EM Case Presentation

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EM Case Presentation
Nic Granzella MSIV, Albert Einstein College of
Medicine
2
ED Triage Note 725AM
-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/
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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
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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
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Physical Exam
Vitals T 98.3, HR 98, BP 116/66, RR 18, 98 on
RA, BMI 23.8 Gen 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 AOx3, CN2-12 intact, no focal
deficits, gait wnl
http//heart-symptoms.org/heart-palpitations-at-ni
ght.html
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Labs/Imaging
BMP 141/4.5 108/16.8 30/1.8 Glucose 64
CBC 9.1 gt 11.2 / 35.0 lt 296, MCV 101.3, RDW
13.6 Coags INR 2.6, PT 27.9, aPTT
32.5 Troponins 0.007 (nl lt0.09) 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
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Labs/Imaging, cont'd
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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
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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. a- and ß-
adrenergic activation. Enhances platelet
activation and aggregation.
http//atforum.com/SiteRoot/pages/current_pastissu
es/winter2000.shtml
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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/coca
ine-history/
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Palpitation Dx/Tx
http//www.aafp.org/afp/2005/0215/p743.html
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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 SBPlt100.
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
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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 gt
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)
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Take Home Points
Any drug toxicity history is important,
especially if multiple comorbidities/meds
(iatrogenic vs. illicit) Cocaine toxicity does
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.
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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-in
toxication?sourcesee_linkH8.
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Additional Literature re beta-blockers
Cocaine and ß-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 ß-adrenergic antagonists in
patients with cocaine use who were admitted to
either telemetry or the ICU. Undoubtedly, this
article will renew the controversy surrounding
ß-adrenergic antagonists and cocaine and find
support of others who continue to write of the
benefits of ß-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 is generally 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 ß-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.
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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).