In this issue of JNN, Letzkus and colleagues1 report the findings of a pilot study conducted among children to explore the environmental nociceptive stimuli that could hinder recovery of paroxysmal sympathetic hyperactivity (PSH) after severe brain injury. The authors have identified this study as the first to explore potential contributing environmental factors in children who develop PSH, and thus, this article is a great resource for critical care pediatric nurses.

Study Purpose

The purpose of this study was to identify environmental nociceptive stimuli that could impact recovery of children who experience PSH after brain injury.

Significance

Paroxysmal sympathetic hyperactivity presents with autonomic instability such as recurrent hyperthermia, hypertension, tachypnea, tachycardia, diaphoresis, and/or dystonia in individuals after brain injury. This condition is associated with poor recovery, higher morbidity, healthcare costs, longer hospitalization, and rehabilitation length. Although studies have reported the outcomes of PSH, no study has explored potential contributing environmental nociceptive factors in children who develop PSH.

Developmental care that includes interventions such as reducing noise and light, minimal handling, and promoting rest is designed to allow optimal neuroprotection during a vulnerable period of brain development. Noxious environmental stimuli such as noise, bright lights, and frequent disruptions are less conducive for healing.

Method

Children were recruited from a level 1 trauma center in a tertiary academic center in central Virginia. Children included in the study were younger than 18 years, had experienced severe brain injury with traumatic or nontraumatic etiology, and had not regained consciousness. A PSH episode was defined as a cluster of symptoms, which include hyperthermia without a source of infection, hypertension, tachycardia, tachypnea (based on age-appropriate vital sign parameters), diaphoresis, and/or dystonia.

The study used a naturalistic prospective mixed-method design. Demographic data were obtained from medical records. The team developed an environmental assessment form, which was completed daily over a period of 7 days when a child met inclusion criteria. An additional environmental assessment was conducted if a child experienced PSH symptoms. The Pyle photometer light meter was used to measure light, and a Plusbuyer phonometer was used to obtain sound levels. Semistructured interviews were conducted among 2 caregivers, and informal interviews were performed with 7 nurses of children experiencing PSH. Nonparticipant observation field notes describing observations of surrounding, interactions among families and caregivers, and pertinent information related to the physical environment were documented.

Analysis

Environmental variables were analyzed using descriptive statistics. [chi]² Tests were used to compare percentages of PSH across levels of environment variable. Qualitative data underwent thematic analysis.

Results

Eight children between the ages of 5 weeks and 13 years were enrolled in the study. Paroxysmal sympathetic hyperactivity events were captured on 3 subjects. Two environmental factors such as lower room temperature (P = .002) and blanket application (P = .009) were associated with PSH. Although noise levels exceeded the US Environmental Protection Agency recommendation, it was not associated with PSH events. The light levels were within reference limits. The findings note opportunities to standardized noise and light levels. The 3 themes that were related to potential triggers of PSH included auditory stimuli, tactile stimuli, and visual stimuli.

Implications

This pilot study demonstrates evidence of potential impact of environmental factors on PSH. Ensuring that the physical environment is conducive for recovery should be considered a nursing priority when caring for children who have experienced brain injury.

Reference