I published 3 tutorials on Local Anesthetics this Month. These are part of a new series of Anesthesiology Tutorials.
Tutorial 1 looks at the basic pharmacology of local anesthetics
Tutorial 2 looks at the various different drugs that we use, the volume and concentration. I discuss the maximum safe doses at the end of the tutorial.
Tutorial 3 looks at the history of, the diagnosis of and the treatment of Local Anesthetic Systemic Toxicity (LAST)
This is a longer version of the lecture that I delivered at the 2025 College of Anaesthesiologists of Ireland Annual Scientific Meeting.
This tutorial, from the Introduction to Critical Care Series, looks at perioperative anaphylaxis. It covers topics that are relevant to practitioners in the OR, ICU, ED and wards.
This HI-Impact tutorial looks at the common questions relating to commencement and route of nutrition in critical care. Is TPN good, bad or indifferent. Is enteral feed better than parenteral? When should we start feeding? Is it useful to add parenteral feed to enteral if the patients’ caloric goals have not been met? When should patients achieve their isocaloric goals. I guarantee you’ll learn something.
This is a trio or tutorials on Acute Myocardial Ischemia, Acute Coronary Syndromes and Cardiogenic Shock.
This is the second tutorial in the nutrition series. Previously I looked at metabolism in critical illness. In this tutorial I start to answer many of the questions that arise on rounds principally: how many calories does the patient need? How much protein? What are the routes of food administration? Is there a benefit to post pyloric feeding tubes? Should I feed the stomach continuously or by bolus? Should I check gastric residual volumes? I provide you with the answers to these questions using the best available evidence.
Patients who spend significant time in critical care may lose a staggering amount of weight, particularly lean body mass. In early critical illness glucose is used as the principle energy source in the stress response; glycogen is rapidly exhausted and glycogenic amino acids are mobilized from muscular protein to generate glucose via gluconeogenesis, to maintain plasma glucose levels to feed, principally red blood cells. This has a major impact on muscle mass and in particular muscular strength, that may take years, perhaps a decade to restore. The most effective mechanism of preventing the development of critical illness cachexia is to curtail the duration of the stress response, by rapid source control, deresuscitation and early mobilization. In general, patients should be receiving full nutrition and be mobilized by day 8 following injury.
This tutorial looks at the devastating problem that is neurogenic shock. A young male is involved in a motor vehicle crash. He cannot move his legs at the scene. Not long after arrival to the emergency room he becomes hypotensive and bradycardic. This tutorial looks at the mechanisms behind spinal cord injury, the pathophysiology and the management. Neurogenic shock involves disruption of the autonomic nervous system. It manifests as vasoplegia, and is treated, once the patient has been adequately resuscitated, with norepinephrine. Injuries above the T4 spinal level may also be associated with bradycardia, due to loss of the cardiac accelerator nerves. In that situation, chronotropic agents may also be required (epinephrine, dopamine etc). Neurogenic shock usually resolves over a 72 hour period but may persist for weeks and months as autonomic dysreflexia.
In November 2024 six tourists died of suspected Methanol Poisoning in Laos, and several more were hospitalized. Methanol, or methyl alcohol, is an industrial chemical used to thin paints, as a precursor for medley chemicals and for fuel cells. It is passed off as “vodka” (odorless, tasteless, clear) to unsuspecting victims.
Methanol is metaboized by the same pathways as ethanol, but to formaldehyde and formate. Although small amounts of methanol may be found in the body, due to gut bacterial fermentation, methanol poisoning is a life threatening problem. Formate causes a widened anion gap metabolic acidosis, blindness, brain damage and interferes with mitochondrial function resulting in cytotoxic hypoxia.
The treatment for methanol poisoning is fomipazole given 12 hourly intravenously, folate, intravenous fluids and, if necessary, renal replacement therapy. Fomipazole competitively antagonizes the metabolism of methanol by the enzyme alcohol dehyrogenase. If fomipazole is unavailable, ethanol can be given as an emergency measure, intravenously or orally.
ORtoICU 