Neonatology, perinatology and neonatal resuscitation developed to a great extent during the 1970’s in response to an epidemic of litigation involving birth brain injury; fetal monitoring was detecting fetal distress in utero, and specialized perinatal intensive care promised great improvement in neonatal morbidity and mortality.
(All referenced images will open in new windows by clicking their names)
Neonatology, perinatology and neonatal resuscitation developed to a great extent during the 1970’s in response to an epidemic of litigation involving birth brain injury; fetal monitoring was detecting fetal distress in utero, and specialized perinatal intensive care promised great improvement in neonatal morbidity and mortality. Today, in US hospitals, if a child is born alive, the chances of it dying within a few days are virtually zero; even some babies without a heartbeat are resuscitated. Perhaps one third of all neonates receive some form of resuscitation treatment, and the success in terms of mortality is excellent. About 6% to 10% of all neonates are “morbid” and need NICU care – many of these are preemies; again, NICU mortality is extremely rare; however, in terms of neurological and mental disability, especially in NICU babies, long-term morbidity is anything but rare.  The life-saving procedures of neonatal resuscitation and NICU care are much less successful in preserving brains. If resuscitation does not result in a five minute Apgar of 7 or more, neurological impairment is likely. 
The term “resuscitation” implies restoration of deficient life support systems, especially respiration; in the depressed newborn, that deficiency is in the placenta and cord, as the lungs have not yet begun to function. The rationale on which current resuscitation is based is that early detection of fetal asphyxia combined with rapid delivery and rapid establishment of pulmonary respiration (reversal of asphyxia) will prevent brain injury. If brain damage (neuron necrosis) has occurred in utero, resuscitation will not heal it; however, overt brain damage seldom is evident at birth, and it often appears after resuscitation. Hypoxic ischemic encephalopathy usually is diagnosed hours after birth when the child convulses; germinal matrix hemorrhage in preemies may develop a day or two after birth; mental and behavioral problems may not surface for years.
The general consensus is that birth “asphyxia” is the cause of the brain damage; hypoxia is a more precise term, although asphyxia implies arrest of respiration – respiration includes oxygen supply and removal of carbon dioxide. Iatrogenic resuscitation usually corrects this asphyxia promptly by initiating pulmonary ventilation; most organs survive superbly, all except the brain. This strongly implies that there are other factors active in neonatal “depression” besides hypoxia and acidosis that must be corrected during “resuscitation”. The placenta is much more than a respiratory organ. Correction of the placental / cord deficiency that caused the depression, and support of placental function are thus rational priorities in revival of a depressed neonate, just as they are in the “resuscitation” of the “distressed” fetus in utero.
In utero, the normal blood supply of the fetal brain is relatively hypoxic. Umbilical vein blood is fairly well oxygenated, but it is mixed in the inferior vena cava and in the heart with de-oxygenated blood from the venae cavae; this is then circulated systemically. The color of a normal newborn is purple – it has been purple for nine months – circulating a mixture of hemoglobin (blue) and oxyhemoglobin (red). It turns pink only after the fetal circulation is changed to the adult circulation, and is combined with aeration of the lungs. The fetal brain thus grows and develops with a copious blood supply that is only partially oxygenated, but which readily removes products of aerobic and anaerobic respiration and excretes them through the placenta. The fetal kidneys and gut thrive on blood with the same oxygen partial pressure as the blood flowing to the placenta to be oxygenated. The newborn brain and other organs are therefore relatively immune to pure hypoxic injury  as long as organ and placental perfusion are copious.
The same basic principles apply to the adult brain; five minutes or more of cardiac arrest will produce some brain damage or brain death; occlusion of a cerebral artery rapidly results in infarction (death) of the supplied tissue. On the other hand, five minutes or more of pure anoxia (e.g. breathing pure nitrogen) will produce unconsciousness that is fully reversible without brain damage provided that brain perfusion is not impaired. The integrity of the newborn brain is maintained (by perfusion and oxygenation) at normal (physiological) birth; therefore the physiological mechanisms that ensure these functions (perfusion and oxygenation) should be supported and/or duplicated during iatrogenic resuscitation if brain damage is to be avoided.
The severely depressed/asphyxiated newborn typically shows not only no sign of breathing, but also lack of muscle tone and reflexes needed to initiate breathing, as well as signs of hypoxia such as cyanosis; in the most severe cases, pallor indicates vasomotor collapse. Such a child has obviously suffered a major respiratory insult prior to or during birth; the cause of that insult and its specific effects are factors that must be corrected, if possible, in the resuscitation process. In any and every case of newborn depression, if a child is born alive – with a heart beat and a pulsating cord – the placental life support system has not failed completely; utilization of this system in resuscitation and transition to “adult” life support systems in the depressed newborn is essential in restoring the physiological state – health – without the incursion of organ damage, primary or secondary, from “birth asphyxia.” With early detection of fetal distress and with rapid delivery, the neonate’s central nervous system should be undamaged at birth; the objective of therapy should be that it remains so.
Normal (Physiological) Resuscitation at Birth – Transition
At normal (physiological) birth, the child “resuscitates” itself:
There is no period of asphyxia or hypo-perfusion.  However, this description is very simplistic and incomplete.
The switch from placental to lung “breathing” is only a portion of the whole; the switch from placental alimentation and placental excretion to the newborn’s alimentary and excretory organs is also part of “natural” resuscitation. To initiate and establish the newborn functions of the lungs, gut, kidneys, and other systems, including the brain, continuous copious perfusion of these organs is required; a large transfusion of placental blood during natural childbirth “resuscitates,” or more correctly “activates” all these organ systems as the massive flow of blood through the placenta (40% of the fetal cardiac output) is diverted to these organs during physiological closure of the cord vessels.
Cord closure abruptly halts the placental supply of glucose to the brain (used in aerobic and anaerobic respiration); the neonatal liver (glycogen stores) must begin to maintain blood glucose levels. A major portion of the liver’s blood supply is from the hepatic portal vein that derives its blood from the mesenteric arteries. If the gut (and hence the liver) is not “copiously perfused,” hypoglycemia may result in a neonatal convulsion. Deficient perfusion of the liver may also be a factor in bilirubin excretion and “physiological” jaundice.
Copious perfusion of the neonatal kidneys with adequate blood pressure is required for solute excretion, fluid, electrolyte and acid-base regulation after the placenta ceases to function.
During the third stage of labor while the cord is pulsating, warm blood from the placenta courses through the newborn. After cord closure, temperature regulation is suddenly required of the neonate; switch of blood flow to and from the epidermis requires a copious amount of blood to regulate heat loss and heat retention.
In the fetus, pulmonary circulation is minimal; after the adult circulation is established, the entire cardiac output flows through the lungs. A major portion of the placental transfusion is utilized in establishing pulmonary blood flow after birth. Jaykka demonstrated that perfusion of the fetal lung “erected” the alveoli and actually initiated aeration;  the high colloid osmotic pressure of the circulating blood rapidly absorbs amniotic fluid from the erected alveoli. Thus adequate “copious perfusion” of the lungs may result in pulmonary oxygenation before any muscular respiratory effort occurs.
Respiratory effort is reflexively controlled through the central nervous system; hypoxia and increased concentration of carbon dioxide are strong stimulants for receptors. For the reflex to function, copious perfusion of the reflex circuit is required, as is copious perfusion of the respiratory muscles.
Third stage placental function and placental transfusion were dramatically demonstrated by Gunther . In Figure 1., this particular child lived outside the uterus for nearly ten minutes without starting to “breathe”; the child was wrapped in a warm blanket and deprived of the “cold crying reflex.” This non-breathing newborn with an intact cord and placenta is in no distress and is not asphyxiated; note how it “kicked the bed.” Uterine systoles and diastoles produce virtual tidal waves of placental transfusion and blood loss during continuous placental circulation until pulmonary respiration is established; (Figure 1) thereafter, transfusion proceeds in a step-wise manner, each uterine transfusion being arrested by sphincter closure of the umbilical vessels, resulting in plateaus until the final blood volume is attained and permanent cord closure occurs.
Yao  demonstrated that full placental transfusion, impelled by gravity, occurred within 30 seconds if the child was held 40 cms below the level of the placenta. The natural position adopted by “primitive” mothers is squatting, and the child is delivered downwards; such a child receives very rapid “resuscitation” from gravitational placental transfusion. Ventilation of the lungs, which reflexively relaxes pulmonary arterioles, greatly facilitates placental transfusion and pulmonary perfusion. Whether the placental transfusion is effected by gravity or by uterine contraction or by both, it is regulated and terminated reflexively by the child and results in a blood volume that is optimal for survival; those reflexes have been honed to perfection by natural selection over millions of years.
An additional factor in “normal” resuscitation/transition is increased systemic blood pressure  caused by placental transfusion, the cold pressor reflex and closure of the umbilical arteries; this may reverse blood flow in the ductus arteriosus and increase “erection” of lung tissue. Increased blood pressure also increases glomerular filtration in the kidneys and causes increased fluid loss into the extra-cellular space resulting in hemo-concentration. The consequent increase in plasma colloid osmotic pressure prevents pulmonary edema and dries up the lungs. After crying started in Figure 1, the child received a transfusion of nearly 100 mls of blood within one minute; this was forced (by maternal uterine contraction) into the venae cavae, liver, heart and lungs of the child at high pressure – see Figure 2. Jaykka’s “erection” of alveoli could well be done by pressure generated by the maternal uterus or gravity, not the neonate’s heart.
Thus natural “resuscitation” is the physiological switch from the placental life support system to all the independent corresponding organ systems of the newborn; it involves much more than ventilation of the lungs. The most important factor is the placental transfusion that increases the newborn’s blood volume by 30% to 50%, the additional blood being utilized to activate and establish the functioning of these organ systems. Comprehension of this physiology is essential for elucidating the factors in neonatal depression and in iatrogenic resuscitation that produce the variety of pathology seen in the NICU following incomplete recovery of the depressed newborn.
The routine procedure for resuscitating an “at risk” or depressed newborn is immediate clamping of the umbilical cord followed by transfer to a warmer where the child’s airway is cleared (by visualization of the vocal cords and tracheal suction in cases of meconium staining) and the baby is stimulated by rubbing the skin. If respiration does not occur within 30 seconds or so, bag-mask ventilation is started; if this fails to produce spontaneous respiration, endo-tracheal intubation is performed with positive pressure ventilation.
Immediate cord clamping produces the major deviations from “natural resuscitation”; placental oxygenation, placental acidosis regulation, placental glucose supply and placental transfusion are all abruptly aborted and the child is subjected to a period of complete asphyxiation until the lungs function. The warmer deprives the child of the cold crying and cold pressor reflexes. Bag-masking or intubation ventilation readily aerates the alveoli; this reflexively dilates pulmonary arterioles and promotes pulmonary perfusion and the switch from fetal to adult circulation; however, without additional blood volume that is normally supplied by placental transfusion, less than optimal pulmonary perfusion may occur resulting in less than optimal gas exchange and incomplete closure of the foramen ovale and the ductus arteriosus. 
The immediately clamped newborn has, in effect, been subjected to a massive hemorrhage,  losing up to 50% of its blood volume; however, the actual amount of blood loss varies greatly with the circumstances of the particular birth and with the speed with which the cord is clamped. At normal, spontaneous delivery, the contracting uterus may squeeze blood into the child during the second stage of labor; if the child cries before the trunk is delivered, the contraction that delivers the child may also deliver a “full” placental transfusion before the clamp can be applied. Similarly, a mother who delivers in the squatting position will usually transfuse the child fairly adequately by gravity before the clamp can be applied. A normal, spontaneous delivery (with the mother supine) followed by immediate placement of the child on the mother’s abdomen may result in considerable gravitational blood loss into the placenta if the clamp is placed during uterine diastole. Rarely, when a clamp happens to be placed during a strong uterine contraction, the child may be over-transfused with blood that would have drained back into the placenta had the clamp not been placed. In general, most newborns that breathe immediately after a normal vaginal delivery will not lose a critical amount of blood volume from early cord clamping.
This, no doubt, has led to complacency about immediate cord clamping; however, many immediately clamped newborns, especially those that are apneic, have much less than an optimal blood volume, and some are very blood volume deficient. After a “normal” birth and immediate cord clamping, they may develop infant anemia months later,  and years later, in grade school, they may be found to be mentally deficient. 
The apneic child that is delivered above the level of the placenta that is in a relaxed uterus will suffer gravitational blood loss into the placenta. This fact is used as rationale for immediate clamping at cesarean section. The procedure certainly prevents immediate newborn blood loss, but the sectioned child thus delivered is routinely hypovolemic from loss of placental transfusion. Sectioned newborns have a higher incidence of RDS and persistent fetal circulation (PFC) than do vaginal deliveries; Landau  completely prevented RDS in sectioned babies by leaving the placenta attached and suspending it above the child like an I.V. A significant number of perfectly normal, term babies die from PFC following elective c-section. 
Premature babies are routinely immediately clamped for transfer to resuscitation. The premature placenta is relatively large in relation to the fetus and contains a correspondingly larger portion of the feto-placental blood volume. The blood loss from immediate clamping is, therefore, correspondingly greater. All such preemies develop anemia. Shock lung (RDS/ hyaline membrane disease [HMD]) is a common complication. Kinmond  prevented RDS in preemies by gravitational placental transfusion and also eliminated the need for red cell transfusion. The routine use of physiological cord closure has NEVER been reported; there are many indications that such preemies would be healthier than those of Kinmond.  In the extremely immature infant, preservation of the placental circulation with immersion of the placenta in an appropriate nutrient medium would appear to be rational therapy to support the immature life support systems. RDS and HMD are readily produced in newborn foals by immediate cord clamping and in newborn rabbits and puppies by removal of blood volume.  It would appear that adequate blood volume at birth is essential for normal lung function. RDS/HMD from hypovolemia may occur at any age regardless of the presence or absence of surfactant in the lungs.
The most common cause of fetal distress in labor is cord compression (cord around the neck, cord prolapse, knot in the cord, oligohydramnios), and measures to relieve cord compression (re-positioning the patient, amnio-infusion, elevation of the presenting part, stopping labor with uterine relaxants) may succeed in returning the fetal heart tracing to normal – may resuscitate the fetus. If these measures do not succeed, the child is born “depressed,” its cord is clamped immediately, and it is transferred to the resuscitation table. Intra-partum cord compression impedes cord venous blood flow (oxygenated, non-acidotic) to the child while allowing cord arterial flow (high pressure) to engorge the placenta. Thus the very “depressed” child (following cord compression) is born in hypovolemic shock, complicated by hypoxia and acidosis – limp and pallid. Immediate cord clamping seals its fate.
If the cord is not clamped and the compression is relieved, (knot loosened, cord unwound from the neck) and the child is lowered, blood drains from the engorged placenta into the child and the hypovolemic, hypoxic shock is reversed within 30 seconds with transfusion of oxygenated, non-acidotic blood; placental respiration reverses the “depression.” This third stage therapy mimics successful intra-uterine resuscitation.
If the cord compression has been of some duration (“intra-uterine asphyxia,” Linderkamp ), e.g. oligohydramnios, the high hydrostatic pressure in the placental capillaries may have dehydrated the fetus, causing marked hemoconcentration. This situation is often reversed in utero by amnioinfusion; if it is not corrected, the immediately clamped neonate is prone to develop the “hyper-viscosity syndrome,” a combination of dehydration, hypovolemia and hemoconcentration.  While placental circulation and placental transfusion (delayed clamping) may help in this situation, in the more severe cases, the cord vessels are constricted and little placental blood is available; intravenous hydration may also be needed to restore physiology.
In asphyxia caused by placental abruption, increase in carbon dioxide may dilate placental and cord vessels, causing a shift in blood volume from the fetus; in the pre-term fetus, the more premature the child, the higher is the placental portion of the feto-placental blood volume. In nearly all “risk” deliveries subjected to immediate cord clamping, there is strong potential for severe hypovolemia at birth.
The neonate reacts to hypovolemia with massive generalized vaso-constriction that shifts volume circulation from less vital organs to the heart and brain. Depending on the degree of hypovolemia, the clinical signs vary from weakness to those of hypovolemic shock: pallor, hypotension, hypothermia, oliguria / anuria, metabolic acidosis, anemia and respiratory distress syndrome (RDS) otherwise known as “shock lung.” Hypoglycemia caused by deficient liver perfusion has already been mentioned. These signs and symptoms and their related pathology are present to some degree in practically every child admitted to the NICU. They are seldom recognized for what they are, because neonatologists are indoctrinated with the concept that placental transfusion is a pathological event and that an immediately clamped newborn has a normal blood volume. Many neonatologists have never seen a newborn that has closed its cord physiologically.
There are many consequences of this conceptual error – the insufficient and tardy use of blood volume expanders and blood transfusion in ischemic encephalopathy; the use of medication (vasoconstrictors) to maintain blood pressure in hypovolemic shock while vasoconstriction is causing oliguria and ischemic necrosis of the bowel – necrotizing entero-colitis; the use of surfactant to treat RDS (shock lung) while the hypovolemic shock remains untreated and lungs are under-perfused. All of these and other consequences, and especially those consequences relating to brain damage,  become irrelevant when the conceptual error is corrected and rational management of neonatal depression is employed.
In the late 1960’s and the early 1970’s, Windle  and Myers  published papers on brain damage in Rhesus monkeys produced by timed periods of birth asphyxia. Necrosis of basal nuclei, brain stem nuclei and the cerebral cortex was induced by various means of birth asphyxia, all of which included disruption of the placental circulation at birth. The clinical results varied from spastic paralysis / decerebrate rigidity to memory dysfunction without obvious neurological impairment; these were correlated with autopsy examination of the brain, sometimes done years after birth. Myers published two very significant recordings of resuscitation.
The newborn monkey in Figure A was perfectly normal until its cord was clamped. Its heart rate dropped immediately and precipitously; its blood pressure rose momentarily (due to umbilical artery closure), then fell immediately (due to decreased venous return), recovered (due to endogenous epinephrine release) and then fell to zero during the interval that the experimenters prevented pulmonary respiration. Ten minutes after immediate clamping, the blood pressure was so low that there was effective cardiac arrest, despite the persistent electrical cardiac activity. At this stage, the brain was not being perfused and was undergoing necrosis. When resuscitation (pulmonary ventilation) was started 25 minutes after immediate clamping, much brain damage had already occurred. Massive doses of Epinephrine, cardiac massage and ventilation produce “life”; however, this monkey was already brain dead. Autopsy findings confirm brain death. Multiple other studies using the same technique and shorter periods of asphyxia and hypotension produced regular patterns of basal nuclear necrosis and brain stem nuclear necrosis at autopsy that were preceded by corresponding neurological defects in surviving monkeys.
In Figure B, depriving the mother of oxygen asphyxiates this monkey fetus; gradual (and severe) fetal bradycardia follows, but blood pressure does not fall significantly and brain perfusion is maintained despite severe bradycardia. Blood pressure is the product of cardiac output and peripheral resistance; bradycardia indicates less cardiac output; vasoconstriction in all organs except the heart and brain is maintaining brain perfusion. Ventilation with the placental circulation intact results in full recovery of blood pressure and heart rate – there is no loss of blood volume; cord clamping (3.5 minutes after birth) causes an increase in blood pressure. This newborn monkey is normal, however, delay in resuscitation with prolonged hypoxia/anoxia will eventually reduce cardiac output and blood pressure, resulting in brain damage. Windle produced asphyxia (and brain damage) by abruption of the placenta and leaving the fetus inside the sac; he did not record the time of cord clamping. Some mildly depressed neonates recovered with no permanent neurological deficit, however, memory and attention deficit dysfunction was demonstrated and necrosis of the inferior colliculus was seen at autopsy.
Several factors are contrasted in these two charts. In 'A' the newborn is not hypoxic at birth – brain damage occurs after birth; in 'B' the newborn is markedly hypoxic at birth, but incurs no brain damage. Resuscitation in 'A' is started much later than in 'B'. Resuscitation (extreme) in 'A' results in rapid oxygenation, but blood pressure levels never attain pre-birth levels despite intense vasoconstriction. Resuscitation (early and minimal) in 'B' results in gradual restoration of oxygenation; blood pressure levels never fall significantly and blood pressure rises as pulmonary oxygenation improves. The effects of cord clamping contrast vividly: In ‘A’, clamping before the lungs are ventilated results in bradycardia and eventual loss of blood pressure. In ‘B’, clamping after ventilation produces a rise in blood pressure and an increase in heart rate. Gasping in ‘A’ is against a closed endo-tracheal tube that ensures asphyxia. Had those gasps been functional, the newborn might have survived; the following paragraphs elucidate that possibility.
Peltonen, using fluoroscopic filming of the thorax at birth, describes in detail the hazards of clamping the cord before the first breath. He notes immediate marked decrease in cardiac size due to incomplete filling of the ventricles. The umbilical vein is as large as the inferior vena cava and returns 40% of the cardiac output. Loss of this massive venous return from the placenta results in virtual cardiac collapse and is relieved only by blood flow through the lungs.  Peltonen’s comment on this is decisive:
“On the basis of these observations, it would seem that the closing of the umbilical circulation before aeration of the lungs has taken place is a highly unphysiological measure, which should thus be avoided. Although the normal infant survives without harm, under certain unfavorable conditions, the consequences may be fatal.”
From this language, it would seem that Peltonen witnessed an irreversible cardiac arrest following immediate cord clamping on a depressed newborn; he had good reason to proscribe the procedure universally. Myers’ recording of the precipitous drop in heart rate (and cardiac output) immediately following cord clamping in Fig. A is confirmatory evidence for the recommendation. Peltonen then notes the strong correlation between clamping before the first breath and the severity of RDS, and comments on the continuing function of the placental circulation during the third stage of labor:
“There is thus good reason in cases of resuscitation to keep the umbilical circulation intact.”
Yet, today, every premature child, every compromised child, every newborn “at risk” has its cord clamped immediately in the panicked rush to the resuscitation table. Very, very few die following the procedure, but RDS is a common sequel; many incur neurological impairment  and many more remain disabled and dependent on others for the rest of their lives. Growth and development of the brain continues for years after birth, and optimal nutrition and sustenance are required for optimal growth and development. A hiatus in this progress caused by loss of a large amount of blood volume at birth and subsequent anemia may not become apparent for years.   The following comment of Windle applies to all immediately clamped newborns:
“A child with a slight brain defect often appears no different from a normal child. His intelligence quotient may lie in the range considered normal, but one never knows how much higher it would have been if his brain had escaped damage in the uterus or during birth.” 
Peltonen  and Linderkamp  published the two most comprehensive review articles on placental transfusion; both noted the strong correlation between immediate cord clamping and infant anemia. Linderkamp concluded:
“It may be speculated that the prevention of severe iron deficiency in infants living under primitive conditions is more important than the risk of circulatory overload shortly after birth. In civilized countries, a medium placental transfusion appears to be more appropriate in order to avoid the risk of hyperviscosity, whereas iron deficiency in later infancy is probably less dangerous.”
Within a few years, multiple reports [14, 15] of infant anemia being associated with learning and behavioral disorders and mental deficiency in grade school children filled the literature, but none of these authors have made the association of anemia / mental defects with immediate cord clamping at birth. The broad spectrum of brain injury, from neonatal death through spastic paraplegia to memory and mental dysfunction, produced in monkeys by Windle and Myers has been and is being reproduced repeatedly in human neonates by means of immediate cord clamping and current methods of neonatal resuscitation. Today, an epidemic of immediate cord clamping correlates with an epidemic of PDD and autism.
Discussion and Commentary
During the third stage of labor, transition from placental dependency to self-sufficiency in life support is well understood by most midwives, lay and professional; the term used is “transing.” Most physicians think (and are taught) that this physiological process is pathological. For the midwife-home-delivered baby, the pulsating cord is routinely allowed to close itself regardless of the condition of the child at birth. Few if any of these neonates need NICU admission; this is a strong indication that delayed cord clamping – transing - is not a routine cause of pathology (jaundice, polycythemia, hypervolemia, hyperviscosity). In the depressed home-delivered neonate, transing is used as an essential factor in resuscitation; again, the paucity of NICU admissions attests to its value in these cases. On the other hand, that paucity may be due to home deliveries being very selective and of the low risk variety; however, the complexity of the transition process, however perfect, does make it prone to accidents.
The baby inadvertently delivered en route to the hospital is routinely healthy on arrival despite the lack of a cord clamp; on the other hand, the fetus that arrives with a prolapsed cord protruding from the vulva is routinely dead. The results of early detection of cord prolapse / fetal distress and treatment by immediate section are usually good, but not routinely so. No rational person would clamp the prolapsed cord in the vagina; rational therapy aims at relieving the cord compression. The only purpose of emergency delivery of the “at-risk” fetus is to establish pulmonary respiration before impaired cord /placental function injures the child; what contorted logic can sanction immediate destruction of the child’s only life support system before pulmonary respiration is established? The procedure of immediate cord clamping is universally condemned in obstetrical literature, yet it is practiced routinely. 
The ultimate example of this irrationality is ACOG’s Obstetrical Practice Bulletin 138  that advocates immediate cord clamping for arterial cord blood sampling and pH studies in all at risk deliveries; this practice is widespread in the western world. The purpose of the cord blood studies is to (medico-legally) document the oxygenation/asphyxia status of the child at the moment of birth. The results have no bearing on the immediate treatment or resuscitation of the child; they have no correlation with the oxygenation/asphyxia status of the child in the hours and minutes before birth (prenatal scalp pH studies do); however, they do document that the neonate has been deprived of a portion of its natural blood volume and that it was subjected to a period of complete asphyxia until its lungs became functional. Immediate cord clamping does correlate with neonatal hypotension, hypovolemia, RDS, cerebral palsy  and infant anemia that correlates with mental deficiency. 
The costs of birth injury in terms of parental agony are matched by the enormous medical and medico-legal economic burdens it generates. Bulletin 138  is an extreme example of legal defensive medical malpractice – an injurious procedure that results in or accentuates the very pathology that it supposedly documents. Kinmond  came to a very significant and pertinent conclusion regarding the use of delayed clamping / placental transfusion at premature delivery (the transfused preemies were much less morbid (injured) than those immediately clamped):
“This intervention at preterm deliveries has clinical and economic benefits.”
Perinatologists, neonatologists and trial lawyers have pointedly ignored the study. Kinmond’s economic benefits of routinely converting a potentially morbid preemie into a healthy small baby would render these professions virtually redundant. The use of “transing” at every delivery, especially at “risk” deliveries and during resuscitation would produce even more of these economic benefits for patients, but not for these professions. The economic impact of downsizing or closing NICU’s nation-wide and the virtual disappearance of birth injury lawsuits will not occur without strong resistance from those being economically impacted; the campaign of silence and misinformation regarding the cord clamp and placental transfusion from the medical, legal, insurance and hospital professions and the peer review press has succeeded well for many years.
“Another thing very injurious to the child, is the tying and cutting of the navel string too soon; which should always be left till the child has not only repeatedly breathed but till all pulsation in the cord ceases. As otherwise the child is much weaker than it ought to be, a portion of the blood being left in the placenta, which ought to have been in the child.” - Erasmus Darwin, Zoonomia, 1801 
Regarding cutting a cord that is around the neck:
“Let the loop be loosened to enable it to be cast off over the head. … [or] by slipping it down over the shoulders. … If this seems impossible, it should be left alone; and in the great majority of cases, it will not prevent the birth from taking place, after which the cord may be cast off. … Should the child be detained by the tightness of the cord, as does rarely happen, … the funis may be cut … Under such a necessity as this, a due respect for one’s own reputation should induce him to explain, to the bystanders, the reasons which rendered so considerable a departure from the ordinary practice so indispensable. I have known an accoucheur’s capability called harshly into question upon this very point of practice. I have never felt it necessary to do it but once. … The cord should not be cut until the pulsations have ceased.” - Charles D Meigs, M.D. Professor of Midwifery Philadelphia, 1842 
Placental function was the only resuscitative option available to the above authors, and its preservation was of obvious value. Destruction of the infant’s only functioning life support system was clearly understood to be injurious not only for the child, but for the physician’s reputation. Destruction of physiology invariably produces pathology. Immediate cord clamping (ICC) can destroy the physiology that activates all the life support systems of the newborn child; while ICC may impair the function of various organs, the most vulnerable are the metabolically active areas of the brain where ischemic necrosis produces a lifelong defect. ICC is a very injurious and irrational procedure; those that use it put the newborn, themselves and their profession in jeopardy. Those that use, advocate and promote ICC  are invited to explain their morality.
Rational neonatal resuscitation primarily involves the restoration and maintenance of adequate circulation through the brain and all feto-placental life support organs and systems. Amputation of a functioning placenta, and the blood volume contained in it, is an obviously injurious procedure; the organ most vulnerable to permanent injury is the brain.
Copyright February 9, 2003, George Malcolm Morley, MB ChB FACOG
Figure 1 - Weight changes in baby lying at level of vulva, with cord pulsating for 19 minutes. Note weight changes induced by uterine contraction and relaxation.
Figure 2 - Umbilical/placental venous pressure recorded in mms. of Hg. with a catheter inserted in the vein after cutting and clamping the cord 45 seconds after delivery. The first contraction is about one minute post partum (1) as the uterus closes round the placenta. Successive contractions (2 & 3) generate pressures of over 100 mms. of Hg. until the placenta is separated during contraction (4). A fifth contraction pushes the placenta through the lower segment into the vagina (5) followed by sharp peaks of pressure due to maternal effort which eventually expels the placenta from the vulva (6). This third stage of labor followed a spontaneous term labor and delivery. No medication was used.
Figure A - Heart rate and blood pressure changes (above) and gasp pattern (below) associated with 25 minutes of total asphyxia in Term Fetus 1735. Fifteen minutes of resuscitation are also represented. The gasp pattern is identifiable in the cardiotachometer and blood pressure recordings as well as in the bar graph. Efforts at cardiac massage during the twenty-sixth and twenty-seventh minutes also appear. Epinephrine, 0.1 mg was injected intra-arterially at the beginning of resuscitation during the twenty-sixth minute. Gasping reappeared during the fifth minute of resuscitation.
Figure B - Rapid cesarean section delivery of an asphyxiated monkey fetus. During delivery and intubation, severe bradycardia and hypotension developed. However, with 100 per cent oxygen ventilation, the heart rate and blood pressure again increased toward normal values. Umbilical cord clamping after resuscitation led to a sudden jump in the mean blood pressure (65 -> 74 mm. Hg.).