The Risks of Surgery: John Carlisle

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SMACC Conference

John Carlisle asks the big question – what is the risk of surgery? It is a big question that holds implications for everyone involved in caring for patients. Like John, patients want to live a long and happy life. They would like to know whether the chances of living a long and happy life are enhanced by having surgery or not. They do not generally care whether they will be alive in 30 days or not. John explored whether or not we can accurately answer the question – what are the risks of a given surgery? Prognostic models based on a single surgical cohort are very vulnerable to chance and variation. This is even the case with large cohorts. The reason is that mortality is not that common. Therefore, the range of uncertainty in any one model is big. John explores this concept in the context of surgical intervention for abdominal aortic aneurysms. He highlights the perils prognosticating by describing the trials that influences the treatment guidelines for abdominal aortic aneurysms. John describes the current data, and the flaws in the recommendations currently being offered. John then describes a tool he has developed relating to this particular question. The tool also explains how one piece of research has been misunderstood, a misunderstanding that has resulted in two general mistakes: surgeons operating on aneurysms when they should not; surgeons not operating on aneurysms when they should. For more like this, head to our podcast page. #CodaPodcast

Health & Medicine

SURGERYWhat’s the risk?

AAA
Don’t operate unless > 55 mm

UK Small Aneurysm Trial (1993): 46 mm

UK Small Aneurysm Trial (1993): 46 mm

UK Small Aneurysm Trial (1993): 46 mm

UK Small Aneurysm Trial (1993): 46 mm
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Operate if > 46 mm?

UK Small Aneurysm Trial (1993): 46 mm
initial monthly mortality 0.40%
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UK Small Aneurysm Trial (2016): 46 mm
initial monthly mortality 0.20%

UK Small Aneurysm Trial (2016): 46 mm
initial monthly mortality 0.20%
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Operate if > 41 mm?

AAA size, mortality hazard & survival
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AAA size, mortality hazard & survival

AAA size, mortality hazard & survival
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Operate if > your MLE threshold?

SURGERYWhat’s the risk?

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Stephen Bernard shares his thoughts and the current evidence for using oxygen for cardiac arrest patients. Oxygen is ubiquitous in society! You can buy it in bottles and there are even oxygen cafes. This is especially true in hospitals where oxygen is used frequently and often without much thought. Oxygen is a natural substance. So surely, a short time on 100% oxygen can’t be harmful, right? Stephen wants to challenge that idea. In this talk he presents the data on why oxygen might be harmful to your patients, particularly following a cardiac arrest. Out-of-hospital cardiac arrest (OHCA) is common and carries a high mortality rate. In Victoria, Australia, approximately 50% of patients with an initial cardiac rhythm of VF achieve a return of spontaneous circulation (ROSC) and 30% overall survive to hospital discharge. The outcome for patients is improving. This is due mainly to faster ambulance response times and increased rates of bystander CPR. What is done in the hospital has altered the patient’s outcomes in the same way. Currently, OHCA patients who have achieved ROSC but who remain unconscious routinely receive 100% oxygen for several hours in the ambulance, ED, cardiac catheterisation laboratory until admission to ICU. However, there is now evidence from laboratory studies and preliminary observational clinical studies that the administration of 100% oxygen during the first few hours following resuscitation may increase both cardiac and neurological injury. Clinical trials are underway to test whether titrated oxygen to a target oxygen saturation of 90-94% in the immediate hours after ROSC results in improved outcomes compared with 100% oxygen. Join Stephen as he makes you think twice about blindly using oxygen for patients following a cardiac arrest.

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Ah, but you don't look like a professor! A recent statement from a (female) patient says it all, doesn't it? Since the first women were admitted to medical schools – quite a while ago in most countries, the participation of women in clinical and academic medicine has increased steadily. Overall, women represent the majority of health care workers and also medical students in most countries of the world today. SMACC audience is almost 50% female. However, only few women make it to the top, and with each step up the career ladder, the proportion of women decreases substantially, a phenomenon called the “glass ceiling” or the „leaky pipeline“. This is particularly true for some medical specialties such as critical care or trauma surgery, as opposed to specialties like endocrinology, pediatrics or gynecology. Although often subtle, gender discrimination against women continues to be a problem – for instance, it has been shown that a ficticious student named “John” would receive a higher salary and find a mentor easier than “Jennifer”. A manuscript written by “John” is judged more favourably than one that is authored by “Joan”, and female grant applicants with the same scientific productivity are given substantially lower scores than male applicants by reviewers (men and women). Sheryl Sandberg’s statements are as true in clinical and academic medicine as in other areas. This talk will definitely raise your awareness for the topic.

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The application of ‘CPR-for-all’ is the ultimate evidence drift. A treatment that is completely appropriate for dropping dead whilst running a marathon has almost no place in acute healthcare facilities where chronic irreversible complex co-morbidities abound. 90% of doctors would not choose CPR for themselves, yet 100% are trained in how to administer it to patients. Defaulting to ‘CPR-for-all’ removes a patients’ ability to provide informed consent for assault whilst they die from another disease. Remember - 2 weeks in ICU can spare you 5 minutes of difficult conversation. vs. Across the globe, patients are assumed to be full code to allow for prompt resuscitation, until code status can be discussed and clarified. There are numerous excellent reasons for this. Can you imagine if our systems decreed that DNR was the default? “Let’s not shock that VF, until we can clarify his code status.” Or, “let’s not resuscitate that child, after all, DNR is the default and her mother isn’t here yet!” Making DNR the default is not a good solution to ICU or hospital over-crowding. Let’s not mandate DNR, let’s mandate having reasonable code discussions early and often.

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SMACC Conference

Scott Weingart discusses post-intubation sedation – a topic that tends to aggrieve him on a regular basis. Scott explains in simple terms why he is bemused at the lack of understanding surrounding intubated patients who become agitated or aggressive. How would you like a piece of plastic placed down your throat? The problem, as Scott explains, is that sedation does not blunt pain. Sedation without analgesia leads to delirium. In simple terms delirium leads to poor outcomes and death. Moreover, concerningly, the early sedation strategy of intubated patients has long term and far-reaching outcomes during their course of critical illness. So, what can be done? Scott explains that we need patients properly sedated, however not too deeply sedated. The goal needs to be a patient who is oriented, safe and with a normal sleep-wake cycle. Paralysis is not the answer. What is the answer? Scott walks you through A1 sedation – meaning analgesia first. Once pain is controlled, then sedation comes in to play. Scott stresses with analgesia first, the sedation needed is less. He explains how he achieves this in practice in detail. He then provides some clinical examples and how he would approach them including which specific medications he uses in practice. Scott’s main points are simple. Control the pain and very few patients will need a lot of sedation. In addition, if you adequately control the pain, very few patients will have delirium in the Emergency Department. Join Scott as he passionately discusses post-intubation sedation. For more like this, head to our podcast page. #CodaPodcast

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Haney Mallemat discusses the treatment for PEA cardiac arrest. Patients who present with pulseless electrical activity (PEA) arrest have a high mortality. The treatment of PEA requires finding and reversing the underlying cause; therefore a simple and rapid approach is required. Traditionally we were taught to use the H’s and the T’s, but this diagnostic tool is cumbersome and of questionable utility overall. Haney discusses the problems with the traditional H’s and T’s as well as focusing on newer approaches to PEA arrest. Haney makes the point that PEA is not a diagnosis, but a ‘waste basket term’ for a lot of possible diagnoses. Rather than assisting a clinician in the assessment and treatment of a patient, it acts on to lead to pontification. To that end, Haney wants us to do away with the H’s and T’s. The problem with the algorithm of diagnosing a PEA, as Haney explains, is the reliance on feeling a pulse. It lacks sensitivity and specificity, largely linked to using fingers. They should not be used in resuscitation scenarios – as the guidelines say we should. Haney makes the point that despite all the advances in medicine, resuscitation has stayed essentially the same for decades. He describes two ways in which he thinks we can advance our care. The first involves the QRS complex. Ask the question – is the QRS complex narrow or wide. Narrow (< 0.12 seconds) leads you to consider mechanical problems, such as tension pneumothorax or tamponade. If it is wide (> 0.12 seconds), then consider metabolic problems such as hypokalaemia. If the QRS is narrow, and you are thinking a mechanical problem then there is electrical activity, and the heart is still beating underneath. The step should be to use ultrasound immediately to find the focused cause. If it is wide, and you are considering metabolic causes, this is more aligned with a true PEA. Calcium bicarbonate should be considered in the first instance. Haney describes the limitations with the algorithm that includes the trauma patient or those with underlying cardiac conditions. Next Haney describes a second algorithm - PREM (pulseless with rhythm and echo motion) and PRES (pulseless with a rhythm and echo standstill). The use of ultrasound is central to this pathway. In PREM the left ventricle is not strong enough to produce a pulse. Does this patient get adrenaline or chest compressions? Haney discusses the options. In PRES there is electrical activity, but the heart is not squeezing. Maybe these people should get adrenaline and compressions! The ECG should still play a part in this algorithm. Haney puts it all together for you and takes you through the algorithm he uses when faced with a patient with PEA. He includes some tips for using the ultrasound probe during cardiac arrest resuscitation scenarios. A Revised Algorithm for PEA Cardiac Arrest: Haney Mallemat For more like this, head to our podcast page. #CodaPodcast

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In sub-Saharan Africa, where infectious diseases and nutritional deficiencies are common, severe anaemia is a common cause of paediatric hospital admission, yet the evidence to support current treatment recommendations is limited. The TRansfusion and TReatment of severe Anaemia in African Children: (TRACT ISRCTN84086586) is a 3x2x2 factorial controlled trial involving 3954 children (aged 2m to 12y) with severe anaemia (haemoglobin <6g /><4g /><6g/dl if accompanied by complications)); and how volume to transfuse in each transfusion event?. Q3 and 4: Since the major factors related to poor longer term outcome are micronutrient deficiencies and sepsis would post-discharge multi-vitamin multi-mineral supplementation versus routine care (folate and iron) for 3 months and/or cotrimoxazole prophylaxis for 3 months versus no prophylaxis improve outcome and prevent relapse. Primary outcome is cumulative mortality to 4 weeks for the transfusion strategy comparisons, and to 6 months for the nutritional support/antibiotic prophylaxis comparisons.

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Maxime Valois and John Christian Fox argue the role of POCUS in critical care. Maxime makes the case for POCUS being a problem. POCUS changes everything. It has helped physicians throughout the world to make easier, more accurate and faster diagnoses. It has contributed to enhance the diagnostic possibilities in resource-scarce environments However, as it gains more widespread acceptance, its use is becoming more and more common. Maxime contests that this poses a problem. No longer is ultrasound only in the domain of specialists and technology-eager early adopters of the technology. He proposes that this will lead to difficulties as non-specialists take up the technology. Maxime warns against being hypnotised against the seductive nature of ultrasound. Research and use of fancier, new or more advanced applications are likely to help the global advancement of POCUS and even medicine in general. But as POCUS enters fully in its stage of normal science, this will inevitably induce some degree of scientific esotericism. This has been the case of all past scientific revolutions. Point-of-care ultrasound is already generating some important difficulties. If these go unattended, Maxime believe POCUS itself might rapidly be a problem. John on the other hand claims in no way is POCUS a problem. It is maybe only a problem for the radiologist holding down their turf in a small hospital that has been shielded from the world wide web. John argues that POCUS is changing the way medicine is practiced for the better. John makes the point that ultrasound makes the clinician better, faster, and stronger. It does so without exposing patient to harmful radiation. Furthermore, John contends that POCUS enables the physician to bridge the gap between patient and doctor in increasingly complex healthcare system. It allows him to spend more time at the bedside and in doing so deliver better care for his patients. John makes his point with a range of clinical situations, driving his point home that POCUS certainly has a place in the future of medicine. Is Point of Care Ultrasound (POCUS) a problem? For more like this, head to our podcast page. #CodaPodcast

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SMACC Conference

Scott presents the argument that whilst Emergency Physicians are amazing, as it stands, Emergency Medicine is failing. Scott presents the system as it should be. This involves stabilising the critically ill before admission to the ICU, seeing sick patients in appropriate time and seeing the less sick patients as you can. The issue as it stands, is when this system breaks down. He talks about the ‘boxes’ which now includes the ‘not sick at all’ patient. This leads to Emergency Physician’s not doing what they are trained to do. Scott discusses the issues with the outcome measurements of Emergency Departments. Hospitals measure patient satisfaction and wait times. Moreover, Scott argues that a trip to the ED should be the worst day in a patient’s life and measuring their satisfaction is misleading. A good medical outcome should be the indication of success. Scott also discusses the issue of Emergency Physicians not dealing with emergencies for most of their practice. This, in Scott’s eyes, leads to cognitive dissonance, where ED doctors are not doing what they are trained to do. Simon argues that Emergency Medicine is not a failed paradigm. Emergency Physicians are trained to help people, when people feel that they need to be treated. He claims that doctors in this speciality want to treat a wide variety of people across a wide spectrum of disease. Evidently, Simon discusses a ‘revolution’ in Emergency Medicine. An increasing number of people are attending Emergency Departments across the world. The generalist approach of Emergency Medicine is critical in triaging, treating, and helping these people in their moment of need. The skills, breadth of knowledge and wisdom and ability to work across a range of specialties and in uncertainty is what makes Emergency Medicine and the physicians who work in it special. Join in the debate as Scott and Simon argue for and against the place of Emergency Medicine. Finally, for more like this head to our podcast page. #CodaPodcast

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Anthony Holley and Marietjie ‘MJ’ Slabbert debate the value of prehospital doctors in trauma. Anthony argues that doctors in the prehospital setting add little value. He does so with the upmost respect for prehospital doctors and having worked in this setting himself. He makes the point that across the globe, the employment of doctors in the prehospital setting is a rarity. Working in this environment is diverse and every situation encountered requires a different skillset. This presents a logistical challenge. Anthony continues to discuss the evidence, or lack thereof, in this space. He raises the point of competing interests from paramedics, flight nurses and doctors themselves. This leads to apples being compared to oranges most of the time. Anthony goes on to suggest all the advanced clinical interventions that are necessary in prehospital situations can be competently undertaken by paramedics. MJ argues for the negative. In doing so, she concedes that the evidence base for prehospital medicine is scarce. This is due to inherent biases, the difficulty of gathering data and the issues with methodology. However, MJ believes that care provided outside of the hospital should be of the same level as care received in hospital. This provides a seamless patient journey from the prehospital setting into the hospital and improving the chain of survival. Furthermore, MJ posits that prehospital doctors not only improve care of patients outside of the hospital, but care for those in the hospital and clinics too. Prehospital physicians add value wherever they practise. They bring leadership, knowledge, additional skills, and training as well as innovation and collaboration. Tune in as Anthony and MJ debate over the value of prehospital doctors in trauma. For more like this, head to our podcast page. #CodaPodcast

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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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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

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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.

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SMACC Conference

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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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SMACC Conference

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SMACC Conference

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SMACC Conference

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SMACC Conference

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SMACC Conference

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EEG and Status Eplilepticus by Tania Farrar

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.

Browne Neuro symposium.pptx

Browne Neuro symposium.pptx

Browne Neuro symposium.pptx

SMACC Conference

Paediatric Stroke by Shree Basu

Paediatric Stroke by Shree Basu

Paediatric Stroke by Shree Basu

SMACC Conference

After spinal cord injury (SCI), there aren’t many interventions we have available that actually make a difference. Augmenting blood pressure to increase spinal cord perfusion pressure is an attractive concept that may improve neurological outcomes following SCI. We know that hypotension can make SCI worse. Clinical studies looking at blood pressure augmentation are mostly old, retrospective and flawed in various ways. Aiming for a MAP of > 85 for 5-7 days is recommended by guidelines but why this pressure and duration are good questions. Hypertensive therapy is relatively safe and easy to implement but not without risk. Tessa discusses the pros and cons, how this is managed practically and what the future may hold in this area.

Hypertensing Spinal Cord Injury - gold standard or wacky?

Hypertensing Spinal Cord Injury - gold standard or wacky?

Hypertensing Spinal Cord Injury - gold standard or wacky?

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.

Optimal Cerebral Perfusion Pressure

Optimal Cerebral Perfusion Pressure

Optimal Cerebral Perfusion Pressure

SMACC Conference

The Power of Words - Death and Language.ppt

The Power of Words - Death and Language.ppt

The Power of Words - Death and Language.ppt

SMACC Conference

Appropriate use of antimicrobials is primarily a patient safety issue, and is the key aim of an effective antimicrobial stewardship program. We discuss the challenges in the management of a patient with sepsis, and how decision-making is usually done in the absence of effective diagnostics. Time dependent protocols and the knowledge that undertreatment of a patient with sepsis will lead to poor outcomes will lead to prescribing that may be driven by fear. Antimicrobial resistance is associated with over-use of antimicrobials but is usually not the immediate concern. Antimicrobial stewardship programs should work closely with sepsis teams to ensure that sepsis pathways are implemented across the whole hospital, and that key principles of judicious use are embedded within the clinical pathway.

Sepsis and Antimicrobial Stewardship - Two Sides of the Same Coin

Sepsis and Antimicrobial Stewardship - Two Sides of the Same Coin

Sepsis and Antimicrobial Stewardship - Two Sides of the Same Coin

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.

Brain injury outcomes and predictors

Brain injury outcomes and predictors

Brain injury outcomes and predictors

SMACC Conference

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Precision Medicine in Acute Brain Injury

Precision Medicine in Acute Brain Injury

Precision Medicine in Acute Brain Injury

CSD by Jeffcote Coda 22.pdf

CSD by Jeffcote Coda 22.pdf

CSD by Jeffcote Coda 22.pdf

Subdural Haemorrhage and MMA embolisation

Subdural Haemorrhage and MMA embolisation

Subdural Haemorrhage and MMA embolisation

Andy Neill - More neuroanatomy pearls for neurocritical care

Andy Neill - More neuroanatomy pearls for neurocritical care

Andy Neill - More neuroanatomy pearls for neurocritical care

The BONANZA Trial and PbTO2 Monitoring

The BONANZA Trial and PbTO2 Monitoring

The BONANZA Trial and PbTO2 Monitoring

Dilating the Dogma of Vasospasm

Dilating the Dogma of Vasospasm

Dilating the Dogma of Vasospasm

EVD Tips and Tricks

EVD Tips and Tricks

EVD Tips and Tricks

There is no such thing as mild, moderate and severe TBI - by Andrew Udy

There is no such thing as mild, moderate and severe TBI - by Andrew Udy

There is no such thing as mild, moderate and severe TBI - by Andrew Udy

TBI Debate - Mild, moderate and severe categories work

TBI Debate - Mild, moderate and severe categories work

TBI Debate - Mild, moderate and severe categories work

TBI: when to stop and when to give time

TBI: when to stop and when to give time

TBI: when to stop and when to give time

Ketamine in Brain Injury by Toby Jeffcote

Ketamine in Brain Injury by Toby Jeffcote

Ketamine in Brain Injury by Toby Jeffcote

Managing Complications of Chronic SCI by Bonne Lee

Managing Complications of Chronic SCI by Bonne Lee

Managing Complications of Chronic SCI by Bonne Lee

EEG and Status Eplilepticus by Tania Farrar

EEG and Status Eplilepticus by Tania Farrar

EEG and Status Eplilepticus by Tania Farrar

Browne Neuro symposium.pptx

Browne Neuro symposium.pptx

Browne Neuro symposium.pptx

Paediatric Stroke by Shree Basu

Paediatric Stroke by Shree Basu

Paediatric Stroke by Shree Basu

Hypertensing Spinal Cord Injury - gold standard or wacky?

Hypertensing Spinal Cord Injury - gold standard or wacky?

Hypertensing Spinal Cord Injury - gold standard or wacky?

Optimal Cerebral Perfusion Pressure

Optimal Cerebral Perfusion Pressure

Optimal Cerebral Perfusion Pressure

The Power of Words - Death and Language.ppt

The Power of Words - Death and Language.ppt

The Power of Words - Death and Language.ppt

Sepsis and Antimicrobial Stewardship - Two Sides of the Same Coin

Sepsis and Antimicrobial Stewardship - Two Sides of the Same Coin

Sepsis and Antimicrobial Stewardship - Two Sides of the Same Coin

Brain injury outcomes and predictors

Brain injury outcomes and predictors

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The Risks of Surgery: John Carlisle

1. SURGERYWhat’s the risk?

2.

3.

4.

5.

6.

7.

8. AAA Don’t operate unless > 55 mm

9.

10. UK Small Aneurysm Trial (1993): 46 mm

11. UK Small Aneurysm Trial (1993): 46 mm

12. UK Small Aneurysm Trial (1993): 46 mm

13. UK Small Aneurysm Trial (1993): 46 mm 0 0.1 0.2 0.3 0.4 0.5 0.6 0.7 0.8 0.9 1 0 1 2 3 4 5 6 7 8 9 10 11 12

14. AAA Operate if > 46 mm?

15.

16.

17. UK Small Aneurysm Trial (1993): 46 mm initial monthly mortality 0.40% 0 0.1 0.2 0.3 0.4 0.5 0.6 0.7 0.8 0.9 1 0 1 2 3 4 5 6 7 8 9 10 11 12

18. UK Small Aneurysm Trial (2016): 46 mm initial monthly mortality 0.20%

19. UK Small Aneurysm Trial (2016): 46 mm initial monthly mortality 0.20% 0 0.1 0.2 0.3 0.4 0.5 0.6 0.7 0.8 0.9 1 0 1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 18

20. AAA Operate if > 41 mm?

21.

22.

23. AAA size, mortality hazard & survival 0.01 0.1 1 20 30 40 50 60 70 80 90Monthlymortalityhazard(%) Aneurysm diameter (mm)

24. 0.01 0.1 1 20 30 40 50 60 70 80 90Monthlymortalityhazard(%) Aneurysm diameter (mm) AAA size, mortality hazard & survival

25. AAA size, mortality hazard & survival 0.01 0.1 1 20 30 40 50 60 70 80 90Monthlymortalityhazard(%) Aneurysm diameter (mm)

26. AAA Operate if > your MLE threshold?

27.

28.

29. SURGERYWhat’s the risk?