Flower on an iconoclastic view of neuro-icu
•
4 likes•1,199 views
Oli Flower gives an iconoclastic view of neurocritical care. This is a talk that was given at the College of Intensive Care Medicine's ASM in Wellington in June 2013. It focuses on three aspects of traumatic brain injury management: - Prognostication - Transfusion thresholds - The role of ICP monitoring
Report
Share
Report
Share
Download to read offline
Recommended
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.
Subdural Haemorrhage and MMA embolisation
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.
Recommended
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.
Subdural Haemorrhage and MMA embolisation
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 care
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"!
The BONANZA Trial and PbTO2 Monitoring
Andrew Udy talks about Brain Tissue Oxygen Monitoring:
It’s Not What You’ve Got It’s What You Do With It
The BONANZA Trial
Andrew Udy talks about the ongoing BONANZA Trial which is assessing whether an algorithm that incorporates both ICP and brain tissue oxygen (PbTO2) can improve outcomes after traumatic brain injury (TBI). Like with all monitoring, how the PbTO2 is interpreted and managed is critical and the devil is in the detail!
More on BONANZA here
More on BOOST3 here
Dilating the Dogma of Vasospasm
R. Loch Macdonald, M.D., Ph.D.
Community Neurosciences Institute
Fresno, California, USA
Angiographic vasospasm and more accurately, delayed cerebral ischemia, continue to contribute to morbidity and mortality in patients with aneurysmal subarachnoid hemorrhage (SAH). It is known that angiographic vasospasm is common after SAH, occurring in two-thirds of patients. Cerebral infarctions that developed days after the SAH have been attributed to angiographic vasospasm, occuring in about a third of patients, although this has always been controversial. Angiographic vasospasm theoretically can only damage the brain by restricting blood flow but there is no easy, accurate, widely available method to measure cerebral blood flow and this is not the measurement we need. Blood flow depends on metabolic demand so what we need to know to determine if angiographic vasospasm is causing ischemia is oxygen extraction fraction in the brain tissue supplied the the spastic artery. Without this measurement, the attribution of ischemia to vasospasm is subjective. Since angiographic vasospasm is essentially the only detectable delayed phenomenon after SAH, we focus on it and apply tremendous resources to preventing or reversing the vasospasm. Undoubtedly angiographic vasospasm can cause cerebral infarctions, but it has to be severe and flow limiting. But SAH is a complex disease. There are many other causes for cerebral infarctions after SAH, the most common being due to the aneurysm repair procedure. And a given degree of vasospasm may cause infarction in a volume-depleted patient with poor collateral blood supply but not in a patient without these things. There also are hypodense brain lesions after SAH that are due to intracerebral hemorrhages. There can be hypodensities in the brain directly under usually thick SAH where the brain dies. This observation in particular supports a role for cortical spreading depolarizations/ischemia as a cause of infarction after SAH. Other macromolecular processes that are hypothesized to cause brain damage after SAH include microthromboembolism, changes in the microcirculation, delayed brain cell apoptosis and capillary transit time heterogeneity. Determining the importance of these things is hindered by the lack of an easy way to detect them in patients. It is also known that poor grade patients, who presumably have more early brain injury and ischemia than good grade patients, are more prone to delayed cerebral ischemia, suggesting increased sensitivity to secondary insults of the already injured brain. We also assume delayed neurological deterioration when attributed to vasospasm or delayed cerebral ischemia, is purely due to ischemia. While knowledge about what happens pathophysiologically after SAH is increasing, management of delayed cerebral ischemia still focuses on detecting angiographic vasospasm and then augmenting the blood pressure to improve cerebral blood flow or dilating the spastic arteries with balloons or drugs.
EVD Tips and Tricks
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 Udy
Part 2 of a debate over the classification of TBI. Andrew Udy then argues that this classification is fundamentally flawed. He discusses the issues with the Glasgow Coma Scale, and therefore the follow-on issues in TBI classification, including all the confounders to the GCS, the issues with timing of the score as well as GCS not taking baseline function or specifics subtypes of TBI into account. He makes teh argument that biomarkers may better categorise the diffuse entity we call TBI.
TBI Debate - Mild, moderate and severe categories work
Andrew Chow, Intensivist with a neurosurgical background, argues that the current categorisation system for traumatic brain injury (TBI) works, and makes sense! He tackles us through the history of this system, and why it’s important to differentiate different types of TBI. The arguments in favour of this categorisation include the consistency and benefits of a universal language, the implications for triage and management, and the fact that this system has been endorsed by all major organisations
TBI: when to stop and when to give time
Dr Nick Little is an experienced Neurosurgeon who's looked after patients with traumatic brain injury for his whole career. Here he discusses the difficulties of prognostication following traumatic brain injury (TBI). He talks about the statistics of outcomes following mild, moderate and severe TBI and then goes on to tackle the harder topic of how we try to work out what an individual would want if they knew the spectrum of outcomes that they may face. The issues with the clinical examination findings we use to prognosticate are covered, as well as which imaging findings he finds most helpful. He also mentions the difficulties with current prognostic calculators.
Ketamine in Brain Injury by Toby Jeffcote
Historically, when it came to brain injury, ketamine had a bad rap. Much of that dogma was dispelled in the last decade, and ketamine is now frequently used as an induction agent in acute brain injury, especially traumatic brain injury, due to it’s favorable effects on haemodynamics.
However a new application of ketamine is now being explored - whether ketamine may be able to reduce secondary brain injury.
Managing Complications of Chronic SCI by Bonne Lee
20 million people around the world are living with a spinal cord injury (SCI). The medical issues they develop over the years differ to any other patient cohort.
These complications include autonomic dysreflexia, management of pressure areas, specific infections, nuanced peri-operative care and highly specific issues such as baclofen pump management and syringomyelia
Do look at the NeuroResus section on this and listen to Spinal Rehab Specialist Bonne Lee talk about this side of SCI care.
Keywords
SCI, spinal, spinal cord injury, autonomic dysreflexia, pressure areas, infection, peri-operative care, baclofen pump, syringomyelia, chronic SCI, spinal trauma, spinal rehab, incomplete SCI
EEG and Status Eplilepticus by Tania Farrar
Tania is a neurologist and epileptologist with expertise in continuous EEG (cEEG) and status epilepticus (SE). This talk covers what a seizure is, what status is, including focal and generalised status epilepticus.
So why do we do cEEGs for patients with suspected SE?
To confirm the diagnosis
To see if patient just post ictal or still seizing
To establish that the clinical and electric seizures have stopped
To see if burst suppression is achieved
To exclude other differential diagnoses
She makes a good argument for why cEEG is such an important tool in managing SE.
In the questions after the talk, the issue of availability of cEEG in the Australian setting was discussed. Limited montage EEGs are discussed including their pros and cons.
Browne Neuro symposium.pptx
Stuart Browne is a Neuro Rehab specialist from Sydney. These slides accompany a talk he gave at the Brian Symposium in 2023. He discusses what "severe disability" really means.
Severe disability is more common than many realise - about 6% of the Australian population.
Stuart discusses how health is more than simply physical recovery and how it is a multidimensional construct. He covers how permanent disability doesn't necessarily equate to a poor quality of life. He also discusses the long timespan of recovery, which is often much longer than appreciated.
He specifically discusses "Locked-in Syndrome" and how the survivors have surprisingly positive self-reported health-related quality of life and well-being.
Stuart also covers how severely disabled people face various forms of discrimination.
Paediatric Stroke by Shree Basu
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?
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.
Optimal Cerebral Perfusion Pressure
Mark Weedon takes us through the increasingly utilised concept of an optimal cerebral perfusion pressure (CPPopt) for each unique patient. He discusses the background to CPPopt, including intrcranial pressure (ICP), the Monroe Kelly hypothesis, neurovascular coupling, and cerebral autoregulation in health and following brain injury. He shows how intracranial pressure is affected by intracranial compliance and how this affects ICP waveforms. Cerebral perfusion pressure in relation to the Brain Trauma Foundation guidelines is covered including management of elevated ICP (EICP). The currently recommended tiered approach to managing cerebral perfusion pressure and EICP is mentioned citing recent guidelines. He uses a clinical case of a TBI to illustrate how the CPPopt can be ascertained and used to guide therapy, including the easy to perform “MAP Challenge”. Mark also describes the Pressure Reactivity Index (PRx) and how it can be used as a target for therapy. Finally, he covers the exciting results of the preliminary COGiTATE pilot study.
The Power of Words - Death and Language.ppt
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 Coin
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.
Brain injury outcomes and predictors
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.
Knee anatomy and clinical tests 2024.pdf
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.
More Related Content
More from SMACC Conference
Andy Neill - More neuroanatomy pearls for neurocritical care
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"!
The BONANZA Trial and PbTO2 Monitoring
Andrew Udy talks about Brain Tissue Oxygen Monitoring:
It’s Not What You’ve Got It’s What You Do With It
The BONANZA Trial
Andrew Udy talks about the ongoing BONANZA Trial which is assessing whether an algorithm that incorporates both ICP and brain tissue oxygen (PbTO2) can improve outcomes after traumatic brain injury (TBI). Like with all monitoring, how the PbTO2 is interpreted and managed is critical and the devil is in the detail!
More on BONANZA here
More on BOOST3 here
Dilating the Dogma of Vasospasm
R. Loch Macdonald, M.D., Ph.D.
Community Neurosciences Institute
Fresno, California, USA
Angiographic vasospasm and more accurately, delayed cerebral ischemia, continue to contribute to morbidity and mortality in patients with aneurysmal subarachnoid hemorrhage (SAH). It is known that angiographic vasospasm is common after SAH, occurring in two-thirds of patients. Cerebral infarctions that developed days after the SAH have been attributed to angiographic vasospasm, occuring in about a third of patients, although this has always been controversial. Angiographic vasospasm theoretically can only damage the brain by restricting blood flow but there is no easy, accurate, widely available method to measure cerebral blood flow and this is not the measurement we need. Blood flow depends on metabolic demand so what we need to know to determine if angiographic vasospasm is causing ischemia is oxygen extraction fraction in the brain tissue supplied the the spastic artery. Without this measurement, the attribution of ischemia to vasospasm is subjective. Since angiographic vasospasm is essentially the only detectable delayed phenomenon after SAH, we focus on it and apply tremendous resources to preventing or reversing the vasospasm. Undoubtedly angiographic vasospasm can cause cerebral infarctions, but it has to be severe and flow limiting. But SAH is a complex disease. There are many other causes for cerebral infarctions after SAH, the most common being due to the aneurysm repair procedure. And a given degree of vasospasm may cause infarction in a volume-depleted patient with poor collateral blood supply but not in a patient without these things. There also are hypodense brain lesions after SAH that are due to intracerebral hemorrhages. There can be hypodensities in the brain directly under usually thick SAH where the brain dies. This observation in particular supports a role for cortical spreading depolarizations/ischemia as a cause of infarction after SAH. Other macromolecular processes that are hypothesized to cause brain damage after SAH include microthromboembolism, changes in the microcirculation, delayed brain cell apoptosis and capillary transit time heterogeneity. Determining the importance of these things is hindered by the lack of an easy way to detect them in patients. It is also known that poor grade patients, who presumably have more early brain injury and ischemia than good grade patients, are more prone to delayed cerebral ischemia, suggesting increased sensitivity to secondary insults of the already injured brain. We also assume delayed neurological deterioration when attributed to vasospasm or delayed cerebral ischemia, is purely due to ischemia. While knowledge about what happens pathophysiologically after SAH is increasing, management of delayed cerebral ischemia still focuses on detecting angiographic vasospasm and then augmenting the blood pressure to improve cerebral blood flow or dilating the spastic arteries with balloons or drugs.
EVD Tips and Tricks
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 Udy
Part 2 of a debate over the classification of TBI. Andrew Udy then argues that this classification is fundamentally flawed. He discusses the issues with the Glasgow Coma Scale, and therefore the follow-on issues in TBI classification, including all the confounders to the GCS, the issues with timing of the score as well as GCS not taking baseline function or specifics subtypes of TBI into account. He makes teh argument that biomarkers may better categorise the diffuse entity we call TBI.
TBI Debate - Mild, moderate and severe categories work
Andrew Chow, Intensivist with a neurosurgical background, argues that the current categorisation system for traumatic brain injury (TBI) works, and makes sense! He tackles us through the history of this system, and why it’s important to differentiate different types of TBI. The arguments in favour of this categorisation include the consistency and benefits of a universal language, the implications for triage and management, and the fact that this system has been endorsed by all major organisations
TBI: when to stop and when to give time
Dr Nick Little is an experienced Neurosurgeon who's looked after patients with traumatic brain injury for his whole career. Here he discusses the difficulties of prognostication following traumatic brain injury (TBI). He talks about the statistics of outcomes following mild, moderate and severe TBI and then goes on to tackle the harder topic of how we try to work out what an individual would want if they knew the spectrum of outcomes that they may face. The issues with the clinical examination findings we use to prognosticate are covered, as well as which imaging findings he finds most helpful. He also mentions the difficulties with current prognostic calculators.
Ketamine in Brain Injury by Toby Jeffcote
Historically, when it came to brain injury, ketamine had a bad rap. Much of that dogma was dispelled in the last decade, and ketamine is now frequently used as an induction agent in acute brain injury, especially traumatic brain injury, due to it’s favorable effects on haemodynamics.
However a new application of ketamine is now being explored - whether ketamine may be able to reduce secondary brain injury.
Managing Complications of Chronic SCI by Bonne Lee
20 million people around the world are living with a spinal cord injury (SCI). The medical issues they develop over the years differ to any other patient cohort.
These complications include autonomic dysreflexia, management of pressure areas, specific infections, nuanced peri-operative care and highly specific issues such as baclofen pump management and syringomyelia
Do look at the NeuroResus section on this and listen to Spinal Rehab Specialist Bonne Lee talk about this side of SCI care.
Keywords
SCI, spinal, spinal cord injury, autonomic dysreflexia, pressure areas, infection, peri-operative care, baclofen pump, syringomyelia, chronic SCI, spinal trauma, spinal rehab, incomplete SCI
EEG and Status Eplilepticus by Tania Farrar
Tania is a neurologist and epileptologist with expertise in continuous EEG (cEEG) and status epilepticus (SE). This talk covers what a seizure is, what status is, including focal and generalised status epilepticus.
So why do we do cEEGs for patients with suspected SE?
To confirm the diagnosis
To see if patient just post ictal or still seizing
To establish that the clinical and electric seizures have stopped
To see if burst suppression is achieved
To exclude other differential diagnoses
She makes a good argument for why cEEG is such an important tool in managing SE.
In the questions after the talk, the issue of availability of cEEG in the Australian setting was discussed. Limited montage EEGs are discussed including their pros and cons.
Browne Neuro symposium.pptx
Stuart Browne is a Neuro Rehab specialist from Sydney. These slides accompany a talk he gave at the Brian Symposium in 2023. He discusses what "severe disability" really means.
Severe disability is more common than many realise - about 6% of the Australian population.
Stuart discusses how health is more than simply physical recovery and how it is a multidimensional construct. He covers how permanent disability doesn't necessarily equate to a poor quality of life. He also discusses the long timespan of recovery, which is often much longer than appreciated.
He specifically discusses "Locked-in Syndrome" and how the survivors have surprisingly positive self-reported health-related quality of life and well-being.
Stuart also covers how severely disabled people face various forms of discrimination.
Paediatric Stroke by Shree Basu
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?
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.
Optimal Cerebral Perfusion Pressure
Mark Weedon takes us through the increasingly utilised concept of an optimal cerebral perfusion pressure (CPPopt) for each unique patient. He discusses the background to CPPopt, including intrcranial pressure (ICP), the Monroe Kelly hypothesis, neurovascular coupling, and cerebral autoregulation in health and following brain injury. He shows how intracranial pressure is affected by intracranial compliance and how this affects ICP waveforms. Cerebral perfusion pressure in relation to the Brain Trauma Foundation guidelines is covered including management of elevated ICP (EICP). The currently recommended tiered approach to managing cerebral perfusion pressure and EICP is mentioned citing recent guidelines. He uses a clinical case of a TBI to illustrate how the CPPopt can be ascertained and used to guide therapy, including the easy to perform “MAP Challenge”. Mark also describes the Pressure Reactivity Index (PRx) and how it can be used as a target for therapy. Finally, he covers the exciting results of the preliminary COGiTATE pilot study.
The Power of Words - Death and Language.ppt
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 Coin
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.
Brain injury outcomes and predictors
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.
More from SMACC Conference (20)
Andy Neill - More neuroanatomy pearls for neurocritical care
Andy Neill - More neuroanatomy pearls for neurocritical care
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
Managing Complications of Chronic SCI by Bonne Lee
Managing Complications of Chronic SCI by Bonne Lee
Hypertensing Spinal Cord Injury - gold standard or wacky?
Hypertensing Spinal Cord Injury - gold standard or wacky?
Sepsis and Antimicrobial Stewardship - Two Sides of the Same Coin
Sepsis and Antimicrobial Stewardship - Two Sides of the Same Coin
The importance of communication in pain management
The importance of communication in pain management
Recently uploaded
Knee anatomy and clinical tests 2024.pdf
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.
A Classical Text Review on Basavarajeeyam
Basavarajeeyam is a Sreshta Sangraha grantha (Compiled book ), written by Neelkanta kotturu Basavaraja Virachita. It contains 25 Prakaranas, First 24 Chapters related to Rogas& 25th to Rasadravyas.
How to Give Better Lectures: Some Tips for Doctors
Talk given to Koronadal Internists Society, Marbel, South Cotabato as part of the Continuing Medical Education (CME) series.
CDSCO and Phamacovigilance {Regulatory body in India}
The Central Drugs Standard Control Organization (CDSCO) is India's national regulatory body for pharmaceuticals and medical devices. Operating under the Directorate General of Health Services, Ministry of Health & Family Welfare, Government of India, the CDSCO is responsible for approving new drugs, conducting clinical trials, setting standards for drugs, controlling the quality of imported drugs, and coordinating the activities of State Drug Control Organizations by providing expert advice.
Pharmacovigilance, on the other hand, is the science and activities related to the detection, assessment, understanding, and prevention of adverse effects or any other drug-related problems. The primary aim of pharmacovigilance is to ensure the safety and efficacy of medicines, thereby protecting public health.
In India, pharmacovigilance activities are monitored by the Pharmacovigilance Programme of India (PvPI), which works closely with CDSCO to collect, analyze, and act upon data regarding adverse drug reactions (ADRs). Together, they play a critical role in ensuring that the benefits of drugs outweigh their risks, maintaining high standards of patient safety, and promoting the rational use of medicines.
Basavarajeeyam - Ayurvedic heritage book of Andhra pradesh
Basavarajeeyam is an important text for ayurvedic physician belonging to andhra pradehs. It is a popular compendium in various parts of our country as well as in andhra pradesh. The content of the text was presented in sanskrit and telugu language (Bilingual). One of the most famous book in ayurvedic pharmaceutics and therapeutics. This book contains 25 chapters called as prakaranas. Many rasaoushadis were explained, pioneer of dhatu druti, nadi pareeksha, mutra pareeksha etc. Belongs to the period of 15-16 century. New diseases like upadamsha, phiranga rogas are explained.
How STIs Influence the Development of Pelvic Inflammatory Disease.pptx
STIs may cause PID. For the both disease, herbal medicine Fuyan Pill can be a solution.
Dehradun #ℂall #gIRLS Oyo Hotel 9719300533 #ℂall #gIRL in Dehradun
Dehradun #ℂall #gIRLS Oyo Hotel 9719300533 #ℂall #gIRL in Dehradun
Physiology of Special Chemical Sensation of Taste
Title: Sense of Taste
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 structure and function of taste buds.
Describe the relationship between the taste threshold and taste index of common substances.
Explain the chemical basis and signal transduction of taste perception for each type of primary taste sensation.
Recognize different abnormalities of taste perception and their causes.
Key Topics:
Significance of Taste Sensation:
Differentiation between pleasant and harmful food
Influence on behavior
Selection of food based on metabolic needs
Receptors of Taste:
Taste buds on the tongue
Influence of sense of smell, texture of food, and pain stimulation (e.g., by pepper)
Primary and Secondary Taste Sensations:
Primary taste sensations: Sweet, Sour, Salty, Bitter, Umami
Chemical basis and signal transduction mechanisms for each taste
Taste Threshold and Index:
Taste threshold values for Sweet (sucrose), Salty (NaCl), Sour (HCl), and Bitter (Quinine)
Taste index relationship: Inversely proportional to taste threshold
Taste Blindness:
Inability to taste certain substances, particularly thiourea compounds
Example: Phenylthiocarbamide
Structure and Function of Taste Buds:
Composition: Epithelial cells, Sustentacular/Supporting cells, Taste cells, Basal cells
Features: Taste pores, Taste hairs/microvilli, and Taste nerve fibers
Location of Taste Buds:
Found in papillae of the tongue (Fungiform, Circumvallate, Foliate)
Also present on the palate, tonsillar pillars, epiglottis, and proximal esophagus
Mechanism of Taste Stimulation:
Interaction of taste substances with receptors on microvilli
Signal transduction pathways for Umami, Sweet, Bitter, Sour, and Salty tastes
Taste Sensitivity and Adaptation:
Decrease in sensitivity with age
Rapid adaptation of taste sensation
Role of Saliva in Taste:
Dissolution of tastants to reach receptors
Washing away the stimulus
Taste Preferences and Aversions:
Mechanisms behind taste preference and aversion
Influence of receptors and neural pathways
Impact of Sensory Nerve Damage:
Degeneration of taste buds if the sensory nerve fiber is cut
Abnormalities of Taste Detection:
Conditions: Ageusia, Hypogeusia, Dysgeusia (parageusia)
Causes: Nerve damage, neurological disorders, infections, poor oral hygiene, adverse drug effects, deficiencies, aging, tobacco use, altered neurotransmitter levels
Neurotransmitters and Taste Threshold:
Effects of serotonin (5-HT) and norepinephrine (NE) on taste sensitivity
Supertasters:
25% of the population with heightened sensitivity to taste, especially bitterness
Increased number of fungiform papillae
Are There Any Natural Remedies To Treat Syphilis.pdf
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.
Non-respiratory Functions of the Lungs.pdf
These simplified slides by Dr. Sidra Arshad present an overview of the non-respiratory functions of the respiratory tract.
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
Flu Vaccine Alert in Bangalore Karnataka
As flu season approaches, health officials in Bangalore, Karnataka, are urging residents to get their flu vaccinations. The seasonal flu, while common, can lead to severe health complications, particularly for vulnerable populations such as young children, the elderly, and those with underlying health conditions.
Dr. Vidisha Kumari, a leading epidemiologist in Bangalore, emphasizes the importance of getting vaccinated. "The flu vaccine is our best defense against the influenza virus. It not only protects individuals but also helps prevent the spread of the virus in our communities," he says.
This year, the flu season is expected to coincide with a potential increase in other respiratory illnesses. The Karnataka Health Department has launched an awareness campaign highlighting the significance of flu vaccinations. They have set up multiple vaccination centers across Bangalore, making it convenient for residents to receive their shots.
To encourage widespread vaccination, the government is also collaborating with local schools, workplaces, and community centers to facilitate vaccination drives. Special attention is being given to ensuring that the vaccine is accessible to all, including marginalized communities who may have limited access to healthcare.
Residents are reminded that the flu vaccine is safe and effective. Common side effects are mild and may include soreness at the injection site, mild fever, or muscle aches. These side effects are generally short-lived and far less severe than the flu itself.
Healthcare providers are also stressing the importance of continuing COVID-19 precautions. Wearing masks, practicing good hand hygiene, and maintaining social distancing are still crucial, especially in crowded places.
Protect yourself and your loved ones by getting vaccinated. Together, we can help keep Bangalore healthy and safe this flu season. For more information on vaccination centers and schedules, residents can visit the Karnataka Health Department’s official website or follow their social media pages.
Stay informed, stay safe, and get your flu shot today!
NVBDCP.pptx Nation vector borne disease control program
NVBDCP was launched in 2003-2004 . Vector-Borne Disease: Disease that results from an infection transmitted to humans and other animals by blood-feeding arthropods, such as mosquitoes, ticks, and fleas. Examples of vector-borne diseases include Dengue fever, West Nile Virus, Lyme disease, and malaria.
Recently uploaded (20)
How to Give Better Lectures: Some Tips for Doctors
How to Give Better Lectures: Some Tips for Doctors
CDSCO and Phamacovigilance {Regulatory body in India}
CDSCO and Phamacovigilance {Regulatory body in India}
Basavarajeeyam - Ayurvedic heritage book of Andhra pradesh
Basavarajeeyam - Ayurvedic heritage book of Andhra pradesh
How STIs Influence the Development of Pelvic Inflammatory Disease.pptx
How STIs Influence the Development of Pelvic Inflammatory Disease.pptx
Dehradun #ℂall #gIRLS Oyo Hotel 9719300533 #ℂall #gIRL in Dehradun
Dehradun #ℂall #gIRLS Oyo Hotel 9719300533 #ℂall #gIRL in Dehradun
Are There Any Natural Remedies To Treat Syphilis.pdf
Are There Any Natural Remedies To Treat Syphilis.pdf
Maxilla, Mandible & Hyoid Bone & Clinical Correlations by Dr. RIG.pptx
Maxilla, Mandible & Hyoid Bone & Clinical Correlations by Dr. RIG.pptx
Pharynx and Clinical Correlations BY Dr.Rabia Inam Gandapore.pptx
Pharynx and Clinical Correlations BY Dr.Rabia Inam Gandapore.pptx
NVBDCP.pptx Nation vector borne disease control program
NVBDCP.pptx Nation vector borne disease control program
Flower on an iconoclastic view of neuro-icu
- 1. NEUROCRITICAL CARE! an iconoclastic view!
- 4. smacc! GOLD MARCH 2014!
- 7. Image: Nicolas de Camaret!
- 8. Image: Nicolas de Camaret! PaCO2! < 25! THIO! CPP! >70! AEDs! STEROIDS!
- 9. Image: Tiago Vidal Dutra! A STORY!
- 16. FUTILITY!
- 17. GCS! SHOCK! >60!
- 20. push on...!
- 21. Hb 8.8!
- 22. DO2 = [1.39 x Hb x SaO2 + (0.003 x PaO2)] x Q!
- 23. Hb!
- 25. RETROSPECTIVE!
- 26. LUND! 12.5-14! image by Kjell Eriksson! fresh! leukodepleted!
- 27. photo by Dalibor Levicek! BLOOD TRANSPLANT! Text TRANSFUSION ASSAULT!
- 29. MENON! Le ROUX!
- 30. 9!
- 31. CT! CODMAN! ICP 22!
- 32. PARADIGM!
- 33. ICP! image from the BBC!
- 35. BEST ! TRIP! LATIN AMERICA! 324 PATIENTS! ICP vrs No ICP!
- 36. BEST!
- 37. WORST!
- 39. 45%!
- 40. 55%!
- 42. ICP! photo by Glatze mit Kamera
- 43. logic! image by yellowcloud!
- 44. history! image by sciencesque!
- 45. In the beginning...! SURGERY!
- 46. ICPST UMRROIAMGNTUIAECOIhMTRGUeTOAYI ! NBDR !CGTRINAF!YGRG!E!! !
- 47. evidence! image by Robert Cudmore!
- 48. RETROSPECTIVE!
- 54. HOME!
- 55. ICP! image from the BBC!
- 56. it’s not the number! it’s what you do with it!
- 65. do research! prognosticate with IMPACT! transfuse if < 9 g/dL! don’t rely on one number!