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Since there is no report quantifying vibration imposed upon neonates, we prospectively studied the vibration produced during high frequency ventilation (HFV) and compared it with that during conventional mechanical ventilation (CMV) of studied patients and weight matched controls (±250 g) receiving CMV or breathing spontaneously. A non-invasive accelerometric sensor (Analog Devices ADXL05, Norwood, MA, USA) was placed at the mid sternum or postauricular cranium to measure the linear vibration transmitted to the body and head, respectively (amplitude in time and frequency domains expressed in units of “g”).
From April to October 1998 we enrolled seven neonates treated with HFV (mean (SD) weight 2210 (1680) g, gestation 32 (7) weeks) and 14 weight matched controls (CMV group: n=7, 2100 (1730) g, 31 (8) weeks; spontaneous breathing group: n=7, 2230 (1520) g, 32 (7) weeks). The groups were not different with regard to body weight, length, and head circumference. Neonates received HFV at a frequency of 12 Hz, mean airway pressure of 14 (2) cm H2O, amplitude of 39 (10) cm H2O, and back up CMV at 6 breaths/min. Higher amplitudes of vibration were detected during HFV than during CMV (0.098 (0.026)g v0.017 (0.006)g at the chest and 0.011 (0.003)g v 0.007 (0.001)g at the cranium, p<0.05) in six HFV treated neonates. One HFV treated neonate did not tolerate the switch to CMV. The vibrations at the chest and postauricular cranium in seven HFV treated neonates were higher than those of weight matched controls (fig 1, p=0.001), whereas no significant difference was found between the control groups. A higher amplitude of vibration at the chest was found in neonates with an adverse outcome than in normal survivors (0.136 (0.014)g v 0.087 (0.024)g, respectively), while demographic data and the duration and amplitude of HFV were not different. Interestingly, the vibration at the chest exceeded the limit of whole body vibration in adults (0.05g at 12.5 Hz third octave band for 24 hours per ISO 2631).1 The significance of our observations is not known. While cardiovascular instability is commonly observed in neonates during HFV and has been related to a high lung volume ventilation strategy, cardiovascular effects of vibration have been reported in animal2 and clinical studies.3 We speculate that the vibration during HFV may also contribute to the haemodynamic instability in neonates.
Furthermore, the effect of vibration on the developing brain is uncertain. We do not know whether the vibration will compromise the cerebral haemodynamic stability resulting in adverse neurological outcomes, especially in premature neonates who transmit vibration more efficaciously because of less body mass and fat compared with term neonates. Moreover, the combined effects of vibratory stress and environmental noise may contribute to hearing loss.4
Although no definitive vibration disease has been recognised in neonates, we have demonstrated the inadvertent exposure of neonates to excessive vibration. Research is required to examine the significance of HFV induced vibration and to reduce the vibration without compromising its effectiveness in critically ill neonates.
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