Brown Pediatrics

Brown's Pediatric Residency Blog

Month: August 2016

Commercial Sexual Exploitation of Children (CSEC)

Post Created by: Anish Raj, MD

Case: A 15-year-old female, with a history of PTSD, presents to the ED for medical clearance after being AWOL (absent from care) from her group home for the past 3 weeks. What are critical components you should consider prior to making any disposition plans for this patient?

I.) Background (Smith, 2014)

  • Commercial Sexual Exploitation of Children (CSEC): the sexual abuse of a minor (< 18 years old) with remuneration in money, goods, or services—or the promise of money, goods, or services—to the child or a third-party for the sexual use of that child.
  • Note: CSEC is an umbrella term that encompasses child sex trafficking, escorting, survival sex, child pornography, stripping, etc.
  • Domestic Minor Sex Trafficking (DMST): the inducement of a commercial sex act of anyone under the age of eighteen by a controlling party (i.e. trafficker/exploiter/pimp) that takes place within U.S. borders and involves a child who is a U.S. citizen.
  • Note: Per the Trafficking Victims Protection Act (TVPA), in cases of child sex trafficking, the inducement of a commercial sex act of a minor (< 18 years old) is enough to meet criteria for trafficking. Force, fraud, or coercion do NOT have to be demonstrated.

 

II.) Epidemiology (IOM, 2013)

  • No consensus on estimates of incidence and prevalence
  • Most widely cited national estimate: 244,000-325,000 children are at risk for CSEC
  • Average age of initial involvement: 15 years old (Gibbs et al., 2015)
  • Rhode Island preliminary data: ~70 suspected cases over the past 3 years

 

III.) Risk Factors

  • *History of sexual abuse*: up to 70-90% of CSEC victims (Bagley & Young, 1987)
  • History of running away and/or truancy: 70% of street youth estimated to be involved in CSEC at some point (Estes & Weiner, 2001)
  • Child welfare (e.g. DCYF) involvement: 50-80% of CSEC victims (Walker, 2013)
  • Juvenile justice system (e.g. RITS) involvement
  • Adult (> 18 years old) “boyfriend”/“girlfriend”
  • Multiple sexual partners at present
  • Positive STI testing
  • Substance use

 

IV.) Physical Exam

tattoo

  • Observation: are clothing and accessories congruent with age/time/season?
  • Tattoos: name branding? explicit? gang insignia?
  • Note: In Rhode Island, individuals must be > 18 years old to receive a tattoo or piercing in a licensed parlor.
  • Signs of physical abuse (including but not limited to head trauma, oral trauma, genital trauma, and cutaneous injuries)

 

V.) Screening Examples (no brief, validated screening tool currently exists)

  • Have you or any of your friends ever exchanged sex for money, a place to stay, food, or drugs?
  • Has anyone ever asked you to have sex with someone else or made you have sex when you didn’t want to?
  • Has anyone ever taken sexual pictures of you or posted such pictures on the internet? (Greenbaum et al., 2015)

 

VI.) What To Do If You Suspect CSEC

  • Understand that it is very common for patients to NOT disclose
  • Notify Aubin Center (i.e. page on-call physician) of suspected CSEC
  • Determine need for forensic evidence collection if acute assault has taken place
  • Consult Psychiatry for evaluation
  • Confirm with law enforcement that missing persons report was filed if patient had been missing
    • If no report was filed, communicate this information to DCYF due to concern for possible neglect by caregiver
  • File report expressing concern for suspected CSEC to DCYF Hotline
  • Complete PRE without hold and fax to DCYF
  • Order screening labs: urine pregnancy, urine gonorrhea, urine chlamydia, urine trichomonas, urine toxicology screen, RPR, hepatitis C, hepatitis B, and HIV
  • Consider administration of empiric STI antibiotic treatment (e.g. ceftriaxone, azithromycin, and metronidazole)
  • Consider administration of Plan B
  • Consider administration of HIV post-exposure prophylaxis (PEP) on a case-by-case basis in coordination with Aubin Center +/- Infectious Disease team
  • Determine safe disposition plan
    • Ensure patient has an outpatient appointment at Aubin Center if being discharged
  • Consult social work and Aubin Center if patient is admitted

 

Faculty Reviewer: Christine Barron, MD

 

References:

  • Smith, Holly Austin. Walking Prey: How America’s Youth Are Vulnerable to Sex Slavery. New York: St. Martin’s, 2014. Print.
  • Institute of Medicine and National Research Council. Confronting commercial sexual exploitation and sex trafficking of minors in the United States. Washington, DC: The National Academies Press; 2013. Print.
  • Gibbs, D., Walters, J., Lutnick, A., Miller, S., & Kluckman, M. (2015). Evaluation of Services for Domestic Minor Victims of Human Tracking. Manuscript submitted for publication. Retrieved August 12, 2016, from https://www.ncjrs.gov/pdffiles1/nij/grants/248578.pdf.
  • Bagley, C., & Young, L. (1987). Juvenile Prostitution and Child Sexual Abuse: A Controlled Study. Canadian Journal of Community Mental Health, 6(1), 5-26. doi:10.7870/cjcmh-1987-0001.
  • Estes, R., & Weiner, N. (2001). The Commercial Sexual Exploitation of Children in the U.S., Canada and Mexico. Retrieved August 12, 2016 from http://www.gems-girls.org/Estes%20Wiener%202001.pdf.
  • Walker, K. (2013). Ending the Commercial Sexual Exploitation of Children: A Call for Multi-System Collaboration in California (USA, California Child Welfare Council). Retrieved August 12, 2016, from http://www.chhs.ca.gov/Child Welfare/Ending CSEC-ACallforMulti-SystemCollaborationinCA-February2013.pdf.
  • Greenbaum, J., & Crawford-Jakubiak, J. E. (2015). Child Sex Trafficking and Commercial Sexual Exploitation: Health Care Needs of Victims. Pediatrics, 135(3), 566-574. doi:10.1542/peds.2014-4138.

Image of the Week: 8/9/2016

Case:

A 16 year-old male presents to the ED after a syncopal episode. He currently feels well and wants to go home. Below is his EKG, what do you think?

 

Brugada-type-1

 

Discussion:

The above presentation (syncopal event) paired with this EKG is concerning for the Brugada syndrome.

Epidemiology:

  • The Brugada syndrome was first described in 1992 by Drs. Pedro and Josep Brugada in a case report of 8 patient with aborted sudden cardiac death (SCD), though cases of sudden unexplained nocturnal death (SUND) had been described previously in various southeast Asian populations (Juang JM et al, 2004).
  • Some estimate that 4-12% of SCD can be attributed to the syndrome, with a higher prevalence in SE Asian populations (Gourraud JB et al, 2016)
  • Median age of presentation is 41, though has be reported in neonates through the elderly.
  • While many mutations have been described, the Brugada syndrome appears to result from mutations in the Na+ channel, affecting the SCN5A gene (Behere SP et al, 2015)
    • Note: Only 20% of patients with Brugada syndrome have a documented mutation in the SCN5A gene. Studies show a autosomal dominant transmission with incomplete penetrance  (Juang JM et al, 2004).

Clinical Presentation:

  • In the original description of the syndrome, the Brugada brothers noted that all patients presented with syncope, with 5/7 progressing immediately to cardiac arrest and the other 2 progressing to cardiac arrest over the next 2 weeks
    • Registry data indicates that almost 1/3 present with syncope, 6% with SCD, though >60% were asymptomatic at the time of diagnosis (Probst V et al, 2010)
      • NOTE: Registry listed above excluded children, so interpret with caution
  • Sustained Polymorphic Ventricular Tachycardia is the most common rhythm noted to precipitate SCD

EKG Findings and Diagnosis

  • ST elevation in V1-3 with right bundle block morphology is common, with “coved pattern” in V1-3  negative T wave (referred to as “Type 1;” this is the only pathognomonic EKG pattern)
    • In most cases, no reciprocal ST-depression noted (Juang JM et al, 2004).
  • EKGs in Brugada syndrome tend to be variable and at times are even normal
  • In patients with normal EKG, class Ia or Ic antiarrhythmic drugs ( potently blocks Na channel) may unmask the Brugada pattern (Juang JM et al, 2004).
  • Two other patterns have been described, though are considered less significant
  • To be considered diagnostic of Brugada syndrome the EKG findings must be combined with the following clinical findings:
    • Polymorphic ventricular tachycardia
    • syncope
    • ventricular fibrillation
    • Family history of early sudden cardiac death (<45)
  • Workup must also exclude other causes that lead to ST-elevation (e.g. acute pericarditis, arrhythmogenic right ventricular dysplasia (ARVD), Prinzmetal angina, etc).

Treatment

  • Implantable cardioverter-defibrillator (ICD) is the only strategy to prevent SCD
  • Patients should also be advised to avoid alcohol, certain drugs, and treat fevers aggressively (Refaat MM, 2016).
Resident Reviewer: Vanessa Tommey, MD

References

  1. Brugada P, Brugada J. Right bundle branch block, persistent ST segment elevation and sudden cardiac death: a multicenter report. J Am Coll Cardiol 1992;20:1391–6
  2. Juang JM et al. “Brugada syndrome–an under-recognized electrical disease in patients with sudden cardiac death.” Cardiology. 2004;101(4):157-69
  3. Gourraud JB et al. “The Brugada Syndrome: A Rare Arrhythmia Disorder with Complex Inheritance.” Front Cardiovasc Med. 2016 Apr 25;3:9.
  4. Behere SP et al. “Inherited arrhythmias: The cardiac channelopathies.” Ann Pediatr Cardiol. 2015 Sep-Dec; 8(3): 210–220.
  5. Probst V et al. “Long-Term Prognosis of Patients Diagnosed With Brugada Syndrome.” Circulation. 2010;121(5):635-643.
  6. Alley P. “What is Brugada Syndrome?” http://lifeinthefastlane.com/what-is-brugada-syndrome/

EKG Basics

Created on 8/4/2016 by Hiral Mehta, MD

CASE:

Griffin is a 5 y/o boy who comes into the ER. Parents state that earlier today he began complaining of his “heart running fast” and his chest hurting. His cardiac exam is unremarkable. You decide to get an EKG as part of your work up.

What should I know when interpreting a pediatric EKG?

EKGs are simple, relatively straightforward to obtain, and provide a great deal of important information- if you are able to interpret them!

First: Lead placement

There are several different types of lead set ups. Intuitively, more leads generally provide more information. Remember, EKGs are vector representations of electrical depolarization. The more “viewpoints” you have, the more information you can gather.

 

5 Lead-ECG: This is what we generally have on our hospitalized kids who are on CRM (cardio-respiratory monitoring).

5-electrode-ECG

http://i1.wp.com/lifeinthefastlane.com/wp-content/uploads/2010/05/5-electrode-ECG.jpg

 

Think “smoke (black) over fire (red), snow (white) over grass (green)” and “white on right”.

12-lead EKG: This is the standard 12 lead EKG that we order. In pediatrics, we use the “V4R lead” to better assess the right ventricular potentials because the RV extends to the right of the sternum in children. This gets confusing- you should still use the leads that the machine labels “V1”-”V6” in that order (R->L anatomically), but start V1 further to the right (and relabel the EKG when it prints out).

precordial_V4R

http://www.ems12lead.com/wp-content/uploads/sites/42/2008/10/precordial_V4R.jpg

How do I interpret this EKG?

Good general guidelines: have a systematic approach. Look at as many EKGs as possible to start getting a sense of what is “normal”, especially at various ages. One standard approach is to think through EKGs as an approach of “rate, rhythm, and axis” but really, everyone tends to develop their own methodology.

It is helpful to think of the EKG as a “graph” of electrical activity on the “Y-axis” and time on the “X-axis.” (For more in depth explanation, please see videos at end of the post). 

  • The standard speed of paper is 25mm/sec, but it is always helpful to make sure EKG strips you are looking at are run at the standard speed
  • A “small box” is 0.04 seconds on the time axis and 0.1mV on the electrical axis
  • A “big box” is 0.2 seconds on the time axis and 0.5mV on the electrical axis
Basic components of Interpretation:

Rate

  1. For regular rhythms (more below on how to determine this), Rate = 300/ #of big boxes between 2 consecutive R waves
  2. For faster rhythms (infants), Rate = 1500/ #small boxes between 2 consecutive R waves
  3. For irregular rhythms, Rate = number of complexes on rhythm strip (usually lead II), multiplied by 6

Rhythm

  1. P waves: absent or present?
  2. Relationship between p- waves and QRS
    1. For sinus rhythm, there is a 1-1 relationship between p waves and QRS
  3. Regular vs Irregular (are intervals consistent across the rhythm strip)?
    1. If Irregular, is it regularly irregular (classically A-flutter) or irregularly irregular (classical atrial fibrillation)
  4. QRS morphology
    1. Narrow (sinus or junctional origin)
    2. Wide (ventricular origin)

Axis: There are multiple ways of determining the “axis.” Below highlights 1 of these methods. “Normal” axis changes with age, with infants having a “rightward” axis. As children grow older, the axis becomes more leftward.

successive-approximation

http://i2.wp.com/lifeinthefastlane.com/wp-content/uploads/2012/01/successive-approximation.jpg

Waves and Intervals:

waves-of-the-ecg

http://i0.wp.com/lifeinthefastlane.com/wp-content/uploads/2011/01/waves-of-the-ecg.gif?w=407

 

  • P wave- represents atrial depolarization
  • QRS complex- represents ventricular depolarization
  • T wave- represents ventricular repolarization

(Note: In case you were wondering, there is an atrial repolarization wave, but it is “hidden” in the QRS complex).

Note: Remember, standard speed of paper is 25mm/sec, therefore, a “small box” is 0.04 seconds on the time axis and 0.1mV on the electrical axis and a “big box” is 0.2 seconds on the time axis and 0.5mV on the electrical axis

 

PR interval: This reflects conduction from the SA node AV node.

  • Normally thought of as 0.12- 0.2 sec (one “big box”) for adults; however in children it varies with age and HR.

QRS interval: Represents ventricular depolarization. The Q wave reflects depolarization from L -> R across the interventricular septum, the R wave reflects depolarization through the thick ventricular walls, and the S wave reflects depolarization of the Purkinje fibers. Again, normal intervals vary by age.

QT interval: Represents the time it takes for ventricular depolarization and repolarization. This is one of the intervals that can’t really be obtained just by reading off what the EKG machine calculates, since QT varies with the HR and the individual RR intervals. This will be expanded upon in a future topic, but for now:

  • The calculated “corrected QT” interval (QTc) is most commonly derived with Bazett’s Formula:
    • QTc=QT√RR
    • Use the RR interval preceding the QT interval that you’re looking at. This formula is most accurate for HRs 60-100!
    • Infants normally have a longer QTc (under 6 months, QTc of <490 msec is considered normal). Children older than 6 months should have a QTc <440msec.
    • MD Calc

 

For reference, here is a table with some normal EKG values for children (adapted from Sharieff et al, 2006):

intervals

 

Videos From around the web:

Basics of EKG leads

The Limb Leads

The Precordial Leads

 

Faculty Reviewer: Sara Ford, MD

Resident Reviewer: Brian Lee, MD

References:

“ECG Basics.” http://lifeinthefastlane.com/ecg-library/basics/

“Paediatric ECG Interpretation.” http://lifeinthefastlane.com/ecg-library/paediatric-ecg-interpretation/

Sharieff GQ, Rao SO. The pediatric ECG. Emerg Med Clin North Am 2006;24:196.

 

Image of the Week: 8/3

Created on 8/3/2016 by Vanessa Hand, MD

Case:

A 17 year-old male in obvious distress is brought the ED by his sister. She states that  this morning he woke up with a fever and a sore throat. However, over the next few hours his voice has been changing and is now more “hoarse.” She notes that during this time he also developed difficulty breathing. Below is an x-ray obtained upon presentation. What are you most concerned about?

epiglottitis

Case courtesy of Dr Maxime St-Amant, Radiopaedia.org. From the case rID: 26840

 Radiology Findings: Typical findings of epiglottitis with enlarged epiglottis and aryepiglottic folds.

Diagnosis: Acute Epiglottitis

Presentation:

  • Combination of sore throat, dysphagia, “hot potato” voice and high fevers classically described
  • Difficulty with breathing may be most common chief complaint (Mayo-Smith et al, 1995)
  • Symptoms progress rapidly, usually over hours (Stroud et al, 2001)
  • Physical Exam Shows:
    • Vitals: Febrile, Tachypnea
    • Visibly Distressed Child; “Tripoding” position
    • Muffled or hoarse voice

Epidemiology (Shah at al, 2004)

  • Historically caused by H. Influenza type B, however vaccination has largely shifted etiology to other organisms
  • Rate dropped from 5/100,000 to 0.6-0.8/100,000 (immunized)
  • Increased age of presentation from 3 yo to 6-12 yo 

Causative Organisms

  • H. influenzae, penicillin resistant S. pneumoniae, S. Aureus, β-hemolytic strep

Treatment

  • Minimize stimuli, stressful procedures
  • Maintain airway, anesthesia/ENT intubate in OR
  • Antibiotics: Ceftriaxone or Ampicillin/Sulbactam; add Vancomycin or Clindamycin if concern for MRSA

Faculty Reviewer: Brian Alverson, MD

References

Mayo-Smith MF et al. “Acute Epiglottitis. An 18-year experience in Rhode Island.” Chest. 1995;108(6):1640-7

Shah RK et al. “Epiglottitis in the Hemophilus influenzae Type B Vaccine Era: Changing Trends.” The Laryngoscope. 2004;114(3): 557-60

Stroud RH et al. “An update on inflammatory disorders of the pediatric airway: epiglottitis, croup, and tracheitis.” Am J Otolaryngology.  2001;22(4):268-275

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