Polycythemia in the newborn: do asymptomatic babies need exchange transfusion?

A total of 2288 infants were screened for hematocrit over a period of 15 months. Polycythemia was diagnosed in 27 cases (1.2%). Preterm and term babies had more or less equal risk to develop polycythemia (1.5% and 1.1% respectively) while postterm infants had at least three times increased risk (3.4%) when compared to their term counterparts. Large-for-dates (LFDs) and small-for-dates (SFDs) infants had increased risk of manifesting polycythemia which was nearly four times (2.2%) and twenty-five times (13.2%) respectively, as compared to appropriate-for-dates (AFDs) babies (0.5%). About one-third of polycythemic infants had one or more symptoms. The most common symptoms observed was jitteriness (25.9%) followed by respiratory distress (14.8%) and lethargy (11.1%). The mean (+/- SD) hematocrit of symptomatic newborns (76.0 +/- 4.04) was found to be significantly higher (p less than 0.001) as compared to asymptomatic babies (70.84 +/- 2.73). Partial exchange transfusion with plasma was performed in all the symptomatic cases within 8 hours of onset of symptoms. No such intervention was performed in asymptomatic cases. On neurodevelopment follow-up, the development indices (MDI and PDI) of both asymptomatic and symptomatic cases were found to be comparable.     

Effects of maternal labetalol on the newborn infant.

Forty eight neonates, born to mothers suffering from pregnancy induced hypertension and receiving labetalol for control of blood pressure, were studied for the possible adverse effects of the drug. These were compared with eighty one neonates matched for gestation and weight and born to mothers with pregnancy induced hypertension treated with drugs other than labetalol. Incidence of birth asphyxia and intrauterine growth retardation (IUGR) in the study population was 10.4 and 22.9%, respectively and in the control group 5 and 19.7%, the difference between two groups was not statistically significant (p > 0.05). However, the incidence of hypoglycemia was significantly higher (p < 0.01) in the study group (47.9%) as compared to the control group (17.2%). Two-thirds of the hypoglycemic babies in the study population were asymptomatic and they were managed with sugar-fortified milk feeds. In the study population, the symptomatic hypoglycemic babies had hypoglycemia for prolonged duration of 43.3 +/- 23.3 hours as compared to 11.5 +/- 6.3 hours in symptomatic hypoglycemic babies of the control group (p < 0.01). The mothers of the symptomatic babies in the study group received higher doses of labetalol in the range of 287.6 +/- 142.3 mg/day while rest of the mothers in the same group whose babies had either asymptomatic hypoglycemia or normal blood glucose levels, received 239.5 +/- 118.5 mg/day, though the difference was not statistically significant. It is concluded that maternal labetalol therapy is associated with increased risk of neonatal hypoglycemia.     

Hypoglycemia in small for gestational age babies

The main objectives of the study were to find the incidence and risk factors associated with development of hypoglycemia in small for gestational age (SGA) babies, to compare haemoglucotest strips (Boehringer Mannheim) with the standard laboratory method (glucose-hexokinase) for estimation of blood glucose, and to measure the insulin and cortisol responses of SGA babies. This was a prospective longitudinal study. The sample included SGA babies and over a period of six months, 127 consecutively born small for gestational age babies were investigated prospectively for development of hypoglycemia in first 48 hrs of life. Plasma samples were taken during episodes of hypoglycemia for insulin and cortisol estimation and compared with non-hypoglycemic controls. The overall incidence of hypoglycemia was 25.2% in SGA babies and 98% of the episodes occurred within first 24 hrs. Compared to non-hypoglycemics, mothers of hypoglycemic babies had higher incidence of receiving i.v. fluids (5% dextrose) during labour. The hypoglycemic babies were more likely to be sick and oral feeds had been initiated by one hour of life in only 37% of them compared to 63% of non-hypoglycemic babies. Plasma insulin/glucose ratio was significantly higher in hypoglycemic than non-hypoglycemic babies, whereas the cortisol levels were similar. Small for gestational age babies are highly prone to develop hypoglycemia in first 24 hrs of life.     

糖尿病母亲婴儿低血糖发生情况及其与脑损伤的关系

目的探讨糖尿病母亲婴儿（IDMS）低血糖的发生情况及其与脑损伤的关系。方法分析86例IDMS低血糖的发生情况、母亲孕期血糖控制与低血糖持续时间的关系。分析其脑损伤发生及严重程度与低血糖持续时间、并其他疾病和症状性低血糖的关系。结果短暂性低血糖75例（87.2%）,反复发作性低血糖11例（12.8%）。母亲孕期血糖反复发作性低血糖发生率控制不满意组为19.4%,满意组为8%。反复发作性低血糖组脑损伤总发生率及重度脑损伤发生率高于短暂性低血糖组,并其他疾病组48.5%和无临床症状组57.4%,均有显著性差异（Pa〈0.05）。结论低血糖的持续时间与母亲妊娠期血糖控制情况及脑损伤发生、严重程度有关;低血糖并其他疾病会加重脑损伤,症状性低血糖时常存在严重脑损伤。     

Hypoglycemia in newborn infants: Features associated with adverse outcomes

The purpose of this review article is to document from the literature values of blood/plasma glucose concentration and associated clinical signs and conditions in newborn infants (both term and preterm) that indicate a reasonable clinical probability that hypoglycemia is a proximate cause of acute and/or sustained neurological injury and to review the physiological and pathophysiological responses to hypoglycemia that may influence the ultimate outcome of newborns with low blood glucose. Our overall conclusion is that there is inadequate information in the literature to define any one value of glucose below which irreparable hypoglycemic injury to the central nervous system occurs, at any one time or for any defined period of time, in a population of infants or in any given infant. Clinical signs of prolonged and severe neurological disturbance (coma, seizures), extremely and persistently low plasma/blood glucose concentrations (0 to <1.0 mmol/l [0 to <18-20 mg/dl] for more than 1-2 h), and the absence of other obvious central nervous system (CNS) pathology (hypoxia-ischemia, intracranial hemorrhage, infection, etc.) are important for the diagnosis of injury due to glucose deficiency. Specific conditions, such as persistent hyperinsulinemia with severe hypoglycemic episodes that include seizures, also contribute to the diagnosis of hypoglycemic injury. Such lack of definitive measures of injury specific to glucose deficiency indicates that clinicians should be on the alert for infants at risk of hypoglycemia and for clinical signs and conditions that might herald severe hypoglycemia; they should have a low threshold for investigating and diagnosing 'hypoglycemia' with frequent measurements of plasma/blood glucose concentration; and they should treat low glucose concentrations promptly and maintain them in a safe range. Because there is no conclusive evidence or consensus in the literature that defines an absolute value or duration of 'hypoglycemia' that must occur, with our without related clinical complications, to produce neurological injury, clinicians should consider the information currently available, determine a 'target' plasma or blood glucose concentration that is acceptable, and treat infants with glucose concentrations below this value accordingly. Our intent in this review article is to highlight the studies relevant to this issue and help clinicians formulate a safe and, hopefully, effective strategy for the diagnosis and treatment of hypoglycemia.     

血清脑红蛋白评估新生儿低血糖脑损伤的临床价值

目的探讨血清脑红蛋白（NGB）在新生儿低血糖脑损伤评估中的临床应用价值。方法选择100例低血糖新生儿为研究对象。根据振幅整合脑电图（aEEG）结果和/或临床表现，分为3组：症状性低血糖脑损伤组（n=22）、无症状性低血糖脑损伤组（n=37）和低血糖无脑损伤组（n=41）。比较各组患儿血糖、低血糖持续时间、NGB及神经元特异性烯醇化酶（NSE）水平、改良aEEG评分；分析NGB与NSE水平、改良aEEG评分之间的相关性并绘制受试者工作特征（ROC）曲线等。结果症状性低血糖脑损伤组血糖、改良aEEG评分低于无症状性低血糖脑损伤组及低血糖无脑损伤组（P < 0.05），NGB、NSE、低血糖持续时间高/长于无症状性低血糖脑损伤组及低血糖无脑损伤组（P < 0.05）。无症状低血糖脑损伤组血糖、改良aEEG评分低于低血糖无脑损伤组（P < 0.05），NGB、NSE及低血糖持续时间高/长于低血糖无脑损伤组（P < 0.05）。NGB与NSE、低血糖持续时间呈正相关（分别r=0.922、0.929，P < 0.05），与血糖、改良aEEG评分呈负相关（分别r=-0.849、-0.968，P < 0.05）；NGB、NSE、改良aEEG评分的ROC曲线下面积分别为0.894、0.890、0.941，NGB最佳截断值为108 mg/L，敏感度80.8%，特异度95.8%。结论血清NGB与NSE、改良aEEG评分比较，同样可作为评估低血糖新生儿脑损伤的特异性指标，具有一定的临床应用价值。     

Hypoglycemic brain injury

Hypoglycemia frequently occurs in newborn infants who previously have suffered asphyxia, who are offspring of diabetic mothers, or who are low birthweight for gestational age (IUGR). Many infants who are hypoglycemic do not exhibit clinical manifestations, while others are symptomatic and at risk for the occurrence of permanent brain damage. This review emphasizes the clinical, neuropathologic, and neuro-imaging features of hypoglycemia in newborn infants, especially those who are symptomatic. Neurologic morbidity occurs particularly in those infants who have suffered severe, protracted, or recurrent symptomatic hypoglycemia. Experimental observations emphasize the resistance of the immature brain to the damaging effect of hypoglycemia; such resistance occurs as a consequence of compensatory increases in cerebral blood flow, lower energy requirements, higher endogenous carbohydrate stores, and an ability to incorporate and consume alternative organic substrates to spare glucose for energy production. Hypoglycemia combined with hypoxia-ischemia (asphyxia) is more deleterious to the immature brain than either condition alone.     

Meconium-stained amniotic fluid and hypoglycemia among term newborn infants

To evaluate whether meconium-stained amniotic fluid (MSAF) is a risk factor for neonatal hypoglycemia. Retrospective recording of medical charts of full-term infants born following observation of meconium-stained amniotic fluid to examine glucose levels in the first hours of life. Out of 803 infants of the study group, 68 (8.5%) had glucose levels lower than 47 mg/dl. Most (6.7%) had mild hypoglycemia, and 14 (1.8%) had moderate or severe hypoglycemia (1.4% and 0.4% respectively). No infant developed clinical signs clearly related to hypoglycemia. Low-risk infants born following meconium-stained amniotic fluid are not at increased risk for neonatal hypoglycemia.     

Metabolic events in infants of diabetic mothers during first 24 hours after birth. I. Changes in plasma glucose, insulin and glucagon

Changes in plasma glucose, nonantibody-bound insulin and glucagon concentrations were studied in 32 newborn infants of diabetic mothers (IDM) during the first 24 hours after birth. Ten infants were born to White class A mothers and 22 to class B-F mothers. The infants were kept fasting during the investigative period and blood was sampled from an umbilical artery catheter. At birth, plasma glucose and glucagon levels were similar in the class A and B-F infants, whereas nonantibody-bound insulin levels were approximately 15-fold higher in the class B-F infants than in the class A infants (p less than 0.001). After birth, plasma glucose fell in all infants, the nadir being reached at two hours (p less than 0.01). Plasma glucose fell by approximately 35% in the class A infants and 63% in the class B-F infants (p less than 0.01). Eight IDM had asymptomatic hypoglycemia (plasma glucose less than 1.9 mmol/l) and four of these infants had glucose levels below 1.7 mmol/l and were withdrawn from further study. In the remaining four hypoglycemic IDM, plasma glucose was about 1.6-fold higher (p less than 0.01) and insulin about 11-fold higher (p less than 0.001) at birth compared to the 24 normoglycemic IDM. The hypoglycemia was attended by unchanged insulin levels in the class A infants, whereas insulin fell in the class B-F infants (p less than 0.01). However, during the whole investigative period, plasma insulin of the class B-F infants was higher than that of the class A infants (p less than 0.01). After birth, plasma glucagon increased slowly in all IDM and peak values were reached after 12 hours in the class A infants (p less than 0.05) and 24 hours in the class B-F infants (p less than 0.01). Only those infants who became hypoglycemic after birth exhibited a significant increment in plasma glucagon from 0.2 hours (p less than 0.05). These results suggest that neonatal hypoglycemia of IDM results from high plasma levels of nonantibody-bound insulin together with a very retarded increment in plasma glucagon levels. The degree of neonatal hypoglycemia and hyperinsulinemia of an individual IDM seems to be positively correlated to the severity of the diabetes of the mother.     

Neonatal hypoglycemia caused by hyperinsulinism and subsequent epilepsy

A historical cohort study was undertaken to determine the risk of epilepsy in a population of 18 newborns with neonatal hypoglycemia due to insulin excess. Follow-up was 3 years 8 months (range 7 years-1 year 3 months). Insulin excess was associated with maternal diabetes in 13 infants, with an isolated macrosomia in 2 infants, in one case with probable Langerhans hyperplasia, and in 2 newborns only prolonged beta-sympathomimetic therapy was the possible cause of insulin excess. Newborns with anoxia, brain malformation or small for date were excluded. Two newborns had hypoglycemia with epileptic clonic seizures, but only one was later epileptic. In this case, hypoglycemia was severe and persistent (16 hours). Hyperinsulinism was related to Langerhans hyperplasia. CT scan made at ages one and 6 months showed large hypodensity of the frontal and occipital white matter. Visual evoked responses were also abnormal. Visual evoked responses and CT scan normalized at 1 year. In other children, asymptomatic hypoglycemia (n = 11) or symptomatic hypoglycemia without epileptic seizures (n = 5) did not increase the epileptic risk as none of them had epileptic seizure later on. Thus, seizures associated with neonatal hypoglycemia alone seem to increase the epileptic risk with duration and severity of hypoglycemia being also essential prognostic factors.     

胎龄≤32周早产儿低血糖的危险因素分析

目的 探讨胎龄≤32周早产儿出生后发生低血糖的危险因素。方法 回顾性纳入2017年1月至2020年6月入住新生儿重症监护病房的86例胎龄≤32周低血糖早产儿作为低血糖组,随机选取同期住院监测血糖正常的早产儿172例为对照组。采用单因素分析与多因素logistic回归分析筛选早产儿低血糖的危险因素。结果 研究期间早产儿共计515例,其中低血糖86例（16.7%）。低血糖组小于胎龄儿（SGA）、剖宫产出生、孕母高血压、产前使用激素的比例均高于对照组（P < 0.05）,而出生体重及血糖检测前已静脉使用葡萄糖的比例均低于对照组（P < 0.05）。SGA（OR=4.311,95% CI：1.285~14.462）、孕母高血压（OR=2.469,95% CI：1.310~4.652）和产前使用激素（OR=6.337,95% CI：1.430~28.095）为早产儿低血糖的危险因素（P < 0.05）,静脉使用葡萄糖（OR=0.318,95% CI：0.171~0.591）为早产儿低血糖的保护因素（P < 0.05）。结论 SGA、孕母高血压和产前使用激素可增加胎龄≤32周早产儿早期发生低血糖的风险;对胎龄≤32周早产儿,建议生后尽早静脉使用葡萄糖,以减少低血糖的发生。     

Hypoglycemia in pediatric renal allograft recipients

Symptomatic hypoglycemia developed 5 to 45 months after transplantation in nine children who had renal transplants before 6 years of age. During hypoglycemia, serum glucose levels ranged from 14 to 39 mg/dl (0.8 to 2.1 mmol/L). Hypoglycemic episodes occurred between 1.7 and 7.5 years of age. Six patients had generalized seizures; the remaining three had diaphoresis with stupor or lethargy. None of the children had serious infections, diabetes, congenital defects of glucose metabolism, or a history of treatment with insulin or oral hypoglycemic agents. Six patients had hypoglycemic symptoms after a prolonged fast, and at least four had ketosis. Eight of the nine patients were receiving propranolol when hypoglycemia occurred. No differences in the daily prednisone dose, the number of transplant rejection episodes, or the frequency of treatment with medications other than propranolol were noted between hypoglycemic patients and 56 normoglycemic age-matched renal transplant recipients. All hypoglycemic patients were subsequently treated with frequent feedings and discontinuation of propranolol. No further hypoglycemic episodes have occurred in eight of nine patients. Symptomatic hypoglycemia should be recognized as a potentially devastating complication of pediatric renal transplantation.     

Perinatal outcome of infants born to diabetic mothers.

Two hundred and sixty three pregnant diabetic mothers' perinatal outcome was evaluated. Two hundred and twenty five infants were born to gestational diabetic mothers (IGDM) and 38 infants to mothers with established diabetes mellitus (IDM). In IGDM group, 34 babies (15%) were preterm and 45 (20%) were low birth weight (less than 2500 g). Thirty eight babies (17%) were large-for-dates (LFD) and 14 (6.2%) were small-for-dates (SFD). Among IDM group, 8 (21%) babies were preterm and 8 (21%) were low birth weight (less than 2500 g). Fifteen babies (39.5%) were LFD and 3 (8%) were SFD. Out of all babies, hypoglycemia occurred in 43 (16%), birth asphyxia in 24 (9%) and respiratory distress in 21 (8%). Nearly half of respiratory distress were due to hyaline membrane disease. Perinatal mortality rate was significantly higher (p less than 0.001) in IDM (237/1000 live birth) as compared to IGDM (40/1000 live birth).     

The Relationship between Decreased Iron Stores, Serum Iron and Neonatal Hypoglycemia in Large-for-Date Newborn Infants

ABSTRACT. We assessed the relationship between neonatal hypoglycemia and newborn iron status in 15 hypoglycemic, large-for-date newborn infants, 12 of whom were infants of diabetic mothers. These infants had significantly lower mean serum iron concentrations, ferritin concentrations, percent iron-binding saturation and calculated iron stores, and significantly higher mean transferrin concentrations, total iron-binding capacity concentrations and mid-arm circumference: head circumference ratios when compared with either 15 euglycemic large-for-date or 15 euglycemic appropriate-for-date control infants ( p < 0.001 for all comparisons). All hypoglycemic infants had ferritin concentrations below the 5th percentile as compared to 3 % of controls ( p < 0.001), and 67 % had transferrin concentrations above the 95th percentile (controls: 0 %; p < 0.001). Only the hypoglycemic infants demonstrated a significant negative linear correlation between ferritin and transferrin concentrations ( r =−0.83; p < 0.001). Decreased serum iron concentrations were associated with size at birth ( r =−0.60; p = 0.01) and with increased red cell iron ( r =−0.60; p = 0.01), implying a redistribution of iron dependent on the degree of fetal hyperglycemia and hyperinsulinemia. Infants with increased red cell iron had more profound neonatal hypoglycemia. These results show a significant association between decreased iron stores and neonatal hypoglycemia in macrosomic newborn infants associated with a significant shift of iron into red blood cells.     

The relationship between decreased iron stores, serum iron and neonatal hypoglycemia in large-for-date newborn infants

We assessed the relationship between neonatal hypoglycemia and newborn iron status in 15 hypoglycemic, large-for-date newborn infants, 12 of whom were infants of diabetic mothers. These infants had significantly lower mean serum iron concentrations, ferritin concentrations, percent iron-binding saturation and calculated iron stores, and significantly higher mean transferrin concentrations, total iron-binding capacity concentrations and mid-arm circumference:head circumference ratios when compared with either 15 euglycemic large-for-date or 15 euglycemic appropriate-for-date control infants (p less than 0.001 for all comparisons). All hypoglycemic infants had ferritin concentrations below the 5th percentile as compared to 3% of controls (p less than 0.001), and 67% had transferrin concentrations above the 95th percentile (controls: 0%; p less than 0.001). Only the hypoglycemic infants demonstrated a significant negative linear correlation between ferritin and transferrin concentrations (r = -0.83; p less than 0.001). Decreased serum iron concentrations were associated with size at birth (r = -0.60; p = 0.01) and with increased red cell iron (r = -0.60; p = 0.01), implying a redistribution of iron dependent on the degree of fetal hyperglycemia and hyperinsulinemia. Infants with increased red cell iron had more profound neonatal hypoglycemia. These results show a significant association between decreased iron stores and neonatal hypoglycemia in macrosomic newborn infants associated with a significant shift of iron into red blood cells.     

新生儿低血糖脑损伤临床特征与脑电图监测

目的探讨新生儿低血糖脑损伤(HBD)时的脑电图(EEG)改变与临床预后关系,为HBD的诊断及预防提供依据。方法监测住院新生儿血糖并描记入院后24～72 h的EEG,低血糖新生儿于入院后2周再次EEG检查。分析比较低血糖新生儿与正常血糖新生儿,以及无症状性与症状性低血糖患儿EEG的异常率以及预后。结果入组100例新生儿,其中低血糖组52例,正常血糖组48例;低血糖组新生儿中症状性低血糖25例,无症状性低血糖27例。EEG异常率低血糖组新生儿73.1%(38/52),正常血糖组12.5%(6/48),两者差异有统计学意义(χ2=37.17,P<0.05)。低血糖组新生儿中,症状性低血糖组EEG异常率96%(24/25),无症状性低血糖组51.9%(14/27),两者差异有统计学意义(χ2=10.7,P<0.05)。新生儿血糖越低、持续时间越长,则EEG异常越严重。EEG中重度异常新生儿,大多遗留认知障碍、癫疒间、脑瘫等后遗症。结论新生儿HBD与低血糖的严重程度及持续时间密切相关。EEG能客观、直接地反映脑细胞的功能状态及损害程度,有助于早期评估脑损伤的程度及预后。     

METABOLIC EVENTS IN INFANTS OF DIABETIC MOTHERS DURING FIRST 24 HOURS AFTER BIRTH I.

ABSTRACT. Changes in plasma glucose, nonantibody-bound insulin and glucagon concentrations were studied in 32 newborn infants of diabetic mothers (IDM) during the first 24 hours after birth. Ten infants were born to White class A mothers and 22 to class B-F mothers. The infants were kept fasting during the investigative period and blood was sampled from an umbilical artery catheter. At birth, plasma glucose and glucagon levels were similar in the class A and B-F infants, whereas nonantibody-bound insulin levels were approximately 15-fold higher in the class B-F infants than in the class A infants (p<0.001). After birth, plasma glucose fell in all infants, the nadir being reached at two hours (p<0.01). Plasma glucose fell by approximately 35 % in the class A infants and 63 % in the class B-F infants (p<0.01). Eight IDM had asymptomatic hypoglycemia (plasma glucose <1.9 mmol/l) and four of these infants had glucose levels below 1.7 mmol/l and were withdrawn from further study. In the remaining four hypoglycemic IDM, plasma glucose was about 1.6-fold higher (p<0.01) and insulin about 11-fold higher (p<0.001) at birth compared to the 24 normoglycemic IDM. The hypoglycemia was attended by unchanged insulin levels in the class A infants, whereas insulin fell in the class B-F infant (p<0.01). However, during the whole investigative period, plasma insulin of the class B-F infants was higher than that of the class A infants (p<0.01). After birth, plasma glucagon increased slowly in all IDM and peak values were reached after 12 hours in the class A infants (p<0.05) and 24 hours in the class B-F infants (p<0.01). Only those infants who became hypoglycemic after birth exhibited a significant increment in plasma glucagon from 0-2 hours (p<0.05). These results suggest that neonatal hypoglycemia of IDM results from high plasma levels of nonantibody-bound insulin together with a very retarded increment in plasma glucagon levels. The degree of neonatal hypoglycemia and hyperinsulinemia of an individual IDM seems to be positively correlated to the severity of the diabetes of the mother.     

Hyperammonemia in hypoglycemic preterm neonates

Plasma glucose, blood urea nitrogen, and ammonia were measured simultaneously in 44 newborns a few hours after birth. When the concentration of plasma glucose was below 30 mg/dl, plasma ammonia concentration was significantly higher (129 +/- 67 mumol/l) than in normoglycemic infants (74 +/- 33 mumol/l; p less than 0.01). Blood urea nitrogen was slightly lower in hypoglycemic infants (3.65 +/- 0.7 mmol/l) than in the control group (4.5 +/- 1 mmol/l) but the difference was not significant. These data show that hyperammonemia can be associated to hypoglycemia in low birth weight infants. Therefore, further investigations are required to determine the link between urea and glucose production rates in hypoglycemic newborns and whether hyperammonemia participates in the deleterious effects of hypoglycemia on the neonatal brain.     

Neonatal hypoglycemia in a growth hormone registry: incidence and pathogenesis

OBJECTIVE: To examine the characteristics of infants with neonatal hypoglycemia treated with growth hormone (GH) in order to gain insights into factors aiding in the identification of and timely treatment of hypopituitary neonates. STUDY DESIGN: The National Cooperative Growth Study (NCGS) database was examined to identify infants with neonatal hypoglycemia started on GH by 6 months of age. 169 infants (100 males, 69 females) were found and their data analyzed for physical characteristics, the presence of other hormone deficits, and the diagnostic methods used. RESULTS: Mean +/- SD baseline length standard deviation score (SDS) was -1.5 +/- 1.8. 148/169 infants had hypopituitarism. Twelve had isolated GH deficiency (GHD). Nine had hypoglycemia without hypothalamic or pituitary pathology. Structural central nervous system (CNS) lesions and/or midline facial defects were present in 66/169. 55/100 males had micropenis. Although 158 infants had GHD, only 90 infants had it documented by stimulation testing (80) or a critical sample when hypoglycemic (10). Multiple hormone replacement therapy was necessary in 89% of the hypoglycemic infants. CONCLUSIONS: The great majority of these hypoglycemic infants had GHD, usually secondary to hypopituitarism. Over 1/3 had structural lesions of the hypothalamic-pituitary area or midline facial defects. Although lengths may be normal in these infants, physical features such as micropenis or cleft lip and/or palate should suggest pituitary dysfunction as the etiology of their hypoglycemia. A critical blood sample for GH taken during hypoglycemia is a quick and definitive diagnostic tool.     

Pilot study of a model-based approach to blood glucose control in very-low-birthweight neonates

ABSTRACT: BACKGROUND: Hyperglycemia often occurs in premature, very low birthweight infants (VLBW) due to immaturity of endogenous regulatory systems and the stress of their condition. Hyperglycemia in neonates has been linked to increased morbidities and mortality and occurs at increasing rates with decreasing birthweight. In this cohort, the emerging use of insulin to manage hyperglycemia has carried a significant risk of hypoglycemia. The efficacy of blood glucose control using a computer metabolic system model to determine insulin infusion rates was assessed in very-low-birth-weight infants. METHODS: Initial short-term 24-hour trials were performed on 8 VLBW infants with hyperglycemia followed by long-term trials of several days performed on 22 infants. Median birthweight was 745g and 760g for short-term and long-term trial infants, and median gestational age at birth was 25.6 and 25.4 weeks respectively. Blood glucose control is compared to 21 retrospective patients from the same unit who received insulin infusions determined by sliding scales and clinician intuition. RESULTS: Reduction in hyperglycemia towards the target glucose band was achieved safely in all cases during the short-term trials with no hypoglycemic episodes. Lower median blood glucose concentration was achieved during clinical implementation at 6.6 mmol/L (IQR: 5.5 - 8.2mmol/L, 1,003 measurements), compared to 8.0 mmol/L achieved in similar infants previously (p < 0.01). No significant difference in incidence of hypoglycemia during long-term trials was observed (p = 0.51). Percentage of blood glucose within the target range was increased by 83% compared to the retrospective cohort (p < 0.01). CONCLUSIONS: A computer model that accurately captures the dynamics of neonatal metabolism can provide safe and effective blood glucose control without increasing hypoglycemia.