Pearl of The Day: Disposition of Atrial Fibrillation

Disposition of Atrial Fibrillation For other pearls of the day regarding afib, follow the links here: Rhythm Control and Cardioversion Holiday Heart Syndrome Ottawa Aggressive Protocol

Admit - indications: hyperthyroidism, ischemia, infectious process, CHF, difficulty with rate control - ablation therapy indications: difficulty with controlling ventricular rate, LV dysfunction, rate-related cardiomyopathy, refractory symptomatic paroxysmal afib

Discharge - stable patients may be discharged with outpatient follow up if rate-controlled and absence of structural heart disease - if required medications for rate control during ED stay, prescribe same class of medications when discharged (e.g., metoprolol tartrate 50 mg PO BID or dilitiazem ER 120 mg or 180 mg PO daily) - risk of stroke is equal for paroxysmal and persistent afib, and so anticoagulation should always be considered based on CHA2DS2VASc score

CHA2DS2VASc Score - congestive heart failure - hypertension - age > 74 (2 points) - diabetes - previous TIA/CVA (2 points) - vascular diseases (e.g., CAD, MI, PVD) - age 65 - 74 - female - score 0 = low risk - score 1 = low-moderate risk (consider antiplatelet or anticoagulation) - score 2 = moderate-high risk (anticoagulation indicated) - consider bleeding risk for patients prior to starting (ATRIA Bleeding Risk Score)

Anticoagulation - oral anticoagulation preferred: apixaban, dabigatran, rivaroxaban, warfarin - patients not suitable for anticoagulation (if not due to risk of bleed) -> clopidogrel and ASA (81 mg - 325 mg) - afib + mitral stenosis -> warfarin - afib + stable CAD -> warfarin - afib > 48h -> warfarin OR heparin OR dabigatran for at least 3 weeks prior to cardioversion

Resources LITFL, Atrial Fibrillation: https://lifeinthefastlane.com/ccc/atrial-fibrillation/ Anticoagulation Dosing: http://www.acc.org/tools-and-practice-support/clinical-toolkits/atrial-fibrillation-afib/anticoagulant-dosing-table Emergency Medicine Cases: https://emergencymedicinecases.com/episode-20-atrial-fibrillation/ Ann Arbor Afib Algorithm: https://www.acep.org/_QIPS-Section-Microsite/Improving-and-Standardizing-Care-of-Patients-with-Atrial-Fibrillation-in-a-Community-Emergency-Department/#sm.0000o9mbwcinmefstkr1zrovyb3vu

Pearl of the Day: Cannabinoid Hyperemesis Syndrome

Cannabinoid Hyperemesis Syndrome (CHS) Background - prodromal phase (months to years): early morning nausea, fear of vomiting, abdominal discomfort - hyperemetic phase (24 - 48 hours): paroxysms of intense vomiting and abdominal pain, can have marked weight loss - recovery phase (days to months): normal eating patterns, regular weight gain - can be confused with cyclic vomiting syndrome, which is usually more associated with increased gastric emptying rates, psychological comorbidities, history of migraine headaches - in GI tract, cannabinoids activate CB1 receptors -> inhibits gastric acid secretion, relaxes lower esophageal sphincter relaxation, reduces gastric motility, delays gastric emptying

Signs and Symptoms - recurrent episodes of nausea, vomiting, dehydration - begins several years after start of chronic marijuana abuse, usually with daily use and often > 3 - 5 times per day

Diagnosis - proposed clinical criteria: long-term weekly cannabis use, abdominal pain, severe cyclic nausea and vomiting, relief of symptoms with hot showers

Treatment - may require hospitalization during hyperemetic phase for supportive therapy - traditional antiemetic therapy provides minimal improvement - hot showers provide relief through unknown mechanism (one theory:  heat corrects cannabis-induced disequilibrium of thermoregulatory system of hypothalamus) - topical capsaicin cream to abdomen has successfully treated CHS in multiple case reports - capsaicin binds to TRPV1 receptors with high specificity -> impairs substance P signaling - most effective treatment:  cessation

Resources Galli JA, Sawaya RA, Friedenberg FK. Cannabinoid Hyperemesis Syndrome. Current drug abuse reviews. 2011;4(4):241-249. https://www.aliem.com/2017/11/trick-trade-treatment-cannabinoid-hyperemesis/

Related Reading https://www.nytimes.com/2018/04/05/well/a-perplexing-marijuana-side-effect-relieved-by-hot-showers.html?smid=fb-nytimes&smtyp=cur

Pearl of the Day: Metformin Toxicity

Metformin Toxicity Background - metformin decreases glucose utilization, increases lactate production by hepatocytes - metformin toxicity manifests as lactic acidosis - in absence of acute overdose, rarely develops in patients without comorbidities (e.g., renal/hepatic insufficiency, acute infection) - unclear what minimum dose leads to toxicity

Signs/Symptoms - nausea, abdominal pain, other GI complaints - altered mental status, dyspnea, hypotension, tachycardia

Work-up - BGM - EKG,  acetaminophen, salicylate levels to rule out other coningestants - blood gas, BMP, serum lactate - serum metformin levels often do not correlate with severity of poisoning, but negative level rules out toxicity

Management - if acute, GI decontamination with activated charcoal - if hypoglycemic, dextrose 0.5 - 1 g/kg IV, though should seek other causes as metformin itself should not cause hypoglycemia - sodium bicarbonate for severe metabolic acidosis (pH < 7.15) - hemodialysis indications:  lactate > 20 mmol/L, pH < 7.0, failure to improve with supportive care within 2 - 4 hours - early consultation with nephrologist and toxicologist

Disposition - patients who appear well and have normal acid-base status after 6 - 8 hours may be medically cleared - asymptomatic patients with persistent acidosis require further observation - symptomatic patients should all be admitted

Resources Metformin Poisoning, UpToDate