SMACCForce: E-CPR - Panel
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SMACCForce: E-CPR - Panel by Brian Burns, Paul Gowens, Lional Lamhaut, Steve Bernard, Nikki Stamp, Alice Hutin
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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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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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CSD by Jeffcote Coda 22.pdf
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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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It’s Not What You’ve Got It’s What You Do With It
The BONANZA Trial
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More on BONANZA here
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R. Loch Macdonald, M.D., Ph.D.
Community Neurosciences Institute
Fresno, California, USA
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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.
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So why do we do cEEGs for patients with suspected SE?
To confirm the diagnosis
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To establish that the clinical and electric seizures have stopped
To see if burst suppression is achieved
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She makes a good argument for why cEEG is such an important tool in managing SE.
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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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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?
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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.
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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.
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Local Advanced Lung Cancer: Artificial Intelligence, Synergetics, Complex Sys...
Overall life span (LS) was 1671.7±1721.6 days and cumulative 5YS reached 62.4%, 10 years – 50.4%, 20 years – 44.6%. 94 LCP lived more than 5 years without cancer (LS=2958.6±1723.6 days), 22 – more than 10 years (LS=5571±1841.8 days). 67 LCP died because of LC (LS=471.9±344 days). AT significantly improved 5YS (68% vs. 53.7%) (P=0.028 by log-rank test). Cox modeling displayed that 5YS of LCP significantly depended on: N0-N12, T3-4, blood cell circuit, cell ratio factors (ratio between cancer cells-CC and blood cells subpopulations), LC cell dynamics, recalcification time, heparin tolerance, prothrombin index, protein, AT, procedure type (P=0.000-0.031). Neural networks, genetic algorithm selection and bootstrap simulation revealed relationships between 5YS and N0-12 (rank=1), thrombocytes/CC (rank=2), segmented neutrophils/CC (3), eosinophils/CC (4), erythrocytes/CC (5), healthy cells/CC (6), lymphocytes/CC (7), stick neutrophils/CC (8), leucocytes/CC (9), monocytes/CC (10). Correct prediction of 5YS was 100% by neural networks computing (error=0.000; area under ROC curve=1.0).
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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
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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.
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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.
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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.
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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.
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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.
SMACCForce: LIVE EMS Nation Podcast - "Feeding the Flame"
SMACCForce: LIVE EMS Nation Podcast - "Feeding the Flame" by Faizan Arshad , Raed Arafat, Lamhaut and Anne Creaton
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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Introduction
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Editor's Notes
- BRIAN: E-CPR Panel Nikki Stamp, Steve Bernard, Lamhaut, Alice Hutin, Paul Gowens
- BRIAN: This has been quite a day! We’ve hopefully challenged you a bit. CONOR: We hope we have made you think. ASH: But most of all, hopefully you walk away knowing that prehospital medicine makes a difference. BRIAN: Today we came together as a family, and while you’ve seen a lot of us, SMACCFORCE would be nothing without Jason at the helm, and our ATACC team. Thanks to you, thanks to our faculty and the SMACCFORCE team for your commitment! GO FORTH AND TAKE CARE!