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The Ethics Behind Assessment

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The Ethics Behind Assessment

Consider the following scenarios:

As an advanced practice nurse, you will run into situations where a patient’s wishes about his or her health conflict with evidence, your own experience, or a family’s wishes. This may create an ethical dilemma. What do you do when these situations occur?

In this Lab Assignment, you will explore evidence-based practice guidelines and ethical considerations for specific scenarios.



· A 49-year-old woman with advanced stage cancer has been admitted to the emergency room with cardiac arrest. Her husband and one of her children accompanied the ambulance.


. What necessary information would need to be obtained about the patient through health assessments and diagnostic tests?

. Consider how you would respond as an advanced practice nurse. Review evidence-based practice guidelines and ethical considerations applicable to the scenarios you selected.

Write a detailed one-page narrative (not a formal paper) explaining the health assessment information required for a diagnosis of your selected patient (include the scenario number). Explain how you would respond to the scenario as an advanced practice nurse using evidence-based practice guidelines and applying ethical considerations. Justify your response using at least three different references from current evidence-based literature.

The International Journal of Sports Physical Therapy | Volume 9, Number 2 | April 2014 | Page 242

Purpose/Background: In 2010, the American Academy of Pediatrics officially adopted the recommended return
to play guidelines proposed by the International Conference on Concussion in Sport. The guidelines include a
six-step process that provides structure to guide an athlete who is recovering from a concussion in a gradual
return to play (RTP) by allowing participation in increasingly difficult physical activities. Unfortunately, the
guidelines fail to take into account the variability that occurs within different sports and the resulting challenges
medical professionals face in making sure each athlete is able to withstand the rigors of their specific sport,
without return of symptoms. Therefore, the purpose of this clinical commentary is to expand upon the current
general consensus guidelines for treatment of concussed pediatric athletes and provide sport specific RTP

Description of Topic: The intention of the sport specific guidelines is to maintain the integrity of the current
six-step model, add a moderate activity phase highlighted by resistance training, and to provide contact and lim-
ited contact drills specific to the athlete’s sport and/or position. The drills and activities in the proposed seven-
step programs are designed to simulate sport specific movements; the sports include: football, gymnastics,
cheerleading, wrestling, soccer, basketball, lacrosse, baseball, softball, and ice hockey. These activities will pro-
vide sports specific challenges to each athlete while simultaneously accomplishing the objectives of each stage
of the RTP progression. The final RTP determination should occur with documented medical clearance from a
licensed healthcare provider who has been trained in the evaluation and management of concussions.

Discussion/Relation to Clinical Practice: There have been significant strides in the management and care of
concussed athletes. However, there continues to be a lot of confusion among, athletes, parents, and coaches
regarding the proper management of an athlete with a concussion, particularly in the pediatric population. In
an effort to eliminate ambiguity and help further promote adherence to the RTP guidelines, the authors devel-
oped several sports-specific RTP guidelines.

Level of Evidence: 5

Keywords: Concussion, pediatric, return to play guidelines, sports


Keith H. May, PT, DPT, SCS, ATC, CSCS1

David L. Marshall, MD1

Thomas G. Burns, PsyD, ABPP/CN1
David M. Popoli, MD1

John A. Polikandriotis, PhD, MBA, MPH, FACHE1

1 Children’s Healthcare of Atlanta, Atlanta, GA, USA

Keith H. May, PT, DPT, SCS, ATC, CSCS
Clinical Outcomes Project Manager Sports
Medicine Program
Children’s Healthcare of Atlanta
5445 Meridian Mark Rd. NE Atlanta, GA 30342
offi ce # (404) 785-5701

The International Journal of Sports Physical Therapy | Volume 9, Number 2 | April 2014 | Page 243

Attention to sports related head injuries, specifically
concussions, has increased over the last ten years.1
The increased interest is likely multi-factorial, occur-
ring due to the impact of concussions on high profile
professional athletes coverage in the popular media,
and the large number of teens participating in con-
tact and collision sports. More than half of all high
school students, over 7.7 million boys and girls, par-
ticipated in sports during the 2012-2013 school year
compared to 6.8 million during the 2002-2003 school

Consequently, the overall number of reported head
injuries continues to rise. In fact, Langlois et al
reported that at least 1.6-3.8 million sports related
concussions occur each year in the United States.3
While the majority of concussion symptoms resolve
within 10 days to two weeks,4 the consequences
of returning an athlete to play too soon following
a concussion are now beginning to be understood.
For example, there is a significant risk for a second
concussion whose compounding effects can be det-
rimental to the adolescent athlete.5-13

In 2001, a multidisciplinary group of sport and medi-
cal professionals met in Vienna, Austria at the Inter-
national Conference on Concussion in Sport (ICCS)
and has since met three additional times with the
specific objective of improving the evaluation, man-
agement, and return to play of concussed athletes.14-17
Interestingly, the pediatric and adolescent athlete
was not considered until the 2008 conference that
occurred in Zurich, Switzerland where three sig-
nificant questions were raised: 1) Which symptom
reporting scale is the most appropriate for this age
group?; 2) Which tests are useful and how often
should baseline testing be performed?; and 3) What
are the most appropriate return to play criteria for
the elite and non-elite child and adolescent athlete?
In 2012 and in response to the 2008 conference, the
ICCS developed the child SCAT 3 (for ages 5-12) for
sideline use, recommended that neurophysiological
testing be used broadly the same as adults with con-
sideration made toward age appropriate cognitive
development, recommended that children make a
complete return to school prior to a return to play,
and recommended a more conservative return to
play progression, secondary to a child’s physiologi-

cal response to a head injury and their tendency to
take longer to recover.17

In 2010, the American Academy of Pediatrics (AAP)
published basic concussion management guidelines
for children and adolescents, adapted from the ICCS
recommendations that emphasized a graduated
return to play (RTP) protocol and the importance of
having an athlete follow a stepwise progression in
their RTP.18 Table 1, adapted from the AAP guide-
lines, shows the recommended RTP progression.

According to the recommended protocol, a concussed
athlete begins the 6-step protocol and moves through
the progression at 24-hour intervals as long as no
symptoms occur. If an athlete develops symptoms
the progression should be stopped and the athlete
must be returned to the previous phase. The final
RTP determination should occur with documented
medical clearance from a licensed healthcare pro-
vider who has been trained in the evaluation and
management of concussions.

It is important to recognize that the mechanisms of
concussive injury and force of collision vary among
sports. In football, for example, helmet-to-helmet col-
lisions are common, whereas contact from a stick,
puck or ball can occur in ice hockey, lacrosse, or
soccer. For this reason, every concussion is unique
and athletic medical providers should consider sport
specific RTP guidelines utilizing symptom reports,
as well as cognitive and balance examination data to
track recovery. Ultimately, this will assist in develop-
ing detailed understanding regarding how and when
to return pediatric athletes back their sports activi-
ties. Therefore, the purpose of this clinical commen-
tary is to expand upon the current general consensus

Table 1. Graduated Return-to-Play Protocol, with
additional Step 618

The International Journal of Sports Physical Therapy | Volume 9, Number 2 | April 2014 | Page 244

guidelines for treatment of concussed pediatric ath-
letes and provide sport specific RTP guidelines.

The following sports specific RTP criteria developed
by a multidisciplinary sports medicine team at Chil-
dren’s Healthcare of Atlanta was written and imple-
mented into the Atlanta, GA metro service area in
2012 (Appendices 1-10). The intention was to main-
tain the integrity of the current 6-step basic progres-
sion suggested by the ICCS and adopted by the AAP,
spanning the time period from no physical activity
to full RTP. The authors propose adding a moderate
activity step highlighted by resistance training and
modifying steps three and four to include noncon-
tact and limited contact drills specific to the athlete’s

Assessing an athlete’s tolerance to resistance
training is important because weight training can
increase intracranial pressure and exacerbate post
concussive symptoms.19 Resistance training should
be introduced with low weight/high repetition exer-
cises.20 The specific sports chosen for this new 7-
step program were known to be of high risk for head
injury and included football, gymnastics, cheerlead-
ing, wrestling, soccer, basketball, lacrosse, baseball,
softball and ice hockey. Each sport was considered
for drills and activities that could be completed by
the athlete that would simulate sport specific move-
ments while simultaneously accomplishing the
objectives of each stage of the RTP progression. As
with the basic guidelines, each step represents a 24-
hour period unless an athlete develops symptoms. A
pediatric or adolescent athlete should begin the RTP
progression once they have achieved a full return
to school (cognitive activities). If symptoms occur,
the progression should be stopped and the athlete
returned to the previous phase where symptoms did
not occur. A list of common concussion symptoms
described by the AAP is included in Table 2.

To reiterate, the final RTP determination should
occur with documented medical clearance from a
licensed healthcare provider who has been trained
in the evaluation and management of concussions.
This could include a physician, nurse practitioner,
physician assistant, certified athletic trainer, or
board certified sports physical therapist.

The pathophysiology, recognition and treatment of
concussions are becoming far better understood than
in years past. Most concussion management pro-
grams now stress cognitive rest, physical rest, the use
of neurocognitive testing, and utilization of return to
play guidelines. Despite these improvements in the
care of athletes, there continues to be a lot of confu-
sion among athletes, parents, and coaches as to the
proper management of a concussion, particularly
those that occur in children. In an effort to elimi-
nate ambiguity and help further promote adherence
to the RTP guidelines, the authors developed these
sequential sports-specific RTP guidelines. Further
research is warranted in order to validate these
guidelines and their potential impact on return to
play adherence and overall success. Adherence to
even the current general return to play recommen-
dations continues to be a challenge in the pediatric
and adolescent sporting community. In 2009, Yard
and Comstock found that one in six athletes failed
to follow a standardized RTP guideline and thus fre-
quently returned to their sport prematurely.21 Fur-
thermore, Hollis et al reported that in a group of 296
rugby athletes with suspected concussions only 66
returned to play with medical clearance.12 Similarly,
Sye et al reported 145 of 187 rugby players were only
compliant with the initial rest period.23

Of special concern is that there are currently no sug-
gested RTP guidelines for athletes under the age of
13. The consensus guidelines are described to be
applicable for adolescents 13 years of age and older.
An age appropriate physical, cognitive testing and
symptom checklist is recommended as a component
of the assessment as patients below age 13 tend to
report concussion symptoms different from adults.17
Consensus in the literature is that those who man-
age a younger athlete with a concussion should be
prepared to extend the recovery timeline.17,24 The

Table 2. Signs and Symptoms of a Concussion18

The International Journal of Sports Physical Therapy | Volume 9, Number 2 | April 2014 | Page 245

extended time is a product of the different physi-
ological response that children and adolescents
demonstrate as a result of a concussion (e.g. diffuse
cerebral swelling). The actual recovery time may
vary based on the individual patient.17,24 Additionally,
RTP guidelines may need to be adjusted for those
who have experienced a prior head injury. Multiple
authors have described that those who have suffered
a prior injury have up to a 5.8 fold increased rate of
re-injury.6-13 Therefore, treating an athlete with mul-
tiple concussions involves emphasizing the need to
consider the long-term consequences and recovery
prior to RTP.25-27

Lastly, many states have passed legislation designed
to address the growing concern of traumatic brain
injuries and concussion among young athletes. In
addition to the legislative efforts that may govern
RTP guidelines, a team approach that involves health
care providers, parents, athletes, and coaches is key
for the long-term health of the athlete.

1. Graham R, Rivara FP, Ford MA, Spicer CM, eds.

Sports Related Concussions in Youth: Improving the
Science, Changing the Culture. Washington DC:
National Academies Press; 2014.

2. National Federation of State High School
Associations. 2012-2013 high school athletics
participation survey.
Accessed September 8, 2013.

3. Langlois JA, Rutland-Brown W, Wald MM. The
epidemiology and impact of traumatic brain injury: a
brief overview. J Head Trauma Rehabil. 2006 Sep-

4. D`Hemecourt P. Subacute symptoms of sports-
realted concussion: outpatient management and
return to play. Clin Sports Med. 2011;30:63-72.

5. McCrea M, Guskiewicz K, Randolph C, et al. Effects
of a symptom free waiting periods on clinical
outcome and risk of reinjury after sport-related
concussion. Neurosurgery. 2009;65(5):876-882.

6. Schulz MR, Marshall SW, Mueller FO et al. Incidence
and risk factors for concussion in high school
athletes, North Carolina, 1996-1999. Am J Epidemiol

7. Colvin AC, Mullen J, Lovell MR, et al. The role of
concussion history and gender in recovery from
soccer-related concussion. Am J Sports Med.

8. Emery C, Kang J,Shrier I, et al. Risk of injury
associated with bodychecking experience among
youth hockey players. CMAJ 2011;83:1249-56.

9. Guskiewicz KM, Marshall SW,Bailes J, et
al. Recurrent concussion and risk of depression in
retired professional football players. Med Sci Sports
Exerc. 2007;39:903-9.

10. Guskiewicz KM, McCrea M, Marshall SW, et
al. Cumulative effects associated with recurrent
concussion in collegiate football players: The NCAA
concussion study. JAMA 2003;290:2549.

11. Guskiewicz KM, Weaver NL, Padua DA, et al. Jr.
Epidemiology of concussion in collegiate and high
school football players. Am J Sports Med. 2000;28:

12. Hollis SJ, Stevenson MR, McIntosh AS, et
al. Incidence, risk, and protective factors of mild
traumatic brain injury in a cohort of Australian
nonprofessional male rugby players. Am J Sports
Med. 2009;37:2328-33.

13. Kristman VL, Tator CH, Kreiger N, et al. Does the
apolipoprotein epsilon 4 allele predispose varsity
athletes to concussion? A prospective cohort study.
Clin J Sport Med. 2008;18:322-8.

14. Aubry M, Cantu R, Dvorak J, et al. Summary and
agreement statement of the fi rst international
conference on concussion in sport, Vienna 2001. Br J
Sports Med. 2002;36:6-7.

15. McCrory P, Johnston K, Meeuwisse W, et al.
Summary and agreement statement of the 2nd
International Conference on Concussion in Sport,
Prague 2004. Br J Sports Med. 2005;39:196-204.

16. McCrory P, Meeuwisse W, Johnston K, et al.
Consensus Statement on Concussion in Sport: the
3rd International Conference on Concussion in Sport
held in Zurich, November 2008. Br J Sports Med.
2009;43 Suppl 1:i76-90.

17. McCrory P, Meeuwisse W, Aubry M, et al. Consensus
statement on Concussion in Sport-The 4th
International Conference on Concussion in Sport
held in Zurich, November 2012. J Sci Med Sport

18. Halstead ME, Walter KD, and the Council on Sports
Medicine and Fitness. Sports-Related Concussion in
Children and Adolescents. Pediatrics. 2010; 126(3):

19. Haykowsky M, Eves N, Warburton D, et al.
Resistance exercise, theValsalva maneuver, and
cerebrovascular transmural pressure. Med Sci Sports
Exerc. 2003;35:65-68.

The International Journal of Sports Physical Therapy | Volume 9, Number 2 | April 2014 | Page 246

20. Kissick J, Johnston KM. Return to play after a
concussion principles and practice. Clin J Sport Med.

21. Yard EE, Comstock RD. Compliance with return to
play guidelines following concussion in US high
school athletes, 2005-2008. Brain Inj. 2009;23:888-98.

22. Jack K, McLean SM, Moffett JK, Gardiner E.
Barriers to treatment adherence in physiotherapy
outpatient clinics: A systematic review. Man Ther.

23. Sye G, Sullivan SJ, McCrory P. High school rugby
players’ understanding of concussion and return to
play guidelines. Br J Sports Med. 2006;40:1003-5.

24. Karlin AM. Concussion in the pediatric and
adolescent population: “Different population,
different concerns”. Pm&R. 2011;3:S369-79.

25. Harmon KG, Drezner JA, Gammons M, et al.
American Medical Society for Sports Medicine
position statement: concussion in sport. Br J Sports
Med. 2012;47:15-26.

26. Laker SR. Return-to-play decisions. Phys Med Rehabil
Clin N AM. 2011;22:619-34.

27. Doolan AW, Day DD, Maerlender AC, Goforth M,
Gunnar Brolinson P. A Review of Return to Play
Issues and Sports-Related Concussion. Ann Biomed
Eng. 2011;40:106-13.

Appendix 1

The International Journal of Sports Physical Therapy | Volume 9, Number 2 | April 2014 | Page 247

Appendix 2

The International Journal of Sports Physical Therapy | Volume 9, Number 2 | April 2014 | Page 248

Appendix 3

It is recommended that you seek further medial a�en�on if you fail more than 3 a�empts to pass a stage

The International Journal of Sports Physical Therapy | Volume 9, Number 2 | April 2014 | Page 249

Appendix 4

The International Journal of Sports Physical Therapy | Volume 9, Number 2 | April 2014 | Page 250

Appendix 5

The International Journal of Sports Physical Therapy | Volume 9, Number 2 | April 2014 | Page 251

Appendix 6

The International Journal of Sports Physical Therapy | Volume 9, Number 2 | April 2014 | Page 252

Appendix 7

The International Journal of Sports Physical Therapy | Volume 9, Number 2 | April 2014 | Page 253

Appendix 8

The International Journal of Sports Physical Therapy | Volume 9, Number 2 | April 2014 | Page 254

Appendix 9

The International Journal of Sports Physical Therapy | Volume 9, Number 2 | April 2014 | Page 255

Appendix 10

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Sudden cardiac deaths in young people are
devastating and personally tragic events,
which fortunately occur uncommonly.1–7
Unsuspected genetic or congenital heart dis-
eases, as well as blunt trauma and c ommotio
cordis, have been recognized as causes of
sudden cardiac deaths for >30 years.1–3,5,8,9
Considerable public debate has arisen in
the lay and medical communities about
establishing the most effective strategies for
reducing or eliminating these events.6,10–25
For competitive athletes, much attention has
been directed towards reducing head trauma
and concussions in contact sports such as
football,26–28 but also in devising prepartici-
pation screening approaches for identifying
potentially lethal cardiovascular diseases.6 In
the process, a vast literature has been assem-
bled, comprising both original data and a
myriad of editorial commentaries.6

Although initially regarded as personal
and family tragedies, the sudden deaths of
young competitive athletes have become
highly reported events over the past few

decades, achieving prominence in the public
consciousness.1,5,6,10 Indeed, the sudden
deaths of young people are counterintuitive
and inconsistent with our expectations for
sports competition. This discourse has been
driven by the ubiquity of traditional and new
social media, creating an exaggerated impres-
sion of the incidence of these events that is
disproportionate to the true effect that such
deaths have on overall public health. Indeed,
the strong influence of the media might have
even fuelled the misconception that deaths
are more common on athletic fields than they
actually are, that these events might be largely
limited to athletes, and that they are abso-
lutely preventable by electro cardiographic
screening.6,29 In this Perspectives article, we
place many of these issues into the appro-
priate context, with particular focus on the
ethical considerations related to the prac-
tice of limiting cardiovascular screening to
c ompetitive athletes.

Historical context
Interest in the preferential screening of
young athlete populations (lately with
electro cardiograms) has been justified on
the assumption that sudden death owing to

underlying and unsuspected cardiovascular
disease is largely explained by the physi-
cally vigorous and stressful lifestyle to which
young athletes are uniquely exposed by
virtue of competition and systematic training
regimens—that these deaths occur in athletes
because they are athletes.6,30,31 However, the
data supporting a strong link between com-
petitive sports participation and the risk of
sudden death remains incomplete.6,32–37 For
example, sudden arrhythmic deaths were
reported in 2014 to be most common at rest
or during sleep.38

In the USA, a long-standing customary
practice is to screen young people before
they engage in sanctioned competitive
sports in high school or college, using a
personal and family history and physical
examination, such as the 14 elements recom-
mended by the AHA/ACC.6 This process has
generally included all student athletes (at
high school or college), independently of
their level of achievement and performance.
Indeed, Israel, Italy, and the USA are the
only countries with systematic, broad-based
screening of the athlete population.5,6,10,22,


Mass population screening with the
12-lead electrocardiogram (including on a
national basis) has been heavily promoted
by Italian cardiologists,5,10,17–19 and by some
in the US sports medicine community,16,31
despite the lack of both conclusive evidence
and general agreement that adding electro-
cardiograms to the screening examination
substantially reduces cardiovascular mortality
(Figure 1).6,23,25,37 Indeed, the Italian proposal
has triggered a decade-long debate among
cardiologists, paediatricians, and family prac-
titioners about the merits of various cardio-
vascular screening strategies.4,6,7,15–25,30 Many
in the US cardiology community,1,4,7,20,21,23,24
including the AHA/ACC, regard mass
electro cardiographic screen ing as excessive,
if not inadvisable.6,39 This view is predicated
on the considerable number of expected
false-positiv e and false-negative test results,
and the costs triggered by secondary ‘down-
stream’ diagnostic testing (largely, but not
necessarily, limited to echocardiography),
which is wasteful of resources that could
otherwise be used to promote improved
pop ulation health.40 These factors, as well
as other obstacles associated with limited
resources, have led to the view that national


Ethics of preparticipation cardiovascular
screening for athletes
Barry J. Maron, Richard A. Friedman and Arthur Caplan

Abstract | Preparticipation screening for unsuspected cardiovascular disease is a
controversial topic in the medical and lay communities. Much attention has been
directed towards young competitive athletes, particularly the proposed strategy of
incorporating 12‑lead electrocardiograms into the screening process, even on a
national or worldwide basis. However, sudden deaths of young athletes owing to
genetic or congenital heart diseases have a low incidence in the general population.
Furthermore, young people not engaged in competitive sports can harbour the same
conditions that cause sudden death in athletes, which has gone largely unrecognized.
Notably, sudden deaths from these diseases are numerically far more common in
the much larger population of nonathletes. In this Perspectives article, we propose
that an ethical dilemma has emerged, raising the important public‑health issue
of whether young individuals should be arbitrarily excluded from potentially life‑
saving clinical screening evaluations because they do not engage in competitive
sports programmes.

Maron, B. J. et al. Nat. Rev. Cardiol. 12, 375–378 (2015); published online 24 February 2015;

Competing interests
The authors declare no competing interests.


© 2015 Macmillan Publishers Limited. All rights reserved

376 | JUNE 2015 | VOLUME 12

or mandated universal electrocardiographic
screening is impractical and imprecise, if
not potentially unethical when arbitrarily
c onfined to athletes.6,32,33

Incidence and proportionality
Most data on the incidence and causes of
sudden death in young people come from
the athlete community, because these events
can be easily tabulated owing to their trad-
itionally extensive exposure in the public
domain.29 By contrast, sudden deaths occur-
ring in nonathletes or participants in infor-
mal recreational sports are not regularly
identified publically. As a consequence, the
highly-charged deaths of individual young
athletes have come to dominate, or even
overwhelm, larger and potentially more
substantial public-health issues.4


Based on the considerable assembled data,
sudden deaths as a result of cardio vascular
disease in young athletes are among the
least common causes of death in this age
group (Figure 2).6,24 We wish to empha-
size that these events are several hundred-
fold less common than the major causes of
death, such as motor vehicle accidents or
suicide, and occur with a similar frequency
to that of fatal lightning strikes (Figure 2).
For example, athlete data from Minnesota,
USA,4 Denmark,33,34 and the Veneto region
of Italy 5 all indicate that the  absolute
numbers of these sudden death events are
in the range of one to two annually, with

an incidence in most studies of 1:80,000
to 1:200,000.6

Nationwide comparative data from
Denmark32–36,40 and France41 show that
cardio vascular-related sudden deaths occur
uncommonly in competitive athletes, and
less frequently than in either recreational
sports participants or the general popula-
tion. This finding was the basis for the deci-
sion by Danish health authorities to reject
the European proposal to screen all com-
petitive athletes with electrocardiograms.
Resources can be redirected to other, more
effective societal initiatives to reduce sudden
deaths in young people (athletes and non-
athletes alike),40 such as prevention of
suicide, reduction of illicit drug use and the
number of motor vehicle accidents and fatal-
ities, as well as increased use of automated
external d efibrillators for out-of-hospital
cardiac arrest.40

An ethical dilemma
The current situation, in which the oppor-
tunity to detect potentially lethal cardio-
vascular diseases is confined to those
students who engage in organized or sanc-
tioned competitive athletic programmes,
unavoidably raises an ethical dilemma.
With this practice, students or others not
involved in competitive sports are arbitrar-
ily excluded from the potentially impor-
tant (and possibly life-saving) benefits of
screening. In effect, this practice confers

preferential attention on competitive ath-
letes solely because of their vigorous lifestyle
and often public prominence.42 However,
substantially more young people partici-
pate in recreational or noncompetitive ath-
letic activities,43 but nevertheless are also at
risk of sudden death owing to unsuspected
cardiovascular disease.41,44 For example, 70%
of high school students and 98% of college
students do not participate in competitive
athletics, but often engage in other sports-
related activities at some level, which can be
vigorous and intense.45–48

Genetic and congenital heart diseases, such
as hypertrophic cardiomyopathy, congenital
coronary artery anomalies, arrhyth mo genic
right ventricular cardiomyopathy, and ion
channelopathies, which can cause sudden
deaths in young people, do not have a unique
predilection for trained athletes. Conversely,
these diseases occur in both athletes and
non athletes alike, and can cause sudden
death whether they occur on the field during
competition, in a myriad of recreational
sporting activities, or even when associated
with seden tary lifestyle.6,41 Given that only
a minority of students choose to be trained
competitive athletes,45–48 the absolute number
of sudden deaths expected in nonathletes nec-
essarily exceeds—by at least eightfold—that
in competitive athletes, because non athletes
greatly out number students in organized and
s anctioned sports programmes.

Well-meaning clinicians and advo-
cacy groups have persistently been strong
advocates for universal 12-lead electro-
cardio graphic testing in young competitive
athletes.5,10,15–19,31 In many European coun-
tries, in which interest in electrocardiographic
screening is greatest, the effort to identify
potentially lethal cardiovascular disease
has mostly been extended only to the small
subgroups of elite or professional athletes at
the highest level of performance. Therefore,
after considering all viewpoints, we are com-
pelled to pose this novel question: is it ethical
to restrict cardiovascular screening to only
those young people who elect to participate in
competitive sports, and in the process deprive
others who might be at similar or greater risk
of sudden death from access to potentially
life-saving clinical evaluations and testing? In
2015, is it appropriate for competitive young
athletes to be p rivileged at the expense of
other young people?

Future perspectives
We wish to emphasize that we do not mean
to suggest or justify abandoning long-
standin g systematic screening of high school












































Nature Reviews | Cardiology

Veneto, Italy
Minnesota, USA

P = 0.88

Figure 1 | Effect of preparticipation screening on cardiovascular mortality in competitive
athletes.37 The graph shows annual athlete mortality per 100,000 person‑years in the
Veneto region of Italy (history, physical examination, and 12‑lead electrocardiogram) and
Minnesota, USA (history and physical examination only), with the two strategies compared over
21 years (1985–2005). No significant difference exists in mortality between the two populations
with the different cardiovascular screening strategies. The Italian national preparticipation
screening programme began in 1981. Reprinted from Maron, B. J. et al. Comparison of U.S.
and Italian experiences with sudden cardiac death in young competitive athletes and
implications for preparticipation screening strategies. Am. J. Cardiol. 104 (2), 276–280 ©
2009, with permission from Elsevier.

© 2015 Macmillan Publishers Limited. All rights reserved


and college student athletes or others in the
USA.6 Indeed, history and physical exami-
nation screening have been practised in the
USA for >50 years, with proven efficacy in
identifying many young individuals with
potentially lethal cardiac disease.48 However,
consideration should be given to more wide-
spread availability of the personal and family
history (and possibly physical examination)
to those students not engaged in competi-
tive sports, using the 14 target elements from
the AHA/ACC to raise suspicion of cardio-
vascular abnormalities.6 We concede that
extending this approach to larger popula-
tions of nonathletes would be an ambitious
strategy, undoubtedly fraught with logistical

challenges. Nevertheless, a precedent for
such a process in large populations does
exist. Mandated under the School Health
Law in Japan, general population cardio-
vascular screening largely with history and
physical examination has been performed
systematically in thousands of children
in the first, seventh, and tenth grades.49,50
However, the reported results are rudimen-
tary and do not indicate whether mortality
was reduced.

In this Perspectives article, we recommend
that the ongoing cardiovascular screening
debate be refocused beyond the fairly small

population of competitive athletes to other,
larger groups of active young people who
might also be at risk of sudden premature
death. In principle, little ethical justification
exists for arbitrarily excluding such people
from clinical evaluations that could diag-
nose lethal cardiovascular diseases, either
because of their decision to forgo partici-
pation in competitive sports, or the lack of
physical talent to perform in such activi-
ties. We suggest devoting greater energy
and resources to cardiovascular screening
(without noninvasive testing), extended to
larger segments of the youthful population
beyond competitive athletes, as part of an
expanded public-health policy.

Hypertrophic Cardiomyopathy Center,
Minneapolis Heart Institute Foundation,
Suite 620, 920 East 28th Street, Minneapolis,
MN 55407, USA (B.J.M.). Cohen Children’s
Medical Center of New York, 269‑01 76th
Avenue, New York, NY 11040, USA (R.A.F.).
Division of Medical Ethics, NYU Langone
Medical Center, 455 1st Avenue, New York,
NY 10016, USA (A.C.).
Correspondence to: B.J.M.

1. Maron, B. J. Sudden death in young athletes.
N. Engl. J. Med. 349, 1064–1075 (2003).

2. Maron, B. J., Doerer, J. J., Haas, T. S.,
Tierney, D. M. & Mueller, F. O. Sudden deaths in
young competitive athletes: analysis of 1866
deaths in the United States, 1980–2006.
Circulation 119, 1085–1092 (2009).

3. Maron, B. J., et al. Sudden death in young
competitive athletes: clinical, demographic,
and pathological profiles. JAMA 276, 199–204

4. Maron, B. J., Haas, T. S., Ahluwalia, A.
& Rutten‑Ramos, S. C. Incidence of
cardiovascular deaths in Minnesota high school
athletes. Heart Rhythm 10, 374–377 (2013).

5. Corrado, D. et al. Trends in sudden
cardiovascular death in young competitive
athletes after implementation of a
preparticipation screening program. JAMA 296,
1593–1601 (2006).

6. Maron, B. J. et al. Assessment of the
12‑lead electrocardiogram as a screening
test for detection of cardiovascular disease in
general healthy populations of young people
(12–25 years of age). J. Am. Coll. Cardiol. 64,
1479–1514 (2014).

7. Maron, B. J., Haas, T. H., Murphy, C. J.,
Ahluwalia, A. & Rutten‑Ramos, S. Incidence
and causes of sudden death in U.S. college
athletes. J. Am. Coll. Cardiol. 63, 1636–1643

8. Maron, B. J. & Estes, N. A. 3rd. Commotio
cordis. N. Engl. J. Med. 362, 917–927 (2010).

9. Maron, B. J., Roberts, W. C., McAllister, H. A.,
Rosing, D. R. & Epstein, S. E. Sudden death in
young athletes. Circulation 62, 218–229 (1980).

10. Corrado, D. et al. Cardiovascular pre‑
participation screening of young competitive
athletes for prevention of sudden death:
proposal for a common European protocol.
Consensus Statement of the Study Group of

0 1 2 3
Number of deaths per year (×103)
4 5 6 7 8 9 10 11 12 13





Major CV diseases


Motor vehicle accidents

US athletes—CV

Accidental �rearm


US athletes—all causes

Cystic �brosis



Lightning strike fatalities

NCAA athletes
—all causes (forensic)


NCAA athletes
—CV (non-forensic)

Dry sand collapse

NCAA athletes
—CV (forensic)

NCAA athletes—CV*

Sickle cell trait (athletes)

Minnesota high school

Nature Reviews | Cardiology






















Minnesota high school
athletes—CV* 0.2

Figure 2 | Causes of sudden death in young people (aged <25 years) in the USA.6 *Detectable by electrocardiographic screening. In Denmark, the risk of sudden death from CV disease in young competitive athletes is low (1.5 deaths per year). Abbreviations: CV, cardiovascular; NCAA, National Collegiate Athletic Association. Reprinted from Maron, B. J. et al. Assessment of the 12‑lead ECG as a screening test for detection of cardiovascular disease in healthy general populations of young people (12–25 years of age): a scientific statement from the American Heart Association and the American College of Cardiology. J. Am. Coll. Cardiol. 64 (14), 1479–1514 © 2014, with permission from Elsevier and the American College of Cardiology; and reprinted from Maron, B. J. et al. Assessment of the 12‑lead ECG as a screening test for detection of cardiovascular disease in healthy general populations of young people (12–25 years of age): a scientific statement from the American Heart Association and the American College of Cardiology. Circulation 130 (15), 1303–1334 (2014).

© 2015 Macmillan Publishers Limited. All rights reserved

378 | JUNE 2015 | VOLUME 12

Sport Cardiology of the Working Group of
Cardiac Rehabilitation and Exercise Physiology
and the Working Group of Myocardial and
Pericardial Diseases of the European Society of
Cardiology. Eur. Heart J. 26, 516–524 (2005).

11. Baggish, A. L. et al. Cardiovascular screening
in college athletes with and without
electrocardiography: a cross‑sectional study.
Ann. Intern. Med. 152, 269–275 (2010).

12. Glover, D. W. & Maron, B. J. Profile of
preparticipation cardiovascular screening for
high school athletes. JAMA 279, 1817–1819

13. Corrado, D., Basso, C., Schiavon, M.
& Thiene, G. Screening for hypertrophic
cardiomyopathy in young athletes. N. Engl. J.
Med. 339, 364–369 (1998).

14. Pfister, G. C., Puffer, J. C. & Maron, B. J.
Preparticipation cardiovascular screening for
US collegiate student‑athletes. JAMA 283,
1597–1599 (2000).

15. Myerburg, R. J. & Vetter, V. L.
Electrocardiograms should be included in
preparticipation screening of athletes.
Circulation 116, 2616–2626 (2007).

16. Drezner, J. A. ECG screening in athletes:
time to develop infrastructure. Heart Rhythm 8,
1560–1561 (2011).

17. Corrado, D. & Thiene, G. Protagonist: routine
screening of all athletes prior to participation
in competitive sports should be mandatory to
prevent sudden cardiac death. Heart Rhythm 4,
520–524 (2007).

18. Thiene, G., Corrado, D., Schiavon, M. & Basso, C.
Screening of competitive athletes to prevent
sudden death: implement programmes now.
Heart 99, 304–306 (2013).

19. Corrado, D., Basso, C., Schiavon, M.,
Pelliccia, A. & Thiene, G. Pre‑participation
screening of young competitive athletes for
prevention of sudden cardiac death. J. Am. Coll.
Cardiol. 52, 1981–1989 (2008).

20. Chaitman, B. R. An electrocardiogram should
not be included in routine preparticipation
screening of young athletes. Circulation 116,
2610–2614 (2007).

21. Estes, N. A. 3rd & Link, M. S.
Preparticipation athletic screening including
an electrocardiogram: an unproven strategy
for prevention of sudden cardiac death in the
athlete. Prog. Cardiovasc. Dis. 54, 451–454

22. Viskin, S. Antagonist: routine screening of all
athletes prior to participation in competitive
sports should be mandatory to prevent sudden
cardiac death. Heart Rhythm 4, 525–528

23. Thompson, P. D. Preparticipation screening
of competitive athletes: seeking simple
solutions to a complex problem. Circulation
119, 1072–1074 (2009).

24. Maron, B. J. Counterpoint: mandatory ECG
screening of young competitive athletes.
Heart Rhythm 9, 1646–1649 (2012).

25. Steinvil, A. et al. Mandatory electrocardiographic
screening of athletes to reduce their risk for
sudden death proven fact or wishful thinking?
J. Am. Coll. Cardiol. 57, 1291–1296 (2011).

26. Kerr, Z. Y. et al. Impact locations and
concussion outcomes in high school football
player‑to‑player collisions. Pediatrics 134,
489–496 (2014).

27. Nordström, A., Nordström, P. & Ekstrand, J.
Sports‑related concussion increases the risk
of subsequent injury by about 50% in elite
male football players. Br. J. Sports Med. 48,
1447–1450 (2014).

28. Thomas, M. et al. Epidemiology of sudden
death in young competitive athletes due to
blunt trauma. Pediatrics 128, e1–e8 (2011).

29. Maron, B. J., Murphy, C. J., Haas, T. S. &
Garberich, R. F. Strategies for assessing the
prevalence of cardiovascular sudden deaths in
young competitive athletes. Int. J. Cardiol. 173,
369–372 (2014).

30. Corrado, D., Basso, C., Rizzoli, G., Schiavon, M.
& Thiene, G. Does sports activity enhance the
risk of sudden death in adolescents and young
adults? J. Am. Coll. Cardiol. 42, 1959–1963

31. Harmon, K. G., Asif, I. M., Klossner, D. &
Drezner, J. A. Incidence of sudden cardiac death
in National Collegiate Athletic Association
athletes. Circulation 123, 1594–1600 (2011).

32. Maron, B. J. Diversity of views from Europe
on national preparticipation screening for
competitive athletes. Heart Rhythm 7,
1372–1373 (2010).

33. Holst, A. G. et al. Incidence and etiology of
sports‑related sudden cardiac death in
Denmark—implications for preparticipation
screening. Heart Rhythm 7, 1365–1371 (2010).

34. Risgaard, B. et al. Sports‑related sudden
cardiac death in a competitive and a
noncompetitive athlete population aged 12 to
49 years: data from an unselected nationwide
study in Denmark. Heart Rhythm 11, 1673–1681

35. Winkel, B. G. et al. Nationwide study of sudden
cardiac death in persons aged 1–35 years.
Eur. Heart J. 32, 983–990 (2011).

36. Winkel, B. G. et al. Sudden cardiac death in
children (1–18 years): symptoms and causes
of death in a nationwide setting. Eur. Heart J.
35, 868–875 (2014).

37. Maron, B. J., Haas, T. S., Doerer, J. J.,
Thompson, P. D. & Hodges, J. S. Comparison
of U.S. and Italian experiences with sudden
cardiac deaths in young competitive athletes
and implications for preparticipation screening
strategies. Am. J. Cardiol. 104, 276–280

38. Mellor, G. et al. Clinical characteristics and
circumstances of death in the sudden
arrhythmic death syndrome. Circ. Arrhythm.
Electrophysiol. 7, 1078–1083 (2014).

39. Maron, B. J. et al. Recommendations and
considerations related to preparticipation

screening for cardiovascular abnormalities
in competitive athletes: 2007 update:
a scientific statement from the American
Heart Association Council on Nutrition,
Physical Activity, and Metabolism: endorsed
by the American College of Cardiology
Foundation. Circulation 115, 1643–1655

40. Maron, B. J., Winkel, B. G. & Tfelt‑Hansen, J.
Perspectives on cardiovascular screening.
JAMA 313, 31–32 (2015).

41. Marijon, E. et al. Sports‑related sudden death
in the general population. Circulation 124,
672–681 (2011).

42. Daniels, N. & Sabin, J. E. Setting Limits Fairly.
Can We Learn to Share Medical Resources?
(Oxford University Press, 2002).

43. Maron, B. J. & Zipes, D. P. Introduction:
eligibility recommendations for competitive
athletes with cardiovascular abnormalities—
general considerations. J. Am. Coll. Cardiol. 45,
1318–1321 (2005).

44. Berdowski, J. et al. Exercise‑related out‑
of‑hospital cardiac arrest in the general
population: incidence and prognosis.
Eur. Heart J. 34, 3616–3623 (2013).

45. Rutten‑Ramos, S., Garberich, R. F., Haas, T. S.
& Maron, B. J. Cardiovascular death in
student‑athletes and in the general
population: are trained athletes really at higher
risk? [abstract] Circulation 128, A18424

46. Colabianchi, N., Johnston, L. & O’Malley, P. M.
Bridging the Gap. Sports Participation in
Secondary Schools: Resources Available and
Inequalities in Participation [online], http://

47. National College Athletic Association.
1981–82—2012–13 NCAA Sports
Sponsorship and Participation Rates Report

48. Adabag, A. S, Kuskowski, M. A. & Maron, B. J.
Determinants for clinical diagnosis of
hypertrophic cardiomyopathy. Am. J. Cardiol. 98,
1507–1511 (2006).

49. Tasaki, H., Hamasaki, Y. & Ichimaru, T.
Mass screening for heart disease of school
children in Saga city: 7‑year follow up study.
Jpn. Circ. J. 51, 1415–1420 (1987).

50. Haneda, N. et al. Heart diseases discovered
by mass screening in the schools of Shimane
Prefecture over a period of 5 years. Jpn. Circ. J.
50, 1325–1329 (1986).

Author contributions
All the authors researched data for the article,
contributed to discussion of content, and
wrote, reviewed, and edited the manuscript
before submission.

© 2015 Macmillan Publishers Limited. All rights reserved

Reproduced with permission of the copyright owner. Further reproduction prohibited without

  • c.nrcardio.2015.21
  • nrcardio.2015.21
    Ethics of preparticipation cardiovascular screening for athletes
    Barry J. Maron, Richard A. Friedman and Arthur Caplan
    Historical context
    Figure 1 | Effect of preparticipation screening on cardiovascular mortality in competitive athletes.37 The graph shows annual athlete mortality per 100,000 person-years in the Veneto region of Italy (history, physical examination, and 12‑lead electrocardi
    Incidence and proportionality
    An ethical dilemma
    Future perspectives
    Figure 2 | Causes of sudden death in young people (aged <25 years) in the USA.6 *Detectable by electrocardiographic screening. In Denmark, the risk of sudden death from CV disease in young competitive athletes is low (1.5 deaths per year). Abbreviations: Author contributions

Current Topics in Care

A Case of Inappropriate Apolipoprotein E
Testing in Alzheimer’s Disease Due to
Lack of an Informed Consent Discussion

Christian D. Furman, MD, MSPH, AGSF1,
Lori A. Earnshaw, MD2, David J. Doukas, MD3,
Lindsay A. Farrer, MD4, and Robert P. Friedland, MD3

Background/Objective: Apolipoprotein E (APOE) genetic testing is used to assist in the diagnosis of Alzheimer’s Disease (AD).
Whenever genetic testing is performed, an informed consent process should occur. Methods: In this case, a patient with memory
loss presented to the neurologist. The neurologist ordered a lumbar puncture (LP). The LP was performed by a neuroradiologist
who also ordered APOE genetic testing. The patient received no genetic counseling, nor was an informed consent document
offered. Results: After the testing was completed, the neurologist faced an ethical dilemma. His solution was to offer the genetic
testing to the patient in order to have an informed consent process. It was clear that the patient and her adult children did not
want the genetic testing and that they would have been burdened with the results. The neurologist opted not to disclose the
results. Conclusion: Genetic counseling and a signed informed consent document are required prior to any genetic testing. In
this case, neither occurred and it led to an ethical dilemma that was ultimately resolved by the neurologist. As the population ages
and AD becomes more prevalent, there is a need to expand the workforce of genetic counselors and educate physicians who
commonly treat AD about genetic testing.

genetic testing, Alzheimer’s disease, ethics, informed consent


Twenty years ago, the apolipoprotein E (APOE) e4 allele was
found to confer susceptibility to late-onset Alzheimer’s dis-

ease (AD) in caucasians.1 This association was extended to

noncaucasian populations, and the APOE-associated risk of

AD was demonstrated to vary with age and sex.2 Although the

presence of the e4 allele in a person with dementia increases
the probability of AD, this finding is not ‘‘diagnostic’’ of the

disease because more than one-half of e4 carriers surviving
to age 80 years do not develop AD.2,3 Thus, APOE e4 is best
viewed as a genetic risk factor for AD rather than a genetic

marker of the disease4 because the risk of developing AD for

individuals with at least 1 e4 allele by age 80 years is esti-
mated to be 29% compared to 9% for individuals lacking e4.5

Among caucasians, the odds of developing AD are 2 to 3 times

higher for e4 heterozygotes and 12 to 14 times higher for e4
homozygotes compared to persons who are APOE 3/3, the most

common genotype.2 However, these risks are dependent on age

and gender and are lower in some ethnic groups including African

Americans, Indians, and Israeli Arabs.2,6-9 Further, the APOE risk

appears to be attenuated by adequate control of hypertension.10

The 2/3 genotype is associated with an approximately 40%

decreased risk of AD compared to 3/3 genotype,2 and the 2/4

genotype has a similar risk as those with 3/3 genotype.2,11

Consensus exists among members of the scientific commu-

nity that the value of APOE genotyping as a predictive test for

AD in asymptomatic individuals is currently limited, with the

weight of professional opinion against offering the test as part

of a routine medical examination.12 Physicians may order

APOE genetic testing in symptomatic patients in order to assist

1 Department of Family and Geriatric Medicine, University of Louisville School

of Medicine, Louisville, KY, USA
2 Department of Internal Medicine, University of Louisville School of Medicine,

Louisville, KY, USA
3 University of Louisville School of Medicine, Louisville, KY, USA
4 Boston University Schools of Medicine and Public Health, Boston, MA, USA

Corresponding Authors:

Christian D. Furman, MD, MSPH, AGSF, Department of Family and Geriatric

Medicine, University of Louisville School of Medicine, 401 E. Chestnut St. Ste.

170; Louisville, KY, USA.


Lori A. Earnshaw, MD, Department of Internal Medicine, 550S. Jackson St,

3rd Fl ACB, Louisville, KY, USA.


American Journal of Alzheimer’s
Disease & Other Dementias®

2014, Vol. 29(7) 590-595
ª The Author(s) 2014
Reprints and permission:
DOI: 10.1177/1533317514525829

in the clinical diagnosis of AD. For some clinicians, APOE
genetic testing is considered a supportive adjunct to the clinical

diagnosis of AD. Alternatively, some clinicians believe that

APOE genetic testing should be offered to patients as a matter
of respect for the informed choice of the patient and family.13

Although the value of APOE testing is generally viewed as

limited, testing can have efficacy in some circumstances. Early

diagnosis of symptomatic AD may be beneficial because some

treatment options are most effective in the early stages, and

patient awareness may provide psychological relief, incentive

to pursue financial and advance care planning, access to early

counseling, and the option to participate in research.14

However, when genetic testing is performed, patients must

be fully informed as to the risks and benefits. Genetic testing

should be conducted with a protocol for pretest and posttest

counseling that affords the opportunity to fully explore the per-

sonal meaning regarding a positive or negative test result and to

make an informed decision about obtaining the test.4 Testing

involves potential risks to patients, including the fact that the

results could be emotionally upsetting and stressful, might

influence the patient’s ability to obtain insurance, and may

affect employment.14 Patients may misunderstand a test result

and think a positive or negative result is absolute assurance that

they will or will not develop dementia. In addition, long-term

care insurance may discriminate based on the results of the

genetic testing. Genetic testing affects children of the patient,

potentially causing psychological distress if they find out they

are at greater risk of a debilitating and terminal condition. The

informed decision discussion should also include logistical

issues, such as costs and planning for future care contingencies.

If genetic testing is performed, counseling must be com-

pleted and documented with a signed informed consent docu-

ment placed in the medical record. The laboratories that

perform genetic testing should not process any specimen with-

out a written informed consent. Unfortunately, many labora-

tories will conduct the test without proper documentation,

even when it violates their own corporate policies.15

In 2011, patients could bypass their providers for testing by

purchasing a home genetic testing kit.16 This kit contained

basic information about what the genetic testing means but did

not provide the level of detail that would be communicated by a

physician who is familiar with the genetic, statistical, and psy-

chological aspects of APOE testing. In addition, the kit did not

provide any posttest consultation and counseling. The Food and

Drug Administration recently suspended this program because

of the inherent problems with not having a physician involved

in genetic testing.

With the current increase in genetic testing, primary care

providers, geriatricians, neurologists, and neuroradiologists

need to be well-versed in the details of genetic testing and

counseling for AD. A lack of awareness can cause significant

suffering to patients and their families due to the possible dis-

closure of unwanted medical information. The following case

subsequently illustrates the potential for adverse effects when

genetic counseling and informed consent protocols are not


Case Presentation

A 55-year-old white female with short-term memory loss for

2 years presented to the neurologist, as a referral from her

primary care physician for confirmation of the diagnosis of

frontotemporal dementia. She had neuropsychological testing

3 months before presentation to the neurologist, which showed

frontal dysfunction suggestive of frontotemporal dementia with

deficits in attention, concentration, and working memory as

well as slow processing speed. The patient reported difficulty

recalling conversations and trouble with finances. Her husband

observed episodes of staring and eyelid fluttering. Electroence-

phalogram showed bitemporal epileptiform activity, worse on

the left. She was started on antiseizure medication. Magnetic

resonance imaging (MRI) of the brain was read as normal.

Folstein Mini-Mental Status Examination was 23 of 30.17

Buschke Memory Impairment Screen was 4 of 8, indicative

of poor memory, and she had poor topographical orientation

on a map of the United States.18 Clock drawing task was unre-

markable except hands were of equal size. Spontaneous speech

was normal but she had trouble naming object parts. Her ability

to perform simple calculations was poor. Her eye movements

were full and conjugate; however, pursuit movements were

jerky in the horizontal and vertical directions. The remainder

of the neurological examination was normal.

During the neurologist’s interview, the following history

was obtained from the patient and family: the patient held a

master’s degree in psychology. She never smoked nor drank

alcohol. The patient was married and had 3 children who were

in their 20s without medical problems. She lived at home with

her husband. The patient’s mother, age 79, was alive and

healthy. Her father, age 85, was alive but with kidney prob-

lems. She had 2 brothers and 4 sisters, ranging in age from

50 to 62 years old, with no neurological or psychiatric history.

The initial working diagnosis was frontotemporal dementia.

Since the patient was relatively young, the neurologist ordered

the following: a positron emission tomography (PET) scan with

18-F fluorodeoxyglucose; complete blood count; comprehen-

sive metabolic profile; folate level; antithyroglobulin and

antithyroperoxidase antibodies; thyroid stimulating hormone;

antinuclear antibody; C-reactive protein; vitamin B12 level;

Lyme titer; and a fluoroscopy-guided lumbar puncture with

fluid sent for total protein, glucose, venereal disease research

laboratory test, culture, and cell count, and the Athena Diag-

nostics Phospho-Tau/Total-Tau/Ab 42 CSF Analysis & Inter-

pretation to measure cerebrospinal fluid (CSF) amyloid-b
(Ab) 1-42 and t levels.19 It is important to note that the Athena
Alzheimer’s panel was completely paid for by the patient’s


During the lumbar puncture, performed under fluoroscopic

guidance, the neuroradiologist ordered APOE genetic testing

(without the knowledge or agreement of the neurologist or con-

sent of the patient). Blood was obtained and sent to Athena

Diagnostics for analysis. The patient received no genetic coun-

seling before the blood was drawn, and there was no documen-

ted informed consent. Per the referring neurologist, the patient

Furman et al 591

had sufficient decision-making capacity for medical decisions.

Additionally, the family was not consulted about the genetic

testing. The neurologist was unaware that the test had been

ordered until the results became available.

The PET scan showed diminished glucose metabolism in the

bilateral parietal and temporal regions suggestive of AD. The

CSF Athena panel showed low Ab 1-42 and high t, strongly
indicative of AD. The APOE test revealed that the patient’s

genotype was e4/4. Other laboratory tests were normal. These
results indicate that AD was the likely cause of the dementia.

Assuming both of the patient’s parents are e4 heterozygotes,
each of the patient’s siblings has a 75% chance of having at
least 1 e4 allele (100% if either parent is 4/4). Each of the
patient’s children has a 100% chance of having at least 1 APOE
e4 allele. The cause of AD in this case was unlikely due to a
rare autosomal dominant mutation since both of her parents are

living without signs of dementia, and there is no family history

of the disease.

The neurologist did not request APOE genetic testing

because it would not substantially increase diagnostic accu-

racy. Additionally, he perceived that it could cause undue stress

for her children if the genotype was 4/4 and could generate a

sense of guilt in the patient and/or her parents for transmitting

the e4 allele. At the second visit, following the acquisition
of the laboratory results, the neurologist debated whether to

inform the patient and her family of the genetic testing results

because (1) he did not order the genetic testing; (2) the patient

and family had not given their consent for the test to be done;

and (3) the information may not be of value to the adult chil-

dren, as there is nothing that one can do with the APOE geno-

type information to lower one’s Alzheimer risk, other than

widely-recommended healthy behaviors regarding diet and

exercise that should be recommended to everyone.10 However,

the neurologist was concerned about his responsibility not to

withhold information from the family.

The neurologist met with the patient and her adult children,

informing them that the diagnosis was highly likely to be AD,

based solely on the MRI, PET scan, and CSF findings. He

reviewed all of these test results and then told them about the

availability of APOE genetic testing and the risks and benefits

of such testing whether the results are positive or negative. He

explained the risks of undue stress, no cure, no preventive mea-

sures, and no guarantee of predictability. He explained the ben-

efits of potentially knowing the diagnosis with even more

certainty and helping future generations. He informed them

that the results of this genetic test would not change the cur-

rent treatment course or the diagnosis. Based on the neurolo-

gist’s recommendation, the patient and adult children

declined genetic testing. The neurologist concurred with their

decision. The neurologist did not inform the patient and the

family of the existence or results of the APOE genetic testing.

He also consulted with the insurance company who paid for

the test and was informed that they had not informed the

patient that the test had been completed. He consulted with

a geneticist on faculty at the University who concurred that

it was not indicated to inform the children as the neurologist

had told them about the availability of this test, and they had

not indicated an interest. The neurologist also spoke with the

Ethics Committee and the patient’s primary care provider who

all agreed that it was not indicated to disclose these results.

The neurologist’s perspective was that not disclosing this

information, especially when not requested, mitigated genetic

testing harm, as described by Karlawish.20

Ethical Considerations

The ethical considerations in this case are manifold. The main

concerns are on the ethical principles of respecting persons

(patient autonomy), promoting the patient’s benefit (benefi-

cence), avoidance of harm (nonmaleficence), justice, and the

virtue-based considerations of truth-telling and trust.21 When

ordering an APOE genetic blood test, a signed informed con-

sent document must be explained to the patient and verified for

their understanding of the test under consideration by an evi-

denced means of consent (in this case, a signature on the form).

The neuroradiologist did not provide this information nor was a

form offered for signature. It was later determined that the neu-

roradiologist independently devised the protocol whereby he

would always perform APOE genetic testing automatically

(without patient consent) when AD testing for CSF was per-

formed. Motives of the neuroradiologist can be inferred, such

as (1) consent was received for the more invasively procured

CSF studies (Ab 1-42 and t levels) and that blood testing is
implied or (2) that the informed consent would be done by the

neurologist later. Yet, these cases inadequately safeguard the

patient’s autonomous right to consent to a test that has far-

reaching meaning not only for her but also for her descendants.

Regardless of whether the neuroradiologist rationalized this

practice as easier or implied, it cannot be ethically defended

as it violates the patient’s autonomy. Each APOE genetic test

requires explicit consent, given the ramifications of a positive

test, requiring pretest genetic counseling and a valid signed

informed consent process. There was no demonstrable urgency

or ethical rationale for not providing such consent to the

patient. Even worse, it was subsequently learned that similar

abridgements of consent had occurred by this neuroradiologist

with other patients in drawing APOE blood testing without

their consent. Because of this case study, the neuroradiologist

ended the protocol to draw the genetic test automatically and

agreed that he should not unilaterally order genetic testing

at any time. This protocol was a clear violation of the standard

of care regarding respect for persons in genetic testing (see


The patient was at risk of harm in such a circumstance,

rather than benefit as the testing was done without her permis-

sion, a violation of beneficence and nonmaleficence claims.

The ‘‘assault’’ (unknown by the patient) is the invasion of pri-

vacy of removal of bodily fluids with knowledge gained that

will have far-reaching impact that could be harmful. The neu-

rologist did not feel that the results should be removed from the

chart as it would be unethical to alter a medical record. Elec-

tronic health records, and medical records generally, have a

592 American Journal of Alzheimer’s Disease & Other Dementias® 29(7)

propensity for moving information in unintended ways—the

patient’s genetic risk noted in the medical record is now acces-

sible by the patient’s physician and potentially by a proxy, her

offspring, and their insurers. The consequences of a positive

test, once errantly discovered, could be emotionally devastat-

ing, with the shock of such news being more harmful than if

valid consent had been received. The patient’s offspring could

also be harmed through receiving test results that reveal risk of

future AD. If the patient, her family, or any third party ever

requests her records, then they would see the results of the

genetic testing. The adult children would then know that they

are carriers of an e4 allele and that this information was not
shared with them—with the resultant consequences of a breach

of trust. Also, if a new provider requests medical records, then

the new provider may reveal the genetic test results. The harm

of this land mine of unrequested medical knowledge could

have a detrimental impact on their concept of future health,

their insurability, and their perceived trust in the medical


In the aftermath of the neuroradiologist’s actions, the refer-

ring neurologist believed that offering the now known APOE

genetic testing safeguarded his responsibility to honor the

patient’s autonomous consent or refusal of the APOE test, with-

out revealing what had been done by the neuroradiologist.

Since patient and family refused the test, he believed that the

completed result offered no benefit to the patient or her chil-

dren). His perception was that all parties could be harmed,

rather than helped, by learning the results of the APOE genetic

testing. The neurologist made the diagnosis of AD before the

genetic test results were available. This decision makes the vir-

tues of truth-telling and fidelity to trust relevant, as the family

trusted the neurologist, who had already made the clinical diag-

nosis of AD in the patient and who had strong suspicions that

this was indeed the correct diagnosis to be validated by the

requested laboratory testing. As such, family members may

then have the opportunity to gain from this metaphorical ‘‘fruit

from the poisonous tree’’ in order to better prepare themselves

for the future risk of Alzheimer’s and to consider proactive

treatment when such opportunities avail themselves in future

medical interventions.

One might question whether the neurologist had a duty to

report the genetic testing results to the patient and family.

Some might suggest that he did not.12,14 After all, there is

no duty to report information that will not impact the diagno-

sis or course of treatment for the patient or to cause the off-

spring unnecessary worry. The decision to perform genetic

testing should be a personal one between the physician and the

patient. One could also argue that the neurologist also had an

autonomy-based obligation to divulge this information (as the

genetic test results are the property of the patient).22 Further,

there is a virtue-based obligation (see earlier) to divulge the

protocol of the neuroradiologist that the test had been per-

formed without permission, that the results were available if

requested, and that the system-based errors that resulted in the

ethical and procedural lapses had been addressed by the insti-

tution. By extension, the family had a right to know that such

knowledge could impact their future health, by both justice-

based consideration and family-based consideration.23 A pre-

ventive ethics strategy in genetic testing would be to utilize a

family covenant, a health care agreement between physician,

patient, and family members, to proactively set parameters of

how knowledge is shared within the family and how it should

be disseminated.24

Standard of Care Considerations

In June 2011, guidelines were published by the American Col-

lege of Medical Genetics and the National Society of Genetic

Counselors to assist health care providers in making decisions

about appropriate management of genetic concerns related to

AD.25 The guidelines state that ‘‘genetic testing for AD should

only occur in the context of genetic counseling and support by

someone with expertise in this area.’’25 The guidelines gener-

ally discourage APOE testing in asymptomatic people but do

allow for testing ‘‘at the clinician’s discretion.’’25 These guide-

lines had not yet been issued at the time the case occurred.

However, the principles within these guidelines were available

as standard of care since 1997 when a consensus statement

explained that ‘‘except for autosomal dominant early-onset

families, genetic testing in asymptomatic individuals is unwar-

ranted. Use of APOE genetic testing as a diagnostic adjunct in

patients already presenting with dementia may prove useful

but it remains under investigation. The premature introduction

of genetic testing and possible adverse consequences are to be

avoided.’’26 Therefore, home genetic testing in asymptomatic

people is not recommended.

In 2009, the Risk Evaluation and Education for Alzheimer’s

Disease (REVEAL) Study Group randomly assigned 162

asymptomatic adults who had a parent with AD to receive the

results of their own APOE genotyping or not to receive such

results. The REVEAL Study Group found that the disclosure

of APOE genotyping did not result in significant short-term

psychological risks to the patient.27 The REVEAL study also

found that persons who learned about their APOE genotype

through an education-and-disclosure protocol did not have

greater symptoms of anxiety, depression, or test-related distress

than those not receiving such information.27 However, the

patient in this case did not have any education about testing and

there was no disclosure protocol in place to ensure minimal

psychological harm. Therefore, when the test results came back

to the neurologist, he did not immediately disclose the results.

Instead, he educated the patient and family about the genetic

testing options in order to prevent potential anxiety, depression,

or distress.

Conclusion and Practical Considerations

In the case presented, the neuroradiologist, who was not an

expert in AD, inappropriately performed APOE genetic test-

ing without requisite or genetic counseling or informed con-

sent. Further, Athena Diagnostics performed the genetic

testing without a signed informed consent document,

Furman et al 593

violating their own protocol. The genetic testing demon-

strated a case in which multiple errors resulted in a genetic

test finding with potentially negative consequences for the

patient and family, which then required redress by the neurol-

ogist regarding whether the test ever would have been wanted,

and whether it bore relevance to the patient’s future health or

that of her progeny.

There may be a large number of people who will want

genetic testing for AD as there is more concern over the illness.

A study published in 2004 showed that 24% of contacted par-
ticipants wanted genetic counseling regarding AD and 64% of
self-referred participants wanted the counseling.28 Predictive

genetic testing performed by those not trained in genetics will

very likely recur, as in this case. Yet, genetic testing should

never be performed unless the patient has been given the oppor-

tunity to consent to such testing by a professional with funda-

mental genetics training on the meaning of the test offered.

Situations exist when genetic testing and counseling are appro-

priate, with the ideal setting of counseling always being pro-

vided by a genetic counselor or a geneticist. However, there

is a significant shortage of genetic counselors and geneticists

in the United States.14 Most nongenetics professionals do not

believe that they are prepared to provide genetic counseling

and testing unless they receive further requisite training to do

so. Therefore, health care providers need to know the guide-

lines surrounding their responsibilities on genetic testing and

counseling and should be educated about the risks and benefits

of their playing this role in the absence of a genetic counselor.

Only with this training can providers mitigate the harm genetic

testing can do to their patients and their patients’ children.

There is a need to educate physicians and train more genetic

counselors about genetic testing for Alzheimer’s dementia

because this is a disease that is becoming more prevalent as our

population ages.

This case confirms that safeguards to genetic testing should

be generally established as standards of care and that APOE

testing is a herald case. Formal education should be provided

to primary care physicians, geriatricians, neurologists, and neu-

roradiologists regarding the proper ethical and clinical uses of

genetic testing. Genetic testing should always be preceded by a

genetic counseling discussion between the patient, his/her fam-

ily, and a provider experienced in the discussion, as well as an

informed consent from a patient with known decisional capac-

ity or from the health care surrogate. These safeguards will pre-

vent future inappropriate genetic testing due to lack of an

informed consent discussion.


The authors would like to thank Sharon Barrer, RN and Margaret

Feldman for their editorial assistance.

Declaration of Conflicting Interests

The authors declared no potential conflicts of interest with respect to

the research, authorship,

and/or publication of this article.


The authors received no financial support for the research, authorship,

and/or publication of this article.


1. Corder EH, Saunders AM, Strittmatter WJ, et al. Gene dose of

apolipoprotein E type 4 allele and the risk of Alzheimer’s disease

in late onset families. Science. 1993;261(5123):921-923.

2. Farrer LA, Cupples LA, Haines JL, et al. Effects of age, sex, and

ethnicity on the association between apolipoprotein E genotype and

Alzheimer disease. A meta-analysis. APOE and Alzheimer disease

meta analysis consortium. JAMA. 1997;278(16):1349-1356.

3. Farrer LA, Cupples LA, van Duijn CM, et al. Apolipoprotein E

genotype in patients with Alzheimer’s disease: implications for

the risk of dementia among relatives. Ann Neurol. 1995;38(5):


4. Mayeux R, Schupf N. Apolipoprotein E and Alzheimer’s disease:

the implications of progress in molecular medicine. Am J Public

Health. 1995;85(9):1280-1284.

5. Seshadri S, Drachman DA, Lippa CF. Apolipoprotein E epsilon 4

allele and the lifetime risk of Alzheimer’s disease. What physicians

know, and what they should know. Arch Neurol. 1995;52(11):


6. Bowirrat A, Friedland RP, Chapman J, Korczyn AD. The very

high prevalence of AD in an Arab population is not explained

by APOE epsilon4 allele frequency. Neurology. 2000;55(5):731.

7. Chandra V, Pandav R, Dodge HH, et al. Incidence of Alzheimer’s

disease in a rural community in India: the Indo-US study. Neurol-

ogy. 2001;57(6):985-989.

8. Ganguli M, Chandra V, Kamboh MI, et al. Apolipoprotein E poly-

morphism and Alzheimer disease: the Indo-US Cross-National

dementia study. Arch Neurol. 2000;57(6):824-830.

9. Chandra V, Ganguli M, Pandav R, Johnston J, Belle S, DeKosky

ST. Prevalence of Alzheimer’s disease and other dementias in rural

India: the Indo-US study. Neurology. 1998;51(4):1000-1008.

10. Guo Z, Fratiglioni L, Viitanen M, et al. Apolipoprotein E geno-

types and the incidence of Alzheimer’s disease among persons

aged 75 years and older: variation by use of antihypertensive med-

ication? Am J Epidemiol. 2001;153(3):225-231.

11. Corder EH, Saunders AM, Risch NJ, et al. Protective effect of

apolipoprotein E type 2 allele for late onset Alzheimer disease.

Nature genetics. 1994;7(2):180-184.

12. American College of Medical G. Statement on use of apolipo-

protein E testing for Alzheimer disease. American college of

medical genetics/American society of human genetics working

group on ApoE and Alzheimer disease. JAMA. 1995;274(20):


13. Mayeux R, Saunders AM, Shea S, et al. Utility of the apolipo-

protein E genotype in the diagnosis of Alzheimer’s disease.

Alzheimer’s disease centers consortium on apolipoprotein E

and Alzheimer’s disease.[Erratum appears in N Engl J Med.

1998;338(18):1325]. N Engl J Med. 1998;338(8):506-511.

14. Kapp MB. Physicians’ legal duties regarding the use of genetic

tests to predict and diagnose Alzheimer disease. J Leg Med.


594 American Journal of Alzheimer’s Disease & Other Dementias® 29(7)

15. McGovern MM, Benach MO, Wallenstein S, Desnick RJ,

Keenlyside R. Quality assurance in molecular genetic testing

laboratories. JAMA. 1999;281(9):835-840.

16. 23andMe I. 2011;

Accessed December 27, 2011.

17. Folstein MF, Folstein SE, McHugh PR. ‘‘Mini-mental state’’. A

practical method for grading the cognitive state of patients for the

clinician. J Psychiatr Res. 1975;12(3):189-198.

18. Kuslansky G, Buschke H, Katz M, Sliwinski M, Lipton RB.

Screening for Alzheimer’s disease: the memory impairment

screen versus the conventional three-word memory test. J Am

Geriatr Soc. 2002;50(6):1086-1091.

19. Athena Diagnostics. 2011;

test-catalog. Accessed September 18, 2011.

20. Karlawish J. Addressing the ethical, policy, and social chal-

lenges of preclinical Alzheimer disease. Neurology. 2011;77(15):


21. Giarelli E.Ethical issues in genetic testing. The experiences of one

family diagnosed with an inherited cancer syndrome. J Infus Nurs.


22. Arribas-Ayllon M. The ethics of disclosing genetic diagnosis for

Alzheimer’s disease: do we need a new paradigm? Br Med Bull.


23. Parker M, Lucassen AM. Genetic information: a joint account?

BMJ. 2004;329(7458):165-167.

24. Doukas DJ, Berg JW. The family covenant and genetic testing.

Am J Bioeth. 2001;1(3):3-10.

25. Goldman JS, Hahn SE, Catania JW, et al. Genetic counseling and

testing for Alzheimer disease: joint practice guidelines of the

American college of medical genetics and the national society

of genetic counselors. Genet Med. 2011;13(6):597-605.

26. Post SG, Whitehouse PJ, Binstock RH, et al. The clinical intro-

duction of genetic testing for Alzheimer disease. An ethical per-

spective. JAMA. 1997;277(10):832-836.

27. Green RC, Roberts JS, Cupples LA, et al. Disclosure of APOE

genotype for risk of Alzheimer’s disease. N Engl J Med. 2009;


28. Roberts JS, Barber M, Brown TM, et al. Who seeks genetic sus-

ceptibility testing for Alzheimer’s disease? Findings from a multi-

site, randomized clinical trial. Genet Med. 2004;6(4):197-203.

Furman et al 595

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