Jeffrey Pomerance, MD, MPH

Case 23: Asphyxia Prior to Hospital Admission

The mother was a 41-year-old, gravida 4, para 3, aborta 0, with an intrauterine pregnancy at 42 0/7 weeks gestation. (1) She com- plained of decreased fetal movement beginning the day before admission and felt no fetal movement on the morning of admission. At the hospital, she had uterine contractions every five to seven minutes; her cervix was five cm dilated, completely effaced, and at zero station. The FHR was 140 bpm, without decelerations but with absent variability. After one hour, the patient had an uncomplicated vaginal delivery of a male infant with Apgar scores of 3 and 6 at one and five minutes, respectively. Amniotic fluid wasclear. The placenta was not sent to pathology.

FIGURE

Cord blood gas results were as follows: 

	BD (mmol/L)	Umbilical Vein
pH	7.35	-1
Umbilical Artery	7.31	0
Pco2 (mmHg) (kPa)	48 6.40	52 6.93
Po2 (mmHg) (kPa)	21 2.80	14 1.87

Blood gases obtained from the infant at 30 minutes of age were as follows:

	CBG
pH	7.33
Pco2 (mmHg) (kPa)	42 5.60
Po2 (mmHg) (kPa)	41 5.47
BD (mmol/L)	4

The NRBC count was not elevated. Subsequently, the infant had a seizure in the neonatal intensive care unit and showed signs of moderate renal failure, from which he ultimately recovered.

Interpretation

Both the umbilical venous and arterial cord blood gas results are entirely normal. In the presence of FHR monitoring that continues until close to the time of delivery and in the absence of significant FHR decelerations, intrapartum fetal asphyxia can be excluded. However, in the presence of low Apgar scores, it is prudent to obtain a follow-up blood gas directly from the infant soon after birth to document the infant’s blood gas status. One would expect complete cord occlusion (both venous and arterial), a complication that could explain normal or near-normal cord gas values, to have resulted in severe fetal bradycardia. However, bradycardia was not observed, and the follow-up capillary blood gas was normal. This infant was not suffering from asphyxia at the time of delivery.

Intrapartum asphyxia is not the only cause of low Apgar scores. Another cause of Apgar score depression is recent antenatal, but not intrapartum, moderate to severe in utero asphyxia with acid-base recovery before delivery. Such a baby may have neurological findings during the neonatal period. This deficit would correspond with the maternal history of decreased fetal movement and the absence of variability in an otherwise stable heart rate pattern. Usually, but not always, problems of uteroplacental insufficiency increase over time. Occasionally, uteroplacental insufficiency or a cord problem may injure the fetus, allowing fetal acid-base recovery before delivery.

In this case, the neonatal clinical course strongly suggests hypoxic-ischemic encephalopathy and acute tubular necrosis with recovery. The FHR tracing on the day of admission, the normal umbilical cord blood gas values, and the normal follow-up capillary blood gas shortly after delivery suggest the insult occurred before fetal monitoring was initiated. Absent variability on the fetalmonitoring strip, right from the beginning of the tracing, confirms this. The absence of an elevation in the NRBC count (2) suggests the insult was relatively acute and was not ongoing during labor and delivery. It is highly unlikely that earlier delivery during fetal monitoring would have resulted in a baby with a different clinical course or a better outcome.

The differential diagnosis of normal or near-normal cord gases associated with low Apgar scores is the rare finding of complete cord occlusion (both venous and arterial), without a widened umbilical cord venoarterial pH difference. However, there was no associated evidence of a vulnerable cord, such as variable decelerations or severe fetal bradycardia prior to delivery.

Key Point

• Even in the presence of low Apgar scores, absence of significant decelerations on FHR monitoring, presence of normal or near-normal umbilical cord blood gas values, and a normal follow-up blood gas soon after delivery all suggest the absence of intrapartum asphyxia and likely recent antepartum asphyxia.

Case 24: Renal Agenesis with Hypoplastic Lungs

The mother was a 27-year-old, gravida 2, para 1, aborta 0, with an intrauterine pregnancy at 40 1/7 weeks gestation. (3) The mother reported spontaneous rupture of membranes five hours before admission with the escape of a small amount of clear fluid. The FHR monitor showed variable decelerations. Over the next several hours, the patient’s cervix became completely dilated and effaced, and the head was at plus two station. The FHR monitor revealed deep variable decelerations that lasted 60-90 seconds. The infant was delivered vaginally 30 minutes later. Apgar scores were 2, 2, and 3 at one, five, and 10 minutes.

[READ FULL CASE 24 DESCRIPTION IN ARTICLE BELOW]

Figure 1. Amnion nodosum in the placenta of a newborn with renal agenesis. Note the uniform presence of fine granules, mostly sparing the vessel surfaces and not present on the cord. (From Benirschke K, Kaufman P: Placental Membranes in Pathology of the Human Placenta, 2nd ed. New York, Springer-Verlag, 1990, p160. Reproduced with permission.)

References:

1. Pomerance J. Umbilical cord blood gas casebook: Interpreting umbilical cord blood gases, Part IV. J Perinat 1999;19:158.

2. Phelan JP, Ahn MO, Korst LM, Martin GI. Nucleated red blood cells: A marker for fetal asphyxia? Am J Obset Gynecol 1995:173:1380-4. DOI: 10.1016/0002-9378(95)90620-7

3. Pomerance J. Umbilical cord blood gas casebook: Interpreting umbilical cord blood gases, part VI. J Perinat 1999;19:608-9.

4. Benirschke K, Kaufman P. Placental membranes. In: Pathology of the Human Placenta. 2nd ed. New York: Springer-Verlag; 1990, p160.