Parent satisfaction with acute pediatric pain treatment at home.

OBJECTIVES: Outpatient pain management after acute injuries is an important part of emergency department (ED) care, but there is little evidence to support best practice. Satisfaction with care is one way to assess the effectiveness of current practice. This study describes the outpatient pain experience for children with an arm fracture and explores the variables associated with parents' dissatisfaction with pain treatment for 2 analgesics after ED care. METHODS: As a part of a randomized clinical trial assessing pain treatment after an arm fracture, parents and their children completed daily diaries recording pain scores, function disruption (play, school, sleep, eating), and adverse effects for 3 days after discharge from the ED. Parents and children also completed the Total Quality Pain Management Instrument on the third day to assess pain experience. Parents' satisfaction was defined with an arm fracture lowest reported satisfaction during the study period. RESULTS: A total of 244 children with complete diaries were analyzed. More than half of children reported pain at home that was present "all the time" or "quite a bit." Thirty-two percent of parents were not satisfied with home pain treatment for their child. Parents' dissatisfaction was strongly associated with inadequate pain relief. It was also independently associated with nausea, disruption in play and sleep, and increased doses of medication. DISCUSSION: Children with arm fractures experience noteworthy pain in the outpatient setting. Parents' dissatisfaction with home pain management for children suggests that more research is needed to evaluate the factors that result in improvements in both parent and child satisfaction and the most effective way of producing those changes.

The endoplasmic reticulum stress response factor CHOP-10 protects against hypoxia-induced neuronal death.

Hypoxia-induced gene expression is a critical determinant of neuron survival after stroke. Understanding the cell autonomous genetic program controlling adaptive and pathological transcription could have important therapeutic implications. To identify the factors that modulate delayed neuronal apoptosis after hypoxic injury, we developed an in vitro culture model that recapitulates these divergent responses and characterized the sequence of gene expression changes using microarrays. Hypoxia induced a disproportionate number of bZIP transcription factors and related targets involved in the endoplasmic reticulum stress response. Although the temporal and spatial aspects of ATF4 expression correlated with neuron loss, our results did not support the anticipated pathological role for delayed CHOP expression. Rather, CHOP deletion enhanced neuronal susceptibility to both hypoxic and thapsigargin-mediated injury and attenuated brain-derived neurotrophic factor-induced neuroprotection. Also, enforced expression of CHOP prior to the onset of hypoxia protected wild-type cultures against subsequent injury. Collectively, these findings indicate CHOP serves a more complex role in the neuronal response to hypoxic stress with involvement in both ischemic preconditioning and delayed neuroprotection.