الفهرس 
coverOnly 14 pages are availabe for public view
 |  | from | 143 |  |  |
| | | from | 143 | | |
Abstract
Bronchopulmonary dysplasia continues to be an important problem in premature infants despite improved facilities of care, monitoring and treatment. The etiology of BPD is still unknown but large number of factors is suggested to be involved in the development of the disease and thought to be of multifactorial origin of which oxygen is one factor.
This prospective study presents some possible risk factors for BPD development. The study population consisted of 50 preterm infants admitted to NICU, Obstetric & Gynecology hospital, Ain Shams University from May 2009 to May 2010 with gestational age equal to or less than 32 weeks and need to oxygen support.
Enteral feeding, Fluid intake and total calories were also recorded.
Serum electrolytes levels were recorded.
Blood gases and acidosis were recorded.
Respiratory data was recorded; mode of assisted ventilation, pressure, mean Fio2, flow rate, PIP, PEEP, Surfactant use was not noted.
Echocardiography for detection of PDA if suggested. Transcranial U/S for detection of intracranial hemorrhage if suggested.
Chest X-ray was done for detection and grading of RDS, detection and staging of bronchopulmonary dysplasia.
Sepsis was diagnosed by using clinical and hematological results.
Respiratory failure scores in 1st day were calculated for mechanically ventilated newborns
The pulmonary score, calculated on 28th day for detection of bronchopulmonary dysplasia severity.
Preterm neonates were followed up in the NICU for development of BPD defined as oxygen therapy ≥ 28 days to maintain an adequate range of oxygen saturation.
Those who did not develop chronic lung disease were included in group I(completely cured ), they were 21 neonate, their mean birth weight was 1.379 ±0.167 (kgm), male/female was 3/18 and mean gestational age was 30.95 ±1.12 (weeks).
While those who developed bronchopulmonary dysplasia were included in group II (cured with BPD), they were 16 neonates, mean birth weight was 1.249±0.246 (kgm), male/female was 9/7 and mean gestational age was 29.50 ±2.191 (weeks).
Those who died were included in group III (non survivors), they were 13 neonates, mean birth weight was 1.202 ±0.305 (kgm), male/female was 8/5 and mean gestational age was 30.00 ±2.160 (weeks).
The results showed that:
• Group I 21 neonates didn’t develop BPD and survived (100%). Group II 16 neonates developed BPD (32%) needed specific intervention and group III13 infants died (26 %).
• There was significant association between BPD and gestational age. Obviously, the more immature infants, the higher risk for BPD.
• There was significant association between BPD and increased CPAP-Fio2 and CPAP duration.
• There was significant association between BPD and high IMV-Fio2, IMV rate and IMV duration
• There was significant association between BPD and PDA.
• There was significant association between BPD and increased blood products transfusion, decreased caloric intake and late sepsis.
• There was significant association between BPD and positive C-reactive protein.
• There was significant association between BPD and increased total fluid intake.
• There was significant association between BPD and acidosis on 7th day.
• Unvaried analysis showed no significant association between BPD and early sepsis, blood gases, mode of delivery, sex, maternal DM, maternal infection, preclamsia, PROM, antepartum Hge, serum Na, serum K.
• Higher respiratory failure scores in 1st day were significantly associated with BPD development.
• The pulmonary score calculated on 28th day reflects BPD severity.
The pulmonary score calculated on 28th day had a positive correlation with IMV-PIP.