Fever management practices of neuroscience nurses: what has changed?

Current evidence shows that fever and hyperthermia are especially detrimental to patients with neurologic injury, leading to higher rates of mortality, greater disability, and longer lengths of stay. Although clinical practice guidelines exist for ischemic stroke, subarachnoid hemorrhage, and traumatic brain injury, they lack specificity in their recommendations for fever management, making it difficult to formulate appropriate protocols for care. Using survey methods, the aims of this study were to (a) describe how nursing practices for fever management in this population have changed over the last several years, (b) assess if institutional protocols and nursing judgment follow published national guidelines for fever management in neuroscience patients, and (c) explore whether nurse or institutional characteristics influence decision making. Compared with the previous survey administered in 2007, there was a small increase (8%) in respondents reporting having an institutional fever protocol specific to neurologic patients. Temperatures to initiate treatment either based on protocols or nurse determination did not change from the previous survey. However, nurses with specialty certification and/or working in settings with institutional awards (e.g., Magnet status or Stroke Center Designation) initiated therapy at a lower temperature. Oral acetaminophen continues to be the primary choice for fever management, followed by ice packs and fans. This study encourages the development of a stepwise approach to neuro-specific protocols for fever management. Furthermore, it shows the continuing need to promote further education and specialty training among nurses and encourage collaboration with physicians to establish best practices.

The role of norepinephrine in differential response to stress in an animal model of posttraumatic stress disorder.

BACKGROUND: Posttraumatic stress disorder (PTSD) is a prevalent psychiatric disorder precipitated by exposure to extreme traumatic stress. Yet, most individuals exposed to traumatic stress do not develop PTSD and may be considered psychologically resilient. The neural circuits involved in susceptibility or resiliency to PTSD remain unclear, but clinical evidence implicates changes in the noradrenergic system. METHODS: An animal model of PTSD called Traumatic Experience with Reminders of Stress (TERS) was developed by exposing C57BL/6 mice to a single shock (2 mA, 10 sec) followed by exposure to six contextual 1-minute reminders of the shock over a 25-day period. Acoustic startle response (ASR) testing before the shock and after the last reminder allowed experimenters to separate the shocked mice into two cohorts: mice that developed a greatly increased ASR (TERS-susceptible mice) and mice that did not (TERS-resilient mice). RESULTS: Aggressive and social behavioral correlates of PTSD increased in TERS-susceptible mice but not in TERS-resilient mice or control mice. Characterization of c-Fos expression in stress-related brain regions revealed that TERS-susceptible and TERS-resilient mice displayed divergent brain activation following swim stress compared with control mice. Pharmacological activation of noradrenergic inhibitory autoreceptors or blockade of postsynaptic α(1)-adrenoreceptors normalized ASR, aggression, and social interaction in TERS-susceptible mice. The TERS-resilient, but not TERS-susceptible, mice showed a trend toward decreased behavioral responsiveness to noradrenergic autoreceptor blockade compared with control mice. CONCLUSIONS: These data implicate the noradrenergic system as a possible site of pathological and perhaps also adaptive plasticity in response to traumatic stress.