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Selected Abstracts from Hot Topics in Neonatology Meeting, Washington DC, December 2000
Neonatal Hypoglycemia:
Marvin Cornblath, MD
This presentation summarized Dr. Cornblath’s half century of study of the problem of glucose homeostasis in the neonate. He reported no new randomized controlled trials, but did offer some interesting suggestions which merit our attention.
In 1959, Dr. Cornblath defined hypoglycemia as having 1) clinical manifestations, 2) a reliable blood glucose of < 20-25 mg/dl, 3) a response to treatment, and 4) usually in SGA, males, born to toxemic mothers. Since that time, the advent of glucometers, statistical surveys, a series of case reports and retrospective analyses led to a number of arbitrary decisions, an increasing number of lawsuits, and an increase in the glucose values defined as hypoglycemic. From the late 1950’s, the definition of hypoglycemia has increased from 20-25mg, to 1970-88 when it became 40-45, to the 1988-1998 period when it rose to 48, to the 1999-2000 era when it is 60.
In late 2000, hypoglycemia is 1) any blood glucose value <60 mg/dl; 2) screening glucometer values are of the same value as laboratory determination; 3) one value is sufficient for diagnosis; 4) response to therapy not necessary and often ignored and 5) secondary hypoglycemia not investigated.
In response to the generalized state of confusion regarding what is normoglycemia, Dr. Cornblath offered an interesting proposal. He suggests that we abandon the term "hypoglycemia", which implies disease, and substitute "operational threshold", which implies action. Operational Thresholds should be considered 1) an indication for action; 2) NOT diagnostic of disease, and 3) should reflect conservative estimates of tolerable lower limits for normoglycemia. These thresholds will be different for specific infants, different at specific ages, and different under established conditions. He proposes the following thresholds for intervention. 1)Asymptomatic: <30-35 mg/dl in AGA term or preterm neonates, lower in breast fed newborns with elevated ketone levels. 2) Symptomatic: <45 mg/dl, where clinical signs clear with glucose. 3) Sick Neonates: <45 mg/dl, includes any infant with HIE, suspected sepsis, or on IV support. At > 24 hours of age the threshold level increases to 40-50 mg/dl, and at any age, glucose level of <20-25 mg/dl should receive parenteral glucose therapy promptly.
Comment: While not supported by any great weight of evidence, Dr. Cornblath’s preeminence in this field lends a certain degree of credibility to his suggestions. Certainly the concept of "Operational Thresholds" would remove the concept of "disease" from our efforts to support glucose homeostasis. It may make diagnostic coding decisions easier, and might even lead to a decrement in the number of lawsuits, which, as Dr. Cornblath points out, are continuing to multiply, and succeed.
Griffith E. Quinby M.D.
UserName: G. M. Morley MB ChB FACOG
Institution: Retired Obstetrician
telephone: (231) 386-9655
email: gmmorley@webtv.net
Date: 26 Oct 2001
Time: 16:45:59
Neonatal hypoglycemia has a cause, and its lawsuits have a cure.
Inside the fetal abdomen, 60% of umbilical blood flows through the ductus venosus, 40% goes to the liver where blood glucose is converted to stored glycogen.
At normal birth (without a cord clamp), placental transfusion boosts the blood volume and establishes the adult circulation in the lungs AND IN THE GUT; the ductus venosus and the umbilical vein close. The liver's main blood supply now comes from the functioning gut via the portal vein and glycogen is readily converted to blood glucose to prevent neonatal hypoglycemia - IF GUT/HEPATIC BLOOD FLOW IS ADEQUATE.
Immediate cord clamping (to obtain a cord pH) stops placental oxygenation (causing asphyxia) and aborts placental transfusion. The resulting hypovolemia causes general vaso-constriction; blood flow through the gut (and hence the liver) is markedly reduced preventing glycogen conversion to blood glucose and causing hypoglycemia. Hypovolemic shock lung (RDS) causes hypoxia; there is no placental oxygenation; vaso-constriction, hypotension and hypoglycemia all combine to cause hypoxic, ischemic, hypoglycemic encephalopathy. Immediate cord clamping is a trial lawyer's dream come true.
Until neonatologists insist that every newborn be resuscitated with the placental circulation intact, and that cords be clamped only after the child is pink and after the cord at the umbilicus is pulseless and bloodless, their hypoglycemic nightmare lawsuits will continue.
P.S. Deficient liver perfusion also causes hepato-cellular jaundice. Placental transfusion prevents jaundice and has produced normal babies for millions of years.