Hinds: More Cases from the Races

Oct 6, 2015Download as PPTX, PDF0 likes7,884 views

John Hinds gives his last talk - on the subject he was most passionate about. Back with popular demand, More Cases from the Races.

Mechanism matters.
Speed mostly ��Ǳ��’t.

Traumatic cardiac arrest:
A tale of two frenchmen

Dr Grace Leo shares her cornerstones for developing a powerful presentation: passion, purpose and practice. This workshop talk from the social media and critical care conference 2014 also includes some of her tips and strategies to turn an average presentation into one with style. This slide deck is best viewed in conjunction with audio which can be found at www.intensivecarenetwork.com/leo-powerful-presentation

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Dr Victoria Brazil discusses the Dunning-Kruger Effect, Imposter Syndrome and quality improvement. Vic starts the podcast reminiscing about her initial days as a resuscitationist. She talks about the two psychological phenomena noticed in people working in pre-hospital care. The Dunning-Kruger effect, where people tend to think they are better at a job than they are, and imposter syndrome, where people tend to think they are worse than they are at doing a particular job. People's perception of their performance can impact their chances of improvement. She suggests scientific methods to reduce this gap in perception. Resuscitation quality improvement (RQI) is a machine-based assessment method to improve the quality of chest compressions that helps doctors and nurses assess and improve their chest compression skills. An example is a person trying to intubate a patient while wearing a camera. This highlights how different his perception is of what he is doing. According to Vic, an important tool to improvement and reduce the gap in perception is feedback between the person in the field and the consultant. This is because according to Dunning, though we do not assess ourselves correctly, we are good at assessing others. For the feedback loop to be effective it is essential to follow three basic rules. Firstly, be honest. Secondly, do it often and thirdly be good at extracting feedback. Vic suggests that everyone should start practising giving feedback by assessing speakers. She suggests that rather than giving vague comments like “Good talk mate”, people should make an effort to give speaker specific comments about the talk. This could include what they liked and what could be improved. Vic demonstrates live feedback of her 47-year-old self giving her younger self, Registrar Vic, some feedback with help from the audience. Through this act she shows how to give effective feedback and how to extract good feedback. For more like this, head to our podcast page. #CodaPodcast

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Tor Ercleve's slides from his smaccGOLD workshop talk on Resuscitating Art - diving into the world of infographics, symphonies and battle planning. You'll leave this talk refreshed and inspired to reinvent the way you communicate information as a health care professional. The talk was recorded at the smaccGOLD Get Creative Workshop and is available at www.intensivecarenetwork.com/tor-ercleve-resuscitating-art

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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.pdfSMACC Conference

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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.

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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

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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.

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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.

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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.

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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.

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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 FarrarSMACC Conference

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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.pptxSMACC Conference

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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.

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Hypertensing Spinal Cord Injury - gold standard or wacky?SMACC Conference

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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 PressureSMACC Conference

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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.

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Sepsis and Antimicrobial Stewardship - Two Sides of the Same CoinSMACC Conference

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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 predictorsSMACC Conference

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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 managementSMACC Conference

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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 HistorySMACC Conference

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Blood Gas InterpretationSMACC Conference

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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.

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The shoulder complex acts as in coordinated fashion to provide the smoothest and greatest range of motion possible of the upper limb. Combined motion of GH and ST joint of shoulder complex helps in: Distribution of motion between other two joints. Maintenance of glenoid fossa in optimal position. Maintenance of good length tension Although some amount of glenohumeral motion may occur while the other shoulder articulations remain stabilized, movement of the humerus more commonly involves some movement at all three shoulder joints.

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