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Oxygenation response to NO in newborns with severe pulmonary hypertension

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S S j c a k u m a r B. Reddy V. Absorption o f labelled vitamin A in childi-en during infection. Hr J N u t r 1972: 27: 299-304

6. Hunie E M . Ki-cbs H A . Vitamin A requirement of h u m a n adults: an experimental study of vitamin A deprivation in inan. M R C Spec Rep 1949: 264: I - 145

Received Jan. 5 , 1996. Accepted i n revised form J L I I K 27. I996

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F~rc~rtltjr, Lkptrrrr77cwr 0 / Pucv/itr/ric,s. Oh500 H ~ w i ~ l i ~ r , A / / / i t / r ( / , 7 i / r / < c i ,

Oxygenation response to NO in newborns with

se ve re p ulm

o

nary hyper t e n s

i o

n

Sir,

We read with interest the article by Turbow et al. in

which a sub-group of infants (6 out of 13) with severe

persi s t e n t p u lin on a r y hypertension of the new born

( P P H N ) presented an improvement in oxygenation beyond a 30 min exposure period to inhaled nitric

oxide (NO). They suggested that the clinical challenge

was to identify these infants, since the response time to

NO inhalation is multifactorial and dependent on the

disease process associated with PPHN (1).

Our protocol includes the evaluation of the response to

NO at 6 h of therapy before considering other alterna-

tive treatments such as extracorporeal membrane oxy- genation (ECMO). I n 16 consecutive neonates (median gestational age 38 weeks, range 27-41; median birth- weight 2530g, range 550--4100) with P P H N , N O (mean 12.3 parts per million, range 5-40) caused an overall

significant decrease in mean oxygenation index (OI),

f r o m 7 4 ( r a n g e 2 7 ~ - 1 3 l ) t o 4 2 ( l l - l 2 7 ) ; p

<

0.04. How-

ever, the oxygenation improvement markedly varied in relation to the underlying disease associated with

PPHN: in the group of patients with asphyxia or

sepsis (n.6) mean 01 significantly decreased, from 87

(40-131) to 16 ( I 1-35) ( p

<

0.03); 0 1 moderately

improved in premature patients with hyaline membrane

disease ( / I = 6), from 56 (27-72) to 40 (16-80)

( p = NS); however, in newborn infants with pulmonary

hypoplasia (congenital diaphragmatic hernia, n = 3,

and oligohydramnios, n = 1 ) 0 1 worsened from 83

(72-91) to 100 (62-127) and this group of patients

also showed no response to N O inhalation 30min

after onset of therapy, three of them undergoing ECMO.

Since N O enhances oxygenation by a selective

pulmonary vasodilation (2) and an improvement in

ventilntion-perfusion matching ( 3 ) , we suggest that alveolar diseases, with collapsed and non-ventilated

regions may limit inhaled NO to reach blood vessels in

thcse terminal lung units, thus blunting its potential

eflect, whereas a scarce response to N O treatment in

patients with severe bilateral hypoplastic lungs could be

related to an early arrest in the development o f their

peripheral vascular and bronchial tree, associated with

surfactant deficiency (4, 5 ) .

In agreement with Turbow et al. we believe that some

infants may benefit from a trial of NO therapy that

exceeds 30 min since the response to NO treatment is

multifactorial and dependent on the disease process. Nevertheless, infants with pulmonary hypoplasia

could represent a distinct clinical sub-group of non-

responders, early identifiable after onset of NO inhala-

tion. In fact, in our series of early non-responders, 2

RDS infants out of 3 showed an 01 improvement 6 h

later, while the remaining 4 patients with PPHN secondary to hypoplastic lung persisted hypoxic.

The exact reasons for this lack of acute response are

still controversial. However, our data suggest that the absence of an acute N O response in this specific struc- tural pulmonary disease may be an early predictor of poor outcome, prompting alternative treatments.

References

I . Turbow R, WafTarn F, Yang L, Sills J. Hallman M . Variable oxygenation response t o inhaled niti-ic oxide in secere persistent pulmonary hypertension of the newborn. Acta Pnediatr I995:84: 1305-8

2. Roberts JD. Polaner DM. Lang P. Zapnl W M . Inhaled nitric ouide in persistent pulmonary hypcrtenuon 01' the newborn. Lancet

I992;340:8 18 9

3. Roissanl R. Falke K J , Lopaz F. Slania K. Pison U . Zapol W M . Inhaled nitric oxide lor the adult respiratoi-y disti-css s) ndrome. N Engl J Med 1993;328:399 405

4. Bohn D, Taniura M , Perrin D, Barker G, Rabinocitch M . Venti- latory predictors of pulmonary hypoplasia in congenital diaphrng- inatic hernia, confirmed by morphologic iisscssnient. J Pcdiatr l987;l I l:423 31

5 . Karanianoukian HL. Glick PL, Zayek M. Steinhorn RH. Zwass MS. Fineman J R , Morin FC. Inhaled nitric oxide in congenital hypoplasia of the lungs d u e to diaphragmatic hcrnia o r oligo- hydramnios. Pediatrics 1994:94:715 8

I1 Tr~i.s(7riu/o, P F ~ r t / r ~ , P Bihtrir. P C ' t ~ 7 r t ~ w / ; , I ' A U I U ~ ~ / I I , Dcpoi'rriicrit of Pctlir/trics. Ptrdirtr liriiwi,.\i/J., l'iri G i i / . s / i / i m i i . 3 . 3.7 I AS

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