What does this month’s journal club have to do with astrophysics? Want to grasp the literature for this month’s journal club and get inside what the attendings are thinking about analgesics, stroke therapy, and PE prevalence? Listen to this month’s podcast!
In this video cast I try to sort through some of the differences between a simple CHF exacerbation and acute decompensated heart failure. I discuss the wet/dry warm/cold approach, use of BNP and NTproBNP in decision making, high dose nitro, ACE inhibitors, BiPAP, and the proper timing of diuretics.
Here is the videocast.
Click below for the podcast – audio only.
“The Road to Character” by David Brooks. As an academic physician climbing my “second mountain”, I am really connecting with the message this book offers. I was moved and inspired by his talk at #AAMC2017
The old 6 hour rule to differentiate mushrooms with limited toxicity (early i.e. < 6 hr GI symptoms) from those that cause serious end organ damage (late >6 hr GI symptoms) has been busted by the recognition of two additional mushrooms that cause both early GI symptoms and late end organ toxicity. Furthermore, another mushroom has been added to the group with late GI symptoms and delayed end organ damage. Hope this mnemonic and vodcast will help sort them out for you!
Enjoy the vodcast!
Dr. David Vearrier, Program Director Medical Toxicology Fellowship Drexel University College of Medicine, joins me to discuss the physiology of opioid withdrawal and approaches to treatment including suboxone and other approaches.
Outline of the show can be found here:
The Opioid Crisis _Treating Opioid Withdrawal in the ED
Check back for another podcast on our lessons learned when we initiate the program.
Thanks for listening!
My guest is Suraj Rajasimhan PharmD – Suraj is our brilliant EM Clinical Pharmacist and is an indispensable part of the ED. Follow him @Sraj726
Today we talk about the “Banana Bag”
You can enjoy the podcast here:
The Banana Bag – what is it? It usually contains dextrose, thiamine, folate, multivitamins, +/_ magnesium. Why? Acute alcohol intoxication is often accompanied by acute and chronic nutritional deficiencies
Dextrose
Alcoholic ketoacidosis should be suspected in patients with binge drinking and poor nutrition (acutely – ie no meals recently). Do not need to be an alcoholic to get it. Alcohol binge in a healthy patient with few meals can leade to AKA. Symptoms include nausea & vomiting, malaise, abdominal pain, dizziness, tremulousness, tachypnea, tachycardia, and hypotension. Urine ketones may be falsely negative or only trace positive in alcoholic ketoacidosis. Alcohol metabolism depletes NAD, leaves excess NADH (so called reducing metabolic state). This skews ketoacids / beta-hydroxybutyrate and alpha-ketoglutarate toward beta-hydroxybutyrate. Although
AKA patients have depleted glycogen stores, serum glucose level can be often within the normal range. Lactic acidosis forms from a combination of dehydration and the impaired lactate dehydrogenase thus unable to convert lactate to pyruvate, thus impairing gluconeogenesis.
What is WE and Korsakoff Psychosis?
Wernicke’s encephalopathy and Korsakoff syndrome are linked disease states that are often under recognized in the critically ill and acutely intoxicated. Typically referred to as “Dry Beriberi” because of their lack of cardiovascular symptoms. Wet beriberi is presents with congestive heart failure from dilated cardiomyopathy.
Thiamine B1 is a cofactor for several essential enzymes in the Krebs cycle and the pentose phosphate pathway – alpha-ketoglutarate dehydrogenase, pyruvate dehydrogenase, and transketolase. alpha-ketoglutarate dehydrogenase, pyruvate dehydrogenase. The result is increases lactic acid production and impaired glucose metabolism especially in the CNS
Prevalence
Autopsy studies suggest that 12% of alcoholics have a Wernicke’s encephalopathy. Alcohol affects thiamine uptake and utilization. Also found in prolonged starvation, hyperemesis gravidarum, bariatric surgery (bariatric beriberi), and (HIV)/ (AIDS).
The most typical clinical manifestation was an altered mental status in patients with identified Wernicke’s encephalopathy at autopsy. Only 20% of these patients have received a clinical diagnosis of WE. Only 10% had a complete triad of symptoms of altered mental status, ophthalmoplegia, and ataxia.
Making the diagnosis
Thiamine levels are difficult to turn around and there is not a thiamine level that will result in WE in all patients. Thiamine levels are reduced in up to 80% of alcohol users.
Thus clinical recognition and prophylactic treatment are necessary.
According to the European Federation of Neurologic Societies the criteria for Wernicke’s encephalopathy he and Korsakoff syndrome should have 2 of the following 4 features
1) a nutritional deficiency is present (they look malnourished),
2) ocular abnormalities,
3) ataxia (i.e. cerebellar dysfunction), or
4) mental status changes or memory impairment
Unfortunately alter mental status occurs in virtually all patients who are acutely intoxicated or admitted to intensive care
The condition is not always 100% reversible, although ataxia and ophthalmoplegia usually resolve within hours after receiving thiamine if given early. Confusion improves but memory and learning difficulties often persist. Progression to Korsakoff psychosis usually results in permanent neurologic dysfunction.
| Supplement | Evidence level for routine use in critically ill patients | Signs and symptoms in alcohol withdrawal (you can apply to acute alcohol intoxication) | Dose |
| Dextrose | Adequate | nausea & vomiting, malaise, abdominal pain, dizziness, tremulousness, tachypnea, tachycardia, and hypotension | D5 ½ NS run at maintenance (do not delay for thiamine) |
| Thiamine | Adequate | Altered MS, WE, KP, metabolic dysfunction | 200 – 500 mg IV every 8 hrs |
| Folic Acid | Reasonable but weak | Megaloblastic anemia, confusion, depression, psychosis, seizures, sleep disturbance | 0.4 to 1 mg day |
| Magnesium | Reasonable but weak | QT prolongation, altered MS, seizures, tremors, hyper-reflexia | 64/ mg/kg on day 1, followed by 32 mg/kg on days 2 to 4 |
| Multivitamin
Phosphorous Potassium Riboflavin Selenium Vit A Vit C Zinc |
NO
NO NO NO NO NO NO |
||
What do we recommend?
First of all – Keep the Dextrose.
All the rest is patient specific – but start with clinical evaluation and a high index of suspicion.
Thiamine
Wernicke’s Triad = mental status changes, ophthalmoplegia, and ataxia
Other sx: hypothermia, vestibular dysfunction, nystagmus
These are vague and can be difficult to differentiate or use for diagnosis amongst alcoholic cerebellar degeneration and other comorbidities
Patients with chronic alcohol use are at risk for thiamine deficiency due to:
Decreased dietary intake
Impaired absorption
Decreased conversion to active form
Poor Absorption of Oral Thiamine
In HEALTHY adults, the MAX absorbed from a 30 mg dose was 4.5 mg
Thiamine absorption in alcoholics is reduced to 30-98% below the lower limit of normal
In alcoholics, 5 mg of a 100 mg TID PO regimen is estimated to be absorbed in 24 hours
How Much Thiamine?
100 MG IV dose in banana bags was chosen arbitrarily
Landmark study in patients with confirmed WE receiving 50-100 mg IV thiamine/day
84% developed Korsakoff Syndrome and long-term impairments
Minimum dose recommended to prevent/treat WE:
Royal College of Physicians: >500 mg IV QD or BID
European Federation of Neurological Societies: 200 mg IV TID
One study suggested that at least 200 mg IM thiamine daily may be required to improve symptoms
Thiamine Pharmacokinetics
Thiamine is transported into the brain by both an active, saturable mechanism AND a passive mechanism
Goal would be to achieve a steep concentration gradient between serum and CNS
This is the justification for high IV doses
Single 50 mg IV dose has plasma ½ life of 1.5 hours and returns to initial levels within 6-12 hours
Optimal dosing interval = 8-12 hours
200 mg dose only costs $3
Recommendations
Take the thiamine out of the routine banana bag! If you are concerned about the possibility of WE – treat with the full dose of 200 mg at least.
200-500 mg IV Q8h for at least 72 hours or until WE is ruled out
Folic acid (folate)
Folate 400 -1000 mcg IV for several days
“Conversion to oral therapy is reasonable if no concomitant alcohol consumption will occur”
Magnesium
Magnesium 1 mEq/kg on the first day (in divided doses) and 0.5 mEq/kg/day over the next 3 days
Deficiency is common since EtOH use increases magnesium elimination
Multivitamins
MVI
No substantial treatment effect
Better to target specific deficiencies
Cost $10 per vial
References:
Latt N, Dore G. Thiamine in the treatment of Wernicke encephalopathy in patietns with alcohol use disorders. Internal Medicine Journal 2014:44;911-915.
Glavin R, Brathen G, Ivashynka A, Hillbom M, Tanasescu R, Leone MA. EFNS guidelines for diagnosis, therapy and prevention of Wernicke encephalopathy. European Journal of Neurology 2010:17;1408-1418.
Thomson AD; Cook CC; Touquet R; Henry JA; The Royal College of Physicians report on alcohol: guidelines for managing Wernicke’s encephalopathy in the accident and Emergency Department. Alcohol Alcohol. 2002; 37(6):513-21 (ISSN: 0735-0414)
In this podcast I am joined by Rick McKnight PhD author of Victim, Survivor, Navigator and Curt Woolford MA E-RYT. Rick, Curt, and I held a Workshop/Retreat for my Department last month with the goal of building resilience using mindfulness techniques.
The basic approach we took was to have all participants take a Maslach-Burnout Inventory and begin using a few apps (Mood Meter, Provider Resilience) before the retreat. The day of the retreat we started with a review of the groups Maslach-Burnout Inventory and then each individual opened the envelope with their results. It had a fairly powerful attention getting effect. We then moved to various small group sharing and transitioned to Mindful Resilience Training specifically focusing on individual based techniques (e.g. meditation, breathing exercises, etc). Finally, we created workshop like approach to identify best practices for Team Resilience. Four specific scenarios were discussed that typically result in interpersonal stress on teams in the Emergency Department (a few examples – an angry patient confronts a colleague, a difficult patient keeps calling for help, a colleague is not seeing enough patients or carrying an appropriate load, a rude consultant, a colleague appears to becoming distressed dealing with a violent patient). What should our response be? How would we want our colleagues to respond if it we were in distress, being attacked, treated rudely etc? This generated a lot of great discussion.
In the podcast we reviewed some of the important take home themes from the retreat. Social connectivity and a sense of not being alone in feelings of stress goes a long way to restoring a sense of balance and calm. Resilience is not about hardening you to be resistant to stress, resilience is about developing the attributes that make you and your team someone who thrives in stressful environments. Choosing to navigate the challenges and stress that EM has to offer leads to a much better outlook and a happier and enjoyable practice. Remaining a victim at worst or a survivor at best is not the path to a satisfying relationship with the practice of EM.
Finally we take a look at this brand new paper Psychological Skills to Improve Emergency Care Providers’ Performance Under Stress.This papers develops the BTSF (Breath, self Talk, See (mental rehearsal), Focus with trigger word) mnemonic that is discussed at EMCrit and is specifically focused on high stakes performance. Somewhat different from our retreat topic, but still the same technique.
Just for fun – here are some of my favorite self talk, trigger word performance enhancing practices from the movies!
Inner Space – a fun favorite from way back when that has one of favorites “Zero Defects”
For the Love of the Game – the story of Billy Chapel – “Clear the Mechanism” dramatizes how weirdly personal a trigger word can be – and how effective. They say many of the great athletes had the ability to focus and eliminate distractions. This scene is perfect for EM physicians because I think on just about every shift I am trying to concentrate on something while being heckled (okay – distracted) by someone who thinks I need to do something else (get a phone call, hear about a case, read an ECG, get them food, the list goes on…).
Enjoy the podcast and leave your comments on how you build resilience personally and with your teams!!!
Here’s a video cast of the talk I gave at the Association of Academic Chairs of Emergency Medicine Annual Retreat March 22, 2017. The purpose of the talk was to inform EM academic chairs about the social media in medicine movement. The theory of the talk is that our hero, your average EM physician, is in crisis. They are leaving patient care because they feel their autonomy threatened, they struggle to maintain mastery of the complexity of clinical practice, and they feel that they have lost a sense of purpose. Social Media is the found pilot of emergency medicine – building social capital, accelerating knowledge translation, and enabling personal learning networks. The net effect is to give EM physicians a restored sense of themselves. EM physicians engaged in social media feel empowered to defend their autonomy and have a stronger sense of purpose and mastery. I hope you enjoy the talk and would love to hear your feedback! I want to thank Ken Milne and K Kay Moody for taking time to speak to me about their ideas on social media – and more importanly for being social media pioneers that have made a difference. These and so many others are the found pilots of our specialty! #getonboard
O’Connor and Dornfield “The Moment You Can’t Ignore”
In this podcast, Dr. Rita McKeever and I try to use some recent evidence to see if we can hasten the throughput of self-poisoning patients in the ED.
First let’s look at:
The short answer is NO! If you suspect acetaminophen overdose then you should properly identify a time or range for a 4 hr level and obtain the specimen at that time.
However – “Only very low to undetectable acetaminophen concentrations prior to 4 hours reliably excluded a subsequent concentration over the treatment line.” We can use this to our advantage for patients who we do NOT suspect to have an acetaminophen overdose!
In this UK study, none of the 136 patients who denied taking acetaminophen had a detectable level at 4 hours.
In another UK study, less than 10% (13 of 155) of patients who denied taking acetaminophen had any detectable level and none required antidote.
So although you can lower the prior probability of acetaminophen poisoning when the patient denies ingestion, you cannot completely exclude the diagnosis without an acetaminophen level. However, you can save a few hours of ED time – here’s how:
When you do NOT suspect an acetaminophen overdose (prior probability is close to zero!) , an undetectable level before 4 hrs (at 2 hours and even as soon as 1 hour) post ingestion will reliably exclude acetaminophen toxicity (likelihood ratio of zero!). If you draw a < 4hr level and it shows detectable acetaminophen – it must be repeated at 4 hours to determine if it needs treatment.
If you DO suspect an acetaminophen overdose, obtain only a 4 hour level to guide NAC therapy.
Hopefully this will help with a more rapid throughput of patients with self poisoning who need to be medically cleared for further psychiatric evaluation. Of course, this represents one opinion based on a review of the literature. A prospective trial would be needed to prove this conclusively.
Enjoy the Podcast!
In this podcast Dr. Rita McKeever and I review the recent article entitled Do heroin overdose patients require observation after receiving naloxone? from our toxicology friends at Washington University – Michael W. Willman, David B. Liss, Evan S. Schwarz & Michael E. Mullin. They reviewed the literature to try and answer the following questions:
(1) What are the medical risks to a heroin user who refuses ambulance transport after naloxone?
(2) If the heroin user is treated in the emergency department with naloxone, how long must they be observed prior to discharge?
(3) How effective in heroin users is naloxone administered by first responders and bystanders? Are there risks associated with naloxone distribution programs?
We also take a look at Ed Boyer’s article Management of Opioid Analgesic Overdose and an important but older article entitled Early discharge of patients with presumed opioid overdose: development of a clinical prediction rule.
The clinical prediction rule that may predict safe discharge is as follows:
1) can mobilize as usual; 2) have oxygen saturation on room air of >92%; 3) have a respiratory rate >10 breaths/min and <20 breaths/min; 4) have a temperature of >35.0 degrees C and <37.5 degrees C; 5) have a heart rate >50 beats/min and <100 beats/min; and 6) have a Glasgow Coma Scale score of 15
We conclude that if the patient demonstrates all six features carefully applied WITH the caveat that there be no verbal or tactile stimulation prior to the evaluation, then the patient is likely to be safe to discharge after reversal with naloxone. This concept has not been strictly tested in the literature, but the article in Clinical Toxicology supports this practice. And now on to the podcast … let us know what you think!
The Hot Stove League of EM/Tox 