Author: Don Stader, MD
- Fluoroquinolones can cause connective tissue disruption leading not only to tendon rupture but also aortic dissection.
- Retrospective study from Taiwan showed over a 2x higher rate of dissection when exposed to fluoroquinolones (1.6% vs 0.6%).
- Remember to think about aortic dissection when you have a patient with chest pain that travels and/or involves neurologic symptoms.
- Try to use fluoroquinolones when no other appropriate antibiotic exists as they have significant other side effects as well.
Editor’s note: In July 2018, the FDA required strengthening of warning labels on fluoroquinolones about the risks of mental health effects and hypoglycemia
Lee CC, Lee MG, Hsieh R, Porta L, Lee WC, Lee SH, Chang SS. Oral Fluoroquinolone and the Risk of Aortic Dissection. J Am Coll Cardiol. 2018 Sep 18;72(12):1369-1378. doi: 10.1016/j.jacc.2018.06.067. PubMed PMID: 30213330.
Khaliq Y, Zhanel GG. Fluoroquinolone-associated tendinopathy: a critical review of the literature. Clin Infect Dis. 2003 Jun 1;36(11):1404-10. Epub 2003 May 20. Review. PubMed PMID: 12766835.
Summary by Travis Barlock, MS4 | Edited by Erik Verzemnieks, MD
Author: Don Stader, MD
- 8014 patients with out-of-hospital cardiac arrest randomized to epinephrine vs placebo
- 30-day survival was not dramatically better between groups (3.2%in the epinephrine group and 2.4% in the placebo group)
- Functional neurological outcome was nearly identical at 2.2% and 1.9% of patients
- Adds to literature that epinephrine provides little important benefit in cardiac arrest – focus on chest compressions and early defibrillation
Editor’s note: NNT for epinephrine to prevent one death in this study was 115 – compared to bystander CPR (NNT 15) and defibrillation (NNT 5) from prior studies.
Perkins GD et. al. . A Randomized Trial of Epinephrine in Out-of-Hospital Cardiac Arrest. N Engl J Med. 2018 Aug 23;379(8):711-721. doi: 10.1056/NEJMoa1806842. Epub 2018 Jul 18.
Kitamura T, Kiyohara K, Sakai T, et al. Public-access defibrillation and out-of-hospital cardiac arrest in Japan. N Engl J Med 2016;375:1649-1659.
Hasselqvist-Ax I, Riva G, Herlitz J, et al. Early cardiopulmonary resuscitation in out-of-hospital cardiac arrest. N Engl J Med 2015;372:2307-2315.
Hagihara A, Hasegawa M, Abe T, Nagata T, Wakata Y, Miyazaki S. Prehospital epinephrine use and survival among patients with out-of-hospital cardiac arrest. JAMA. 2012 Mar 21;307(11):1161-8. doi: 10.1001/jama.2012.294. PubMed PMID: 22436956.
Sanghavi P, Jena AB, Newhouse JP, Zaslavsky AM. Outcomes after out-of-hospital cardiac arrest treated by basic vs advanced life support. JAMA Intern Med. 2015 Feb;175(2):196-204. doi: 10.1001/jamainternmed.2014.5420.
Author: Michael Hunt, MD
- Toxicity happens from local anesthetics being given too fast, too much, or in the unintended spot
- Systemic toxicity manifests first with neurologic symptoms like circumoral numbness, tinnitus, blurred vision, nausea, and even seizures. Severe toxicity can then progress to arrhythmias and cardiac arrest.
- Maximum doses of lidocaine: 4 mg/kg; and with epinephrine: 7mg/kg.
- Maximum dose of bupivacaine: 2mg/kg; with epinephrine 3mg/kg
Editor note: treat seizures with benzodiazepines and avoid propofol for sedation; severe toxicity can also be treated with a 20% lipid emulsion, though there is debate on its efficacy
Dickerson DM, Apfelbaum JL. Local anesthetic systemic toxicity. Aesthet Surg J. 2014 Sep;34(7):1111-9. doi: 10.1177/1090820X14543102.
Neal JM, Mulroy MF, Weinberg GL; American Society of Regional Anesthesia and Pain Medicine.. American Society of Regional Anesthesia and Pain Medicine checklist for managing local anesthetic systemic toxicity: 2012 version. Reg Anesth Pain Med. 2012 Jan-Feb;37(1):16-8. doi: 10.1097/AAP.0b013e31822e0d8a.
Vasques F, Behr AU, Weinberg G, Ori C, Di Gregorio G. A Review of Local Anesthetic Systemic Toxicity Cases Since Publication of the American Society of Regional Anesthesia Recommendations: To Whom It May Concern. Reg Anesth Pain Med. 2015 Nov-Dec;40(6):698-705. doi: 10.1097/AAP.0000000000000320.
Author: Don Stader, MD.
- A baby can be born dependent on opioids but not addicted to them.
- Opioid addiction (Opioid Use Disorder) is a disease of mature brains and is characterized by compulsive drug use despite adverse consequences.
- Opioid addiction is a disease that affects the reward center of the brain
- Pregnant patients struggling with addiction do better when started on buprenorphine or methadone. This treatment will cause opioid withdrawal syndrome in newborns, but not the long term morbidity and mortality of illicit opioids.
Gowing L, Farrell MF, Bornemann R, Sullivan LE, Ali R. Oral substitution treatment of injecting opioid users for prevention of HIV infection. Cochrane Database of Systematic Reviews 2011, Issue 8: CD004145. DOI: 10.1002/14651858.CD004145.pub4.
Volkow ND, Koob GF, McLellan AT ( 2016). “Neurobiologic Advances from the Brain Disease Model of Addiction.” New England Journal of Medicine. 374 (4): 363?371.
Author: Rachel Beham, PharmD
- Tenecteplase is more specific for fibrin and has a longer half-life than alteplase.
- In setting of ischemic stroke, tenecteplase before thrombectomy was associated with a statistically higher incidence of reperfusion and better functional outcome than alteplase.
Bruce C.V. Campbell B et al (2018). Tenecteplase versus Alteplase before Thrombectomy for Ischemic Stroke. New England Journal of Medicine. 378:1573-1582
Author: Dylan Luyten, MD
- Most important questions to answer with low potassium are 1. What are their symptoms? 2. Can they take potassium by mouth?
- Oral repletion is faster, cheaper, and more effective than IV repletion.
- Give IV potassium when patients have K < 2.5 mmol/L or present with arrhythmias and/or characteristic EKG changes (flattened T waves).
- Most patients who are hypokalemic are hypomagnesemic and require magnesium supplementation. Checking a level is unnecessary.
Ashurst J, Sergent SR, Wagner BJ, Kim J. Evidence-based management of potassium disorders in the emergency department. Emerg Med Pract. 2016 Nov 22;18(Suppl Points & Pearls):S1-S2
Whang R, Flink EB, Dyckner T, et al. Magnesium depletion as a cause of refractory potassium repletion. Arch Intern Med 1985; 145:1686.
Check out this episode!
Author: Nick Hatch, MD
- Recent study argues that CHF patients receiving furosemide within 60 minutes of arrival had a lower in-hospital mortality than those receiving it after (2.3% vs. 6.0%, p=0.002).
- A flaw in the study is that there were significant baseline differences between groups.
Matsue Y et al. Time-to-Furosemide Treatment and Mortality in Patients Hospitalized With Acute Heart Failure. JACC 2017. PMID: 28641794
Author: Nick Hatch, MD
- The sodium-glucose cotransporter in the gut is essential for rehydration.
- Oral rehydration therapies require an equimolar concentration of glucose and sodium to be effective.
- ORT has saved millions of lives globally.
- Consider using ORT in patients with dehydration. Especially useful in resource limited settings.
Victora CG, Bryce J, Fontaine O, Monasch R. Reducing deaths from diarrhoea through oral rehydration therapy. Bull World Health Organ. 2000; 78:1246.
Santillanes G, Rose E. Evaluation and Management of Dehydration in Children. Emerg Med Clin North Am. 2018. 36(2):259-273. doi: 10.1016/j.emc.2017.12.004.
Author: Rachel Beham, PharmD
- Some synthetic cannabinoids have been contaminated with Brodifacoum. Brodifacoum is a Vitamin K antagonist and can present with a severe coagulopathy.
- Brodifacoum is commonly known as “superwarfarin” and has a very long half life of 120+ days.
- Check PT/INR in patients with a bleeding diathesis in setting of synthetic cannabinoid use.
- Treatment is activated charcoal and large doses of Vitamin K (10mg Q6H for months).
Lipton R.A.; Klass E.M. (1984). “Human ingestion of a ‘superwarfarin’ rodenticide resulting in a prolonged anticoagulant effect”. JAMA. 252: 3004?3005.
La Rosa F; Clarke S; Lefkowitz J. B. (1997). “Brodifacoum intoxication with marijuana smoking”. Archives of Pathology & Laboratory Medicine. 121: 67?69
Author: Gretchen Hinson, M.D.
- Controversial topic.
- Pathophysiology – acidosis leads to an extracellular potassium shift. Patients in DKA will be intracellularly potassium deplete, but will have a falsely normal/elevated serum potassium.
- 3 risk of giving bicarb in DKA – alkalosis will drive potassium intracellularly but can overshoot (hypokalemia) and increase risk of arrhythmias; bicarb slows clearance of ketones and will transiently increase their precursors; bicarb can cause elevated CSF acidosis.
- 3 instances when appropriate to give bicarb in DKA: DKA in arrest; hyperkalemic in DKA with arrhythmia; fluid and vasopressor refractory hypotension.
Bratton, S. L., & Krane, E. J. (1992). Diabetic Ketoacidosis: Pathophysiology, Management and Complications. Journal of Intensive Care Medicine, 7(4), 199-211. doi:10.1177/088506669200700407
Chua, H., Schneider, A., & Bellomo, R. (2011). Bicarbonate in diabetic ketoacidosis – a systematic review. Annals of Intensive Care, 1(1), 23. doi:10.1186/2110-5820-1-23