`Volume 129, Number 1
`
`Editorial correspondence
`
`1 8 3
`
`inhaled nitric oxide can cause
`
`Neurodevelopmen’ral outcome in
`
`severe systemic hypotension
`
`To the Editor.-
`
`Inhaled nitric oxide (NO) is a promising and now widely used
`pulmonary vasodilator for neonates with persistent pulmonary
`hypertension of the newborn (PPHN) because of its alleged lack
`of systemic hypotensive side effects.l We describe a term baby
`with PPHN and left ventricular dysfunction caused by birth
`asphyxia, in whom marked systemic hypotension developed after
`exposure to NO. The condition reversed when NO therapy was dis—
`continued.
`
`The baby, born at 38 weeks of gestation, was referred to our in—
`stitution at 5 hours of age for cardiac assessment to exclude cyan—
`otic heart disease. An cchocaidiogram showed a structurally normal
`heart, severe left ventricular dysfunction. and a patent ductus arte-
`riosus (PDA) with bidirectional flow. This suggested that the sys-
`temic perfusion was dependent on the right-to-left shunt through the
`PDA, and therefore the prostaglandin E2 infusion, started at the re—
`ferring hospital, was continued to maintain ductal palency. A dob—
`utaminc infusion was commenced to provide inouopic support to
`the left ventricle.
`
`The baby was given a trial of NO 6 hours later because of wors—
`ening hypoxemia (saturation of arterial oxygen intermittently fall-
`ing to 50%). Exposure to N0 (20 ppm) resulted in an immediate fall
`in the mean systemic arterial blood pressure from 48 to 35 mm Hg,
`which reversed when NO therapy was discontinued. This hypoten-
`sive episode was thought to have been caused by the NOS rovers-
`ing the right-to~left shunt duough the PDA on which the systemic
`circulation depended.
`Thirty hours later, after recovery of left ventricular function
`(clinically and on cchocardiography), a second trial of NO (20 ppm
`for 30 minutes) resulted in a marked improvement in oxygenation,
`from an arterial oxygen tension of 16 to 420 mm Hg without a
`change in the systemic arterial blood pressure. The baby was suc-
`cessfully weaned from N0 during a period of 30 hours, and extu-
`bation was successful 2 days later.
`This case demonstrates that although N0 is a selective pulmonary
`vasodilator, it can nonetheless cause severe systemic hypotension
`in babies with PPHN associated with severe left ventricular
`
`dysfunction. N0 should therefore be administered with caution to
`such babies.
`
`There Henrichsen, Cami Med
`Allan P. Goldman, MRCP
`Duncan J. Mocme, FRCA
`Cardiac Intensive Care Unit,
`
`Great Omtond Street Hospital for Children NHS Trust
`London WCl N 31H, United Kingdom
`9.3373314
`
`extracorporeal membrane
`
`oxygenation survivors
`
`To the Editor:
`
`The long-term outcome for critically ill neonates requiring extra-
`corporeal membrane oxygenation (ECMO) reflects not only the in-
`herent risk of the procedure but also the underlying disease state,
`the aggressive conventional therapy required, and the child’s fain-
`ilyfhome environment. The recent article by Glass et al' has been
`helpful in delineating the 5—year neurodevelopmental outcome for
`ECMO—treated survivors. However, these 103 ECMO-treated sub-
`jects include 61% of discharged survivors, leaving an almost 40%
`of loss-Io—follow-up rate, particularly among those requiring
`extended travel. and hence raising the possibility of selection bias
`along ut'banfrural. or nearidistant lines. Comparison subjects num—
`bered less than one third of study subjects and were not adequately
`matched for a case-control study; notably they had a significantly
`longer gestation with a narrower standard deviation, suggesting that
`the ECMO-trcatcd children had a greater range of gestational age.
`This is particularly important because the authors previously sug-
`gested a possible association between gestational age and outcome.2
`Nonetheless. die report of 42% of nonretarded ECMO-treatcd chil-
`dren at risk of school failure is clinically very imponant.1 The pro—
`portion of reported behavioral concern in this Washington popula-
`tion is high and requires further evaluation. In view of recent reports
`of undetected neurosensory hearing loss after infancy in both
`ECMO survivors and children with persistent pulmonary hyperten-
`sion?" ‘ and the link of undetected hearing loss with poor neurobe—
`havioral performance and school failure, further evaluation of
`childhood hearing should be carried out in fl'iis population.
`We ask the authors of this article, if at all possible, to reanalyze
`their data for the ECMO—treated study group, using famityihome
`environment and underlying respiratory diagnostic variables to
`predict the risk of academic failure. in view of the complexity of
`insults of ECMO—treated survivors, it is strongly recommended that
`subsequent comparisons use a comparable ‘ ‘control’ ’ group of crit—
`ically ill infants not treated with ECMO to assess the safety and ef-
`fectiveness of ECMO therapy. Because most nontrcated ECMO
`candidates do not survive, the choice of control groups is not idea];
`however,
`those with documented hypoxemia are preferable to
`healthy children as control subjects.
`Po-Yr'n Cheating, MBBS, MRCPfUK), DCH
`Charlene M. T. Robertson. MD, FRCPt‘C}
`Neonatal Follow—up Clinic,
`Gtem'ose Rehabilitation Hospital,
`University ofAlberra
`Edmonton, Alberta, Canada
`935173300
`
`REFERENCE
`
`REFERENCES
`
`1. Kinsella IP, Neish SR, Ivy DD, Shaffer E, Abman SH. Clin-
`ical responses to prolonged treatment of persistent pulmonary
`hypertension of the newborn with low doses of inhaled nitric
`oxide. 1 Pediatr 1993;123:103-8.
`
`1. Glass P, Wagner AE. Papero PH, et a]. Neurodevelopmental
`stems at age five years of neonates heated with extracorporeal
`membrane oxygenation. J Pediatr 1995;127:44'l—5'l.
`2. Glass P, Miller M, Short B. Morbidity for survivors of extra-
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