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ROP description
Eugenics against oxygen
Slandering oxygen
Oxygen study frauds  
Alleged study results

Later deaths >>>

Futility and harm
Fluorescent ROP lamps
Damaging irradiance
Preemie vulnerabilities
Studies of light and ROP
Frauds in LIGHT-ROP
Coverup stonewalling

 

Related items

Protect your baby

Baby-blinding lights
LIGHT-ROP Manual
Macular degeneration
Preemie Pain
Parent Concerns

Re-Tuskegee

Bioethics LIGHT-ROP

Bioethics SUPPORT

Bioethics own violations

Bioethics Consent

Bioethics 1955 Oxygen

Unethical Bioethics 1

Unethical Bioethics 2

Unethical Bioethics 3

Unethical Bioethics 4

Hypocritical Nature

False Medical Denials

Pre-Nuremberg Bioethics

Protect Humans in Research

Avaaz Petition to WHO

 


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Footnotes :

 

[1]  Starr P. The Social Transformation of American Medicine: The rise of a sovereign profession and the making of a vast industry. Basic Books, New York, 1982, page 347, second half: The relaxing in the 1960s of the American Medical Association's previously very tight restrictions on the nation's supply of physicians may be another instance of  that cultural trend towards greater permissiveness at work.

 

[2]  Silverman WA: Retrolental fibroplasia: a modern parable. Grune & Stratton, Inc., New York, 1980, pages 56-58.

 

[3]  Weiter JJ. Phototoxic Changes in the Retina, in Miller D. (ed.): Clinical Light Damage to the Eye, Springer Verlag, New York, 1987, pages 79-125, see pages 86 and 122.

 

[4]  Meanwhile, a new technology marketed by Hamamatsu claims to offer “a simple, painless way to monitor oxygen levels in the brain directly – using only light”, as advertised in Scientific American, August, 2005, page 11.  However, even if this technique made it now possible to measure the oxygenation levels in the retinal vessels, the results would be irrelevant because that oxygenation is not the trigger for ROP and can at worst only enhance the light damage which causes it.

 

[5]  Kinsey VE, Arnold HJ, Kalina RE, Stern L, Stahlman M, Odell G, Driscoll JM, Elliott JH, Payne J, Patz A. PaO2 Levels and Retrolental Fibroplasia: A Report of the Cooperative Study. Pediatrics, November 1977, 60: 5: 655-68.

 

[6]   As described in Kalina RE, Karr DJ. Retrolental fibroplasia - Experience over two decades in one institution. Ophthalmology, February 1982 89: 2: 91-5, see page 95 top left.

 

[7]  Silverman WA. Retrolental fibroplasia: a modern parable. Grune & Stratton, Inc., New York, 1980, page 143 middle

 

[8]  Avery ME, Taeusch HW, Floros J. Surfactant Replacement. New Engl J Med, Sept 25, 1986, 315: 13: 825-826.

 

[9]  Eidelman AI. Economic Consequences of Surfactant Therapy. Journal of Perinatology, 1993, 13: 2: 137-139.  See page 138 right top for cost approaching a half billion dollars, page 138 left, bottom, for higher neurological damage, page 137 right, end of first paragraph, for 1200 extra survivors, and Table 1, page 138 right, top, for up to 3750 additional survivors.

 

[10]  Bancalari E, Flynn J, Goldberg RN, Bawol R, Cassady J, Schiffman J, Feuer W, Roberts J, Gillings D, and Sim E. Influence of Transcutaneous Oxygen Monitoring on the Incidence of Retinopathy of Prematurity. Pediatrics, May 1987, 79: 5: 663-669, see page 664 right, middle.

 

[11]  Silverman WA. Retrolental fibroplasia: a modern parable. Grune & Stratton, Inc., New York, 1980, footnote b on page 60.

 

[12]  Phelps DL. National Eye Institute Grant Application No. 1 U10 EY09962-01,  Draft Manual of Procedures, Multicenter Trial of Supplemental Therapeutic Oxygen for Prethreshold Retinopathy of Prematurity (STOP-ROP).  Draft 1/27/92, Exhibit 2-3: Arterial PaO2 Values in Various Subjects, page 2-8.

 

[14]  Phelps DL. National Eye Institute Grant Application No. 1 U10 EY09962-01,  Draft Manual of Procedures, Multicenter Trial of Supplemental Therapeutic Oxygen for Prethreshold Retinopathy of Prematurity (STOP-ROP).  Draft 1/27/92, pages 7-2,3.

 

[15]  Phelps DL. National Eye Institute Grant Application No. 1 U10 EY09962-01,  Draft Manual of Procedures, Multicenter Trial of Supplemental Therapeutic Oxygen for Prethreshold Retinopathy of Prematurity (STOP-ROP).  Draft 1/27/92, page 2-9.

 

[16]  Phelps DL. National Eye Institute Grant Application No. 1 U10 EY09962-01,  Draft Manual of Procedures, Multicenter Trial of Supplemental Therapeutic Oxygen for Prethreshold Retinopathy of Prematurity (STOP-ROP).  Draft 1/27/92, page 2-8.

 

[17]  Bancalari E, Flynn J, Goldberg RN, Bawol R, Cassady J, Schiffman J, Feuer W, Roberts J, Gillings D, and Sim E. Influence of Transcutaneous Oxygen Monitoring on the Incidence of Retinopathy of Prematurity. Pediatrics, May 1987, 79: 5: 663-669, see page 665 right, near bottom, for correlation of oxygen monitoring and increased mortality rate: "The excess mortality in the continuous monitoring group infants was due mainly to massive intracranial hemorrhage and necrotizing enterocolitis.  It can be speculated that the use of transcutaneous oxygen monitoring may have increased the risk of these complications in the continuous monitoring group, but the fact that the difference was only observed in the larger infants makes this possibility less feasible." On the other hand, it seems just as likely that the smallest infants, whose mortality rate was not as much affected by the monitoring, suffered from so many other problems of immaturity that they tended to die anyway from severe ailments other than only their lack of oxygen, whereas the larger babies were more ready to live and would have needed only a little more breathing help to put them over the threshold of viability. To dismiss this possibility despite its high statistical probability seems a biased ad hoc interpretation incompatible with rational inquiry.

 

[18]  Rothman K., identified as an epidemiologist from Boston University: the cookbook recipe concept of significance is "a clumsy substitute for thought [that can] blind the investigators to the informa­tion in their data", as quoted in Newsweek, March 22, 1993, in an article about the pending Supreme Court decision on "junk" science versus "good" science, page 63 middle right.

 

[19]  Phelps DL. Vitamin E and Retinopathy of Prematurity: The Clinical Investigator's Perspective on Antioxidant Therapy: Side Effects and Balancing Risks and Benefits. Birth Defects: Original Article Series, 1988, 24: 1: 209-218, see page 214 top:  the number of babies born in 1985 with birth weights of less than 1500 grams is here given as 42,000, and that of survivors among them as 26,200.

 

[20]  Phelps DL. National Eye Institute Grant Application No. 1 U10 EY09962-01,  Draft Manual of Procedures, Multicenter Trial of Supplemental Therapeutic Oxygen for Prethreshold Retinopathy of Prematurity (STOP-ROP).  Draft 1/27/92, page 2-4: Estimates of ROP morbidity for 1991: 4,479 with cicatricial disease and 777 totally blind if no cryotherapy is used; this is reduced to 2,060 cicatricial and 412 blind if cryotherapy works as expected.

 

[21]  Tin W, Wariyar U: “Giving small babies oxygen: 50 years of uncertainty”, Semin Neonatol, October 2002, 7(5):361-7.

 

[22] Chow LC, Wright KW, Sola A, and the CSMC Oxygen Administration Study Group: “Can changes in clinical practice decrease the incidence of severe retinopathy of prematurity in very low birthweight infants?”, Pediatrics, February 2003, 111(2):339-345.

 

[22a] Support Study Group of the Eunice Kennedy Shriver NICHD Neonatal Research Network: "Target Ranges of Oxygen Saturation in Extremely Preterm Infants", NEJM, May 127, 2010, http://www.nejm.org/doi/full/
10.1056/NEJMoa0911781

 

[22b] http://www.nejm.org/doi/full/
10.1056/NEJMc1007912

 

[23]   Florence Nightingale: “Notes on Nursing”, 1859, as quoted by Marianne Szegedy-Maszak in her Los Angeles Times article of November 28, 2005: “As noise rises, so do the dangers: The constant clatter in hospitals stresses both patients and staff”.  Szegedy-Maszak discusses several recent studies which all found that routine noise levels in hospitals, particularly in pediatric intensive care units, are a serious public health problem and trigger “a whole set of physiological changes, such as increased levels of adrenaline and noradrenaline, which are associated with increased blood pressure and inflammatory responses that are implicated in heart disease and heart attacks.” 

 

[24]  Lawson JR: “Standards of Practice and the Pain of Premature Infants”, Zero to Three, The Bulletin of the National Center for Clinical Infant Programs, December 1988, pages 1 to 5; this article is posted on the Preemie Pain page of this site.


 


 

  

 

  

 Baby-harming medical research frauds

 

about retinopathy of prematurity

by H. Peter Aleff, 2005 

 
 

 

 

2.8: Later deaths from restricting oxygen

Beginning in the mid to late 1960s, in tune with the then cultural climate of relaxing overly tight restrictions[1], the oxygen withholding became slowly and gradually and tacitly a little less Draconian[2], and the death rates slowly and gradually and less tacitly began to decrease again. 

The bogus Cooperative Study of 1953/54 had only recorded the percentage of oxygen in the breathing mix but not how this translated into blood oxygenation for the baby. A few years later, actual measurements of arterial oxygen tensions became possible, and some nursery doctors incorrectly assumed these to be an indicator of the retinal oxygenation.  

They did so although it had already been known since 1924 that the retina has the highest rate of oxygen consumption among all the tissues in the entire body, and that it can auto-regulate its local oxygen levels as needed, independent of the arterial oxygen concentrations[3]. This auto-regulation disconnects the levels of oxygen in the retinal vessels from the arterial oxygen tension, and trying to extract the former out of the latter is therefore as doomed to fail as trying to drag the reflection of the moon out of the water[4]

Despite this long known impossibility of measuring or controlling the oxygen levels in the retina where alone they would matter in the oxygen theory for ROP, another Cooperative Study was launched in 1969 to nail down the supposed relationship between arterial oxygen levels and ROP risk, although this time in only five hospitals.  Two of its authors had also been members of the Coordinating Committee for the earlier bogus oxygen study, so it was to be expected that the new study would not try to expose the fraud and flaws in its predecessor. 

On the other hand, try as they might, the authors of the new study were unable to confirm either the accusation against oxygen or the safety of its withholding, or to obtain any result whatsoever. Their trial, published in 1977[5], failed to show any correlation between arterial oxygen concentrations and any measure for the development of ROP[6], and it also did not answer any question about the risk of brain damage and death from low oxygen levels. 

Silverman described these non-results from 1977 in his book about the epidemic:

"... the design of the study doomed it from the start.  Measurements were made of oxygen in the blood of infants who received supportive treatment according to individual physician prescription (the ‘active’ observations approach) rather than by random assignment to prescribed conditions of blood oxygen (the experimental approach).  At the end of eight years of effort (3 years of observations and 5 years of analysis of the results!), there were no interpretable findings. To this day, when oxygen is administered to premature infants, they are exposed to the intertwined risks of brain damage, death and RLF with nothing more than authoritative guessing as protection."[7]

The guessing continues, but none of it is authoritative or offers any protection to those infants.

Meanwhile, the more recently developed technique of introducing surfactant preparations into the preemies' lungs every few hours[8] helps the expansion and deflation of the alveoli and allows many of the smaller preemies to absorb the incoming low-oxygen air more efficiently, almost as well as if they had been given higher concentrations of oxygen to begin with. 

This surfactant treatment partly cancels the effects of the elaborate oxygen rationing efforts and so helps an estimated 1200 to 3750 more babies a year to stay alive, although with a higher rate of neurological damage among the survivors, and at a monetary cost in the U.S. that approached in the early 1990s a half billion dollars per year for this one treatment and is probably higher now[9].

Despite these changes, a study at the University of Miami/Jackson Memorial Medical Center, published in the May 1987 issue of Pediatrics, suggests that some babies still died unnecessarily from oxygen rationing.  That article, five pages from ten co-authors who expressed no concern about the harm their experiment had done to the babies, showed that their closer monitoring of the then recommended more generous oxygen rationing levels seems to have killed about one extra baby in twelve among those with very low birth weights.      

In one of two matched groups with birth weights up to 1300 grams, the experimenters had continuously monitored the babies' arterial oxygen concentrations to maintain them as much as possible in a predetermined range of 50 to 70 mm Hg[10]

This is far below the normal values for healthy preemies with mature lungs. The arterial oxygen tensions of these range from about 60 mm Hg at birth to about 100 mm at 54 hours of age[11]. By that time, their “normal” is the same as for adults, or 80 to 100 mm Hg[12].  Levels below 80 mm Hg are defined as hypoxia, a condition in which the body or some of its parts are deprived of adequate oxygen and which can lead, depending on its severity, to headaches, fatigue, shortness of breath, nausea, unsteadiness, and sometimes seizures and coma, or even brain death. 

Brain cells are extremely sensitive to oxygen deprivation and can begin to die within five minutes after their oxygen supply has been cut off [13].  Even marginal hypoxia is likely to weaken the patient and his ability to heal, but intensive care nurseries in the USA have typically tried to maintain preemies between only 45 to 85 mm Hg for ninety percent of the time[14]

This low level corresponds to blood oxygen saturations of only 90 to 95%, less than the at least 96% an infant with more mature lungs is supposed to obtain from room air before her oxygen supplementation is discontinued[15], and it is far from the optimum needed to help a preemie recover from the many complications caused by his early birth.  For comparison, the preemies whose lives oxygen routinely saved before its marsupial condemnation in 1954 had been typically maintained at about 200-275 mm Hg[16].

The babies in the control group of the Miami study had received standard care which means their oxygen was also rationed with the intent to keep it in the same low hypoxic range of 50 to 70 mm Hg, but their oxygen levels were monitored only about a third of the time, and thus less tightly. Nurses, like those in the Gallinger Hospital above, and parents often turn the oxygen flow up when the baby is gasping or starts to breathe irregularly, so this group received probably higher though unrecorded oxygenation. 

Like the prior studies of oxygen and ROP, this one failed again to show any convincing relationship between oxygen levels and either the incidence or the severity of ROP.  The tighter monitoring and constant taping of painfully hot electrode pad sensors to the few not-yet-reddened spots on the tender skin of the preemies had not helped them at all against the blinding or in any other way, but these procedures appear to have killed many of them. 

The mortality figures from that study revealed the deaths of twelve extra babies out of the 148 in the continuously monitored group, or 8% more than in the control group.  For the babies with birth weights above 900 grams, the death rate in the monitored subgroup was over 11% higher than among those who had received oxygen a little more freely. 

The authors computed the probability that this difference might be due to chance as 6% which means a 94% probability that the extra deaths were related to the monitoring[17]. However, none of the investigators or their reviewers expressed any concern or raised any alarm about the fatal outcomes that were so strongly associated with the ROP-neutral monitoring and the constant hot-pad pain. 

Medical doctors are taught to regard correlations between treatments and effects as "not significant" until that probability of a chance result reaches or becomes smaller than 5%. Unfortunately, many apply this cookbook recipe, which has been called a "clumsy substitute for thought"[18], also to the evaluation of harmful side effects.  

This inverted logic, which passes in America today for medical science, confirms the wisdom of the ancient Greeks who said that their healing god Asklepius held a vial in each hand, one with a curing potion and one full of poison, and that he often confused the two. If medical ethics had made any progress since then, the doctors in that nursery should have told the parents honestly that there were 16 chances out of 17 that their baby’s risk of dying would increase from the oxygen withholding, and that there was no demonstrable practical or even theoretical benefit whatsoever to expect from this drastic increase in fatal danger. 

The relative differences in mortality between babies with different accuracies of oxygen rationing in this trial allow no proper estimate about the nation­wide toll from the practices in that one nursery because the oxygen policies and their enforcement were no longer as uniform across the country as they had been in the early years of the most severe oxygen withholding. 

However, a hypothetical extrapolation can help to illustrate the potential consequences from just a small turn of the oxygen valve for the most vulnerable preemies: If a similar relative tightening of each hospital's oxygen monitoring produced a similar 8% rise in mortality for the estimated 42,000 American children born in 1985 with similarly low birth weights[19], then this slight further restriction of the already rationed oxygen supply would have led to the deaths of about 3,360 extra babies in that year, roughly as many as were said at that time to suffer vision problems from ROP[20]. There is no way to tell how many more preemies would survive and avoid brain damage if their oxygen was not rationed at all.

Unfortunately, the pendulum seems now to swing from the temporary relaxation of the oxygen restrictions back towards tighter rationing, again in parallel with the cultural trend back towards less permissive attitudes. For instance, in October, 2002, a pair of British neonatologists gushed gullibly in the abstract for their paper “Giving small babies oxygen: 50 years of uncertainty” how admirably the early oxygen-blaming studies had “banished all residual doubt” that oxygen "caused" ROP, and they proposed to now ask whether the breathing help for the youngest babies could be further reduced:

“A small landmark trial in 1952 showed that excess oxygen use might well be causing a major epidemic of retinal blindness in preterm babies.  That a single study of just 65 babies was enough to throw doubt on a long-standing treatment strategy revealed just how powerful a tool the randomized controlled trial could be.  Confirmatory evidence from a cooperative trial involving a further 212 babies banished all residual doubt just four years later, and it remains a major reproach that we have still not learnt, after 50 years, how to optimize the delivery of oxygen to the preterm baby with further help from this powerful tool.  Two well-conducted trials have recently shown that avoiding subclinical hypoxaemia (fractional SaO(2) < 92%) in babies more than a month old does nothing to improve later growth or development.  It is now time the same question was asked of babies less than a month old, because we might reduce their need for ventilatory support.  This is particularly important in babies of less than 28 weeks’ gestation, who remain currently at serious risk of chronic lung disease and permanent retinal scarring.”[21]

With this totally uncritical approach to the alleged benefits of oxygen withholding, while completely ignoring its well documented fatal dangers, the answer to that question about further reducing the oxygen support given to the youngest babies is foreordained.  Such attitudes are now bound to lead to a re-tightening of the oxygen faucets and thereby to more deaths as well as brain damage among current and future preemies.

A recent study, published in the February, 2003, issue of Pediatrics, reported no rise in mortality from its stricter enforcement of the clinical oxygen withholding parameters by trying to keep the babies between 85% and 93% of blood saturation (or 95% for larger babies) to “avoid undesired episodes of high oxygen saturation levels”[22]. To the contrary, it found a rise in the survival rate of the preemies which had been 81% in the “before” year 1997. After the change to tighter rationing, that rate climbed slowly to 83% in 1998 and 85% in 1999, then it jumped to 93% in 2000 and leveled to 90% in 2001. 

The authors of that study also described in their abstract a “consistent” decrease in the severe ROP stages three and four from 12.5% in 1997 to 2.5% in 2001, and a complete elimination of the need for surgical treatment which 4.5% of the babies had required in 1997.

However, that decrease was not “consistent” but slow in coming, and it did not coincide with the start of the stricter oxygen enforcement: the ROP rate remained at 9% in 1998 and 5.5% in 1999, and it fell to the 2.5% level only for 2000 and 2001.  The break after the second year of the restrictions is even clearer for the babies with birth weights under 750 gram who are those with the highest risk of ROP.  Their incidence went from 35% in 1997 with little change to 30% in both 1998 and 1999, and then only did it fall to 10% in 2000 and about 12% in 2001.

The authors speculated that this delay between implementation and results might have been due to staff resistance against the oxygen throttling, to the point that all nursery personnel had to sign statements of mandatory compliance. This resistance echoes that of the nurses at the above Gallinger Hospital trial who did not want to kill the babies, and it reflects the continued compassion among today’s nurses for the preemies’ often desperate struggle to catch their breath. 

The authors also stated that their switch to more user-friendly monitoring equipment may have led to better compliance, while noting elsewhere that different monitors do not measure exactly the same values of saturation under the same conditions in the same infant, and also that the duration of out-of-range readings was not accurately quantified for each baby. They further changed the protocol of ROP screening for the “after” years, meaning the data from the “before” year are not necessarily comparable, and they admitted that they could not exclude several other confounding factors in their “before-and-after” study with only one “before” year.

Despite all these caveats, the authors speculated that even lower values of oxygen saturation could have been of more benefit to the babies in the lowest birth-weight group. They also say, against all experience with oxygen-deprived brains, that there is no evidence that the normal oxygen saturation levels of 95% to 100% are needed for the very-low-birth weight babies, and they assert, again without any evidence, that these normal levels are potentially dangerous. 

Their dangerous speculations about the supposed benefits of  low oxygen saturations were debunked by a more recent study of 1316 preemies born at up to almost 28 weeks of gestation and assigned randomly to two different target levels of  oxygen saturation: 85 to 89 per cent in the low-oxygen  group and 91 to 95 per cent in the other. The authors of this study, published in the May 27, 2010, issue of the New England Journal of Medicine, found that

"Death before discharge occurred more frequently in the lower-oxygen saturation group (in 19.9% of infants vs. 16.2% ... p =0.04) whereas severe retinopathy among survivors occurred less often in this group (8.6%vs. 17.9% ... p =<0.001)." [22a]

In a response to a reader question, they also added:

"Our preliminary unadjusted analysis indicates that infants who died spent a higher proportion of time (P<0.001) with saturations below 80%." [22b]

The additional babies in the low-oxygen group who had such immature lungs that they died from the lack of oxygen had most likely also the most immature eyes and were therefore most susceptible to develop severe ROP if they had survived.

In other words, the lower incidence of severe ROP in that group appears to have been partly due to the oxygen restrictions having killed those babies who would otherwise have survived with severe eye damage. Rationing the oxygen is therefore the equivalent of saying "better dead than blind", and all those who hold this to be an absurd position will find it hard to justify exposing the preemies to the fatal risk of asphyxiation while attempting to prevent a non-fatal condition.

This confirms again the dangers of oxygen rationing which the designers of the mid-1950s oxygen trial had tried to hide with their late-enrollment trick, and the 2010 authors concluded more honestly:

"The increase in mortality is a major concern, since a lower target range of oxygen saturation is increasingly being advocated to prevent retinopathy of prematurity."

For a discussion of this 2010 study's ethics-violating tradeoff using death to reduce blindness, see my 2011 letter to Professor Amy Gutmann, Chair of the Presidential Commission for the Study of Bioethical Issues, and several additional pages about that cruel experiment conducted without informing the parents about the risks.

Compared with this 2010 study in NEJM, the abrupt changes in both the survival rates and the ROP incidence from year two to year three of the restrictions in that above 2003 paper from Pediatrics suggest clearly that some other uncontrolled or unappreciated change(s) in the nursery routines may have taken place around that later time. 

One such change could well have been the switch to better monitoring equipment, though not, as the authors propose, by making compliance with the oxygen restrictions easier. The benefit from the better monitoring equipment could rather have come from disturbing the babies less often with ear-piercing alarms: 

The trial policy had been to not turn off the monitor alarms after increasing the oxygen flow until the baby’s blood gas levels returned to the preset range, so the affected babies as well as all their nursery neighbors must have been often exposed to shrieking noise levels even higher than the already dangerous ones that are unfortunately common in many intensive care nurseries. If the new monitors produced less false alarms, as the authors asserted, then the preemies would have been able to get more rest and even some fortifying sleep which is essential for all healing and recuperating. This effect alone could easily have accounted for the babies’ better survival, and also for their apparently greater resistance to the retinal damage from ROP.

Most parents try instinctively to protect their babies from loud noises that make them cry and cranky. Unfortunately, the typical intensive care nurseries in America are run not like baby bedrooms but like outdated rustbelt factories.  

Already Florence Nightingale had warned that

“unnecessary noise is the most cruel abuse of care which can be inflicted on either the sick or the well.”[23]

Yet, the routine noise levels in hospital nurseries are often even higher today than in modern industrial settings that now usually guard their workers against such damaging and unnecessary stressors. Babies are much more vulnerable to all environmental insults and require more protection from them than those adult workers, not less. 

From the dawn of recorded history, and probably already long before some ancient Sumerian wrote down the first surviving lullaby, sensible people have tried to provide peace and quiet and soothing sounds for their babies to help them have a pleasant and healthy sleep. This instinctive “shhh...” reaction to shield a baby from anything startling or harsh, particulalrly when the baby is sick and needs this rest even more, comes naturally to most humans, at least to those not made reckless by medical arrogance.

Unfortunately, many of the medical doctors in charge of intensive care nurseries are so smitten with their alleged science that they seem to forget their patients are humans. They routinely used to vivisect babies without anesthesia, even for major surgery, until 1988 when a mother discovered and exposed this barbarian inflicting of unnecessary pain that was based on nothing but the cult-like pediatric delusion that babies don’t feel pain[24].  The same insensitivity to their fellow humans’ pain still manifests itself in the neonatologist approach to nursery noise.

There is not one shred of justification for the often earsplitting cacophony of sharp and unnecessary sounds that most preemies must endure and that greatly imperil them by denying them their much needed rest. No aspect of humane infant care needs a blaring radio next to the baby’s bed, or monitors beeping and shrieking. Caring nurses would also hear a discreet chime or see the warning lamp that should replace the audio alarm, but many neonatologists appear to prefer the busy-sounding noises that add drama to their “heroic” treatments of “miracle babies”, even though many studies have warned against the permanent harm these high noise levels cause to many babies.

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