Please read the article it isn’t long- the rash (the basis of “the scientist” if that’s even a job role) is what she claims puts into disrepute Dr Lee stating he never saw a case of a rash with an air embolism. The rash was 4 days prior to the babies collapse and resuscitation and it also wasn’t seen at a time that is classed as decompensation. In fact the baby was given fluids and was fine 10 minutes later. The baby was also found to have an air embolism in the heart when he passed 4 days later- how is this an accurate comparison to baby A. Let’s also presume they were obviously accurately monitoring rashes etc- then it backs up what Dr Lee said- there was no rash with the air embolism.
I'm actually very familiar with this article as it was part of a literature review I did for my work last year. The air in his chest was seen on his first day of life, directly following the transient skin discoloration. He stabilized initially but then began to decomoensate after 24 hours. Later imaging was consistent with him having previously experienced air embolism. But he did not die until day of life 3, after suffering a pulmonary hemorrhage. He did not die of air embolism. The air embolism resolved. The damage caused was left behind and that damage is likely what led to his fatal pulmonary hemorrhage.
"Case 1
A male infant with a birth weight of 1 770 g was born by
normal vaginal delivery at 31 weeks' gestation. The infant
manifested significant respiratory distress from birth. Initial
chest radiograph confirmed severe respiratory distress
syndrome (RDS). A peripheral intravenous infusion was
inserted and infusion of Neolyte (Intramed, South Africa) was
initiated. The infant was intubated and transported to the
neonatal intensive care unit for mechanical ventilation. En
route, the infant's skin turned blue-black with blotchy redness.
The feet were extremely pale. The attending physician thought
that this was a 'reaction' to the intravenous fluid and replaced
it with 0.2% saline and glucose 5%. Over the next 10 minutes
central perfusion returned to normal, but the hands and feet
remained bluish. At this time an umbilical venous line was
inserted. No air could be withdrawn. The infant's condition
stabilised. Over the next 4 hours his mean blood pressure
varied between 30 and 48 mmHg and his pulse rate between
150 and 165/min. He received surfactant treatment and routine
intravenous penicillin. An anteroposterior chest radiograph did.
not reveal the classic picture of a pneumothorax or
pneumopericardium. However, an area of hyperlucency was
noted behind/within the left cardiac border (Fig.1). An
anterolateral chest radiograph revealed the presence of air in
the retrosternal area, anterior to the heart, as well as a
hyperlucent area within the heart border. In the retrocardiac
ORIGINAL ARTICLES
Fig. 1. Anteroposterior chest radiograph: No evidence for
pneumothorax or pneumopericardium. An area of hyperlucency is
noted behind/within the left cardiac border.
area a triangular shadow, representing aerated lung or free air,
was present. A diagnosis of a pneumomediastinum and
intracardiac air was entertained. The infant's clinical condition
stabilised, but within 24 hours of birth he developed
generalised myoclonic convulsive movements of all four limbs
and was treated with phenobarbitone. The cranial ultrasound
scan showed striking evidence of cerebral air embolism (Fig. 2),
as manifested by an echogenic density in the right lateral
Fig. 2. Cranial ultrasonography evidence of cerebral air embolisation.
An echo genic density in the right lateral ventricle created acoustic
shadowing with no through transmission.
December 2003, Vol. 93, No. 12 SAMJ
ventricle, which created an acoustic shadow with no through
transmission.' A C-reactive protein and a blood culture were
negative. On day 3 of life, the infant developed generalised
oedema and a metabolic acidosis, followed by a severe acute
pulmonary haemorrhage. Despite extensive resuscitation
efforts the infant died. An autopsy was refused."
