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EM Case Presentation

EM Case Presentation. Nic Granzella MSIV, Albert Einstein College of Medicine. ED Triage Note – 7:25AM. -70M BIB ambulance after calling 911 for “palpitations after drinking and drug use last night.” -HR 98, FS 62, afebrile, other VSS -Intermittent palpitations -No pain, non-distressed

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EM Case Presentation

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  1. EM Case Presentation Nic Granzella MSIV, Albert Einstein College of Medicine

  2. ED Triage Note – 7:25AM -70M BIB ambulance after calling 911 for “palpitations after drinking and drug use last night.” -HR 98, FS 62, afebrile, other VSS -Intermittent palpitations -No pain, non-distressed -HIV+ http://thebsreport.wordpress.com/2009/12/02/woman-steals-ambulance-that-brought-her-to-the-hospital/

  3. History HPI: - Woke up at 6am → upon awakening he felt dizzy and noticed his heart beating quickly. - Heart rate would stay elevated for minutes at a time, then return to normal. Cannot identify any alleviating or exacerbating factors since waking up. - Last night reports drinking 5-6 beers and 5-6 [shrugs] “or more” vodka drinks and taking 5-10 hits from his crack pipe - Similar symptoms “a few months ago” - Denies: chest/arm pain, tightness, SOB, HA, syncope, episodes of N/V/D, weakness, fevers, heat intolerance

  4. More History PMH: HIV (CD4 = ~500), HepC, HTN, Afib (on warfarin), DM2, asthma (no intubations), hiatal hernia, +/- 1 mild MI (details unknown) PSH: Hiatal hernia repair x2 Meds: statin, metoprolol, aspirin, inhaled corticosteriod & B-agonist, HAART, glyburide, warfarin, diclofenac Allergies: NKDA Social:Cocaine 1x/month for 30 years, ~1 pint of vodka/month, never smoked cigarettes, lives in Bx apt, has home health aide 4hrs/day, rarely sees kids, bored at home

  5. Physical Exam Vitals: T 98.3, HR 98, BP 116/66, RR 18, 98% on RA, BMI 23.8Gen: pt awake & alert in bed, NAD, well-appearing HEENT: NCAT, PERRL, EOMI, MMM, nasal septum intact & midline, non-injected pharynx, clear conjunctivae CV: +/- tachy, regular rhythm, no m/r/g, nl s1s2 Resp:CTAB, equal air entry b/l Abd:soft, NTND, +BS, no HSM Extr:no c/c/e, no track marks, no calf tenderness Neuro:A&Ox3, CN2-12 intact, no focal deficits, gait wnl http://heart-symptoms.org/heart-palpitations-at-night.html

  6. Labs/Imaging BMP: 141/4.5 108/16.8 30/1.8 Glucose 64 CBC: 9.1 > 11.2 / 35.0 < 296, MCV 101.3, RDW 13.6 Coags: INR 2.6, PT 27.9, aPTT 32.5 Troponins: 0.007 (nl <0.09) EtOH: 55.0 CK, LFTs, amylase, lipase: wnl CXR:large hiatal hernia (unchange from previous), no enlargement of cardiac silhouette, no acute cardiopulmonary abnormality, no interval change http://www.flutrackers.com/forum/showthread.php?t=92343

  7. Labs/Imaging, cont'd

  8. Differential Diagnosis Cardiopulm: cardiac arrhythmias (PVCs, SVT, Afib/flutter, WPW, MAT, others), cardiomyopathy, CHF, atrial myxoma, valvulopathies/prolapse, pericarditis, PE Endo/metabolic: hyperthyroidism, hypoglycemia, pheo Psyc: anxiety/panic attack Drugs/Meds: numerous, including beta-agonists, sympathomimetics, digoxin, theophylline, cocaine, diet pills, caffeine, many others

  9. Cocaine - Background What it is: extract from coca plants (erythroxylum coca). Chewed by South American Indians to relieve hunger and fatigue. Also topical anesthetic. Sympathomimetic/ psychomotor stimulant. http://en.wikipedia.org/wiki/Erythroxylum_coca Mechanism: blocks reuptake of DA, 5-HT, catecholamines. Peripheral blockage of epi/norepi reuptake→ vasoconstriction. α- and β- adrenergic activation. Enhances platelet activation and aggregation. http://atforum.com/SiteRoot/pages/current_pastissues/winter2000.shtml

  10. Cocaine - Background Acute effects: low doses: euphoria, paranoia, hyperthermia, HTN, tachycardia. High doses: seizures, arrhythmias, respiratory arrest, coronary (and other vessel) vasospasm, LV dysfunction, rhabdo. Also GI, endo, renal, sexual effects Chronic effects: accelerated atherosclerosis, LVH, cardiomyopathy, myocarditis, myocardial fibrosis Metabolism: plasma cholinesterase...also metabolizes succinylcholine! So don't use succ if intubation is needed! http://www.homehealthtesting.com/blog/2010/07/cocaine-history/

  11. Palpitation Dx/Tx http://www.aafp.org/afp/2005/0215/p743.html

  12. Managing Cocaine Toxicity Dx/severity: history, vitals, EKG, troponins/cardiac biomarkers, CXR, can confirm with Utox (+/-). Initial treatment: can give O2 -Benzos if HTN/tachy/agitated (5mg diazepam or 1 mg lorazepam q5 min). -Nitroglycerin if HTN (0.4 mg q5 min max 3 doses). -ASA(325mg) and/or phentolamine(1-5 mg) if ischemia/HTN. -Hold phentolamine if SBP<100. Later/dispo: -uncomplicated: agitation + sympathomimetic tox = benzos → obs until asymptomatic → d/c -w/ chest pain/palps: if nl/unchanged ekg → repeat trops and ecg at 6 hours → d/c -complicated: end-organ toxicity = admit

  13. What does the research show? Beta blockers? 2008 study by Dattilo et al suggested they have a benefit. Multiple responses suggest this study was flawed. Then in 2010, Rangel et al found no evidence of increase rates of adverse events with beta-blockers. Again, suggestions of study flaws arose. Current recommendations = don't give beta blockers. Benzos: 2003 study by Honderick et al found that lorazepam + nitroglycerin > nitroglycerin alone in terms of pain relief during cocaine-associated chest pain. No differences in complications (none occurred). Phentolamine:alpha-adrenergic antagonist. Study: during cardiac cath, pts given low-dose cocaine which caused 8-12% CA narrowing, increased HR & BP, and decreased coronary sinus blood flow. Phentolamine reversed these (Lange et al, 1989, NEJM)

  14. Take Home Points Any drug toxicity = history is important, especially if multiple comorbidities/meds (iatrogenic vs. illicit) Cocaine toxicitydoes not always = chest pain. Cocaine can affect most organ systems. Initial eval: history, vitals, EKG, troponins, CXR, FS Initial treatment: O2, benzos/nitro/phentolamine, no beta-blockers (yet). Avoid succinylcholine if possible. Watch out for:missing dx in cases of mild chest pain, young pts, or pts with no obvious cardiac history. Infrequent monitoring. Incomplete chart review for previous cardiac work-up (e.g. pt's baseline EF if CHF). Complications: pneumothorax 2/2 “crack lung,” and aortic dissection.

  15. References Abbot, A. “Diagnostic approach to palpitations.” American Family Physician 2005; 71(4)743-750. Cotran, RS et al (1999). Pathologic basis of disease; Chapter 9. Environmental and Nutritional Pathology. Pages 425-426. Fung, SC. “Response to 'Beta-blockers are associated with reduced risk of MI after cocaine use' by Dattilo et al.” Annals of Emergency Medicine, 2008; 52(1)88. Hoffman, R. “Cocaine and beta-blockers: should the controversy continue?” Annals of Emergency Medicine, 2008; 51(2)127. Nelson, L. “Cocaine: acute intoxication.” Uptodate, 2012; http://www.uptodate.com/ contents/cocaine-acute-intoxication?source=see_link#H8.

  16. Additional Literature re: beta-blockers Cocaine and β-Blockers: Should the Controversy Continue? Robert S. Hoffman, MD In this issue of Annals, Dattilo et al offer a retrospective view of the use of β-adrenergic antagonists in patients with cocaine use who were admitted to either telemetry or the ICU. Undoubtedly, this article will renew the controversy surrounding β-adrenergic antagonists and cocaine and find support of others who continue to write of the benefits of β-adrenergic antagonists. [28] and [29] On closer examination, however, significant limitations in study design interfere with conclusions about safety, efficacy, and applicability. Previous studies [19], [20] and [21] enrolled patients with cocaine use and chest pain, whereas in the present study less than half the patients had chest pain. Additional concerns about this cohort can be best appreciated in the mortality table, which highlights the differences between a prospective evaluation of patients with cocaine-related chest pain and a retrospective review of ICU and telemetry admissions for various illnesses in recent cocaine users. Furthermore, whereas previous studies used a history of recent cocaine use (often confirmed by urine screening), here the criterion standard is a urine test that is positive for cocaine. Although it isgenerally accepted that urine remains positive for 2 to 3 days after intermittent cocaine use, chronic users can have positive urines for up to 2 weeks at the cutoff value selected by Dattilo et al. Although rare cases of myocardial infarction have been attributed to cocaine many days after their last use, nearly 90% of patients with documented cocaine-associated myocardial infarctions present within 24 hours of their last cocaine use. Given these limitations, it is unclear how these patients compare with those reported in the prospective studies described earlier. Because the majority of patients with cocaine-associated chest pain will continue to use cocaine after discharge, giving these patients β-adrenergic antagonists will not only repeat a practice abandoned by its pioneers nearly 30 years ago for good reason but also subject an unpredictable subset of these individuals to the lethal drug interaction so well described in controlled animal investigations.

  17. Additional Literature re: beta-blockers Response to: Beta-Blockers Are Associated With Reduced Risk of Myocardial Infarction After Cocaine Use (2008) by Dattilo et al. By: Sze Chun Albert Fung, MBChB, FHKCEM, FHKAM (Emergency Medicine), Yiu Cheung Chan, MBBS., FHKCEM, FHKAM (Emergency Medicine), Fei Lung Lau, MBBS., MRCP, FHKAM (Emergency Medicine) To the Editor: We read with interest the article by Dattilo et al.1 However, we found several limitations in the data calculation which may affect the interpretation and conclusion of this study. First of all, 33 out of the 60 patients (55%) receiving beta-blockers had troponin measured. On the other hand, 277 out of the 288 patients (96%) not receiving beta-blockers had troponin levels measured. This may imply that the baseline characteristics of these 2 groups were different. The group not receiving beta-blockers might have more clinical features suggestive of cardiac problems which led to more frequent troponin testing. Besides, such a high “drop-off” rate in the beta-blocker group would affect the interpretation of the results. Moreover, the authors calculated myocardial infarction risk in the group receiving beta-blockers and the group not receiving beta-blockers as 6% (2/33) versus 26% (72/277), respectively. They excluded the 31 patients with myocardial infarction in the beta-blocker group who had a raised troponin before the use of beta-blockers but included those same 31 patients in the denominator when calculating the risk. If we excluded those 31 patients, the calculated risk of myocardial infarction in the beta-blocker group would become 100% (2/2).

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