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Objective: The purpose of this study was to assess the incidence of perinatal factors that are associated with severe intracranial hemorrhage in a large and recent multicenter experience., Study Design: Retrospective analyses of nonanomalous newborns who were admitted to 100 neonatal intensive care units from 23 to 34 6/7 weeks' gestation were analyzed by multiple regression., Results: There were 12,578 premature newborns with a mean (+/- SD) gestational age of 31.3 +/- 2.9 weeks and a birth weight of 1685 +/- 571 g, respectively. The overall incidence of severe intracranial hemorrhage was 2.9%; in 4575 newborns who weighed < or = 1500 g the incidences of intracranial hemorrhage was 7.1%. Factors with positive and negative associations with severe intracranial hemorrhage are listed in order of decreasing statistical significance: gestational age (negative), surfactant (positive), antenatal indomethacin (positive), neonatal transport (positive), cesarean birth (negative), poor prenatal care (positive), 5-minute Apgar score of < 7 (positive), chorioamnionitis (positive), antenatal terbutaline (negative), preterm premature rupture of fetal membranes (negative), and abruption (positive)., Conclusion: The incidence of severe intracranial hemorrhage has dramatically declined over the past 2 decades. Antenatal steroids were not associated with reductions in severe intracranial hemorrhage.

In recent years, survival of the extremely low birthweight infant has dramatically improved. Morbidity, both short- and long-term, however, remains very high Costs in the currency of pain and suffering for the newborn, stress and financial burdens for the family, and dollars for society are extensive. The controversial questions that are discussed include: How small is too small? How much is too much? How far should we go? How much can we afford? Who should decide? What strategies should be followed to ensure such decisions are just?

End-tidal PCO2 (PETCO2) measurements from two commercially available neonatal infrared capnometers with different sampling systems and a mass spectrometer were compared with arterial PCO2 (PaCO2) to determine whether the former could predict the latter in mechanically ventilated rabbits with and without lung injury. The effects of tidal volume, ventilator frequency and type of lung injury on the gradient between PETCO2 and PaCO2 (delta P(a-ET)CO2) were evaluated. Twenty rabbits were studied: 10 without lung injury, 5 with saline lavage and 5 with lung injury by meconium instillation. Paired measurements of PETCO2 by two infrared capnometers and a mass spectrometer were compared to PaCO2. In the rabbits without lung injury, the values from the infrared capnometers and mass spectrometer correlated strongly with PaCO2 (r > or = 0.91) despite differences in the slopes of the linear regression between PETCO2 and PaCO2 and in delta P(a-ET)CO2 (P < 0.05). Values from the mainstream IR-capnometer more closely approximated the line of identity than the regression between the sidestream IR-capnometer values or the mass spectrometer and PaCO2, but tended to overestimate PaCO2. The delta P(a-ET)CO2 was similar at all tidal volumes and ventilator frequencies, regardless of capnometer type. In the rabbits with induced lung injury, while there was a positive correlation between the slopes of the regression between PETCO2 and PaCO2 for both capnometers (r > or = 0.70), none of the regression slopes approximated the line of identity. The delta P(a-ET)CO2 was greater in rabbits with injured than noninjured lungs (P < 0.05). The delta P(a-ET)CO2 was similar among capnometers regardless of tidal volume, ventilator frequency, or type of lung injury. The 95% confidence interval of plots PaCO2 against PETCO2 was large for rabbits with injured and noninjured lungs.(ABSTRACT TRUNCATED AT 250 WORDS)

Twelve liveborn anencephalic infants were serially examined to determine if they would meet our clinical criteria for whole brain death within a 7-day period: Protocol 1 infants (6) received intensive care including intubation from birth; and Protocol 2 infants (6) received intensive care during the period in which death was imminent. Brain death was determined by absence of brainstem function, including loss of all cranial nerve responses and sustained apnea (PCO2 greater than 60 torr) for 48 hours with confirmation of findings by an outside consulting child neurologist. The initial examinations of these 12 infants revealed spontaneous movements and startle myoclonus (12), suck, root, and gag responses (7), increased tone (8), deep tendon reflexes (9), absent pupillary responses (9), absent oculocephalic and corneal responses (6), absent auditory/Moro responses (7), and nonvisualization of the optic nerve (8). Mild depression of neurologic function occurred during the first several days of life; subsequently, the infants' responses were easier to elicit and more sustained. Only 2 infants met the clinical criteria for brain death. Neuropathologic findings indicated that observed complex motor responses were not based upon cortical activity because no infant had a normally-formed cerebrum. Brainstem neuronal activity may have accounted for these motor responses in some patients but even at this level neurons were scanty or absent. Our findings suggest that, although rare, clinical brain death can be determined in liveborn anencephalic infants; ophthalmologic and otologic developmental abnormalities may confound examination of cranial nerve function; and absence of cortical neurons supports the widely held opinion that these infants do not experience sensation.

To determine whether there are significant alterations in cerebral blood flow patterns in infants with a patent ductus arteriosus and whether these alterations correlate with alterations in aortic blood flow, we performed range-gated pulsed-Doppler examinations of the aorta and cerebral arteries in 20 infants. Ten infants had a PDA and ten control infants did not. We analyzed these flow patterns quantitatively by calculating the pulsatility index (peak systolic frequency minus trough diastolic frequency)/peak systolic frequency. In the ten control infants and in three infants with a small PDA, there was no significant diastolic flow in the descending aorta; flow in the cerebral arteries was antegrade throughout systole and diastole (PI = 0.75 +/- 0.03 for control infants and 0.73 +/- 0.07 for small PDA infants). In seven infants with a large PDA, there was retrograde diastolic flow in the descending aorta. This pattern was not seen after PDA closure. In the cerebral arteries of the seven infants with a large PDA, diastolic flow was retrograde in three and decreased or absent in four, and PI was significantly higher (PI = 0.96 +/- 0.06. P less than 0.001 vs controls). After PDA closure, cerebral diastolic flow was antegrade in all seven infants (PI = 0.74 +/- 0.04). We conclude that a large PDA can cause abnormal flow patterns in the descending aorta and cerebral arteries. These flow patterns may predispose these infants to CNS ischemia or intraventricular hemorrhage.

The evaluation of pharmacologic effects in perinatal medicine is dependent on our clinical methods for measurement and monitoring of the mother, the fetus, and the newborn infant. The development of a noninvasive continuous method of measuring PO2, the transcutaneous PO2 electrode, has greatly enhanced the ability to assess effects of drugs on the cardiorespiratory system. During labor, diazepam and meperidine have been documented to cause respiratory depression and significant decreases in PO2. The advantageous effect of epidural anesthesia on the oxygen-cardiorespirogram of mothers in labor has also been demonstrated. Both fetal and maternal tcPO2 have been successfully assessed during the administration of peridural catheter anesthesia (carticaine) and during suppression of labor with fenoterol. In the newborn infant, monitoring of tcPO2 has been helpful in assessing the residual effects of drugs administered during labor and delivery, in prescribing the appropriate and safe dose of oxygen, and in defining the effects of theophylline on the oxygen-cardiorespirogram. We have also demonstrated the effect of furosemide on PO2 in the treatment of pulmonary edema accompanying bronchopulmonary dysplasia and of indomethacin for the management of patent ductus arteriosus. Use of tcPO2 measurements for clinical pharmacologic evaluation is a promising addition to our research techniques.

The authors review the function, reliability, risks, and clinical applications of skin surface blood gas monitoring that have become evident during the first decade of its clinical use. Also discussed is the problem of data expression and the recent developments in this area.

Recent advances have made organ transplantation in newborns feasible, but the paucity of organs small enough for this age group remains a major limitation. Because anencephalic infants can survive for no more than a few weeks, they have been considered as possible organ donors for other infants. Under current law, however, they cannot be used as donors until their brain-stem activity ceases and the criteria for total brain death are thereby met. If anencephalic infants receive customary care, their solid organs usually undergo irreversible hypoxic injury during the process of dying and become unsuitable for donation by the time of death. We modified the medical care of 12 live-born anencephalic infants for one week to determine whether organ viability could be maintained and whether the criteria of total brain death could be met. Six received intensive care from birth, and six only when signs of imminent death developed. Only two infants met the criteria for total brain death within one week, and no solid organs were procured. Most organs were suitable for transplantation at birth. When intensive care was provided from birth, organ function was maintained; however, brain-stem activity ceased in only one infant within the first week. When intensive care was delayed until death was imminent, most organs were damaged to an extent that made them no longer suitable for transplantation. Our findings suggest that it is usually not feasible, with the restrictions of current law, to procure solid organs for transplantation from anencephalic infants.

We studied the effects of six different head positions on intracranial pressure and cerebral blood flow velocity in six infants with a recent history of asphyxia and eight without. ICP was measured noninvasively using a transfontanel pressure transducer, and CBF was assessed using the continuous-wave Doppler method. We found that ICP was lowest with the head elevated and in the midline (P less than 0.01), and that ICP was higher in all infants in the dependent position (P less than 0.001). This increase was significantly greater in those who had had an episode of asphyxia during the 48 to 72 hours prior to the study (P less than 0.02). Therefore, we recommend a head elevation of 30 degrees in the midline in any infant with increased ICP or at high risk for cerebral injury, and caution against the use of the dependent position in these infants.

Continuous monitoring of oxygenation in sick newborns is vitally important. However, transcutaneous PO2 measurements have a number of limitations. Therefore, we report the use of the pulse oximeter for arterial oxygen saturation (SaO2) determination in 26 infants (birth weights 725 to 4,000 g, gestational ages 24 to 40 weeks, and postnatal ages one to 49 days). Fetal hemoglobin determinations were made on all infants and were repeated following transfusion. SaO2 readings from the pulse oximeter were compared with the SaO2 measured in vitro on simultaneously obtained arterial blood samples. The linear regression equation for 177 paired measurements was: y = 0.7x + 27.2; r = .9. However, the differences between measured SaO2 and the pulse oximeter SaO2 were significantly greater in samples with greater than 50% fetal hemoglobin when compared with samples with less than 25% fetal hemoglobin (P less than .001). The pulse oximeter was easy to use, recorded trends in oxygenation instantaneously, and was not associated with skin injury. We conclude that pulse oximetry is a reliable technique for the continuous, noninvasive monitoring of oxygenation in newborn infants.

Transcutaneous PO2 (tcPO2) monitoring offers a new approach to the evaluation of drug effects. We investigated the effect of theophylline on ten premature infants with apnea. Theophylline was administered as aminophylline, 8 mg/kg per rectum every 12 hours for two doses and 4 mg/kg every 12 hours for a total of two or five days (short and long courses). The tcPO2, heart rate (beat-to-beat), and thoracic impedance were continuously monitored during each of three 4-hour study periods: 12 hours before theophylline administration, 12 hours after initiation of theophylline therapy, and 24 to 48 hours after discontinuing the drug's use. Plasma levels were measured by a radioimmunoassay developed in our laboratory. Polygraphic recordings were analyzed without knowledge of treatment for frequency of apneic spells, mean duration of apneas, total duration of hypoxemia (tcPO2 less than or equal to 40 torr), total duration of hyperoxemia (tcPO2 greater than or equal to 100 torr), basal tcPO2, heart rate, and respiratory rate. In each case during theophylline use, cardiorespiratory patterns were altered, respirations were more regular, apneic spells were reduced, PO2 was stabilized with less hypoxia and hyperoxia, and bradycardic episodes were decreased. There was considerable variation in the response of the ten infants and a significant difference in the frequency of return of symptoms between those receiving short-term therapy and those receiving the longer course.

In summary, our findings support and confirm the concerns of many investigators that present methods of cardiorespiratory monitoring are inadequate for the detection of many forms of apnea. Nurses underrecord both the frequency and duration of apneic episodes. Bradycardia is an unreliable index of hypoxemia. Thoracic impedance monitors are unreliable because they detect only a fixed duration of respiratory pause and are sensitive to many artifacts unavoidable in a clinical setting. Finally, ineffective breathing patterns such as disorganized breathing, obstructive apnea, and paradoxical breathing are undetectable by thoracic impedance monitoring. We warn against the reliance on heart rate and thoracic impedance monitoring alone for infants with recurrent apnea.

The clinical usefulness of the transcutaneous O2 electrode was investigated in 30 sick infants; 159 simultaneous measurements of arterial PO2 and transcutaneous PO2 were made. During the comparisons, arterial blood pressure, heart rate, and thoracic impedance were continuously recorded, and skin axillary and environmental temperatures and hematocrit were noted. Despite a wide range of arterial blood pressure and hematocrits, arterial PO2 and transcutaneous PO2 were similar (slope, 0.963), except for 2 groups of sick infants. Some infants with severe, persistent pulmonary hypertension who were receiving an intravascular infusion of tolazoline and infants with mean arterial blood pressures more than 2.5 SD less than the predicted average had values for transcutaneous PO2 that were lower than PO2. The surface O2 electrode is safe and relatively easy to use and provides data that can help in the management of most sick infants.

In summary, the pulse oximeter provides a reliable, continuous assessment of oxygenation in newborn infants. Its rapid response time and ease of use make it a practical device for use on all sick newborns. To avoid hyperoxia it should be used in conjunction with arterial blood gas measurements and we recommend a high SaO2 alarm of 92% in infants with predominantly fetal hemoglobin. Finally, it is an improved way of monitoring oxygenation in very immature infants and in infants with bronchopulmonary dysplasia.