The condition we now refer to as attention-deficit/hyperactivity disorder (ADHD) was first recognized in England in 1902 by eminent physician Dr George Still (eg, Still’s Disease = Juvenile Rheumatoid Arthritis). Dr Still identified and reported in the journal 

 several boys who seemed normal physically and intellectually but who struggled with symptoms of “restlessness, inattention, and hyper-arousal.” The cause was then unknown.

Following the pandemic of influenza in 1918, similar findings in children and adolescents were labeled “post-encephalitic syndrome” or “minimal brain damage,” later changed to “minimal brain dysfunction” when no obvious brain deficits were noted. Hyperactivity also led to the term “the hyperactive child.” Essentially, all the cases were male.

In the 1980s, emphasis was placed on the most universal trait, inattentiveness, and the term attention deficit disorder (ADD) was adopted. This gave rise to the diagnosis in females, who, though often “fidgety” are usually not grossly “hyperactive.” 

The Diagnostic and Statistic Manual of Mental Disorders, Fourth Edition (DSM-IV)

 distinguished 3 subtypes: inattentive only, hyperactive/impulsive only, and combined type, (inattentive, hyperactive, and impulsive), and changed the terminology to ADHD.

The Diagnostic and Statistic Manual of Mental Disorders, Fifth Edition (DSM-5)

, published in 2013, made these changes in diagnostic criteria: (paraphrased). 1) ADHD was defined as a “neurodevelopmental disorder” rather than a “neurobehavioral disorder,” putting emphasis on the developmental rather than the behavioral, opening the door for educational interventions, as well as other advantages. 2) For adolescents aged 17 years and older, and adults, only 5 out of the 9 criteria for inattention, or hyperactivity/impulsivity are required for diagnosis, versus 6 in 

. 3) Several of the inattentive/hyperactive/impulsivity symptoms must present before age 12. (

 required symptoms prior to age 6: Females a year after 6, more likely to be the inattentive type, often did not meet diagnostic criteria. 4) 

 specified that ADHD may coexist with a diagnosis of autistic spectrum disorder (ASD) since some children have overlapping symptoms, allowing more clarity of diagnosis, and therapeutic options.

The American Academy of Pediatrics, who had initially published Guidelines for Diagnosis and Treatment of ADHD in 2011, published a guideline update in November 2019.

 Though the earlier guidelines were not significantly altered, the following rules were re-emphasized: (paraphrased)

1. ­Any child aged 4-18 years, who manifests academic or behavioral issues, symptoms of inattention, and/or hyperactivity/impulsivity, should be assessed for ADHD.

2. ­To make a diagnosis, the primary care clinician (PCC) should verify that 

 symptom criteria have been met, to a degree causing impairment, including documentation of symptoms in at least 2 environments (eg, school, home), as reported by caregivers, teachers or other school personnel, and/or mental health persons involved in the child’s care.

3. ­The evaluation for ADHD should include a screening process to rule out other comorbid conditions (see table) which can “mimic” the symptoms of ADHD, or be a coexistent condition. (Note: studies have shown that as many as 75% of children/adolescents diagnosed with ADHD fulfill criteria for another 

 condition, such as specific learning disorder (SLD), anxiety, and/or depression, oppositional defiant disorder, etc. The term “ADHD Complex” is now being used to describe those children/adolescents.)

4.­ Since ADHD is a chronic condition, the PCC should manage the child in the same manner used to manage any child with special care needs, using the principles of the chronic care model.

Miscellaneous “pearls” re: diagnosing

Pre-school child: can be challenging to diagnose accurately, eg, mistaken for delayed maturational skills versus inadequate parenting. Always withhold diagnosis until parents have attended a thorough parenting class or 1:1 parenting help and are practicing good parenting skills. If significant improvement, perhaps is not ADHD. Lack of adequate response to behavioral interventions can then lead to consideration of medication trial and presumptive diagnosis of ADHD.

Phone call to teacher. Invaluable. An experienced teacher can be extremely helpful to help decide whether child’s inattention is due to learning difficulty or more boredom/disinterest? (than ADHD).

Thorough medical history, as noted earlier: There are 30 or more conditions that can cause symptoms which mimic ADHD.

Medical: eg, obstructive sleep apnea, traumatic brain injury, lead, medications, hypoxemia, near-drowning, prematurity etc.

Developmental: eg, ASD, SLD, speech/language disorders, lower IQ

Environmental: eg, abuse, neglect, death in family, divorce/separation

Mental/behavioral: eg, anxiety, depression, trauma

About 2/3 of children/adolescents diagnosed with ADHD are combined typed (mostly males) and 1/3 are females, mostly inattentive type. Males are often diagnosed early, in kindergarten or first grade due to overactivity and impulsive behavior. Girls are frequently not diagnosed until later eg, start of middle school, when they fail to turn in assignments in a timely manner.

In July 2016 the US Department of Education classified ADHD as a “specific disability” under the Civil Rights Law, which helps obtain special services for children and adolescents with ADHD.

The proper testings/screenings, of course, are only half the battle. However, once a conclusive diagnosis of ADHD has been made, there are a number of medications and tools to help your child navigate the healthiest and happiest childhood and adolescence possible (see 

1) Wolraich ML, Hagan, JF, Allan C, et al. Clinical practice guidelines for the diagnosis, evaluation, and treatment of attention deficit/hyperactivity disorder in children and adolescents. 

. October 2019;144(4). doi:10.1542/peds.2019-2528

ADHD Complex: Practicing Mental Health in Primary Care.

3) Langberg JM et al. Clinical utility of the Vanderbilt ADHD Rating Scale for ruling out comorbid learning disorders. 

 October 2010;126(5).
doi:10.1542/peds.2010-1267

Articles

Attention-deficit/hyperactivity disorder (ADHD) was first recognized over 100 years ago, but the diagnostic criteria has changed over the years. Here's a look at the latest guidance for diagnosing ADHD.

The Dx of ADHD

Once attention-deficit/hyperactivity disorder (ADHD) has been diagnosed, the well-researched treatment approach for children with ADHD continues to have parent behavior management training (PBMT), school-based interventions, and medication as the main tools for reducing symptoms and impairment. There are newly emerging treatment modalities to be considered, that will briefly be discussed here. An additional key piece of the puzzle in caring for children and adolescents with ADHD is the way that their care is delivered.

The American Academy of Pediatrics has divided ADHD treatment recommendations into 3 age groups: children aged 4 years to their sixth birthday; children aged 6 years through their 12th birthday; and adolescents aged 12 to 18 years. First-line treatment for children under the age of 6 years is PBMT. Medication recommendations at this age are reserved for children with moderate to severe symptoms that are not improving with PBMT, or when there are safety concerns due to their ADHD symptoms. It may also be indicated in children whose families are not able to access PBMT, or in children who have been expelled from multiple school or child-care settings. When medication is necessary in this age group, initiation of methylphenidate is recommended, which is off-label use in children aged younger than 6 years old. For children aged 6 years to their 12th birthday, treatment recommendations include PBMT, US Food and Drug Administration (FDA)-approved medication, and school interventions. For adolescents, FDA-approved medication is a treatment strongly recommended. Parent behavioral management training, organizational skills training, and school interventions are also helpful.

When caring for children with ADHD, knowing what resources are available and reputable for providing PBMT in your area is an important task. The most intensive PBMT with evidence-based benefits for children in this age group is parent child interaction therapy (PCIT). This involves real time interaction between a parent-child dyad and a trained therapist. This may not be available in all areas, or may not be accessible for some families.

 Group programs for parents of preschool age children to learn about behavior management techniques are available in many areas.

 During the COVID-19 pandemic, many mental health providers have moved their services to a virtual format, that may be more accessible for some families, but may present new barriers for other families. At minimum, it is crucial to be aware of books like 1-2-3 Magic

 to recommend to families for behavioral management education and support.

School-based interventions for patients with ADHD are integral to their treatment plan. Most often, these interventions should be formalized with a Section 504 Plan or an Individual Education Plan (IEP). Providing parents with information that they can use to request evaluation for a 504 Plan or an IEP from their child’s school is important when developing an ADHD treatment plan. A range of resources can be expected in the educational setting. Children with uncomplicated ADHD will likely qualify for a 504 Plan to provide support and accommodations such as daily report cards to enhance communication regarding the child’s progress, preferential classroom seating, or a quieter environment for taking tests. Children and adolescents with ADHD and co-occurring conditions such as learning disorders may require additional support in the academic environment with a more detailed IEP.

 Schools are working to provide special education services in a virtual format for children who do not attend school in person during the pandemic. Clinicians can check in with families to be sure services are being provided.

The FDA-approved medications for ADHD treatment are listed in Tables 1 and 2. Stimulant medications have the most evidence

 The use of non-stimulant medication is to be considered when stimulants are contraindicated, when patients have experienced intolerable side effects on stimulant medication, or, for the alpha-agonists, as adjunctive treatment along with stimulant medication. Careful investigation is needed when starting stimulant or non-stimulant medication in patients with significant personal history or family history of cardiac disease. This investigation may include testing such as an electrocardiogram or referral to pediatric cardiology.

There are many formulations of stimulant medications available. The process of selecting a formulation for your patient needs to take several factors into consideration. How many hours of the day will symptom relief be needed? It is worthwhile to spend some time understanding the patient’s daily routines: when medication will be given, how long they need the medication to be working for school, homework, extracurricular activities, or work responsibilities, and when they will be going to sleep. Providing treatment for adolescents with ADHD when they are driving is important, as they have increased risk of moving violations and crashes compared to adolescents who do not have ADHD.

 There is less abuse potential with longer-acting stimulants compared to shorter-acting stimulants, so use of these medications is recommended in most circumstances. Having familiarity with 2 or 3 of the longer-acting formulations from each stimulant class that are covered by the insurance programs common in your practice is usually sufficient. Determining how patients prefer to take the medication (if they are able to swallow pills or prefer a different method of administration) will also impact the formulation that is chosen.

Tips for prescribing stimulant medications

1. ­In most cases, the long-acting form of the medication is desirable

3. ­Titrate weekly to the most effective dose with acceptable side effects

4.­ Follow up by phone or electronic messages, or virtual visits with weekly titration, utilizing trained office staff and/or templates for obtaining information.

5.­ Follow up visit within 30 days including height, weight, pulse, blood pressure, physical exam

6.­ Use rating scales to measure improvement in ADHD symptoms and impairment

7.­ If intolerable side effects on first class of stimulants initiated, switch to the other class of stimulant medication.

Decreased appetite, difficulty with sleep onset, stomach ache, and headache are the most common side effects with stimulant medications.

 When initiating non-stimulant medication, symptom improvement is not expected as quickly. In this circumstance, less frequent contact is acceptable in the first month, but a follow-up visit is expected within the first 30 days.

During the COVID-19 pandemic, many students have less face-to-face contact with their teachers. Providers will need to increase their communication with patients, families, and school professionals when necessary to understand how effective the recommended treatments are in these new educational settings. At a minimum, progress reports from teachers on how students are doing with completion of their coursework may be helpful, in addition to use of the standardized questionnaires completed by those who have the opportunity to observe the child’s behavior. Providers, patients, families, teachers, mental health professionals, and mentors in the community will need to work together to provide the best possible care for ADHD.

During follow-up care for children and adolescents with ADHD there must be monitoring for co-occurring mental health disorders, and careful observation for conditions that may mimic ADHD. When primary care providers are uncertain about the presence of co-occurring or mimicking disorders, referral to subspecialists or mental health providers is recommended.

 When a co-existing mental health condition is identified, treatment of the most impairing condition is the highest priority. When possible, this treatment can be started by the primary care provider or, if necessary, referral to a mental health specialist.

Primary care visits are recommended every 6 months for children receiving treatment for ADHD, more frequently with medication changes, intolerable medication side effects, appearance of new or worsening symptoms, or concern for new co-occurring mental health disorders.

Newly emerging treatment modalities for ADHD include trigeminal nerve stimulation (TNS) and digital therapeutics. Trigeminal nerve stimulation for treatment of ADHD was evaluated in a double-blind, sham-controlled study supported by the National Institutes of Mental Health and showed few side effects and modest effect size in children.

 The TNS device gained FDA approval for treatment of ADHD in children aged 7-12 years that are not on medication.

 A new game-based digital therapeutic was given FDA approval following a randomized controlled trial that showed minimal side effects and some improvement with inattention in children aged 8-12 years that were not on medication.

 Although they have low risk of side effects in early studies and have gained FDA approval, these new modalities do not have studies proving adequate effectiveness to replace existing treatments.

These new treatment modalities are likely to have appeal to patients and families, with low risk of side effects. There are a number of other proposed treatments patients and families may ask about or may have tried such as dietary changes, nutritional supplements, neurofeedback, play therapy, etc, that have perceived lack of side effects, but lack of proven effectiveness.

 Discussion about these treatments help families understand that PBMT, school interventions, and FDA-approved medication have proven effectiveness, whereas these other treatments do not have adequate evidence to support routine use.

Providing appropriate assessment and evidence-based treatment for children and adolescents with ADHD is rewarding work. The COVID pandemic presents challenges to all. Working together to provide ongoing care will require increased communication. Parent behavioral management training, school-based interventions, and medication continue to be the most important treatments to reduce the symptoms and the impairment due to ADHD.

For more information on ADHD, visit our sister publication, 

1. Wolraich ML, Hagan JF, Allan C, et al. Clinical practice guidelines for the diagnosis, evaluation, and treatment of attention-deficit/hyperactivity disorder in children and adolescents. 

1-2-3 Magic: 3-Step Discipline for Calm, Effective, and Happy Parenting

3. CHADD: Understanding ADHD, For Parents and Caregivers. Accessed August 27,2020. 

4. Wolraich ML, Chan E, Froehlich T, et al. ADHD diagnosis and treatment guidelines: a historical perspective. 

5. Curry AE, Yerys BE, Metzger KB, et al. Traffic crashes, violations, and suspensions among young drivers with ADHD. 

6. NCQA: Measuring Quality. Improving Health Care. Accessed August 27, 2020. 

https://www.ncqa.org/hedis/measures/follow-up-care-for-children-prescribed-adhd-medication/

7. McGough JJ, Sturm A, Cowen J, et al. Double-Blind, Sham-Controlled, Pilot study of Trigeminal Nerve Stimulation for Attention-Deficit/Hyperactivity Disorder. 

8. US Food and Drug Administration (FDA). Accessed Augusst 27, 2020. 

https://www.fda.gov/news-events/press-announcements/fda-permits-marketing-first-medical-device-treatment-adhd

9. Kollins SH, DeLoss DJ, Canadas E et al. A novel digital intervention for actively reducing severity of paediatric ADHD (STARS-ADHD):a randomised controlled trial. 

https://www.fda.gov/news-events/press-announcements/fda-permits-marketing-first-game-based-digital-therapeutic-improve-attention-function-children-adhd

11. ADHD Medication Guide. Accessed September 6, 2020.

http://www.adhdmedicationguide.com/pdf/adhd_med_guide_022020_1434.pdf

12. Micromedex. Accessed September 6, 2020. 

https://www.micromedexsolutions.com/micromedex2/librarian

Following the diagnosis of attention-deficit/hyperactivity disorder (ADHD), the next step is treatment, which can include parent behavior management training, school-based interventions, and medication. Here's a look at the latest in ADHD treatments.

The Rx of ADHD

A 3720g (75th percentile) female infant was born at 40 weeks and 3 days gestation to a 30-year-old female following and uncomplicated pregnancy with regular prenatal care. Her length and head circumference were measured at 50 cm (60th percentile) and 35 cm (75th percentile), respectively. Her initial newborn examination revealed a non-erythematous, midline, suprapubic dimple located 5 cm below the level of the umbilicus (Figures 1, 2). The remainder of her examination was unremarkable, including head/scalp, eyes, ears, heart, back, umbilicus, anus, and genitalia. She had no hepatosplenomegaly and no skin lesions.

On the day of birth, white discharge was removed from this dimple. On the second day of life, she had a wet diaper with urine appearing to originate from 2 separate sources, including the dimple (Figure 3). However, using gentle manual palpation, examiners were unable to express urine through the dimple. Patient had 2 wet diapers in the first day of life and 4 wet diapers on the second day of life. She had 4 stools in the first 48 hours of life.

Our patient underwent abdominal ultrasound, which noted a fluid-filled tract from the lower anterior bladder to the suprapubic lower anterior abdominal wall, measuring approximately 2 mm in thickness/diameter and appearing to communicate with the bladder (Figures 4-7). The bladder wall was mildly and diffusely thickened. Renal sonography revealed normal kidneys without evidence of hydronephrosis, calculi, or masses. The remainder of the bladder appeared normal. Urology was consulted and recommended outpatient follow up for a voiding cystourethrogram (VCUG) and eventual surgical excision of the tract. No laboratory tests were recommended by the urologist given the normal renal ultrasonography and the normal urination. She was placed on amoxicillin at 10 mg/kg/day for urinary tract (UTI) prophylaxis, as the tract was in communication with the bladder and the bladder was already showing signs of wall thickening.

: Needle puncture during fetal life as a complication of diagnostic amniocentesis can result in skin dimpling that can occur anywhere on the body, in which case obtaining history of amniocentesis and ruling out other cases is key to diagnosis.

Every newborn should be inspected for any abnormalities, some of which may be benign and/or transient. Some abnormalities may point to an underlying pathology that needs further evaluation.

 are small indentations located anterior to the helix and superior to the tragus of the ear. They are present bilaterally in 25% to 50% of cases. They are common and occur in approximately 1% of white, 5% of black, and 10% of Asian children. Associated congenital anomalies occur in approximately one-third of the sporadic cases. In approximately one-third of the sporadic cases. Renal ultrasound should be performed in patients with isolated pre-auricular pits or in patients with other ear anomalies accompanied by 1 or more of the following: other malformations or dysmorphic features; a family history of deafness; auricular and/or renal malformations; or a maternal history of gestational diabetes. Our patient did not have any pre-auricular pits or auricular malformation.

 appear as a small opening, skin tag, or dimpling in the upper part of the neck anterior to the sternocleidomastoid. Branchial cleft cysts are remnants of embryonic development and result from a failure to obliterate one of the branchial clefts. First branchial cleft cysts are usually found near the auricle; second branchial cleft cysts are found just below the angle of the mandible and anterior to the sternocleidomastoid muscle (SCM). The third branchial cleft cysts are also found anterior to the SCM but lower in the neck as compared to the second branchial cleft cysts. Patient did not have any dimples near the auricle, at the angle of the jaw, or in her neck.

 are skin dimples in congenital rubella that generally occur over each patella, the radial styloid process, the lower end of the ulna at each wrist, the bony medial and lateral epicondyles at each elbow, and/or 1 over each superior and inferior posterior iliac spine.

 Our patient did not have skin dimpling over any bony prominence and had no other findings to suggest intrauterine rubella infection. She did not have microcephaly, hepatosplenomegaly, purpura, or a heart murmur.

Midline skin dimpling in the back can be seen in congenital derma sinus tracts or 

 (2 hemicords due to a congenital longitudinal split in spinal cord from an osseous or fibrous band). Small sacral dimples that overlie the coccyx and have well-visualized intact bases are considered benign variants. Dimples associated with excess hair, pigmentation, skin tags, or vascular anomalies need further ultrasound or magnetic resonance imaging to check for neural tube defects. Our patient did not have any midline back dimpling.

Skin dimpling may occur secondary to injury during amniocentesis.

 Amniocentesis is generally performed under ultrasonography during the second trimester when the ratio of viable to nonviable cells in the amniotic fluid is greatest. It is usually done on older pregnant women who are at greatest risk for delivering babies with genetic disorders. Our patient’s mother was 30 years old and did not undergo amniocentesis.

Our patient had a midline suprapubic dimple but the rest of her physical exam was normal. She did not have any other physical findings suggestive of congenital rubella as her dimpling was located midline on her lower abdomen and not over patella, near the radius, ulna, elbow, or iliac spine. The mother’s history and laboratory tests did not indicate an intrauterine rubella infection. Our patient did not have any midline back dimpling to suggest congenital dermal sinus tract or underlying neural tube defect. Also, our patient did not have any periauricular, below the angle of the mandible, or anterior neck dimpling to suggest branchial cleft cysts. Evidence of urine seeping out of the pit pointed to a diagnosis of vesical fissures, confirmed with abdominal ultrasonography.

Bladder exstrophy occurs when normal embryological abdominal wall development fails.

 In this anomaly, there is a failure of the infraumbilical mesenchyme to migrate caudally and invade between the endoderm and ectoderm of cloacal membrane. As a result, the cloacal membrane becomes unstable and prone to rupture. Rupture of the cloacal membrane after the gastrointestinal tract and genitourinary tracts separate is a defining embryological etiology event in bladder exstrophy.

 Patients classically present with bladder mucosa that is open and exposed in the midline of the abdominal wall. The incidence for bladder exstrophy ranges from 2 to 4 per 100,000 live births.

 This condition is often diagnosed during prenatal ultrasound and can be associated with other abnormalities in the development of the bladder, abdominal wall, pelvic bones, anus, and genitalia.

 Several variants of classical bladder exstrophy have been described.

 On this variant, the bladder mucosa is not exposed through the opening of the abdominal wall but has a communicating tract from the bladder to the skin. In 1 series of classic exstrophy only 1 vesical fissure was found among 72 patients.

Detection of vesical fissure requires examination in a well-lit room with careful attention to any unusual diaper findings. Evaluation of a midline suprapubic dimple found on physical examination requires an ultrasound of the abdominal wall and a renal ultrasound to check for any communicating tract between the anterior abdominal wall and the lower abdominal bladder and to check for any other renal anomalies. Evaluation with a VCUG for the urinary system is recommended. Plain radiograph of the pelvis is done to check for widening of the symphysis pubis. Our patient had a normal renal ultrasound and X-rays of the pelvis. The abdominal ultrasound showed a tract from the lower anterior bladder to the suprapubic lower anterior abdominal wall. A UTI prophylaxis was recommended for potential exposure of the bladder to abdominal wall mucosa. Patient followed up with urology for surgical excision of the tract.

Unlike patients with bladder exstrophy, patients with vesical fissure have a normal urethra and no problems with urinary incontinence. Because in vesical fissure there is no exposed bladder mucosa, risk of adenocarcinoma of the bladder is absent. This risk of adenocarcinoma of the bladder is present in bladder exstrophy because of bladder mucosa on the anterior abdominal wall; it typically appears between the third and sixth decade of life.

At 4 months our patient underwent excision of the tract, with a normal exam 2 months later. She continued to track at the 75th percentile for weight and 60th percentile for height and achieved developmental milestone appropriately.

1. Kulshrestha S, Kulshrestha M, Yadav A. Complete bladder exstrophy with a normal phallus: a variant of superior vesical fissure. 

2. TE Herman, MJ Siegel, and PF Austin. Superior vesical fissure; variant classical bladder exstrophy

3. Siffel C, Correa A, Amar E. Bladder exstrophy: an epidemiologic study from the international clearinghouse for birth defects surveillance and research, and an overview of the literature. 

4. Maruf M, Benz K, Jayman J, Kasprenski M, Michaud J, Di Carlo Heather, Gearhart J. Variant Presentations of the exstrophy-epispadias complex: a 40 year experience. 

5. DeRiese W, Warmbold H. Adenocarcinoma in exstrophy of the bladder. A Case Report and Review of the Literature: 

6. Bruce S, Duffy JO, Wolf JE Jr. Skin dimpling associated with midtrimester amniocentesis. 

7. Kumar A, Kanojia R, Saili A. Skin dimples. 

During a newborn's initial examination, doctors discovered a non-erythematous, midline, suprapubic dimple located 5 cm below the level of the umbilicus. The remainder of the examination was unremarkable. On the second day of life, the newborn had a wet diaper with urine appearing to originate from 2 separate sources, including the dimple. What's the diagnosis?

Vesical fissure in a newborn female: A variant of bladder exstrophy

You are asked to evaluate a healthy 15-year-old boy with transverse bruise-like marks on his back (Figure 1).

A 15-year-old male first noticed the marks on his back during a recent vertical growth spurt. On exam there are multiple horizontal violaceous linear striae on his back. He is otherwise healthy and denies any history of back injury or exposure to topical or systemic steroids.

Differential diagnosis for bruises on lower back

The differential diagnosis includes striae distensae in addition to bruising from skin injury. There are various triggers for striae distensae including both topical and oral steroid usage, obesity, excessive marijuana use, and rapid weight gain or loss.

 Another less common cause of striae in adolescents is Cushing syndrome, which is often associated with metabolic weight gain, high blood pressure, and Cushingoid facies.

Diagnosis: Transverse striae distensae (also known as stretch marks)

Striae distensae during adolescence are a common physiological change associated with rapid pubertal growth spurts. These pink-silver thin streaks are seen in up to 35% of girls and 15% of boys between 9–16 years of age.

 In females, the marks commonly occur on the breasts, thighs, shoulders, and buttocks.

 In males, the marks tend to be on the back, thighs, and calves.

 Recent studies on patient demographics have found that striae distensae in adolescents are often associated with tall stature, childhood obesity, and a family history of striae distensae.

 These striae initially appear as violaceous, flat plaques called striae rubra that progress over the course of months into permanent pink and hypopigmented scar-like depressions called striae alba.

Although the exact pathogenesis remains unknown, striae distensae of adolescence result from dermal breaks in connective tissue following physical stress and skin stretching.

 Pubertal growth spurts are a common time for physiologic skin stretching in teenage boys. It is also thought that reduced levels of the genes encoding collagen and fibronectin result in a thinning of the connective tissue and atrophic appearing striae.

 Histological analysis of striae reveals collagen fibers stacked horizontally in straight bundles whereas in normal skin, collagen is arranged randomly into wavy and thick collagen fibers.

In general, treatment of striae distensae is not necessary in otherwise healthy adolescent males. Lesions often stop progressing at the end of pubertal growth spurts in healthy teenagers who have normal body surface area. Lesions also tend to pale in color and shrink once the growth spurt is complete. Thus, management typically begins with reassurance and patient education of the benign nature of the course. In patients with risk factors for striae distensae, such as obesity with high body mass index (BMI), a healthy diet and exercise regimen is a good place to start for further management.

Although not a necessity in adolescent males with striae likely to improve after puberty, patients interested in improving the cosmetic appearance of striae can opt for initial therapy with 0.1% topical retinoic acid. Laser therapy, more specifically pulse-dye laser, has also been shown to work as initial therapy for inflammatory marks in the striae rubra stage.

 Other interventions including phototherapy, chemical peels, cocoa butter, and vitamin supplements are of limited evidence in the current literature.

Of note, striae located on the lower back are commonly mistaken for bruises from child abuse, as mentioned in the differential diagnosis. Patients are often referred to social services due to this misdiagnosis. This highlights the importance of raising awareness among providers regarding the appearance of these benign striae.

This patient was diagnosed with striae distensae based on clinical and physical exam findings. No further lab workup was necessary. We suggested observation of the patient’s back and regular sunscreen use. The patient felt that no further treatment was needed at this time.

1. Salter SA, Kimball AB. Striae gravidarum. Clin Dermatol. 2006; 24(2), 97-100. doi:10.1016./j.clindermatol.2005.10.008

2. Elshimy N, Gandhi A. A teenager with lumbar striae distensae (when a bruise is not a bruise). Case Reports. 2013;bcr2013201962. doi:10.1136/bcr-2012-201962

3. Lokhande AJ, Mysore V. Striae distensae treatment review and update. Indian Dermatol Online J. 2019;10(4):380-395. doi:10.4103/idoj.IDOJ¬¬_336_18

4. Maguire S, Mann MK, Sibert J, Kemp A. (2005). Are there patterns of bruising in childhood which are diagnostic or suggestive of abuse? A systematic review. Arch Dis Child. 2005;90(2): 182-186. doi:10.1136/adc.2003.044065

5. Stratakis CA. Skin manifestations of Cushing’s syndrome. Rev Endocr Metab Disord., 2016;17(3), 283-286. doi:10.1007/s11154-016-9399-3

6. Lause M, Kamboj A, Faith EF. Dermatologic manifestations of endocrine disorders. Transl Pediatr. 2017;6(4), 300-312. doi:10.21037/tp.2017.09.08

7. Al‐Himdani S, Ud-Din S, Gilmore S, Bayat A. "Striae distensae: a comprehensive review and evidence‐based evaluation of prophylaxis and treatment." Br J

8. Boozalis E, Grossberg, AL, Puttgen KB, Heath CR, Cohen BA. Demographic characteristics of teenage boys with horizontal striae distensae of the lower back. Pediatr Dermatol. 2018;35(1) (2018): 59-63. doi:10.1111/pde.13329

9. Burk CJ, Pandrangi B, Alvarez Connelly E. Picture of the Month—Quiz Case. Arch Pediatr Adolesc Med. 2008;162(3):277 doi:10.1001/archpediatrics.2007.61-a

A 15-year-old male first noticed the marks on his back during a recent vertical growth spurt. On exam there are multiple horizontal violaceous linear striae on his back. He is otherwise healthy and denies any history of back injury or exposure to topical or systemic steroids. What's the diagnosis?

Bruise-like marks on a healthy teenage male’s back

To find out the cause of a transient loss of consciousness (TLOC), your best bet may be to evaluate the youngster’s presymptoms and then administer appropriate tests, according to a retrospective study conducted in Korea. In this study of 160 children and adolescents, TLOC most often resulted from vasovagal syncope and epileptic seizures.

Investigators analyzed the medical records of participants who visited the hospital for “syncope and collapse,” noting age, sex, pre-symptoms (such as dizziness, headache, nausea, and blurred vision), accompanying signs (such as the presence of an aura, eye deviation, convulsions, or cyanosis), and trigger factors (such as standing up, exercise, emotional stress, urination, and defecation). They also took note of cardiographic and neurologic evaluations that were performed, including electrocardiograms, computed tomography scanning, magnetic resonance imaging, electroencephalograms, echocardiograms, and head-up tilt tests (HUTTs). Participants then were divided into 3 groups according to their final diagnoses: vasovagal syncope (63.8% of participants), epileptic seizures (10.6%), and “others” (25.6%). Mean age of onset did not differ significantly among the vasovagal syncope, epileptic seizure, or others groups: 14, 12.7, and 13.5 years, respectively.

A comparative analysis showed that presymptoms and accompanying signs often pointed the way to a diagnosis. Specifically, patients with a final diagnosis of vasovagal syncope were more likely than others to have pre-symptoms of dizziness or light-headedness and blurred vision, whereas patients diagnosed with epileptic seizures were more likely to have convulsions as an accompanying sign. Additionally, standing up was the most significant trigger factor for TLOC among those diagnosed with vasovagal syncope.

As for testing, the vasovagal syncope group had the greatest proportion of positive HUTT results, with 95% of patients with positive results diagnosed with vasovagal syncope. Head-up tilt tests showed high sensitivity (95.1%), positive predictive value (95.1%), and accuracy (91.8%), far better results than other group tests performed. Electroencephalograms, on the other hand, proved to be the test of choice for patients with epileptic seizures; they demonstrated a sensitivity, specificity, and accuracy of 80.0%, 70.6%, and 80.0%, respectively (

It is not clear that investigators in this study ever followed my preferred approach, which is to do no testing if the history suggests vasovagal syncope, especially for a first faint. The teenager who faints on a hot day (not during exercise or the like) and has prodromal symptoms does not require a work-up to my mind.

A study examines whether examining presymptoms can help clinicians find the cause of transient loss of consciousness.

Determining the cause of transient loss of consciousness

Oral challenge tests (OCTs) in 60 children referred to a clinic in Turkey with a suspected history of acetaminophen hypersensitivity verified hypersensitivity to the drug in 8 patients. Conversely, skin tests for acetaminophen hypersensitivity produced only 1 positive reaction, which turned out to be a false positive.

Skin prick tests with acetaminophen were administered to participants, who had a median age of 8.5 years, with positivity defined as producing a wheal with a diameter at least 3mm or larger than the negative control after 20 minutes. Investigators also checked for delayed type reactions. For the OCTs, 4 escalating doses of the culprit drug (either acetaminophen or acetaminophen/ibuprofen) were administered orally at 30-minute intervals until a cumulative dose was reached without triggering any symptoms. The OCT was considered negative if it produced no reaction during the test or when patients continued to take the drug for 3 days at home. The cumulative doses were 15mg/kg/dose and 10mg/kg/dose for acetaminophen and ibuprofen, respectively.

In those with verified acetaminophen hypersensitivity, an OCT with a strong COX-1 inhibitor was performed to classify the type of the reaction as either selective- or cross-intolerance-hypersensitivity. A subsequent OCT with a selective COX-2 inhibitor was performed in those cross-intolerant patients to find a safe alternative drug (

I have 2 points to make here. First, although I was aware that aspirin allergy is well known, I had not heard of allergy being an issue with acetaminophen. Second, this study is a reminder that the true test for an ingestion allergy, when doubt exists, is an OCT (done in a safe setting).

A study examines using oral challenges to diagnose acetaminophen ingestion allergies.

Study confirms oral challenge as gold standard for diagnosing ingestion allergies

An extensive literature review relating to the clinical features, causes, diagnosis, and treatment of cases of dermatoses resulting from playing video games revealed many reports of video game-related dermatologic conditions. Primarily localized to the extremities, especially the palms and fingers, these conditions generally are associated with repetitive friction and trauma, along with allergic contact sensitivities. Video game consoles, personal computers, laptop computers, mobile phones, and tablets all were implicated in the reported cases. For example, conditions associated with PlayStation, a video game console, include palmar hidradenitis (papules and/or nodules on the palms), “PlayStation thumb,” (a repetitive strain injury manifesting as painful blisters on the tips of the thumbs) and “PlayStation lip” (ulceration and bleeding of the lower lip associated with intense biting, chewing, and sucking on the lower lip during games). Early recognition and removal of the associated device usually resolves symptoms (

This is a fun article, worth reading for the discussion and pictures. The conditions described are minor, but you can impress and reassure parents (as well as encouraging cutting back on video use, perhaps) if you make one of these diagnoses correctly right in the office.

An extensive literature review looks at the dermatoses that are connected to video game play.