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Objectives: Hospital closures promote latent factors putting patients at risk for medical errors. Our goal was to maintain safe patient care in our Neonatal Intensive Care Unit (NICU) by preventing any increase in neonatal mortality or hospital-based complications prior to hospital closure., Methods: Interventions included expanding TeamSTEPPS huddles and Leadership WalkRounds TM . Measurements of safety domains were conducted using the Safety Attitudes Questionnaire. A run chart tracked neonatal mortality. We compared hospital-based complications for all neonatal admissions in 2019 with our own past outcomes., Results: Teamwork climate scores increased from an average score of 24.6-28.3 (maximum score 30, P < 0.05, CI 6.7-0.9). Quarterly neonatal mortality and neonatal outcomes did not worsen. The frequency of transfer did not increase., Conclusions: A strong teamwork climate with resilient leadership may mitigate safety concerns under calamitous circumstances.

Objective: Utilizing passive radio frequency identification (RFID) tags embedded in knitted smart-garment devices, we wirelessly detect the respiratory state of a subject using an ensemble-based learning approach over an augmented Kalman-filtered time series of RF properties., Methods: We propose a novel approach for noise modeling using a "reference tag," a second RFID tag worn on the body in a location not subject to perturbations due to respiratory motions that are detected via the primary RFID tag. The reference tag enables modeling of noise artifacts yielding significant improvement in detection accuracy. The noise is modeled using autoregressive moving average (ARMA) processes and filtered using state-augmented Kalman filters. The filtered measurements are passed through multiple classification algorithms (naive Bayes, logistic regression, decision trees) and a new similarity classifier that generates binary decisions based on current measurements and past decisions., Results: Our findings demonstrate that state-augmented Kalman filters for noise modeling improves classification accuracy drastically by over 7.7% over the standard filter performance. Furthermore, the fusion framework used to combine local classifier decisions was able to predict the presence or absence of respiratory activity with over 86% accuracy., Conclusion: The work presented here strongly indicates the usefulness of processing passive RFID tag measurements for remote respiration activity monitoring. The proposed fusion framework is a robust and versatile scheme that once deployed can achieve high detection accuracy with minimal human intervention., Significance: The proposed system can be useful in remote noninvasive breathing state monitoring and sleep apnea detection.

Imaging of human tissue using noninvasive techniques has been of great interest in biomedical fields. Optical imaging has attracted a lot of attention because of its portability and economy. The possibility that a highly portable, fast, safe, and affordable imaging system which could obtain interpretable images of brain function for pre- and full-term neonates in a few seconds, has been explored in this article. We have used a sensitive optical topography system, termed phased array, in which a pair of equal-amplitude and antiphase light sources are applied to generate a sharp amplitude null and phase transition plane. This two-wavelength (750 and 830 nm), frequency encoded (50 and 52 MHz) phased array imaging system can indicate the blood concentration and oxygenation changes in blood model studies and during parietal brain activation in neonates. Significant functional responses, particularly to parietal stimulation in normal and pathological states of neonatal brain, have been revealed in our study. The preliminary clinical results are presented in this article.

Imaging of the human body by any non-invasive technique has been an appropriate goal of physics and medicine, and great success has been obtained with both Magnetic Resonance Imaging (MRI) and Positron Emission Tomography (PET) in brain imaging. Non-imaging responses to functional activation using near infrared spectroscopy of brain (fNIR) obtained in 1993 (Chance, et al. [1]) and in 1994 (Tamura, et al. [2]) are now complemented with images of pre-frontal and parietal stimulation in adults and pre-term neonates in this communication (see also [3]). Prior studies used continuous [4], pulsed [3] or modulated [5] light. The amplitude and phase cancellation of optical patterns as demonstrated for single source detector pairs affords remarkable sensitivity of small object detection in model systems [6]. The methods have now been elaborated with multiple source detector combinations (nine sources, four detectors). Using simple back projection algorithms it is now possible to image sensorimotor and cognitive activation of adult and pre- and full-term neonate human brain function in times < 30 sec and with two dimensional resolutions of < 1 cm in two dimensional displays. The method can be used in evaluation of adult and neonatal cerebral dysfunction in a simple, portable and affordable method that does not require immobilization, as contrasted to MRI and PET.

A multicenter, randomized, double-blind, placebo-controlled trial of synthetic surfactant therapy for premature infants with respiratory distress syndrome (RDS) and birth weights of 700 to 1350 gm demonstrated a reduction in severity of RDS, morbidity, and neonatal and 1-year mortality. Of the 419 infants who were entered in the study, 80% of the surviving infants in both the air placebo group (122) and the synthetic surfactant group (138) returned for the follow-up evaluation at 1-year adjusted age. The only significant difference observed at follow-up was a reduction in the incidence of mild cerebral palsy in the synthetic surfactant group (air placebo group, 8 of 122 (7%); synthetic surfactant group, 3 of 138 (2%); relative risk 0.306; 95% confidence interval 0.094, 0.999). No differences were observed between the air placebo and synthetic surfactant treatment groups with respect to health status of the infants, including the incidence of retinopathy of prematurity and neurodevelopmental delays. The difference in the overall incidence of impairment among the 1-year survivors in the air placebo group (43 of 122 (35%)) and in the synthetic surfactant group (40 of 138 (29%)) was not statistically significant. The results of this 1-year follow-up study show that rescue treatment with synthetic surfactant in infants weighing 700 to 1300 gm is not associated with adverse developmental consequences despite the improvement in survival.

Newborns delivered to cocaine-abusing mothers are often exposed to other concurrently consumed illicit drugs, which may alter the hemodynamic and cerebral response to cocaine. This study examined the interaction of ethanol, morphine or barbiturate with cocaine on mean arterial pressure (MAP), cerebral blood flow (CBF) and cerebral metabolic rate of oxygen (CMRO2) in newborn pigs. CBF, CMRO2 and cerebral O2 extraction (CEO2) were measured before and 4 and 10 min after cocaine (1.5 mg/kg i.v.) was administered in piglets that were awake, or pretreated with morphine, ethanol or pentobarbital. In awake piglets, cocaine increased CMRO2 and CEO2 while it had no significant effect on CBF. Conversely, in morphine- and ethanol-pretreated piglets, cocaine decreased CMRO2, decreased CBF and had not effect on CEO2. In awake piglets, cocaine increased MAP, whereas in morphine- or ethanol-pretreated piglets, cocaine decreased MAP. In the pentobarbital group, cocaine had no effect. These data demonstrate that other drugs of abuse alter the hemodynamic and cerebral effects of cocaine in the immature animal and may contribute to the central nervous system abnormalities in 'crack babies'.

Non-immune hydrops fetalis (NIHF) is due to many different causes. Fetal hypomobility has been alluded to as a possible cause. We present a preterm fetus with NIHF secondary to fetal hypomobility. Fetal movements were undetected after the 20th week of gestation. The infant was born 8 weeks later and was edematous, had pleural effusions, and no spontaneous movements. He died on day four of life. Diffuse massive central nervous system (CNS) destruction found on post-mortem examination was thought to be the origin of the hypomobility. As all other causes of NIHF were eliminated, we propose that the NIHF in this infant was due to the hypomobility. This case then gives support to the assertion that fetal hypomobility is another cause of NIHF. The cause of the CNS catastrophy remains unelucidated.

The effect of cocaine on brain cell membrane structure and function was studied in the fetal guinea pig. We tested the hypothesis that cocaine, a potent vasoconstrictor, would result in brain cell membrane dysfunction as determined by altered activity of Na+,K(+)-ATPase and the appearance of products of membrane lipid peroxidation (conjugated dienes (CD) and fluorescent compounds (FC)). A total of 14 pregnant guinea pigs were studied at term (60 days). One hour prior to delivery, the pregnant guinea pigs were divided into 3 groups as follows: cocaine, 30 mg/kg i.p., saline placebo i.p., or 7% FiO2 for 1 h. Following cocaine, brain Na+,K(+)-ATPase activity decreased (mean +/- S.D., 25.6 +/- 9.2 vs. 54.6 +/- 3.4 mumol Pi/mg protein/h, cocaine vs. control, respectively, P < 0.01) and was similar to the hypoxia group (21.9 +/- 2.8 mumol Pi/mg protein/h). The products of lipid peroxidation did not change significantly following cocaine whereas hypoxia resulted in a rise in CD from 0 to 0.175 +/- 0.015 mumol/g brain, control vs. hypoxia, (P < 0.01), and FC from 1.13 +/- 0.15 to 1.88 +/- 0.13 micrograms quinine sulfate/g brain, control vs. hypoxia, (P < 0.01). These data show that acute fetal cocaine exposure, unlike hypoxia alone, results in a significant decrease in Na+,(K+)-ATPase activity without a significant increase in the products of lipid peroxidation, suggesting the mechanism by which cocaine affects brain cell membrane integrity is distinct from hypoxia. Inhibition of the enzyme activity may be due to a direct action of cocaine on the enzyme or due to enzyme regulation by cocaine-induced alterations in neurotransmitters.

Cocaine abuse by pregnant women is often associated with neurological injury in the newborn. To explore a vascular-related mechanism of injury, we investigated the effect of cocaine on the cerebral circulation in newborn pigs. During normoxic conditions, cocaine administration (1.5 mg/kg i.v.), resulting in peak plasma cocaine levels on the order of 10(-6) M, decreased cerebral blood flow (CBF) by 14%, as measured by the tracer microsphere method. To elicit the mechanisms by which cocaine decreased CBF, closed cranial windows were placed and the diameter of pial arterioles was measured by intravital microscopy while cocaine (10(-6) M) was applied onto the cortical surface. Topically applied cocaine decreased pial arteriolar diameter by 9%. Vasoconstriction induced by topically applied cocaine was blocked by tetrodotoxin (10(-7) M, Na+ channel blocker), whereas phentolamine (10(-5) M, noradrenergic receptor blocker) had no effect on the arteriolar response to cocaine, which suggested that cocaine effected constriction by an anesthetic and not a sympathomimetic mechanism. To evaluate this hypothesis further, cerebral vessels in the right hemibrain were sympathetically denervated while those in the left hemibrain remained innervated. During normoxia, cocaine (1.5 mg/kg i.v.) decreased CBF equally in both hemibrains, confirming the non-sympathomimetic mechanism. During asphyxia, cocaine administration attenuated cerebral hyperemia in both hemibrains, but in innervated more than in denervated, indicating that anesthetic and sympathomimetic vasoconstriction occurred during asphyxia. We conclude that cocaine constricts the immature cerebrovasculature and decreases CBF by an anesthetic mechanism during normoxic conditions and by both sympathomimetic and anesthetic mechanisms during asphyxia.

The present study investigated the effect of cocaine (COC) on cerebral circulation (CBF) and oxidative metabolism (CMRO2) in the newborn piglet and aimed to relate pharmacokinetics of cocaine to cerebrovascular effects. COC decreased CBF and CMRO2 from 75 to 64 and 4.27 to 3.91 ml/min/100 g, respectively, at 4 min with reduced flow to all brain regions (p < 0.05) which returned to baseline by 10 min. COC was rapidly metabolized with a t1/2 of 43 min and peak plasma concentration of 1,172 ng/ml. Norcocaine (NOR) appeared in plasma and CSF within 3 min of cocaine administration and remained elevated for the duration of the study along with COC in the CSF. These data show that the timing of the peak plasma COC level is associated with maximal decreased CBF. Further, the stable elevated level of COC and NOR in the CSF suggests that biotransformation does not occur in the brain. As a result, accumulation of these drugs may occur in the brain with successive COC use and affect the developing CNS in a deleterious manner.

In a multicenter, double-blind, placebo-controlled trial conducted at 23 hospitals in the United States, a single prophylactic 5 ml/kg dose of a synthetic surfactant (Exosurf Neonatal) or air placebo was administered shortly after birth to 215 infants with birth weights of 500 to 699 gm. Despite stratification at entry by birth weight and gender, by chance female infants predominated in the air placebo group and male infants predominated in the surfactant group. Among infants receiving synthetic surfactant, improvements in oxygen requirements were significant at 2 hours after birth (p = 0.014) and persisted for 3 days (p = 0.001); improvements in the alveolar-arterial partial pressure of oxygen gradient were significant at 6 hours after birth (p = 0.01) and persisted for 3 days (p = 0.008). Improvements in mean airway pressure were not significant at 2 or at 6 hours after birth (p = 0.622 and 0.083, respectively), but became significant thereafter and persisted for 3 days (p = 0.002). Pneumothorax was reduced by slightly more than half (25 vs 11; p = 0.014); death from respiratory distress syndrome (RDS) was also reduced (26 vs 15; p = 0.046). Overall neonatal mortality, however, was not significantly reduced (58 vs 46; p = 0.102). Other complications of RDS and prematurity were not altered, except that pulmonary hemorrhage occurred significantly more frequently in infants receiving synthetic surfactant (2 vs 12; p = 0.006). These findings indicate that a single prophylactic dose of synthetic surfactant in infants weighing 500 to 699 gm at birth improves lung function, incidence of air leak, and death from RDS but not overall mortality. The only safety problem identified was an increase in pulmonary hemorrhage.

In order to define longitudinal data in premature infants, impedance pneumograms were performed weekly on 23 healthy premature infants. Studies were performed while infants remained hospitalized and at the discretion of the attending physician following discharge. A total of 97 studies were obtained on the study group. The recordings were analyzed for percentage of sleep time spent in periodic breathing, apnea density, and duration of longest apneic pause. Infants in this study demonstrated decreased percent of periodic breathing and decreased apnea density with increased maturation; longest pause per recording was independent of postconceptional age. Results from this study provide data to assist in the evaluation of pneumograms in the premature infant.

Pregnancy is associated with altered liver function, particularly in serum enzymes. Anabolic steroids are responsible to some degree in mediating the physiologic and biochemical changes that occur during an uncomplicated pregnancy. However, several liver disorders are unique to pregnancy and include intrahepatic cholestasis of pregnancy, acute fatty liver of pregnancy, and hepatic dysfunction associated with pre-eclampsia and eclampsia. It is imperative for the clinician to diagnose these liver disorders in a timely manner and to institute appropriate management as maternal and fetal outcome are affected in an adverse manner if these conditions are left untreated.

The growth and development of inborn very low birth weight infants was evaluated in 50 of 60 survivors from 132 babies weighing less than or equal to 1,250 gm born July 1974 to December 1977. Mean +/- SE birth weight and gestation was 1,066 +/- 19.3 gm and 29.5 +/- 0.3 weeks, respectively, with 13 infants small-for-gestational age. Of the survivors, 26% weighed less than or equal to 1,000 gm. Male to female ratio was 1:1.4. Apgar scores less than or equal to 5 at five minutes occurred in 16% of the infants. Respiratory distress syndrome occurred in 56%, but only 10% (5/50) required mechanical ventilation. At 1 year, 46% small for gestational age (SGA) and 8% appropriate for gestational age (AGA) infants were less than the third percentile for weight. Major neurologic abnormality occurred in three infants (6%), one of whom is also blind. Grade V retrolental fibroplasia occurred in two others. Severe developmental delay (development quotient < 80, Gesell) occurred in these five infants and two other neurologically normal babies. Of 15 infants weighing less than or equal to 1,000 gm, two had major handicaps. Eight percent of the AGA infants and 30% of the SGA infants had major handicaps. These data indicate that infants born and treated in a perinatal center have a decreased incidence of asphyxia and severe respiratory distress syndrome and that the incidence of major handicaps is reduced, especially in the appropriate for gestational age baby.

An epidemic of adenovirus 7a in our neonatal intensive care nursery and intermediate care nursery in July and August 1987 caused the death of two patients. Significant symptomatic infection possibly due to the virus occurred in nine patients, ten staff, and three parents, of whom three patients, three staff, and one parent were positive by culture. As a direct consequence of the outbreak, 58 staff days of work were lost; the intensive care nursery had to be closed to admissions for 19 days and the intermediate care nursery for 14 days. Seventeen newborns were transferred to other hospitals and four mothers were sent elsewhere for delivery. Control measures, which included cohorting of patients, use of gloves, gowns and goggles, and exclusion of symptomatic staff from the unit, appeared effective. Rapid immunofluorescence testing of virological specimens was of little use in monitoring the outbreak, largely because of poor specimen quality. This outbreak further underlines the ease of transmission and high morbidity of neonatal adenovirus infection.

The present study uses the glabellar reflex and reflex modification procedures to assess acoustic and tactile sensory processing capabilities in the human neonate. Fourteen term infants and 28 clinically stable preterm infants were given identical test paradigms. Augmentation testing consisted of a 16 V dc tap presented simultaneously with a 90 dB SPL tone; inhibition testing consisted of a 16 V tap preceded 900 msec. by an identical tap. All 14 term infants showed augmentation with 8 of 14 at p less than 0.05 level and eleven of 14 showed significant inhibition at the 900 msec intertap interval. However, only 12 of 28 preterm infants demonstrated significant augmentation and none showed reliable inhibition. These data indicate that areas of the central nervous system that process sensory stimuli are not fully developed at the time of birth even in the term infant. Further, the neural system for augmentation and inhibition may be independent of each other.

In human adults the eyeblink elicited by a given stimulus can be inhibited if that stimulus is preceded by another stimulus at an appropriate lead interval. In the present work, pairs of eyeblink-eliciting stimuli separated by 300-1200 msec were presented to sleeping preterm and full-term infants as well as to adults. Preterm infants did not exhibit reliable inhibition at any interval. Full-term infants did so, but they required longer interstimulus intervals than were needed for inhibition in the adult subjects. Results imply that the neural systems that mediate reflex inhibition are functional at birth, but that they are relatively slow to act.

Nineteen infants (mean +/- SD gestational age 30 +/- 2 weeks, birth weight 1.28 +/- 0.53 kg) with Staphylococcus epidermidis bacteremia were found on retrospective chart review to have had signs and symptoms of acute enterocolitis. This S. epidermidis-associated enterocolitis constituted 37% of the 51 cases of enterocolitis and 23% of the 81 cases of S. epidermidis sepsis during the study period. S. epidermidis-associated enterocolitis was relatively mild compared with other forms of enterocolitis. Although abdominal radiographs showed markedly abnormal bowel gas patterns with distended bowel loops and bowel wall edema, only one infant had pneumatosis intestinalis and none had portal venous or free intraperitoneal gas. Only three infants had neutropenia, and five had thrombocytopenia. None of these infants required surgical intervention. Although bloody stools often persisted for weeks, none of the neonates had prolonged feeding intolerance or development of a stricture. We conclude that S. epidermidis infection is commonly associated with a mild form of enterocolitis in the neonate and that this association should be considered when selecting antibiotics for therapy.

Two infants with clinical and radiologic features of metatropic dwarfism presented in the neonatal period with episodes of cyanosis. Diagnostic studies to determine the etiology of these spells, including electrocardiogram, electroencephalogram, arterial blood gases, and metabolic and sepsis studies, were unremarkable. Chest roentgenograms revealed the characteristic long, narrow thoracic cage with no evidence of parenchymal disease. Cervical spine stability evaluation, pulmonary function studies, and chest impedance monitoring with qualitative air flow thermistor studies and transcutaneous oxygen monitoring were carried out. Both patients demonstrated a significant increase in resistance of the respiratory system following passive maneuvering of the head from a neutral position, suggestive of hypopharyngeal air flow obstruction. Obstructive sleep apnea resulting in cyanosis was documented in both patients. All other studies failed to yield a cause for the episodes of cyanosis. Our investigation failed to alter the clinical course which resulted in respiratory arrest and death by 7 months of age. A table is presented for the differentiation of skeletal dysplasias presenting in the perinatal period.

The amplitude of the human eyeblink elicited by a mild tap between the eyebrows can be increased if a brief tone is presented simultaneously with the tap. In two experiments we examined how this reflex augmentation effect varies with changes in the frequency characteristics of the tone and with changes in the intensity of the tap. We also examined how these effects change in the course of development. For newborn infants and for adults, fixed intensity tones with frequencies of either 1, 2, or 4 kHz produced equivalent amounts of reflex augmentation. Furthermore, while blink amplitude was an increasing function of tap intensity in both populations, the amount of reflex augmentation engendered by a simultaneously presented tone was independent of the intensity of the tap.

To examine why newborn infants frequently cannot maintain adequate levels of plasma glucose in the interval between delivery and the time they are first fed, circulating metabolic fuel and regulatory hormone concentrations were determined in 44 healthy infants at the end of an eight-hour postnatal fast. Plasma glucose fell below 40 mg/100 ml prior to eight hours in four of 24 term-appropriate-for-gestational-age (AGA), two of nine preterm-AGA, five of six term-small-for-gestational-age (SGA), and three of five preterm-SGA infants. Fuel and hormone patterns in the premature and SGA infants were not different from those found in term-AGA infants. Results in these neonates differed in two areas from the response to fasting seen later in life. In fasted term-AGA infants, ketones were low (beta-hydroxybutyrate 0.29 +/- 0.04 mM/liter) despite elevated concentrations of fatty acid precursors (1.4 +/- 0.07 mM/liter), and the group of infants studied failed to demonstrate the increase in plasma ketones with lower glucose levels (r = ".23, P = .07) which is found in older children. Levels of glucose precursors were two to three times higher in term-AGA infants (lactate 2.9 +/- 0.2 mM/liter; alanine 0.48 +/- 0.02 mM/liter) than levels found beyond the neonatal period and, in contrast to older children and adults, were not diminished in infants with lower plasma glucose (lactate, r = -.28, P less than .035; alanine, r = -33, P less than .02). These differences between the responses to postnatal fasting and those seen beyond the neonatal period suggest that the capacity for both hepatic ketone synthesis and gluconeogenesis is not fully developed at birth.

Based on a three year surveillance in the neonatal intensive and transitional care nurseries (NICU) at the Hospital of the University of Pennsylvania (HUP), an analysis of all cases of nosocomial bacteremia was made. From January 1982 to September 1984, a total of 57 nosocomial bacteremic episodes were identified. This gave a rate of 3.6 episodes per 100 NICU admissions or 6.5 per 1000 live hospital births. While coagulase-negative staphylococci (CNS) accounted for approximately 40 percent of all positive blood cultures, it was responsible for 73 and 66 percent of the nosocomial bacteremias in 1982 and 1983, respectively. In 1984, coagulase-negative staphylococcus was the responsible pathogen for 92 percent of all nosocomial bacteremic episodes. Of 139 infants weighing less than or equal to 1250 g at birth, 30 (22 percent) developed CNS bacteremia. The risk of coagulase-negative staphylococcus bacteremia was associated with low birth weight, respiratory distress, prolonged hyperalimentation, and multiple supportive measures. Infants were treated with vancomycin hydrochloride, as most of the CNS were resistant to methicillin and/or gentamicin. There were no deaths related to coagulase-negative staphylococcal septicemia.

The relative contribution of transfusions of adult blood to the development of retrolental fibroplasia (RLF) in very low-birth-weight infants was examined. Five years of experience with the expanded use of replacement and exchange transfusions in 90 infants with birth weight less than or equal to 1,250 gm was reviewed. Twenty percent of the infants developed cicatricial RLF. Exchange transfusion was not related to development of cicatricial RLF. The incidence of RLF in infants receiving greater or equal to 130 ml of packed red blood cells per kilogram of birth weight as replacement blood transfusion (RBT) was significantly higher (42.9%) than that in infants receiving 61 to 131 ml of packed red blood cells per kilogram (15.4%) and infants receiving less than or equal to 60 ml of packed red blood cells per kilogram (0%), P less than .001. The need for RBT, however, was strongly correlated (r = .85, P less than .001) with increasing duration of O2 therapy. When O2 therapy was controlled for, the association between RBT and RLF did not achieve statistical significance (P = .07). The association between RBT and RLF remained significant when adjusted for duration of therapy in fractional inspired oxygen (FIO2) greater than 0.4. Further detailed studies of large numbers of susceptible infants are warranted to assess the magnitude of the contribution of transfusions of adult blood to development of RLF.

Sequential lung function was measured in 12 very low-birth weight infants (less than or equal to 1,250 g) within 14 hours of birth, and at daily intervals thereafter for the first week of life, using an esophageal balloon and pneumotachograph system. All infants were clinically free of respiratory distress syndrome and radiographically showed no evidence of atelectasis or pulmonary edema. The alveolar-arterial oxygen tension gradient was high at birth and remained elevated over the period during which arterial blood gases were monitored. Increases of lung compliance and tidal volume between the first day and the end of the first week of life were not significant. Day-to-day determinations of lung compliance revealed an individual and group variability without a definite pattern. Lung resistance measurements indicated no clear trend for the group as a whole, but inspiratory resistance was generally lower than expiratory resistance. Possible causes, in addition to technical factors, that may account for the variability in the pulmonary mechanics of these small infants include an instability of lung volume and uneven distribution of pleural pressure due to chest wall distortion, differences in sleep-state, and alteration in the distribution of body fluids, resulting in a change in lung water. Any or all of these mechanisms may result in an unstable lung, even in an apparently clinically stable very low-birth weight infant.

Three premature infants with zinc deficiency who had an unusual presentation with generalized edema and hypoproteinemia between 5 and 9 weeks of age are described. The infants were fed their own mother's milk, supplemented with a proprietary formula after the first 2 to 3 weeks of life. None of the infants had diarrhea, liver disease, or urinary protein loss. Treatment with oral zinc supplements led to rapid resolution of the edema, with an increase in values for serum proteins, alkaline phosphatase, and zinc. There was no recurrence of symptoms following discontinuation of zinc therapy 1 month later. At 1-year follow-up, all infants were doing well and had normal growth and development. As zinc plays a critical role in nucleic acid and protein synthesis, it is postulated that dietary zinc deficiency in the phase of rapid postnatal growth precipitated edema and hypoproteinemia in these infants. Zinc deficiency should be included in the list of causes of generalized edema in the low-birth-weight infant.

The effect of prenatal cocaine on acoustic sensorineural reactivity was assessed using reflex modification procedures in infants born to mothers with cocaine abuse (C-exposed). Reflex modification was tested using a controlled eyeblink-eliciting tap to the glabella presented either alone or with a 90-dB SPL tone. The results from 19 C-exposed infants were compared to 19 healthy matched drug-free infants. ANOVA comparison of the two groups showed C-exposed infants were more reactive in general, as indicated by a larger glabellar reflex, and more responsive to auditory stimuli, as indicated by an increased blink when the tone accompanied the tap (p less than 0.05). These data suggest that in utero cocaine exposure may have a direct effect on sensorineural processing and may place these infants at risk for cognitive and/or neurological sequelae.

Reflex modification procedures were used to test sensory processing in premature infants to examine the relationship between respiratory abnormalities and brainstem neuronal function. A total of 73 premature infants at risk for apnea and/or infants receiving methylxanthine therapy was given a 12-h pneumocardiogram and reflex modification test at a comparable postconceptional age, before discharge. Reflex modification was tested using a controlled eyeblink-eliciting tap to the glabella presented either alone or with a 1 kHz 90-dB SPL tone. The amplitude of the glabellar tap eyeblink and acoustically modified blink were lower in infants discharged on cardiac/apnea monitors (n = 36) than in the unmonitored group (1.44 and 1.59 volts versus 2.15 and 2.39 V, p less than 0.005, respectively). At follow-up, 12 monitored infants had clinically significant apnea after discharge. The records of this subgroup of infants revealed a significantly lower augmentation of the glabellar eyeblink response when compared to all infants screened for respiratory abnormalities and to the other monitored babies (p less than 0.01). The data suggest that abnormalities of the ventilatory pattern and occurrence of clinical apnea in preterm infants may in some measure be related to acoustic sensory processing, implying an alteration of brainstem neuronal function and organization.

Behavioral and physiological work in animals and adult humans have established the sensitivity of various procedures and allowed delineation of the neuroanatomical pathways involved in sensory processing. Herein we used the glabellar reflex and reflex modification procedures to assess acoustic sensory processing capabilities in the term newborn infant. The eyeblink-eliciting device consisted of a miniature solenoid which could deliver a controlled tap. A photoreflective densitometer attached to a TDH-39 earphone assessed the eyeblinks. A total of 98 term infants was studied to determine how a response to a reflex-eliciting event (tap) was modified (either augmented or inhibited) by a mild exteroceptive stimulus (tone) which was presented at an appropriate lead interval. Ninety adult subjects were given identical testing procedures and their data were compared to that of the infants. The results of this study showed that newborn infants reliably exhibited an eyeblink response after a tap to the glabella. With fixed intensity tones, frequencies from 1 to 4 kHz produced equivalent amounts of reflex augmentation in infants and adult subjects. Blink amplitude increased as a function of increased tap and tone intensity in both infants and adults. State change was shown to affect the amplitude of the reflexive eyeblink, but not the augmentation effect. However, neonates failed to show inhibition to either acoustic lactile stimuli at an interstimulus interval that produced significant inhibition in the adult. These data indicate that reflex modification procedures provide an objective assessment of acoustic sensory processing in the term neonate.(ABSTRACT TRUNCATED AT 250 WORDS)