Analgesia for neonatal circumcision: a randomized controlled trial of EMLA cream versus dorsal penile nerve block.

OBJECTIVE: To compare the efficacy of the dorsal penile nerve block (DPNB) with a less invasive form of local anesthesia, eutectic mixture of local anesthetic (EMLA) cream, for reduction of pain during neonatal circumcision. DESIGN: Prospective, blinded, randomized, controlled trial. SETTING: Tertiary referral, neonatal intensive care nursery in a university teaching hospital. PATIENTS: Fifty infants >/=341/2 weeks postmenstrual age and stable for discharge at time of circumcision; gestational age at birth 25 to 41 weeks; birth weight 600 to 4390 g; age at study 3 to 105 days. An additional cohort of term newborns (n = 20), who were not randomized, were circumcised without anesthesia. INTERVENTIONS: Administration of either EMLA cream (0.5 g topically 1 hour before circumcision) or 1% lidocaine (0.7-1.0 mL subcutaneously 3 minutes before circumcision). OUTCOME MEASURES: Primary: Neonatal Infant Pain Scale (NIPS) score; secondary: heart rate, respiratory rate. All outcome measures were assessed by an individual who was blinded to the group assignment and did not perform the circumcision. RESULTS: NIPS scores were significantly lower in the DPNB infants (2.3 +/- 1.8) compared with the EMLA infants (4.8 +/- 0.7). NIPS scores in patients circumcised without anesthesia indicated severe pain. There was a significantly greater increase in heart rate over the duration of the circumcision in the EMLA group than in the DPNB group (49 vs 9 beats per minute). Adverse effects included small hematomas at the site of injection in DPNB infants (10/23), mild erythema at 1 and/or 24 hours after circumcision in the EMLA infants (3/21), and penile edema noted 5 days after circumcision requiring removal of the circumcision bell in 1 DPNB infant. CONCLUSIONS: DPNB provides better pain reduction during neonatal circumcision than EMLA cream. EMLA cream may provide pain reduction compared with no anesthesia during neonatal circumcision.

Effects of neonatal exposure to caffeine on adenosine A1 receptor ontogeny using autoradiography.

The ontogeny of adenosine A1 receptor density was assessed via autoradiographical analysis of [3H]cyclohexyladenosine ([3H]CHA) binding in brains of 14-31-day-old rats as a function of exposure to caffeine over postnatal days 2-6. This exposure period was analogous to the period during which human infants are administered caffeine as treatment for apnea of prematurity. [3H]CHA binding was greatest in CA1 and CA3 hippocampus in both caffeine-exposed and control rats across all ages. Within the anterior, ventral, lateral and medial regions of the thalamus of unmanipulated rats, [3H]CHA binding did not change with age. In caffeine-exposed rats, however, [3H]CHA binding increased significantly within these thalamic subregions as the rats aged. In addition, with age in both treatment groups, the molecular and granular layers of the cerebellum and the CA1 and dentate gyrus of the hippocampus displayed increasing [3H]CHA density. Furthermore, regardless of age, [3H]CHA binding was decreased in the molecular layer of neonatally caffeine-exposed animals as compared to controls. Thus, limited exposure to caffeine within the first postnatal week altered the subsequent expression of adenosine A1 receptors in most subregions of the thalamus and in the molecular layer of the cerebellum.

Aging-related changes in brain metabolism are altered by early developmental exposure to diazepam.

To study the long-term effects of prenatal diazepam (DZ) exposure, 31P NMR (nuclear magnetic resonance) spectra and levels of thiobarbituric acid (TBA)-reactive material were measured in the brains of rats from 3 to 26 months of age. In control rats, there were aging-related increases in levels of TBA-reactive material, decreases in intracellular pH (pHi) and alterations in phosphocreatine (PCr) utilization. Prenatal (late gestational) DZ exposure induced lasting, dose-related and age-related alterations in levels of TBA-reactive material and pHi. The results indicate that the prenatal chemical environment can influence cellular metabolism throughout the lifetime of the organism, and that the process of aging can in turn interact with the consequences of prenatal drug exposure.