Ventilation with an inappropriate tidal volume (Vt) triggers lung inflammation, an important predisposing factor of bronchopulmonary dysplasia. It still remains uncertain what the appropriate starting target Vt should be during the acute phase of respiratory distress syndrome (RDS). Our aim was to evaluate lung inflammation in preterm infants undergoing synchronized intermittent positive-pressure ventilation (SIPPV) with two different tidal volumes Vt during the acute phase of RDS. Thirty preterm infants (gestational age, 25-32 weeks) with acute RDS were randomly assigned to be ventilated with Vt = 5 ml/kg (n = 15) or Vt = 3 ml/kg (n = 15). Proinflammatory cytokines (interleukin-6 (IL-6), interleukin-8 (IL-8), and tumor necrosis factor (TNF)-alpha) were determined in the tracheal aspirate on days 1, 3, and 7 of life. IL-8 and TNF-alpha levels collected on day 7 were significantly higher (P < 0.05), and mechanical ventilation lasted longer in the group with Vt = 3 ml/kg (16.8 +/- 4 vs. 9.2 +/- 4 days; P = 0.05). In conclusion, our data show significantly higher lung inflammation in preterm infants ventilated with Vt = 3 ml/kg, suggesting a role for Vt = 5 ml/kg in reducing both inflammatory response during the acute phase of RDS and the length of ventilation. Whether the use of this starting Vt prevents bronchopulmonary dysplasia requires further study.
Volutrauma and pulmonary inflammation are thought to be the most important predisposing factors of chronic lung disease (CLD), a major complication of prematurity. A new option in patient-triggered ventilation (PTV), the volume guarantee (VG), a volume-targeted ventilation, seems to be a promising approach in reducing the risk of CLD, by limiting lung inflammatory injury and volutrauma. Our aim was to evaluate lung inflammatory response in preterm infants with respiratory distress syndrome (RDS), mechanically ventilated with and without VG, as measured by proinflammatory cytokines (IL-6, IL-8, and TNF-alpha) in tracheobronchial aspirate (TA) fluid. Fifty-three preterm infants (GA = 25-32 weeks) with RDS were randomized at birth to be ventilated using pressure support ventilation (PSV) with VG (Vt = 5 ml/kg) (n = 30) and without VG (n = 23) (Draeger Babylog 8000 Plus, 5.n). IL-6, IL-8, and TNF-alpha were determined by ELISA in TA samples on days 1, 3, and 7 of life. We observed a significant difference (ANOVA) in IL-8 and IL-6 levels on day 3 between the two groups (P < 0.05), and an increasing significative trend in IL-8 values in PSV group (P < 0.05). Mechanical ventilation lasted longer in the PSV group (12.3 +/- 3 vs. 8.8 +/- 3 days) (P = no significance). In conclusion, these preliminary data suggest a role for volume-targeted ventilatory strategy in reducing acute inflammatory response in preterm infants with RDS. Further studies are required in order to define whether this ventilatory strategy prevents lung injury.
Background: Perinatal asphyxia remains one of the most devastating neurologic processes. There is experimental and clinical evidence that cerebral cooling may suppress the biochemical cascades leading to delayed cerebral damage. Objective: To determine if hypothermia started soon after delivery reduces cerebral damage in term infants. Design/Methods: Retrospective chart analysis with historical controls. Ten asphyxiated newborns treated with hypothermia between October 1998 and October 1999 were compared to 11 asphyxiated newborns admitted from September 1997 to September 1998. Characteristics at birth of infants of the two groups (control and hypothermia) were comparable. After obtaining parental consent, whole-body hypothermia was induced before the 6th hour of life by placing a cold blanket (Polar Air, Augustine Medical Inc., model 600) around the body of the patients. Rectal temperature was maintained between 32 and 34°C for 72 h. Outcome was assessed by neurological evaluation at birth and every 3 months up to the 12th month. Brain MRI was performed in the 2nd month. We had no evidence of severe adverse events related to hypothermia. In the hypothermic group there was a significant (p < 0.05) reduction of major neurologic abnormalities at follow-up and abnormal MRI findings. Conclusions: Hypothermia appears to be safe. Our results on morphological damage evaluated by brain MRI and neurological outcome are encouraging: randomized controlled trials are needed to confirm this experience.
Background: Several studies have demonstrated the efficiency and safety of mild hypothermia (33°C) used for treating moderate encephalopathy. In animal models, deep hypothermia proved to be neuroprotective. Objectives: To determine the safety of whole-body deep hypothermia between 30 and 33°C in moderate-severe hypoxic-ischemic encephalopathy in newborn term infants. Methods: Mortality rates, incidence of brain damage detected by magnetic resonance imaging (MRI) and neurological outcomes of 39 term asphyxiated infants were retrospectively compared. A first group of patients (control group C) was treated with routine standard methods, a second group (MH) was treated with mild whole-body hypothermia (32–34°C) and a third group (DH) was treated with deep whole-body hypothermia (30–33°C), for 72 h. Mean arterial pH, basic excess (BE) and lactic acid in the blood were measured. Laboratory and clinical side effects of hypothermia were investigated. A conventional brain MRI was performed after the second week of life. Results: 39 term asphyxiated newborns were enrolled in the study: 11 in group C, 10 in group MH, and 18 in group DH. During the first 72 h, disseminated intravascular coagulation was recorded in 2 cases (18%) in group C, pulmonary hypertension in 2 patients (20%) in group MH, and pneumonia in 3 cases (16%) in group DH. Severe cerebral lesions and poor neurological outcome were observed in 4 cases (36%) in group C, 1 case (10%) in group MH, and 1 case (5%) in group DH. A statistically significant difference in brain damage and major clinical neurological abnormalities was observed between group C and groups MH and DH, whereas no differences were demonstrated between asphyxiated infants treated with mild or deep hypothermia. Conclusions: The results support the safety of deep hypothermia. Further studies are needed to confirm these results and the neuroprotective effect of this approach.
Background: Oxygen (O2) plays a critical role in the O2-reduction reactions indispensable for life, but can produce free radicals that are involved in many diseases. Coenzyme Q10 (CoQ10), acting as a redox carrier in the respiratory chain, occupies a central position in the energy metabolism and oxidative defence. Neonates seem to be very subjected to oxidative stress because of their deficient antioxidant systems. Design/Methods: The aim of the study was to verify whether the mode of delivery may affect CoQ10 levels in the mother and neonate, and thus influence the risk of oxidative damage in the newborn. We measured CoQ10 levels in maternal plasma and cord blood at birth after three different modes of delivery (45 term healthy pregnancies): (1) vaginal in room air (VD) (n = 15); (2) elective caesarean section with general anaesthesia (50% O2 and 50% N2O) (CSg) (n = 15), and (3) elective caesarean section with spinal anaesthesia without O2 (CSs) (n = 15). Our results showed higher levels of Q10 in mothers and neonates with VD (1.29 ± 0.43 and 0.15 ± 0.06 µg/ml, respectively) or CSs (1.15 ± 0.28 and 0.24 ± 0.06 µg/ml, respectively) when compared to CSg (0.74 ± 0.28 and 0.07 ± 0.03 µg/ml, respectively) (p < 0.01). Conclusions: These data demonstrate that the mode of delivery may affect CoQ10 levels in mothers and neonates, and thus influence the risk of oxidative damage in the newborn.
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