Not all bleeding stops: acute coagulopathy of trauma by Brohi
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Karim Brohi highlights the pitfalls of fluid resuscutation and the deadly spiral of coagulopathy in severe trauma.
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Tranexamic Acid in Trauma by Karim Brohi
WARNING: This talk will be ineffective if you have no sense of humour.
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WARNING: This talk will be ineffective if you have no sense of humour.
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- IMRT may be beneficial for large or centrally-located tumors but further study is needed due to the study's retrospective nature and heterogeneous patient population.
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Pancholy SB 2014
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Precision Medicine in Acute Brain Injury
Systematic review of 26 studies with 55,792 patients found that dedicated neurocritical care (NCC) was associated with decreased risk of mortality (17% relative risk reduction) and decreased risk of poor functional outcomes (17% relative risk reduction) in critically ill brain-injured adults. A survey of Australian ICUs found limited availability of NCC, with only 4 centers specializing in it and 9 employing an intensivist subspecializing in NCC. Continuous EEG monitoring was found to have higher sensitivity for detecting nonconvulsive seizures than routine EEG monitoring, and was associated with reduced in-hospital mortality, though barriers to its universal use include infrastructure and personnel requirements.
CSD by Jeffcote Coda 22.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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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
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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.
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By Catherine Bell and Andrew Udy
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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.
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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.
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Stuart Browne is a Neuro Rehab specialist from Sydney. These slides accompany a talk he gave at the Brian Symposium in 2023. He discusses what "severe disability" really means.
Severe disability is more common than many realise - about 6% of the Australian population.
Stuart discusses how health is more than simply physical recovery and how it is a multidimensional construct. He covers how permanent disability doesn't necessarily equate to a poor quality of life. He also discusses the long timespan of recovery, which is often much longer than appreciated.
He specifically discusses "Locked-in Syndrome" and how the survivors have surprisingly positive self-reported health-related quality of life and well-being.
Stuart also covers how severely disabled people face various forms of discrimination.
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?
This document discusses the concept of maintaining higher blood pressure levels, known as hypertension, after a spinal cord injury to improve spinal cord perfusion pressure and reduce secondary injury. It notes that while animal studies and some human trials have shown improved neurological outcomes, the evidence is still limited. It calls for larger randomized controlled trials in humans that also incorporate multi-modal monitoring and standardized outcome measures to further evaluate if inducing hypertension after spinal cord injury should be considered the gold standard of care.
Optimal Cerebral Perfusion 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
Undertreatment of sepsis can lead to mortality, while overdiagnosis and overtreatment can increase future risk of antimicrobial resistance. Antimicrobial stewardship aims to balance these risks by prioritizing patient safety and appropriate antimicrobial use. Data shows variability in appropriateness of antimicrobial prescribing between different types of hospitals. Embedding antimicrobial stewardship principles throughout sepsis diagnosis and treatment, from initial microbiology testing to post-treatment review, can help standardize care and optimize outcomes.
Brain injury outcomes and 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.
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These lecture slides, by Dr Sidra Arshad, offer a quick overview of the 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 lead (limb II)
4. Differentiate between intervals and segments
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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. Chapter 3, Cardiology Explained, https://www.ncbi.nlm.nih.gov/books/NBK2214/
7. ECG Basics, http://www.nataliescasebook.com/tag/e-c-g-basics
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Not all bleeding stops: acute coagulopathy of trauma by Brohi
- 1. ACUTE TRAUMATIC COAGULOPATHY Centre for Trauma Sciences Queen Mary University of London www.c4ts.qmul.ac.uk Royal London Major Trauma Centre Barts Health NHS Trust KARIM BROHI, FRCS FRCA Professor of Trauma Sciences, QMUL
- 3. 0% 20% 40% 60% 0 - 3 4 - 7 8 - 11 12 - 15 16 - 19 20 - 23 24 - 27 28 - 31 Mortality(%) PRBCs in 24 Hours
- 17. HAEMOSTATIC Resuscitation 1. Early haemorrhage control (DCS) 2. Permissive hypotension 3. Limit fluid infusions (dilution) 4. Target coagulopathy
- 18. Hallmarks of ATC
- 20. -100 -80 -60 -40 -20 0 20 40 60 80 100 0 10 20 30 40 50 60 Firmness[mm] Time [min] exTEM PTr Comparison EXTEM PTR<1.2 EXTEM PTR>1.2
- 21. ATC: CA5 < 36mm
- 27. CRYOSTAT
- 28. CRYOSTAT Mortality a Standard: Y 7/22 : 32% Early CRYO: 3/21 : 14%
- 32. -100 -80 -60 -40 -20 0 20 40 60 80 100 0 10 20 30 40 50 60 Firmness[mm] Time [min] exTEM PTr Comparison EXTEM PTR<1.2 EXTEM PTR>1.2
- 33. 0% 20% 40% 60% 80% 100% ≤15 16 - 50 >50 %ofPatients % Maximum Lysis
- 36. Occult Fibrinolysis Normal %ML + PAP 1500-7000ng/ml Severe Occult Fibrinolysis Normal %ML + PAP >7000ng/ml Overt Fibrinolysis %ML >15%
- 37. 0% 20% 40% 60% Normal Occult Severe Occult Overt %ofPatients Hyperfibrinolysis
- 40. Mechanism of ATC
- 41. Systemic Activation of Protein C
- 45. VIIa IXa Xa +++ + XIIa XIa TM TM TM TM Thrombin Fibrin + platelet Thrombin-TM Fibrinogen
- 46. VIIa IXa Xa + XIIa XIa aPC PC - Thrombin-TM - Thrombin Fibrin + platelet TM TM TM TM Fibrinogen
- 50. VIIa IXa Xa + XIIa XIa aPC PC - Thrombin-TM - Thrombin Fibrin + platelet TM TM TM TM Fibrinogen
- 51. VIIa IXa Xa + XIIa XIa aPC PC - Thrombin-TM - FDPs Plasmin tPA + Thrombin Fibrin + platelet + Fibrinogen
- 52. VIIa IXa Xa + XIIa XIa aPC PC - Thrombin-TM - FDPs Plasmin tPA + Thrombin Fibrin + platelet + Fibrinogen -
- 53. VIIa IXa Xa + XIIa XIa aPC PC - Thrombin-TM - FDPs Plasmin tPAPAI-1 + - - Thrombin Fibrin + platelet + Fibrinogen -