Selective Aortic Arch Perfusion -
Summary by: Jim Manning
Selective Aortic Arch Perfusion (SAAP) is an endovascular-extracorporeal perfusion resuscitation technique designed specifically to treat cardiac arrest. SAAP involves the blind insertion of a large-lumen balloon occlusion catheter into the descending thoracic aortic arch via a femoral artery. With the SAAP catheter balloon inflated in the thoracic aorta, the heart and brain are relatively isolated for resuscitative perfusion through the SAAP catheter lumen with an oxygen-carrying fluid (such as blood, hemoglobin-based oxygen carrier or fluorocarbon emulsion). SAAP promotes restoration of spontaneous circulation (ROSC) by the heart while protecting the brain from further ischemic insult. SAAP can be used to treat both hemorrhage-induced traumatic cardiac arrest and medical, non-traumatic cardiac arrest.
In traumatic cardiac arrest, SAAP provides the combination of (1) thoracic aortic balloon occlusion for control of hemorrhage below the diaphragm, (2) rapid volume replacement in hemorrhage-induced hypovolemia to restore normovolemia and (3) perfusion of the heart and brain in an effort to achieve ROSC. SAAP also allows titration of small doses of intra-aortic adrenaline or other medications to achieve ROSC.
In medical cardiac arrest, SAAP catheter balloon occlusion of the thoracic aorta limits the distribution of oxygenated perfusate toward the heart and brain. Since medical cardiac arrest patients are not typically hypovolemic, SAAP with an exogenous oxygen-carrier is a volume loading intervention that can only be used for a short time period (5-10 min). If ROSC is not achieved with the limited volume of exogenous oxygen-carrier, femoral venous access during initial SAAP infusion allows venous blood withdrawal for continued SAAP support to promote ROSC without further volume loading (autologous blood SAAP or, essentially, aortic arch ECMO). Intra-aortic adrenaline and anti-reperfusion agents can also be used. Even if ROSC is not rapidly achieved, SAAP serves as a bridge that limits hypoperfusion until cannulation for full body ECMO can be achieved.
Stroke is a leading cause of death and disability. All doctors should have a basic knowledge about stroke management. This presentation gives a summary of treatment options in acute brain stroke.
Stroke is a leading cause of death and disability. All doctors should have a basic knowledge about stroke management. This presentation gives a summary of treatment options in acute brain stroke.
Research guru and PI for the ARISE study, college examiner and semi-professional forrest-based carpenter, Anthony always gives a fascinating talk. This time he gives an intelligent and considered breakdown on the nebulous topic of cerebral protection.
Shay McGuinness talks about what ECMO is, the history of its use in New Zealand and how their ECMO retrieval system works there. This was recorded live at the inaugural ICN NZ meeting, with support from ANZICS NZ.
Budding cardiothoracic intensivists will enjoy this talk by Brian Plunkett on thoracic aortic dissection given at Bedside Critical Care Conference 4. For the audio access and similar talks, head over to intensivecarenetwork.com
Research guru and PI for the ARISE study, college examiner and semi-professional forrest-based carpenter, Anthony always gives a fascinating talk. This time he gives an intelligent and considered breakdown on the nebulous topic of cerebral protection.
Shay McGuinness talks about what ECMO is, the history of its use in New Zealand and how their ECMO retrieval system works there. This was recorded live at the inaugural ICN NZ meeting, with support from ANZICS NZ.
Budding cardiothoracic intensivists will enjoy this talk by Brian Plunkett on thoracic aortic dissection given at Bedside Critical Care Conference 4. For the audio access and similar talks, head over to intensivecarenetwork.com
Christine Bowles takes on the big issue of Sex in critical care. In 2015, why is sexual equality in the workplace even an issue and how can we address it? Listen to the talk recorded live at SMACC Chicago.
Associate Professor Vincent Pellegrino is a Senior Intensive Care Specialist at The Alfred Hospital and head of the ECMO Clinical Service. He has had a lead role in the development of ECMO services at The Alfred since 2003. From the ECMO CPR ICN Victoria meeting he discusses how to get patient selection and outcomes right for eCPR.
A patient's death maybe certain but the timing isn’t.
Ashley Shreves discusses the difficult subject of dying and how best to understand and help diagnose when the battle is lost.
Shreves explores the correlating patterns present in the functional decline in end of life patients, with particular reference to the type of disease a patient is suffering from. Understanding these patterns is paramount to understanding the care and medical intervention require, at certain points of a patients disease lifecycle.
Are You as Good as You Think?
Simon Carley has us asking ourselves some confronting questions about our abilities in his SMACC Chicago talk ‘Are You as Good as You Think?’. Carley has us delve into our confidence, competencies and whats makes for a good self learning environment.
Initially Carley asks us how good we think we are at driving? He then sites studies of Australian and European driver responses, of which 93% of Aussies and 69% europeans rated themselves as above average drivers. Carley uses this example to suggests that, as individuals we are not particlarly good at rating ourselves, and inexperienced people tend to rate themselves more highly than experienced one - Illusory Superiority Cognitive Bias. Carley asks since you can’t have awesome without average... How do we measure ourselves?. He offers us the following tools and processes to establish better self learning and teaching processes, such as;
Reflection Diaries - revisit it (clinically and physically), follow up.
Peer reviews: 1:1 feedback doesn’t work. It needs to planned with clear goals and objectives such as;
Clarify expectations
review logistics
focus lens
plan feedback
observe event (i.e teaching)
debrief and action
Clinical Feedback
Follow up - not just the exceptionally sick patients, but follow up with the routine ones.
Build Peer Reviews into your practice.
Carley finishes by asking us to choose on of the items below and commit ourselves to making happen within the month.
I am going to …
Organise Trainee Feedback
Focused 360 Assessment
Keep a Patient/Teaching Diary
Be Peer Reviewed
Reflect
Develop Team Feedback
Follow up with Patients
Something Else
Nothing I am already Awesome!
What have you committed too?
POCUS is a problem? Really? For who? Maybe a radiologist holding down their turf in a small hospital that has been shielded from the world wide web. Will paint a broad picture of the wide multi-specialty impact POCUS has made in clinical care citing key references and case examples.
Bare Knuckle Trauma Debate: There's no denying it - Prehospital doctors add p...SMACC Conference
Ever wondered if prehospital doctors add LITTLE or LOTS of value in trauma? Ever wondered if an Amazonian Warrior Girl can take on a Kangaroo Aussie Military Man? If you are looking for level-1 evidence on either of these topics, you are in the wrong room! But stick around, it will sure be entertaining & enlightening. Show me anyone who doesn't like a full-contact bare knuckle debate. Bring it on!
Dr Anne Creaton talks about the healthcare capacity building in Fiji.
Fiji was struck by Cyclone Winston in 2016. It caused widespread devastation and the impact will be felt for a long time in the future.
The most important thing that Fiji has taught her is faith, patience and persistence.
Anne begins by talking about the three Rs that are essential in trainees who want to work in Fiji or similar situations.
The three Rs being: Realistic, Resilient and Resourceful.
Emotional intelligence is also very important. Most of the people are highly trained, but always in a high resource environment. Dysfunctional systems in places like Fiji, can impact the clinician’s welfare and performance.
Critical care systems are made up of multiple building blocks with doctors playing a small part. Anne compares critical care systems in Fiji to a game of Jenga. This is because multiple blocks that are essential for critical care systems are non-existent.
Anne divides the Jenga blocks of a critical care system into three: a pre-hospital block, a hospital block, and an administration and governance block.
The pre-hospital block consists of scene care, transport care, communication, hazmat, decontamination and retrieval.
The hospital blocks consist of factors like triage, medical assessment, equipment, drugs and patient flow.
The administrative and governance block provides data, audits, leadership and human resource activities such as training, recruitment and retention.
All these blocks put together form the critical care system. This illustrates how when the different blocks in critical care services are removed, it makes it very difficult to successfully treat a patient.
She explains how doctors face multiple difficulties like faulty equipment, untrained staff, lack of timely transport vehicles, inaccessibility to interventional cardiology, lack of risk management and quality improvement. They also lack hazmat, decontamination, personal protective equipment (PPE), proper communication.
Anne then gives an example of using the three Rs technique to reduce VF arrest by early defibrillation.
Realistic: Automatic external defibrillator (AED) for all health facilities.
Resilient: Placed all AEDs in pelican cases.
Resourceful: Acquired the AEDs via Twitter.
Anne ends by saying that life is about expectation management and you need to understand that there will be a gap between the type of care you want to provide and what you will be able to provide in situations like Fiji.
So, are you ready to play critical care Jenga?
For more like this, head to our podcast page. #CodaPodcast
Peter McCanny is part of the LearnECMO team. In this podcast he explains some of the background and history of ECMO CPR, what evidence there is to support its use and where we're heading in the future.
Evidence Based Medicine in Prehospital ResuscitationSMACC Conference
Marius Rehn examines the difficulties and importance of evidence based medicine in prehospital resuscitation. Notably, combining academic activity with pre- and in-hospital clinical practice is hard work. Being an academic in a flight suit can be quite lonely.
Marius wants this to change and is passionate about increasing the quantity and quality of prehospital research.
Prehospital research that examines patient pathophysiology should dictate care – as it does in the hospital environment. However, Evidence based practice pertaining to the prehospital environment is minimal. This needs to change.
Evidence based medicine in the prehospital setting can dictate care, critically appraise practice and enable improvements in process and cost effectiveness whilst decreasing harms.
Evidently, in-hospital evidence is different to the field application. Ultimately, prehospital research is critical, 5.8 million people die from injury every year – around 10% of the world’s deaths. Unfortunately, pre-hospital research is underfunded.
So, how can we take interventions from the hospital to the streets?
Marius shares three important steps:
The research that is needed
How to interpret the evidence
Why all research is important to consider (from case studies to randomised controlled trials)
Moreover, Marius highlights the need to lean on other members of the scientific community when conducting your own research. For example, a statistician is worth their weight in gold in observational studies when fleshing out regression analysis.
Finally, Marius discusses the importance of information dissemination across all platforms, including peer reviewed journals and informal FOAMed platforms such as Twitter. They all have their place.
For more like this, head to our podcast page. #CodaPodcast
It's all about function NOT movement re-education!Kate Allatt
Function then movement re-education
Don't lower patient expectations
Mind-blowing stories
Future research ideas
www.kateallatt.com
Practical OT presentation
Resuscitation in Paediatric Cardiac Patients: Michele DomicoSMACC Conference
Michele Domico presents a talk on the pitfalls of common paediatric resuscitative manoeuvres in paediatric cardiac patients. Emergency and critical care physicians are all well accustomed to items such as oxygen, bolus adrenaline, intubation and cardioversion. However, as Michele explains, these ‘go to’ interventions may in fact be harmful for the paediatric cardiac patient presenting to the emergency department in extremis. Due to the physiology of certain complex congenital heart diseases, the usual resuscitation manoeuvres may in fact kill the patient instead of helping.
Supplemental oxygen can worsen the pulmonary to systemic blood flow ratio in single ventricle patients and cause them to have rising lactate levels and cardiac arrest from low systemic cardiac output. Intubation and positive pressure ventilation may impede pulmonary blood flow in patients with a Glenn shunt and the patient can become more desaturated. With increasing PEEP and higher respiratory rates, the patients will continue to deteriorate and desaturate. Regular dosing of adrenaline boluses in patients with single ventricle physiology who are nearly arrest, can worsen their systemic output by increasing systemic vascular resistance and promoting pulmonary overcirculation. Cardioversion of a previously healthy paediatric patient might be tempting when you see what looks like a stable ventricular tachycardia. This wide complex rhythm has fooled many people into shocking it. You might in fact be dealing with something else and can make the patient infinitely worse by shocking.
In her talk, Michele highlights the importance of understanding the physiology of your patients. This particularly applies to paediatric cardiac patients. In this population, the change from typical physiology means standard models of care are harmful. Tune in to hear what not to do!
For more like this, head to our podcast page. #CodaPodcast
Details of Cerebrospinal Fluid special reference to cell count and alteration of CSF Hydrodynamics explained in brief and Different Diagnostic parameters to Hydrocephalus
ICN Victoria presents Dr Aiden Burrell talking on the diagnosis, clinical features and treatment of right ventricular failure for the Intensive Care Specialist
Extracorporeal membrane oxygenation, also known as extracorporeal life support (ECLS), is an extracorporeal technique of providing prolonged cardiac and respiratory support to persons whose heart and lungs are unable to provide an
adequate amount of gas exchange or perfusion to sustain life. The technology for ECMO is largely derived from cardiopulmonary bypass, which provides shorter-term support with arrested native circulation.
This intervention has mostly been used on children, but it is seeing more use in adults with cardiac and respiratory failure. ECMO works by removing blood from the person's body and artificially removing the carbon dioxide and oxygenating red blood cells. Generally, it is used either post-cardiopulmonary bypass or in late stage treatment of a person with profound heart and/or lung failure, although it is now seeing use as a treatment for cardiac arrest in certain centers, allowing treatment of the underlying cause of arrest while circulation and oxygenation are supported.
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.
Celia Bradford takes us through the latest on the management of subdural haemorrhage (SDH). She covers acute SDH, chronic SDH and middle meningeal artery embolisation, a novel treatment for chronic SDH management in certain circumstances.
Andy Neill - More neuroanatomy pearls for neurocritical careSMACC Conference
Andy Neill shares some more neuroanatomy wisdom that's highly practical for anyone working with neuro emergencies. This time he covers brain herniation syndromes, hydrocephalus, extradural vs subdural haematomas, cervical spinal imaging, vertebral artery dissection and "things you read on CT reports but don't know what they mean"!
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
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.
By Catherine Bell and Andrew Udy
Catherine Bell takes us through how to troubleshoot problems commonly encountered when looking after patients who have an external ventricular drain (EVD) in situ. Issues with using brain tissue oxygen monitors are also discussed. A highly practical session aimed at bedside clinicians.
There is no such thing as mild, moderate and severe TBI - by Andrew UdySMACC 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 workSMACC 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
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.
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 LeeSMACC 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
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.
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.
Shree Basu is a Paediatirc Intensivist in Sydney. These slides from the Brain Symposium 2023 accompany the talk she gave. She discusses how Paediatric stroke presents, what neuroimaging is required and what interventions are available, including thrombolysis and the role of endovascular thrombectomy.
Hypertensing Spinal Cord Injury - gold standard or wacky?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.
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.
Social Worker Victoria Whitfield and Bereavement councilor Louise Sayers discuss the power of words when health professionals are communicating topics around of death and serious injury with relatives and patients in critical care. They use role plays to bring theories to life.
Sepsis and Antimicrobial Stewardship - Two Sides of the Same CoinSMACC 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.
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.
New Drug Discovery and Development .....NEHA GUPTA
The "New Drug Discovery and Development" process involves the identification, design, testing, and manufacturing of novel pharmaceutical compounds with the aim of introducing new and improved treatments for various medical conditions. This comprehensive endeavor encompasses various stages, including target identification, preclinical studies, clinical trials, regulatory approval, and post-market surveillance. It involves multidisciplinary collaboration among scientists, researchers, clinicians, regulatory experts, and pharmaceutical companies to bring innovative therapies to market and address unmet medical needs.
ARTIFICIAL INTELLIGENCE IN HEALTHCARE.pdfAnujkumaranit
Artificial intelligence (AI) refers to the simulation of human intelligence processes by machines, especially computer systems. It encompasses tasks such as learning, reasoning, problem-solving, perception, and language understanding. AI technologies are revolutionizing various fields, from healthcare to finance, by enabling machines to perform tasks that typically require human intelligence.
Pulmonary Thromboembolism - etilogy, types, medical- Surgical and nursing man...VarunMahajani
Disruption of blood supply to lung alveoli due to blockage of one or more pulmonary blood vessels is called as Pulmonary thromboembolism. In this presentation we will discuss its causes, types and its management in depth.
New Directions in Targeted Therapeutic Approaches for Older Adults With Mantl...i3 Health
i3 Health is pleased to make the speaker slides from this activity available for use as a non-accredited self-study or teaching resource.
This slide deck presented by Dr. Kami Maddocks, Professor-Clinical in the Division of Hematology and
Associate Division Director for Ambulatory Operations
The Ohio State University Comprehensive Cancer Center, will provide insight into new directions in targeted therapeutic approaches for older adults with mantle cell lymphoma.
STATEMENT OF NEED
Mantle cell lymphoma (MCL) is a rare, aggressive B-cell non-Hodgkin lymphoma (NHL) accounting for 5% to 7% of all lymphomas. Its prognosis ranges from indolent disease that does not require treatment for years to very aggressive disease, which is associated with poor survival (Silkenstedt et al, 2021). Typically, MCL is diagnosed at advanced stage and in older patients who cannot tolerate intensive therapy (NCCN, 2022). Although recent advances have slightly increased remission rates, recurrence and relapse remain very common, leading to a median overall survival between 3 and 6 years (LLS, 2021). Though there are several effective options, progress is still needed towards establishing an accepted frontline approach for MCL (Castellino et al, 2022). Treatment selection and management of MCL are complicated by the heterogeneity of prognosis, advanced age and comorbidities of patients, and lack of an established standard approach for treatment, making it vital that clinicians be familiar with the latest research and advances in this area. In this activity chaired by Michael Wang, MD, Professor in the Department of Lymphoma & Myeloma at MD Anderson Cancer Center, expert faculty will discuss prognostic factors informing treatment, the promising results of recent trials in new therapeutic approaches, and the implications of treatment resistance in therapeutic selection for MCL.
Target Audience
Hematology/oncology fellows, attending faculty, and other health care professionals involved in the treatment of patients with mantle cell lymphoma (MCL).
Learning Objectives
1.) Identify clinical and biological prognostic factors that can guide treatment decision making for older adults with MCL
2.) Evaluate emerging data on targeted therapeutic approaches for treatment-naive and relapsed/refractory MCL and their applicability to older adults
3.) Assess mechanisms of resistance to targeted therapies for MCL and their implications for treatment selection
Title: Sense of Smell
Presenter: Dr. Faiza, Assistant Professor of Physiology
Qualifications:
MBBS (Best Graduate, AIMC Lahore)
FCPS Physiology
ICMT, CHPE, DHPE (STMU)
MPH (GC University, Faisalabad)
MBA (Virtual University of Pakistan)
Learning Objectives:
Describe the primary categories of smells and the concept of odor blindness.
Explain the structure and location of the olfactory membrane and mucosa, including the types and roles of cells involved in olfaction.
Describe the pathway and mechanisms of olfactory signal transmission from the olfactory receptors to the brain.
Illustrate the biochemical cascade triggered by odorant binding to olfactory receptors, including the role of G-proteins and second messengers in generating an action potential.
Identify different types of olfactory disorders such as anosmia, hyposmia, hyperosmia, and dysosmia, including their potential causes.
Key Topics:
Olfactory Genes:
3% of the human genome accounts for olfactory genes.
400 genes for odorant receptors.
Olfactory Membrane:
Located in the superior part of the nasal cavity.
Medially: Folds downward along the superior septum.
Laterally: Folds over the superior turbinate and upper surface of the middle turbinate.
Total surface area: 5-10 square centimeters.
Olfactory Mucosa:
Olfactory Cells: Bipolar nerve cells derived from the CNS (100 million), with 4-25 olfactory cilia per cell.
Sustentacular Cells: Produce mucus and maintain ionic and molecular environment.
Basal Cells: Replace worn-out olfactory cells with an average lifespan of 1-2 months.
Bowman’s Gland: Secretes mucus.
Stimulation of Olfactory Cells:
Odorant dissolves in mucus and attaches to receptors on olfactory cilia.
Involves a cascade effect through G-proteins and second messengers, leading to depolarization and action potential generation in the olfactory nerve.
Quality of a Good Odorant:
Small (3-20 Carbon atoms), volatile, water-soluble, and lipid-soluble.
Facilitated by odorant-binding proteins in mucus.
Membrane Potential and Action Potential:
Resting membrane potential: -55mV.
Action potential frequency in the olfactory nerve increases with odorant strength.
Adaptation Towards the Sense of Smell:
Rapid adaptation within the first second, with further slow adaptation.
Psychological adaptation greater than receptor adaptation, involving feedback inhibition from the central nervous system.
Primary Sensations of Smell:
Camphoraceous, Musky, Floral, Pepperminty, Ethereal, Pungent, Putrid.
Odor Detection Threshold:
Examples: Hydrogen sulfide (0.0005 ppm), Methyl-mercaptan (0.002 ppm).
Some toxic substances are odorless at lethal concentrations.
Characteristics of Smell:
Odor blindness for single substances due to lack of appropriate receptor protein.
Behavioral and emotional influences of smell.
Transmission of Olfactory Signals:
From olfactory cells to glomeruli in the olfactory bulb, involving lateral inhibition.
Primitive, less old, and new olfactory systems with different path
Explore natural remedies for syphilis treatment in Singapore. Discover alternative therapies, herbal remedies, and lifestyle changes that may complement conventional treatments. Learn about holistic approaches to managing syphilis symptoms and supporting overall health.
Tom Selleck Health: A Comprehensive Look at the Iconic Actor’s Wellness Journeygreendigital
Tom Selleck, an enduring figure in Hollywood. has captivated audiences for decades with his rugged charm, iconic moustache. and memorable roles in television and film. From his breakout role as Thomas Magnum in Magnum P.I. to his current portrayal of Frank Reagan in Blue Bloods. Selleck's career has spanned over 50 years. But beyond his professional achievements. fans have often been curious about Tom Selleck Health. especially as he has aged in the public eye.
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Introduction
Many have been interested in Tom Selleck health. not only because of his enduring presence on screen but also because of the challenges. and lifestyle choices he has faced and made over the years. This article delves into the various aspects of Tom Selleck health. exploring his fitness regimen, diet, mental health. and the challenges he has encountered as he ages. We'll look at how he maintains his well-being. the health issues he has faced, and his approach to ageing .
Early Life and Career
Childhood and Athletic Beginnings
Tom Selleck was born on January 29, 1945, in Detroit, Michigan, and grew up in Sherman Oaks, California. From an early age, he was involved in sports, particularly basketball. which played a significant role in his physical development. His athletic pursuits continued into college. where he attended the University of Southern California (USC) on a basketball scholarship. This early involvement in sports laid a strong foundation for his physical health and disciplined lifestyle.
Transition to Acting
Selleck's transition from an athlete to an actor came with its physical demands. His first significant role in "Magnum P.I." required him to perform various stunts and maintain a fit appearance. This role, which he played from 1980 to 1988. necessitated a rigorous fitness routine to meet the show's demands. setting the stage for his long-term commitment to health and wellness.
Fitness Regimen
Workout Routine
Tom Selleck health and fitness regimen has evolved. adapting to his changing roles and age. During his "Magnum, P.I." days. Selleck's workouts were intense and focused on building and maintaining muscle mass. His routine included weightlifting, cardiovascular exercises. and specific training for the stunts he performed on the show.
Selleck adjusted his fitness routine as he aged to suit his body's needs. Today, his workouts focus on maintaining flexibility, strength, and cardiovascular health. He incorporates low-impact exercises such as swimming, walking, and light weightlifting. This balanced approach helps him stay fit without putting undue strain on his joints and muscles.
Importance of Flexibility and Mobility
In recent years, Selleck has emphasized the importance of flexibility and mobility in his fitness regimen. Understanding the natural decline in muscle mass and joint flexibility with age. he includes stretching and yoga in his routine. These practices help prevent injuries, improve posture, and maintain mobilit
Knee anatomy and clinical tests 2024.pdfvimalpl1234
This includes all relevant anatomy and clinical tests compiled from standard textbooks, Campbell,netter etc..It is comprehensive and best suited for orthopaedicians and orthopaedic residents.
Lung Cancer: Artificial Intelligence, Synergetics, Complex System Analysis, S...Oleg Kshivets
RESULTS: Overall life span (LS) was 2252.1±1742.5 days and cumulative 5-year survival (5YS) reached 73.2%, 10 years – 64.8%, 20 years – 42.5%. 513 LCP lived more than 5 years (LS=3124.6±1525.6 days), 148 LCP – more than 10 years (LS=5054.4±1504.1 days).199 LCP died because of LC (LS=562.7±374.5 days). 5YS of LCP after bi/lobectomies was significantly superior in comparison with LCP after pneumonectomies (78.1% vs.63.7%, P=0.00001 by log-rank test). AT significantly improved 5YS (66.3% vs. 34.8%) (P=0.00000 by log-rank test) only for LCP with N1-2. Cox modeling displayed that 5YS of LCP significantly depended on: phase transition (PT) early-invasive LC in terms of synergetics, PT N0—N12, cell ratio factors (ratio between cancer cells- CC and blood cells subpopulations), G1-3, histology, glucose, AT, blood cell circuit, prothrombin index, heparin tolerance, recalcification time (P=0.000-0.038). Neural networks, genetic algorithm selection and bootstrap simulation revealed relationships between 5YS and PT early-invasive LC (rank=1), PT N0—N12 (rank=2), thrombocytes/CC (3), erythrocytes/CC (4), eosinophils/CC (5), healthy cells/CC (6), lymphocytes/CC (7), segmented neutrophils/CC (8), stick neutrophils/CC (9), monocytes/CC (10); leucocytes/CC (11). Correct prediction of 5YS was 100% by neural networks computing (area under ROC curve=1.0; error=0.0).
CONCLUSIONS: 5YS of LCP after radical procedures significantly depended on: 1) PT early-invasive cancer; 2) PT N0--N12; 3) cell ratio factors; 4) blood cell circuit; 5) biochemical factors; 6) hemostasis system; 7) AT; 8) LC characteristics; 9) LC cell dynamics; 10) surgery type: lobectomy/pneumonectomy; 11) anthropometric data. Optimal diagnosis and treatment strategies for LC are: 1) screening and early detection of LC; 2) availability of experienced thoracic surgeons because of complexity of radical procedures; 3) aggressive en block surgery and adequate lymph node dissection for completeness; 4) precise prediction; 5) adjuvant chemoimmunoradiotherapy for LCP with unfavorable prognosis.
These lecture slides, by Dr Sidra Arshad, offer a quick overview of 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 leads (limb II)
4. Differentiate between intervals and segments
5. Enlist some common indications for obtaining an ECG
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. ECG Basics, http://www.nataliescasebook.com/tag/e-c-g-basics
Couples presenting to the infertility clinic- Do they really have infertility...Sujoy Dasgupta
Dr Sujoy Dasgupta presented the study on "Couples presenting to the infertility clinic- Do they really have infertility? – The unexplored stories of non-consummation" in the 13th Congress of the Asia Pacific Initiative on Reproduction (ASPIRE 2024) at Manila on 24 May, 2024.
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- Video recording of this lecture in English language: https://youtu.be/lK81BzxMqdo
- Video recording of this lecture in Arabic language: https://youtu.be/Ve4P0COk9OI
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The prostate is an exocrine gland of the male mammalian reproductive system
It is a walnut-sized gland that forms part of the male reproductive system and is located in front of the rectum and just below the urinary bladder
Function is to store and secrete a clear, slightly alkaline fluid that constitutes 10-30% of the volume of the seminal fluid that along with the spermatozoa, constitutes semen
A healthy human prostate measures (4cm-vertical, by 3cm-horizontal, 2cm ant-post ).
It surrounds the urethra just below the urinary bladder. It has anterior, median, posterior and two lateral lobes
It’s work is regulated by androgens which are responsible for male sex characteristics
Generalised disease of the prostate due to hormonal derangement which leads to non malignant enlargement of the gland (increase in the number of epithelial cells and stromal tissue)to cause compression of the urethra leading to symptoms (LUTS
TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Ve...kevinkariuki227
TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Verified Chapters 1 - 19, Complete Newest Version.pdf
TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Verified Chapters 1 - 19, Complete Newest Version.pdf
TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Ve...
Jim Manning - Selective Aortic Arch Perfusion
1. Is Selective Aortic Arch Perfusion
the Answer?
James E. Manning, MD
Departments of Emergency Medicine and Surgery
University of North Carolina at Chapel Hill School of Medicine
SMACC 2015
Chicago, IL
June 25, 2015
Disclosure: Inventor on patents for the Selective Aortic Arch Perfusion assigned to the
University of North Carolina at Chapel Hill. Co-Founder of Resusitech, Inc., a medical
device company developing resuscitation technologies.
3. Selective Aortic Arch Perfusion
Selective Aortic Arch Perfusion
is a resuscitationtechnique that
involves the blind insertionof a
large-lumenballoon occlusion
catheter into the descending
thoracic aortic arch via a
femoral artery. With the
balloon inflated, the heart and
brain are relativelyisolated for
resuscitative perfusionwith an
oxygen-carrying fluid in an
effort to promote restoration of
spontaneous circulationby the
heart while protecting the brain
from further ischemic insult.
6. Resuscitation Medicine
Key Concept: The “Chain of Survival”
Early Recognition
& Activation(911)
Early CPR
Rapid
Defibrillation
ACLS &
Transport
Post-Resuscitation
ICU/Neuro Care
7. Two Principles
In Order to Improve Cardiac Arrest Survival:
(1)We Need Better Methods of Artificial Perfusion
(2)We Need Better Monitoring Technology
8. Selective Aortic Arch Perfusion
Time-critical pre-hospital / in-hospital resuscitation
intervention intended to compensate for “weak links”
in the Chain of Survival
.…an effort to “turn back the clock” in cardiac arrest
9. “Endovascular-Extracorporeal Resuscitation Era”
Momentum from two different directions
(1) Endovascular hemorrhage control:
Trauma / Severe Hemorrhagic Shock
REBOA ………/ SAAP ……../ EPR
(2) Extracorporeal perfusion:
Medical Cardiac Arrest / Sudden Death
CPB / EMCO / ECLS / ECPR ….…./ SAAP
12. Selective Aortic Arch Perfusion for Medical Cardiac Arrest/Sudden Death
Manning et al, Ann Emerg Med 1992; 21:1068-1065
Medical Cardiac Arrest:
Aortic balloon occlusionallows
relativelyisolatedperfusion of
the heart and brain
Heart and brain perfusion with
an oxygen-carrying fluid
Hemoglobin-based(HBOC)
Fluorocarbon emulsion(PFC)
Blood (allogeneic / autologous)
Intra-aortic drug administration
- Epinephrine / vasoactive agents
- Ischemia-reperfusion agents
- Hemostatic products
Rapid hypothermia induction
20. A
SAAP catheter: 11.5 Fr OD, 7.3 Fr ID of infusion lumen
ECMO arterial cannulas: 15 Fr & 19 Fr
21. Sequential Invasive Resuscitation Interventions in
Medical/Non-Trauma Cardiac Arrest
If initial CPR, Defibrillation, ACLS is unsuccessful (No ROSC)
Femoral artery SAAP balloon catheter insertion &
initiate SAAP with O2 carrier (HBOC, PFC, WB/pRBC)
(obtain venous access during this initial SAAP phase)
If ROSC not achieved, venous blood W/D & transition
to SAAP with Autologous Blood (partial ECMO/ECLS)
If ROSC not achieved, larger femoral arterial cannula
& convert to whole body ECLS/ECPR
If ROSC not achieved, Consider: Cardiac Cath
for PCI, LVAD, VIR, CT/Vasc Surgery,
profound hypothermia (?), and
cessation of resuscitation efforts
23. Aortic Hemostasis and Resuscitation
AHR
NCTH/decompensated Hemorrhage-induced
hemorrhagic shock Traumatic Cardiac Arrest (HiTCA)
but NOT impending
CV collapse/CA if CA occurs
REBOA SAAP ROSC not achieved
ROSC but EPR
myocardial dysfx
ECLS ECLS inadequate
(ECMO)
REBOA – Resuscitative Endovascular Balloon Occlusion of the Aorta
SAAP – Selective Aortic Arch Perfusion
EPR – Emergency Preservation & Resuscitation
ECLS – Extracorporeal Life Support (Extracorporeal Membrane Oxygenation)
24. Selective Aortic Arch Perfusion for Hemorrhage-Induced Cardiac Arrest
Manning et al, Crit Care Med 2001; 29:2067-2074
Trauma / Hemorrhagic Shock:
Aortic balloon occlusionto
limit abdominal/pelvic blood
loss caudal to the balloon
(functional aortic cross-clamp)
Perfusion of the heart & brain
with an oxygenated solution
(HBOC, fluorocarbon, whole
blood) to ROSC & to restore
intravascular volume rapidly
Intra-aortic administration
- Epinephrine / vasoactive agents
- Ischemia-reperfusion agents
- Hemostatic products
Temperature regulation(??)
25.
26. Oxygen-Carrier Perfusate for SAAP:
PFCs & HBOCs – still “future capability” in the USA
Present capability
Whole Blood
Packed RBCs
(citrate anticoagulant issue)
SAAP in Hemorrhage-induced Cardiac Arrest
27. Selective Aortic Arch Perfusion with Hemoglobin-BasedOxygen Carrier-201
for resuscitationfrom exsanguination cardiac arrest in swine
Manning et al. Crit Care Med 2001; 29:2067-2074
SAAP with oxygenated HBOC-201 vs. SAAP with oxygenated LR
Swine liver lacerationmodel, rapid exsanguination, cardiac arrest at 10-13 mins
Sustained ROSC in 6/6 SAAP – HBOC-201 1-hour survival in 5/6
Transient ROSC in 2/6 SAAP – LR (with Ao-Epi) 1-hour survival in 0/6
ROSC time for SAAP – HBOC-201 was 1.9±1.0 min
28. Oxygen-Carrier Perfusate for SAAP:
PFCs & HBOCs – still “future capability” in the USA
Present capability
Whole Blood
Packed RBCs
(citrate anticoagulant issue)
SAAP in Hemorrhage-induced Cardiac Arrest
38. Is Selective Aortic Arch Perfusion the answer?
Maybe, in part……
SAAP is one of the interventions we could have in
our “resuscitation toolkit” to help us save the lives
of our cardiac arrest patients….before it’s too late.