Contributor: Travis Barlock MD Educational Pearls:   Alcohol binds the GABA receptor, which produces an inhibitory response, hence the “depressive” effects of ethanol beverages.   Over time, alcohol downregulates the GABA receptors, leading to unopposed glutamate activity. Given that glutamate is excitatory, this can lead to seizures.   Alcohol also suppresses REM sleep; in patients with chronically suppressed REM sleep, the brain starves for dream sleep and it spills over into the wakeful state, inducing a dream-like state when someone is awake.   The awake dream-like state of delirium tremens (DT) differs from alcohol hallucinosis    Alcohol hallucinosis presents with visual hallucinations in a wakeful state   DT presents with a generalized clouding of the sensorium and a dream-like state    Treatment for DT is better achieved with phenobarbital due to predictable pharmacology    Phenobarbital acts on GABA and NMDA receptors    References 1. Davies M. The role of GABAA receptors in mediating the effects of alcohol in the central nervous system. J Psychiatry Neurosci. 2003;28(4):263-274. 2. Fujimoto J, Lou JJ, Pessegueiro AM. Use of Phenobarbital in Delirium Tremens. J Investig Med High Impact Case Reports. 2017;5(4):4-6. doi:10.1177/2324709617742166 3. Walker, M. Chapter 13: iPads, Factory Whistles, and Nightcaps In: Walker, M, Why We Sleep. Scribner; 2017, pg. 272.  4. Zarcone V. Alcoholism and sleep. Adv Biosci. 1978;21:29-38. Summarized & Edited by Jorge Chalit, OMSII  

Podcast 861: Alcohol Withdrawal and Delirium Tremens

Our near daily podcasts move quickly to reflect current events, are inspired by real patient care, and speak to the true nature of what it’s like to work in the Emergency Room or Pre-Hospital Setting.  Each medical minute is recorded in a real emergency department, by the emergency physician or clinical pharmacist on duty – the ER is our studio and everything is live.

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Contributor: Aaron Lessen MD Educational Pearls:   Lorazepam (Ativan) is dosed at 0.1 mg/kg up to a maximum of 4 mg in status epilepticus    Some ED protocols only give 2 mg initially    The maximum recommended dose of levetiracetam (Keppra) is 60 mg/kg or 4.5 g   In one retrospective study, only 50% of patients received the correct dose of lorazepam    For levetiracetam, it was only 35% of patients    Underdosing leads to complications    Higher rates of intubations   More likely to progress to refractory status epilepticus    References 1. Cetnarowski A, Cunningham B, Mullen C, Fowler M. Evaluation of intravenous lorazepam dosing strategies and the incidence of refractory status epilepticus. Epilepsy Res. 2023;190(November 2022):107067. doi:10.1016/j.eplepsyres.2022.107067 2. Sathe AG, Tillman H, Coles LD, et al. Underdosing of Benzodiazepines in Patients With Status Epilepticus Enrolled in Established Status Epilepticus Treatment Trial. Acad Emerg Med. 2019;26(8):940-943. doi:10.1111/acem.13811 Summarized by Jorge Chalit, OMSII | Edited by Meg Joyce & Jorge Chalit  

Episode 901: Underdosing in Status Epilepticus

Contributor: Travis Barlock MD Educational Pearls: Ketamine is an NMDA receptor antagonist with a wide variety of uses in the emergency department. To dose ketamine remember the numbers 0.3, 1, and 3. Pain dose   For acute pain relief administer 0.3 mg/kg of ketamine IV over 10-20 minutes (max of 30 mg).   Note: There is evidence that a lower dose of 0.1-0.15 mg/kg can be just as effective.   Dissociative dose   To use ketamine as an induction agent for intubation or for procedural sedation administer 1 mg/kg IV over 1-2 minutes.   IM for acute agitation   If a patient is out of control and a danger to themselves or others, administer 3 mg/kg intramuscularly (max 500 mg).   If you are giving IM ketamine it has to be in the concentrated 100 mg/ml vial.   Additional pearls   Pushing ketamine too quickly can cause laryngospasm.   Between .3 and 1 mg/kg is known as the recreational dose. You want to avoid this range because this is where ketamine starts to pick up its dissociative effects and can cause unpleasant and intense hallucinations. This is colloquially known as being in the “k-hole”.   References   Gao, M., Rejaei, D., & Liu, H. (2016). Ketamine use in current clinical practice. Acta pharmacologica Sinica, 37(7), 865–872. https://doi.org/10.1038/aps.2016.5   Lin, J., Figuerado, Y., Montgomery, A., Lee, J., Cannis, M., Norton, V. C., Calvo, R., & Sikand, H. (2021). Efficacy of ketamine for initial control of acute agitation in the emergency department: A randomized study. The American journal of emergency medicine, 44, 306–311. https://doi.org/10.1016/j.ajem.2020.04.013   Stirling, J., & McCoy, L. (2010). Quantifying the psychological effects of ketamine: from euphoria to the k-Hole. Substance use & misuse, 45(14), 2428–2443. https://doi.org/10.3109/10826081003793912   Summarized by Jeffrey Olson MS2 | Edited by Jorge Chalit, OMS II

Episode 900: Ketamine Dosing

Contributor: Travis Barlock MD Educational Pearls:   Thrombolytic therapy (tPA or TNK) is often used in the ED for strokes   Use of anticoagulants with INR > 1.7 or  PT >15    Warfarin will reliably increase the INR    Current use of Direct thrombin inhibitor or Factor Xa inhibitor     aPTT/PT/INR are insufficient to assess the degree of anticoagulant effect of Factor Xa inhibitors like apixaban (Eliquis) and rivaroxaban (Xarelto)     Intracranial or intraspinal surgery in the last 3 months    Intracranial neoplasms or arteriovenous malformations also increase the risk of bleeding    Current intracranial or subarachnoid hemorrhage    History of intracranial hemorrhage from thrombolytic therapy also contraindicates tPA/TNK    Recent (within 21 days) or active gastrointestinal bleed   Hypertension    BP >185 systolic or >110 diastolic   Administer labetalol before thrombolytics to lower blood pressure    Timing of symptoms    Onset > 4.5 hours contraindicates tPA    Platelet count < 100,000   BGL < 50    Potential alternative explanation for stroke-like symptoms obviating need for thrombolytics    References 1. Fugate JE, Rabinstein AA. Absolute and Relative Contraindications to IV rt-PA for Acute Ischemic Stroke. The Neurohospitalist. 2015;5(3):110-121. doi:10.1177/1941874415578532 2. Powers WJ, Rabinstein AA, Ackerson T, et al. Guidelines for the Early Management of Patients with Acute Ischemic Stroke: 2019 Update to the 2018 Guidelines for the Early Management of Acute Ischemic Stroke a Guideline for Healthcare Professionals from the American Heart Association/American Stroke Association. Vol 50.; 2019. doi:10.1161/STR.0000000000000211 Summarized by Jorge Chalit, OMSII | Edited by Jorge Chalit

Episode 899: Thrombolytic Contraindications

Contributor: Ricky Dhaliwal, MD Educational Pearls:   Takotsubo cardiomyopathy, also known as "broken heart syndrome,” is a temporary heart condition that can mimic the symptoms of a heart attack, including troponin elevations and mimic STEMI on ECG.   The exact cause is not fully understood, but it is often triggered by severe emotional or physical stress. The stress can lead to a surge of catecholamines which affects the heart (multivessel spasm/paralysed myocardium).   The name "Takotsubo" comes from the Japanese term for a type of octopus trap, as the left ventricle takes on a distinctive shape resembling this trap during systole. The LV is dilated and part of the wall becomes akenetic. These changes can be seen on ultrasound.   The population most at risk for Takotsubo are post-menopausal women.   Coronary angiography is one of the only ways to differentiate Takotsubo from other acute coronary syndromes.   Most people with Takotsubo cardiomyopathy recover fully.   References   Amin, H. Z., Amin, L. Z., & Pradipta, A. (2020). Takotsubo Cardiomyopathy: A Brief Review. Journal of medicine and life, 13(1), 3–7. https://doi.org/10.25122/jml-2018-0067   Bossone, E., Savarese, G., Ferrara, F., Citro, R., Mosca, S., Musella, F., Limongelli, G., Manfredini, R., Cittadini, A., & Perrone Filardi, P. (2013). Takotsubo cardiomyopathy: overview. Heart failure clinics, 9(2), 249–x. https://doi.org/10.1016/j.hfc.2012.12.015   Dawson D. K. (2018). Acute stress-induced (takotsubo) cardiomyopathy. Heart (British Cardiac Society), 104(2), 96–102. https://doi.org/10.1136/heartjnl-2017-311579   Kida, K., Akashi, Y. J., Fazio, G., & Novo, S. (2010). Takotsubo cardiomyopathy. Current pharmaceutical design, 16(26), 2910–2917. https://doi.org/10.2174/138161210793176509   Summarized by Jeffrey Olson MS2 | Edited by Jorge Chalit, OMSII

Episode 898: Takotsubo Cardiomyopathy

Contributor: Ricky Dhaliwal MD Educational Pearls:   Primary adrenal insufficiency (most common risk factor for adrenal crises)    An autoimmune condition commonly known as Addison's Disease   Defects in the cells of the adrenal glomerulosa and fasciculata result in deficient glucocorticoids and mineralocorticoids   Mineralocorticoid deficiency leads to hyponatremia and hypovolemia    Lack of aldosterone downregulates Endothelial Sodium Channels (ENaCs) at the renal tubules   Water follows sodium and generates a hypovolemic state    Glucocorticoid deficiency contributes further to hypotension and hyponatremia    Decreased vascular responsiveness to angiotensin II   Increased secretion of vasopressin (ADH) from the posterior pituitary     An adrenal crisis is defined as a sudden worsening of adrenal insufficiency    Presents with non-specific symptoms including nausea, vomiting, fatigue, confusion, and fevers   Fevers may be the result of underlying infection    Work-up in the ED includes labs looking for infection and adding cortisol + ACTH levels   Emergent treatment is required    100 mg hydrocortisone bolus followed by 50 mg every 6 hours   Immediate IV fluid repletion with 1L normal saline    The most common cause of an adrenal crisis is an acute infection in patients with baseline adrenal insufficiency    Often due to a gastrointestinal infection    References 1. Bancos I, Hahner S, Tomlinson J, Arlt W. Diagnosis and management of adrenal insufficiency. Lancet Diabetes Endocrinol. 2015;3(3):216-226. doi:10.1016/S2213-8587(14)70142-1 2. Bornstein SR, Allolio B, Arlt W, et al. Diagnosis and Treatment of Primary Adrenal Insufficiency: An Endocrine Society Clinical Practice Guideline. J Clin Endocrinol Metab. 2016;101(2):364-389. doi:10.1210/jc.2015-1710 3. Cronin CC, Callaghan N, Kearney PJ, Murnaghan DJ, Shanahan F. Addison disease in patients treated with glucocorticoid therapy. Arch Intern Med. 1997;157(4):456-458. 4. Feldman RD, Gros R. Vascular effects of aldosterone: sorting out the receptors and the ligands. Clin Exp Pharmacol Physiol. 2013;40(12):916-921. doi:10.1111/1440-1681.12157 5. Hahner S, Loeffler M, Bleicken B, et al. Epidemiology of adrenal crisis in chronic adrenal insufficiency: the need for new prevention strategies. Eur J Endocrinol. 2010;162(3):597-602. doi:10.1530/EJE-09-0884  Summarized by Jorge Chalit, OMSII | Edited by Meg Joyce & Jorge Chalit  

Podcast 861: Alcohol Withdrawal and Delirium Tremens

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