Tasty Morsels of Critical Care

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.

This episode delves into the complexities of pulmonary hypertension, emphasizing the need to quantify and categorize the condition. The discussion highlights the importance of defining the severity and cause of PH, and categorizing patients into distinct groups for effective management. With a focus on diagnosis and treatment options, the episode provides a detailed overview of PH classification and management strategies in critical care settings.

Exploring the management of hyponatremia in critical care, focusing on the use of hypertonic saline for seizures caused by low sodium levels. The podcast discusses the challenges of administering treatment in emergency situations and the importance of cautious approach to avoid rapid sodium rise.

Explore the risks of osmotic demyelination syndrome with rapid sodium corrections in hyponatremia. Learn about brain adaptability to lower sodium levels and the complexities of diagnosing different types of hyponatremia based on clinical context and osmolality.

The podcast discusses the thyroid gland and its role in causing emergencies. It covers the physiology of thyroid hormones, underactive thyroid, and thyroid storm. It also discusses the diagnosis and treatment of thyroid storm, as well as thyroid emergencies in critical care.

This podcast discusses VV ECMO, a therapy used in intensive care to support patients with compromised lung function. It explores the process of removing blood from the veins, oxygenating it, and returning it, as well as the challenges in drainage and pipe placement. The chapters cover factors to consider, indications for use, and the role of VVECMO in treating hypoxia and struggling right ventricles.

This podcast explores the effects and mechanisms of vasopressin, highlighting its maxed-out effect at low doses and its role as a pure pressor at high doses. They also discuss its potential advantages as a vasopressor in ICU patients, its use in treating septic shock, and the findings of several trials and a meta-analysis.

The podcast explores dynamic LV outflow tract obstruction, a condition that reduces LV outflow and affects blood pressure. They discuss the clinical context and risk factors, as well as the role of echocardiography in diagnosis. They also delve into the clinical presentation and management in sepsis and cardiac surgery patients.