Secrets – Pediatric: Adolescent Medicine editing
1. What are the three leading causes of mortality in adolescents?
1. Unintentional injury is the leading cause of death with the majority of injuries caused by car crashes. The fatal crash rate per mile driven for 16- to 17-year-olds is about 3 times greater than the rate for drivers 20 and older.
2. Violence, specifically homicide, is the second leading cause of death among 15- to 24-year-olds and the leading cause for black males in this age range. In 2013, about 28% of males compared with 8% of females reported having carried a weapon (gun, knife, or club) on at least 1 day in the previous month.
3. Suicide is the third leading cause of death in adolescents aged 10 to 19 years.
Highway Loss Data Institute, 2014: www.iihs.org. Accessed Oct. 29, 2014.
Heron M: Deaths: leading causes for 2010. National vital statistics reports: from the Centers for Disease Control and Prevention, National Center for Health Statistics, Natl Vital Stat System, 62:1–97, 2013.
Kann L, Kinchen S, Shanklin SL, et al: Youth risk behavior surveillance—United States, 2013, MMWR, 63:4,2014.
2. How common is dating violence among adolescents? Dating VIOLENCE, also referred to as intimate partner violence (IPV), can be defined as being hit, slapped, or intentionally physically hurt by a boyfriend or girlfriend. Almost 10% of high school students have reported IPV and 7% report having ever been forced to have sexual intercourse.
Kann L, Kinchen S, Shanklin SL, et al: Youth risk behavior surveillance—United States, 2013, MMWR 63:4,2014.
3. Which sports cause the greatest number of concussions in teenagers?
Among individuals 15 to 24 years of age, sports are second only to motor vehicle crashes as the leading cause of concussions. In 2012, the majority of concussions resulted from participation in football, followed by girls’ soccer. The most common mechanism of injury was player-player contact. In gender-comparable sports, girls had a higher concussion rate (OR¼ 1.7) than boys.
Marar M, McIlvain NM, Fields SK, et al:. Epidemiology of concussions among United States high school athletes in 20 sports, Am J Sports Med 40:747–755, 2012.
4. Which diagnoses require mandatory disclosure regardless of confidentiality?
Most states require:
• Notification of child welfare authorities under state child-abuse (physical and sexual) reporting laws
• Notification of law enforcement officials of gunshot and stab wounds
• Warning from a psychotherapist to a reasonably identifiable victim of a patient’s threat of violence
• Notification to parents or other authorities if a patient represents a reasonable threat to himself or herself (i.e., suicidal ideation)
5. How does the “HEADS” mnemonic assist in adolescent interviewing? This mnemonic allows for a systematic approach to the evaluation of multiple health issues and risk factors that affect teenagers:
H–Home (living arrangement, family relationships, support) E–Education (school issues, study habits, achievement, expectations) A–Activities (recreation, friends, exercise, employment)
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D–Drugs (alcohol, tobacco, marijuana, cocaine, pills, etc.)
Depression
S–Sexuality (sexual activity, sexual orientation)
Self-esteem (body image)
Safety (abuse, intimate partner violence, risk of self-harm)
Suicidality
6. When does sexual orientation usually emerge?
Sexual orientation emerges before or in early adolescence. Sexual minority youth are often referred to as LGBTQ or Lesbian, Gay, Bisexual, Transgender, and Questioning youth. Sexual experimentation is common in adolescence and may not predict future sexual orientation.
7. What characterizes gender identity, gender expression, and gender dysphoria?
• Gender identity is how one identifies one’s own gender.
• Gender expression is the outward display of gender characteristics. This usually conforms to anatomic sex for both heterosexual and homosexual teenagers.
• Gender dysphoria refers to the emotional stress of having a gender identity that is different from natal or anatomic sex.
Levine DA: Office-based care for lesbian, gay, bisexual, transgender, and questioning youth, Pediatrics 132: e297–313, 2013.
8. What health disparities are particular to LGBTQ youth?
LGBTQ youth have higher rates of being bullied, stigmatization, and/or parental rejection. This may result in issues with self-esteem, depression, and suicidality. LGBTQ youth have also been found to have higher rates of drug and alcohol use, STIs (particularly human immunodeficiency virus [HIV]), and homelessness. Protective factors include family connectedness, caring adults, and school safety.
9. How may social media impact adolescent behavior?
Social media (e.g., Facebook, Instagram, Snapchat, YouTube) can strongly influence adolescents’ attitudes and behavior. It has become an integral part of many adolescents’ lives. Many teens use the Internet daily to communicate with friends and maintain and form new social relationships. Teens often post on social media venues pictures of risky behaviors that reflect their actual behavior. They may display postings of risky sexual behaviors, substance use, or violence. Their peers may perceive these public displays as acceptable, and this false perception may entice others to engage in such high-risk behaviors as well.
Moreno MA, Parks MR, Zimmerman FJ, et al: Display of health risk behaviors on MySpace by adolescents: prevalence and associations, Arch Pediatr Adolesc Med 163:27–34, 2009.
10. What is cyberbullying?
Cyberbullying is using the Internet, cell phones, or social media venues to communicate false, embarrassing, or hostile information about someone else. This can range from insults to peer exclusion to sexual harassment. Cyber victims can develop emotional, behavioral, and school-related problems.
Suzuki K, Asaga R, Sourander A, et al: Cyberbullying and adolescent mental health. Int J Adolesc Med Health
24:27–35, 2012.
11. Which teenagers <18 years can give consent for their medical care?
Those who are <18 years old must be considered “emancipated” or “mature” minors in order to give consent. However, the definition varies from state to state. Emancipated minors include those who are
married, are parents themselves, are members of the armed forces, are living apart from their parents, and/or those who have evidence of independence (financial or otherwise).
Berlan ED, Bravender T: Confidentiality, consent and caring for the adolescent patient, Curr Opin Pediatr 21:450–456, 2009. Bruce CR, Berg SL, McGuire AL: Please don’t call my mom: pediatric consent and confidentiality, Clin Pediatr 48:243–246, 2009.
EATING DISORDERS
12. How is the diagnosis of anorexia nervosa made?
Anorexia NERVOSA consists of a spectrum of psychological, behavioral, and medical abnormalities. The 2013 Diagnostic and Statistical Manual of Mental Disorders, 5th Edition (DSM-5) lists three components needed for the diagnosis:
1. Restriction of energy intake RELATIVE to requirements, leading to a significantly low body weight—a weight that is less than minimally expected. (This replaces the older criterion of refusal to maintain a weight that is >85% of expected weight for height.)
2. Intense fear of gaining weight or of becoming fat or persistent BEHAVIOR that interferes with
weight gain, even though the affected individual is at a significantly low weight. Often, adolescents insist that they are trying to gain weight but are unable to do so.
3. Disturbances of perception of body shape and size, undue influence of body weight or shape on self- evaluation, or persistent lack of recognition of the seriousness of the current low body weight.
The presence of amenorrhea is no longer necessary for the diagnosis of anorexia nervosa in postmenarchal girls.
American Psychiatric Association: Diagnostic and Statistical Manual of Mental Disorders, ed 5. Washington, DC, 2013, American Psychiatric Association.
13. What are signs of anorexia nervosa on physical examination?
• Sinus bradycardia (or other dysrhythmias)
• Hypothermia
• Orthostatic changes in blood pressure and heart rate
• Dull, thinning hair
• Dry skin, lanugo (downy hair on body)
• Cachexia (especially facial wasting)
• Acrocyanosis (cold, bluish hands and feet)
• Extremity edema
• Heart murmur (mitral valve prolapse)
• Growth retardation
• Pubertal delay or arrest
14. What are the differential diagnoses that one must consider when evaluating a patient with anorexia nervosa?
One should consider gastrointestinal disorders (inflammatory bowel, celiac, or peptic ulcer disease), occult malignancies, endocrine disorders (hyperthyroidism, diabetes), and infection (tuberculosis, HIV). Depression, anxiety, obsessive–compulsive disorder, and substance abuse can also present with weight loss. Superior mesenteric artery (SMA) syndrome is a consequence of severe weight loss but can present like anorexia.
15. What are good and bad prognosticators for recovery from anorexia?
Good: Early age at onset (<14 years), supportive family, shorter duration of illness
Bad: Late age at onset, purging behavior, more significant weight loss, family dysfunction, comorbid
mental illness, longer duration of illness
16. Why are adolescent girls with anorexia nervosa at risk for low bone mineral density? Decreased FSH and LH levels result in anovulation and subsequent low levels of serum estrogen. Because estrogen is necessary to incorporate calcium into bone, osteopenia may be a consequence.
17. What are the clinical differences between males and females with anorexia nervosa?
It is estimated that less than 5% of anorexia nervosa involves boys. Males are more likely to:
• Have been obese before the onset of symptoms
• Be ambivalent regarding the desire to gain or lose weight
• Have more issues about gender and sexual identity
• Involve dieting with sports participation
• Engage in “defensive dieting” (avoiding weight gain after an athletic injury)
Domine F, Berchtold A, Akre C, et al: Disordered eating behaviors: what about boys? J Adolesc Health
44:111–117, 2009.
18. What electrolyte disturbances occur in patients with severe anorexia nervosa and what are the potential clinical effects?
Hypocalcemia: Muscle spasm and tetany, stridor, seizures
Hyponatremia: Seizures, coma, death
Hypokalemia: Dysrhythmias, poor gut motility, skeletal muscle myopathy, nephropathy Hypomagnesemia: Muscle cramps, weakness, irritability, psychosis, seizures, dysrhythmias Hypophosphatemia: Muscle weakness, paresthesia, central nervous system (CNS) disturbances
(e.g., irritability, delirium, seizures)
Norrington A, Stanley R, Tremlett M, Birrell G: Medical management of acute severe anorexia nervosa, Arch Dis Child Educ Pract Ed 97:48–54, 2012.
19. What causes sudden death in patients with anorexia nervosa?
The main cause of sudden death is related to cardiac complications. Chronic malnutrition, prolonged hypokalemia, low serum albumin, and prolonged QT intervals on electrocardiogram are related to sudden cardiovascular death in eating disorder patients. Cardiovascular complications include bradycardia, orthostatic hypotension, dysrhythmias (often related to prolonged QT interval), and decreased left ventricular mass and myocardial contractility.
Jauergui-Garrido B, Jauregui-Lobera I: Sudden death in eating disorders, Vasc Health Risk Manag
8: 91–98, 2012.
20. What are indications for hospital admission for a patient with anorexia nervosa?
• Refusal to eat with ongoing weight loss despite intensive management
• Dehydration and orthostatic changes in pulse (>20 beats per minute) or blood pressure (>10 mm Hg)
• Electrolyte abnormalities (e.g., hypokalemia, hyponatremia, hypophosphatemia)
• Heart rate less than 50 beats per minute during the day, less than 45 beats per minute overnight
• Systolic blood pressure < 80 mm Hg
• Temperature < 96° F
• Cardiac dysrhythmia
• Acute medical complication of malnutrition (syncope, seizure, congestive heart failure, pancreatitis)
• Severe coexisting psychiatric disease (e.g., suicidality, psychosis)
Rosen DS: American Academy of Pediatrics Committee on Adolescence: Identification and management of eating disorders in children and adolescents, Pediatrics 126:1240–1253, 2010.
21. What are the medical complications of bulimia nervosa?
Electrolyte abnormalities: Hypokalemia, hypochloremia, and metabolic alkalosis may occur.
The hypokalemia can cause a prolonged QT interval and T-wave abnormalities.
Esophageal: Acid reflux with esophagitis and (rarely) Mallory-Weiss tear may be found.
Central nervous system: Neurotransmitters can be affected, thereby causing changes in the patient’s perceptions of satiety.
Miscellaneous: Enamel erosion, salivary gland enlargement, cheilosis, and knuckle calluses are signs of recurrent vomiting.
Mehler PS: Bulimia nervosa, N Engl J Med 349:875–881, 2003.
22. An 11-year-old with weight loss due to avoidance of food because of its sensory characteristics has what condition?
AVOIDANT/RESTRICTIVE Food Intake Disorder (ARFID). This is a new DSM-5 diagnostic category of eating disorder not explained by a concurrent medical condition or a mental disorder. The condition is distinct from anorexia nervosa or bulimia nervosa. Children and younger teens in this category may avoid foods because of problems with digestion, they may have an aversion to colors or textures, or they may eat in very small portions because of previous frightening episodes of choking or vomiting. The food restriction leads to weight loss, nutritional deficiencies, or interference with psychosocial functioning.
23. What is the primary biochemical feature of the refeeding syndrome? Hypophosphatemia. The refeeding syndrome is a potentially fatal process that results from fluid shifts and electrolyte abnormalities, which occurs when someone who has been chronically malnourished is refed, either orally or parenterally. In starvation, total body phosphorus is depleted although the serum phosphorus level usually remains normal because of adjustments in renal excretion. When carbohydrates are added through feeding, insulin is secreted, which stimulates anabolic protein synthesis and enhances the intracellular uptake of glucose, phosphate, and water. This can lead to significant extracellular hypophosphatemia. Because phosphate is needed for metabolic processes, potentially fatal cardiac, respiratory, and neurologic complications can ensue.
Mehanna HM, Moledina J, Travis J: Refeeding syndrome: what it is, and how to prevent and treat it, BMJ
336:1495–1498, 2008.
24. Name the three features that constitute the “female athlete triad.”
Low energy availability (with or without disordered eating), menstrual dysfunction, and low bone mineral density. This triad can present in active girls and young women, particularly in those who engage in sports that emphasize leanness such as gymnastics, ballet, or diving. Diagnosis is based on history, physical examination, and laboratory evaluation. The basic laboratory workup should include a urine pregnancy test, thyroid-stimulating hormone, prolactin, FSH, LH, and estradiol. Evaluation for bone mineral density and vitamin D levels may be helpful. Ongoing counseling regarding eating behaviors and need for adequate weight gain is important. The use of oral contraceptives may give patients a false sense of security by inducing menses, but it has not been shown to increase bone mineral density.
DeSouza MJ, Nattiv A, Joy E: 2014 Female athlete triad coalition consensus statement on treatment and return to play of the female athlete triad, Br J Sports Med 48:289, 2014.
KEY POINTS: EATING DISORDERS
1. Eating disorders can affect both females and males and young people of all ethnicities and from all socioeconomic backgrounds.
2. Eating disorders put young people at risk for serious electrolyte disturbances, as well as for other physiological, metabolic, and hormonal disturbances.
3. Anorexia nervosa has the highest mortality of any psychiatric disorder.
4. When treating a patient with anorexia nervosa on an inpatient unit, be on the lookout for fluid overload, and monitor electrolytes in order to avoid refeeding syndrome.
5. Treatment for a patient with an eating disorder is best done using a collaborative approach and involving a mental health professional and a nutritionist.
MENSTRUAL DISORDERS
25. What is the median age of menarche in the United States?
12.4 years. Non-Hispanic black females experience menarche slightly earlier than non-Hispanic white and Mexican-American females. Menstruation typically begins 2 to 2.5 years after breast development begins and occurs at sexual maturity rating (SMR) 3 to 4.
Gray SH: Menstrual disorders, Pediatr REV 34:6–17, 2013.
26. How do you define a normal menstrual cycle?
• INTERVAL: count from the first day of one period to the first day of the next period; range is from 21 to 45 days in adolescents
• Duration: 3 to 7 days; more than 8 days is considered prolonged
• Quantity: average is about 30 mL per cycle; >80 mL of blood loss is considered excessive (but can be hard to quantify). Changing a blood-soaked pad or tampon every 1 to 2 hours, bleeding through clothing, and using secondary protection are all signs of excessive bleeding.
ACOG Committee on Adolescent Health Care: ACOG Committee Opinion No. 349, November 2006: Menstruation in girls and adolescents: using the menstrual cycle as a vital sign, Obstet Gynecol 108:1323–1328, 2006.
27. What is the physiology of a normal menstrual cycle?
Three phases: follicular (proliferative), ovulation, and luteal (secretory phase) See Figure 1-1.
28. What is the difference between primary and secondary amenorrhea?
Primary amenorrhea is the failure to achieve menarche by 15 years or no menses by 3 years after the development of secondary sex characteristics.
Secondary amenorrhea is ≤3 months of amenorrhea after achievement of menarche.
29. What is the value of a progesterone challenge test in a patient with amenorrhea? If bleeding ensues within 2 weeks after the administration of oral medroxyprogesterone (5 to 10 mg daily for 5 to 10 days), the test is positive. This indicates that the endometrium has been primed by estrogen and that the outflow tract is functioning. No response indicates hypothalamic-pituitary dysfunction, anatomic obstruction, or ovarian failure.
30. What are some of the causes of amenorrhea in adolescents?
Causes of amenorrhea in adolescents include pregnancy, contraceptive use, stress, chronic illness, iatrogenic (i.e., medications, chemotherapy), disordered eating (e.g., anorexia nervosa), female athlete triad, anatomic anomalies (e.g., imperforate hymen, vaginal septum, uterine or vaginal agenesis), and endocrinologic causes. Endocrine disorders that can result in amenorrhea include hypothalamic/pituitary dysfunction, ovarian pathology, thyroid abnormalities, adrenal abnormalities, androgen insensitivity syndrome, and polycystic ovarian syndrome (PCOS).
Talib HJ, Coupey SM: Excessive uterine bleeding, Adolesc Med State Art REV 23:53–72, 2012.
31. How do you define the different types of “rrhagias”?
• Menorrhagia: large quantity of bleeding
• Metrorrhagia: irregular interval bleeding
• Menometrorrhagia: heavy and irregular bleeding
32. What is the differential diagnosis of heavy menstrual bleeding?
Heavy menstrual bleeding, also sometimes referred to as abnormal uterine or vaginal bleeding, was formerly called dysfunctional uterine bleeding (DUB). This is usually caused by anovulation secondary to an immature hypothalalmic-pituitary-ovarian axis. However, the differential diagnosis also includes pregnancy (ectopic, miscarriage), bleeding disorders (such as von Willebrand disease, often with onset of first menstrual cycle and affecting about 1% of the population), PELVIC infection (gonorrhea, chlamydia), foreign body/trauma, and endocrinopathies (PCOS, thyroid disease).
33. You see an 18-year-old female who comes to your office complaining of 10 days of heavy menstrual bleeding, including soaking through a pad every 2 hours and passing clots. What are key points in the assessment of this patient?
• Vital signs: look for orthostatic hypotension, tachycardia
• Physical exam:
• Skin for acne, hirsutism, striae consistent with PCOS
• Petechiae/bruising suggestive of a bleeding disorder
• Palpation of abdomen to evaluate for undetected pregnancy
• If sexually active: pelvic/bimanual exam to examine for infection and PID
• Labs: complete blood count (CBC) (assessing for anemia and platelet count), reticulocyte count, TSH, pregnancy test
34. What are the two key clinical features that determine the management of abnormal uterine bleeding?
Hemoglobin concentration (i.e., anemia) and signs of orthostatic hypotension. The more severe the clinical feature, the more urgent and aggressive the management must be, particularly in the setting of acute hemorrhage.
35. How would you treat a patient with heavy menstrual bleeding?
Treatment is based on extent of bleeding. First, it is important to stabilize the endometrium by giving estrogen (hemostasis) and progestin (for endometrial stability). This can be done by using a combined birth control pill. Iron replacement should be given. Consider a blood transfusion if the patient is hemodynamically unstable. An alternative is to use an antifibrinolytic agent such as tranexamic acid to prevent breakdown of blood clots, especially if the patient has a contraindication to estrogen-containing medication.
36. You see a 16-year-old overweight female who reports having irregular periods, acne, and having to remove hair on her upper lip and chin. What is her most likely diagnosis?
Polycystic ovary syndrome (PCOS), which can affect up to 10% of reproductive age women, is the most likely diagnosis. Symptoms include amenorrhea/oligomenorrhea, hyperandrogenism (hirsutism, acne), overweight/obesity, and polycystic ovaries on ultrasound. Not all patients with PCOS will have all of these symptoms. Endocrinologic abnormalities may include insulin resistance (with elevated blood insulin levels), elevated LH/FSH ratios, and elevated free and total testosterone. It is important to rule out other causes of symptoms by obtaining DHEA-S (marked elevation suggests a possible adrenal tumor), TSH, prolactin (elevation suggests a possible pituitary tumor), and a morning 17-hydroxyprogesterone (to rule- out late-onset congenital adrenal hyperplasia). Long-term risks and sequelae of PCOS include infertility, endometrial cancer, metabolic syndrome, and diabetes.
37. How common is dysmenorrhea?
Up to 90% of adolescents are affected by primary dysmenorrhea (pain during menses). The condition remains the single greatest cause of lost school hours in females. However, fewer than 15% of teenage females with dysmenorrhea will seek medical care, so it is important to screen for the problem. Most cases are primary, but about 10% of patients with severe dysmenorrhea symptoms will have uterine or pelvic abnormalities, such as endometriosis.
Harel Z: Dysmenorrhea in adolescents and young adults: an update on pharmacological treatments and management strategies, Expert Opin Pharmacother 13:2157–2170, 2012.
38. Does dysmenorrhea occur more commonly in early or late adolescence? Dysmenorrhea occurs almost entirely with ovulatory cycles due to prostaglandin release. Menstrual periods shortly after the onset of menarche are usually anovulatory. With the establishment of more regular ovulatory cycles after 2 to 3 years, primary dysmenorrhea becomes more likely.
39. What is the difference between primary and secondary dysmenorrhea?
Primary dysmenorrhea, also called functional dysmenorrhea, is pain in the absence of pelvic disease. This usually presents in the second to third year after menarche; occurs with ovulatory cycles due to prostaglandin release and uterine hyperactivity; and may be associated with nausea, vomiting, and/or diarrhea. Pain is usually in the lower abdomen, back, or upper thighs.
Secondary dysmenorrhea is dysmenorrhea due to a pathologic process. Some of these processes include endometriosis (endometrial tissue outside the uterus), pelvic infections, intrauterine device (IUD)-related pain (specifically from the nonhormonal copper IUD), pregnancy (either pregnancy-related bleeding or complication such as miscarriage), and genital tract anomalies (especially if dysmenorrhea has been present since menarche).
Gray SH: Menstrual disorders, Pediatr REV 34:6–17, 2013.
40. What two classes of medications are most commonly used for dysmenorrhea?
• Nonsteroidal anti-inflammatory drugs (NSAIDs): These limit local prostaglandin production. Naproxen or ibuprofen may be effective in up to 80% of patients.
• Hormonal therapies: Oral contraceptives act by reducing endometrial growth, which limits the total production of endometrial prostaglandin. Ovulation is suppressed, which also minimizes pain. A combined estrogen-progestin pill is preferred. Improvement may not be seen for up to 3 months.
41. What is a common cause of chronic pelvic pain in adolescents without a history of pelvic inflammatory disease (PID)?
Endometriosis. This condition results from the implantation of endometrial tissue in areas of the peritoneum outside the uterine cavity. It is reported in 25% to 38% of adolescents with chronic pelvic pain. The pain can be noncyclic (may occur with intercourse or defecation) or cyclic (often most severe just before menses, and dysmenorrhea is common). Studies show that endometriosis can be diagnosed in 50% to 70% of patients with dysmenorrhea who do not respond to NSAIDs. Definitive diagnosis is made by laparoscopy and biopsy. Therapy can be surgical (e.g., excision, coagulation, laser vaporization) and/or medical (e.g., gonadotropin-releasing hormone analogues [GnRHa], combination oral contraceptives, medroxyprogesterone acetate).
Hickey M, Ballard K, Farquhar C: Endometriosis, BMJ 348:1752, 2014.
42. What is the peak age for ovarian torsion?
National data reveal that almost 90% of those with ovarian torsion are >11 years old, with a mean age of
14.5 years and an estimated incidence of approximately 5 per 100,000 females aged 1 to 20 years old.
A pubertal peak of ovarian torsion is thought to be due to the increasing likelihood of the development of ovarian cysts by the maturing reproductive hormonal axis. These cysts then act as lead points for torsion. Ovarian torsion should be considered in the evaluation of abdominal pain in an adolescent.
Guthrie BD, Adler MD, Powell EC: Incidence and trends of pediatric ovarian torsion hospitalizations in the United States, 2000-2006, Pediatrics 125:532–538, 2010.
43. In what setting should ectopic pregnancy be suspected?
Amenorrhea with unilateral abdominal or pelvic pain, irregular vaginal bleeding, and a positive pregnancy test is indicative of ectopic pregnancy until proven otherwise. A teenager with a ruptured ectopic pregnancy can present with features of shock (hypotension, tachycardia) and rebound tenderness.
Sequential hCG levels can help with differentiating an ectopic from an intrauterine pregnancy. For a viable intrauterine pregnancy, the doubling time of hCG levels is about 48 hours; in ectopic pregnancy, there is usually a significant lag. Other causes of lag include missed abortion and spontaneous abortion. Ultrasound is the first-line imaging modality for diagnosis. Laparoscopy may be necessary if the diagnosis remains unclear.
Barnhart KT: Ectopic pregnancy, N Engl J Med 361:379–387, 2009.
KEY POINTS: MENSTRUAL DISORDERS
1. Consider von Willebrand disease for abnormally heavy bleeding at menarche or unusually long menstrual periods.
2. Irregular menstrual bleeding patterns are common in early adolescence because regular ovulatory menstrual cycles typically do not develop for 2 to 3 years after the onset of menarche. If irregularity continues >2 years after menarche, consider a workup for PCOS or other causes.
Continued on following page
KEY POINTS: MENSTRUAL DISORDERS (Continued)
3. Always consider pregnancy in a patient with secondary amenorrhea.
4. Signs of androgen excess (hirsutism and/or acne) in the setting of menstrual irregularities suggest polycystic ovarian syndrome.
5. Ask about dysmenorrhea; it affects >50% of teenage girls and causes considerable school absence.
PCOS, Polycystic ovarian syndrome.
OBESITY
44. What is the body mass index (BMI)?
BMI (weight [kg]/height [m2]). BMI is an indicator of body fat, is age and sex-specific, and is recommended by the Centers for Disease Control and Prevention (CDC) as the main screening tool
for obesity. When plotted on standard charts for age and gender, a BMI from the 85th to 95th percentile indicates “overweight” and a BMI> 95th percentile indicates “obese.” Data from 2011 to 2012 show that among 12- to 19-year-olds, 35% are overweight, and 21% are obese. BMI growth charts for
age and gender are available at http://www.cdc.gov/growthcharts/.
Centers for Disease Control: http://www.cdc.gov/growthcharts/. Growth charts accessed on Dec. 3, 2014. Ogden CL, Carroll MD, Kit BK, et al: Prevalence of childhood and adult obesity in the United States, 2011-2012, JAMA 311:806–814, 2014.
Endocrine Society: http://obesityinamerica.org. Accessed on Mar 19, 2015.
45. How predictive is early childhood obesity of later adolescent obesity?
An overweight 5-year-old is 4 times as likely to be an overweight teenager, which highlights the importance of addressing obesity at an early age.
Cunningham SA, Kramer MR, Narayan KMV: Incidence of childhood obesity in the United States, N Engl J Med
370:403–411, 2014.
46. What are some of the health risk factors related to obesity?
A variety of physical, social, and emotional potential problems are involved (Fig. 1-2).
Psychosocial
Poor self-esteem
Depression Quality of life
Pulmonary Asthma Sleep apnea
Exercise intolerance
Renal
Glomerulosclerosis
Proteinuria
Gastrointestinal
Paniculitis Steatohepatitis Liver fibrosis Gallstones
Risk for cirrhosis
Risk for colon cancer
Musculoskeletal Forearm fracture Blount’s disease Slipped capital femoral
epiphysis Flat feet
Risk for degenerative
joint disease
Neurologic Pseudotumor cerebri Risk for stroke
Cardiovascular Dyslipidemia Hypertension
Left ventricular hypertrophy Chronic inflammation Endothelial dysfunction Risk of coronary disease
Endocrine
Type 2 diabetes Precocious puberty Polycystic ovary syndrome (girls)
Hernia Hypogonadism (boys) DVT/PE
Stress incontinence
Risk of GYN malignancy
Figure 1-2. Complications of adolescent obesity. DVT/PE, Deep vein thrombosis/pulmonary embolism; GYN, gynecologic; (From Slap GB: Adolescent Medicine: The Requisites in Pediatrics. Philadelphia, 2011, ELSEVIER Mosby, p 67.).
47. What variety of factors may contribute to obesity?
Both genetic and ENVIRONMENtal factors are associated with obesity in most cases. Endocrine disorders and genetic syndromes leading to obesity are uncommon. An emerging area of interest is epigenetics, which is defined as the study of heritable changes in gene expression that occur without a change in the deoxyribonucleic acid (DNA) sequence. Epigenetic mechanisms would include alterations in DNA methylation, histone modifications, or other epigenetically related processes that might increase susceptibility to weight gain.
• Genetic factors may explain the variance of fat distribution and metabolism rate.
• Genetic syndromes include Prader-Willi, Cohen, and Bardet-Biedl syndromes and are rare.
• ENVIRONMENTAL factors include increased caloric intake and decreased physical activity.
• Psychological disordered eating may result in obesity.
• Endocrine causes such as hypothyroidism, Cushing’s syndrome, and growth hormone deficiency are rare.
Marinez JA, Milagro FI, Claycombe KJ, et al: Epigenetics in adipose tissue, obesity, weight loss and diabetes, ADV Nutr
5:71–81, 2014.
Martos-Moreno GA, Vincente Barrios, Munoz-Calvo, et al: Principles and pitfalls in the differential diagnosis and management of childhood obesity, ADV Nutr 5:2995–3055, 2014.
48. What features on physical examination are particularly important in the evaluation of the obese patient?
• Blood pressure (hypertension)
• Acanthosis nigricans (type 2 diabetes)
• Hirsutism (polycystic ovarian syndrome)
• Thyroid (goiter, possible hypothyroidism)
• Right upper quadrant (RUQ) tenderness (gallbladder disease)
• Striae (Cushing syndrome)
• Tonsils (hypertrophy; potential for obstructive sleep apnea)
• Facial dysmorphic features (evidence of genetic syndrome)
• Limited hip range of motion (slipped capital femoral epiphysis)
• Small hands and feet, cryptorchidism (Prader-Willi syndrome)
• Lower-leg bowing (Blount disease)
49. How does sleep affect weight? Lack of sleep increases the risk of obesity, and with each hour of sleep lost, the odds of becoming obese increase. People who sleep fewer hours also seem to prefer eating foods that are higher in calories and carbohydrates, which can lead to overeating, weight gain, and obesity. Sleep helps maintain a healthy balance of the hormones that regulate hunger (ghrelin) or satiety (leptin). Insufficient sleep causes levels of ghrelin to increase and levels of leptin to decrease. Sleep also affects the body’s response to insulin and lack of sleep results in a higher than normal blood glucose level, increasing the risk for diabetes.
National Institutes of Health: “What causes overweight and obesity?” Accessed at http://www.nhlbi.nih.gov/health/health- topics/topics/obe/causes.html on Oct. 1, 2014.
50. What are the diagnostic criteria for the metabolic syndrome?
For children age 10 or older, metabolic syndrome can be diagnosed by abdominal obesity (using waist circumference percentiles >90%) and the presence of two or more other clinical features: triglycerides
>150 mg/dL, HDL <40 mg/dL, BP systolic 130/diastolic 85 mm Hg, and known type 2 diabetes or
elevated glucose.
Zimmer P, Alberti KG, Kaufman F, et al: The metabolic syndrome in children and adolescents—an IDF consensus report,
Pediatr Diabetes 8:299–306, 2007.
51. Why is a short obese 11-year-old of more clinical concern than a tall obese 11-year-old?
Being overweight is associated with an advanced skeletal age in preadolescents and younger adolescents, and thus, increased height compared with nonobese peers. Therefore, you expect them to be taller. Short stature in an obese 11-year-old could be a sign of possible endocrine disease.
52. What are some key points when discussing weight reduction counseling and management with a teenager?
It is important to assess current diet history, encourage healthy dietary practices, and identify problem areas and behaviors. Providers should:
• Help the adolescent set small attainable goals
• Discourage the use of food as reward/comfort and avoid emotional eating
• Encourage physical activity
• Encourage family mealtimes; involve the family to help modify behaviors and lifestyle
• Limit screen-time, including TV, videogames, Internet, and cell phone use when not related to school work, and discourage a TV in the teen’s bedroom
Centers for Disease Control and Prevention: “How much physical activity do children need? Accessed at http://www.cdc. gov/physicalactivity/everyone/guidelines/children.html on October 1, 2014.
53. What are the indications for bariatric surgery in adolescents?
Surgery can be considered when adolescents have a BMI 35 kg/m2 with a severe comorbid condition (i.e., type 2 diabetes mellitus, severe obstructive sleep apnea (OSA), pseudotumor cerebri, or severe steatohepatitis) or a BMI >40 kg/m2 with mild comorbidities (mild OSA, hypertension, insulin resistance, dyslipidemia, impaired quality of life). The patient must be Tanner stage IV or V; have completed at least 95% of skeletal maturity; be able to understand diet and lifestyle changes after surgery; and have
evidence of mature decision making, social support, and motivation to comply with preoperative and postoperative treatments. Many experts also recommend that before surgery a patient should have failed sustained organized efforts through lifestyle intervention to lose weight. Assent from the adolescent should always be obtained separately from the parents to avoid coercion.
Black JA, White B, Viner RM, et al: Bariatric surgery for obese children and adolescents: a systematic review and meta-analysis, Obes REV 14: 634–644, 2013.
Apovian CM, Baker C, Ludwig DS, et al: Best practice guidelines in pediatric/adolescent weight loss surgery, Obes Research 13: 274–282, 2005.
KEY POINTS: OBESITY
1. Obesity is the most common chronic condition in children.
2. With obesity and short stature, think thyroid abnormalities and evaluate thyroid-stimulating hormone and T4 levels.
3. Only 5% of obese children have an identifiable underlying pathologic cause.
4. If a child is at risk as a result of family history, the earlier the modifications (e.g., limiting television time, encouraging exercise, and healthy diet), the better.
5. Keep weight reduction or stabilization goals reasonable; if too unrealistic, discouragement and weight cycling are more likely.
SEXUAL DEVELOPMENT
54. What is Tanner staging for boys?
In 1969 and 1970, Dr. James Tanner categorized the progression of stages of puberty, (Table 1-1). It is now commonly referred to as sexual maturity rating (SMR) staging of sexual development. Separate
Table 1-1. Tanner Staging for Boys
STAGE DESCRIPTION
Pubic Hair
I None
II Countable; straight; increased pigmentation and length; primarily at base of penis
III Darker; begins to curl; increased quantity
IV Increased quantity; coarser texture; covers most of pubic area
V Adult distribution; spread to medial thighs and lower abdomen
Table 1-1. Tanner Staging for Boys (Continued )
STAGE DESCRIPTION
Genital Development
I Prepubertal
II Testicular enlargement (>4 mL volume); slight rugation of scrotum III Further testicular enlargement; penile lengthening begins
IV Testicular enlargement continues; increased rugation of scrotum; increased penile breadth V Adult
scales define staging for males based on pubic hair and genital appearance. Of note, the limitation of this rating system is that it relies only on visual inspection. Accurate staging requires palpation for assessment of testicular volume.
55. What is the normal progression of sexual development and growth for boys during puberty?
Nearly all boys begin puberty with testicular enlargement. This is followed in about 1 to 1.5 years by pubic hair and then about 12 months later by phallic enlargement. For boys, puberty lasts an average of
3.5 years and begins an average of 2 years later than it does in girls (Fig. 1-3).
56. What are the ranges of normal in the stages of pubertal development in girls?
Tanner divided pubertal development in girls according to pubic hair and breast development (Table 1-2).
Table 1-2. Tanner Stages for Girls
STAGE DESCRIPTION
Pubic Hair
I None
II Countable; straight; increased pigmentation and length; primarily on medial border of labia III Darker; begins to curl; increased quantity on mons pubis
IV Increased quantity; coarser texture; labia and mons well covered
V Adult distribution; with feminine triangle and spread to medial thighs
Breast Development
I Prepubertal
II Breast bud present; increased areolar size
III Further enlargement of breast; no secondary contour
IV Areolar area forms secondary mound on breast contour
V Mature; areolar area is part of breast contour; nipple projects
57. What is the normal progression of sexual development and growth for girls during puberty?
The majority of girls typically begin puberty with thelarche, or breast development. The appearance of breast buds may initially be asymmetric. Pubic hair usually starts to appear 1 to 1.5 years
later, although this may occur first or simultaneously in some girls. In about 15% of girls, axillary hair may appear first. Menarche usually occurs about 18 to 24 months after the onset of breast development. For girls, the duration of puberty is about 4.5 years, which is longer than that for boys (Fig. 1-4).
Figure 1-4. Summary of pubertal development in girls. (From Rosen DS: Physiologic growth and DEVELOPMENT during adolescence, Pediatr Rev 25:198, 2004.)
58. Has the age of menarche declined in the United States during the century? Survey data of women over the last several decades indicate a general decline in age over this time period for the initiation of puberty by about 15 months for black girls, 12 months for Mexican-American girls, and 10 months for white girls. A variety of factors may be contributing, including environmental (dietary changes and increasing obesity), socioeconomic, and genetic. Currently the average age of menarche is
12.6 years in white girls and 12.1 years in black girls of normal weight, and Mexican-American girls falling intermediate to this range.
McDowell MA, Brody DJ, Hughes JP: Has age at menarche changed? Results from the National Health and Nutrition Examination Survey (NHANES), J Adolesc Health 40:227–231, 2007.
59. When do boys develop the ability to reproduce?
The average age of spermarche (as demonstrated by the presence of spermatozoa in the first morning urine) is 13.3 years or at Tanner stage (SMR) 3. Unlike what occurs in girls (in whom menarche follows the peak height velocity), in boys, spermarche occurs before the growth spurt. Ejaculation usually occurs by Tanner stage (SMR) 4.
60. How is delayed puberty defined?
Delayed puberty is defined as the absence of testicular enlargement (>4 cm) in boys and absence of breast development in girls at an age that is 2 to 2.5 standard deviations later than the population mean. This has traditionally been defined as age 14 years in boys and age 13 in girls, but given downward trends in pubertal timing in the United States and racial and ethnic disparities, some experts have advocated for younger age cutoffs.
Palmert MR, Dunkel L: Delayed puberty, N Engl J Med 366:443, 2012.
61. Why should the sense of smell be tested in a teenager with delayed puberty? Kallmann syndrome is characterized by a defect in gonadotropin-releasing hormone [GnRH] with resultant gonadotropin deficiency and hypogonadism. Maldevelopment of the olfactory lobes also occurs, with resultant anosmia or hyposmia. Less commonly, cleft palate, congenital deafness, kidney malformation, pes cavus, and color blindness can co-occur. Boys who have GnRH deficiency often have a small phallus and testes, but physical exam may be significant only for sexual immaturity. Delayed bone age is the only consistent lab finding. These patients require hormonal therapy to achieve puberty and fertility.
62. What is the most common cause of delayed puberty? Constitutional delay of growth and puberty (CDGP) is the cause of delayed puberty in 70% to 90% of cases, boys more commonly than girls. This is a form of hypogonadotropic hypogonadism in
which there is delayed secretion of GnRH and activation of the gonadal axis. Fifty percent to 75% of children with CDGP have a family history of late-onset puberty, which indicates a strong genetic component. Children often are small for their age (5%) but have grown steadily. Bone age is delayed. Once puberty does begin, its progression is normal. Although it is considered a normal
variant of growth, there are some consequences to adult height. Once the pubertal growth spurt occurs, its duration and peak height velocity achieved are both reduced, resulting in a reduction in total pubertal height gain.
Frank Graeme. Growth Disorders. In Martin M, Alderman E, Kreipe R, Rosenfeld W, editors: Textbook of Adolescent Health Care. Elk Grove Village, IL, 2011, American Academy of Pediatrics, pp 656–666.
63. What features suggest constitutional delay of puberty?
• Family history of delayed puberty
• Short stature (boys are usually below the 10th percentile for height)
• Slowed growth velocity (4 to 5 cm/year in preadolescent girls and 3.5 to 4.5 cm/year in preadolescent boys) compared with same-age, same-sex peers (8 to 11 cm/year)
• Delayed bone age (from 1.5 to 4 years) compared with chronologic age; bone age is typically 12 to
13.5 years before the onset of puberty
• Normal prepubertal anatomy, sense of smell, and prepubertal LH, FSH levels
64. Which laboratory tests should you consider in a boy or girl with delayed puberty? If history or physical examination does not suggest an underlying cause (e.g., anorexia nervosa, chronic disease), tests should include LH, FSH, testosterone (male), and bone age. These tests help categorize the condition as hypergonadotropic with increased GnRH, FSH, and LH (implying possible gonadal defects, androgen insensitivity, or enzyme defects) or hypogonadotropic with decreased GnRH and low to normal FSH and LH (implying constitutional delay or primary hypothalamic-pituitary problems). Most cases involve decreased GnRH.
65. What is the most common cause of primary gonadal failure in boys? Klinefelter syndrome. The frequency of this condition is 1:1000 males. It is characterized in adolescence by gynecomastia and small, firm testes with seminiferous tubule dysgenesis. It is found in more than 80% of XXY males (i.e., males with 47 chromosomes). Onset of puberty is usually not delayed, and testosterone levels are usually adequate to initiate pubertal development. Levels of FSH and LH are elevated in these patients after the onset of puberty.
66. Can puberty be safely accelerated?
In some teenagers—more commonly boys—the constitutional delay in puberty has significant psychological effects. Studies have shown that, in boys, puberty can be accelerated without any compromise in expected adult height. In boys older than 14 years with plasma testosterone levels of less than 10 ng/dL, intramuscular testosterone can be given every 2 to 4 weeks for 4 to 6 months. Treatment for girls who are constitutionally delayed is less well studied. Conjugated estrogen or estradiol for
4 to 6 months has been used in girls older than 13 years without breast buds.
Palmert MR, Dunkel L: Delayed puberty, N Engl J Med 366:443–453, 2012.
67. How do you evaluate a breast lump noted by a teenage girl on self-examination? Although the incidence of cancerous lesions is extremely low in adolescents, breast lumps do require careful evaluation. Fibrocystic changes (i.e., the proliferation of stromal and epithelial elements,
ductal dilation, cyst formation) are common in later adolescence and are characterized by variations in size and tenderness with menstrual periods. Cystic changes will often resolve over 1 to 2 menstrual cycles. Reassurance and observation should be provided. The most common tumor (70% to 95%) is a fibroadenoma, which is a firm, discrete, rubbery, smooth mass that is usually found laterally. This is the most surgically treated or biopsied mass in adolescents. Other causes of masses include lipomas; hematomas; abscesses; simple cysts; and rarely, adenocarcinomas (especially if a bloody nipple discharge is present).
The size, location, and other characteristics of a mass should be documented and reevaluated over the next one to three menstrual periods. A persistent or slowly growing mass should be evaluated with fine-needle aspiration. Ultrasound can be helpful for distinguishing cystic from solid masses.
Mammography is a very poor tool for identifying distinct pathologic lesions in teenagers because the breast density of adolescents makes interpretation difficult.
Huppert JS, Zidenberg N: Breast disorders in females. In Slap GB, editor: Adolescent Medicine: The Requisites in Pediatrics. Philadelphia, 2008, Mosby Elsevier, pp 146–151.
68. Should breast self-examination be taught and emphasized for all teenage girls? Because the incidence of malignancy is very low in this age group, no data support benefits for breast self-examination, and it may cause unnecessary anxiety and testing. Exceptions would be all adolescents with a history of malignancy, those who have had radiation therapy to the chest more than 10 years ago, and adolescents 18 to 21 years old whose mothers carry the BRCA1 or BRCA2 gene.
Huppert JS, Zidenberg N: Breast disorders in females. In Slap GB, editor: Adolescent Medicine: The Requisites in Pediatrics. Philadelphia, 2008, Mosby Elsevier, p 150.
KEY POINTS: SEXUAL DEVELOPMENT
1. If there are no signs of puberty by age 13 in girls and age 14 in boys, evaluate for an underlying medical cause.
2. Most cases of late puberty are constitutional delay.
3. Nearly all boys begin puberty with testicular enlargement; 85% of girls begin puberty with breast enlargement.
4. Following onset, puberty lasts about 4.5 years for girls and 3.5 years for boys.
5. Mean time between the onset of breast development and menarche is slightly more than 2 years.
SEXUALLY TRANSMITTED INFECTIONS
69. How does the prevalence of sexually transmitted infections (STIs) in adolescents compare with that of adults? Among sexually active people, adolescents have a higher likelihood than adults of being infected with an STI. About 25% of adolescents contract at least one STI by the time of high school graduation. Reinfection is also more common in adolescents. About 40% of the annual incidence of chlamydia or gonorrhea infections occurs in teens previously infected with the causative organism. Many adolescents are reinfected within a few months of the index infection. Reasons for the increased susceptibility in teens include the following:
• Cervical ectropion: Neisseria gonorrhoeae and Chlamydia trachomatis more readily infect columnar epithelium, and the adolescent ectocervix has more of this type of epithelium than does that of an adult.
• Cervical metaplasia in the transformation zone (from columnar to squamous epithelium) is more susceptible to human papillomavirus (HPV) infection.
• There is less frequent use of barrier methods of contraception among this population.
• Adolescents and young adults account for approximately one fourth of new human immunodeficiency virus (HIV) infections in the United States. In general, the number of cases of HIV is increasing among youth ages 13 to 24 years.
70. What is the best way to screen for STIs?
Nucleic acid amplification tests (NAATs), such as polymerase chain reaction or transcription-mediated amplification, are highly sensitive and specific, primarily for chlamydial and gonococcal infections.
Advantages of NAATs include more rapid results and less invasiveness. Disadvantages include higher costs and lack of antibiotic sensitivity testing.
The gold standard for STI diagnosis in cases of possible sexual abuse has traditionally been culture.
However, as fewer laboratories perform culture tests and more use NAATs for diagnosis, the recommendations are evolving. The American Academy of Pediatrics now recommends the use of NAATs for such evaluations.
Crawford-Jakubiak JC, Committee on Child Abuse and Neglect of the American Academy of Pediatrics: The evaluation of children in the primary care setting when sexual abuse is suspected, Pediatrics 132:e558–e567, 2013.
71. What is the most common STI in sexually active adolescent females?
Among females, the most common STI is HPV infection followed by chlamydial infection.
72. How should we screen for STIs in adolescent females?
For all sexually active females younger than 25 years, the CDC recommends screening annually
for chlamydia. High risk adolescent females should also be screened yearly for gonorrhea. Universal screening for HIV is recommended. Screening for syphilis and hepatitis B is on a case-by-case basis. Routine screening for other STIs such as trichomoniasis, herpes simplex virus (HSV), and HPV is not recommended. Risky sexual behaviors should determine screening frequency. Other populations, such as pregnant or HIV-infected adolescent females, may require more thorough evaluation.
CDC: Sexually Transmitted Diseases Treatment Guidelines, 2010, MMWR 59 (No. RR-12), 2010. Screening for HIV: Clinical Summary of U.S. Preventive Services Task Force, 2013.
AHRQ Publication No. 12-05173-EF-4: Accessed at http://www.uspreventiveservicestaskforce.org/uspstf13/hiv/hivfinalrs. htmon Dec. 3, 2014.
73. How should we screen for STIs in adolescent males? National recommendations for STI screening among sexually active heterosexual males have not yet been officially determined. Annual gonorrhea and chlamydia screening should be considered in sexually active adolescent males. Universal screening for HIV is now also recommended. For males who have had sex with males, the CDC recommendations include annual HIV and syphilis serologies, with more frequent screening based on specific sexual practices.
74. Are pelvic examinations with specula always required to obtain specimens for STI diagnosis in teenagers?
Trends in screening for STIs in teenage girls have shifted from endocervical sampling to urine-based and vaginal swab collection. Optimal specimen type for NAATs in females is a vaginal swab.
• The chlamydia load in females has been found to be greater in vaginal fluid than in urine.
• Vaginal specimens obtained without the use of a speculum have a high screening validity for trichomonas, bacterial vaginosis, and yeast infections.
• Self-collection by teenagers of vaginal specimens has yielded comparable results compared with physician-obtained cervical specimens when nucleic acid amplification testing was used.
• Urine testing for chlamydia and gonorrhea is also useful if a vaginal specimen is not obtainable or if the adolescent resists obtaining a vaginal swab sample. Urine-based screening tests (NAATS) also have good sensitivity and specificity similar to that of specimens obtained using a speculum.
Fang J, Husman C, DeSilva L, et al: Evaluation of self-collected vaginal swab, first void urine, and endocervical swab specimens for the detection of Chlamydia trachomatis and Neisseria gonorrhoeae in adolescent females, J Pediatr Adolesc Gynecol 21:355–360, 2008.
Michel CE, Sonnex C, Carne CA, et al: Chlamydia trachomatis load at matched anatomic sites: implications for screening strategies, J Clin Microbiol 45:1395, 2007.
75. Which STI is most closely linked to cervical cancer?
Human papillomavirus. HPV affects 20% to 40% of sexually active adolescent females. More
than 100 HPV types have been identified, of which about 30% are known to infect the genital tract. They differ in their clinical presentation. Types 6 and 11 classically cause 90% of genital warts.
Types 16 and 18 cause the majority of cervical cancers. Because of this association, HPV vaccination is recommended by the Advisory Committee on Immunization Practices for boys and girls beginning at the 11- to 12-year visit. Catch-up vaccination is also recommended for unvaccinated adolescents.
http://www.cdc.gov/hpv/ (Accessed Mar 23, 2015).
76. What are the manifestations of HPV infection? HPV infection is typically subclinical, but infection can present with anogenital condyloma acuminata (genital warts). Cervical HPV infection may lead to cervical dysplasia and cervical cancer. Other complications may include vulvar and vaginal cancers. HPV is also a cause of nonsexually
transmitted disease, including deep plantar warts, palmar warts, and common warts.
Cervical infection with both the low-risk and the high-risk types of HPV in adolescent girls often clears spontaneously over a 6- to 8-month period. In males, HPV infection has been associated with anal cancers, particularly among men who have sex with men (MSM) and patients
who are HIV infected. Oropharyngeal and penile cancers have also been associated with HPV infection.
77. When are Pap smears indicated in teenagers?
The American College of Obstetricians and Gynecologists recommends that routine cervical cytology screening (Pap smear) for healthy women begins at age 21. Only in certain circumstances (HIV infection, immunocompromised state) are pap smears indicated in younger women. This is because most HPV infections in healthy adolescents self-resolve.
Whitlock EP, Vesco KK, Eder M, et al: Liquid based cytology and human papillomavirus testing to screen for cervical cancer: a systematic review for the U.S. Preventive Services Task Force, Ann Intern Med 155:687–697, 2011.
78. Describe the appearance of condylomata acuminata
Condyloma acuminata (anogenital warts) are soft, fleshy, polypoid or pedunculated papules that appear in the genital and perianal area (Fig. 1-5). They may coalesce and take on a cauliflower-like appearance. Visualization of anogenital warts can be enhanced by wetting the area with 3% to 5% acetic acid (vinegar), which whitens the lesions. They may be located in the urethra or on the penis, scrotum, or perianal area of men and on the vulva, perineum, vagina, cervix, periurethral, or perianal area in women. They may also be found periorally.
Figure 1-5. Perianal condylomata acuminata. (From Gates RH: Infectious Disease Secrets, ed 2. Philadelphia, 2003, Hanley & Belfus, p 221.)
79. What is the natural history of genital warts?
Left untreated, 40% of genital warts may spontaneously resolve, but the timing is unpredictable (months to years). The lesions are not oncogenic and will not progress to malignancy. Treatment, often done for cosmetic purposes or symptoms of itching or burning, consists of topical products, cryotherapy, or surgical removal. Recurrence can occur in as many as one third of cases and usually manifests within the first 3 months after therapy.
80. What is the typical presentation of chlamydial genital infections in both female and male teenagers?
Most are asymptomatic (up to 80% in females and 75% in males) and infection can persist for several months. Those with asymptomatic infection contribute to the high rates of transmission, which is the reason for screening asymptomatic adolescents. In females with symptoms, chlamydia should be suspected if vaginal discharge and bleeding are noted, especially after intercourse. This may be due to endocervical friability. In males, the most typical symptoms are dysuria and a penile discharge, which is usually scant and watery or mucoid. Occasionally penile itching or tingling may occur without discharge. Less frequently, urinary frequency, dysuria, hematuria, or hematospermia may occur.
Siqueira LM: Chlamydia infections in children and adolescents, Pediatr REV 35;145–154. 2014.
81. What is the typical appearance of N. gonorrhoeae on Gram stain?
Intracellular gram-negative diplococci (Fig. 1-6) are found on Gram stain.
Figure 1-6. Gram stain of Neisseria gonorrhoeae. (From Gates RH: Infectious Disease Secrets, ed 2. Philadelphia, 2003, Hanley & Belfus, p 207.)
82. What are the minimal criteria for the diagnosis of PID?
Pelvic or lower abdominal pain with no other cause likely other than PID and one or more of the following must be present:
• Uterine tenderness
• Cervical motion tenderness
• Adnexal tenderness
83. What additional criteria support the diagnosis of PID?
• Oral temperature> 38.3°C (101 ° F)
• Abnormal cervical or vaginal discharge (with leukocytes> epithelial cells)
• Elevated erythrocyte sedimentation rate (usually >15 mm/hr)
• Elevated C-reactive protein
• Cervical infection with N. gonorrhoeae or C. trachomatis
Because no single clinical aspect or laboratory test is definitive for PID, a constellation of findings is used to support the diagnosis. Of note, tests for gonorrhea and chlamydia are often negative in PID because, although the disease is in the upper genital tract, specimens are typically obtained from the lower tract.
CDC: Sexually transmitted diseases treatment guidelines, 2010, MMWR Recomm Rep 59 (RR-12), 1–110, 2010.
84. Which adolescents with PID should be hospitalized for intravenous antibiotics?
Those with any of the following conditions:
• Surgical emergency (e.g., appendicitis or ectopic pregnancy [or if such a diagnosis cannot be excluded])
• Severe illness (e.g., overt peritonitis, vomiting, high fever)
• Tubo-ovarian abscess
• Pregnancy
• Immunodeficiency
• High suspicion for unreliable compliance or timely follow-up within 72 hours
• Failure of outpatient therapy These are the same criteria that are used for older women when considering hospitalization for PID.
No evidence is available that supports adolescents have better outcomes from hospitalizations for treatment for PID as compared with adults if none of these conditions are present.
American Academy of Pediatrics: Pelvic inflammatory disease. In Pickering LK, editor: 2012 Red Book, ed 28. Elk Grove Village, IL, 2012, American Academy of Pediatrics, p 550.
85. What are the common causative pathogens for PID?
PID is typically a polymicrobial ascending infection causing endometritis, salpingitis, and oophoritis. It is most commonly caused by gonococcal or chlamydial infections. Other pathogens include Gardnerella species, Haemophilus influenza, gram negative rods, mycoplasma, Ureaplasma urealyticum, and cytomegalovirus.
86. A sexually active 17-year-old girl with adnexal and RUQ tenderness probably has what condition?
Fitz-Hugh–Curtis syndrome. This is an infectious perihepatitis that is caused by gonococci or by chlamydia. It should be suspected in any patient with PID who has RUQ tenderness. It may be mistaken for acute hepatitis or cholecystitis. The pathophysiology is thought to be the direct spread from a pelvic infection along the paracolic gutters to the liver, where inflammation develops and capsular adhesions form (the so-called violin-string adhesions seen on surgical exploration). If RUQ pain persists despite treatment for PID, ultrasonography should be done to rule out a perihepatic
abscess.
87. What are the sequelae of PID?
Twenty-five percent of patients with a history of PID will have one or more major sequelae of the disease, including the following:
• Tubo-ovarian abscess
• Recurrent PID (about 1 in 5 patients)
• Chronic abdominal pain: May include exacerbated dysmenorrhea and dyspareunia related to pelvic adhesions in about 20% of patients with PID
• Ectopic pregnancy: Risk is increased 6- to 10-fold
• Infertility: Up to 21% after 1 episode of PID, 30% after 2 episodes, and 55% after 3 or more episodes
Trent M, Haggerty CM, Jennings JJ, et al: Adverse adolescent reproductive health outcomes after pelvic inflammatory disease, Arch Pediatr Adolesc Med 165:49–54, 2011.
Bortot AT, Risser WL, Cromwell, PF: Coping with pelvic inflammatory disease in the adolescent, Contemp Pediatr
21:33–48, 2004.
88. How are the genital ulcer syndromes differentiated?
Genital ulcers may be seen in herpes simplex, syphilis, chancroid, lymphogranuloma venereum, and granuloma inguinale (donovanosis). Herpes and syphilis are the most common, and granuloma inguinale is very rare. Although there is overlap, clinical distinction is summarized in Table 1-3.
Table 1-3. Differentiation of Genital Ulcer Syndromes
HERPES SIMPLEX SYPHILIS (PRIMARY, SECONDARY)
CHANCROID LYMPHO- GRANULOMA VENEREUM
Agent Herpes
simplex virus Treponema pallidum Haemophilus ducreyi Chlamydia trachomatis
Primary lesions Vesicle Papule Papule-pustule Papule-vesicle
Size (mm) 1-2 5-15 2-20 2-10
Table 1-3. Differentiation of Genital Ulcer Syndromes (Continued )
HERPES SIMPLEX SYPHILIS (PRIMARY, SECONDARY)
CHANCROID LYMPHO- GRANULOMA VENEREUM
Number Multiple, Single Multiple (coalesce T) Single
clusters
(coalesce
T)
Depth Superficial Superficial or deep Deep Superficial or deep
Base Erythematous, nonpurulent Sharp,
indurated, nonpurulent Ragged border, purulent, friable Varies
Pain Yes No Yes No
Lymphadenopathy Tender,
bilateral Nontender, bilateral Tender, unilateral, may suppurate, unilocular fluctuance Tender, unilateral, may suppurate, multilocular fluctuance
From Shafer MA: Sexually transmitted disease syndromes. In McAnarmey ER, Kreipe RE, Orr DP, et al, editors: Textbook of Adolescent Medicine. Philadelphia, 1992, WB Saunders, p 708.
89. What are risk factors for the acquisition of genital ulcer disease?
• Lack of circumcision in males
• High-risk sexual behaviors (unprotected sex, MSM have a 6-fold increased risk)
• Unprotected skin-skin contact with ulcers
• Infection with HIV
Braverman PK: Genital ulcer disease: herpes simplex virus, syphilis, and chancroid. In Slap GB, editor: Adolescent Medicine: The Requisites in Pediatrics. Philadelphia, 2008, Mosby Elsevier, p 211.
Roett MA, Mayor MT, Uduhiri KA: Diagnosis and management of genital ulcers, Am Fam Physician 85:254–262, 2012.
90. What are the main differences between HSV-1 and HSV-2?
HSV-1 is typically associated with gingivostomatitis. It is usually transmitted nonsexually through contact with oral secretions (i.e., kissing) during childhood, whereas HSV-2 is associated with genital infection acquired via genital-genital contact. HSV-1 is being increasingly recognized as a cause of genital herpes in industrialized countries in adolescents and college students, which may result from oral sex in the setting of a declining prevalence of early childhood acquisition of HSV-1. This means more young people are susceptible to genital HSV-1 infection.
Bradley H, Marowitz LE, Gibson T, et al: Seroprevalence of herpes simplex virus types 1 and 2—United States, 1999-2010,
J Infect Dis 209:325–333, 2014.
91. How do recurrent episodes of genital herpes simplex infections compare with the primary episode?
• Usually less severe, with faster resolution
• Less likely to have prodromal symptoms (buttock, leg, or hip pain or tingling)
• Less likely to have neurologic complications (e.g., aseptic meningitis)
• More likely to have asymptomatic infections
• Duration of viral shedding is shorter (4 versus 11 days)
Chayavichitsilp J, Buckwalter JV, Krakowski AC, et al: Herpes simplex, Pediatr REV 30:119–129, 2009. Kimberlin DW, Rouse DJ: Genital herpes, N Engl J Med 350:1970–1977, 2004.
92. How are the three most common causes of postpubertal vaginitis clinically distinguished?
Candidal vaginitis: Vulvar itching, erythema and excoriations, vaginal discharge (thick, white, curdlike, lack of odor)
Trichomonal vaginitis: Vulvar itching and soreness and erythema, vaginal discharge (gray, yellow-green, frothy; rarely malodorous)
Bacterial vaginosis: Minimal erythema, vaginal discharge (malodorous fishy smell; thin white discharge clings to vaginal walls)
93. How does the vaginal pH help determine the cause of a vaginal discharge? Ordinarily, the vaginal pH in a pubertal girl is less than 4.5 (compared with 7.0 in prepubertal girls). If the pH is greater than 4.5, infection with trichomonas or bacterial vaginosis should be suspected.
94. How does evaluation of the vaginal discharge help identify the etiology?
See Table 1-4.
Table 1-4. Evaluation of Vaginal Discharge
CANDIDAL VAGINITIS TRICHOMONAL VAGINITIS BACTERIAL VAGINOSIS
pH ≤4.5 >4.5 >4.5
KOH prep Mycelia
pseudohyphae Normal Fishy odor (positive
“whiff” test)
NaCl prep Few WBCs Many WBCs; motile trichomonads Clue cells
KOH ¼ Potassium hydroxide; NaCl ¼ sodium chloride (salt); WBCs ¼ white blood cells.
95. How is trichomoniasis diagnosed?
Wet mount microscopy has been the most common method of diagnosis. For a wet mount, a sample of vaginal fluid is rolled onto a glass slide, and normal saline is added; look for the lashing
flagella and jerky motility of the trichomonads (Fig. 1-7). Wet mounts, however, can be falsely negative in up to one third of cases. Nucleic acid amplification tests are now available for detection of Trichomonas VAGINALIS, with higher sensitivities than the wet mount.
Gallion HR, Dupree LJ, Scott TA, et al: Diagnosis of Trichomonas VAGINALIS in female children and adolescents evaluated for possible sexual abuse: a comparison of the InPouch Trichomonas VAGINALis culture method and wet mount microscopy, J Pediatr Adolesc Gynecol 32:300–305, 2009.
Figure 1-7. Wet mount of vaginal secretions with leukocytes and flagellated trichomonads. (From Mandell GL, Bennett JE, Dolin R, editors: Principles and Practice of Infectious Diseases, ed 6. Philadelphia, 2004, Churchill LIVINGSTONE,
p 1361.)
96. If a patient is receiving a standard treatment for a trichomonal infection, why should alcohol be avoided?
The recommended treatment is single dose administration of metronidazole or tinidazole. Both medications interfere with the processing of ingested alcohol and may cause a disulfiram-like reaction in patients who drink alcohol within 24 hours of dosing. Symptoms may include abdominal pain, cramps, nausea/vomiting, facial flushing, and headaches.
97. What are “clue cells”?
Clue cells are vaginal squamous epithelial cells to which many bacteria are attached. This gives the cell a stippled appearance when viewed in a normal saline preparation (Fig. 1-8). Clue cells are characteristic—but not diagnostic—of bacterial vaginosis.
Figure 1-8. “Clue cells” are squamous cells with folded cytoplasm and numerous bacteria (typically Gardnerella VAGINALis) attached to their surface. (From Mandell GL, Bennett JE, Dolin R, editors: Principles and Practice of Infectious Diseases, ed 6. Philadelphia, 2004, Churchill
LIVINGstone, p 1366.)
98. What is the etiology of bacterial vaginosis?
Formerly called nonspecific, Gardnerella, or Haemophilus vaginitis, bacterial vaginosis is the replacement of normal vaginal lactobacilli with a variety of bacteria, including Gardnerella VAGINALIs, genital mycoplasmas, and an overgrowth of anaerobic species.
99. What are the criteria for the diagnosis of bacterial vaginosis?
Clinical diagnosis requires three of the four following criteria (Amsel criteria):
• Homogeneous thin white or gray homogeneous vaginal discharge
• Discharge pH greater than 4.5
• On wet mount, more than 20% of cells are clue cells
• Positive “whiff” test: addition of 10% KOH to discharge results in fishy odor
Hwang LY, Shafer M-A: Vaginitis and vaginosis. In Neinstein LS, editor: Adolescent Health Care, ed 5. Philadelphia, 2008, Wolters Kluwer, pp 728–729.
100. What is expedited partner therapy? Expedited partner therapy is treating the patient’s sexual partner(s) for presumed infection of gonorrhea or chlamydia without examining the partner(s) before dispensing treatment. The CDC has recommended this option to facilitate partner treatment. The legality of this practice is determined by each state.
101. What are CDC treatment recommendations for common STIs?
See Table 1-5.
Table 1-5. CDC STI treatment guidelines
COMMON INFECTION RECOMMENDED TREATMENT
Gonorrhea urethritis/cervicitis Ceftriaxone 250 mg intramuscular (IM), single dose PLUS
Azithromycin 1 g orally, single dose
Chlamydia urethritis/cervicitis Azithromycin 1 g orally, single dose
Continued on following page
Table 1-5. CDC STI treatment guidelines (Continued )
COMMON INFECTION RECOMMENDED TREATMENT
PID Ceftriaxone 250 mg IM, single dose
PLUS
Doxycycline 100 mg orally twice daily for 14 days
WITH or WITHOUT
Metronidazole 500 mg orally twice daily for 14 days
PARENTERAL REGIMEN:
Cefotetan 2 g IV every 12 hrs OR Cefoxitin 2 g IV every 6 hrs
PLUS
Doxycycline 100 mg oral or IV every 12 hours
OR
Clindamycin 900 mg IV every 8 hrs
PLUS
Gentamycin (loading) 2 mg/kg IV once, followed by 1.5 mg/kg
IV every 8 hrs
Genital HSV PRIMARY LESION:
Acyclovir 400 mg orally three times a day for 7-10 days
OR
Valacyclovir 1 g orally twice a day for 7-10 days
EPISODIC THERAPY FOR RECURRENT GENITAL HERPES:
Acyclovir 800 mg orally twice a day for 5 days
OR
Valacyclovir 1 g orally once a day for 5 days
SUPPRESSION:
Acyclovir 400 mg orally twice a day
OR
Valcyclovir 1 g orally once a day (decrease to 500 mg once a
day if <10 outbreaks/year)
Primary Syphilis Benzathine Penicillin G 2.4 million units IM in a single dose
HSV Herpes simplex virus; IM intramuscular; IV intravenous; PID pelvic inflammatory disease; STI sexually transmitted infection.
http://www.CDC.GOV/STD/TREatment/update.htm (Accessed Mar 23, 2015).
KEY POINTS: SEXUALLY TRANSMITTED INFECTIONS
1. Regardless of the pathogen, most sexually transmitted infections (STIs) can be asymptomatic.
2. Nucleic acid amplification tests for chlamydia and gonorrhea are particularly useful when screening for STIs in males and females.
3. STI screening in girls is best done via vaginal swab or urine collection rather than through endocervical sampling. Vaginal samples are the most sensitive.
4. No single symptom, exam finding, or laboratory test is definitive for PID.
5. Cultures are often negative in PID because the disease is in the upper genital tract and specimens are obtained from the lower tract.
6. Despite high rates of STIs in adolescents, clinicians frequently do not inquire about sexual activity, risk factors, or means of reducing risks.
SUBSTANCE ABUSE
102. What are the categories of abused drugs?
• Sedative-hypnotics: Alcohol, barbiturates, benzodiazepines, γ-hydroxybutyrate, flunitrazepam (Rohypnol), other sedatives
• Stimulants: Caffeine, cocaine, amphetamines, decongestants
• Tobacco
• Cannabinoids: Marijuana, hashish, synthetic cannabinoids
• Opioids: Heroin, opium, pharmaceutical opioid painkillers including methadone and oxycodone/ oxycodone derivatives
• Hallucinogens: Lysergic acid diethylamide (LSD), phencyclidine, mescaline, psilocybin, hallucinogenic mushrooms, methylenedioxy-methamphetamine (MDMA, ecstasy, Molly)
• Inhalants: Aliphatic, halogenated, and aromatic hydrocarbons; nitrous oxide; ketones; esters
• Steroids
Liepman MR, Calles JL, Kizilbash L, et al: Genetic and nongenetic factors influencing substance abuse by adolescents,
Adolesc Med 13:375–401, 2002.
103. What is the CRAFFT screen?
This is a six-item screening test for adolescent substance abuse. Two or more “yes” answers indicate with more than 90% sensitivity and more than 80% specificity potential significant substance abuse. A number of screening instruments are available for interviewing adolescents, and the search for alcohol or drug use should be part of routine medical care.
• Car: Have you driven a car (or ridden with a driver) under the influence of drugs or alcohol?
• Relax: Do you use drugs or alcohol to relax, feel better, or fit in?
• Alone: Do you use drugs or alcohol while you are alone?
• Forget: Do you sometimes forget what you did while using drugs or alcohol?
• Family/Friends: Do they ever tell you to cut down on drug or alcohol use?
• Trouble: Have you gotten into trouble when using drugs or alcohol?
American Academy of Pediatrics, Committee on Substance Abuse: policy statement—alcohol use by youth and adolescents: a pediatric concern, Pedatrics 125: 1078–1087, 2010.
104. What are characteristic physical signs of illicit drug use?
See Table 1-6.
Kaul P, Coupey SM: Clinical evaluation of substance abuse, Pediatr REV 23:85–94, 2002.
Table 1-6. Physical Signs of Illicit Drug Use
PHYSICAL SIGN DRUG OF ABUSE
Hypothermia Phencyclidine, ketamine
Hyperthermia Mescaline, LSD
Increased heart rate Amphetamine, cocaine, marijuana, MDMA, LSD
Increased blood pressure Amphetamine, cocaine, phencyclidine, MDMA, LSD
Decreased gag reflex Heroin, morphine, oxycodone, other opiates, benzodiazepines
Conjunctival redness Marijuana
Pinpoint pupils Heroin, morphine, oxycodone, other opiates
Sluggish pupillary response Barbiturates
Irritation/ulceration of nasal mucosa Intranasal cocaine, heroin, inhalants
Oral sores/burns, perioral pyodermas Inhalants
Cutaneous scars (“tracks)” Intravenous use
Gynecomastia, small testes Marijuana
Subcutaneous fat necrosis Intravenous and intradermal use
Continued on following page
Table 1-6. Physical Signs of Illicit Drug Use (Continued )
PHYSICAL SIGN DRUG OF ABUSE
Tattoos in antecubital fossa Intravenous use
Skin abscesses and cellulitis Intravenous and intradermal use
LSD ¼ Lysergic acid diethylamide; MDMA ¼ methylenedioxy-methamphetamine.
105. Should an adolescent be screened for drug abuse without his or her consent?
The American Academy of Pediatrics (AAP) advises against involuntarily drug testing of adolescents. The AAP recommends that pediatricians discuss who will receive results with adolescents and their parents before ordering a drug test. Others have argued that a teenager’s right to privacy and confidentiality does not supersede potential risks for serious damage from drug abuse, particularly if there is strong clinical suspicion or parental concern. Drug screening may be obtained without consent in cases of emergency where the minor is unable to give consent and/or the course of management may be dependent on the drug screen results. The legal ramifications are evolving and vary from state to state. In 1995, the U.S. Supreme Court ruled that random drug testing of high-school athletes and participants in extracurricular activities is legal.
Levy S, Siqueira LM and Committee on Substance Abuse: Testing for drugs of abuse in children and adolescents, Pediatrics 133:e1798–e1807, 2014.
106. How long do illicit drugs remain detectable in urine specimens?
There is variability depending on a patient’s hydration status and method of intake, but, as a rule, metabolites can be detected after ingestion, as shown in Table 1-7. Most urine screens are very sensitive and may detect drugs up to 99% of the time in concentrations established as analytic cutoff points. However, the screens can be much less specific, sometimes with false-positive rates of up to 35%. Therefore, second tests using the analytic methodology most specific for the suspected drug should be used. Furthermore, the use of urine drug screening is of limited value because many drugs are not included in screening panels.
Levy S, Siqueira LM, and Committee on Substance Abuse: Testing for drugs of abuse in children and adolescents,
Pediatrics 133:e1803, 2014.
Table 1-7. Detection of Illicit Drug Metabolites
Alcohol 7-12 hours
Amphetamines 1-3 days
Barbiturates (short acting) 4-6 days
Benzodiazepines (short acting) 1 day
Cocaine 1-3 days
Heroin <24 hours up to 1-2 days
Marijuana 1-3 days for single use; 3-5 weeks after last use for chronic smoker
Methadone 1-7 days
Morphine 1-2 days
Oxycodone 2-4 days
Phencyclidine 2-8 days for casual use; several weeks for chronic use
107. What is the genetic predisposition for alcoholism?
A male child of an alcoholic father is five times more likely to become an alcoholic than a child with a nonalcoholic father. Twin studies have demonstrated heritability patterns to be between 50% to 75%.
108. What are other individual risk factors for alcohol abuse?
Risk factors include poor school performance, conduct disorder, and untreated attention-deficit/ hyperactivity disorder (ADHD). Mood disorders and psychiatric conditions such as anxiety, depression, schizophrenia and bulimia tend to co-occur with alcohol abuse.
109. Which type of substance abuse is more common in younger adolescents than older adolescents?
Inhalant abuse. These substances are used at a higher rate among 12- to 13-year-olds as compared with older adolescents. Household products are typically abused, including aliphatic hydrocarbons (e.g., gasoline, butane in cigarette lighters), aromatic hydrocarbons (e.g., benzene and toluene in glues and acrylic paints), alkyl halides (e.g., methylene chloride and trichloroethylene in paint thinners and spot removers), and ketones (e.g., acetone in nail polish remover). Inhalants are the first illicit drugs used in about 6% of adolescents. Marijuana and pain relievers are the next most common drug types to be used for the first time by adolescents. Inhalants have short durations of action and usually cannot be detected by toxicology screen.
110. What is the leading cause of fatality related to inhalant abuse?
Fatal arrhythmias. The volatile hydrocarbons sensitize the myocardium to the effect of epinephrine and also affect depolarization of the myocardial cell membranes. Abnormal propagation of impulses can occur, sometimes associated with adrenaline surge (as when hallucinating or running from an authority figure), resulting in fatal arrhythmias. In adolescents who die from this entity, about 1 in 5 is using inhalants for the first time. This phenomenon may be referred to as Sudden Sniffing Death Syndrome.
Crocetti M. Inhalants, Pediatr REV 29; 33–34. 2008.
Williams JF, Storck M: Inhalant abuse, Pediatrics 119:1009–1017, 2007.
111. What are the toxicities of chronic marijuana use?
Pulmonary: Decreased pulmonary function. Compared with cigarette smoke, marijuana smoke contains more carcinogens and respiratory irritants and produces higher carboxyhemoglobin levels and greater tar deposition. Studies have demonstrated premalignant changes in those who smoke marijuana but not tobacco. The long-term significance of this has not yet been determined. Chronic use is associated with symptoms of chronic bronchitis.
Endocrine: Decreased sperm count and motility in boys. Marijuana use may interfere with hypothalamic-pituitary function and increase the likelihood of anovulation in girls. Chronic use also antagonizes insulin, which may affect diabetic management. Marijuana use may also impair cortisol and growth hormone secretion but the clinical implications are not yet known.
Neurologic/behavioral: Diminished short-term memory, concentration, and ability for complex decision making. Reaction time and motor coordination may be affected as well. There may also be interference with learning, possible “amotivational syndrome.” Use early in adolescence may alter brain development and result in cognitive impairment. Regular use is associated with an increased risk of anxiety and depression (although causality has not been established).
112. Is marijuana a “gateway” drug? A gateway drug is one with apparent less deleterious side effects, which is believed to lead to future risks of the use of more dangerous drugs. Epidemiologic and preclinical data indicate that marijuana use by adolescents could influence multiple addictive behaviors in adulthood. Additionally, long-term marijuana use itself can lead to addiction. One in 6 who starts using marijuana as a teenager and 25% to 50% among those who smoke marijuana daily will become addicted.
Volkow ND, Baler RD, Compton WM, Weiss SRB: Adverse health effects of marijuana use, N Engl J Med
370:1724–1731, 2014.
113. What performance-enhancing drugs are used by teenagers?
The different classes of these drugs include anabolic steroids (e.g., androstenedione), nutritional supplements (e.g., creatine, protein shakes), stimulants (e.g., ephedrine, caffeine, or guarana), and others,
including human growth hormone and blood-enhancing products. Many adolescents using these products do not participate in sports, but take these products in an effort to improve their appearance.
Dandoy C, Gereige RS: Performance-enhancing drugs. Pediatr REV 33;265–271, 2012.
114. What are the potential side effects of anabolic steroids?
See Table 1-8.
Table 1-8. Potential Side Effects of Anabolic Steroids
Endocrine In males—testicular atrophy, oligospermia, gynecomastia
In females—amenorrhea, breast atrophy, clitoromegaly
Musculoskeletal Premature epiphyseal closure
Dermatologic Acne, hirsutism, striae, male pattern baldness
Hepatic Impaired excretory function with cholestatic jaundice, elevated liver function test results, peliosis hepatis (a form of hepatitis in which hepatic lobules have microscopic pools of blood), benign and malignant tumors
Cardiovascular Hypertension, decreased high-density lipoprotein, thrombosis
Psychological Aggressive behavior, mood swings, depression
Smith DV, McCambridge TM: Performance-enhancing substances in teens, Contemp Pediatr 26:41, 2009.
115. When does cigarette smoking begin?
In the United States, about three fourths of daily adult smokers started smoking when they were between the ages of 13 and 17 years. Nearly 9 out of 10 smokers begin by age 18 years; worldwide, the average age is lower. Cigarette smoking remains the major preventable cause of premature death in the world. In the United States, rates for teenagers younger than 18 years have been declining since the late 1990s. In 2014, 14% of 8th graders and 34% of high school seniors reported any lifetime use of cigarettes.
http://monitoringthefuture.org//pressreleases/14drugpr_complete.pdf (Accessed Mar 23, 2015).
116. What are the main reasons that cigarette smoking begins?
• Peer pressure (the strongest influence)
• Curiosity or wanting to experiment
• Family member smoking
• As a method of weight control by girls
• As a way of risk-taking by boys
• Low self-esteem and depression
• LGBTQ youth smoke over 50% more than their straight counterparts and are more likely to use smokeless tobacco products as well.
117. What are the risks of chewing tobacco? As a result of the decreased gingival blood flow caused by nicotine, chronic ischemia and necrosis can occur. Chronic use results in gingival recession and inflammation, periodontal disease, and oral leukoplakia (a premalignant change). The risk for oral and pharyngeal cancer is increased. Although more commonly used by males, smokeless tobacco used by pregnant females may be associated with low-birth-weight infants and premature birth. Chewing tobacco, like cigarettes, is addictive.
Lenney W, Enderby B: “Blowing in the wind”: a review of teenage smoking, Arch Dis Child 93:72–75, 2008.
118. What are the risks of E-cigarette use among adolescents?
E-cigarettes electronically aerosolize nicotine and therefore have a similar side effect profile to that of cigarettes. Little is known about their long-term health effects; however, because e-cigarettes contain
concentrated nicotine, there is a greater risk of nicotine overdose. The Food and Drug Administration (FDA) has not approved their sale to teenagers, given these safety concerns.
119. What are the 5 “A’s” of smoking cessation counseling?
• Ask about tobacco use
• Advise to quit
• Assess willingness to attempt quitting
• Assist in attempt to quit (e.g., pharmacotherapy such as nicotine gum or patch)
• Arrange follow-up
Klein JD, Camenga DR: Tobacco prevention and cessation in pediatric patients, Pediatr REV 25:17–26, 2004. www.smokefree.gov: This is the national site with information for individuals interested in quitting, including smoking quitlines. Accessed May 2, 2014.
120. Are tattoos a tip-off to high-risk behaviors?
Yes. Permanent tattoos are obtained by 10% to 16% of adolescents between the ages of 12 and
18 years in the United States. The more tattoos an adolescent has, the stronger is the association with high-risk behaviors, including substance abuse, early initiation of sexual intercourse, interpersonal violence, and school failure.
Owen DC, Armstrong ML, Koch JR, Roberts AE. College students with body art: well-being or high risk behavior?
J Psychosoc Nurs Ment Health SERV 51(10):20–28, 2013.
Desai NA, Smith ML: Body art in adolescents: paint, piercings, and perils. Adolesc Med State Art REV
22:97–118, 2011.
Roberts TA, Ryan SA: Tattooing and high-risk behavior in adolescents, Pediatrics 110:1058–1063, 2002.
TEENAGE MALE DISORDERS
121. How common is gynecomastia in teenage boys? As many as 60% to 70% of adolescent boys have some breast development. In most, it spontaneously resolves in 1 to 2 years; 25% have persistence 2 years. It occurs most commonly during Tanner stages II and III, and it usually consists of subareolar enlargement (breast bud). It may be unilateral or bilateral. The breast bud may be tender, which indicates the recent rapid growth of tissue. Obese boys often have breast enlargement due to the deposition of adipose tissue, and differentiation from gynecomastia (true breast budding) is sometimes difficult.
Bell DL, Breland DJ, Ott MA: Adolescent and young adult male health: a review, Pediatrics 132:540, 2013.
Cakan N, Kamat D: Gynecomastia: evaluation and treatment recommendations for primary care providers, Clin Pediatr
46:487–490, 2007.
122. Why does gynecomastia occur so commonly in young teenage boys? Early during puberty, the production of estrogen (a stimulator of ductal proliferation) increases relatively faster than does that of testosterone (an inhibitor of breast development). This slight imbalance causes the breast enlargement. In obese teenagers, the enzyme aromatase (found in higher concentrations in adipose tissue) converts testosterone to estrogen.
123. Which boys with gynecomastia warrant further evaluation?
• Prepubertal or postpubertal boys
• Pubertal-age boys with little or no virilization and small testes
• Boys with hepatomegaly or abdominal mass palpated
• Boys with CNS complaints
Evaluation may include testing for hypothalamic or pituitary disease, feminizing tumors of the adrenal or testes, and genetic abnormalities (e.g., Klinefelter syndrome). Although breast cancer is extremely rare in men (0.2%), the rate increases to 3% to 6% in patients with Klinefelter syndrome. Benign cases of gynecomastia should be managed with reassurance.
Plastic surgery is a last resort option if the gynecomastia does not resolve and is causing significant distress.
124. What are the clinical manifestations of testicular torsion? Testicular torsion in adolescents usually presents with acute-onset hemiscrotal pain that may radiate to the groin and lower abdomen. Nausea and vomiting are also common. The testis is acutely tender and may be elevated, indicating a twisted and foreshortened spermatic cord. The cremasteric
reflex (the testicle retracts after light stroking of the ipsilateral thigh) is typically absent. Many patients report previous episodes of severe acute scrotal pain.
125. When is testicular torsion likely to occur?
Testicular torsion has a peak incidence at ages 15 to 16, with two thirds of cases occurring between ages 12 to 18. The most common underlying factor leading to testicular torsion is a congenital malformation called the “bell-clapper” deformity. The bell-clapper deformity refers to an abnormal fixation of the tunica vaginalis to the testicle, resulting in a horizontal lie of the testis
and increased mobility of the testis. Of note, the other peak of testicular torsion occurs in the neonatal period.
Sharp VJ, Kieran K, Arlen AM: Testicular torsion: diagnosis, evaluation, and management, Am Fam Physician 88:835- 840, 2013.
126. How is testicular torsion diagnosed?
Because salvage of the testis depends on the timely restoration of blood flow, imaging studies should not delay surgical exploration if symptoms and physical exam findings strongly suggest torsion.
Ultrasound with color Doppler is sensitive and specific, fast to perform, and often readily available, making it the modality of choice for imaging if the presentation warrants further investigation.
Low or absent blood flow to the testis seen on Doppler is suggestive of torsion.
127. How is testicular torsion treated?
Manual detorsion of the spermatic cord may be attempted if prompt surgical intervention is not available. However, surgical exploration is still required for fixation to prevent recurrence. Bilateral orchiopexy should be performed because the bell-clapper deformity is bilateral in up to 80%
of cases.
Gatti JM, Murphy JP: Acute testicular disorders, Pediatr REV 29:235–240, 2008.
128. If complete testicular torsion has occurred, how long is it before irreversible changes develop?
Irreversible changes develop in 4 to 8 hours. Reported testicular salvage rates are 90% to 100% if surgical exploration occurs within 6 hours of symptoms, 50% if symptoms are present for more than 12 hours, and less than 10% if symptom duration is 24 hours or longer.
129. How is testicular torsion clinically differentiated from other causes of the acute painful scrotum?
• Epididymitis: An inflammatory process that is usually slower in onset; pain is initially localized to epididymis, but as inflammation spreads, whole testis may become painful; may be associated with nausea, fever, abdominal or flank pain, dysuria, and/or urethral discharge; pain does not usually radiate to the groin; often caused by C. trachomatis and N. gonorrhoeae; history of STIs is suggestive; unusual in non–sexually active teenagers
• Orchitis: Usually slower in onset; often systemic symptoms (nausea, vomiting, fever, chills) as a result of diffuse viral infection; in patients with mumps, occurs about 4 to 8 days after parotitis; bilateral involvement more common, most commonly affects 7- to 12-year-olds
• Torsion of appendix testis: Sudden onset of pain; localized, isolate tenderness at the superior aspect of the testicle (occasionally with bluish discoloration, the so-called blue-dot sign); nausea and vomiting uncommon; more common in prepubertal boys; cremasteric reflex is usually present
• Incarcerated hernia: Acute onset; pain not localized to hemiscrotum; usually palpable inguinal mass; testes not painful; symptoms and signs of bowel obstruction (vomiting, abdominal distention, guarding, rebound tenderness)
Yin S, Trainor JL: Diagnosis and management of testicular torsion, torsion of the appendix testis, and epididymitis, Clin Pediatr Emerg Med 10:38–44, 2009.
130. How does the Prehn sign help distinguish between epididymitis and testicular torsion?
Relief of pain with elevation of the testis (POSITIVE Prehn sign) is associated with epididymitis, whereas persistent pain (NEGATIVE Prehn sign) is more indicative of testicular torsion. However, this relatively nonspecific sign should be interpreted in the context of other signs and symptoms.
131. What is the most frequent solid cancer in older adolescent males? Testicular cancer. Testicular cancer is most common in males 15 to 35 years of age. Those with a history of cryptorchidism (undescended testicle) are at increased risk, as are males with a history of hypospadias. The most common type is a seminoma, which, if detected when confined to the testicle (stage I), has a cure rate of up to 97% with orchiectomy and radiation. There is currently no evidence that testicular self-exam is associated with improved outcomes in testicular cancer and is therefore controversial.
Bell DL, Breland DJ, Ott MA: Adolescent and young adult male health: a review, Pediatrics 132:535–546, 2013.
132. What is the significance of a varicocele in a teenager? A VARICOCELE is an enlargement of either the pampiniform or cremasteric venous plexus of the spermatic cord, which results in a boggy enlargement (“bag of worms)” of the upper scrotum. These are rare before puberty. About 15% of boys between the ages of 12 to 18 have a varicocele, and about 10% of those are symptomatic (pain, discomfort). Longitudinal studies of adolescents show that large varicoceles may interfere with normal testicular growth and result in decreased spermatogenesis.
133. Which varicoceles warrant surgical intervention? It is controversial whether surgery can prevent the potential fertility consequences. Referral for possible intervention is warranted in the following situations:
• Varicocele with testicular atrophy (>20% volume difference)
• Large varicocele
• Bilateral varicoceles (higher potential for infertility)
• Scrotal pain
Fine RG, Poppas DP: Varicocele: standard and alternative indications for repair, Curr Opin Urol 22:513–516, 2012. Hayes JH: Inguinal and scrotal disorders, Surg Clin North Am 86:371–381, 2006.
134. On which side do varicoceles more commonly occur?
The left side: The left spermatic vein drains into the left renal vein at a right angle, and the right spermatic vein drains into the inferior vena cava at an obtuse angle. These hemodynamics favor higher left-sided pressures, which predispose patients to left-sided varicoceles. Unilateral left-sided varicoceles are the most common type, occurring in 90% of patients; the remainder are bilateral.
A unilateral right-sided lesion is rare, and many experts consider its presence a reason to search for other causes of venous obstruction, such as a renal or retroperitoneal tumor.
135. What is the difference between phimosis and paraphimosis? Phimosis is constriction of the prepuce orifice that prevents the foreskin from being withdrawn to reveal the glans penis. It can be secondary to minor inflammation from normal erections and from poor hygiene. Treatment is initially conservative with topical steroid creams, but circumcision may be considered in resistant cases.
Paraphimosis, on the other hand, is retraction of the foreskin behind the glans with inability to reposition it back. This is a medical emergency and requires surgical intervention. If untreated, paraphimosis can lead to penile ischemia.
136. What are pearly penile papules and should a teen worry about them?
Pearly penile papules (hirsuties coronae glandis) are 1- to 3-mm papules of the same size and shape distributed symmetrically along the corona of the glans penis. These papules are an anatomic variation and not infectious. They occur in about 15% to 20% of adolescent boys. There is a higher incidence in uncircumcised males. No treatment is indicated. Providers should reassure the teen that this is a normal finding.
Leung AK, Barankin B: Pearly penile papules, J Pediatr 165:409, 2014.
TEENAGE PREGNANCY AND CONTRACEPTION
137. What are trends in teenage pregnancy in the United States?
Teenage pregnancy rates have fallen steadily from 1990 to 2009, except for a brief increase between 2006 and 2007. Pregnancy rates fell 51% for non-Hispanic white and non-Hispanic black teenagers and 40% for Hispanic teenagers between 1990 and 2009. However, U.S. teen pregnancy rates are among the highest in the developed world. Teen pregnancy rates for black and Hispanic teens remain consistently at least twice that of white teenagers. About 80% of teen pregnancies are unintended and about one-third end in abortion. The teenage abortion rate in 2008 was the lowest since abortion was legalized (in 1973). About half of U.S. teen pregnancies progress to delivery.
Curtain SC, Abma JC, Ventura SJ, et al: Pregnancy Rates for U.S. Women Continue to Drop. NCHS Data Brief 136:1–8, 2013.
138. What factors make it more likely that a teenager will become pregnant?
• Early initiation of sexual intercourse: Risk factors for early initiation include low socioeconomic status, low future-achievement orientation, and academic difficulties.
• Influence from peers and sisters: If surrounded by sexually active friends and siblings, a teenager is more likely to engage in sexual behavior. For many teens, pregnancy is not viewed as a negative experience.
• History of physical or sexual abuse
• Family history of adolescent pregnancy
• Lack of family support and structure
• Barriers to contraception: Inaccurate information, lack of accessibility, improper use
• History of pregnancy
• History of negative pregnancy tests
• Race: Blacks and Hispanics have higher rates of pregnancy than whites, although rates significantly vary by race according to socioeconomic status.
Cox JE: Teenage pregnancy. In Neinstein LS, editor: Adolescent Health Care, ed 5. Philadelphia, 2008, Wolters Kluwer, pp 565–569.
139. If a teenager has been pregnant once, how likely is she to become pregnant again during her teenage years?
Repeat adolescent pregnancy is common. Studies show that 28% to 63% of teen mothers will have a repeat pregnancy within 18 months and about 40% will have a repeat pregnancy within 2 years. Factors associated with a repeat teen pregnancy include young age at first conception, intended first pregnancy, lack of contraceptive use, poor outcome of first birth, low school achievement, regular use of alcohol or drugs, poor family involvement, low level of parental education, and being the product of a teen pregnancy.
Crittenden CP, Boris NW, Rice JC, et al: The role of mental health factors, behavioral factors, and past experiences in the prediction of rapid repeat pregnancy in adolescence, J Adolesc Health 44:25–32, 2009.
140. What are the risks for infants of teenage mothers? Babies born to young teenage mothers are more likely to be preterm, have low birth weight, or be small for gestational age. In addition, infant mortality is greater for the infants of teenage mothers. It is unclear whether these risks are due to physiologic effects of adolescent pregnancy or to sociodemographic factors associated with teenage pregnancy (e.g., poverty, inadequate prenatal care).
Ganchimeg T, Ota E, Morisaki N, et al: Pregnancy and childbirth outcomes among adolescent mothers: a World Health Organization multicountry study, BJOG 121:40–48, 2014.
141. How soon after conception will a urine pregnancy test become positive?
Human chorionic gonadotropin (hCG) is a glycoprotein that is produced by trophoblastic tissue. Urine pregnancy tests can detect pregnancy by measuring total hCG, hyperglycosolated hCG, or the free
β subunit of hCG. Urine levels of 25 mIU/mL hCG are detectable by the most sensitive tests by about 7 days after fertilization. Although many home pregnancy tests can detect these low levels, some are
less sensitive and can only accurately diagnose pregnancy by about 3 days after the missed menstrual period.
Cole LA: The utility of 6 over-the-counter (home) pregnancy tests, Clin Chem Lab Med 49:1317–1322, 2011.
142. Which contraceptive methods are appropriate for adolescents? All available reversible methods of contraception are appropriate for use in adolescents, barring specific medical contraindications.
• Long-acting reversible contraception (LARC): Long-acting reversible contraceptive methods available include IUDs and subdermal implants. In the past, myths about the safety of IUD use in adolescents and in nulliparous women discouraged providers from taking advantage of these highly effective methods. However, it is now known that methodologic flaws in prior studies exaggerated the risks in the adolescent population and that these methods are safe for use in teens. IUDs do not significantly increase the risk of PID, outside of the 3 weeks after insertion, and do not cause infertility.
• Progestin-only injectable contraception: The injectable progestin-only contraception available in the United States (Depo-Provera®) is a common type of hormonal contraception used by adolescents. It is dosed every 3 months. Weight gain and intermenstrual bleeding are side effects associated with this method. While bone mineral loss may be associated with this method, users do not appear to have an increased risk of fractures.
• Combined hormonal contraception: Combined estrogen and progestin contraception methods include the combined oral contraceptive pill (COC), patch, and vaginal ring. These methods have the same mechanism of action, but vary in their delivery systems and dosing intervals, from daily dosing (COCs) to monthly dosing (vaginal ring). Despite excellent efficacy with perfect use, failure rates for typical use are about 9 pregnancies per 100 women and may be higher for adolescents because missed doses are common.
• Barrier methods: The male and female condoms are the only contraceptive methods that also provide protection against STIs. However, condoms have relatively high typical use failure rates for pregnancy prevention and therefore dual contraceptive method use (i.e., hormonal contraception together with a barrier method) should be encouraged.
Upadhya KK: Contraception for adolescents, Pediatr REV 34:384–394, 2013.
143. What are contraindications to the use of estrogen-containing contraceptive methods?
Estrogen is the hormonal component of contraception with the greatest number of medical contraindications. Absolute contraindications that should be screened for before starting an estrogen-containing method include:
• Migraine headaches with aura
• Personal history of deep venous thrombosis
• Known thromboembolic disorder, including lupus with antiphospholipid antibody syndrome and familial factor V Leiden deficiency
• Untreated hypertension (>160/100)
• Major surgery with prolonged immobilization
• Complicated valvular heart disease
• Coronary artery disease
• Stroke
• Acute or chronic liver disease with abnormal liver function
• Breast, endometrial, or other estrogen-sensitive cancer
Straw F, Porter C: Sexual health and contraception, Arch Dis Child Educ Pract Ed 97:177–184, 2012.
144. How likely are teenagers to use contraception?
About 25% of teenagers use no contraception at the time of first intercourse and about two-thirds report using condoms, with or without another contraceptive method. Among sexually experienced adolescent females ages 15 to 19, the majority report having used a contraceptive method, with the condom being the most popular method used (96%), followed by withdrawal (57%), and then the
contraceptive pill (56%). The approximate time between first sex and seeking family planning services for adolescent females is just over 1 year.
145. Is a pelvic examination mandatory before starting a patient on contraception?
No. Numerous professional organizations, including the American College of Obstetricians and Gynecologists, concur that a pelvic examination is not required for safe initiation of contraception. A large percentage of teenagers will delay seeking contraceptive care if they believe a pelvic examination is required. Routine pelvic examination and pap smears should begin at age 21, regardless of sexual activity or contraceptive use.
ACOG Committee Opinion No. 463: Cervical cancer in adolescents: screening, evaluation, and management, Obstet Gynecol 116:469–472, 2010.
146. What oral treatment is most commonly used for emergency postcoital contraception?
Levonorgestrel (Plan B® and generics) is a U.S. FDA-approved progestin-only method, now available in a one-pill formulation (1.5 mg of levonorgestrel) taken as soon as possible after intercourse. This method has been approved for over-the-counter sale (without a prescription) in the United States to all women, regardless of age. Progestin-only emergency contraception acts by inhibiting or delaying ovulation, disrupting follicular development, thickening cervical mucus to impede sperm penetration, and affecting the maturation of the corpus luteum. Levonorgestrel can reduce the risk for pregnancy by at least 75% when given within 72 hours of unprotected intercourse, and studies show that it maintains good efficacy when taken up to 120 hours later. Ulipristal acetate (Ella®) is another FDA-approved emergency contraceptive method available by prescription only in the United States. This method maintains stable efficacy up to 5 days following intercourse. The copper IUD can also be used as emergency contraception when inserted within 5 days of unprotected intercourse and is the most effective method of emergency contraception.
Upadhya KK: Contraception for adolescents, Pediatr REV 34:384–394, 2013.
TEENAGE SUICIDE
147. What is the main predictor of suicidal ideation in teenagers?
Depression. Up to 85% of adolescents with major depressive disorder (MDD) or dysthymia (less severe chronic depression) will report suicidal ideation. About one-third will make a suicide attempt sometime during adolescence or young adulthood. This is one of the reasons the AAP has advised screening for depression, including the use of various screening tools, at ages 11 through 21 at all well- visits.
Committee on Practice and Ambulatory Medicine: 2014 Recommendations for Pediatric Preventive Health Care, Pediatrics 133:568–570, 2014.
Cash SJ, Bridge JA: Epidemiology of youth suicide and suicidal behavior, Curr Opin Pediatr 21:615, 2009.
148. How often do adolescents attempt suicide in the United States? Suicide is the third leading cause of death in youth ages 15 to 24 in the United States, killing about 4600 youth each year. About 12% to 16% of adolescents report ever having contemplated suicide, and 4% to 8% report ever having made a suicide attempt. Among high school students in the United States, the prevalence of suicide attempt remained fairly stable between 1991 through 2011, although suicidal ideation has decreased over the same time period. About 15% to 30% of teens who attempt suicide will re-attempt within 1 year. Suicide attempt is a significant risk factor for completed suicide.
Nock MK, Green JG, Hwang I, et al: Prevalence, correlates, and treatment of lifetime suicidal behavior among adolescents: results from the National Comorbidity Survey Replication Adolescent Supplement, JAMA Psychiatry 70:300–310, 2013.
149. Who are more likely to attempt suicide, males or females? Females have greater odds of both suicidal ideation and suicide attempt compared with males. However, males (particularly white males) are much more likely to succeed, due in large part to the choice of more lethal methods (especially firearms). In younger patients (10 to 14 years), suffocation (such as hanging) is the most common method used.
150. Which adolescents are at increased risk for suicide?
Those with any of the following characteristics:
• History of previous attempts, especially those involving very lethal methods and those within the past 2 years
• Psychiatric disorder, especially MDD, bipolar disorder, conduct disorder
• Easy access to firearms (most common location for teenage suicide involving firearms is in the home)
• Substance abuse (both illicit drugs and alcohol)
• Family history of suicide and depression
• Family discord
• Loss of a parent to death or divorce
• History of impulsive aggression (tendency to react to frustration with hostility or aggression)
• Sexual minority (LGBTQ) adolescents, especially if unsupportive family or hostile school environment
• History of physical and/or sexual abuse
Cash SJ, Bridge JA: Epidemiology of youth suicide and suicidal behavior, Curr Opin Pediatr 21:613–619, 2009.
BONUS QUESTIONS
151. Is a 16-year-old female able to give consent for treatment of a sexually transmitted infection (STI) in most states?
Yes. Many states waive the legal requirement of parental consent for patients under age 18 for care related to STIs, contraception services, pregnancy-related care, substance abuse treatment, mental health services, and treatment for rape or sexual assault. Additionally, many states allow that adolescents access these services confidentially, if requested.
152. What drugs are associated with gynecomastia?
The drugs that cause this effect can be easier to recall using the CHEST acronym:
• Calcium-channel blockers: verapamil, nifedipine
• Hormonal medications: anabolic steroids, oral contraceptives
• Experimental/illicit drugs: marijuana, heroin, amphetamines, methadone
• pSychoactive drugs: diazepam, methyldopa, phenytoin, tricyclic antidepressants
• Testosterone antagonists: spironolactone, flutamide, cimetidine, ketoconazole
Goldman RD: Drug-induced gynecomastia in children and adolescents, Can Fam Physician 56:344–345, 2010.
153. What is the Maudsley Method for treating anorexia nervosa?
This is a family-based treatment intervention initially used at the Maudsley Hospital in London. With this therapy, parents are told to treat anorexia like any other illness. They are asked to be responsible for feeding their adolescent and limiting other behaviors that may result in weight loss. After some weight gain is obtained, responsibility for feeding and eating gradually transitions back to the adolescent.
154. If a teenager has infectious mononucleosis (IM), how likely is she to develop chronic fatigue syndrome (CFS)?
Six months after IM, 13% of adolescents (mainly girls) meet the criteria for CFS. At 12 months, the number has fallen to 7% and at 24 months to 4%
Katz BZ, Jason LA: Chronic fatigue syndrome following infection in adolescents, Curr Opin Pediatr 25:95–102, 2013.
155. What is binge eating disorder?
The DSM-5 now places binge eating disorder in its own category. It can be diagnosed when a person displays the following:
• Recurrent episodes of binge eating (large amounts of food in a short period of time accompanied by a feeling of loss of control)
• These episodes must be accompanied by at least 3 of the following:
• eating much more rapidly than normal
• eating until feeling uncomfortably full
• eating large amounts when not feeling physically hungry
• eating alone because of embarrassment
• feeling disgusted with oneself, depressed, or guilty afterward
• Marked distress regarding binge eating is present.
• Behavior must occur at least once a week for 3 months.
• With binge eating disorder, there is no compensatory purging.
156. A teenage girl develops migratory polyarthritis, fever, and scattered petechial lesions several days before menses. What condition should be suspected? Gonococcal-arthritis-dermatitis syndrome (GADS). After a migratory polyarthritis or polyarthralgia, the arthritis settles in one or two large joints. The patient then develops painful tenosynovitis over the tendon sheaths in addition to a characteristic crop of embolic skin lesions over the trunk and extremities. Diagnosis is confirmed by culturing gonococci from blood, synovial fluid, and/or rectal or genitourinary sites.
157. How is the diagnosis of PID definitively made?
• Endometrial biopsy with histopathologic evidence of endometritis (rarely done in teenagers because of the low likelihood of endometrial cancer)
• Transvaginal or abdominal ultrasonography revealing tubo-ovarian abscess or fallopian tube abnormalities (e.g., thickened, fluid-filled fallopian tubes with or without free pelvic fluid)
• Laparoscopy revealing abnormalities consistent with PID
American Academy of Pediatrics: Pelvic inflammatory disease. In Pickering LK, editor: 2012 Red Book, ed 28. Elk Grove Village, IL, 2012, American Academy of Pediatrics, p 549.
158. What are the two subtypes of anorexia nervosa?
RESTRICTIVE and binge/purge. Distinction is based on the predominant behaviors exhibited over the prior 3 months.
159. What hormonal abnormalities may be seen in anorexia nervosa? Amenorrhea is seen in most cases as a result of hypothalamic and pituitary dysfunction with very low levels of luteinizing hormone (LH) and follicle-stimulating hormone (FSH). Twenty-five percent of affected girls experience amenorrhea before significant weight loss occurs, which suggests that there is a psychological effect on physiology. Symptoms that are suggestive of hypothyroidism—constipation, cold intolerance, dry skin, bradycardia, and hair or nail changes—are common. Thyroid studies, however, tend to be normal, except for a low triiodothyronine (T3) and an increased reverse T3 (rT3), which is a less active isomer.
Other abnormalities include loss of diurnal variation in cortisol, diminished plasma catecholamine levels, normal or increased growth hormone levels, and flattened glucose tolerance curve.
160. How is the diagnosis of bulimia nervosa made?
According to the DSM-5, bulimia nervosa is diagnosed when a person engages in the following:
• Recurrent episodes of binge eating (characterized by eating an abnormally large amount of food in a short period of time associated with a feeling of a lack of control)
• Recurrent inappropriate compensatory weight-loss BEHAVIORS (such as vomiting, laxative or diuretic abuse, fasting or excessive exercising)
• These behaviors must occur at least once a week for a period of 3 months
• Self-evaluation is unduly influenced by body weight/shape
• These behaviors cannot occur exclusively in the context of anorexia nervosa
161. What modalities are used to treat eating disorders?
For milder cases, a physician can provide outpatient treatment with help from a therapist and a nutritionist. More severe cases are best managed by a specialized eating disorder treatment
team. Outpatient day-treatment or inpatient residential treatment may be necessary in more recalcitrant cases. Treatment for less severe cases should start with nutritional rehabilitation and monitoring on an outpatient basis, with a goal of 1 to 1.25 lb of weight gain a week until ideal weight is achieved. Even hospitalized patients are usually first tried on supervised oral refeeding regimens; if needed calories are refused, then nasogastric feeds are sometimes required for supplementation. The use of antidepressants, particularly selective serotonin reuptake inhibitors (SSRIs), can be helpful in those with bulimia and binge eating disorders. SSRIs can also be used to treat the accompanying depression in patients with anorexia, but they have not been shown to have an effect on weight gain.
Fisher M: Treatment of eating disorders in children, adolescents and young adults, Pediatr REV 27:5–16, 2006. National Eating Disorders Association: http://www.nationaleatingdisorders.org. Accessed December 3, 2014.
162. How should a very anemic teenager with abnormal uterine bleeding and orthostatic signs be managed?
If there are orthostatic changes and the hemoglobin is low (<7 mg/dL):
• Hospitalize for administration of oral combination medications (e.g., 30 μg ethinyl estradiol/0.3 mg
norgestrel every 6 hours until bleeding slows with a medication taper up to 3 weeks); if bleeding persists, begin high-dose intravenous conjugated estrogen therapy (dose 25 mg; may repeat every 4 to 6 hours for up to 4 doses).
• Begin intravenous fluids and consider transfusion (latter usually not required).
• Unresponsive hemorrhage may require dilation and curettage (also rarely required in adolescents).
• Coagulation studies (Because of a higher likelihood of underlying coagulopathy, tests for von Willebrand disease should be drawn before therapy because estrogen may increase the concentration of von Willebrand factor.)
• Begin iron supplementation.
Talib HJ, Coupey SM: Excessive uterine bleeding, Adolesc Med State Art REV 23:53–72, 2012.
Braverman PK, Breech LL: Menstrual disorders. In Slap GB, editor Adolescent Medicine: The Requisites in Pediatrics.
Philadelphia, 2008, Mosby Elsevier, pp 157–160.
163. How effective is treatment for bacterial vaginosis?
Treatment options include oral metronidazole 500 mg twice daily or 0.75% metronidazole gel intravaginally once a day for 5 days. An alternative treatment is 2% clindamycin cream daily for 7 days in cases of metronidazole allergy. Clindamycin cream is oil based, however, and might weaken latex condoms for 5 days after use. Overall, treatment failure is about 15%. Relapse may occur in up to 30% of cases.
164. Why do more ovarian torsions occur on the right than the left?
Multiple studies have noted this asymmetry in location, with nearly two thirds of ovarian torsions occurring on the right. A leading theory is that the relative mobility of the cecum allows for more ovarian motion on the right compared with the relatively fixed sigmoid colon on the left. Because torsion manifests almost 100% of the time with pain, this right-sided preference causes ovarian torsion to be commonly confused with appendicitis. Delays in diagnosis are common, which lessens ovarian salvage rates.
Oltmann SC, Fischer A, Barber R, et al: Cannot exclude torsion—a 15-year review, J Pediatr Surg 44:1212–1217, 2009.
165. Is ultrasonography typically diagnostic in the setting of ovarian torsion?
Ultrasound can correctly diagnose up to three fourths of cases of ovarian torsion with sensitivity over 70% and a specificity over 90%. The definitive diagnostic feature of torsion by ultrasound—visualization of the twisted pedicle—is seen in fewer than 10% of cases. Certain ultrasonographic features can suggest torsion, such as a pelvic mass of 5 cm or larger or diminished or absent arterial or venous (particularly venous) Doppler flow, but they are not diagnostic.
Naiditch JA, Barsness KA: The positive and negative predictive value of transabdominal color Doppler ultrasound for diagnosing ovarian torsion in pediatric patients, J Pediatr Surg 48:1283–1287, 2013.