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Biomedical subjects

J P Phelan

Publications and source records attributed to J P Phelan.

At least 19 recordsLinked to original sources

Fetal heart rate observations in the brain-damaged infant.

The objective of this study was to describe the fetal heart rate patterns and underlying pathophysiologic changes in the brain-damaged fetus. Fetuses with brain damage from hypoxic ischemic encephalopathy do not manifest uniform fetal heart rate patterns. However, these fetuses do show distinct fetal heart rate patterns that permit categorization based on their admission heart rate, subsequent changes in their baseline rate; and neonatal findings. Based on the observations of infants brain damaged in utero because of hypoxic ischemic encephalopathy, the intrapartum fetal management will depend on the admission fetal heart rate pattern, and the subsequent changes in the baseline rate.

Brain Damage, Chronic↗

Neonatal platelet counts in fetal brain injury.

UNLABELLED: The objective of this study was to determine whether neonatal platelet counts can be used in fetal brain injury. The initial platelet counts, expressed as 1000 per mm3, of singleton term infants with and without permanent asphyxial brain injury were compared. Neonates with encephalopathy were divided into 3 groups: I--nonreactive fetal heart rate (FHR) pattern from admission until delivery; II--reactive FHR pattern on admission followed by nonreactivity, tachycardia, a loss of variability and repetitive FHR decelerations; and III--acute: reactive FHR pattern followed by a sudden prolonged FHR deceleration that lasted until delivery. The neonates and platelet counts for each group were as follows: CONTROL: 104 neonates, mean 281 +/- 56, range 154 to 411; I: 60, mean 185 +/- 80, range 28 to 365; II: 34, mean 251 +/- 66, range 100 to 375; and III: 35, mean 267 +/- 93, range 86 to 569. Platelet counts were significantly lower in neonates with encephalopathy (p <0.001). Group I differed statistically from both Groups II and III (p <0.001). These data suggest an association between the FHR pattern, fetal asphyxial brain injury, and the initial platelet count in singleton term neonates. Further investigation should be pursued to clarify the physiological processes leading to this result.

Brain Diseases↗

Neonatal nucleated red blood cell and lymphocyte counts in fetal brain injury.

OBJECTIVE: To determine whether neonatal lymphocyte or nucleated red blood cell (RBC) counts can be used to date fetal neurologic injury. METHODS: Singleton, term infants with hypoxic-ischemic encephalopathy, permanent neurologic impairment, and sufficient laboratory data were divided into two groups: infants with preadmission injury, manifested by a nonreactive fetal heart rate (FHR) pattern from admission until delivery; and infants with acute injury, manifested by a normal FHR pattern followed by a sudden prolonged FHR deceleration. Lymphocyte and nucleated RBC values were compared with published high normal counts for normal neonates: 8000 lymphocytes/mm3 and 2000 nucleated RBCs/mm3. RESULTS: The study population consisted of 101 neonates. In the first hours of life, lymphocyte counts were elevated among injured newborns, and then the counts rapidly normalized. Brain-injured neonates were 25 times more likely to have a lymphocyte count greater than 8000 than were normal neonates (54 [62%] of 87 versus 6 [7%] of 84; odds ratio 25.5; 95% confidence interval 8.8, 80.1; P < .001). The mean lymphocyte count tended to be higher in the preadmission-injury group than in the acute-injury group. In comparison, nucleated RBC values were not correlated as strongly with neonatal hours of life; nucleated RBC counts tended to be higher and persist longer among neonates with preadmission injury than among those with acute injury. CONCLUSION: Compared with normal levels, both lymphocyte and nucleated RBC counts were elevated among neonates with fetal asphyxial injury. Both counts appear to be more elevated and to remain elevated longer in newborns with preadmission injury than in infants with acute injury. However, the rapid normalization of lymphocyte counts in these injured neonates limits the clinical usefulness of these counts after the first several hours of life.

Brain Injuries↗

Uterine activity patterns in uterine rupture: a case-control study.

OBJECTIVE: To determine whether uterine activity patterns are associated with intrapartum uterine rupture. METHODS: Because of the infrequency of uterine rupture, a case-control design was implemented. Cases were women who sustained uterine ruptures during a trial of labor, resulting in a neurologically impaired neonate. Controls were women who had a successful vaginal birth after cesarean (VBAC) or vaginal delivery with no history of uterine scar. The uterine activity patterns of cases were compared with those of each control group for number of contractions per hour, uterine tetany (contraction longer than 90 seconds), and uterine hyperstimulation (five or more contractions in a 10-minute period). RESULTS: The final study population consisted of 18 rupture patients, 35 VBAC patients, and 33 spontaneous vaginal delivery patients. Women in the rupture group had fewer contractions per hour (15.8+/-7.3) than VBAC (19.7+/-5.5) (P < .05) or spontaneous delivery group (19.4+/-6.6) (P < .10). VBAC patients were five times as likely to have 16 or more contractions per hour than were rupture patients, 95% confidence interval [CI] 1.3, 21.3, P < .02). Patients who had spontaneous delivery were 3.5 times more likely to have 16 or more contractions per hour than were rupture patients (95% CI 0.9, 14.1, P = .08). The rupture group had equal or less uterine tetany than did the controls. CONCLUSION: Uterine activity patterns and oxytocin use do not appear to be associated with the occurrence of intrapartum uterine rupture.

Adolescent↗

Permanent Erb's palsy: a lack of a relationship with obstetrical risk factors.

Our objective was to investigate the association between permanent Erb's palsy and the presence of historic obstetrical risk factors. Cases of documented permanent Erb's palsy from our national registry of children with Erb's palsy were extracted and analyzed for the purpose of this descriptive study. Maternal and neonatal records were reviewed for demographic data, prenatal care, labor characteristics, delivery outcome, and long-term follow-up. Sixty-three infants with permanent Erb's palsy were identified. Seventeen (27.0%) mothers were nulliparous. Mean +/- SD (range) gestational age at delivery and birthweight were 39.9 weeks +/- 1.3 (37-43) and 4501 g +/- 625 (3352-6905), respectively. Maternal and perinatal characteristics of these cases were (n [%]): nondiabetic-56 (89%); weight gain <40 lb-48 (76%); normal labor-57 (91%); 2nd stage <2.0 hr-54 (86%); midpelvic procedure-13 (21%); and shoulder dystocia-59 (94%). There were no statistically significant differences between patients with birthweight >4500 g (n = 26 [41%]) and those with birthweight < or =4500 g (n = 37 [59%]). These data suggest that historic risk factors for neonatal brachial plexus injury may not be associated with permanent Erb's palsy.

Adult↗

The fetal admission test and intrapartum fetal death.

Our objective was to describe the admission and subsequent intrapartum fetal heart rate (FHR) patterns in 21 singleton term pregnancies with an intrapartum fetal death. Through a retrospective chart review, 21 pregnancies with a term intrapartum fetal death were divided into 2 groups based on the fetal admission test (FAT): Group I-reactive (one or more FHR accelerations of 15 bpm x 15 sec in the first 30 min of monitoring); and Group II-nonreactive (NR [the absence of accelerations]). The FAT was compared with the subsequent intrapartum FHR pattern. Of the 21 deaths, the FAT was reactive in 7 fetuses (33%) or NR in 14 fetuses (67%). While the demographic features of these groups were statistically similar, Group II had higher rates of meconium (12 out of 14 (86%) vs. 2 out of 7 [29%] p = 0.017) and admission FHR decelerations (9 out of 14 (64%) vs. 1 out of 7 [14%] p = 0.06). In Group I, a sudden catastrophic event such as a uterine rupture produced a prolonged FHR deceleration in six fetuses (86%). One (14%) fetus died after a Hon pattern. In Group II, four patients had a stair steps to death pattern. Intrapartum fetal death can occur after a reactive or NR FAT. With a reactive FAT, a catastrophic event appears necessary to cause fetal death. The higher rates of meconium, FHR decelerations, and stair steps to death patterns in the NR group suggest the underlying basis for the fetal demise was related to preadmission fetal compromise.

Adult↗

Ambulatory obstetrical care: strategies to reduce telephone liability.

The telephone will become the centerpiece of ambulatory care services. As such, a pertinent aspect of office procedures will necessarily include a protocol to manage and document telephone calls. Encourage your office staff to use good telephone manners, as listed in Table 5. The net result should be a reduction in telephone liability risks and an enhanced reputation for your office.

Ambulatory Care↗

Does the onset of neonatal seizures correlate with the timing of fetal neurologic injury?

The onset of seizures after birth has been considered evidence of an intrapartum asphyxial event. The present study was undertaken to determine whether the timing of neonatal seizures after birth correlated with the timing of a fetal asphyxial event. Thus, singleton term infants diagnosed with hypoxic ischemic encephalopathy and permanent brain injury had a mean birth to seizure onset interval of 9.8 +/- 17.7 (range 1-90) hours. When these infants were categorized according to their fetal heart rate (FHR) patterns, the acute group (normal FHR followed by a sudden prolonged FHR deceleration that continued until delivery) tended to have earlier seizures than infants did within the tachycardia group (normal FHR followed by tachycardia, repetitive decelerations, and diminished variability) and the preadmission group (persistent nonreactive FHR pattern intrapartum). These seizure intervals were as follows: acute, 6.6 +/- 18.0 (range 1-90) hours; tachycardia, 11.1 +/- 17.1 (range 1-61) hours; and preadmission, 11.8 +/- 17.9 (range 1-79) hours (p < 0.05). But the range varied widely and no group was categorically distinct. In conclusion, the onset of neonatal seizures after birth does not, in and of itself, appear to be a reliable indicator of the timing of fetal neurologic injury.

Asphyxia Neonatorum↗

Catastrophic shoulder dystocia and emergency symphysiotomy.

We present three cases of shoulder dystocia unrelieved by standard maneuvers, including cephalic replacement. Symphysiotomy was performed in an effort to preserve fetal life. All three infants sustained severe neurologic injury and later died. Maternal morbidity including urinary incontinence was significant but responded to treatment. Symphysiotomy may be the only method of relieving some cases of shoulder dystocia, but its role remains unclear because of operator inexperience and maternal morbidity.

Adult↗

Permanent Erb palsy: a traction-related injury?

Historically, the primary risk factor attributed to brachial plexus injury during birth has been excessive traction applied at delivery to an entrapped anterior shoulder. However, recent evidence has suggested that not all cases of brachial plexus palsy are attributable to traction. We have encountered several cases of permanent Erb palsy associated with birth that were not attributable to traction applied at delivery. We reviewed cases of neonates with documented permanent Erb palsy that occurred either in the absence of shoulder dystocia or in the neonate's posterior arm in the presence of anterior shoulder dystocia. We identified four cases that occurred in the absence of shoulder dystocia and four cases that occurred in the posterior arm of infants with anterior shoulder dystocia. These data further support the notion that the etiology of permanent brachial plexus palsy associated with birth may not be related to traction.

Dystocia↗

Nucleated red blood cells: an update on the marker for fetal asphyxia.

OBJECTIVE: Our goal was to update our experience with nucleated red blood cells as a marker for fetal asphyxia and to determine whether a relationship exists between the presence of nucleated red blood cells and long-term neurologic impairment. STUDY DESIGN: Nucleated red blood cell data from 153 singleton term neurologically impaired neonates were compared with cord blood nucleated red blood cells of 83 term nonasphyxiated newborns. Newborns with anemia, intrauterine growth restriction, and maternal diabetes were excluded. The group of neurologically impaired neonates was separated into the following subgroups: group I, persistent nonreactive fetal heart rate pattern from admission to delivery (n = 69); group II, reactive fetal heart rate on admission followed by tachycardia with decelerations and absent variability (n = 47); group III, reactive fetal heart rate on admission followed by an acute prolonged deceleration (n = 37). The first and highest nucleated red blood cell value and the time of nucleated red blood cell disappearance were assessed. RESULTS: The mean number of initial nucleated red blood cells was significantly higher in the group of neurologically impaired neonates (30.3 +/- 77.5, range 0 to 732 per 100 white blood cells) than in the control group (3.4 +/- 3.0, range 0 to 12 per 100 white blood cells) (p < 0.000001). When the group of neurologically impaired neonates was separated on the basis of timing of the neurologic impairment, distinct nucleated red blood cell patterns were observed. Significant differences were obtained between each of the three groups of neurologically impaired neonates and the normal group, with respect to initial nucleated red blood cells (group I, 48.6 +/- 106.9; group II, 11.4 +/- 9.8; group III, 12.6 +/- 13.4; p < or = 0.000002). Maximum nucleated red blood cell values were higher in group I (mean 51.5 +/- 108.9) than in groups II and III combined (mean 12.7 +/- 11.9) (p = 0.0005). Group I also had a longer clearance time (119 +/- 123 hours) than groups II and III combined (mean 59 +/- 64 hours) (p < 0.001). CONCLUSION: Our ongoing study indicates that nucleated red blood cells identify the presence of fetal asphyxia. When fetal asphyxia is present, distinct nucleated red blood cell patterns are observed that relate to the timing of fetal injury. In general, intrapartum injuries are associated with lower nucleated red blood cell values. Thus our data continue to support the concept that nucleated red blood cell levels may assist in determining the timing of fetal neurologic injury.

Biomarkers↗

Nucleated red blood cells: a marker for fetal asphyxia?

OBJECTIVE: Our purpose was to determine whether a relationship exists between the presence of nucleated red blood cells, hypoxic ischemic encephalopathy, and long-term neonatal neurologic impairment. STUDY DESIGN: Nucleated red blood cell data from 46 singleton term neurologically impaired neonates were compared with cord blood nucleated red blood cells of 83 term nonasphyxiated newborns. The neurologically impaired neonates group was also separated as follows: nonreactive, nonreactive fetal heart rate from admission to delivery; tachycardia, reactive fetal heart rate on admission followed by tachycardia with decelerations; rupture, uterine rupture. The first and highest nucleated red blood cells value and the time to nucleated red blood cells disappearance were assessed. RESULTS: The neurologically impaired neonates group exhibited a significantly higher number of nucleated red blood cells per 100 white blood cells (34.5 +/- 68) than did the control group (3.4 +/- 3.0) (p < 0.00001). When the neurologically impaired neonates are separated as to the basis for the neurologic impairment, distinct nucleated red blood cell patterns were observed. Overall, the nonreactive group exhibited the highest mean nucleated red blood cell (51.4 +/- 87.5) count and the longest clearance times (236 +/- 166 hours). CONCLUSION: In this limited population, nucleated red blood cell data appear to aid in identifying the presence of fetal asphyxia. When asphyxia was present, distinct nucleated red blood cells patterns were identified that were in keeping with the observed basis for the fetal injury. In general, the closer the birth was to the asphyxial event, the lower was the number of nucleated red blood cells. Thus our data suggest that cord blood nucleated red blood cells could assist in the timing of fetal neurologic injury.

Asphyxia Neonatorum↗

Myomas and pregnancy.

At this time, the growth of uterine myomas during pregnancy cannot be predicted. Major complications of pregnancy appear to be related to whether the placenta and the myoma are in contact. The location and number of myomas, especially in the lower uterine segment, increases the likelihood of cesarean birth and malpresentation. Frequent ultrasound evaluations to monitor fetal growth and presentation and the size of the myoma should be considered in pregnant women with uterine myomas. Surgical resection of myomas should be reserved for those pregnant women with symptomatic pedunculated myomas with a small stalk. In those women with a pregnancy complication owing to the myoma, resection should be considered prior to the next pregnancy.

Female↗