Shabih Manzar, MD

Summary:

A case of neonatal hypoxic-ischemic encephalopathy (HIE) is presented. The findings of HIE in association with
chorioamnionitis and fetal acidemia is preceded by a prolonged maternal and fetal tachycardia.

Case:

A male infant was delivered vaginally at 393/7 weeks of gestation. Mother was an eighteen-year-old gravida1, para
1-0-0-0. She had a history of elevated blood pressures. Pregnancy medication included only prenatal vitamins.
All her prenatal labs, including RPR, HIV, hepatitis B, chlamydia, and gonorrhea were negative. Significant history
revealed rupture of membrane nineteen hours prior to delivery, foul-smelling amniotic fluid, and fever with a highest temperature of 102oF (38.9 °C). Fetal heart monitoring showed maternal and fetal tachycardia (Figure).

At delivery, the infant had no cry, poor tone, and poor respiratory effort. He was taken to warmer, dried, stimulated, and bulb suctioned. He was then placed on continuous positive airway pressure (CPAP), oxygen saturations improved, and the infant was transported to the neonatal intensive care unit (NICU). Apgar scores were 5 and 8 at 1
and 5 minutes, respectively. In the NICU, while on CPAP, he developed seizures and was placed on hypothermia
therapy per unit protocol. The cord blood gas showed severe acidemia (Table). The infant’s physical examination
was significant for tachycardia and abnormal muscle tone.

Vital signs showed a temperature of 100.9 °F (38.3 °C) and a heart rate of 191 beats per minute. The rest of the exam
was normal.

The infant transitioned well post warming and started on PO feeds, which he tolerated well. The neurological exam
at discharge was normal. He passed a pre-discharge hearing screen test. The infant was assessed by the pediatric neurologist and was sent home on phenobarbitone with follow up with his primary physician, neurology clinic, developmental clinic, and early steps intervention.

Discussion:

Fetal tachycardia was secondary to maternal tachycardia, which was secondary to high maternal temperature. With
the history of prolonged rupture of membranes and foulsmelling amniotic fluid, the cause of maternal fever was
suspected to be chorioamnionitis. Later, placental pathology showed stage 2, grade 2 chorioamnionitis.

The exact mechanism of fetal tachycardia resulting in acidemia is unknown; however, it could be postulated that
tachycardia increases the oxygen demand of the fetal heart leading to hypoxia. Persistent hypoxemia then generates lactic acid and causes a shift in the buffer system resulting in acidemia. Tachycardia and cardiogenic shock that resulted in acidosis have been reported earlier (1).

Recently Toomey and Oppenheimer (2) showed an association between fetal tachycardia and acidemia. By using a
logistic regression model, they found a tachycardia point estimate of 3.4 (95% CI 1.14-10.14). On careful observation
of fetal heart rate (Figure), we noted a 12- minutes epoch of maternal and fetal tachycardia. Maternal oxygen desaturation down to 88% was also noted that could have lead to poor oxygen delivery to the fetus resulting in severe acidosis as noted in the cord blood gas.

The mechanism of fetal tachycardia secondary to maternal fever and chorioamnionitis, could be explained by the cytokine-mediated fetal inflammatory response, as described by Romero et al. (3).

In conclusion, simultaneous maternal and fetal tachycardia, when seen on antenatal cardiotocography (CTG), is an
ominous sign and a potential risk factor for fetal distress and acidosis.

References:

  1. Viveiros E, Aveiro AC, Costa E, Nunes JL. Cardiogenic shock in a neonate. BMJ Case Rep. 2013. doi: 10.1136/bcr2012-008440
  2. Toomey PC, Oppenheimer L. Prediction of Hypoxic Acidemia in Last 2 Hours of Labour in Low-Risk Women. J Obstet Gyaecol Can. 2019 March 15 pii: S1701-2163(18)31037-5. doi: 10.1016/j.jogc.2018.12.015
  3. Romero R, Chaemsaithong P, Docheva, et al. Clinical chorioamnionitis at term IV: the maternal plasma cytokine profile. J Perinat Med. 2016;44:77-98 doi: 10.1515/jpm-2015-0103.

Disclosure: The author does not identify any relevant disclosures.