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Brief Reports

Indian Pediatrics 2001; 38: 898-901  

Transient Neonatal Hyperglycemia


Nalini K. Pati
Ruchira Maheshwari
Harish Chellani
Ravinder N. Salhan

From the Department of Pediatrics, Safdarjung Hospital, New Delhi 110 029, India.

Correspondence to: Dr. Harish Chellani, Senior Pediatrician, Department of Pediatrics, Safdarjung Hospital, New Delhi 110 029, India.

Manuscript received: March 8, 1999;
Initial review completed: April 8, 1999;
Revision accepted: January 30, 2001.

Hyperglycemia in newborns is usually a transient phenomenon which may result in glycosuria with osmotic diuresis, intraventri-cular hemorrhage and dyselectrolytemia and rarely long term complications like persistent diabetes mellitus and mental retardation (1-3). There is a paucity of data in Indian population where more than 30% babies are low birth weight. The present study was conducted to determine the prevalence and antecedent factors of hyperglycemia among neonates admitted in the neonatal unit.

Subjects and Methods

Babies admitted to the neonatal unit for various problems during January’98 to June’98 were prospectively studied. Babies with gross congenital malformations were excluded. The blood sugar measurement by reagent strip method from capillary blood was done as a routine measure in all babies who required admission in the neonatal unit. Those who were found to be hyperglycemic were included in the study and the data regarding birth weight, gestational age, various stress factors like sepsis, birth asphyxia, respiratory distress syndromes and thermal instability were noted. A detailed drug history of receiving steroids, b2 agonists and phenytoin along with the rate and amount of intravenous administration of glucose, intravenous lipid infusion and other hyperosmolar agents was recorded. Information regarding family history of diabetes mellitus and gestational diabetes, mean duration of persistence of hyperglycemia and its outcome were noted. Neonatal hyper-glycaemia once detected with reagent strip method was confirmed by blood sugar measurements in clinical biochemistry labora-tory using glucose oxidase method. The monitoring of blood sugar in these babies was done by glucose oxidase method every 6 hours for first 48 hours, then every 12 hours during next 7 days or till the hyperglycemia was controlled, which ever was later. Neonatal hyperglycemia was defined as whole blood sugar level ³150 mg/dl in preterms and ³125 mg/dl in term babies(2). Serum insulin and lactate levels were done in 6 and 7 cases respectively.

Results

During the study period, a total of 1171 newborns were admitted in the neonatal unit and of them, 11 (0.94%) were diagnosed to be hyperglycemic. Its prevalence was 2.9% among very low birth weight babies. The mean gestational age and mean birth weight of those hyperglycemic neonates were 29.54 ± 4.18 weeks and 1484.54 ± 518.2 g, respectively. Out of total 11 neonates; 6 (54.5%) babies were below 1500 g. The onset of hyper-glycaemia in all babies was noted within first 48 h of age. Among various stress factors, sepsis, severe birth asphyxia and respiratory distress syndrome were present in 5 (45%), 2 (18%) and 3 cases (27.2%), respectively. None of the babies had received any drugs like steroids, parenteral lipid infusion or any other hyperosmolar agent.

The mean blood glucose level was 271.8 ± 75.33 mg/dl (range 175 to 400 mg/dl) with mean duration of hyperglycemia 60.6 ± 15.44 hours (range 48 to 96 hours). Serum insulin levels done in 6 babies did not show any abnormality. Serum lactate levels were done in 7 babies, of which 4 had shown increased value and these babies were septicemic. In ten babies, the hyperglycemia was controlled with treatment of the underlying condition and reducing the intravenous fluid rate to 4mg/kg/min gradually (2 mg/kg/every 6 hours). One neonate, expired (had developed intra-ventricular hemorrhage at the blood sugar level of 400 mg/dl, had serum osmolality of 320 mosm/l with normal serum electrolyte levels). The mean duration of follow up of ten surviving babies was 14.80 ± 6.44 days.

Discussion

The prevalence of neonatal hyperglycemia was found to be 0.94% among all admissions, and was 2.9% in very low birth weight babies. Others have reported the incidence of less than 2% among all infants, 5% in infants receiving intravenous glucose and 20-40% with glucose infusion in very low birth weight (VLBW) babies, respectively(2,3). The different preva-lence in various studies was due to different patient selection criteria (birth weight, gestational age and rate of glucose infusion). According to a study, glucose infusion @ 10 mg/kg/min or more resulted into various degrees of glucose intolerance in infants of lower gestational age who were significantly more intolerant than the babies of higher gestational age(1). Glucose intolerance in pretern babies was attributed to the immaturity of glucose regulatory systems(2,4). Lilien et al. had reported that hyperglycemia was unrelated to decreased circulatory insulin levels in preterms; rather the insulin level had increased in linear with increased plasma glucose concentration(5). The present study also revealed a normal level of insulin in babies. Hyperglycemia in LBW babies was believed to be due to the secretion of catecholamines, corticosterolds. glucose counter regulatory hormones due to stress or as a result of release of cytokines(2,3,6). Moreover, studies suggested a diminished insulin response to an intravenous glucose load within the first 24 hours of birth in the babies of comparable birth weights leading to a higher risk of hyper-glycemia(7).

Stress factor responsible for causation of hyperglycemia includes sepsis due to E.coli and Group B streptococci. Following sepsis there is liberation of catecholamines, cortico-steroids and cytokines which produce an inadequate insulin response(3). Among drugs, methyl-xanthine which is most often used in preterm babies causes increase in cAMP level resulting in activated liver glycogenolysis(3). While two of our babies received inj. aminophylline, none of them had received any other agents.

The problem of hyperglycemia is manifested due to an increase in the osmolality (1 mosm/litre rise is noted with every 18 mg/dl increase in blood sugar); particularly beyond 300 mosm/lit(7). This is in the form of electrolyte disturbances, osmotic diuresis and in extreme form with intraventricular hemorrhage(3,6). Louik et al. had discussed that fluctuations in cerebral blood flow velocity markedly increase the risk of intraventricular hemorrhage (IVH), and such fluctuations may be partially caused by rapid change in osmolality(8). Whether hyper-glycemia causes IVH or vice versa is still controversial but a plasma glucose level of more than 300 mg/dl is usually associated with a high risk of developing IVH(3).

The management of hyperglycemia has been a challenge to the treating neonatologist. Our babies were managed with decreasing the IV fluid infusion to 5% dextrose at 4-5 mg/kg/min and correcting the underlying condition. This reduction was done gradually at 2 mg/kg/6 hours with necessary electrolyte adjustments and no baby required insulin therapy. While using a hypotonic solution, particularly less than 5% dextrose, a strict vigilance should be adhered to avoid a precipitous fall of blood sugar(3). IV insulin infusions had been used to manage this condition but with limited and conflicting reports(2). With a blood sugar of more than 300 mg/dl, crystalline insulin could be used in a single dose of 0.1-0.5 units/kg (subcutaneous/intravenous)(3,9). Continuous insulin infusions were used in VLBW infants; but chances of complications like metabolic disturbances, hypoglycemia, hypoxemia and electrolyte imbalance were noted(2). Fluid losses should be minimized. Daily weight recording, blood and urine glucose estimation and intake output recording should be used for day to day assessments.

Contributors: HC designed the study and analyzed the data and will act as the guarantor for the manu-script. RNS designed and drafted the manuscript. NKP and RM participated in data collection and helped in drafting the manuscript.

Funding: None.

Competing interests: None stated.

Key Messages

  • Hyperglycemia seen in low birth weight and premature infants is usually a transient phenomenon.

  • The various risk factors are low birth weight, stress factors (sepsis, asphyxia, respiratory distress syndrome and high glucose infusion rate (>6 mg/kg/min).

  • Management includes treatment of underlying condition and reducing the IV infusion slowly (2 mg/kg/every 6 h).

  • Insulin has little role in management.


REFERENCES

1. Stonestreet BS, Rubin L, Pollak A, Cowett RM, William O. Renal functions of low birth weight infants with hyperglycemia and glucosuria produced by glucose infusions. Pediatrics 1980; 66: 561-566.

2. Digiacomo JE, William W, Hary JR. Abnormal glucose homeostasis. In: Effective Care of Newborn Infant, 1st Edn. Eds. Sinclair JC, Bracken MB. New York, Oxford University Press, 1992; pp 591-600.

3. Pildes RS, Lilien LD. Metabolic and endocrine disorders. In: Neonatal Perinatal Medicine, 5th edn. Eds. Fanaroff AA, Martin RJ. Chicago, Mosby, 1992; pp 1152-1179.

4. Cowett RM, William OH, Schwartz R. Persistent glucose production during glucose infusion in the neonate. J Clin Invest, 1983; 71: 467-475.

5. Lillien LD, Rosenfield RC, Baccaro MH, Pildes RS. Hyperglycemia in stressed small premature neonates. J Pediatr 1979; 94: 454-459.

6. Kalhan SC, Saker F. Metabolism of glucose in very LBW infants. In: Neontatal-Perinatal Medicine: Disease of the Fetus and Infant, 6th edn. Eds. Fanaroff AA, Martin RJ, Chicago, Mosby, 1997; pp 1461-1462.

7. Dweck HS, Cassady G. Glucose intolerance in infants of very low birth weight. Incidence of hyperglycemia in infants of birth weight 1100 grams or less. Pediatrics 1974; 53: 189-195.

8. Louik C, Mitchell AA, Epstein MF, Shaprio S. Risk factors for neonatal hyperglycemia associated with 10% dextrose infusion. Am J Dis Child 1985; 139: 783-786.

9. Binder ND, Raschko PK, Benda GI, Reynolds JW. Insulin infusion with parenteral nutrition in extremely low birth weight infants with hyperglycemia. J Pediatr 1989; 114: 273- 280.

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