The effect of profound umbilical artery acidemia in term neonates admitted to a newborn nursery

doi:10.1016/S0022-3476(98)70350-6

The Journal of Pediatrics

Volume 132, Issue 4, April 1998, Pages 624-629

https://doi.org/10.1016/S0022-3476(98)70350-6 Get rights and content

Abstract

Objective: To determine whether there were immediate adverse effects of an umbilical artery pH ≤ 7.0 in term and near-term infants. Study Design: All infants triaged to the newborn nursery with an umbilical artery pH ≤ 7.0 from May 1993 through April 1994 (n = 37) were prospectively identified; 35 of the 37 infants were enrolled and matched with nonacidemic control infants (n = 35). Organ system dysfunction (neurologic, renal, hepatic, gastrointestinal) was evaluated either clinically or biochemically with selected blood and urine parameters. Results: Acidemic and control groups were similar for pregnancy complications before labor, but acidemic infants were more often delivered by cesarean section (20/35 vs 6/35, p = 0.001). No differences existed between acidemic and control infants in gestational age, birth weight, neurologic evaluations, hearing deficits, feeding tolerance, and hepatic function. The acidemic group had a higher mean serum creatinine than control infants on day 2 of life (0.90 ± 0.34 vs 0.71 ± 0.12 mg/dl, p = 0.005) and a greater number of infants with a urine Chemstrip positive for heme (14/35 vs 3/35, p = 0.005). No differences existed between groups in time to first void, urine specific gravity, and number of infants with microscopic hematuria. Conclusion: Term and near-term infants born with an umbilical artery pH ≤ 7.0 and triaged to the newborn nursery on the basis of a stable appearance in the delivery room do not have clinical manifestations of hypoxia-ischemia in the 48 hours after birth. The higher mean serum creatinine for acidemic compared with control groups is presumably prerenal in origin and results from processes responsible for profound fetal acidemia. Infants with an umbilical artery pH ≤ 7.0 and assessed to be clinically well can be treated similar to nonacidemic infants. (J Pediatr 1998;132:624-9)

Section snippets

METHODS

This study was conducted at Parkland Memorial Hospital, which is the sole city/county facility for Dallas County, Texas, and was approved by the Institutional Review Board of the University of Texas Southwestern Medical Center at Dallas. Informed consent was obtained from the parents of infants in the acidemia and control groups. In the delivery room infants were triaged to the NBN either by nursing personnel, nurse practitioner, or houseofficer on the basis of criteria of a gestational age ≥

RESULTS

From May 1, 1993, through April 30, 1994, there were 14,712 deliveries at Parkland Memorial Hospital, and umbilical artery pH and blood gases were measured in 97%. A total of 13,594 infants were triaged to the NBN, and 37 of these infants had an umbilical artery pH ≤ 7.0. Two of the 37 infants were excluded because of parental refusal for consent and recognition of fetal acidemia after transfer to the NICU at 4 hours of age. The umbilical artery pH and blood gases for the 35 acidemic newborns

DISCUSSION

This investigation determined the immediate effects of profound fetal acidemia (umbilical artery pH ≤ 7.0) for term and near-term infants deemed clinically stable. Overall these infants were comparable to control infants without fetal acidemia with regard to neurologic dysfunction, hearing deficits, feeding intolerance, and abnormalities of liver function. The only significant differences between acidemic and control groups were serum creatinine levels and heme-positive urine detected by

Acknowledgements

We wish to thank Ms. Marilyn Dixon for her outstanding secretarial expertise.

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Hypoxic-ischemic injury secondary to asphyxia is a common cause of brain injury in neonates, affecting 1 to 3 infants per 1000 live births. Infants with moderate to severe hypoxic-ischemic injury often have cardiovascular instability and myocardial dysfunction affecting organ perfusion and thus oxygen delivery, which can potentially result in further injury if not identified in a timely manner. Pulmonary hypertension can further complicate the postnatal course. Cerebral autoregulation, often severely impaired by the underlying pathophysiology, can further be affected by therapeutic hypothermia (TH) and rewarming, which in turn can lead to reperfusion injury to the brain. These hemodynamic complications might affect long-term outcomes.
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Pathophysiology of Birth Asphyxia
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Citation Excerpt :
However, even with this degree of acidemia, the likelihood of subsequent brain injury remains low. The majority of these infants (>60%) have an uneventful delivery, remain in the well nursery, and are discharged home without complication.36 Even when infants with severe fetal acidemia are admitted to intensive care (usually because of respiratory difficulties) about 80% to 90% exhibit a benign neurologic course and it is only a small percentage present with encephalopathy.37–39
Short-term outcomes of newborns with perinatal acidemia who are not eligible for systemic hypothermia therapy
2013, Journal of Pediatrics
Citation Excerpt :
Perinatal acidemia is the initial screening component in the sequence of events that culminates in the decision to use hypothermia. The majority of newborns with perinatal acidemia are not cooled because their neurologic examination does not have sufficient abnormalities to classify them as having moderate or severe HIE.17 The outcomes of these infants who are diagnosed with mild or no encephalopathy on an early neurologic examination are not fully known,18 and whether the current assessment of these infants with perinatal acidosis identifies only the more severely affected infants remains to be determined.
To determine short-term outcomes of infants who had perinatal acidemia and were evaluated for hypothermia therapy but did not qualify based on a standardized neurologic examination.
Retrospective, single-site cohort study of inborn infants of ≥36 weeks gestation who had perinatal acidemia from October 2005-September 2008 and had a standardized neurologic examination performed by a certified neonatologist to assess eligibility for hypothermia therapy. An abnormal short-term nursery outcome was defined as death, seizures, brain magnetic resonance imaging consistent with hypoxic-ischemic encephalopathy, abnormal neurologic examination at discharge, gastrostomy tube feeding, or inability to nipple all feeds beyond the first week of age.
One hundred forty-four (0.3%) of 46 887 newborns with perinatal acidemia had a neurologic examination performed that was either normal (n = 29) or consistent with mild encephalopathy (1 or 2 abnormal categories; n = 60). Of the latter infants classified as having mild encephalopathy, 12 (20%) experienced an abnormal short-term outcome (feeding difficulties, n = 8; abnormal neurologic examination at discharge, n = 7; abnormal brain magnetic resonance imaging, n = 6; seizures, n = 5; gastrostomy, n = 1; or death, n = 1).
Twenty percent of newborns with perinatal acidemia and a neurologic examination that revealed only mild encephalopathy had abnormal short-term outcomes that could be attributed to the encephalopathy. Adjunctive tools or biomarkers for optimal assessment of infants with fetal acidemia for hypothermia therapy are needed.
Perinatal acidosis and hypoxic-ischemic encephalopathy in preterm infants of 33 to 35 weeks' gestation
2012, Journal of Pediatrics
Citation Excerpt :
A pH <7.0 reflects the degree of acidosis below which end organ dysfunction is likely to be detected in term infants.10,11 Earlier work from our institution showed that approximately 0.3% of term deliveries are complicated by severe fetal acidosis, and approximately one-third of the newborns required admission to the NICU, and 15% had moderate to severe HIE.12 This study establishes baseline data on which to base future trials of neuroprotective strategies such as hypothermia in this preterm population.13
To determine the frequency of hypoxic-ischemic encephalopathy (HIE) in preterm infants of 33 to 35 weeks’ gestational age on the basis of physiological screening for perinatal acidosis and neurological assessment of encephalopathy and to correlate neurodevelopmental outcomes with brain magnetic resonance imaging findings.
This retrospective cohort study included all inborn infants of 33 to 35 weeks’ gestation admitted to the neonatal intensive care unit at Parkland Memorial Hospital with perinatal acidosis from October 2005 to September 2008. Their medical records were reviewed, and pertinent data were recorded.
Of 1305 newborns, 2.5% (n = 33) had perinatal acidosis, and 27% (n = 9) of these had HIE (2, mild; 4, moderate; 3, severe). Persistence of metabolic acidosis on the first arterial blood gas obtained in the first hour of age was significantly associated with HIE (P < .005). Magnetic resonance imaging results were abnormal in 3 of 4 infants with moderate HIE and in both survivors with severe HIE. Death or disability occurred in no infants with mild or moderate HIE, but in all infants with severe HIE.
Screening criteria for HIE that use biochemical and neurological assessments as performed in term newborns can be applied to preterm infants of 33 to 35 weeks’ gestation.

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^☆: From the University of Texas Southwestern Medical Center, Department of Pediatrics and Otorhinolaryngology and Parkland Memorial Hospital, Women and Children's Services, Dallas, Texas

^☆☆: This work was supported by the Department of Pediatrics and the General Clinical Research Center, USPHS Grant No. M01-RR00633, of the University of Texas Southwestern Medical Center.

^★: Reprint requests: Abbot Laptook, MD, UT-Southwestern Medical Center at Dallas, Department of Pediatrics, 5323 Harry Hines Blvd., Dallas, TX 75235-9063.

^★★: 9/21/82211

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The effect of profound umbilical artery acidemia in term neonates admitted to a newborn nursery☆,☆☆,★,★★

Abstract

Section snippets

METHODS

RESULTS

DISCUSSION

Acknowledgements

Early Hum Dev

Am J Obstet Gynecol

Am J Obstet Gynecol

Am J Obstet Gynecol

Am J Obstet Gynecol

Am J Obstet Gynecol

J Pediatr

J Pediatr

Lancet

Am J Obstet Gynecol