Emergency Medical Minute Emergency Medical Minute

Contributor: Travis Barlock MD
Educational Pearls:
How do you differentiate between compensated and decompensated cirrhosis?
Use the acronym VIBE to look for signs of being decompensated.
V-Volume
Cirrhosis can cause volume overload through a variety of mechanisms such as by increasing pressure in the portal vein system and the decreased production of albumin.
Look for pulmonary edema (dyspnea, orthopnea, wheezing/crackles, coughing up frothy pink sputum, etc.) or a tense abdomen.
I-Infection
The ascitic fluid can become infected with bacteria, a complication called Spontaneous Bacterial Peritonitis (SBP).
Look for abdominal pain, fever, hypotension, and tachycardia. Diagnosis is made with ascitic fluid cell analyses (polymorphonuclear neutrophils >250/mm3)
B-Bleeding
Another consequence of increased portal pressure is that blood backs up into smaller blood vessels, including those in the esophagus.
Over time, this increased pressure can result in the development of dilated, fragile veins called esophageal varices, which are prone to bleeding.
Look for hematemesis, melena, lightheadedness, and pale skin.
E-Encephalopathy
A failing liver also does not clear toxins which can affect the brain.
Look for asterixis (flapping motion of the hands when you tell the patient to hold their hands up like they are going to stop a bus)
Other complications to look out for.
Hepatorenal syndrome
Hepatopulmonary syndrome
References
Engelmann, C., Clària, J., Szabo, G., Bosch, J., & Bernardi, M. (2021). Pathophysiology of decompensated cirrhosis: Portal hypertension, circulatory dysfunction, inflammation, metabolism and mitochondrial dysfunction. Journal of hepatology, 75 Suppl 1(Suppl 1), S49–S66. https://doi.org/10.1016/j.jhep.2021.01.002
Enomoto, H., Inoue, S., Matsuhisa, A., & Nishiguchi, S. (2014). Diagnosis of spontaneous bacterial peritonitis and an in situ hybridization approach to detect an "unidentified" pathogen. International journal of hepatology, 2014, 634617. https://doi.org/10.1155/2014/634617
Mansour, D., & McPherson, S. (2018). Management of decompensated cirrhosis. Clinical medicine (London, England), 18(Suppl 2), s60–s65. https://doi.org/10.7861/clinmedicine.18-2-s60
Summarized by Jeffrey Olson MS2 | Edited by Meg Joyce & Jorge Chalit, OMS II
 

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
 

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

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 BGL 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

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

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