Precision Emergency Medicine & Outcomes by Anand Swaminathan

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Anand Swaminathan brings precision emergency medicine and outcomes in critical care into the light. He will convince you to start calling diseases for what they are and as a result start offering the proper treatments and care. All disease exists on a spectrum. You can’t treat one end of the spectrum the same way you treat the other end. This talk is inspired by a case of Anand’s. An older man who presented to the ED with acute onset shortness of breath and crackles. He was treated with Lasix. More and more Lasix – even though he wasn’t improving. Anand knew this presentation was more than just an exacerbation of heart failure. This was acute pulmonary oedema and this man needed different treatment. Disease is on a spectrum with ‘urgent’ on one end and ‘critical’ on the other. The umbrella term that identifies the disease needs to be spread it out so that it can be placed on this spectrum by you and others around you. Calling a presentation an exacerbation of CHF when it is in fact acute pulmonary oedema is wrong and leads to harm for the patient. We have the medications and treatments for both end of the spectrum. However, they aren’t always used. Too often disease gets miscategorised on the wrong, milder end of the spectrum. Why? First, more patients exist at this end, and we therefore default back to this presentation of the illness. Secondly, there is an inverse relationship between the severity of disease and the research guiding treatment. Therefore, the temptation is to use this research to guide management all along the spectrum. Finally, time and resources are precious. The sicker a patient is, the more of these commodities they use up so err towards an approach for milder disease. To counteract these points Anand wants you to understand the diseases better. How? First, educate yourself and those around you to assess and treat disease properly. Call the disease the right thing and ensure proper allocation of proper and adequate treatment and resources. Secondly, spend more time at the bedside – especially early in your training. This is how you rapidly identify sick patient, and rapidly determine what needs to be done. After this talk Anand hopes you are inspired and can walk into work tomorrow and make a change. Empower each other to act by calling things what they are! For more like this, head to our podcast page. #CodaPodcast

Health & Medicine

This document discusses how humans have evolved mechanisms for coping with critical illness and trauma over thousands of years, as evidenced by survival rates from historical battles and injuries before modern medicine. It notes that minimal organ damage is seen in survivors and non-survivors of critical illness, but the response magnitude varies. Early indicators at 6 hours such as stroke volume can predict outcomes. The signature response is similar in survivors and non-survivors but larger in scale for non-survivors, suggesting predetermination of outcomes and implications for more tailored treatment approaches.

Precision Medicine in Acute Brain Injury

SMACC Conference

Systematic review of 26 studies with 55,792 patients found that dedicated neurocritical care (NCC) was associated with decreased risk of mortality (17% relative risk reduction) and decreased risk of poor functional outcomes (17% relative risk reduction) in critically ill brain-injured adults. A survey of Australian ICUs found limited availability of NCC, with only 4 centers specializing in it and 9 employing an intensivist subspecializing in NCC. Continuous EEG monitoring was found to have higher sensitivity for detecting nonconvulsive seizures than routine EEG monitoring, and was associated with reduced in-hospital mortality, though barriers to its universal use include infrastructure and personnel requirements.

CSD by Jeffcote Coda 22.pdf

SMACC Conference

CORTICAL SPREADING DEPOLARISATION IN NEUROLOGICAL DISEASE – AN INTRODUCTION By Toby Jeffcote Cortical spreading depolarization (CSD) is a spreading loss of ion homeostasis, altered vascular response, change in synaptic architecture, and subsequent depression in electrical activity following an inciting neurological injury. It was first described by Leão in 1944, a disturbance in neuronal electrophysiology has since been demonstrated in a number of animal studies, and recently a few human studies that examine the occurrence of this depolarizing phenomenon in the setting of a variety of pathological states, including migraines, cerebrovascular accidents, epilepsy, intracranial hemorrhages, and traumatic brain injuries. The onset of CSD has been demonstrated experimentally following a disruption in the neuronal environment leading to glutamate-induced toxicity. This initial event leads to pathological changes in the activity of ion channels that maintain membrane potential. Recovery mechanisms such as sodium-potassium pumps that aim to restore homeostasis fail, leading to osmolar shifts of fluid, swelling of the neuron, and ultimately a measurable depression in cortical activity that spreads in the order of millimeters per minute. Equally important is the resulting change in vascular response. In healthy tissue, increased electrical activity is coupled with release of vasodilatory factors such as nitric oxide and arachidonic acid metabolites that increase local blood flow to meet increased energy expenditure. In damaged tissue, not only is the restorative vascular response lacking but a vasoconstrictive response is promoted and the ischemia that follows adds to the severity of the initial injury. Tissue threatened by this ischemic response is then at elevated risk for CSD propagation and falls into a vicious cycle of electrical and hemodynamic disturbance. Efforts have been made to halt this spreading cortical depression using N-methyl-D-aspartate receptor antagonists and other ion channel blockers to minimize the damaging effects of CSD that can persist long after the triggering insult.

Subdural Haemorrhage and MMA embolisation

SMACC Conference

Andy Neill - More neuroanatomy pearls for neurocritical care

SMACC Conference

The BONANZA Trial and PbTO2 Monitoring

SMACC Conference

Andrew Udy talks about Brain Tissue Oxygen Monitoring: It’s Not What You’ve Got It’s What You Do With It The BONANZA Trial Andrew Udy talks about the ongoing BONANZA Trial which is assessing whether an algorithm that incorporates both ICP and brain tissue oxygen (PbTO2) can improve outcomes after traumatic brain injury (TBI). Like with all monitoring, how the PbTO2 is interpreted and managed is critical and the devil is in the detail! More on BONANZA here More on BOOST3 here

Dilating the Dogma of Vasospasm

SMACC Conference

R. Loch Macdonald, M.D., Ph.D. Community Neurosciences Institute Fresno, California, USA Angiographic vasospasm and more accurately, delayed cerebral ischemia, continue to contribute to morbidity and mortality in patients with aneurysmal subarachnoid hemorrhage (SAH). It is known that angiographic vasospasm is common after SAH, occurring in two-thirds of patients. Cerebral infarctions that developed days after the SAH have been attributed to angiographic vasospasm, occuring in about a third of patients, although this has always been controversial. Angiographic vasospasm theoretically can only damage the brain by restricting blood flow but there is no easy, accurate, widely available method to measure cerebral blood flow and this is not the measurement we need. Blood flow depends on metabolic demand so what we need to know to determine if angiographic vasospasm is causing ischemia is oxygen extraction fraction in the brain tissue supplied the the spastic artery. Without this measurement, the attribution of ischemia to vasospasm is subjective. Since angiographic vasospasm is essentially the only detectable delayed phenomenon after SAH, we focus on it and apply tremendous resources to preventing or reversing the vasospasm. Undoubtedly angiographic vasospasm can cause cerebral infarctions, but it has to be severe and flow limiting. But SAH is a complex disease. There are many other causes for cerebral infarctions after SAH, the most common being due to the aneurysm repair procedure. And a given degree of vasospasm may cause infarction in a volume-depleted patient with poor collateral blood supply but not in a patient without these things. There also are hypodense brain lesions after SAH that are due to intracerebral hemorrhages. There can be hypodensities in the brain directly under usually thick SAH where the brain dies. This observation in particular supports a role for cortical spreading depolarizations/ischemia as a cause of infarction after SAH. Other macromolecular processes that are hypothesized to cause brain damage after SAH include microthromboembolism, changes in the microcirculation, delayed brain cell apoptosis and capillary transit time heterogeneity. Determining the importance of these things is hindered by the lack of an easy way to detect them in patients. It is also known that poor grade patients, who presumably have more early brain injury and ischemia than good grade patients, are more prone to delayed cerebral ischemia, suggesting increased sensitivity to secondary insults of the already injured brain. We also assume delayed neurological deterioration when attributed to vasospasm or delayed cerebral ischemia, is purely due to ischemia. While knowledge about what happens pathophysiologically after SAH is increasing, management of delayed cerebral ischemia still focuses on detecting angiographic vasospasm and then augmenting the blood pressure to improve cerebral blood flow or dilating the spastic arteries with balloons or drugs.

EVD Tips and Tricks

SMACC Conference

Part 2 of a debate over the classification of TBI. Andrew Udy then argues that this classification is fundamentally flawed. He discusses the issues with the Glasgow Coma Scale, and therefore the follow-on issues in TBI classification, including all the confounders to the GCS, the issues with timing of the score as well as GCS not taking baseline function or specifics subtypes of TBI into account. He makes teh argument that biomarkers may better categorise the diffuse entity we call TBI.

TBI Debate - Mild, moderate and severe categories work

SMACC Conference

Andrew Chow, Intensivist with a neurosurgical background, argues that the current categorisation system for traumatic brain injury (TBI) works, and makes sense! He tackles us through the history of this system, and why it’s important to differentiate different types of TBI. The arguments in favour of this categorisation include the consistency and benefits of a universal language, the implications for triage and management, and the fact that this system has been endorsed by all major organisations

TBI: when to stop and when to give time

SMACC Conference

Dr Nick Little is an experienced Neurosurgeon who's looked after patients with traumatic brain injury for his whole career. Here he discusses the difficulties of prognostication following traumatic brain injury (TBI). He talks about the statistics of outcomes following mild, moderate and severe TBI and then goes on to tackle the harder topic of how we try to work out what an individual would want if they knew the spectrum of outcomes that they may face. The issues with the clinical examination findings we use to prognosticate are covered, as well as which imaging findings he finds most helpful. He also mentions the difficulties with current prognostic calculators.

Ketamine in Brain Injury by Toby Jeffcote

SMACC Conference

Historically, when it came to brain injury, ketamine had a bad rap. Much of that dogma was dispelled in the last decade, and ketamine is now frequently used as an induction agent in acute brain injury, especially traumatic brain injury, due to it’s favorable effects on haemodynamics. However a new application of ketamine is now being explored - whether ketamine may be able to reduce secondary brain injury.

Managing Complications of Chronic SCI by Bonne Lee

SMACC Conference

20 million people around the world are living with a spinal cord injury (SCI). The medical issues they develop over the years differ to any other patient cohort. These complications include autonomic dysreflexia, management of pressure areas, specific infections, nuanced peri-operative care and highly specific issues such as baclofen pump management and syringomyelia Do look at the NeuroResus section on this and listen to Spinal Rehab Specialist Bonne Lee talk about this side of SCI care. Keywords SCI, spinal, spinal cord injury, autonomic dysreflexia, pressure areas, infection, peri-operative care, baclofen pump, syringomyelia, chronic SCI, spinal trauma, spinal rehab, incomplete SCI

EEG and Status Eplilepticus by Tania Farrar

SMACC Conference

Tania is a neurologist and epileptologist with expertise in continuous EEG (cEEG) and status epilepticus (SE). This talk covers what a seizure is, what status is, including focal and generalised status epilepticus. So why do we do cEEGs for patients with suspected SE? To confirm the diagnosis To see if patient just post ictal or still seizing To establish that the clinical and electric seizures have stopped To see if burst suppression is achieved To exclude other differential diagnoses She makes a good argument for why cEEG is such an important tool in managing SE. In the questions after the talk, the issue of availability of cEEG in the Australian setting was discussed. Limited montage EEGs are discussed including their pros and cons.

Browne Neuro symposium.pptx

SMACC Conference

Stuart Browne is a Neuro Rehab specialist from Sydney. These slides accompany a talk he gave at the Brian Symposium in 2023. He discusses what "severe disability" really means. Severe disability is more common than many realise - about 6% of the Australian population. Stuart discusses how health is more than simply physical recovery and how it is a multidimensional construct. He covers how permanent disability doesn't necessarily equate to a poor quality of life. He also discusses the long timespan of recovery, which is often much longer than appreciated. He specifically discusses "Locked-in Syndrome" and how the survivors have surprisingly positive self-reported health-related quality of life and well-being. Stuart also covers how severely disabled people face various forms of discrimination.

Paediatric Stroke by Shree Basu

SMACC Conference

Hypertensing Spinal Cord Injury - gold standard or wacky?

SMACC Conference

This document discusses the concept of maintaining higher blood pressure levels, known as hypertension, after a spinal cord injury to improve spinal cord perfusion pressure and reduce secondary injury. It notes that while animal studies and some human trials have shown improved neurological outcomes, the evidence is still limited. It calls for larger randomized controlled trials in humans that also incorporate multi-modal monitoring and standardized outcome measures to further evaluate if inducing hypertension after spinal cord injury should be considered the gold standard of care.

Optimal Cerebral Perfusion Pressure

SMACC Conference

Mark Weedon takes us through the increasingly utilised concept of an optimal cerebral perfusion pressure (CPPopt) for each unique patient. He discusses the background to CPPopt, including intrcranial pressure (ICP), the Monroe Kelly hypothesis, neurovascular coupling, and cerebral autoregulation in health and following brain injury. He shows how intracranial pressure is affected by intracranial compliance and how this affects ICP waveforms. Cerebral perfusion pressure in relation to the Brain Trauma Foundation guidelines is covered including management of elevated ICP (EICP). The currently recommended tiered approach to managing cerebral perfusion pressure and EICP is mentioned citing recent guidelines. He uses a clinical case of a TBI to illustrate how the CPPopt can be ascertained and used to guide therapy, including the easy to perform “MAP Challenge”. Mark also describes the Pressure Reactivity Index (PRx) and how it can be used as a target for therapy. Finally, he covers the exciting results of the preliminary COGiTATE pilot study.

The Power of Words - Death and Language.ppt

SMACC Conference

Sepsis and Antimicrobial Stewardship - Two Sides of the Same Coin

SMACC Conference

Undertreatment of sepsis can lead to mortality, while overdiagnosis and overtreatment can increase future risk of antimicrobial resistance. Antimicrobial stewardship aims to balance these risks by prioritizing patient safety and appropriate antimicrobial use. Data shows variability in appropriateness of antimicrobial prescribing between different types of hospitals. Embedding antimicrobial stewardship principles throughout sepsis diagnosis and treatment, from initial microbiology testing to post-treatment review, can help standardize care and optimize outcomes.

Brain injury outcomes and predictors

SMACC Conference

Being able to prognosticate in the aftermath of a traumatic brain injury (TBI) is important as it assists with counselling patients and families. Moreover, it helps rationally allocate healthcare resources. However, due to the heterogenous nature of TBI and variable pre brain injury patient factors and post brain injury course, this has proven to be a difficult task. Large cohort studies have enabled improved accuracy in the prediction of 6 month mortality and unfavourable outcome. Furthermore, many of the factors that contribute to long-term outcome have also emerged. However, it is not yet possible to use them in prediction algorithms or mathematical models. There is emerging evidence that pre injury psychosocial and demographic factors may be of more relevance than injury severity. Moreover, that 'outcome' becomes increasingly subjective and complex as the post injury duration increases. We end with three brief vignettes which highlight the fraught nature of long term outcome prediction.

The importance of communication in pain management

SMACC Conference

In this podcast, Claire discusses the role of clinician communication and its impact on acute pain management. Claire explains how pain management outcomes can be optimised by enhancing patient expectations of benefit via patient-provider communication. Firstly, what we say to patients matters. Secondly, how we say it also matters. Pain is a complex phenomenon and managing expectations of pain and people’s experience of empathy is crucial. As healthcare professionals, we see multiple patients and are often run off our feet, but, as the studies clearly demonstrate… communication matters. And it matters a lot in pain management. This presentation shares research demonstrating the impact of clinician communication. Specifically, this includes how clinicians' talk about pain and pain management. Claire discusses the importance of patients' experience of pain, the effectiveness of pain management and patients' treatment outcomes. From CodaZero Live, tune in to a fascinating discussion on the importance of communication. For more like this, head to https://codachange.org/podcasts/

Brain Death History

SMACC Conference

Blood Gas Interpretation

SMACC Conference

The document provides an overview of analyzing blood gases, including how to assess oxygenation, pH, respiratory and metabolic components, and compensation. Key points discussed include how to evaluate PaO2, A-a gradient, and P:F ratio; what normal pH values indicate; how PaCO2 and HCO3 relate to respiratory and metabolic disorders; how to identify a metabolic component using HCO3 and pH; and factors involved in compensation between acute and chronic conditions. Formulas are given for expected HCO3 changes based on CO2 levels and the delta ratio range in different conditions. Example blood gas results are analyzed in detail.

Timing, Tribes and STEMI's

SMACC Conference

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SMACC Conference

SMACCForce: LIVE EMS Nation Podcast - "Feeding the Flame"

SMACC Conference

Violence against healthcare workers - Paramedics under siege

SMACC Conference

Acts of violence against paramedics is disgraceful but not doing anything about it is much worse. From DAS SMACC, Craig Wylie speaks to us about violence against paramedics in South Africa. In the four years leading up to this talk in 2017, there were 250 attacks against paramedics. In a neighbourhood where there can be up to 100 gunshots in three hours, this almost shouldn’t be surprising. Craig tells a story where he was called out to an emergency where his colleagues were under attack. His first thought? Why didn’t they get a police escort? But in a low to middle income country, it is rarely that straightforward. Where there is a high crime rate and may only be two police vehicles on duty, it isn’t always as easy as waiting for a police escort. Additionally, if paramedics had to rely on police attending their emergencies, is this just introducing another barrier to care? Craig asks three simple questions: 1. Has our management failed our staff members? 2. Have we done enough that the paramedics that we employ can protect themselves? 3. Have we as an EMS system entirely lost the plot towards our paramedics and how we respond to patient emergencies? The solution? Craig suggests it is all in the training. Paramedics need to be trained to understand the situations, to have a strong action plan, to have an exit plan and to involve community leaders. The team need to be trained to understand how to protect themselves so that they can provide care, whilst also looking out for themselves. Tune into a talk from DAS SMACC on Violence against healthcare workers - Paramedics under siege. For more like this, head to our podcast page. #CodaPodcast

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8 Surprising Reasons To Meditate 40 Minutes A Day That Can Change Your Life.pptx

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We’re talking about Vedic Meditation, a form of meditation that has been around for at least 5,000 years. Back then, the people who lived in the Indus Valley, now known as India and Pakistan, practised meditation as a fundamental part of daily life. This knowledge that has given us yoga and Ayurveda, was known as Veda, hence the name Vedic. And though there are some written records, the practice has been passed down verbally from generation to generation.

Cell Therapy Expansion and Challenges in Autoimmune Disease

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There is increasing confidence that cell therapies will soon play a role in the treatment of autoimmune disorders, but the extent of this impact remains to be seen. Early readouts on autologous CAR-Ts in lupus are encouraging, but manufacturing and cost limitations are likely to restrict access to highly refractory patients. Allogeneic CAR-Ts have the potential to broaden access to earlier lines of treatment due to their inherent cost benefits, however they will need to demonstrate comparable or improved efficacy to established modalities. In addition to infrastructure and capacity constraints, CAR-Ts face a very different risk-benefit dynamic in autoimmune compared to oncology, highlighting the need for tolerable therapies with low adverse event risk. CAR-NK and Treg-based therapies are also being developed in certain autoimmune disorders and may demonstrate favorable safety profiles. Several novel non-cell therapies such as bispecific antibodies, nanobodies, and RNAi drugs, may also offer future alternative competitive solutions with variable value propositions. Widespread adoption of cell therapies will not only require strong efficacy and safety data, but also adapted pricing and access strategies. At oncology-based price points, CAR-Ts are unlikely to achieve broad market access in autoimmune disorders, with eligible patient populations that are potentially orders of magnitude greater than the number of currently addressable cancer patients. Developers have made strides towards reducing cell therapy COGS while improving manufacturing efficiency, but payors will inevitably restrict access until more sustainable pricing is achieved. Despite these headwinds, industry leaders and investors remain confident that cell therapies are poised to address significant unmet need in patients suffering from autoimmune disorders. However, the extent of this impact on the treatment landscape remains to be seen, as the industry rapidly approaches an inflection point.

ABDOMINAL TRAUMA in pediatrics part one.

drhasanrajab

Abdominal trauma in pediatrics refers to injuries or damage to the abdominal organs in children. It can occur due to various causes such as falls, motor vehicle accidents, sports-related injuries, and physical abuse. Children are more vulnerable to abdominal trauma due to their unique anatomical and physiological characteristics. Signs and symptoms include abdominal pain, tenderness, distension, vomiting, and signs of shock. Diagnosis involves physical examination, imaging studies, and laboratory tests. Management depends on the severity and may involve conservative treatment or surgical intervention. Prevention is crucial in reducing the incidence of abdominal trauma in children.

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The Electrocardiogram - Physiologic Principles

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These lecture slides, by Dr Sidra Arshad, offer a quick overview of the physiological basis of a normal electrocardiogram. Learning objectives: 1. Define an electrocardiogram (ECG) and electrocardiography 2. Describe how dipoles generated by the heart produce the waveforms of the ECG 3. Describe the components of a normal electrocardiogram of a typical bipolar lead (limb II) 4. Differentiate between intervals and segments 5. Enlist some common indications for obtaining an ECG 6. Describe the flow of current around the heart during the cardiac cycle 7. Discuss the placement and polarity of the leads of electrocardiograph 8. Describe the normal electrocardiograms recorded from the limb leads and explain the physiological basis of the different records that are obtained 9. Define mean electrical vector (axis) of the heart and give the normal range 10. Define the mean QRS vector 11. Describe the axes of leads (hexagonal reference system) 12. Comprehend the vectorial analysis of the normal ECG 13. Determine the mean electrical axis of the ventricular QRS and appreciate the mean axis deviation 14. Explain the concepts of current of injury, J point, and their significance Study Resources: 1. Chapter 11, Guyton and Hall Textbook of Medical Physiology, 14th edition 2. Chapter 9, Human Physiology - From Cells to Systems, Lauralee Sherwood, 9th edition 3. Chapter 29, Ganong’s Review of Medical Physiology, 26th edition 4. Electrocardiogram, StatPearls - https://www.ncbi.nlm.nih.gov/books/NBK549803/ 5. ECG in Medical Practice by ABM Abdullah, 4th edition 6. Chapter 3, Cardiology Explained, https://www.ncbi.nlm.nih.gov/books/NBK2214/ 7. ECG Basics, http://www.nataliescasebook.com/tag/e-c-g-basics

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