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
-HIV+
http://thebsreport.wordpress.com/2009/12/02/woman-stealsambulance-that-brought-her-to-the-hospital/
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
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 & Bagonist, 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
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: A&Ox3, CN2-12 intact, no focal deficits, gait wnl
http://heart-symptoms.org/heartpalpitations-at-night.html
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
Labs/Imaging, cont'd
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
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, 5HT, 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
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/
Palpitation Dx/Tx
http://www.aafp.org/afp/2005/0215/p743.html
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
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)
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 betablockers (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.
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.
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 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 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.
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).