Intrauterine Asphyxia: Clinical Implications for Providers of Intrapartum Care

Abstract

Advances in science and technology have allowed researchers to gain a better understanding of the pathophysiology leading to long-term neurologic damage in newborns. Intrapartum events are now known to be an infrequent cause of adverse neurologic outcome. Clinicians caring for women during labor must have an understanding of the pathophysiology of intrauterine asphyxia as well as an awareness of the capabilities and limitations of available intrapartum fetal assessment tools to diagnose intrauterine fetal asphyxia or predict neurologic outcome. This article reviews the physiology of acid-base balance and fetal gas exchange as well as the current scientific understanding of the role of intrauterine asphyxia in the pathophysiology of neonatal encephalopathy and cerebral palsy. Recommendations for care and documentation are included.

Maternal and fetal acid-base chemistry: A major determinant of perinatal outcome

“…The newborns that had low Apgar scores were significantly more acidotic during labor and delivery and during the 1 st h of life than babies born with high Apgar scores. [242627]…”

Non-reassuring fetal status: Case definition & guidelines for data collection, analysis, and presentation of immunization safety data

“…The fetus is equipped with compensatory mechanisms for transient hypoxia during labor, but prolonged, uninterrupted fetal hypoxia may lead progressively to acidosis with cell death, tissue damage, organ failure and potentially death. In response to hypoxia, fetal compensatory mechanisms include 1) a decrease in heart rate; 2) a reduction in oxygen consumption secondary to cessation of nonessential functions such as gross body movements; 3) a redistribution of cardiac output to preferentially perfuse organs, such as the heart, brain, and adrenal glands; and 4) a switch to anaerobic cellular metabolism [9]. Prolonged fetal hypoxia is associated with significant perinatal morbidity and mortality with particular concern for short- and long-term complications including encephalopathy, seizures, cerebral palsy, and neurodevelopmental delay [10], [11].…”

Asphyxia in the Newborn: Evaluating the Accuracy of ICD Coding, Clinical Diagnosis and Reimbursement: Observational Study at a Swiss Tertiary Care Center on Routinely Collected Health Data from 2012-2015

“…Possible interpretations are that due to the instruction of the existing exclusion term (exclusion of P21) P20 “intrauterine hypoxia” had been encoded instead of P21 “birth asphyxia”. The ACOG, the AAP, the Task Force on Neonatal Encephalopathy and Cerebral Palsy recommend against the use of the term “birth asphyxia” unless there is clear evidence of intrapartum-related causation, as they outlined criteria which together suggest an intrapartum timing, but individually are nonspecific to asphyxia insults [9, 36]. Referring to this recommendation, the onset characteristics could be excluded from the classificatory criteria (“Model Matrix”).…”

“…According to the Committee on Fetus and Newborn, the AAP, and the Committee on Obstetrics Practice, ACOG [39]: “An infant who has had “asphyxia” proximate to delivery that is severe enough to result in acute neurologic injury should have demonstrated all of the following criteria: (a) profound metabolic or mixed acidemia (pH < 7.00) on an umbilical arterial blood sample, if obtained, (b) an Apgar score of 0 to 3 for longer than 5 minutes, (c) neurologic manifestation, e.g, seizure, coma, or hypotonia, and (d) evidence of multiorgan dysfunction”. The 1- minute Apgar score appears to be less useful in the sense of predictability, prognosis and diagnostic accuracy than the 5- minute or 10- minute score [36, 39–49]. …”