What Are Some of the Complications of Shyness?

Patient Presentation
A 5-year-old male came to clinic for his well child examination. He had always been a quieter child who was more reticent to join in peer games, but would readily do so with children and adults he knew. In new situations his parents would allow him to sit next to them for awhile watching and then slowly encourage him to engage with the other children and activities. They reported that it would take him awhile to do so but usually he was having a good time by the end of the activity. They reported that he was nervous about starting school. They had toured the school and met the teachers in the spring. They also had gone to play on the playground during the summer so he would be familiar with it. The past medical history was non-contributory. The family history was positive for maternal post-partum depression.

The pertinent physical exam showed a quiet male who was slow to warm up during the visit but did by the end of it. His vital signs were normal and his growth parameters were 10-50%. His examination was normal. The diagnosis of of a somewhat shy boy was made. The pediatrician suggested that they identify another student who would be riding on the bus with him to be his “bus-buddy” and also maybe identify someone before who would have the same lunch (“lunch buddy”) or recess times. In that way the child would already know someone and hopefully feel a little more comfortable. She also suggested that they go over his routine for getting on and off the bus, especially who would be there to meet him at the bus stop or at home. Additionally the parents could contact the teacher so that the teacher was aware and could look for opportunities to assist the child. A few weeks later, the pediatrician saw the family in the community and they said that the first few days were difficult as he was crying at school and home but then he became more comfortable. He also had joined the local Boy Scout troop because one of his friends was joining and that the first meeting had gone well.

Discussion
Shyness is a temperamental trait that refers to wariness and discomfort in the face of social novelty and/or in situation of perceived social evaluation.” Shy people often avoid or withdraw from familiar and unfamiliar people and situations. Their anxiety prevents them from social life participation when they need or want to.

Social withdrawal, isolation and social anxiety disorders are defined differently.

  • Social withdrawal is the behavioral expression of solitude. It is self-isolation where children and adults isolate themselves from their peer groups. These are non-anxious introverts.
  • Isolation is the result of the peer group rejecting or isolating the affected child or adult. Both social withdrawal and isolation do not necessarily involve fear of negative social evaluation or increased social anxiety as shyness does.
  • Social anxiety disorder, according to the DSM-V, is when the child or adult has significant distress that is out of proportion to the situation in their ordinary activities of daily living that occur in normal social settings such as school or work. The affected individual must also realize that the distress is unreasonable or excessive.

About 30-40% of people label themselves as shy. Shyness is generally a stabile characteristic overtime. Toddlers and preschoolers show more instability, but this trait is generally stabile from early to mid-childhood onward. Shyness may become more disabling and can lead to functional impairments in 13% or more of cases. Shyness affects boys and girls equally but boys are more strongly associated with peer exclusion and rejection than girls. Patients tend to be quiet and have decreased social participation. Infants do have normal increases of stranger anxiety at 9 months or separation anxiety around 18 months, but for shy individuals these tendencies do not disappear. For children who are having complications of shyness, some research supports improvements with exposure (to general or specific environments or situations), social skills training (verbal and non-verbal communication skills, modeling and social problem solving) and peer-mediated interventions (shy and non-shy children engage in joint-task activities together).

Learning Point
Potential complications of shyness include:

  • Anxiety – often significant, and most common
  • Depression
  • Loneliness
  • Poor self esteem
  • Academic impairment
  • “Missing out” on various life opportunities
  • Relationship problems such as exclusion, rejection, neglect or victimization
  • Substance abuse

Questions for Further Discussion
1. What questions could you ask to help determine if a shy child is needs intervention?
2. What are potential treatment options for social anxiety disorder?
3. When should a child with shyness be referred to a mental health professional?

Related Cases

To Learn More
To view pediatric review articles on this topic from the past year check PubMed.

Evidence-based medicine information on this topic can be found at SearchingPediatrics.com, the National Guideline Clearinghouse and the Cochrane Database of Systematic Reviews.

Information prescriptions for patients can be found at MedlinePlus for these topics: Child Development and Child Behavior Disorders.

To view current news articles on this topic check Google News.

To view images related to this topic check Google Images.

To view videos related to this topic check YouTube Videos.

Cheek JM. Shyness in Behavioral and Developmental Pediatrics. Parker and Zukerman B. eds. Little Brown and Co. Boston, MA. 1995;285-288.

Greco LA, Morris TL. Treating childhood shyness and related behavior: empirically evaluated approaches to promote positive social interactions. Clin Child Fam Psychol Rev. 2001 Dec;4(4):299-318.

Rubin KH, Coplan RJ, Bowker JC. Social withdrawal in childhood. Annu Rev Psychol. 2009;60:141-71.

Karevold E, Ystrom E, Coplan RJ, Sanson AV, Mathiesen KS. A prospective longitudinal study of shyness from infancy to adolescence: stability, age-related changes, and prediction of socio-emotional functioning. J Abnorm Child Psychol. 2012 Oct;40(7):1167-77.

American Psychiatric Association. Social Anxiety Disorder. DSM5.org.
Available from the Internet at http://www.dsm5.org/Documents/Social%20Anxiety%20Disorder%20Fact%20Sheet.pdf (rev. 5/2013, cited 8/31/15).

Author

Donna M. D’Alessandro, MD
Professor of Pediatrics, University of Iowa Children’s Hospital

What is the Mortality Rate for Legionellosis in the Pediatric Population?

Patient Presentation
A 3-year-old male came to clinic with a history of coughing and low grade fever for 2 days. He had copious rhinorrhea, coughing that was worse when he was lying down, and fever to 101° F. He slept poorly because of the coughing. His father denied any wheezing, emesis, diarrhea, or rashes. Several children in his daycare had similar symptoms. The past medical history was non-contributory. He was fully immunized including a seasonal influenza vaccine.

The pertinent physical exam showed a tired male in no respiratory distress with copious rhinorrhea. His temperature was 99.8° F., and respiratory rate of 22/minute with the rest of his vital signs being normal. HEENT revealed copious clear rhinorrhea, slightly dull tympanic membranes without fluid bilaterally, and some shoddy anterior cervical lymphadenopathy. His lungs had transmitted upper airway sounds. The rest of his examination was normal. The diagnosis of a viral upper respiratory infection was made and instructions for general support were given to the father. Afterwards the third year medical student had many questions because she had thought the transmitted lung sounds were wheezing. After describing how to distinguish between the two problems, a discussion about community-acquired pneumonia ensued with the attending physician. She asked about when to consider atypical pneumonias and how often they occurred in children. The attending discussed that Mycoplasma was one of the more common atypical pneumonias along with Chlamydia. “What about Legionella? That’s been in the news recently,” she asked.

Discussion
Legionella is often a severe, atypical pneumonia caused by the Legionella pneumophilia. It is a gram-negative bacterium that naturally occurs in water and is transmitted by droplet inhalation. No person-to-person contact has been documented to date. Contaminated water supplies have been documented in cooling tanks, decorative fountains, hot tubs, and large plumbing systems. Household and car air conditioners do not transmit the organism. Risk factors in the pediatric populations for legionellosis are being immunodeficient and exposure. Neonates are at risk from hospital settings.

Clinically legionellosis includes fever, myalgia, cough and radiographic or clinical evidence of pneumonia, along with laboratory confirmation by culture, serum antibody detection or urine antigen detection. Gastrointestinal symptoms can occur in 20-40% of patients. Patient can have mild disease but often it is severe with altered mental status and respiratory failure. Interestingly, children show a faster decline of serum IgM levels than adults. Antigen testing can be difficult to perform and false positive results can occur because of cross-reactivity with other organisms. Another less common clinical presentation is Pontiac Fever which causes less severe symptoms and clinically appears like influenza.

Other common bacterial causes of atypical pneumonia include Mycoplasma pneumoniae and Chlamydia pneumonia.

A differential diagnosis of cough can be reviewed here. Causes of pneumonia and complications can be reviewed here and here. A review of Mycoplasma infections can be found here

Learning Point
A 2015 study of death rates from Legionella during 2000-2010 in the U.S. showed a relatively flat mortality rate of 0.38-0.40/100,000 population, but the absolute numbers of deaths increased from 107 to 135/year. Highest rates were in the July-October time frame. There were no deaths in the 85 year olds. Most deaths occurred in whites but age adjusted mortality was the same for whites and blacks. More deaths occurred in males (63%) and they also had higher age adjusted mortality.

Questions for Further Discussion
1. What are extrapulmonary manifestations of Legionella?
2. What other organisms commonly cause atypical pneumonia?
3. How do you distinguish between wheezing and transmitted upper airway sounds?
4. Why is it called Legionaire’s Disease or Pontiac Fever?

Related Cases

To Learn More
To view pediatric review articles on this topic from the past year check PubMed.

Evidence-based medicine information on this topic can be found at SearchingPediatrics.com, the National Guideline Clearinghouse and the Cochrane Database of Systematic Reviews.

Information prescriptions for patients can be found at MedlinePlus for this topic: Legionaire’s Disease

Information prescriptions for patients can be found at MedlinePlus for these topics: Topics and Topics.

and at Pediatric Common Questions, Quick Answers for this topic: Legionaire’s Diseasec

To view current news articles on this topic check Google News.

To view images related to this topic check Google Images.

To view videos related to this topic check YouTube Videos.

Center for Disease Control. Legionellosis – United States, 2000–2009.
August 19, 2011. 2011:60(32);1083-1086. Available from the Internet at: http://www.cdc.gov/mmwr/preview/mmwrhtml/mm6032a3.htm(cited 8/24/15)

Pancer K. Patients’ age and the dynamics of IgM for L. pneumophila sg1. Przegl Epidemiol. 2014;68(1):21-6, 113-6.

Huong Ple T, Hien PT, Lan NT, Binh TQ, Tuan DM, Anh DD. First report on prevalence and risk factors of severe atypical pneumonia in Vietnamese children aged 1-15 years. BMC Public Health. 2014 Dec 18;14:1304.

Wickramasekaran RN, Sorvillo F, Kuo T. Legionnaires’ disease and associated comorbid conditions as causes of death in the U.S., 2000-2010. Public Health Rep. 2015 May-Jun;130(3):222-9.

Author
Donna M. D’Alessandro, MD
Professor of Pediatrics, University of Iowa Children’s Hospital

What Is Telogen Effluvium?

Patient Presentation
A 3-year-old female came to clinic because of hair loss. The mother said that the child was shedding a large amount of hair over the past 2 weeks with noticeable thinning.
The mother denied any skin changes to the scalp or rest of body. The mother reported that the hairs were not broken and just appeared to pull out from her head easily even when running her fingers through the child’s hair.
The mother said that the hair had a normal texture. “See. I just brushed her hair before we came and look at this brush,” the mother said as she showed a hairbrush with complete hairs of uniform composition and normal hair bulbs on the ends.
The mother also denied any recent illnesses, weight or eating changes, vision, muscle or joint problems. She denied using any other hair care products than a baby shampoo and the patient was not taking any medication or was exposed to toxins.
The past medical history showed a healthy female that did have a viral illness with significant fever about 3 months ago.
The rest of the review of systems was non-contributory.
The family history was positive for atopic dermatitis but negative for any other skin or autoimmune problems.

The pertinent physical exam showed a thin female with growth parameters in the 10%. She had normal weight gain since her prior visit.
Her general physical examination was normal. Her skin showed some bruising on her shins and a 0.5 cm cafe au lait lesion on her back. She had fine hair on her legs and arms and normal eyelashes and eyebrows. Her scalp had thinning hair without localized areas of alopecia. The underlying skin was normal.
A few hairs pulled out easily during finger combing. She had normal dentitia and nails.
The diagnosis of telogen effluvium was made. The mother was counseled regarding the natural history of the problem, physical signs to monitor and reasons to return.

Discussion
Hair is an epidermal appendage. It has a regular cycle of phases where hair grows (anagen), rests (telogen) and has a transition phase (catagen) in between.
Normal hair loss is ~50-100 hairs lost/day on the scalp. Normal hair grows about 2.5 mm/week.

The history should include details about general health, health stressors especially in last 4-6 months including fevers, surgeries, new medication and life events are important.
Review of systems for possible anemia, diabetes, and hypothyroidism and other autoimmune diseases should be obtained including fatigue, constipation, weight changes, night sweats, eye, muscle or other skin changes.
A specific history of drugs and possible toxins is also helpful. On physical examination specific attention should be paid to other dermal appendages (teeth and nails) and a complete skin examination.
Texture of the hair and underlying skin should be noted. Some hair should be pulled to see if it can be pulled out intact, breaks or does not pull out. Exclamation hairs (thinner at base with an abnormal bulb) should be noted.

A review of localized hair loss can be seen here. Some of the most common causes of localized patchy hair loss is tinea capitus, alopecia aerata and tricotillomania.
Alopecia areata causes localized hair loss, with usually round or oval in shape and no inflammation. It is often found on the scalp but may affect other areas of the body. If all of the scalp is involved this is called alopecia totalis and if all of the body hair is involved this is called alopecia universalis. It is often associated with autoimmune diseases.

The differential diagnosis of hair loss or alopecia includes:

  • Congenital (non-scarring)
    • Diffuse
      • Hair shaft anomalies
        • Pili torti
        • Tricchorrhexis nodosa
        • Many others
      • Alopecia congenita
      • Ectodermal dysplasia
    • Localized or patchy
      • Alopecia areata
      • Aplasia cutis congenita
      • Congenital temporal alopecia
      • Nevus sebaceous
      • Triangular alopecia
  • Acquired
    • Non-scarring
      • Diffuse
        • Alopecia areata
        • Anagen effuvium
          • Drugs – often seen with chemotherapy
          • Toxin
          • Radiation
        • Telogen effuvium
      • Physiologic in newborn
      • Parturition
      • Drug induced
      • Hypothyroidism
      • Abnormal nutrition – low protein or zinc levels
      • Stress
        • Anesthesia and surgery
        • Febrile illness
        • Life events
        • Localized or patchy
          • Tinea capitus – broken hairs, scaling and redness
          • Trichotillomania – irregular patches with broken hairs without scaling
          • Traction alopecia – broken hairs of irregular length
          • Alopecia areata – regular, circumscribed patches with exclamation hairs
          • Pressure induced or friction alopecia
      • Scarring
        • Graft vs host disease
        • Incontinentia pigmenti
        • Lichen planus
        • Systemic lupus erythematosus
        • Tinea capitus
        • Trauma

Learning Point
Effluvium means to outflow.
Telogen effluvium is one of the most common causes of diffuse hair loss. Telogen effluvium occurs when there is an abrupt shift from anagen into telogen phases. The hairs are then synchronously shed with more than the normal amount of hair loss over a relatively short period of time.
Diffuse hairs are lost over weeks to months and more hairs are shed if pulled. There is a generalized density decrease in the hair. A wide variety of stresses appear to cause the shift from anagen to telogen with the shedding occurring usually around 3-4 months after the stressor and regrowth generally over the next 6-12 months
Treatment is to treat any underlying process and also reassurance about the normal natural history of the problem.

Questions for Further Discussion
1. What are signs of hypothyroidism?
2. What is the role of trichoscopy in scalp disorders?

Related Cases

To Learn More
To view pediatric review articles on this topic from the past year check PubMed.

Evidence-based medicine information on this topic can be found at SearchingPediatrics.com, the National Guideline Clearinghouse and the Cochrane Database of Systematic Reviews.

Information prescriptions for patients can be found at MedlinePlus for this topic: Hair Loss.

To view current news articles on this topic check Google News.

To view images related to this topic check Google Images.

To view videos related to this topic check YouTube Videos.

Rudolph CD, et. al. Rudolph’s Pediatrics. 21st edit. McGraw-Hill, New York, NY. 2003:1210-1213. – double check reference here.

Lencastre A, Tosti A.Role of trichoscopy in children’s scalp and hair disorders. Pediatr Dermatol. 2013 Nov-Dec;30(6):674-82.

Castelo-Soccio L. Diagnosis and management of alopecia in children. Pediatr Clin North Am. 2014 Apr;61(2):427-42.

Sethuraman G, Bhari N. Common skin problems in children.
Indian J Pediatr. 2014 Apr;81(4):381-90.

Author

Donna M. D’Alessandro, MD
Professor of Pediatrics, University of Iowa Children’s Hospital

When Do Day-Night Circadian Rhythms Really Start for Infants?

Patient Presentation
A 4-day-old male came to clinic for his first well child check after discharge. Although he would awake to feed every 2-2.5 hours, his mother said that he would not latch well and would come off the breast often. She felt that when he did latch well, he would rhythmically suck and she could see his ear moving and see milk in his mouth afterwards. He was urinating 4-5 times/day and was stooling small amounts 5 or more times/day. His mother appeared somewhat disheveled and easily broke into tears saying that “I haven’t slept at all.” The father said that he was trying to help but the mother was very concerned about the feeding and wasn’t sleeping much. The past medical history showed a full term male with uneventful pregnancy or delivery who was discharged on day 2 of life. The family history was non-contributory.

The pertinent physical exam showed a somewhat sleepy infant who would awaken and root. His weight was 3258 grams which was 8% decreased from his birthweight and 2% decreased from his discharge weight. He was mildly jaundiced to the abdomen but the rest of his examination was normal. The work-up of a transcutaneous bilirubin showed a level of 10.2 mg/dL.

The diagnosis of a term male was made and breastfeeding support to help with the infant’s latch was given to the mother by a lactation nurse in the clinic. The pediatrician emphasized that both parents needed to rest and try to sleep when the baby slept. Other family members were available close by to also support the family. “It’s going to be a while before he knows day from night, so you are going to need to sleep or rest as much as you can when he does and leave some of the household chores to other people. Let them take care of you,” he advised. The patient’s clinical course at his next appointment in 2 days showed that the infant’s weight had increased by 30 grams. He was latching better although not perfectly and appeared more contented after eating. He was less jaundiced also. The mother also looked better and said that she had been trying to sleep as she could. They also gave the baby a bottle once at night so that she could sleep for about 4 hours. “It’s going a little better but he still has his days and nights mixed up,” she said.

Discussion
The earth rotates on its axis approximately every 24 hours with corresponding changes in ambient light occurring over that time period. Circadian systems have evolved in almost all living organisms to adapt to the changes in environmental light conditions and include sleep-wake cycles and changes in daily hormone production. In mammals , “[c]ircadian clocks resident in nearly every, if not all, mammalian cells…” and have been detected in embryonic stem cells. The circadian timing system has 3 major components – a central biological clock, input pathways and output pathways.

The central biological clock in the suprachiasmatic nuclei (SCN) isin the anterior hypothalamus just above the optic chiasm. There are peripheral biological clocks such as the liver also but they play less importance. The SCN oscillations (or rhythmic changes) are about 24 hours in length, but not exactly and stimulation is needed daily to reset the SCN and prevent it from drifting or freely running out of phase.

Input pathways are mainly from light which strikes the retina sending messages directly to the SCN or from the retina to the retinohypothalmic tract and then to the SCN. Output pathways are to the hypothalamus and other nonhypothalamic sites that regulate the daily changes of several hormones including melatonin and cortisol, which are two of the most important hormonal circadian regulators. Melatonin is produced in the pineal gland. Melatonin is the main hormone that regulates the daily resetting of the SCN and appears to be a main hormone for circadian rhythm entrainment for neonates and infants.

Primate studies have found that the SCN develops during gestational days 27-48, and metabolic activity is present by the end of gestation. The main SCN day-night settings appear to be set by the end of gestation but need to be entrained after birth. Entrainment appears to be mainly regulated by light cycles in neonates but feeding activities and temperature also appear to play a part of the entrainment. Other maternal time-of-day cues may also play a part.

Learning Point
For term human neonates there are few day-night rhythms detected. Infant activities are evenly distributed over the 24 hour cycle. However by 1-2 months of age, awake activities are consolidating more during daytime hours and by 3 months of age daytime sleeping decreases further with more sleep occurring at night. Day-night melatonin production is detectable by 12 weeks of age and by 3-6 months circadian cortisol variations are seen.

Questions for Further Discussion
1. What are some of the health problems related to inadequate sleep? To review click here.
2. How do circadian rhythms differ for preterm infants relative to full term infants?
3. Does taking melatonin help with jet lag?
4. What are SIDS prevention techniques?

Related Cases

To Learn More
To view pediatric review articles on this topic from the past year check PubMed.

Evidence-based medicine information on this topic can be found at SearchingPediatrics.com, the National Guideline Clearinghouse and the Cochrane Database of Systematic Reviews.

Information prescriptions for patients can be found at MedlinePlus for this topic: Sleep Disorders

To view current news articles on this topic check Google News.

To view images related to this topic check Google Images.

To view videos related to this topic check YouTube Videos.

Rivkees SA. Emergence and influences of circadian rhythmicity in infants. Clin Perinatol. 2004 Jun;31(2):217-28, v-vi.

Feldman R. The development of regulatory functions from birth to 5 years: insights from premature infants. Child Dev. 2009 Mar-Apr;80(2):544-61.

Christ E, Korf HW, von Gall C. When does it start ticking? Ontogenetic development of the mammalian circadian system. Prog Brain Res. 2012;199:105-18.

Sumova A, Sladek M, Polidarova L, Novakova M, Houdek P. Circadian system from conception till adulthood. Prog Brain Res. 2012;199:83-103.

Author
Donna M. D’Alessandro, MD
Professor of Pediatrics, University of Iowa Children’s Hospital