Cerebral magnetic resonance imaging and ultrasonography findings after neonatal hypoglycemia.

OBJECTIVE: The aim of this study was to investigate sequential neuroradiologic changes in the brains of infants after transient neonatal hypoglycemia. We used magnetic resonance imaging (MRI) and ultrasonography (US) head scans. METHODS: Eighteen symptomatic full-term infants whose serum glucose concentrations were

FDG-PET in early infancy: simplified quantification methods to measure cerebral glucose utilization.

UNLABELLED: For further insight into the physiology and pathogenesis of the developing brain, quantification of the cerebral glucose metabolism is needed. Arterial blood sampling or sampling of great volumes of blood is not justified for the purpose of PET studies in children. Therefore, we have developed simplified PET approaches to analyze brain FDG examinations during infancy. METHODS: The study consisted of 18 FDG-PET examinations chosen from our research protocols concerning hypoxicischemic encephalopathy and severe neonatal hypoglycemia. The input function for graphical analysis according to Patlak was derived in two ways: (1) a combined time-activity curve derived from the left ventricular activity concentration (first 7-17 min of the study) and radioactivity concentration in venous whole-blood samples and; (2) activity concentration measured in whole-blood venous blood samples (arterial plasma in one case). As an alternative for semiquantitation, the standardized uptake values (SUV) were calculated and correlated to local cerebral metabolic rates for glucose (LCMRGlc). RESULTS: The influx rate constants (Ki) and LCMRGlc values obtained using the combined curve versus venous curve did not differ statistically (p > 0.05). There was a good correlation between the SUV and LCMRGlc values (r = 0.83, p < 0.001). CONCLUSION: Local cerebral metabolic rates for glucose can be accurately calculated by using the combined curve (left ventricular activity concentration during first 5 min of the study and 2-3 venous whole-blood samples at the end of the study) for even the smallest pediatric patients. When blood samples cannot be obtained, SUV values provide an alternative for estimation of the cerebral glucose uptake and interindividual comparison of the patients.

Estimated radiation dose to the newborn in FDG-PET studies.

UNLABELLED: The aim of this study was to estimate the radiation dose due to intravenous injection of 2-[18F]fluoro-2-deoxy-D-glucose (FDG) for infants studied with PET. METHODS: The radioactivity concentration in the brain and bladder content was measured with PET to determine the cumulated activity in these organs in 21 infant FDG studies. The individual organ masses were estimated according to the whole-body and brain masses, and they were used to calculate the absorbed dose per unit cumulated activity (S values). For organs other than brain and bladder, the cumulated activity was defined from adult studies. For each individual patient, the absorbed dose to the brain, bladder wall and selected organs were calculated. An estimation of the effective dose was determined. RESULTS: Whole-body distribution of FDG in the infants differed from adults: a greater proportion of the injected activity accumulated into the brain (9% versus 7%) and less was excreted to urine (7% versus 20% respectively). The measured cumulated activity in the brain was 0.25 MBq.h/MBq and in the bladder content 0.04 MBq.h/MBq with a large individual variation in latter. The calculated absorbed dose was 0.24 mGy/MBq to the brain and 1.03 mGy/MBq to the bladder wall. The estimated effective dose was 0.43 mSv/MBq. CONCLUSION: The dose to the bladder wall was lower in infants as compared to adults with ordinary amounts of injected activity. The greater amount of activity remaining in the body may increase the dose to other organs. The effective dose was lower compared to adults and conventional nuclear medicine studies of infants. PET can be a valuable tool in pediatric nuclear medicine because of good resolution images, sensitive radiation measurement and a variety of tracers labeled with short-lived isotopes.

Newer techniques to study neonatal hypoglycemia.

Severe neurological sequelae may occur after symptomatic neonatal hypoglycemia. New neuroimaging techniques allow both structural and functional detection of these disturbances. The new diagnostic modalities have shown also transient structural findings associated with neonatal hypoglycemia. The prognostic value of these techniques remains still obscure.

Cerebral metabolic rate for glucose during the first six months of life: an FDG positron emission tomography study.

AIM: To measure the local cerebral metabolic rate for glucose (LCMRGlc) in neonatal brains during maturation using positron emission tomography (PET) and 2-[18F]fluoro-2-deoxy-D-glucose (FDG). METHODS: Twenty infants were studied using PET during the neonatal period. The postconceptional age ranged from 32.7 to 60.3 weeks. All infants had normal neurodevelopment and were normoglycaemic. The development of the infants was carefully evaluated (follow up 12-36 months) clinically, and by using a method based on Gesell Amatruda's developmental diagnosis. LCMRGlc was quantitated using PET derived from FDG kinetics and calculated in the whole brain and for regional brain structures. RESULTS: LCMRGlc for various cortical brain regions and the basal ganglia was low at birth (from 4 to 16 mumol/100 g/minute). In infants 2 months of age and younger LCMRGlc was highest in the sensorimotor cortex, thalamus, and brain stem. By 5 months, LCMRGlc had increased in the frontal, parietal, temporal, occipital and cerebellar cortical regions. In general, the whole brain LCMRGlc correlated with postconceptional age (r = 0.90; P < 0.001). The change in the glucose metabolic pattern observed in the neonatal brain reflects the functional maturation of these brain regions. CONCLUSION: These findings show that LCMRGlc in infants increases with maturation. Accordingly, when LCMRGlc is measured during infancy, the postconceptional age has to be taken into account when interpretating the results.

Cerebral metabolic rate for glucose after neonatal hypoglycaemia.

OBJECTIVE: We studied the effect of neonatal hypoglycaemia on the local cerebral metabolic rate for glucose (LCMRglc). MATERIALS AND METHODS: Eight newborn infants with neonatal hypoglycaemia were studied. The LCMRglc in the whole brain, in five cerebral regions and in skeletal muscles were quantitated using positron emission tomography (PET) and 2-[18F]Fluoro-2-deoxy-D-glucose (FDG). The PET studies were performed at the age of 5.3 +/- 6.2 days during normoglycaemia. The LCMRglc of these infants were compared to the age-adjusted LCMRglc of eight infants with suspected hypoxic-ischaemic brain injury but with normal neurological development. RESULTS: After neonatal hypoglycaemia the age-adjusted LCMRglc in the whole brain was not lower than LCMRglc of the control infants (5.33 +/- 0.60 mumol/100 g/min vs. 6.71 +/- 0.60 mumol/100 g/min). Also the metabolic rate for glucose (MRglc) in the skeletal muscles was similar in hypoglycaemic and control infants (5.56 +/- 2.48 mumol/100 g/min vs. 6.99 +/- 2.41 mumol/100 g/min). CONCLUSION: MRglc in brain and in skeletal muscle seems to be normal after neonatal hypoglycaemia, although larger group of patients with more severe hypoglycaemia are needed to confirm this finding.

Hypoglycemia is common in preterm infants in intensive care.

The blood glucose concentration was measured once daily during the first five days of life in forty appropriate-for-gestational age preterm infants in intensive care. They received human milk and 10% glucose perorally and intravenously. Moderate hypoglycemia (B-Gluc < 2.5 mmol/l) was common in these infants (42%) during the first three days of life. Four infants had severe hypoglycemia (B-Gluc < 0.6 mmol/l) during the first day of life. These data suggest that screening for hypoglycemia will be needed for optimal treatment in preterm infants in intensive care.

Differences in respiratory metabolism during treatment of hypoglycemia in infants of diabetic mothers and small-for-gestational-age infants.

We investigated oxygen consumption and carbon dioxide production during treatment of hypoglycemia in infants of diabetic mothers (IDM) (n=11) and small-for-gestational-age (SGA) infants (n=6). Healthy newborn infants served as controls (n=16). The infants in both groups received normal enteral feedings and they were treated with intravenous glucose at a rate adjusted to increase plasma glucose concentration above 45 mg/dL. Oxygen consumption (VO2) and carbon dioxide production (VCO2) were measured using indirect calorimetry and respiratory quotient (RQ) was calculated. Measurements were performed immediately after the correction of hypoglycemia (6-10 hr), and 24, 72, and 120 hr later. After initiation of treatment, and 24 hr later mean VCO2 and RQ were significantly higher in the IDM and the SGA infants than in healthy infants. 72 and 120 hr after the first measurement, the IDM did not differ from the healthy controls, whereas in the SGA infants mean VCO2 and VO2 were still significantly increased. In the SGA infants, the hypermetabolism was sustained during whole study period. Our results indicate that the metabolic defect resulting in hypoglycemia is different between the SGA and IDM infants. However, the treatment with supplemental glucose is necessary to both groups.