Managing Complications of Chronic SCI by Bonne Lee
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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
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CSD by Jeffcote Coda 22.pdf
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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Community Neurosciences Institute
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R. Loch Macdonald, M.D., Ph.D.
Community Neurosciences Institute
Fresno, California, USA
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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.
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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.
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To confirm the diagnosis
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To see if burst suppression is achieved
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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.
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Hypertensive therapy is relatively safe and easy to implement but not without risk.
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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 management
In this podcast, Claire discusses the role of clinician communication and its impact on acute pain management.
Claire explains how pain management outcomes can be optimised by enhancing patient expectations of benefit via patient-provider communication.
Firstly, what we say to patients matters. Secondly, how we say it also matters.
Pain is a complex phenomenon and managing expectations of pain and people’s experience of empathy is crucial.
As healthcare professionals, we see multiple patients and are often run off our feet, but, as the studies clearly demonstrate… communication matters. And it matters a lot in pain management.
This presentation shares research demonstrating the impact of clinician communication.
Specifically, this includes how clinicians' talk about pain and pain management. Claire discusses the importance of patients' experience of pain, the effectiveness of pain management and patients' treatment outcomes.
From CodaZero Live, tune in to a fascinating discussion on the importance of communication.
For more like this, head to https://codachange.org/podcasts/
Brain Death History
Slides to accompany a podcast on the history of brain death. Describes the history, and some pitfalls in determining brain death. Centres around practice in Australia and New Zealand. These slides make no sense without the accompanying talk.
SMACCForce: E-CPR - Panel
SMACCForce: E-CPR - Panel by Brian Burns, Paul Gowens, Lional Lamhaut, Steve Bernard, Nikki Stamp, Alice Hutin
SMACCForce: LIVE EMS Nation Podcast - "Feeding the Flame"
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Violence against healthcare workers - Paramedics under siege
Acts of violence against paramedics is disgraceful but not doing anything about it is much worse.
From DAS SMACC, Craig Wylie speaks to us about violence against paramedics in South Africa. In the four years leading up to this talk in 2017, there were 250 attacks against paramedics. In a neighbourhood where there can be up to 100 gunshots in three hours, this almost shouldn’t be surprising.
Craig tells a story where he was called out to an emergency where his colleagues were under attack. His first thought? Why didn’t they get a police escort? But in a low to middle income country, it is rarely that straightforward. Where there is a high crime rate and may only be two police vehicles on duty, it isn’t always as easy as waiting for a police escort. Additionally, if paramedics had to rely on police attending their emergencies, is this just introducing another barrier to care?
Craig asks three simple questions:
1. Has our management failed our staff members?
2. Have we done enough that the paramedics that we employ can protect themselves?
3. Have we as an EMS system entirely lost the plot towards our paramedics and how we respond to patient emergencies?
The solution? Craig suggests it is all in the training. Paramedics need to be trained to understand the situations, to have a strong action plan, to have an exit plan and to involve community leaders. The team need to be trained to understand how to protect themselves so that they can provide care, whilst also looking out for themselves.
Tune into a talk from DAS SMACC on Violence against healthcare workers - Paramedics under siege.
For more like this, head to our podcast page. #CodaPodcast
Paediatric intubation
From DAS SMACC, Charles Larson and Andrew Beck discuss intubating sick kids - small holes, big problems.
When intubating a critically ill child we fear that they are going to arrest on induction and we consider the skill required to intubate in difficult circumstances.
The most important thing to remember is that we will never be so good that we won’t make mistakes. The greatest critical care physicians are those that have good skills but that are also able to identify what might go wrong. Understanding the risks and having a plan for when something goes wrong is crucial.
Managing critically ill children is a difficult task. We must understand their physiology, have a plan for induction and have a plan for if things go wrong.
Importantly, we need to consider that it takes several minutes for drugs to kick in for children. What matters more than what drug you give is how you give it. Children don’t follow recipes so nor should you.
Furthermore, some golden rules in managing airways in children:
1. Simulation and training is key: We don’t want to be educating ourselves on our patients, particularly in rare scenarios.
2. We must know our equipment, know our limits and know our support systems. Being able to call down help early is priceless.
3. Assess, plan and communicate with the team.
4. Don’t repeat without change. Trying to put the same size tube down the same size hole will always lead to problems.
5. Training needs to be ongoing and skills need to be revisited. Confidence does not always equal competence.
Charles Larson and Andrew Beck share stories of Paediatric intubation in high pressure scenarios.
For more like this, head to our podcast page. #CodaPodcast
CPR in paediatric congenital cardiac disease
Join Timo de Raad as he discusses the complexities of CPR in paediatric congenital cardiac disease.
Timo introduces the listener to Emma, a 4-year-old cheerful and playful girl. Emma was born with hypoplastic left heart syndrome – a condition where the left side of the heart is poorly formed. As a result, the heart cannot support adequate circulation around the body. 5 out of 10 000 live births in the Netherlands have this congenital heart defect.
Timo was there for Emma’s birth, and he was there for Emma’s death.
Treatment of hypoplastic left heart syndrome is a palliative three stage repair. The first procedure is the Norwood – within the first two weeks. Subsequently the Glenn procedure is undertaken, and finally the Fontan. In this procedure the pulmonary artery and aorta are combined to create one outflow tract from the heart.
In essence, this creates one functional ventricle. As a result, there is a change in the cardiac physiology. This changes the dynamics when considering resuscitation in these patients. In Fontan hearts cardiac output is dependent on the preload which in turn is dependent on how much blood flows through the lungs.
Accordingly, spontaneous breathing is critical for these patients. Constriction of pulmonary veins make it difficult for blood to flow back to the heart.
When dealing with cardiac arrest in these patients Timo suggests treating it the same as any resuscitation – utilising chest compressions and epinephrine (adrenaline). He does suggest one extra thing, that being abdominal compressions.
Timo describes the technique he uses. He pushes between the belly button and sternum. He recommends pushing as hard as if you were palpating the liver. In trials on awake patients, there were no complaints of pain when using this technique. Additionally, Timo discusses the ratio of 1 to 1 chest to abdominal compressions during the resuscitation.
In conclusion, resuscitation of a paediatric congenital heart defect is challenging. Consider the growing evidence base on abdominal compressions whilst acknowledging the differing opinions in this space.
For more like this, head to our podcast page. #CodaPodcast
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Physiology of Chemical Sensation of smell.pdf
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
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Learning objectives:
1. Enlist the non-respiratory functions of the respiratory tract
2. Briefly explain how these functions are carried out
3. Discuss the significance of dead space
4. Differentiate between minute ventilation and alveolar ventilation
5. Describe the cough and sneeze reflexes
Study Resources:
1. Chapter 39, Guyton and Hall Textbook of Medical Physiology, 14th edition
2. Chapter 34, Ganong’s Review of Medical Physiology, 26th edition
3. Chapter 17, Human Physiology by Lauralee Sherwood, 9th edition
4. Non-respiratory functions of the lungs https://academic.oup.com/bjaed/article/13/3/98/278874
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New Directions in Targeted Therapeutic Approaches for Older Adults With Mantl...
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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
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