This paper presents a fully integrated low-power wearable respiration monitoring system using a pyroelectric transducer. Many chronic respiratory diseases such as asthma and apnea are leading causes of death worldwide which are even more critical for premature neonatal infants. Currently, the diagnosis of apnea requires the infants to go through overnight clinical sleep analysis, also known as polysomnography for 12 to 24-hour period. During this process numerous sensors are attached to the sensitive skin of the infants resulting in irritation and inconvenience. To overcome this problem a novel point-of-care respiration monitoring system has been proposed. At the front-end of the sensor a PVDF (Polyvinylidene Fluoride) based pyroelectric transducer is used which could be placed under the nasal cavity or inside a cannula of the subject. The charge generated by the transducer due to the nasal air flow is then converted to a proportional voltage signal by an operational transconductance amplifier (OTA) based charge amplifier. The subsequent signal processing blocks detect and process the signal coming out of the charge amplifier if it lies within the voltage range that corresponds to an apneic event. Once the signal is detected an alarm signal is generated indicating the occurrence of an apneic event. The light-weight design and smaller footprint of the transducer as well as the integrated devices make it suitable as a wearable sensor for non-invasive respiration monitoring. A prototype device with the integrated circuit fabricated using 0.5μm CMOS process is presented in the paper which can prevent many major disorders that can lead to neonatal mortality.

Apnea is one of the leading causes of death not only in the USA but also around the world. It is even more critical for premature neonatal infants. Currently, the diagnosis of apnea requires the infants to go through overnight sleep study involving numerous sensors needed to be attached to the body and the face of the patients causing them a great degree of inconvenience. In order to overcome the complexity of the point-of-care diagnosis of this sleep disorder, a system based on a pyroelectric transducer and the design of a CMOS integrated circuit comprising of readout electronics and signal-processing circuitry is presented. This novel detection system has very small form factor and consumes very small amount of power, which makes it suitable for daily home-based applications.

OBJECTIVE: To compare fluid and electrolyte management in extremely low birth weight (ELBW) infants nursed in humidified versus nonhumidified incubators. STUDY DESIGN: Setting — tertiary intensive care nursery. Subjects — all infants with birth weight <1000 g admitted 1/95 to 1/99 who were treated with incubators and survived for >96 hours ( N =155). Intervention — retrospective comparison of daily weights, fluid intakes, urine outputs, and serum electrolytes between group 1 ( n =70, nonhumidified incubators, born 1/95 to 1/97) and group 2 ( n =85, humidified incubators, born 1/97 to 1/99) over the first 4 days after birth. RESULTS: Despite similar daily weight losses between groups, group 1 infants received higher fluid intakes, had lower urine outputs, and had a higher incidence of hypernatremia, hyperkalemia, and azotemia ( p <0.05). Although no differences in mortality or the incidence of patent ductus arteriosus, bronchopulmonary dysplasia, or the overall rate of nosocomial infections were observed, the proportion of gram-negative isolates increased significantly (62%, p <0.05) following the introduction of humidified incubators. CONCLUSIONS: ELBW weight infants nursed in humidified incubators have lower fluid requirements, improved electrolyte balance, and higher urine outputs during the first 4 days after birth compared to those nursed in nonhumidified incubators.

Objective. To determine appropriate upper limits for gestational age and birth weight when screening infants for retinopathy of prematurity (ROP). Design. Retrospective survey. Setting. Tertiary neonatal intensive care nursery. Patients. Seven hundred seven infants born July 1, 1990 to June 30, 1996 and screened for ROP according to the 1988 to 1996 American Academy of Pediatrics guidelines. Outcome Measures. Maximum stage of ROP with respect to birth weight and gestational age. Results. No ROP more than Stage 1 was observed in infants with gestational ages ≥32 weeks or birth weights ≥1500 g. All cases of threshold and Stage 4 ROP were confined to infants with gestational ages ≤30 weeks or birth weights <1200 g. Conclusions. The latest American Academy of Pediatrics screening guidelines for ROP are discretionary for infants with birth weights >1500 g or gestational ages >28 weeks. If ROP screening is limited to infants with birth weights of ≤1500 g, 34.2% fewer infants would require screening compared with the previous <1800 g recommendation, while missing no cases of ROP more than Stage 1. A gestational age cut-off of ≤28 weeks, however, is less desirable, and could potentially miss several infants with more advanced retinopathy (including Stage 4). If ROP screening criteria were instead modified to include infants of gestational ages <32 weeks, the number of patients requiring screening could be reduced 29.1% compared with the previous recommendation of <35 weeks, again without missing any cases of ROP more than Stage 1. Use of such a screening strategy (birth weight <1500 g or gestational age <32 weeks) is predicted to save in excess of 1.5 million dollars annually in the United States, while missing no cases of ROP more than Stage 1.

We have observed that oxidative phosphorylation (OXPHOS) by isolated mitochondria (MITO) increases at birth in liver and kidney (Ped. Res. 37,214), but not heart (this meeting), and that newborn hypoxia prevents increased OXPHOS. To determine whether initiation of MITO biogenesis is also regulated by oxygen availability pre-term rabbit pups (30-31 days gestation, term=32 days) delivered by C-section were either sacrificed at birth (time zero) or maintained under normoxic (21% O2, NOX) or hypoxic(10% O2, HYPOX) conditions for 4 hours at 35° C. MITO were isolated and in-vitro protein synthesis (PS) determined by measuring 35S methionine incorporation. PS was greater in heart MITO from NOX vs HYPOX or time zero pups (113 ± 18 vs 55.2 ± 20 or 60.0 ± 13 CPM/ mg Prot / 30 min respectively, n=6, p < 0.05) while PS rate was similar for liver (48 ± 13 vs 47 ± 10 or 51.3 ± 11) and kidney (44.1± 15 vs 37.5 ± 20 or 39.5 ± 13) MITO. Nucleotide regulation of PS in NOX and HYPOX pups was also evaluated. PS was reduced by 40-50% (p < 0.05) when isolated MITO from heart, liver and kidney were incubated with 5 mM ATP + 1 mM GTP. Inhibition was similar in MITO from NOX and HYPOX pups. In summary, MITO biogenesis at birth is modulated by nucleotides in all organs and oxygen availability in heart, but not liver or kidney. Taken together these data demonstrate that metabolic adaptation at birth involve increased MITO OXPHOS or biogenesis, changes which are modulated by oxygenation in an organ specific manner.

Intraventricular hemorrhage (IVH) in premature infants may be related to the immaturity of the vascular bed in the germinal matrix. We measured six hemostatic parameters whose alterations may represent an additional risk factor for IVH in preterm infants. On postnatal day 1 there were differences between plasminogen activator inhibitor-1 (PAI-1) activity and antigen, of both full-term and preterm infants with and without IVH (P < 0.05). Preterms with IVH were different to both full-terms and preterms without IVH. No difference was observed in plasma concentrations of fibrinogen, plasminogen and von Willebrand factor. Plasma concentrations of antithrombin III were significantly higher in full-term infants than in preterm infants. The difference between the platelet counts of preterm infants with and without IVH was not significant (P > 0.05). Elevation of crosslinked fibrin degradation products (XDP), determined by the SimpliRED D-dimer test, correlated in four out of five premature infants with the diagnosis of IVH by ultrasonography. No elevation of D-dimer XDP was observed in premature infants without IVH (11/12) and full-term infants (6/6). In conclusion, a hypercoagulable state, indicated by a rise in D-dimer XDP, may be initiated by some types of trauma to fragile blood vessels of the preterm infants who develop IVH. This hypercoagulability is further exacerbated by the increased release of PAI-1 leading to suppressed fibrinolysis.

Lipid inflammatory mediators are thought to play an important role in the pathogenesis of neonatal lung injury and bronchopulmonary dysplasia (BPD). Because preliminary studies from the intensive care nursery of the University of Tennessee Medical Center, Knoxville, revealed linear increases in blood platelet-activating factor (PAF) levels in very low birthweight infants developing chronic lung disease and lower cord blood PAF acetylhydrolase activities in premature infants, it was theorized that altered platelet-activating factor levels and PAF acetylhydrolase activities are associated with increasing severity of BPD. Platelet-activating factor levels (blood and tracheal lavage) and PAF acetylhydrolase activities (blood and tracheal lavage) were measured over days 1 to 2, 3 to 5 and 6 to 7 in 16 ventilated infants and weekly in 9 infants with bronchopulmonary dysplasia. Platelet-activating factor values were normalized per nanogram of lavage blood urea nitrogen. Severity of bronchopulmonary dysplasia was estimated using the scoring system developed by Toce. Mean blood and lavage PAF levels and PAF acetylhydrolase activities were compared in infants developing bronchopulmonary dysplasia with those without the disease over the first seven days of life. Infants developing chronic lung disease were significantly smaller and of younger gestational age, In infants with bronchopulmonary dysplasia, higher PAF levels in blood were seen on days 3 to 5, along with increased lavage acetylhydrolase activities on days 1 to 2. Increased levels of PAF in lavage on days 3 to 5 were associated with increasing severity of bronchopulmonary dysplasia, Altered blood and lavage platelet-activating factor levels and PAF acetylhydrolase activities appear to be associated with the pathogenesis and severity of bronchopulmonary dysplasia.