Perioperative Management and Considerations for Patients With Voltage-Gated Sodium Channel Mutations: A Pediatric Case Report.

A 13-year-old girl with a voltage-gated sodium channel mutation (SCN8A)-associated intractable epilepsy presented for bilateral mastectomy for painful juvenile fibroadenomatosis. Sodium channel mutations are more frequently diagnosed with continued advances in genetic testing. Understanding the effects of sodium channel mutations is important to provide safe anesthetic care to these patients. In this article, we discuss what is known regarding the physiology of SCN8A channels and the anesthetic considerations when caring for patients with an SCN8A mutation.

Aerobic fitness in adolescents with chronic pain or chronic fatigue: parallels and mechanisms?

OBJECTIVE: Chronic fatigue and chronic pain both deter people from participating in exercise, even though exercise is often a key component of treatment. While reasons for this may seem obvious, the extent and mechanism(s) of reduced exercise performance among affected individuals, particularly those with chronic pain, are not well described. We hypothesized that patients with chronic fatigue are more deconditioned than those with chronic pain, due to the nature of their illness or disability. DESIGN: Retrospective chart audit June 2012 to December 2014. SUBJECTS: Adolescents with chronic fatigue (320, 73 males) or chronic pain (158, 30 males). METHODS: Maximal cardiopulmonary exercise test to determine peak oxygen uptake (V̇O2) and work efficiency. RESULTS: Mean (standard deviation (SD)) peakV̇O2 was similar between patients with chronic fatigue and chronic pain: males 36.5 (SD 8.3) vs 34.2 (SD 7.3) ml/kg/min (p = 0.17); females 27.3 (SD 6.1) vs 27.6 (SD 6.6) ml/kg/min (p = 0.67). PeakV̇O2 was < 90% predicted in 80% and 75% of females, or 77% and 83% of males, with chronic fatigue and chronic pain, respectively. Peak O2pulse and work efficiency were likewise similar. CONCLUSION: Patients in both groups manifest exercise responses typical of cardiopulmonary deconditioning and to similar extent. Failure to detect unique cardiopulmonary or muscle pathophysiology suggests a shared pathway to low aerobic work capacity.