Periodical tracheal aspiration in mechanically ventilated patients is necessary to remove mucus from the airways. In children and adults, this procedure causes transient hypoxemia, which may be prevented by hyperoxia and/or hyperventilation. These findings, however, have not been sufficiently assessed in newborn infants. Thus we investigated the usefulness of hyperoxia and/or hyperventilation as antihypoxemic maneuvers before tracheal aspiration in newborn infants. Our design was a prospective, randomized, multiple crossover study. The setting was the NICU of a third-level pediatric hospital in Mexico City. Patients included 15 newborn infants under mechanical ventilation. Within a 12-hr period, every patient received, in random order, three antihypoxemic maneuvers during 1 min just before tracheal aspiration: hyperoxia (10% increase of baseline FiO2), hyperventilation (50% increase of ventilator cycling rate), or both. Additionally, a control (sham) maneuver was also applied. Pulse oximeter saturation (SpO2) was recorded before and after each antihypoxemic maneuver, and at 0, 15, 30, 60, and 300 sec after tracheal aspiration. Basal values of SpO2 (81.5 +/- 1.5%) increased with all three antihypoxemic maneuvers (SpO2 over 90%, P <0.05 to P <0.01). Immediately after tracheal aspiration a drop in the SpO2 could be detected in all infants. However, patients receiving hyperoxia showed higher SpO2 values (87.1 +/- 1.8%) than those observed with the sham maneuver (76.9 +/- 2.3%, P <0.01). From this point on, all newborn infants in all conditions (even those with sham maneuver) had spontaneous increments of SpO2 that at 300 sec were again higher than their respective basal values (P <0.05 to P <0.0005). At this time, SpO2 values from following the hyperoxia maneuver were still higher than those following the sham maneuver (P <0.05). Our results show that, similar to what occurs at other ages, tracheal aspiration in mechanically ventilated newborn infants causes transient hypoxemia, which can be partially prevented by previous application of antihypoxemic maneuvers, especially hyperoxia.
Serum thyrotrophin (TSH), triiodothyronine (T3) and thyroxine (T4) were measured by radioimmunoassay in 165 boys and 171 girls, clinically healthy, aged 6.1 to 16.0 years with normal weight and height, grouped at 12 months' intervals. The TSH values in boys ranged from 5.0 ± 0.6 to 6.1 ± 0.6 μU/ml without significant age differences. In girls, TSH level was 5.3 ± 0.5 μU/ml at the age of 6.0 to 7.0 and 7.4 ± 0.5 μU/ml at the age of 10.1 to 11.0 (P < 0.001). Girls had higher values than boys from 9.1 to 11.0 years (P < 0.025). In boys the T3 level was 182 ± 10 ng/100 ml at age 6.0 to 7.0 and 230 ± 15 ng/100 ml at age 11.1 to 12.0 (P < 0.025). Girls had higher values from the age of 9.1 on (215 ± 12 ng/100 ml), but after 13.1 years they decreased (P < 0.025). Girls had higher T3 levels than boys at age 10.1 to 11.0 (P < 0.025), but this difference disappeared when T3 concentrations in girls of this age were compared to boys aged 11.1 to 12.0. In boys and girls, T4 levels tended to be lower with increasing age (r = −0.860, P < 0.01) and there was a significant difference between the values seen up to 9.0 years and those after 13.1 years (P < 0.025 − < 0.001). Girls had lower values than boys at the age of 8.1 to 9.0; however, this difference disappeared when girls of this age were compared to boys 9.1 to 10.0 years old. It is concluded that previous to and around puberty initiation in both sexes, there is a rise in T3, followed by a progressive decrease in T4 with a rise in TSH only in girls. These changes occurred one year earlier in girls than in boys. These observations may represent transient adaptation responses to the increasing energy needs during periods of rapid growth.
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