Children's Doctor

Injury Prevention

Loss of Consciousness

Victoria L. Vetter, MD, FAAP, FACC

J.K. is an 11-year-old girl who fell off a jungle gym at school. It was unclear if she lost consciousness.

She was taken to the nurse’s office, where she had normal vital signs. Her parents took her to the emergency room. A head CT scan was normal. She was watched for 2 hours and released with a diagnosis of possible concussion. One month later, she was in gym class running laps and felt dizzy. The gym teacher had her rest for a few minutes. She then resumed activities and had no further problems.

A month later, J.K. developed a sore throat and fever. She was prescribed azithromycin. Two days later, while sitting in class, she collapsed and fell from her desk to the floor. She regained consciousness in 2 to 3 minutes.

Discussion: J.K.’s pediatrician referred her to a pediatric cardiologist for further evaluation of syncope. She had an electrocardiogram (ECG), showing a prolonged corrected QT interval (QTc) of 490 milliseconds, with abnormal T wave morphology.

injury-ecg

ECG on patient J.K.

The QTc prolonged with exercise stress testing in the recovery period to 520 milliseconds, confirming the impression of long QT syndrome (LQTS). She was started on 10 mg of nadolol twice daily and was asked to stop competitive swimming. She was advised to avoid caffeine and stimulants, and not to take medications known to further prolong the QT interval. (A list at www.qtdrugs.org includes azithromycin). Genetic testing confirmed a diagnosis of long QT syndrome, type 1, with a mutation in the KCNQ1 gene. J.K. will be followed every 6 to 12 months with exercise stress testing and Holter monitoring and will have medication adjusted as she grows.

Congenital LQTS is an inherited condition characterized by syncope, seizures, and sudden cardiac death (SCD), associated in most people with a prolongation of the QT interval on the electrocardiogram. These patients often have bizarre or notched T wave morphology with prominent U waves or T wave alternans. They develop life-threatening ventricular tachycardia, known as torsades de pointes, or ventricular fibrillation. LQTS results from an ion channel abnormality in the heart, most commonly involving sodium, potassium, or calcium channels. The diagnosis of this syndrome is made from the ECG, clinical associations, family history, and genetic testing, when available. The QTc involves hand measurement of the QT interval with correction for heart rate using Bazett’s formula: QT/√RR interval. A careful history for syncope, seizures, and arrhythmias in the patients and families is essential. Any patient who presents with syncope during or immediately after exercise, or has ventricular tachycardia, especially of the polymorphic or torsades de pointes type or in association with emotional stress, should have an ECG with QTc determined to rule out LQTS. The QTc interval is not always prolonged in long QT syndrome, with 15% of known carriers having normal intervals. The upper limit of normal QTc is 460 ms under 15 years, 470 ms for adult females, and 450 ms for adult males.

Almost 10% of children with LQTS present with a cardiac arrest, 30%with syncope, and 10%with a seizure. Others have arrhythmias or palpitations, or are identified in an evaluation of affected families or when an electrocardiogram is obtained. Precipitating factors for syncope in LQTS include exercise, acute emotions including fear, fright, anger, auditory stimuli, and wakening. Some will have a sudden cardiac arrest during sleep. The incidence of SCD is 10%to 20%in the first year after a syncopal episode and 50% in the first 5 years in untreated patients. The incidence of SCD in untreated individuals is as high as 77%. Treatment with a beta blocker reduces incidence to between 1% and 5%.

The differential diagnosis of LQTS includes seizures or other neurologic disorders, breath-holding spells, metabolic disorders (hypoglycemia), or psychogenic causes (conversion reactions). The most common cause of syncope in teens and pre-teens is neurally-mediated syncope or vasodepressor syncope (VDS). A significantly prolonged QTc interval in the presence of VDS should still prompt an investigation for LQTS. Other cardiac disorders in the differential include cardiomyopathies, structural heart disease, and other electrical disorders.

Treatment is with beta blockers, lifestyle modification, and implantable cardioverter-defibrillators (ICD) in selected patients. All family members of identified cases should be evaluated.

References and Suggested Readings
Roden, DM. Long-QT syndrome.
New Engl J Med 2008; 358: 169-76.

Priori SG, Schwartz PJ, Napolitano C, et al. Risk stratification in the long-QT syndrome
New Engl J Med 2003: 348: 1866-1874.

Schwartz PJ, Priori SG, Spazzolini C, et al. Genotype-phenotype correlation in the long-QT syndrome: gene-specific triggers for life-threatening arrhythmias.
Circulation. 2001; 103:89-95.

Repeated Injury

Angela Smith, MD

Susan, a 14-year-old basketball player, went up for a rebound and twisted her right ankle into inversion as she came down. She heard a cracking sound in her ankle and had to be helped off the court. After the game, she limped home. By bedtime, the ankle was swollen and ecchymotic.

The next morning she went to her local emergency room. X-rays showed no fracture, and her growth plates were closed. She was given a universal-size, stirrup-type brace and told to use crutches until she could walk, then resume her activities as tolerated. On the third day, she discarded her crutches. She couldn’t fit the ankle brace into her sneaker, so she used a pull-on elastic ankle sleeve instead. She had some instability but did not completely roll over. She tried to continue her basketball season, but each time she played it swelled more than baseline. She made it through the season but limped at the end of every game.

Susan went to an orthopaedic surgeon, who learned she had sustained a Salter I fracture of the right distal fibula at 10 years of age, treated for 4 weeks with a below-knee walking cast. Following cast removal, she was instructed to resume sports as tolerated, and she felt entirely back to normal within a month. When she was 12, she sustained a mild twisting injury to her right ankle. She was able to bear weight, but had persistent though mild swelling over the anterolateral ankle for a few weeks.

She walked with a normal gait. She could also walk normally on tiptoes and heels, but when she walked on her tiptoes, there was obvious right calf muscle atrophy. The ankle was moderately swollen, with soft tissue swelling over the anterior talofibular ligament and an ankle effusion. There was no tenderness. The ankle and subtalar joints had full range of motion and the ligaments were stable. She had significant evertor muscle weakness on the right. Skin color, distal circulation, and sensation were intact. X-rays of the ankle were unremarkable.

Susan was fitted with an appropriately sized air stirrup brace (Aircast) that she could lock into a sneaker, so subtalar joint motion was minimized. She began formal physical therapy, with a home program and exercises in a therapy facility. When she returned a month later for a follow-up visit, there was still mild swelling in the region of the anterior talofibular ligament. Her right calf muscles now were almost as developed as the left, and she had only mild evertor weakness. Out of the brace, she could balance almost as well on her right foot as her left, but when she tried to hop, there was still a difference.

She was instructed to continue with her home exercise program. She was allowed to resume working at a sports training facility, wearing the brace for cutting, pivoting, and jumping activities. Six weeks later, Susan still had intermittent, slight swelling over the anterior talofibular ligament, but even out of the brace she felt entirely stable with cutting and pivoting, and her orthopaedist could find no weakness or other asymmetry. She wore a performance-type ankle brace (e.g. AirSport, McDavid) for basketball camp that summer.

Discussion: The most frequently identified cause of an ankle sprain is an incompletely rehabilitated previous ankle or foot injury. Even several years following an unrehabilitated injury, weakness and atrophy may persist. Often, balance and proprioception have not completely recovered.

If an injury has been severe enough that the child required crutches even for a few days, then limped for a few days more, enough muscle could have atrophied to be clinically significant and possibly lead to recurrent injury. It is important to observe muscle size and shape of both the lower legs and the feet to make certain that full rehabilitation has occurred. This can be tested readily by having a young athlete walk away from the examiner on tiptoes and then walk back to the examiner on the heels, taking tiny steps so the muscle contour can be evaluated. Then, if repeated hopping on one foot is also bilaterally symmetric, there is good evidence that functional recovery has been completed.

These are quick tests that easily can be incorporated into the sports preparticipation physical examination. A more thorough examination would include manual muscle testing of each of the major muscle groups around the foot and ankle to make sure normal strength has been attained.

References and Suggested Readings
McHugh MP, Tyler TF, Tetro DT, Mullaney MJ, Nicholas SJ. Risk factors for noncontact ankle sprains in high school athletes: the role of hip strength and balance ability.
Am J Sports Med. 2006 Mar; 34(3):464-70.

Tyler TF, McHugh MP, Mirabella MR, Mullaney MJ, Nicholas SJ. Risk factors for noncontact ankle sprains in high school football players: the role of previous ankle sprains and body mass index.
Am J Sports Med. 2006 Mar; 34(3):471-5.

McGuine TA, Greene JJ, Best T, Leverson G. Balance as a predictor of ankle injuries in high school basketball players.
Clin J Sport Med. 2000 Oct; 10(4):239-44.

Young Passengers at Risk

Flaura KoplinWinston, MD, PhD

A 14-year-old high school freshman calls home before her afternoon soccer practice and tells her mother not to bother picking her up afterward — a group of players are going out for pizza, and then a sophomore teammate will bring her home. The mother is somewhat concerned because the 16-year-old only recently received her driver’s license. Still, the 2 families are friendly, and the mother knows the driver to be a responsible girl.

Discussion: Long before child passengers ever receive a learner’s permit, they begin to exhibit a pattern that looks like the high fatality rates exhibited by teen drivers. Child passengers ages 12 to 17 are more likely to die in a car crash than younger children, according to recent research from The Children’s Hospital of Philadelphia’s Center for Injury Research and Prevention. This risk increases with each teenage year.

Researchers examined 45,560 crashes involving 8- to 17-year-old passengers. Between 2000 and 2005, 9,807 passengers in this age group died in crashes. There was a clear tipping point between ages 12 and 14, where child passengers became far more likely to die in a crash than their younger counterparts.

Of the nearly 10,000 passenger deaths studied, more than half (54.4%) were riding with a driver under age 20; nearly two-thirds were unrestrained; and more than three-quarters of the crashes occurred on roads with posted speed limits above 45 miles-per-hour. Alcohol was also a factor in one-fifth of the fatal crashes. Previous research has shown that as children grow into adolescence, they are more likely to ride in cars with drivers other than their parents, such as classmates, friends, or older siblings.

After controlling for many factors, researchers found key predictors that pose the greatest risk to older child passengers. Knowing the risks allows families to make smart decisions about which rides are safe and which should be off-limits. The 3 biggest factors that contribute to an older child being killed in a car crash are riding with drivers younger than 16 years old, not wearing seat belts, and riding on higher-speed roads. Physicians should start communicating with families about child passenger safety when patients are around age 11, and even earlier if families have older children. (See box.)

Changes in policy, coupled with enforcement, can help to protect teen drivers and their passengers. Optimal graduated driver licensing laws that emphasize a lengthened learner's phase beginning at age 16, as well as nighttime driving and passenger restrictions during the intermediate phase, can help reduce the risk for teens. Primary seat belt laws for all occupants to at least age 18 are also recommended.

Parents, the medical community, and society at large should not accept teen crash deaths as random accidents. These deaths are preventable. Physicians can help develop a culture of safe, smart passengers by providing guidance and reinforcing safe behaviors throughout the teen years.

References and Suggested Readings
For more information to find additional tips for driver and passenger safety, parents can visit http://www.chop.edu/youngdrivers to download a “Teaching Your Teen to Be a Smart Passenger” tip sheet and for video associated with this research.

sResidents’ Corner

C. Jasmine Karalakulasingam, MD

Seeing Stars

A 15-year-old boy comes to your office 2 days after being struck by another player during a football game. He denied loss of consciousness at the time but saw “stars” upon impact, was lightheaded, and had 1 episode of emesis. He was evaluated in the ED, had a negative head CT, and was sent home. He notes mild headaches. His vitals and physical exam are normal, and he is asking your permission to continue playing football.

Discussion: Given the patient’s history and symptoms, he likely has had a concussion, also known as a mild traumatic brain injury (MTBI). MTBI can be caused by a direct blow to the head, or more often an impact that causes a rotational injury to the brain. It is characterized by an acute impairment of neurologic function, which has grossly normal neuroimaging studies and usually resolves spontaneously. Acute symptoms may include loss of consciousness, headache, dizziness, and nausea; and vision, memory, or balance complaints. Red flags include a history of multiple concussions, worsening or prolonged symptoms, or focal neurologic deficits.

Girls are more likely to get injured over boys, as decreased neck muscle strength increases the risk of MBTI. However, boys are more likely to play sports in which they may suffer a concussion. Children and adolescents take longer to recover from MTBI than adults.

MTBI is thought to be due to a mismatch between increased glucose needs by the brain and decreased blood flow to the brain, which slows healing. The idea of treatment — both cognitive and physical rest —is to protect the brain in its vulnerable state, as injured brains are susceptible to more permanent damage if reinjured. Patients should sit out of both school and exercise, and return to play in a graded fashion as the brain heals and symptoms completely resolve. As it is difficult to document complete brain healing, neurocognitive testing may help determine whether an athlete is ready to return to the field. Such testing is done at many sites, including the Sports Medicine and Performance Center at the CHOP Satellite Office in King of Prussia, Pa.

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