2nd Bengt Robertson Memorial Lecture
Neonatology 2010;97:358–365
formerly Biology of the Neonate
DOI: 10.1159/000297765
Useless Perinatal Therapies
Henry L. Halliday 
Department of Child Health, Queen’s University Belfast and Perinatal Medicine, Royal Maternity Hospital,
Belfast, UK
Key Words
Preterm infants ⴢ Perinatal medicine ⴢ Useless or harmful
therapies ⴢ Oxygen ⴢ Thalidomide ⴢ Chloramphenicol ⴢ
Hexachlorophene ⴢ Sodium bicarbonate ⴢ Benzyl alcohol ⴢ
Thyrotrophin-releasing hormone ⴢ Corticosteroids
Abstract
With respect to Professor Bengt Robertson whose research
studies were very instrumental in the development of one of
the most important and evidence-based therapies in perina-
tal medicine, namely surfactant therapy, I thought it might
be appropriate to review some useless or harmful perinatal
therapies. Although the term ‘neonatology’ has only been in
existence for about 50 years, care of the newborn in the 19th
century was largely provided by nurses and obstetricians. As
an example, Pierre Budin, a Parisian obstetrician, was very
aware of the importance of keeping low birth weight babies
warm. More recently however, a number of useless or harm-
ful practices were adopted by those caring for pregnant
women and their babies. These included uncontrolled oxy-
gen supplementation, inadequate temperature control,
withholding feeds, and various drugs such as thalidomide,
chloramphenicol, hexachlorophene, sodium bicarbonate,
Epsom salts, benzyl alcohol, thyrotrophin-releasing hor-
mone and corticosteroids. Even in the modern age, inappro-
priate therapies have been introduced on the basis of short-
term beneficial outcomes without longer-term evaluation.
Sometimes we are slow to learn the lessons of the past.
Copyright © 2010 S. Karger AG, Basel
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Published online: June 10, 2010
Introduction
Perinatal medicine or more accurately perinatal care
probably had its origins in the 19th century. Neonatal
care, in the 19th and the first half of the 20th centuries,
was largely provided by nurses or obstetricians (also
known as accoucheurs) [1]. The Parisian obstetrician
Pierre Budin cared for newborns at the end of the 19th
century, and by careful observation he noted the impor-
tance of keeping low birth weight babies warm [2].
Throughout the early 20th century, paediatricians took a
greater interest in care of the newborn, both in the USA
[3, 4] and in Europe [5–7]. However, infant mortality be-
gan to decrease in developed countries early in the 20th
century well before recognition of the specialty of neona-
tology [8] and this was achieved by improvements in san-
itation, nutrition and socio-economic status rather than
direct medical care. The term ‘neonatology’ was intro-
duced about 1960 by Alexander Schaffer in the first edi-
tion of his textbook Diseases of the Newborn [9]. The
term ‘perinatal medicine’ was probably first used in the
1960s when the fetus became directly accessible for blood
sampling and the first society for perinatal medicine was
founded in Europe [10]. In the UK a perinatal medicine
group was founded in 1976 by about 20 paediatricians led
by Peter Dunn and in 1981 became a multidisciplinary
association of perinatal medicine [11].
The evolution of neonatology has been extensively re-
viewed recently by Alistair Philip including not only the
successes related to better understanding of thermoregu-
Prof. Henry L. Halliday, MD, FRCPE, FRCP, FRCPCH
Perinatal Medicine, Royal Maternity Hospital
Grosvenor Road, Belfast BT12 6BB (UK)
Tel. +44 2890 633 460, Fax +44 2890 236 203
E-Mail h.halliday @ qub.ac.uk
lation, nutrition, respiratory support, cardiopulmonary
support, infection, regionalisation of care, parent-infant
interaction and jaundice, but also the ‘errors in neonatol-
ogy’ [12]. In this paper I will try to go one step further and
review the useless or harmful therapies used in perinatal/
neonatal medicine in the past 100 years or so. My choice
of useless therapies is rather subjective as a literature
search using these key words, whilst unearthing at least
one important publication [13], generally was unhelpful.
I consulted publications by Bill Silverman [14–16] and
Alex Robertson [17–19] and these provided me with use-
ful suggestions for inclusion in this review. I decided to
present my useless perinatal therapies in roughly chrono-
logical order starting from the early 20th century and I
apologise to those whose favourite ‘useless’ therapy has
been left out.
Uncontrolled Oxygen Supplementation
In 1907, Budin [2] recommended giving oxygen to pre-
mature infants with cyanotic attacks. Prior to this in
1780, Chaussier experimented with oxygen for newborn
infants who failed to establish normal respiration after
birth [16]. Prolonged oxygen therapy was advocated for
treatment of cyanotic attacks in 1923 by Bakwin [20] and
for apnoea and perinatal asphyxia in 1934 by Hess [21].
Bill Silverman has stated that ‘the modern era of treat-
ment (routine prolonged exposure of small premature in-
fants to high concentrations of oxygen) began in earnest
… in 1942’ [16]. In the late 1940s, newly designed incuba-
tors were able to administer high concentrations of oxy-
gen for prolonged periods. Although retrolental fibropla-
sia (RLF, now called retinopathy of prematurity, ROP)
was first reported in 1940 [17], it was not until 1951 that
its link with uncontrolled oxygen supplementation was
first recognised by Mary Crosse in Birmingham [22] and
Kate Campbell in Melbourne [23]. The suggestion of a
link between uncontrolled oxygen supplementation and
RLF remained controversial until 18 neonatal units in the
USA undertook a randomised controlled trial in 1953
comparing routine oxygen (150% for 28 days) with cur-
tailed oxygen (only for cyanosis or respiratory difficulty,
!50% until symptoms resolved) [16]. When the results
were presented in 1954 they showed no appreciable in-
crease in mortality with curtailed oxygen and a two-
thirds reduction in the rate of cicatricial RLF [24]. Unfor-
tunately the results of the Cooperative Study were inter-
preted as showing that !40% oxygen was safe for preterm
infants and Silverman [16] reported that it took a further
Useless Perinatal Therapies
5 years to recognise that this was flawed as infants had
not been enrolled in the study until they were 48 hours
old.
The reduction of oxygen concentrations to !40% was
associated with increased mortality of infants with respi-
ratory distress syndrome (RDS) [25] and an increase in
cerebral palsy in surviving preterm infants [26]. It has
been estimated that ‘each sighted infant gained may have
cost some 16 deaths’ [27]. Fortunately, blood gas monitor-
ing was developed in the 1960s, followed by transcutane-
ous monitoring in the 1970s and the concept of titrating
oxygen supplementation based on need led to a reduction
in RLF in all but the most immature infants. With the
introduction of pulse oximetry in the 1990s and increas-
ing survival of very preterm infants there has been a re-
cent increase in ROP [28]. This has led to the conclusion
that neonatologists still do not know what range of oxy-
gen saturations to target in very preterm infants to ensure
optimal survival without disability and the lowest pos-
sible rate of ROP [16, 29, 30]. Indeed there is emerging
evidence that resuscitation of newborn infants with 100%
oxygen increases the risk of neonatal mortality [31].
Inappropriate Thermal Care of Low Birth Weight
Infants
From 1926 to 1933, Blackfan and Yaglou made serial
observations of body temperature and outcomes of pre-
term infants cared for in the Boston Lying-in Hospital
[32]. They found that poor weight gain and mortality
were reduced when body temperature was stabilised with
careful control of humidity but no relationship between
mortality and specific body temperature was found. This
finding of no mortality difference related to body tem-
perature was probably explained by the postnatal age
(most 115 days) and weight (most 11,500 g) of the babies
studied [17]. However, the authors concluded that ‘the
predisposition to a subnormal temperature, particularly
in infants of the low weight group, is believed to be a char-
acteristic of prematurity which should be preserved. At-
tempts to force the body temperature of small infants to
the supposedly normal level of 98.6 ° F (37.4 ° C) should be
discouraged, as in a number of instances such a practice
has been followed by overheating with its resultant seri-
ous consequences.’ This 1933 paper led to preterm babies
being nursed in inappropriately low environmental tem-
peratures until Richard Day in 1943 [33] and Bill Silver-
man in 1959 [34] put the record straight. Silverman [34]
began a randomised controlled trial of incubator humid-
Neonatology 2010;97:358–365 359
ity and temperature in 1954 and this showed that mortal-
ity rates of infants of !1,000 g birth weight were signifi-
cantly higher when nursed in incubator temperatures of
29 versus 32 ° C (50 vs. 14%). Alex Robertson [17] has stat-
ed that ‘it is impossible to know how many babies died
from inappropriate environmental temperature during
the approximately 50 years before newborn temperature
control physiology was understood’.
Withholding Feeds for Preterm Infants
In the 1940s the fear of aspiration led to the practice of
withholding feeds for 72 hours after birth in both the
USA [35] and the UK [36]. Budin in 1907 [2] and later
Ylppo in Finland and Gleiss in Germany [17] advocated
early feeding with breast milk but they were unfortunate-
ly in a minority. From the 1960s there were concerns that
delayed feeding was associated with an increased risk of
neurodevelopmental problems and cerebral palsy [37]
which may have been due to hypoglycaemia and hyper-
bilirubinaemia [38]. A small randomised trial was not
able to confirm the benefits of early feeding [39] and it
was not until the 1970s that it was accepted as appropriate
for preterm infants. Even in recent times, inadequate ear-
ly nutrition of the very preterm baby has been highlight-
ed as a persistent problem [40, 41]. However, Alex Robert-
son [17] has attributed the remarkable improvements in
neonatal mortality over the last 50 years mostly to ade-
quate nutrition, appropriate temperature control, antibi-
otics and assisted ventilation.
Thalidomide as a Sedative in Pregnancy
Thalidomide was developed as a potential antibiotic in
1954 by a small German drug company but it proved to
have no antibiotic activity or any other effects in several
animal models [15]. The company felt that it could be-
come the ideal ‘non-toxic sedative’ and early in 1955 free
samples were distributed to doctors in Germany and
Switzerland. Later the new drug was prescribed for pre-
vention of seizures although no anticonvulsant effects
had been found in animals; however, the sedative effects
of the drug were confirmed in these patients. In 1957, tha-
lidomide was approved and in Germany was sold over the
counter because it was believed to be very safe. A year
later the drug company wrote to all German physicians
to say that thalidomide was the best sedative drug for
pregnant and nursing mothers [15]. Before long, thalido-
360 Neonatology 2010;97:358–365
mide was being marketed as the drug of choice for morn-
ing sickness and nausea. In 1961 there were reports from
Australia [42] and Germany [43] linking thalidomide to
a marked increase in infants born with a variety of birth
defects including limb reductions such as phocomelia.
The German paediatrician Lenz reported 161 infants
with malformations after thalidomide in pregnancy stat-
ing ‘women who took even 1 tablet of thalidomide be-
tween the 20th and 36th day after conception were at risk
of delivering malformed infants [but] beyond that time
thalidomide caused no deformities at all’ [43].
Thalidomide was withdrawn from the German mar-
ket by the end of 1961 [15] but not before it had been used
by pregnant women in many countries worldwide. It has
been estimated that between 8,000 and 12,000 infants
were born with malformations and of these about 5,000
survived beyond childhood. Perhaps the more remark-
able is that thalidomide has made a comeback as a drug
to successfully treat a variety of inflammatory and im-
mune system disorders, and it has potent effects as an
inhibitor of angiogenesis [44].
Chloramphenicol for Neonates
Chloramphenicol was first marketed in 1949 as the
first available broad spectrum antibiotic [18]. In the
1950s, chloramphenicol was given prophylactically to
newborn infants at risk of infection, for example after
preterm rupture of the membranes [45]. These authors
found that mortality among infants with preterm rupture
of the membranes increased from 29/1,000 to 144/1,000
after prophylaxis with chloramphenicol was introduced.
More than 10% of the infants treated with chloramphen-
icol died with ‘grey sickness’ later to become known as the
grey baby syndrome. At about the same time, Sutherland
[46] reported 3 cases of fatal cardiovascular collapse in
neonates given large doses of chloramphenicol. Later, a
randomised trial of combinations of antibiotics versus
no antibiotics found that mortality in infants of 2,001–
2,500 g increased from 2.5 to 45% when chloramphenicol
was given [47]. The grey baby syndrome developed typi-
cally a few days after the start of chloramphenicol treat-
ment when the infants developed abdominal distension,
pallid cyanosis, cold moist skin and a weak pulse with
death occurring shortly afterwards from cardiovascular
collapse [18]. Once the dose of chloramphenicol was re-
duced from 100–150 to 20–50 mg/kg/day about 1960 the
cases of grey baby syndrome disappeared. The toxicity of
the drug was due to impaired glucuronidation and re-
Halliday
duced renal excretion which allowed the drug to accumu-
late although the precise biochemical mechanism of the
toxicity was never fully explained [48].
Hexachlorophene Bathing of Neonates
Staphylococcal skin colonisation and infection was
managed in neonatal units by prophylactic bathing of
each infant with 3% hexachlorophene after effectiveness
was reported in 1952 [49]. The first report of neurotoxic-
ity of hexachlorophene was in 1959 when an infant devel-
oped seizures after 4 days of treatment [18]. Animal stud-
ies later showed spongy degeneration of the white matter
[50]. In 1971, the American Academy of Pediatrics rec-
ommended that hexachlorophene should not be used for
total body washing of newborn infants [18]. Two years
later an autopsy study from the University of Washington
reported vacuolation of the reticular formation of the
brain in 63% of infants who had been washed 3 or more
times with 3% hexachlorophene and !1% in less exposed
infants [51]. When 3% hexachlorophene was withdrawn
from neonatal care, most units reverted to using triple
dye or other antiseptics for cord care.
Epsom Salt Enemas for Respiratory Distress
Syndrome
In October 1964, at a meeting of the American College
of Pathologists, Stowens reported on the beneficial effects
of Epsom salt enemas to treat RDS [18]. As this was the
year after the death of Patrick Bouvier Kennedy (first son
of President John Kennedy) from RDS, this paper was
widely reported in the lay press; indeed on 22nd October
1964 the New York Times [14] reported on its front page
under the headline Fatal Baby Disease Cured:
Respiratory distress syndrome has been cured by giving Ep-
som salt enemas to 28 premature babies in 5 Louisville hospitals.
RDS must be due to too much water in the body and as it tries to
escape through the lungs the babies suffocate and choke. It is not
yet certain that this theory is correct but it is certain that the treat-
ment works as all 28 babies who were suffocating improved dra-
matically and were normal in an hour or less.
When Stowens [52] published his pathological studies
a year later he gave no objective measures of improvement
in the 28 treated infants. However, he also reported mag-
nesium toxicity in a subsequently treated infant and in
1973 others reported a neonatal death [53]. Epsom salt
enemas continued to be used sporadically in the USA to
Useless Perinatal Therapies
treat babies with RDS until at least the mid-1970s, prompt-
ing Alex Robertson [18] to say ‘there is no way of knowing
how many babies died as a result of treatment with Epsom
salt enemas’.
Sodium Bicarbonate in Neonatal Medicine
Sodium bicarbonate has been used for many years to
treat neonatal cardiac arrest and metabolic acidosis [13].
The rationale for use in cardiac arrest was that acidaemia
impairs myocardial function and reduces the beneficial
effects of epinephrine on blood pressure, heart rate and
cardiac output. Standard teaching has been to correct ac-
idosis with sodium bicarbonate before giving epineph-
rine during cardiopulmonary resuscitation [13]. Howev-
er, doubts about the benefits of sodium bicarbonate in
cardiopulmonary resuscitation were first raised in the
1980s when animal studies showed detrimental effects on
myocardial function [54] and myocardial acidosis was
worsened leading to a reduced likelihood of successful
resuscitation [55]. There has been only one small ran-
domised trial of sodium bicarbonate use in neonates with
birth asphyxia and this found no effect on neonatal mor-
tality or abnormal neurological examination at discharge
[56]. There are no studies in neonates showing either
short-term or long-term benefits of sodium bicarbonate
after cardiac arrest [57].
Metabolic acidosis is relatively common in neonatal
units and in 1963, Usher [58] introduced early intrave-
nous administration of glucose and sodium bicarbonate
infusions for preterm infants with RDS reporting im-
proved survival compared to historical controls. Whilst
this was an advance at the time, Usher [59] later showed
that more rapid infusions of hypertonic solutions of so-
dium bicarbonate increased mortality and intracranial
haemorrhage. A later randomised clinical trial showed
that sodium bicarbonate was no more effective in de-
creasing intracranial haemorrhage and mortality than
glucose and water in preterm infants with acidosis [60].
A Cochrane review found only 2 small randomised trials
and neither reported long-term outcomes [61]. Thus,
there is insufficient evidence to determine if infusions of
sodium bicarbonate reduce morbidity or mortality rates
of preterm infants with metabolic acidosis. Indeed, the
situation may be worse than this as there is evidence that
sodium bicarbonate, especially if given rapidly, will in-
crease rates of intracranial haemorrhage [13, 59] and in
addition have potential adverse effects on the developing
myocardium [13, 62]. Aschner and Poland [13] have con-
Neonatology 2010;97:358–365 361
cluded that ‘despite more than 50 years of experience
with sodium bicarbonate, the data do not support a net
beneficial effect of sodium bicarbonate in infants with
metabolic acidosis’.
Benzyl Alcohol as an Excipient
Normal saline containing 0.9% benzyl alcohol as a
bacteriostatic agent was often used to flush arterial lines
[19]. In 1981 there was a report of 5 preterm infants who
presented with severe metabolic acidosis, renal and he-
patic failure with neurological signs and notably gasping
respirations giving rise to the term ‘gasping syndrome’
[63]. As benzyl alcohol is metabolised to benzoic acid it
was believed that this was responsible for the toxicity as
accumulation occurred due to deficient conjugation of
benzoic acid to hippuric acid prior to excretion by liver
and kidneys [19]. In 1982 the Food and Drugs Adminis-
tration in the USA recommended that flush solutions
should no longer contain benzyl alcohol or any other pre-
servatives and the gasping syndrome disappeared after
this. Whether benzyl alcohol was responsible for in-
creased risks of kernicterus and intraventricular hae-
morrhage [64, 65] remains uncertain but it now seems
strange that it was used as a bacteriostatic agent in the
1980s when concerns about displacement of bilirubin
from albumin were raised 10 years earlier [66]. Benzyl
alcohol is only one of many excipients added to preserve
and stabilise drugs used for the newborn and recently
there have been concerns that we do not fully understand
their effects [67]. In a study from Leicester, infants less
than 30 weeks’ gestation were exposed to over 20 excipi-
ents including ethanol and propylene glycol, chemicals
associated with neurotoxicity, during their stay in neona-
tal intensive care [68].
Prenatal Thyrotrophin-Releasing Hormone for Lung
Maturation
Roger Soll and colleagues [69] have recently noted how
Cochrane reviews have been important in identifying
perinatal interventions that are ineffective or harmful.
They chose prenatal thyrotrophin-releasing hormone
(TRH) for fetal lung maturation as the prime example.
Animal studies suggested that TRH might act synergisti-
cally with corticosteroids to reduce the risk of RDS in
preterm infants and the first trials were encouraging [70].
However, subsequent large Australian [71] and American
362 Neonatology 2010;97:358–365
[72] studies and the Cochrane review [73] did not find
any improvement in neonatal outcomes but did uncover
important short-term and long-term adverse effects. The
ACTOBAT study had found an increased risk for RDS
and need for mechanical ventilation in the TRH-treated
infants [71] and at a 12-month follow-up assessment con-
ducted by maternal questionnaire there was also an in-
creased risk of motor delay and sensory impairment in
these infants [74]. Although the ACTOBAT researchers
cautioned that ‘antenatal TRH should only be used in the
context of a clinical trial’, the findings of the follow-up
study remained controversial largely because of the na-
ture of the assessments used. Subsequently, a Cochrane
review containing data from over 4,600 women treated
with TRH concluded that the treatment (added to corti-
costeroids) did not reduce the risk of RDS or chronic ox-
ygen dependence, and did not improve any of the fetal,
neonatal or childhood outcomes assessed by intention-
to-treat analyses [73]. Indeed, there were adverse out-
comes for both infants (increased need for mechanical
ventilation, lower Apgar scores at 5 min and poorer out-
comes at childhood follow-up) and mothers (nausea,
vomiting, light-headedness and raised blood pressure).
Needless to say, prenatal TRH is no longer used to en-
hance fetal lung maturity.
Postnatal Corticosteroids for Chronic Lung Disease
In contrast to the proven beneficial effects of prenatal
corticosteroid therapy [75], controversy exists over the
risks and benefits of postnatal corticosteroid therapy to
prevent or treat neonatal chronic lung disease [19, 69, 76].
Dexamethasone was first used to treat bronchopulmo-
nary dysplasia (BPD) in the neonatal unit of Georgetown
University Hospital in Washington in 1978 [77]. This was
a small uncontrolled study and it was followed in the
1980s by 2 small randomised controlled trials which used
sequential designs [78, 79]. Only 22 infants in total were
enrolled and both studies were terminated early for ben-
efit when lung disease improved or infants could be
weaned from ventilation [77]. Dexamethasone was used
in very large doses of 0.5 mg/kg/day and this was based
upon better responses in 2 infants compared with a dose
of 0.1 mg/kg/day in one of these trials [78]. The authors
of these 2 trials warned of the dangers of using dexameth-
asone to treat BPD: ‘dexamethasone treatment cannot be
recommended without further study of patient selection,
dosage schedules, short- and long-term side effects, and
mechanisms of its action’ [78] and ‘dexamethasone is,
Halliday
however, a dangerous drug with many side effects. In the
long run, risk and benefit must be carefully balanced, lest
the cure be worse than the disease’ [79].
Unfortunately, the cautions given by these authors
went largely unheeded and dexamethasone continued to
be used to prevent and treat BPD albeit mainly in further
randomised controlled trials [80, 81]. By late 1998 over
4,000 preterm infants had been enrolled in randomised
controlled trials of dexamethasone and 29% of very low
birth weight infants in the Vermont-Oxford Network re-
ceived the drug [69]. The situation changed following
publication of Tsu Yeh’s 2-year follow-up study of infants
enrolled in a large randomised trial of a 4-week course of
dexamethasone to prevent BPD [82]. Yeh and his col-
leagues reported that dexamethasone-treated infants had
a significantly higher incidence of neuromotor dysfunc-
tion and lower psychomotor development index scores
than control infants. However, this study did not have a
major impact perhaps because it was published in an elec-
tronic format, and it was not until 2 further follow-up
studies were published in 1999 and 2000 that clinicians
began to seriously worry about the adverse long-term ef-
fects of early dexamethasone therapy [77]. Soll and col-
leagues [69] stated that ‘the use of postnatal corticoste-
roids decreased dramatically since the findings of the Co-
chrane reviews were disseminated’. They noted that by
2005 less than 8% of very low birth weight infants report-
ed to the Vermont-Oxford Network received postnatal
corticosteroids. What the Cochrane reviews did show
was an approximate 70% increased risk of cerebral palsy
in infants treated with dexamethasone in the first week
of life to prevent BPD and little evidence of either harm-
ful or beneficial effects of early hydrocortisone therapy
[80].
A subsequent meta-regression analysis showed the
timing of dexamethasone treatment was less important
than the background risk of developing BPD [83]. When
infants are at low risk of developing BPD (early treatment
preventive studies) the risk of adverse long-term effects of
dexamethasone is highest and vice versa, when the risk of
BPD is high the effect of dexamethasone overall may be
beneficial by allowing earlier extubation and reducing
the severity of chronic lung disease. This means that
postnatal corticosteroid treatment still has a role in the
treatment of BPD although it should not be used in the
first week of life to prevent BPD [80]. More research is
needed to determine which steroid drug should be used,
the lowest effective dose and the route of administration.
If dexamethasone is to be used it seems to be effective in
much lower doses of 0.15 mg/kg/day [84] or even 0.05 mg/
Useless Perinatal Therapies
kg/day [85] and inhaled budesonide is currently being
studied in a large European trial [86]. One of the lessons
from postnatal steroid therapy is that all drugs used in
perinatal medicine have positive as well as negative ef-
fects and short-term benefits do not always translate into
continuing long-term improved outcomes. Randomised
trials of new interventions in perinatal medicine must in-
clude evaluations of long-term outcome in infancy and
childhood.
Conclusions
Space has not allowed me to discuss all the useless or
harmful interventions introduced into perinatal medi-
cine. Some of those I have not mentioned are: sulpha
drugs and kernicterus, increased mortality from feeding
gastrostomies for preterm infants, erythromycin and py-
loric stenosis, intravenous vitamin E and multiorgan
damage, premature infant formulae and lactobezoars, vi-
tamin K prophylaxis and kernicterus, methaemoglobi-
naemia from chemicals used to launder nappies, and no-
vobiocin and kernicterus [12]. Other more recent exam-
ples include inhaled nitric oxide either as rescue therapy
for the very ill ventilated preterm infant or to prevent
BPD in very preterm infants [87, 88] and erythropoietin
therapy to prevent anaemia [89]. Recently there have been
concerns about unwanted adverse effects of erythropoie-
sis-stimulating agents in adults with renal failure who
had increased mortality from myocardial infarctions
[90]. Ohlsson and Aher [89] reported that early erythro-
poietin treatment in very preterm infants reduced the
need for blood transfusions in the short-term but in-
creased the risk of severe ROP to the extent that one extra
case would occur for every 20 treated infants. This brings
us full circle from uncontrolled oxygen supplementation
raising feelings of déjà vu and providing another example
of the need for including long-term follow-up in all stud-
ies of perinatal interventions [14]. I am cognizant of the
fact that I have included only a few examples of useless or
harmful interventions in pregnancy and I recommend
that readers search for examples of these in the excellent
Cochrane Pocketbook on Pregnancy and Childbirth [91].
Neonatology 2010;97:358–365 363
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