Letter to the Editor regarding ACOG Committee Opinion #303, OBSTETRICS & GYNECOLOGY Vol.104, NO. 4: 903-904.




ACOG Opinion 303 confirms confusion about fetal distress, asphyxia and birth brain injury.  Is “fetal distress” more imprecise than “non-reassuring fetal status?”  Why measure hypoxia as a concept “severe enough to result in HIE”?  Why not use oxygen tension or oxyhemoglobin saturation?  In experimental primates, severe hypoxia first causes cardiac arrest from which brain damage results; however, hypoxia does not cause the heart failure that generates human HIE, hypovolemia is the pathogen.


On MRI, HIE is visualized as ISCHEMIC infarction of brain tissue.  HIE lesions occur and progress in oxygenated neonates that never have been “severely” hypoxic.  Cowan [1] states “there is no evidence that brain damage occurs before birth.”  The word “hypoxic” in HIE is invalid.


Most encephalopathic neonates experience an intrapartum “distress” episode like a tight nuchal cord, and cord venous compression engorges the placenta with blood volume from the fetus; these neonates are born very hypovolemic.  Myocardial contractility requires adequate oxygenation.  Cord pulsation indicates oxygenation and perfusion of the heart and brain; a pallid, limp body indicates minimal perfusion of all other organs.  Immediate cord clamping (ICC) at birth for pH studies amputates 50+% of normal blood volume.  Ventilation reflexively fills the pulmonary circulation from the remaining blood volume; systemic blood pressure and cardiac output fall.


Retraction respiration may ensue. This is a reflex effort generated by low central venous pressure; strong negative intra-thoracic pressure (NIP) pulls venous blood into the right heart.  With hypotension, NIP withdraws arterial blood into the thoracic aorta during “gasps” creating cerebral ischemia – and HIE.  Neuron death (infarction) is caused by deficient perfusion regardless of oxygenation.


Metabolic acidosis (ph<7), low 5+ minute Apgar scores, neurological sequelae and multi-organ dysfunction are all readily explained as products of hypovolemic shock and low cardiac output; they are not plausible “signs of hypoxic damage.”  For details see:




Ischemic encephalopathy and CP are preventable by not clamping the cord and by resuscitating with placental circulation intact, especially for “risk, non-reassuring” births.  A massive transfusion of placental blood that fills and activates the child’s lungs, brain and vital organs rapidly changes a pallid, limp body into a bawling, red, vigorous newborn.


ACOG has withdrawn Opinion 138 regarding cord blood procurement; does the Committee still advocate ICC for pH studies?


George M. Morley, MB ChB

Northport, MI






Cowan et al. Origin and Timing of Brain Lesions in Neonatal Encephalopathy.  Lancet, March, 2003, 736-742



ACOG Practice Committee declined comment.  The letter was not printed.