit and the determining factor of endocrine regulation. At a level somewhat below medical student level, calcium is controlled as follows. A low serum Ca stimulates PTH, this in turn stimulates osteoclastic activity and renal reabsorption. It also stimulates renal production of calcitriol (an active metabolite of vitamin D) which encourages gut absorption of calcium. Calcitonin produced by the thyroid acts as a kind of PTH antagonist dampening things down a bit if the calcium level gets too high. Now let’s turn to hypercalcaemia, a fairly common diagnostic issue in the ICU. The major causes to consider are: Malignancy (both from bony mets and probably more commonly from PTHrP that mimics PTH in raising the Ca) High calcium following hypoCalcaemia (eg pancreatitis and recovery from rhabdo) primary hyperPTH granulomatous diseases such as sarcoid Management of high calcium involves 2 mains steps increasing urinary excretion, either with fluids alone or fluids and loop diuretics. Though the addition of loops is somewhat controversial as loops themselves have been known to cause HyperCa. reduction in Ca resorption from bone. This can be done with bisphosphonates working by inhibiting osteoclasts. Or by calcitonin which inhibits osteoclasts and reduces renal reabsorption of calcium. Steroids can be helpful by reducing gut absorption and inhibiting the inflammatory production of calcitriol. Finally on the list is denosumab which as the name suggests is a monoclonal that prevents bone resorption Hypocalcaemia on the other hand produces quite a prolonged differential including citrate (low ionised, high total) massive transfusion (which is just citrate again) high phos sepsis (multiple mechanisms including PTH suppression) thyroid or neck surgery low vitamin D (poor sun exposure, low intake, malabsorption, liver disease, renal failure) drug induced (bisphosphonates, propofol, EDTA, ethylene glycol, protamine, gentamicin) MRI contrast can cause a form of pseudo hypocalcemia  (niche and irrelevant..) Many of the above are associated with alkalosis and indeed a separate differential can be formed for HypoCa in the context of acidosis AKI tumour lysis rhabdomyolysis pancreatitis ethylene glycol hydrofluric acid Management of hypocalcaemia is both straightforward in that you just replace the calcium but at the same time desperately complicated in that you need to treat the cause which is often incredibly challenging. A final mention is warranted of Vitamin D in critical illness given that it has been spread across the literature in recent years and is currently subject to lots of ongoing work. It is thought to have what is best described as “pleiotropic effects”. It is also similar to cortisol in that serum levels probably don’t reflect cellular activity. Either way there is no clear role for it in the ICU as yet. References Oh’s Manual Chapter 63