A targeted noise reduction observational study for reducing noise in a neonatal intensive unit.

BACKGROUND: Excessive noise in neonatal intensive care units (NICUs) can interfere with infants' growth, development and healing.Local problem:Sound levels in our NICUs exceeded the recommended levels by the World Health Organization. METHODS: We implemented a noise reduction strategy in an urban, tertiary academic medical center NICU that included baseline noise measurements. We conducted a survey involving staff and visitors regarding their opinions and perceptions of noise levels in the NICU. Ongoing feedback to staff after each measurement cycle was provided to improve awareness, engagement and adherence with noise reduction strategies. After widespread discussion with active clinician involvement, consensus building and iterative testing, changes were implemented including: lowering of equipment alarm sounds, designated 'quiet times' and implementing a customized education program for staff. INTERVENTIONS: A multiphase noise reduction quality improvement (QI) intervention to reduce ambient sound levels in a patient care room in our NICUs by 3 dB (20%) over 18 months. RESULTS: The noise in the NICU was reduced by 3 dB from baseline. Mean (s.d.) baseline, phase 2, 3 and 4 noise levels in the two NICUs were: LAeq: 57.0 (0.84), 56.8 (1.6), 55.3 (1.9) and 54.5 (2.6) dB, respectively (P<0.01). Adherence with the planned process measure of 'quiet times' was >90%. CONCLUSIONS: Implementing a multipronged QI initiative resulted in significant noise level reduction in two multipod NICUs. It is feasible to reduce noise levels if QI interventions are coupled with active engagement of the clinical staff and following continuous process of improvement methods, measurements and protocols.

Methylxanthines do not affect rhythmogenic preBötC inspiratory network activity but impair bursting of preBötC-driven motoneurons.

Clinical stimulation of preterm infant breathing with methylxanthines like caffeine and theophylline can evoke seizures. It is unknown whether underlying neuronal hyperexcitability involves the rhythmogenic inspiratory active pre-Bötzinger complex (preBötC) in the brainstem or preBötC-driven motor networks. Inspiratory-related preBötC interneuronal plus spinal (cervical/phrenic) or cranial hypoglossal (XII) motoneuronal bursting was studied in newborn rat en bloc brainstem-spinal cords and brainstem slices, respectively. Non-respiratory bursting perturbed inspiratory cervical nerve activity in en bloc models at >0.25mM theophylline or caffeine. Rhythm in the exposed preBötC of transected en bloc preparations was less perturbed by 10mM theophylline than cervical root bursting which was more affected than phrenic nerve activity. In the preBötC of slices, even 10mM methylxanthine did not evoke seizure-like bursting whereas >1mM masked XII rhythm via large amplitude 1-10Hz oscillations. Blocking A-type γ-aminobutyric (GABAA) receptors evoked seizure-like cervical activity whereas in slices neither XII nor preBötC rhythm was disrupted. Methylxanthines (2.5-10mM), but not blockade of adenosine receptors, phosphodiesterase-4 or the sarcoplasmatic/endoplasmatic reticulum ATPase countered inspiratory depression by muscimol-evoked GABAA receptor activation that was associated with a hyperpolarization and input resistance decrease silencing preBötC neurons in slices. The latter blockers did neither affect preBötC or cranial/spinal motor network bursting nor evoke seizure-like activity or mask corresponding methylxanthine-evoked discharges. Our findings show that methylxanthine-evoked hyperexcitability originates from motor networks, leaving preBötC activity largely unaffected, and suggest that GABAA receptors contribute to methylxanthine-evoked seizure-like perturbation of spinal motoneurons whereas non-respiratory XII motoneuron oscillations are of different origin.