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BL is a neonate born at 24 weeks gestation
to a 33-year-old mother, who had one previous pregnancy but
no live births. Eighteen weeks into this pregnancy she experienced
a spontaneous premature rupture of the membranes with clear
fluid. In the 45 days preceding the delivery, BL's mother
was put on antibiotics to prevent and control infections,
bed rest and magnesium sulfate to reduce the risk of premature
labor, and dexamethasone to accelerate maturation of the fetal
lungs and decrease the incidence of neonatal respiratory distress
BL was delivered vaginally with a breech
presentation. After delivery he was placed in a radiant
warmer and resuscitation efforts were begun. He showed no
signs of respiratory effort; heart rate was 100 after 30
seconds; and he had central cyanosis. He was intubated with
a size 2.5 mm endotracheal tube. Paradoxical chest movement
and poor gas exchange were noted with bagging. Apgar scores
were: 1 after 1 minute, 4 after 5 minutes, and 5 after 10
minutes. At this point, he was transported to the neonatal
intensive care unit and placed on high frequency ventilation.
Diagnoses were extreme prematurity, RDS, sepsis, and possible
In the NICU, BL was placed on an oscillator.
Initial settings were:
(mean airway pressure)
||12 Hz (720 bpm)
He was given morphine sulfate for sedation.
BL's initial weight was 935 g and his height
was 34.5 cm. His general appearance was lethargic with gasping
and increased respiratory effort. His initial SpO2 levels
were in the 70s and 80s, but eventually climbed into the
90s. His skin showed bruising in the abdominal area with
sores on the chest wall and lower extremities. In addition,
he had a small chin, deviated nose, and low ears. Initial
arterial blood gas results were:
In response, the Paw was increased to 24
and the delta P was increased to 36.
The initial chest radiograph showed good
placement of the ET tube and UAC and UVC lines. It also
showed developing blebs in all lung fields and a possible
pneumomediastinum. In addition, the lungs appeared hyperinflated
with blunted costophrenic angles. The apparent development
of pulmonary interstitial emphysema (PIE) warranted an immediate
response. The settings on the ventilator were changed, decreasing
the delta P from 36 to 15 over approximately one and a half
hours. This resulted in a progressive decrease in pH from
7.11 to 6.97 and an increase in PaCO2 from 92 to 148. However,
the PaO2 increased from 27 to 50 over the same period.
After the last ventilator change, 3.7 mL
of Survanta was instilled via the surfactant port adapter
of the endotracheal tube. An ABG drawn an hour later showed
no improvement. The decision was made to gradually increase
the delta P to 28 and decrease the Paw to 15. Ninety minutes
later the pH had risen to 7.27 and the PaCO2 had decreased
to 69 while the PaO2 held stable. Two hours later, the ABGs
showed even greater improvement. In response, the delta
P was decreased to 26 and the Paw was decreased to 13.5.
An hour after this, the second dose of
Survanta (3.7 mL) was administered via endotracheal tube
without complications. ABGs continued to improve. Seven
hours later the third and final dose of Survanta was given.
A follow up chest radiograph showed much improvement with
no evidence of blebs and a resolving pneumomdediastinum.
Three hours later, the decision was made
to begin weaning down the oxygen. The FiO2 was decreased
from 100% to 50% over a one hour period with good results.
Follow up ABGs were good. In response, the delta P was weaned
to 23. After this, weaning was continued gradually, and
on day three, he was transferred to pressure control ventilation
with a PIP of 20, PEEP of 5, flow of 8, Paw 8, rate 30,
inspiratory time 46%, and FiO2 40%.
At this point, BL's prognosis is good.
The hope is that with proper nutrition, monitoring, and
other treatment, he will be successfully weaned from all
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