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Introduction
Abration in carbohydrate metabolism in neonates is very frequent but hypoglycemia is
more common than hyperglycemia. These defects should be sought as early as possible to prevent permanent organ damage. Neonatal hyperglycemia is a transient phenomenon and if treated timely there is complete recovery. Neonatal hypoglycemia could be transient or secondary to many causes and they should be diagnosed timely and managed.
Transient DM (Temporary idiopathic neonatal hyperglycemia)
Reversible DM occurs only in neonates. Hyperglycemia occurs in small for gestational
age infants who presents with marked dehydration and wasting but with a history of adequate oral intake and no history of diarrhea and vomittings.
Both males and females are equally affected. A positive family history of DM is present in
one third of cases. The diagnosis is based on glycosuria and hyperglycemia with blood sugar 250 mg%. Ketosis is usually mild. Electrolyte imbalances are common. Several infants suffering from this syndrome had relative hypoinsulinemia i.e. inappropriately low plasma immun ore active insulin values in relation to degree of hyperglycemia. Thus it is hypothesised that a temporary aberration in b-cells function in the islet of lagerhans may be responsible. In a few reported cases hyperglycemia was preceded by episode of hypoglycemia.
These infants differ from true diabetics in the reversibility of disease without recurrence in
follow up of 3-25 years so insulin treatment is optional in these cases. Insulin treatment is certainly indicated if there is marked hyperosmalarity because of blood suger 500-1000 mg%. This hyperosmolar state can pose damage to neurons and renal cortical necrosis. Renal cortical necrosis have been associated with hyperglycemia.
These infants are insulin sensitive and clinical improvement occurs with blood sugar values between 130-200 mg%.
True fetal onset diabetes is very rare and isolated cases have been reported. Liggins
reported one such infant with birth weight of 1800 gm and was permanently diabetic.
Neonatal hypoglycerma
Neonatal hypoglycemia is being defined as whole blood glucose 30 mg% or less than 35
mg'% in serum or plasma in first 72 hours of life or 40 mg% ( 45% in serum or plasma) after 3rd day in full term, full size infant. In low birth weight iritant, the lower limit of normal insulin at 20 mg% for whole blood and 25 mg% from plasma or serum.
Blood sugar should be done as a routine in all infants of diabetic mother and for all LEW
babies having birth weight below 10th percentile of their gestational age. Blood glucose values must be obtained in all infants with haemolytic diseases of newborn before exchange transfusion is given.
Blood glucose must also be determined in hypothermic newborn. Macrosomic especially if
exomphalos persists or associated micropenis or midline defects e.g. cleft lip or palate.
In preterm infants hypoglycemia can occur in usually 1st 24 hours. In erythroflastosis
fetalis frequent blood glucose test is desirable after beginning of exchange transfusion with ACD blood.
Neonatal hypoglycemia has four clinical categories
1. Early transitional - Occurs in 1st 6-12 hours of life and is more common with metarnal
diabetes or delayed feeding. It usually does not recurs after improvement. It is usually
asymptomatic.
2. Secondary - Usually secondary to a specific event. Infant is usually symptomatic.
Causes are usually septicemia, acquired or congenital neurological defects, CHDs,
asphyxia anorexia, hypothermia, drugs administered to mother abrupt cessation of I/V
glucose, endocrinal diseases like hypothyroidism or adrenal hemorrhage, hypocalcemia.
3. Classic, transient hypoglycemia - Infant is symptomatic and usually associated with
toxemia of pregnancy in mother. More common in males and small for date babies.
Symptoms are tremors, cynosis, apnea, irritability and convulsions.
Treatment is vigorous dextrose injection (8-10 mg glucose/kg/min) for 48 to 72 hours.
4. Severe, recurrent or persistent hypoglycemia - associated with absolute or relative
hyper insulemia or specific enzymatic or metabodies abnormalities like glycogen storage
diseases, fructose intolerance, galactosemia etc.
Hyperinsulinism : Hyperinsulinism is the most common cause of intra hypoglycemia
respond 3-4 weeks of age. Persistent hyperinsulinemia in motatal period is associated with either nesidioblastisis, b cell hyperplasia, islet cell adenomas. These infants have recurrent bouts hypoglycemia especially when proteins are introduced in diet. Beckwith - Wiedemann syndrome - hypoglycemia associated with β cell hyerplasia.
These infants require high rates of glucose infusion (7 mg/kg/min) to maintain normal
blood glucose concentration.
Diagnosis is confirmed by obtaining several simultaneous insulin and glucose
measurements when the glucose level is low and insulin to glucose ratio .5. Any measurable insulin at blood glucose ( mg% is abnormal. Serum FA and ketones are low but urine may contain ketones. If tests are equivocal Lencine tolerance test/Teloutannide tolerance test and performed and 50% in blood glucose level tolerance test/Teloutannide tolerance test and performed and 50% in blood glucose level is abnormal.
Infants of diabetic mother : Infants born to diabetic mother may have blood glucose 30
mg% in 1st 2-6 hours of life. It causes no ultrasound effects on the baby and may recover spontaneously. It responds dramatically to glucagon (.3 mg/kg I/M I/V). If patient is symptomatic then I/V dextrose can be given. Usually early oral feeds are sufficient to avoid symptomatic hypoglycemia, of poorly controlled maternal diabetes stimulates fetal pancreatic islet cell and leads to hypersecretion of insulin. These infants are also prone to develop frequent respiratory distress, polyeytemia, hypocalcemia, cong. malformations.
Disturbance in glucose metabolism is easily manageable condition provided that physician
has a insight for correct diagnosis. This can prevent permanent damage to vital organs.
REFERENCES
1. Mary Ellen Alery, H. William Taeusch. In Schaffer's Diseases of New Born. 5th Ed.
W.B. Saunders Co., 1984; 514-521.
2. Barness, Devino, Morrow, Oski, Rudolph. In Advances in Paediatrics Vol. 35. Year
Book Medical Publishers. 1988; 167-189.
3. C. Patrick Mahoney. In the Paediatrics Clinics of North America. Vol. 34, No. 4. W.B.
Saunders Co., Aug. 1984; 961-982.
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