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ARTICLE:
Neil N. Finer, Johnny W. Sun, Wade Rich, Ellen Knodel, and Keith J. Barrington
Randomized, Prospective Study of Low-Dose Versus High-Dose Inhaled Nitric Oxide in the Neonate With Hypoxic Respiratory Failure
Pediatrics 2001; 108: 949-955 [Abstract] [Full text] [PDF]
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[Read P3R] Hypoxic Respiratory Failure: Cause & Prevention
G M Morley   (24 October 2001)

Hypoxic Respiratory Failure: Cause & Prevention 24 October 2001
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G M Morley,
Retired obstetrician
None

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Re: Hypoxic Respiratory Failure: Cause & Prevention

gmmorley{at}webtv.net G M Morley

The pediatric and obstetrical professions, Dr Finer et al. have abandoned the law of cause and effect in their quest to cure the hypoxic newborn. The original cause of hypoxia in this study was not a deficiency of nitrous oxide. Every child in the study, however, being born in the western world, suffered from a deficiency of blood volume due to premature cord clamping and the consequent lack of placental transfusion which, during physiological cord closure, increases the newborn blood volume by 30% - 50%. The extreme example of this hypovolemia in the study is the child which died from hypoxic, ischemic encephalopathy - not enough blood to perfuse or oxygenate the brain. Hypoxic ischemic lesions do not occur in newborns following the normal, massive transfusion of oxygenated placental blood at physiological birth - no cord clamp used.

Most, if not all the 36 patients were suffering from some degree of persistent fetal circulation - incomplete closure of the foramen ovale, a flap valve, which normally is kept closed by pressure in the left atrium being greater than pressure in the right atrium; dilatation of pulmonary arterioles by nitrous oxide aids this closure and decreases cyanosis. At normal birth, the placental transfusion (PT) is an essential part of the switch from fetal to adult circulation. Effected at high presure by gravity and/or the contracting maternal uterus, the PT distends the newborn heart and pulmonary vasculature and supplies the blood voume necessary for optimal perfusion of the newly functioning lungs, gut and kidneys. The full switch mechanism, which has been functioning well for millions of years without cord clamps, is breifly described in my LETTER in OBSTETRICS & GYNECOLOGY, Vol 97, No.6 June, 2001, pages 1025-1026.

Distension of the pulmonary vascular tree "erects" the alveoli and maintains aeration. [Jaykka s. Capillary Erection and Lung Expansion. Acta Paediatr. Scand., 1965; Supp 109]. A very adequate blood volume is needed to maintain this pulmonary circulation and foramen ovale closure; some of the hypovolemic consequences of immediate cord clamping (no PT) are respiratory distress syndrome [1] ("hypovolemic shock lung") and persistent fetal circulation. During the normal third stage of labor, (no cord clamp) placental oxygenation and transfusion continue until pulmonary oxygenation and the adult circulation are well established; this prevents hypoxic brain damage. [Windle, w.f."Brain Damage by Asphyxia at Birth". Scientific American 1969 Oct; 221(4): 76-84.]

Blood tansfusion combined with nitrous oxde therapy might have restored these 36 patients to respiratory and circulatory normalty; it would not have restored the neurons destroyed at birth by ischemia and hypoxia caused by immediate cord clamping. The likelihood of any of these 36 newborns being neurologically perfect is not great.

Until the professions realize that placental transfusion is a normal and necessary physiological event, and that the cord clamp is an extremely dangerous instrument, pediatric reports on treating completely preventable obstetrical tragedies will continue.

Reference: [1] Morley, G.M. Cord Closure: Can Hasty Clamping Injure the Newborn? OBG MANAGEMENT July 1998, 29-36.