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A journal of Dayton Children’s Hospital
Volume 25
Number 1
CME
accredited articles
FREE CME
credits available
Gastroesophageal Reflux Page 3
Bullying Page 6
Update on the Diagnosis and
Management of Obstructive
Sleep Apnea Page 10
A Perplexing Pathogen in a
Neonate with Meningitis
Page 14
News and Updates Page 18
2
Pediatric
Forum
A journal of
Dayton
Children’s
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should only claim credit commensurate with the extent of their participation in the activity.
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The purpose of
Pediatric Forum
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information
and news about
pediatric health
care issues
and to provide
information
about clinical
services and
management
issues of Dayton
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Target audience
This education activity is designed
for pediatricians, family physicians
and related child health
care providers.
Educational objectives
4 Identify the four pediatric
issues covered in this journal
and develop appropriate
intervention.
4 Appropriately use the resources
of Dayton Children’s Hospital
to improve patient care.
Print date: March 2014
Affiliations/disclosures
of authors
Samuel Dzodzomenyo, MD
[email protected]
Dayton Children’s Hospital
Julian Edelschick, MD
[email protected]
Dayton Children’s Hospital
Matthew McRoberts, MD
[email protected]
Dayton Children’s Hospital
Gregory Ramey, PhD
[email protected]
Dayton Children’s Hospital
James Rick, MD
[email protected]
Dayton Children’s Hospital
Author conflict of
interest information
It is the policy of Wright State
University to ensure balance, independence, objectivity and scientific
rigor in all educational activities. All
authors contributing to our programs are expected to disclose any
relationships they may have with
commercial companies whose products or services may be mentioned
so that participants may evaluate
the objectivity of the program. In
addition, any discussion of off-label,
experimental or investigational use
of drugs or devices will be disclosed
by the authors. Contributing authors
reported the following:
Samuel Dzodzomenyo, MD
Dr. Dzodzomenyo has nothing to
disclose with regard to commercial
support. Dr. Dzodzomenyo does not
plan on discussing unlabeled/investigational uses of a commercial product.
Julian Edelschick, MD
Dr. Edelschick has nothing to disclose
with regard to commercial support.
Dr. Edelschick does not plan on
discussing unlabeled/investigational
uses of a commercial product.
Matthew McRoberts, MD
Dr. McRoberts has nothing to disclose
with regard to commercial support. Dr.
McRoberts does not plan on discussing
unlabeled/investigational uses
of a commercial product.
Gregory Ramey, PhD
Dr. Ramey has nothing to disclose
with regard to commercial support.
Dr. Ramey does not plan on discussing
unlabeled/investigational uses of a
commercial product.
James Rick, MD
Dr. Rick has nothing to disclose
with regard to commercial support.
Dr. Rick does not plan on discussing
unlabeled/investigational uses of
a commercial product.
The content and views presented
are those of the author and do not
necessarily reflect those of the
publisher, Dayton Children’s.
Unlabeled use of products may be
mentioned. Before prescribing any
medicine, primary references and
full prescribing information should
be consulted. All planning committee members have disclosed that
they do not have any financial
relationships with commercial
entities that may impact the
content of this publication.
Editorial board
Sherman Alter, MD, chairperson
Lucinda Brown, MSN, RN, CNS
Emmett Broxson, Jr, MD
Lisa Coffey, FACHE
Elvira R. Jaballas, MD
L. David Mirkin, MD
Sherman Alter, MD
Director, Continuing Medical Education
Deborah A. Feldman
President and Chief Executive Officer
Adam G. Mezoff, MD, CPE, AGAF
Vice President for Medical Affairs
Chief Medical Officer
Elizabeth Ey, MD
Chair of the Professional Staff
Dr. Alter is on the speaker’s bureau for
SanofiPasteur. The activity has been
peer reviewed by the remainder of the
planning committee to ensure the absence
of bias. The remainder of the editorial
board/planning committee members
have nothing to disclose.
Gastroesophageal Reflux:
Physiologic Symptoms or Disease Process?
Introduction
There is an increase in the use
of acid suppressive medications to treat esophageal reflux
in infants and children. Not all
patients with esophageal reflux
will need medical therapies
and most benefit from lifestyle
modifications. It is important to
distinguish gastroesophageal
reflux (GER) from gastroesophageal reflux disease (GERD)
so appropriate therapies can
be provided. GER implies the
physiologic passage of gastric
contents into the esophagus.
GERD is defined as esophageal
reflux with the presence of
troublesome symptoms or
complications.
Most babies have GER. The
common manifestation in
infancy is frequent bouts of
Objectives
Following the completion of
this article, the reader should
be able to:
1. Differentiate gastroesophageal reflux (GER) from
gastroesophageal reflux
disease (GERD).
2. Evaluate and manage
both GER and GERD.
3. Recognize that lifestyle
changes are first-line
therapy.
painless, effortless regurgitation
in thriving infants. As a visible
symptom, it is reported daily in
50 percent of infants. In all age
groups, reflux can be associated with vomiting which is the
forceful expulsion of gastric
contents. Esophageal reflux is
also a key component of rumination syndrome, in which the
refluxate consists of ingested
food that is rechewed and
reswallowed. GER resolves in
most infants by 12 to 18 months.
When there are symptoms and/
or complications associated
with GER, then it is classified
as GERD. Conditions can be
esophageal or extra-esophageal.
Esophageal symptoms are
heartburn, abdominal pain,
dysphagia, chest pain, emesis
and poor weight gain/weight
loss. Extra-esophageal manifestations are respiratory (cough,
wheezing, apparent life-threatening events, recurrent pneumonia), laryngitis and dental
erosions. Esophageal mucosal
complications of GERD include
reflux esophagitis, peptic
stricture, Barrett esophagus
and adenocarcinoma.
GERD:
Clinical Features
The presentation of GERD in
pediatric patients is age-dependent. Common symptoms in
infants include regurgitation,
vomiting, irritability and dysphagia. Less common are poor
weight gain due to poor feeding
and excessive loss of calories,
3
respiratory symptoms and obstructive apnea. Rarely, unusual
posturing (back arching and
dystonia), called Sandifer’s
syndrome, can be seen with
severe GERD. From 1 to 5 years
of age, the symptoms of GERD
are similar to infants. GERD is
less common in this age group,
but similar problems of regurgitation, vomiting, anorexia and
abdominal pain occur. Visible
James
reflux is not always seen and
Rick, MD
symptom description is hard,
James Rick, MD,
so diagnosis can be difficult.
is the interim
An aversion to eating due to
medical director
pain may lead to poor weight
of gastroenterology at Dayton
gain or even malnutrition.
Children’s. He is
Older children and adolescents
board certified
with GERD develop symptoms
in pediatrics and
similar to adults. These include
pediatric gastroheartburn, dysphagia, sour
enterology. He is
also associate
burps and/or regurgitation,
professor of
chest pain, nausea and epigaspediatrics at
tric pain. Symptoms are often
Wright State
worse nocturnally when supine
University
for sleeping. Extra-esophageal
Boonshoft
School of
symptoms include nighttime
Medicine.
cough, wheezing, recurrent
pneumonia,
laryngitis and
Table 1: Concerning Symptoms
dental erosions. and Signs
Certain pedi4Bilious vomiting
atric patients
have higher
4Gastrointestinal bleeding
prevalence of
4Consistent forceful
GERD. For invomiting
stance, roughly
4Fevers, lethargy, seizures
65 percent of
children with
4Hepatosplenomegaly
underlying
4Bulging fontanel, macroneurologic
or microcephaly
disorders have
4Abdominal tenderness or
significant
distension
GERD based
on pH probe
4Associated genetic
studies. Factors
syndrome or metabolic
contributing to
disease
GERD include
4Associated other chronic
chronic supine
diseases
position,
under nutrition, chronic constipation, scoliosis, seizures and
spasticity. Concerning clinical
findings among some children
with GERD are noted in
Table 1.
4
Diagnostic
Evaluation
Detailed approaches to assessment and management of GERD
have been published (Vandenplas et al.). History and physical
are essential and, if normal in
the absence of warning signs,
are sufficient to reliably diagnose GER. In the setting of
suspected GERD, testing can
be used to document reflux of
gastric contents, detect complications, establish relationship
between reflux and symptoms,
evaluate treatments and exclude other conditions.
Upper gastrointestinal imaging
(UGI) is key in the evaluation of
vomiting to exclude anatomic
abnormalities in infancy. In older children, it is useful to check
for strictures, hiatal hernia or
esophageal dilation. It should
not be routinely performed for
diagnosis as non-pathologic
GER occurs frequently during
the study.
Esophageal intraluminal pH
monitoring quantifies reflux
and correlates reflux with symptoms. This modality has largely
been replaced by extended pH
monitoring with multi-channel
intraluminal impedance monitoring (pH/MIII). This technology detects both acidic and
non-acidic fluids, solids and
gas movements in the esophagus. Valuable information is
obtained regarding frequency
of GER episodes, duration,
clearance and relationship to
reported GER symptoms. Often,
other etiologies like aerophagia
or rumination syndrome can be
detected. It is often done when
evaluating whether an antireflux surgery is needed.
Upper endoscopy is commonly
used to evaluate patients when
symptoms of GERD are resistant
to treatment, to detect complications of chronic GERD and
exclude other causes of the
symptoms. Endoscopic evaluations may disclose eosinophilic
esophagitis, infectious esophagitis, pill-induced esophagitis, Crohn’s disease, Barrett’s
esophagus, peptic ulcer disease, H pylori gastritis, or other
unexpected esophageal, gastric
or duodenal disease. Biopsies
are routinely done and can
find reflux-induced histologic
esophageal inflammation in up
to 25 percent.
Management
Lifestyle modifications can
reduce symptoms of both GER
and GERD in infants and children, and should be utilized in
all patients with GER and GERD.
Among infants, this involves
feeding changes and positioning. Cow milk protein allergy
can mimic GERD, so a two to
four week trial of maternal cow
milk restriction in breastfed
infants or an extensively hydrolyzed protein may be used in
formula-fed infants. Thickening
of feedings by adding up to one
tablespoon of rice cereal to one
ounce of formula or changing to
a commercially thickened formula is a valid strategy in otherwise healthy infants with GER
or GERD. Smaller volume, more
frequent feedings and frequent
burping are also advocated, yet
no studies have shown these to
be of benefit.
Proper positioning has a role.
Although less GER has been
shown with prone position, it
is clear that the risk of sudden
infant death syndrome while in
the prone position outweighs
this benefit. Thus, prone
position is only recommended
while the infant is observed
and awake and after 1 year of
age. Semi-supine position such
as happens in the car seat or
infant carrier may worsen GER
and should be avoided when
possible, especially after feed-
ing. Lifestyle changes for older
children and adolescents are
similar to adults and include
weight loss in overweight
patients, avoiding smoking and
smoke exposure, limiting alcohol, avoiding triggering foods,
and elevation of the head of
the bed.
Several medications are available to treat GERD in infants
and children. Most commonly
used are acid suppressants
including antacids, histamine-2
receptor antagonists (H2RAs),
and proton pump inhibitors
(PPIs). Antacids are not indicated for chronic use and there is
little data justifying on-demand
use in pediatric population.
H2RAs work by inhibition of histamine-induced acid secretion
by the gastric parietal cell. Little
clinical difference exists among
the various H2RAs. Limitations
include tachyphylaxis reducing
long-term effectiveness, they are
less effective than PPIs in healing of erosive esophagitis, and
may be linked to liver disease
and gynecomastia.
PPIs work by the inhibition
of the hydrogen-potassium
ATPase in the gastric parietal
cell canaliculus. They are the
most effective acid suppressant
agents. Effectiveness is maximized by appropriate timing of
the dose. PPIs should be taken
30 minutes prior to meals and
incorrect timing is associated
with clinical failure. Clinical
trials support the use of PPIs in
esophagitis and GERD symptoms refractory to H2RAs. Concerns about PPIs have emerged.
Overuse in infants with reflux is
reported despite trials showing
no benefit in this population.
Acid suppression may be a risk
factor for pneumonia, gastroenteritis, necrotizing enterocolitis,
candidemia and a variety of
nutritional concerns.
Prokinetic agents are the second
class of drugs used in GERD.
Metoclopramide is the most
common prokinetic agent. It
works by increasing both lower
esophageal sphincter tone and
gastric emptying. Recently, the
FDA issued a black box warning due to adverse events. Other
prokinetics available in the
United States include erythromycin and baclofen. The 2009
NASPGHAN guidelines do not
support the routine use of any
prokinetic agent for treatment
of GER or GERD.
Lastly, surgical therapies are
available for GERD. The most
common is the Nissen fundoplication, which is a 360-degree
wrap of the gastric fundus
around the distal esophagus.
It is an effective procedure, but
should be reserved for those
with severe complications of
GERD who fail other therapy or
those at high risk for aspiration
of gastric contents.
Summary
During infancy, reflux usually
manifests as a physiologic process in healthy babies. Education and reassurance, minimal
testing and treatments with positioning and feeding changes
are recommended. Infants with
complicated GERD especially
in the setting of poor feeding
or growth must be recognized
so evaluation and treatment
can be tailored. Older children
with typical GERD symptoms
may benefit from a trial of acid
suppression. Close follow-up is
essential to ensure response to
treatment and if not responsive,
evaluation for other conditions.
References
1. Couriel J, Bisset R, Miller R.
Assessment of feeding problems in neurodevelopmental
handicap: a team approach.
Arch Dis Child. 1993;69:
609-15.
2. Hassall E. Over-prescription
of acid-suppressing medications in infants: how it came
about, why it’s wrong and
what to do about it. J Pediatr.
2012;160(2):193-198.
3. Lightdale JR, Gremse DA, and
Section on Gastroenterology,
Hepatology and Nutrition.
Gastreoesophageal reflux:
management guidance for
the pediatrician. Pediatrics.
2013;131;e1684-1695.
4. Orenstein SR, Hassal E, Furmaga-Jablonska W, Atkinson
S, Raanan M. Multi-center
double-blinded, randomized, placebo-controlled trial
assessing the efficacy and
safety of proton pump inhibitor lansoprazole in infants
with symptoms of esophageal reflux disease. J Pediatr.
2009;154(4):514-520.e4.
gastroesophageal reflux
clinical practice guidelines:
joint recommendations of the
North American Society for
Pediatric Gastroenterology,
Hepatology and Nutrition
(NASPGHAN) and the European Society for Pediatric
Gastroenterology Hepatology
and Nutrition (ESPGHAN).
J Pediatr Gastroenterol Nutr.
2009;49(4):498-547.
5
CME Questions
1. A 3-month-old is seen for severe reflux.
The child has non-bilious regurgitation
after most feedings. He is growing well,
not fussy and has a normal physical
exam. Your next step is:
a. Provide education, reassurance and
reflux precautions
b. Order a UGI
c. Begin trial of proton pump inhibitor
d. Order a 24-hour pH and impedance
study
5. Rudolph CD, et al. Guidelines
for evaluation and treatment
of gastroesophageal reflux in
infants and children: recommendations of the North
American Society for Pediatric Gastroenterology and Nutrition. J Pediar Gastroenterol
Nutr. 2001;32 Suppl 2:S1-S31.
2. Which of the following would not be
considered a symptom of GERD?
6. Scherer LD, Zikmund-Fisher
BJ, Fagerlin A, Tarini BA.
Influence of “GERD” label
on parent’s decision to
medicate infants. Pediatrics.
2013;131:839-845.
3. A 12-year-old is seen for daily heartburn
and regurgitation of stomach contents.
You suspect GERD. What is your initial
treatment?
7. Vandenplas Y, Rudolph CD,
Di Lorenzo C, et al; North
American Society for Pediatric Gastroenterology,
Hepatology, and Nutrition;
European Society for Pediatric Gastroenterology Hepatology and Nutrition. Pediatric
a. Poor weight gain
b. Irritability
c. Chronic respiratory symptoms
d. Normal feeding behavior
a. Over-the-counter antacids
b. Metaclopramide
c. Refer for a fundoplication
d. Trial of acid suppression
6
Bullying
Gregory
Ramey,
PhD
is a child psychologist at Dayton
Children’s and a
Dayton Daily
News columnist.
His column
FamilyWise is
distributed
through New
York Times wire
service. Dr. Ramey
received his
undergraduate
degree from Lake
Forest College, his
master’s degree
from Harvard
University and his
PhD in psychology
from the University of Massachusetts.
History
While originally used in the
16th century to describe a lover
or friend, the word bully has
morphed to mean a variety
of offensive conduct. While
behaviors intended to intimidate or demean have always
occurred, the
first serious
Objectives
study of bullying
didn’t occur unFollowing the completion of
til the publicathis article, the reader should
tion of “Teasing
be able to:
and Bullying” in
the Pedagogical
1.Identify the prevalence of
Seminary in 1897
childhood bullying.
by Frederic Burk.
This research in2. List three groups that are
vulnerable to bullying.
volved a survey
of teachers with
3. Describe how parents,
many recomschools, and health
mending “flogprofessionals can help
ging or severe
deal with this problem.
punishment”
or “bullying the
bully” as the
cure for this problem.
In the 1970s, Dr. Dan Olweus
from Norway began the first
long-term study of this problem,
prompted by concerns regarding teen suicides. He published
research aimed at helping
schools implement intervention
programs. However, concerns
about bullying didn’t become
widespread until the tragic
events of April 20, 1999. On that
day, Dylan Klebold and Eric
Harris entered Columbine High
School in Littleton, Colorado,
and killed 13 people before committing suicide. Those horrific
events were recorded on the
school’s videotaping system
and the recording eventually
made its way onto the Internet.
The methodical manner in
which these two teenagers
went about their rampage was
incomprehensible. In an effort
to understand the inconceivable, these kids were initially
portrayed as the victims of
bullying who were retaliating
against their aggressors. While
more thoughtful and thorough
studies have concluded that
bullying had nothing to do
with this attack, the school
shootings stimulated a national
discussion on the seriousness
of this problem.
In 2003, increased attention
on bullying was prompted by
a very different kind of event.
Erika Harold was selected as
Miss America and used her
platform to advocate on behalf of the victims of bullying.
Harold spoke eloquently about
the ridicule and humiliation she
experienced from classmates
in the ninth grade due to her
biracial background. “I was very
scared and I felt very helpless
because it seemed as if no one
in the school was willing to
stand up and help me,” Harold
told PBS.1 Harold became a
voice for kids who had suffered
in silence while adults ignored
their plight.
in the prevalence of child
sexual abuse3 and the overall
downward trend in kids thinking about suicide,4 this is the
best time in history to be a
child in America.
Table 1 — Total Victimizations
200
At school
Rate per 1,000
150
100
Professionals like me who take
this problem seriously don’t
deny the overall improvement
in such child welfare metrics,
but point to a plethora of
research indicating that
bullying is more than just
occasional teasing. It is
widespread and has deleterious consequences for both the
victim and the aggressor.
Away from school
50
0
1992
1995
2000
2005
2010
Year
With increased research, the
fear of another Columbine, and
an articulate spokesperson
in Erika Harold, bullying as a
significant problem finally got
America’s attention.
who want to insulate their kids
from the normal harshness of
the world. Kids and adults can
be mean at times and children
need to learn how to deal with
such cruelty without always
seeking protection from adults.
What is Bullying?
Bullying may involve verbal,
social or physical behavior.
Typical verbal bullying may
include name calling, teasing
or even threatening behavior.
Social bullying can be among
the most harmful and includes
embarrassing someone in
public, exclusion or spreading
rumors. Physical bullying
includes hitting, pushing
or violent behavior towards
another.
This perspective cites research
that, in many ways, kids today
have never been safer. Between
1995 and 2009 the number of
children who reported “being afraid of attack or harm at
school” dropped from 11.8 to
3.3 percent. The overall victimization rate per 1,000 students
declined fivefold.2 Combined
with the substantial decrease
How Serious Is
This Problem? The seriousness of bullying has
been debated by both social
scientists and child development experts. Some view this as
nothing more than kids teasing
other children and say the concern about bullying is an overreaction by protective parents
Figure 1 — Percentage of students in grades 9 through 12 who report they thought seriously about attempting suicide,
attempted suicide, and that their suicide attempts required medical attention1, 1991-2011
50
45
Thought seriously about attempting suicide
40
Attempted suicide
Percent
35
30
Suicide attempt, needed medical attention
29
24
25
24
21
20
19
19
17
17
15
10
5
0
7
9
9
8
8
9
9
8
2
3
3
3
3
3
3
2
1991
1993
1995
1997
1999
2001
Year
2003
2005
15
14
7
6
2
2
2007
2009
16
8
2
2011
1
During the past twelve months. Source: Centers for Disease Control and Prevention. Survelilance Summaries. Data for 1991. YRBSS: Youth Online. Comprehensive Results. Retrieved May 24, 2004 from URL:
http://apps.nccd.cdc.gov/lyrbss/; Data for 1993: March 24, 1995. MMWR 1995; 44 (No. SS-1): Table 10; Data for 1995: September 27, 1996. MMWR 1996; 45 (No. SS-4): Table 10: Data for 1997: August 14, 1998.
MMWR: 47 (No.SS-3): Table 10: Data for 1999; June 9, 2000. MMWR 2000; 49 (No. SS-5); Table 12; Data for 2001: June 28, 2002. MMWR 2002: 51 (No. SS-4): Table 12. Data for 2003: May 21, 2004. MMWR 2004; 53
(No. SS-2): Tables 16 and 18. Data for 2005: June 9, 2006. MMWR 2006: 55 (No. SS-6): Table 16. Data for 2007: June 6, 2008. MMWR 2008; 57 (No. SS-4): Tables 21 and 23. Data for 2009: June 4, 2010. MMWR 2010;
69 (No. SS-5): Table 22, 24.
7
8
The ubiquity of social media
and the widespread availability
of smart phones have added
another dimension to this
problem, making it easier to
victimize other kids with a
much wider audience and a
permanent record of such
abuse.
How Often Does
Bullying Occur?
It’s impossible to accurately
measure what cannot be clearly
defined, and researchers have
been plagued by a lack of
consistency in what specific
behaviors constitute bullying.
A consensus has emerged that
bullying behavior must meet
each of the following three
criteria.
Profile of Kids
at Risk for Being
Bullied
Bullying is all about power,
those who have it abusing those
who don’t. The typical victims
are usually kids with little perceived status or influence. Some
groups are more likely the target
of bullies, such as kids who are
obese, have poor social skills,
or are viewed as quiet and
insecure. Kids who are gay or
lesbian get bullied two to three
times as often as other kids.
Bullying is not an innocuous
act. Being a victim of chronic
bullying places kids at risk for
depression, anxiety, anger and
poor school performance.
Profile of Bullies
It is a myth that bullies have low
self-esteem or are rejected by
their peers. Bullies are looking for admiration, status and
dominance. They are typically
aggressive and domineering
with high levels of externalizing
or hyperactive behavior. Bullies
have empathy deficits with little
appreciation for the impact of
their actions. They either don’t
realize that their behavior hurts
others or they just don’t care.
Many of these kids have poor
role models at home with modest adult supervision. In later
years, these kids are more likely
to commit criminal acts, drop
out of school or have serious
drug problems.
First, there must be some
intentionality to cause harm.
Bullying involves an effort to
humiliate or degrade another
individual. Second, bullying
involves a power imbalance
between individuals. This may
be an older child picking on a
younger or smaller child, but
often involves someone ridiculing a child of perceived lower
status. Finally, bullying must
be a repeated event, not an
isolated incident. Researchers
typically define this as repeated
incidents (at least three per
month) occurring over several
months.
Rates of bullying range from the
single digits to over 40 percent,
depending upon the sample
population and the definitions
used in the study. When the
more restrictive criteria delineated above are applied, it is
estimated that 5 to 15 percent
of kids are victims of chronic
bullying, while 7 to 12 percent of
kids are viewed as chronic bullies.5 The most common form of
bullying is verbal, such as name
calling and insults followed by
being the subject of rumors,
particularly cyberbullying.
The typical victims of bullying
are usually kids with little
perceived status or influence.
Can Anything
Be Done?
Schools and families that take
this problem seriously can have
an immediate and substantial
impact. Ohio Revised Code
3313.666 requires that every
school district has a policy to
prohibit harassment, intimidation, and bullying. Successful programs involve not only
increased awareness of the
problem, but setting and enforcing clear standards of behavior
for students and adults. This
involves creating a safe environment for victims to report
abuse, as well as significant
consequences for offenders.
For a busy health care professional, it’s difficult to assess
this problem during a typical
pediatric visit. However, pay
particular attention to patients
who have problems with social
skills, sexual issues or are perceived as different in any way.
Bully offenders are more likely
to present with problems in impulse control or aggression.
Schools are increasingly focusing attention on the culture in
which bullying occurs, recognizing that about 56 percent of
students have observed bullying
behavior. Without an audience
of acceptance, bullying is less
likely to occur.
1. In the Mix: Stop Bullying…
Take a Stand! PBS: Public
Broadcasting Service website.
http://www.pbs.org/inthemix/shows/show_bullying_
erika.html. Accessed 2013.
Parental actions begin with
being a positive role model, but
extend to setting and enforcing expectations of mutual
respect. With kids you mostly
get the behavior that you allow,
so parents need to be educated
that insults and intimidation
among kids are not harmless.
There is increasing attention
on bullying behavior between
siblings, which often has been
inappropriately dismissed as
benign. Cyberbullying places
an increased onus on parents to
teach digital civility and responsibility, and to more carefully
monitor kids’ electronic worlds,
particularly in junior high.
Childhood can be difficult but
loving adults can make it better
by caring enough to take this
problem seriously.
References
2. Indicators of School Crime
and Safety: 2011. National
Center for Education Statistics website. http://nces.
ed.gov/programs/crimeindicators/crimeindicators2011/
figures/figure_02_1.asp. Accessed 2013.
3. Finkelhor, D, Jones, L. Have
Sexual Abuse and Physical
Abuse Declined Since the
1990s? Crimes Against Children Research Center; 2012.
4. Suicidal Teens. Child
Trends Website. http://
www.childtrends.org/
?indicators=suicidal-teens.
Accessed 2013.
5. Bullying: A Model for Teachers. American Psychological
Association Website. http://
www.apa.org/education/k12/
bullying.aspx. Accessed 2013.
9
CME Questions
4. Bullying is primarily defined by…
a.Intentionality to cause harm
b.Power imbalance among
individuals
c. Repeated negative events
d.All of the above
5. Bullies typically have low selfesteem and are rejected by
their peers.
a.True
b.False
6. What is the most common form of
bullying?
a.Postings on YouTube
b.Verbal
c. Physical assaults
d.Physical threats
7. What percent of kids are victims of
chronic bullying?
a.<5 percent
b.5 to 15 percent
c. 20 to 30 percent
d.50 to 60 percent
10
14
Update on the Diagnosis and Management of
Obstructive Sleep Apnea
Objectives
Following the completion of
this article, the reader should
be able to:
Samuel
Dzodzomenyo, MD
Samuel Dzodzomenyo, MD, is the
medical director
of the Pediatric
Sleep Center at
Dayton Children’s.
He is board
certified in
pediatric
neurology and
sleep medicine.
He is also associate professor of
pediatrics and
neurology at
Wright State
University
Boonshoft
School of
Medicine.
1. Recognize the clinical
signs and symptoms of
obstructive sleep apnea
syndrome (OSAS) in children and adolescents.
2. Review the approach to
evaluating patients for
OSAS.
3. Describe treatment
approaches for OSAS.
Definition, etiology
and consequences
of obstructive sleep
apnea syndrome
Obstructive sleep apnea syndrome (OSAS) is a disorder of
breathing during sleep characterized by prolonged partial upper airway obstruction and/or
intermittent complete obstruction that disrupts normal ventilation during sleep and normal
sleep patterns.1 The symptoms
are frequent snoring, labored
breathing during sleep, snorting, gasping, observed apnea,
pauses in breathing, frequent
arousals, cyanosis, sleeping
in unusual positions, daytime
sleepiness, attention deficit/
hyperactivity and morning
headaches. Physical findings
include failure to thrive, being
underweight or overweight,
tonsillar hypertrophy, adenoidal
facies, decreased nasal airflow,
micrognathia, retronathia and/
or high arched palate.
Prevalence rates of OSAS vary
among different populations
and socioeconomic groups, but
generally affect 1 to 5 percent
of children.2 Peak incidence
occurs between 2 and 8 years
of age, likely due to the imbalance between the relative size
of lymphoid tissue to the airway
diameter, as well as airway
neuromotor tone resulting in
upper airway collapse during
sleep.3 Risk factors for pediatric sleep disordered breathing
(SDB) include waist circumference, chronic sinusitis/rhinitis
and minority race.4 Although
most children with OSAS may
have enlarged tonsils, their size
alone is not an independent risk
factor. OSAS is also often seen
in children with neuromuscular disorders, nasal stenosis,
cerebral palsy and prematurity.
Individuals with congenital
anomalies such as might occur
in Down syndrome, Prader-Willi
syndrome, Marfan syndrome,
syndromes associated with micrognathia, mucopolysaccharidoses, Pierre-Robin sequence,
and Hunter’s or Hurler’s syndromes are at risk for OSAS.
Untreated, OSAS is associated
with significant morbidity including failure to thrive, hypertension, cardiac disease and
neurocognitive dysfunction.
The relationship of ADHD and
of obesity with OSAS has drawn
much attention in recent years.
Not all studies have found a
consistent relationship between
OSAS and neurobehavioral outcomes. Also there is not always
a direct relationship between
the degree of the apnea hypopnea index (AHI) and the severity of these outcomes. Some
studies have found an association between primary (habitual)
snoring alone or obesity without OSAS and neurobehavioral
disorders.5
With the current obesity epidemic in the United States, the
prevalence of OSAS is expected
to rise. Physicians may be faced
with finding new ways of treating OSAS to reduce its public
health burden.
Identification and
diagnosis
A careful clinical history is essential. Primary care physicians
are the gateway to recognition
of OSAS. Overnight in-laboratory attended polysomnogram
(PSG) is the gold standard for
evaluating OSAS. A history of
the following warrants performance of a PSG or a referral of
the child to a sleep specialist:
snoring of at least three nights
per week with complaints of
labored breathing, observed
apnea, unusual sleeping
positions, hyperactivity,
daytime sleepiness and
morning headaches.
Physiologic functions measured
during a PSG include pulse
oximetry, oronasal airflow, abdominal and chest wall movements, electroencephalography
(EEG), video recording and partial pressure of carbon dioxide.
The study documents hypopnea, central and/or obstructive
sleep apneas from which the
apnea/hypopnea index (AHI)
is calculated — a number of
complete or partial airway occlusions per hour of sleep. In
the pediatric age an index of
1-5 is considered mild, 6-10 is
moderate and > 10 severe OSA.
Tonsillar size does not always
correlate with severity of OSAS
or the AHI. If a polysomnogram
is not available, sleep video
recordings, nocturnal oximetry
measurement, or use of the
22-item sleep-related breathing
disorder scale of the pediatric
sleep questionnaire are helpful
in screening. The sensitivity and
specificity of these latter assessments are inferior to PSG. PSG
testing should be sought if there
is a strong clinical suspicion of
OSAS after screening.
Home monitoring or ambulatory PSG is difficult to obtain
in young children and has not
been adopted in most pediatric
practices.
Treatment approach
to OSAS
Adenotonsillectomy (AT) is the
first line of treatment for OSAS
in children with adenotonsillar
hypertrophy, even in most obese
individuals. AT requires careful postoperative monitoring
because of the risks of respiratory and other complications.
AT is curative in 70 percent of
patients. Roughly 13 to 30 percent of children have residual
OSAS. There are several reasons
for this.
a. Residual lymphoid tissue
may be present after surgery.
b.Over time some adenoids
may grow back.
c. Other factors such as chronic
rhinitis, craniofacial anomalies and obesity may be
confounding issues.
Children who remain symptomatic even without snoring or
those with severely abnormal
preoperative OSAS should have
postoperative PSG reevaluation.
AT is not for everyone who has
adenotonsillar hypertrophy and
OSAS. Patients with small adenoids and tonsils, particularly
with morbid obesity, bleeding
disorders or medical conditions making them unstable
for surgery, are not good candidates. Adverse events following
AT include nausea, vomiting
and poor oral intake leading
to dehydration. Infrequently,
hemorrhage, velopharyngeal
incompetence, acute upper
airway obstruction, anesthetic
complications and even death
may occur. Respiratory complications are common among
children under 3 years, patients
with lower oxygen saturations
and/or increased end tidal CO2
on PSG, individuals with severe
OSA, children with failure to
thrive, and those with craniofacial anomalies. Patients at
risk require in-house or in-ICU
monitoring after surgery. Postoperative PSG evaluation six to
eight weeks after AT is recommended in at-risk patients and
among those with residual OSA
symptoms.
11
12
Continuous
positive airway
pressure (CPAP)
CPAP is a device that delivers air
by a nasal interface to splint the
upper airway during sleep. It is
used in residual OSAS after AT,
in medical conditions not suitable for AT or in morbidly obese
patients. An overnight laboratory titration is required to
determine a suitable pressure.
Historically, adherence is poor.
It requires several follow-up visits with skilled technicians and
physicians experienced in its
use. Most often pediatric CPAP
users require some form of
behavior modification therapy
to achieve an acceptable level
of compliance of at least four
hours of usage per night during
sleep.6
Bi-level positive airway pressure
(BIPAP) is an alternative mode
of positive airway pressure
delivery more useful in children
with neuromuscular disease,
intrinsic pulmonary disease and
CPAP intolerance.
Weight loss
Weight loss has been shown in
some studies to reduce the AHI
to less than half of pre-polysomnogram AHI in obese children.7
Obese patients with OSAS
who have undergone bariatric
surgery have also been shown
to have decreased severity of
polysomnographic measures
postoperatively.
Other management methods are
being evaluated in OSAS treatment in children. These include:
A. High-flow nasal cannula
This method has been
studied as an alternative to
CPAP. It uses nasal insufflation by delivering warm
humidified air via a nasal
cannula.8 The pressure
delivered is usually enough
to stent the upper airway
during sleep. Studies to
evaluate its tolerance and
acceptance in children are
needed.
B. Anti-inflammatory medications
Intranasal corticosteroids,
such as fluticasone and
budesonide, administered
for a few weeks have demonstrated some efficacy in
reducing the mean AHI
in mild obstructive sleep
apnea. Effects may persist
for only about eight weeks
after discontinuation.9
Tonsillar and adenoidal
tissues express leukotrienes and their receptors
in children with OSAS,
modulating inflammatory
signaling and promoting
proliferation of adenotonsillar tissues. Leukotriene
receptor antagonists show
response in the treatment of
OSAS in selected individuals. More studies, however,
are needed to define effective dosage and treatment
duration.
C. Oral appliances (OA) Unlike in the adult population, studies in children
on the effectiveness of oral
appliance usage for OSAS
have been minimal. Among
adults, mandibular anterior repositioning is widely
utilized with some success.
Oral appliance users require
follow-up visits with a
dental specialist regularly to
monitor patient adherence,
evaluate device deterioration or maladjustment,
assess ongoing health of the
oral structures, and gauge
the integrity of the occlusion. Signs and symptoms
of worsening OSA need
monitoring. Research to
define patient characteristics more clearly for OA
acceptance, success and adherence is needed.10 Rapid
maxillary expansion (RME)
in children with OSAS and
maxillary transverse deficiency (cross-bite) without
enlarged tonsils and adenoids has been shown to
be effective.
D. Positional therapy
Placing a soft material in a
back pouch of a sleep shirt
can avoid sleeping in a
supine position. Success is
best in adults where obesity
is the most frequent cause
of OSAS. The prone position
prevents the tongue from
occluding the upper airway
during sleep. Some authors
report that very young
children breathe better in
supine position, and hence,
may not benefit from positional therapy.
E. Watchful waiting
The Childhood Adenotonsillectomy Trial (CHAT) was
published recently recommending that, although
early AT may reduce symptoms and improve secondary outcomes of behavior,
quality of life, and polysomnographic findings, it may
not significantly improve
attention or executive function as measured by neuropsychological assessments.
As such, watchful waiting
may be appropriate for
selected groups of children
with OSAS.11
In conclusion, OSAS in children
appears to be on the rise. Not all
of the outcomes in children with
OSAS (cardiovascular, inflammatory and neurocognitive
functioning) have been consistently assessed. Some new
treatment modalities of pediatric OSAS have been validated
with randomized controlled
trials. Alternative treatments
such as nasal steroids and
dental manipulations in specialized hands may be of benefit
to some. Importantly, treatment
approaches should be individualized for every patient.
References
1. American Thoracic Society.
Standards and indications for cardiopulmonary
sleep studies in children.
Am J Respir Crit Care
Med.1996;153(920):866-878.
2. Redline S, Tishler PV, et
al. Risk factors for sleepdisordered breathing in
children. Associations with
obesity, race, and respiratory problems. Am J Respir
Crit Care Med. 1999;159(5, pt
1):1527-1532.
3. Marcus CL, Katz ES, et al.
Upper airway dynamic
responses in children with
the obstructive sleep apnea
syndrome. Pediatr Res.
2005;57:99-107.
4. Bixler EO, Vgontzas AN, et
al. Sleep disordered breathing in children in a general
population sample: prevalence and risk factors. Sleep.
2009;32(6):731-736.
5. O’Brien ML, Mervis CB, et
al. Neurobehavioral implications of habitual snoring in children. Pediatrics.
2004;114:41-49.
6. Marcus CL, Rosen G, Ward
SL, et al. Adherence to and
effectiveness of positive
airway pressure therapy in
children with obstructive
sleep apnea. Pediatrics.
2006;117(3):e442-e451.
7. Verhulst SL, Franckx H,
et al. The effect of weight
loss on sleep-disordered
breathing in obese teenagers. Obesity (Silver Spring).
2009;17(6):178-183.
13
8. McGinley B, Halbower A,
et al. Effect of a high-flow
open
nasal
CME Questions
cannula
system on
8. ADHD has been consisobstructently linked with sleep
tive sleep
disordered breathing.
apnea in
children.
a. True
b.False
Pediatrics.
2009;124:
179-188.
9. In obese children with
enlarged tonsils the first
9. Kheiranapproach is:
dish-Gozal L, Ser a. CPAP
pero LD,
b. Tonsillectomy and
Dayyat
adenoidectomy
E, et al.
Cortico c. Wait and see approach
steroids
d.Gastric bypass
suppress
in vitro
tonsillar
10. The most common cause
prolifof obstructive sleep apnea
eration in
in children 2 to 10 years of
children
age is:
with
obstruc a. Cranio-facial anomalies
tive sleep
b. Enlarged tonsils and apnoea.
adenoids
Eur Respir
J. 2009;33:
c. Obesity
1077-1084.
10. Villa MP,
11. Seasonal allergies may be
Bernkopf
responsible for obstructive
E, et al.
sleep apnea.
Random a. True
b.False
ized
controlled
study of
an oral jaw-positioning appliance for the treatment of
obstructive sleep apnea in
children with malocclusion.
Am J Respir Crit Care Med.
2002;165:123-127.
11. Marcus CL, Moore RH, et al.
A randomized trial of adenotonsillectomy for childhood sleep apnea. N Engl J
Med. 2013;368:2366-2376.
14
A perplexing pathogen in a
neonate with meningitis
Objectives
Following the completion of
this article, the reader should
be able to:
Julian
Edelschick,
MD, MBA
Julian Edelschick,
MD, MBA, is a
second year
resident at
Wright State
University Boonshoft School of
Medicine. He
received his
medical school
education at
St. Matthews
University in the
Cayman Islands.
He received his
Masters of Business from Davenport University.
1. Examine the frequency,
epidemiology and clinical presentation of central
nervous system infections
in the newborn caused by
Pasteurella multocida.
2. Understand management
of the child with P. multocida meningitis.
Introduction
Fortunately, meningitis in the
neonate is an uncommon occurrence. In this case report, we
discuss the hospital course of
an infant admitted to the newborn intensive care unit (NICU)
at Dayton Children’s with
bacterial meningitis caused by
an infrequently encountered
microorganism.
Case Description
Matthew
McRoberts,
MD
Matthew McRoberts, MD, is a
second year
resident at
Wright State
University Boonshoft School of
Medicine. He
received his
medical school
education from
the University of
Kentucky.
A 14-day-old female presented
to Dayton Children’s Emergency
Department with a one-day
history of decreased oral intake
and a high fever. Birth history
is pertinent for Mother age 19
years, G1P1. Maternal antenatal culture was positive for
group B streptococcus and was
adequately treated. No other
maternal labs were available at
time of presentation. Pregnancy
was uncomplicated, but meconium was present at rupture
of membranes. The infant was
born by spontaneous vaginal
delivery, APGAR scores were
eight and nine at one and five
minutes respectively, and she
received routine delivery
room care.
Prior to admission the mother
noted that the neonate had poor
oral intake and urine output.
During the day of admission,
fever was noted as high as
100.8° F, measured axillary.
The baby was evaluated by her
physician who referred the child
to Dayton Children’s ED.
In the ED, a normal saline bolus
was administered for concern of
dehydration. The sodium was
131 mEq/L and carbon dioxide
19.1mEq/L. The WBC was 7,000/
µL with a normal differential,
hemoglobin 16.8 gm/dL, and
platelet count 68,000/µL. The
urine had trace blood and slight
protein. The cerebrospinal fluid
(CSF) was milky upon collection. The CSF had a glucose of
<10mg/dL, and protein of 334.3
mg/dL. The spinal fluid had
3850 white blood cells/mm3
with 90 percent neutrophils.
Gram stain of the CSF revealed
gram-negative bacilli. Specimens of blood, urine and CSF
were submitted for bacterial
culture. The baby was admitted
to the Newborn Intensive Care
Unit and intravenous ampicillin, cefotaxime and acyclovir
were administered.
On the third day of hospitalization, cultures of blood and
CSF cultures grew Pasteurella
multocida. IV was continued.
CSF obtained after four days
of therapy and repeat blood
cultures remained sterile. The
patient continued to be febrile
for a number of days. Ampicillin was continued for a full
21-day course. The patient did
well. She had a normal auditory
brainstem response.
The family had a pet dog at
home, but reported that there
was no contact with the infant.
There was no known contact
with cats.
Discussion
Pasteurella multocida infections
are typically associated with
animal bites. Within the genus
Pasteurella, P. multocida is the
major pathogen and is commonly found in the oral flora
of many animals. It occurs in
approximately 70-90 percent of
cats, 25-50 percent of dogs, and
51 percent of pigs.1,2 P. multocida
is a gram negative coccobacillus
and can be initially mistaken
for other gram negative organisms such as Haemophilus and
Neisseria.1–4 P. multocida is a
nonmotile, facultative anaerobe
that grows readily on blood agar
but will not cause hemolysis.5 It
is distinguished from other bacterial species by a characteristic
fermentation pattern.6
Historically Pasteurella species
were known to cause epizootic
infections, including hemorrhagic septicemia or ‘shipping
fever’ in cattle, avian cholera
in birds, snuffles in rabbits,
and pneumonia in goats and
sheep.3,5 The bacteria was characterized by and named after
Louis Pasteur in 1880. The first
report of P. multocida infection
in humans occurred in 1913.
Most infections caused by P.
multocida are due to direct
contact, such as a bite or a
scratch from an infected animal
and result in localized infection.
There are cases of animal bites
to the scalp resulting in direct
inoculation and more invasive
infection as well. The organism
is known to be viable in water
for seven to 25 days and soil for
21 days.2 There are, however,
no documented infections
transmitted from contaminated
food or water sources.5 Of the
invasive P. multocida infections,
it is estimated that 44 percent
are from nontraumatic animal
exposure.1
Other forms of transmission
from animals have been proposed based on reports of P.
multocida infections. These
include respiratory droplets,
exposure to oral secretions of
infected animals, horizontal
vector transmission, and vertical transmission.1,3 There are
documented cases of infection
from intimate contact with
dogs and cats, including licking
around the facial area and from
a vector with a pet licking a
family member’s hands before
handling the infant. It is postulated that the infant, when exposed, will develop pharyngeal
colonization followed by invasion and hematogenous spread
to the meninges. The vertical
route is believed to account for
the other 44 percent of invasive
infections. It occurs mostly from
colonized mothers to neonates
during birth and is an important
risk factor for mortality. Again,
in cases of vertical transmission, the mother often has no
traumatic exposure to animals.1
Cellulitis is the most common
clinical manifestation after a
scratch or bite from an animal
and can be accompanied by
lymphadenopathy, chills and
fever. Local complications can
include septic arthritis, osteomyelitis and tenosynovitis.2
Invasive illness from P. multocida is rare but occurs more
frequently in neonates, with a
reported incidence of 64 percent
compared to 17 percent in studies of adults.1,6 This discrepancy
is attributed to a diminished
host response to infection
in infancy.3 Invasive disease
includes meningitis, endocarditis, appendicitis, hepatic
abscess, urinary tract infection
and ocular infections (such as
conjunctivitis, corneal ulcer,
endophthalmitis).2
Upon review of previous reports, article citations and
cases identified in a PubMed
search, we identified 41 cases
of P. multocida meningitis (not
including our case) between
the years 1950 and the present.
An additional seven cases had
P. multocida pneumonia and
bacteremia.
In a review1, only 25 cases of
invasive infection with P. multocida infection from the years
1950 to 2008 were selected for
a retrospective analysis due to
availability of complete case
documentation. Sixteen of the
25 were true documented cases
of meningitis, while the rest
included mostly bacteremia
and pneumonia. Most cases of
newborn Pasteurella bacteremia
resulted in death within the first
few days of life. The reviewers
proposed that early onset infections resulting in rapid death
did not permit adequate time to
assess the CSF and that a proportion of these infants might
have had meningitis.
The clinical presentation of P.
multocida meningitis in neonates is similar to other causes
of neonatal sepsis, with fever
(80 percent) and irritability/
lethargy (72 percent) as the
main presenting symptoms in
one study.1 Symptoms may also
include apnea, seizures, stiff
neck, full fontanelle and feeding difficulty.
Neonatal infection and meningitis with P. multocida can occur
as either early- or late-onset
disease, similar to other neonatal bacterial infections. Earlyonset is defined as infection
within the first 72 hours of birth
and is associated with a higher
15
16
mortality. Late-onset infection
is postulated to result from a
smaller bacterial inoculum with
longer time to infection, allowing for dissemination to multiple organs including the CNS.
All case mortality of invasive P.
multocida infection is estimated
to be 20 percent.1 Early-onset
disease and birth weight less
than 2500 grams were associated with increased risk of
mortality. Meningitis can result
in development of seizures,
brain abscess, hemiparesis,
hydrocephalus and cervical
osteomyelitis.7
Fortunately empiric antibiotic
coverage for suspected neonatal
pathogens is generally adequate
for treating Pasteurella. Isolates
from humans are nearly always
susceptible to beta-lactam antibiotics.6
Penicillin is the treatment
of choice. Other antibiotics,
however, including ampicillin,
cefuroxime, cefipime, cefpodoxime, doxycycline, and the
fluoroquinolones, are effective
for nonmeningitic infections.
For beta-lactam antibiotic-allergic patients, azithromycin or
trimethoprim-sulfamethoxazole
are acceptable. The recommended duration of treatment
is 7-10 days for local infection,
10-14 for severe disease, 21
for meningitis, and 4-6 weeks
for osteoarticular infections.2
Consultation with an infectious
diseases specialist is recommended for serious disease.
The infrequent occurrence of
invasive Pastuerella infections
combined with the popularity of
household pets suggests zoonotic transmission of the infection is fairly low. Despite this,
serious infections caused by
the organism among newborns
can occur. Nearly all cases of P.
multocida meningitis should
be prevented with appropriate
anticipatory guidance, including separation of young infants
and household pets, avoidance
of contact with saliva of dogs or
cats, and assiduous hand hygiene by all family members.3,6
References
1. Nakwan N, Atta T, Chokephaibulkit K. Neonatal pasteurellosis: a review of
reported cases. Arch Dis
Child Fetal Neonatal Ed. 2009
Sep;94(5):F373–6.
2. Pickering LK, ed. Pasteurella
Infections. In: Red Book. Vol
Red Book. American Academy of Pediatrics; 2012:542–
543.
3. Boocock GR, Bowley JA.
Meningitis in infancy caused
by Pasteurella multocida. J
Infect. 1995 Sep;31(2):161–2.
4. Per H, Kumandaş S, Gümüş
H, Oztürk MK, Coşkun A.
Meningitis and subgaleal,
subdural, epidural empyema
due to Pasteurella multocida. J Emerg Med. 2010
Jul;39(1):35–8.
5. Weber DJ, Wolfson JS, Swartz
MN, Hooper DC. Pasteurella
multocida infections. Report
of 34 cases and review of the
literature. Medicine. 1984
May;63(3):133–54.
6. Miller JJ, Gray BM. Pasteurella multocida meningitis
presenting as fever without
a source in a young infant.
Pediatr Infect Dis J. 1995
Apr;14(4):331–2.
7. Kobayaa H, Souki RR, Trust
S, Domachowske JB. Pasteurella multocida meningitis in
newborns after incidental animal exposure. Pediatr Infect
Dis J. 2009 Oct;28(10):928–9.
CME Questions
12. Pasteurella infections
are typically associated
with animal bites. Within
the genus Pasteurella, P.
multocida is the major
pathogen and is commonly
found in the oral flora of
many animals. It occurs
in approximately what
population?
a.70 to 90 percent of cats
b.10 to 15 percent of dogs
c. 35 percent of pigs
d.25 percent of lizards
13. Fortunately, empiric antibiotic coverage for suspected neonatal pathogens
is generally adequate for
treating Pasteurella. What
is the treatment of choice
for Pasteurella meningitis?
a.Cefepime
b.Doxycycline
c. Penicillin
d.Vancomycin
14. Nearly all cases of P.
multocida meningitis
should be prevented with
appropriate anticipatory
guidance including all of
the following except:
a.Separation of young infants from pets
b.Avoidance of saliva from dogs or cats
c. Assiduous hand hygiene by all family members
d.Frequent dog and cat washing to keep clean
program evaluation
17
1. The material presented in this publication met the mission to enhance
health care delivery in our region through education based on the essentials
and policies of the Accreditation Council for Continuing Medical Education?
c Strongly agree c Agree c Neutral c Disagree c Strongly disagree
2. Did the material presented in this publication meet the educational objectives stated?
c Yes
c No
3. Did the material presented in this publication have a commercial bias?
4.
c Yes
c No
Pediatric Forum
Volume 25
Number 1
Please rate the contents of this issue using the following scale:
1 = Poor, 2 = Fair, 3 = Good, 4 = Very good, 5 = Excellent
(Circle one response for each.) Poor
Excellent
Timely, up-to-date?
1
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Practical?
1
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4
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Relevant to your practice?
1
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4
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5. Please describe any changes you plan to make in your clinical practice based on the information presented in
this program.
______________________________________________________________________________________________
6. Are there any other topics you would like to have addressed in this publication or future educational
programs for health care providers?
c Yes c No If yes, please describe:___________________________________________________________
______________________________________________________________________________________________
7. Please describe how you will incorporate information obtained from this publication into your practice.
______________________________________________________________________________________________
8. Letter to the editor (may be published in next issue)_________________________________________________
______________________________________________________________________________________________
program Test
To obtain CME credit you must:
4 Read and reflect on each article.
4 Answer the questions from each
article and complete this test.
70% correct answers are needed to obtain the full 4 .0 AMA PRA Category 1 CreditsTM.
4 Complete the program
evaluation.
4 Return your completed test and
program evaluation by mail or
fax to: Sue Strader, coordinator
Department of Continuing Medical Education
Dayton Children’s
One Children’s Plaza
Dayton, OH 45404-1815
Fax: 937-641-5931
This sheet must be received by
December 31, 2014, for the
credit to be awarded.
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(Please circle the BEST answer.)
Please type or print clearly
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5.
Street address
True False
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8.
True False
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11.
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Physician
accreditation statement and
credit designation
Wright State
University
(WSU)
Boonshoft
School of
Medicine is accredited by the
Accreditation
Council for
Continuing
Medical Education to provide
continuing
medical education for physicians. WSU
Boonshoft
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with the extent
of their participation in
the activity.
18
news and updates from dayton children’s
Dayton Children’s welcomes new physicians
Arun
Aggarwal,
MD
Todd
Boyd,
DO
Mahesh
Chikkanaiah,
MD
David
Gooden,
DO
Haidar
Kabbani,
MD
Anesthesiology
Newborn Medicine
David Gooden, DO, most
recently completed a fellowship
at Vanderbilt Children’s Hospital in Nashville, Tennessee.
He also completed his residency
training at Dayton Children’s
and at Grandview and Southview Medical Centers in Dayton.
He received his doctorate
of osteopathy at Kirksville
College of Osteopathic Medicine
in Kirksville, Missouri.
Olutoye Osunbunmi, MD,
completed a fellowship in neonatal perinatal medicine at the
University of Texas Southwestern Medical Center in Dallas. He
joins the department of neonatology at Dayton Children’s
after completing a fellowship at
University of Texas’ Southwestern Medical Center. Dr. Osunbunmi received his medical
degree from University of Ilorin
in Ilorin, Nigeria, and completed a pediatric residency at the
Bronx-Lebanon Hospital Center
in Bronx, New York. He is board
certified in pediatrics.
Brandon Roberts, MD,
completed a pediatric anesthesiology fellowship at the
Washington University
Department of Anesthesiology
in St. Louis. He received his
medical degree from Case
Western Reserve University
School of Medicine in
Cleveland.
Gastroenterology
Arun Aggarwal, MD, completed a fellowship in pediatric
gastroenterology at Westchester
Medical Center in New York.
He received his medical degree
from Delhi University’s Maulana
Azad Medical College in India
and completed a residency in
pediatrics at Metropolitan
Hospital in New York. He is
a diplomate of the American
Board of Pediatrics.
Neurology
Mahesh Chikkanaiah, MD,
completed a fellowship in
child neurology at Nationwide
Children’s Hospital. He joins the
department of neurology at Dayton Children’s after completing
a fellowship in child neurology
at Nationwide Children’s Hospital. He received his medical degree from M.S. Ramaiah Medical
College in Bangalore, India, and
completed a pediatric residency
at Flushing Hospital Medical
Center in New York. He has
special interests in headaches
and epilepsy.
Haidar Kabbani, MD, practiced as a consultant pediatric
neurologist and epileptologist
at King Faisal Specialist Hospital and Research Center in
Jeddah, Saudi Arabia. He has
completed a fellowship in
pediatric epilepsy at the Cleveland Clinic. In addition, he
completed a fellowship in child
neurology at Massachusetts
Olutoye
Osunbunmi,
MD
Brandon
Roberts,
MD
Andrew
Smith,
MD
General Hospital and a fellowship in clinical neurophysiology at the University of Kansas
Medical Center. He received his
medical degree from Damascus
University Medical School in
Damascus, Syria. He is certified by the American Board of
Psychiatry and Neurology, with
special qualification in child
neurology and has special
interest in epilepsy.
Pathology
Todd Boyd, DO, practiced as
an assistant professor in the
department of pathology at
Cincinnati Children’s Hospital
Medical Center. He completed
his fellowship training in pediatric pathology at Cincinnati
Children’s. He also completed
his residency in pathology at
the University of Cincinnati and
an internship at Wright State
University. He is board certified in anatomic and pediatric
pathology.
Psychiatry
Andrew Smith, MD, joins Dayton Children’s with the launch
of the new pediatric psychiatry
program as a Wright State Physician and assistant professor at
Wright State University Boonshoft School of Medicine in the
department of psychiatry. He
completed a fellowship in child
and adolescent psychiatry and a
general psychiatry residency at
Wright State University Boonshoft School of Medicine. He
received his medical degree
from the University of Oklahoma. Dr. Smith has special interests in teaching and technology
and medicine.
19
New software reduces radiation exposure
Dayton Children’s Hospital has
implemented new technologies
that significantly reduce radiation exposure in infants and
children during CT and fluoroscopy procedures. These new
technologies are the next steps
in Dayton Children’s long-term
commitment to providing imaging tests that are safer for kids.
The lower radiation dose for CT
scans is made possible by newly
available imaging software that
can mathematically calculate
the image information in CT
using less radiation exposure.
The software, called AIDR 3D by
Toshiba can reduce radiation
exposure by as much as 80 percent. The radiation dose reduc-
tion is greatest when imaging
the neck, chest and abdomen.
3T MRI scanner brings new
functionality to Dayton
Dayton Children’s has implemented a new 3T MRI scanner
that brings functionality and
clearer images to the Dayton
region. This new scanner is the
region’s first 3T MRI scanner
to be implemented. An MRI
is a safe and painless test that
uses a magnetic field and radio
waves to produce detailed
pictures of the body’s organs
and structures.
The “T” in 3T MRI stands for
“Tesla” which refers to the
strength of the magnet used to
Dayton Children’s names vice president
and chief ambulatory officer
Benjamin R. Goodstein has
joined Dayton Children’s as
vice president and chief
ambulatory officer. Goodstein
replaces Gregory Ramey, PhD,
who has been named executive
director of Dayton Children’s
Center for Pediatric Mental
Health Resources.
Goodstein most recently served
as the director of the cardiovascular service line, operations
and business development for
Aurora BayCare Medical Center,
a 167-bed hospital serving the
Green Bay area. As the director, he was responsible for the
cardiac service line for three
hospitals, 45 clinics and two
surgery centers. Prior to joining
Aurora Health Care, Goodstein
served as director of service for
GE Healthcare in Pittsburgh.
He holds a bachelor’s degree
in radiologic technology with
a minor in business management from Marian University in
Fond Du Lac, Wisconsin, and a
master’s in business administration with a finance concentration from Lakeland College in
Sheboygan, Wisconsin.
produce
the diagnostic images. The
hospital
is currently
using a
1.5T MRI
scanner
and by
implementing
the 3T MRI,
the radiologists will
be able to produce images with
twice the quality and clarity
of the 1.5T. This can help find
subtle abnormalities that a 1.5T
scanner is unable to detect.
Dayton Children’s to
invest in new patient
tower
Dayton Children’s board of
trustees recently approved a
long-range facility and campus renewal plan that calls for
transforming the hospital’s
Valley Street campus to improve
the delivery of care to children
in this region for generations
to come.
“Our strategic roadmap, Destination 2020, calls for us to
advance our role as a leader in
children’s health. A thorough
assessment of how we will
achieve this vision has revealed
that new spaces are needed to
provide critical services well
into the future,” says CEO and
President Deborah A. Feldman.
The plan calls for the construction of a 260,000 square-foot,
eight-story patient tower in the
center of the hospital’s current
Valley Street campus. Construction is expected to begin in
spring of 2014 and be completed
sometime in 2017.
Nonprofit Organization
U.S. Postage Paid
Permit Number 323
Dayton, Ohio
20
Dayton Children’s Hospital
One Children’s Plaza
Dayton, Ohio 45404-1815
More pediatric expertise coming
to Springfield through a new
pediatric care alliance
Officials at Dayton Children’s Hospital and Nationwide
Children’s Hospital are pleased to announce a formal
collaboration focused on improving access to highlyspecialized pediatric services for all Springfield area
families.
The Ohio Pediatric Care Alliance is designed to reduce
duplication of services and improve efficiencies and
allow for the two independent children’s hospitals to
work together in the Springfield area to improve access
to subspecialty pediatric care, execute shared initiatives
and evaluate needs for new services.
Dayton Children’s Hospital launches sports medicine service for young athletes
Dayton Children’s Hospital recently announced the
launch of a new service line—sports medicine with a
focus on treatment of sports injuries in young athletes.
The Dayton Children’s sports medicine
team is specially trained in pediatrics
and understands how an injury may
impact growth, or how growth might
impact rehabilitation.
The sports medicine experts offer a multidisciplinary approach
to handling sports injuries in children and teens. Some
conditions the sports medicine clinic will treat are:
4Back pain
4 Muscle strains
4Baseline concussion testing
4 Sports concussions
4Contusions
4 Stress fractures
4Dislocations
childrensdayton.org