Perinatal/Neonatal Casebook

Atypical Variable Decelerations and Intrauterine Growth Restriction

Department of OBGYN, Division of Maternal-Fetal Medicine, Newark Beth Israel Medical Center, Newark, NJ, USA

Correspondence to: Martin L. Gimovsky, MD, Department of OBGYN, Newark Beth Israel Medical Center, 201 Lyons Avenue, Newark, NJ 07112, USA

Abstract

Variable decelerations of the fetal heart rate are the most common changes noted during continuous fetal monitoring. In general, they are presumed to represent a normal response to fetal baroceptor stimulation. When atypical features are present, other considerations are warranted. Journal of Perinatology (2002) 22, 588-591 doi:"10.1038/sj.jp.7210770

CASE REPORT

LA was a 26-year-old gravida 3, para 0020 who presented for induction of labor at 37 weeks' gestation.

Her prenatal course had been significant for Rh negative status for which she had received Rh immune globulin. In addition, she had undergone a glucose tolerance test for an elevated screen. The 1-7 hour glucose remained elevated, but all other values were within normal limits.

Ultrasound examinations during her prenatal course showed a growth pattern consistent with asymmetrical intrauterine growth restriction (IUGR). She was referred for admission for delivery at 37 weeks based on the findings at an ultrasound done for a lag in fundal height growth (Table 1).

On admission to L&D, her cervix was noted to be 1 to 2 cm and 60% effaced (Figure 1). An amniotomy was performed and yielded clear fluid. An internal monitor disclosed a decrease in beat-to-beat variability.

An atypical variable was noted (Figure 2)), which progressed in severity during early labor. This was treated conservatively, with oxygen, position change, and IV fluid bolus; resolution was seen. The oxytocin was resumed, and atypical variable decelerations were again noted (Figure 3)). An amnioinfusion was started, without change in the FHR pattern (Figure 4).

The patient progressed to full dilatation and demonstrated a prolonged FHR deceleration (Figure 5). An emergent cesarean delivery was performed.

A male infant weighing 2490 g (10th centile for estimated gestational age), with Apgar scores of 6 and 8 at 1 and 5 minutes, respectively, was delivered. A loose nuchal cord was noted. The umbilical artery pH was 7.30, with a PCO₂ of 46, and a PO₂ of 45. Theinfant appeared pale but not distressed, and was sent to the normal nursery.

At about 40 hours of life, seizure-like activity as well as hypothermia was noted. Electrolytes and CBC were within normal limits. Definitive seizure activity ensued over the next 12 hours, and an EEG and CT were performed. Phenobarbital was administered.

A large left cerebral infarction was noted in the anterior and middle cerebral arteries. The EEG was interpreted as normal for gestational age. Coagulation studies were normal (including proteins S and C, and antiphospholipids), as was a cardiovascular workup.

An MRI/MRA showed an occlusion at the level of the bifurcation of the left common carotid artery. At follow-up, the infant had a right spastic hemiparesis. He developed normal fine motor adaptive, speech, and social skills.

DISCUSSION

Failure of in utero growth (IUGR) may occur as a result of multiple etiologies with widespread consequences for the newborn. Different patterns of altered fetal growth reflect differing insults with consequent diverse outcome considerations (Table 2).⁴ In asymmetric growth restriction, as in this pregnancy, the fetal abdominal circumference is relatively small for the cranial and long bone parameters.⁵ This is generally the result of less than normal liver growth caused by a lack of glycogen storage, and a decrease in subcutaneous fat. Symmetric patterns of growth restriction, in which there is a "symmetric" reduction in cranial and long bone growth in conjunction with a small abdominal circumference also occur.^5,6 In general, symmetrical growth restriction occurs early in gestation, and may be due to an intrinsic fetal insult, such as a chromosomal aberration, an in utero infection, or exposure to a teratogen. They may be problematic to diagnose, and are commonly confused with errors in pregnancy dating based on the fetal measurements made at ultrasound. Mixed patterns of growth restriction may also be seen, which reflect fetal growth response to both early and late factors. This situation may be seen with maternal systemic processes, such as lupus, Crohn's disease, or during treatment for neoplasms.

Variable decelerations during labor are a common occurrence. Baroceptor mediated responses to periodic interruption of flow through the umbilical veins and artery result in a characteristic rapid decrease and subsequent return in FHR resulting in a narrow "V"-shaped response. These vary in timing with respect to uterine activity. When fetal hypoxemia supervenes, a prolonged recovery phase, with tachycardia and occasional late decelerations, occurs. When hypoxemia is prolonged and results in acidemia, an "overshoot" of the baseline FHR is present during recovery.

The "atypical variable deceleration" presents a different set of characteristics from those normally seen as a result of baroceptor response. There may be a "W," "U," or a widened "V"-shape to the deceleration pattern (Figures 2 and 3).

These more complex responses reflect changes in umbilical cord elasticity and turgidity as well as associations with fetal central nervous system and cardiovascular pathology. Both etiologies have a tendency to represent processes that are chronic in nature.

In this case, on admission, the FHR was normal in baseline rate, and accelerations were present, indicating a normal fetal acid-base status. It may have been critical to the subsequent delivery of the infant in a nonasphyxiated state that the diagnosis of IUGR was made and acted upon in a timely manner. Although there is a lack of beat-to-beat variability on internal monitoring, the initial baseline FHR rate remained normal, and an acceleration is present, both features suggesting normal acid-base balance.

An atypical-appearing variable deceleration occurred and progresses to greater severity. After resolution, atypical variables recurred. There was a mild tachycardia in response to these decelerations and an overshoot pattern developed during return of the FHR to baseline.

Prolonged bradycardia occurred at full dilation and delivery was by emergent cesarean delivery. Fetal/neonatal acid-base was normal at birth as evidenced by the umbilical cord gas. The Apgar scores further indicate a neonate without the need for extensive resuscitation. Thus, this infant was not asphyxiated at the time of delivery.

Prenatal recognition of IUGR resulted in admission for delivery at 37 weeks with the hope that any existing injury to the neonate might be ameliorated. The intrapartum FHR responses noted were not diagnostic of specific fetal injury during labor. They were consistent with a fetus undergoing "stress" and ultimately "intolerance of labor" just before delivery.

The infant's state in the immediate newborn period is most reflective of an injury sustained earlier during pregnancy. The medical care that was provided was very much in keeping with the standard of care. Additionally, the neurologic abnormalities noted during day 2 of life were properly evaluated and led to a timely diagnosis and appreciation of this infant's problem.

Later evaluation revealed the specific neurologic finding, most consistent with an in utero stroke. Infants born with IUGR of either asymmetric or symmetric type are known to be at increased risk for abnormal neurologic development.^1,2,3 Furthermore, diagnosis may often be complicated in situations wherein neonates with mild degrees of growth restriction may not be readily apparent at birth. Early discharge after delivery may further delay the recognition and ultimately the sequelae of injuries that are most likely sustained inutero.

Acknowledgements

The authors appreciate the editorial assistance of Arlene Gimovsky in the preparation of this manuscript.

References

1 Volpe JJ. Neurology of the Newborn 3rd edition Philadelphia, PA: WB Saunders, 1995.

2 Low JA, Handley-Derry MH, Burke SO et al. Association of intrauterine fetal growth retardation and learning deficits at age 9 to 11 years. Am J Obstet Gynecol 1992; 167: 1499-505. MEDLINE

3 Blair E, Stanley F. Intrauterine growth and spastic cerebral palsy: I. Association with birth weight for gestational age. Am J Obstet Gynecol 1990; 162: 229-37. MEDLINE

4 Manning FA. Intrauterine growth retardation: etiology, pathophysiology, diagnosis and treatment. In Fetal Medicine: Principles and Practice Norwalk, CT: Appleton & Lange, 1995.

5 Ferrazzi E, Bellotti M, Galan Het al. . Doppler investigation in IUGR: a review of a collaborative group. Ann NY Acad Sci 2001; 943: 316-25. MEDLINE

6 Baschat AA, Harman CR. Antenatal assessment of the growth restricted fetus. Curr Opin Obstet Gynecol 2001 Apr; 13: 161-8.

7 Alfirevic GR, Neilson JP. Doppler ultrasonography in high-risk pregnancies: systemic review with a meta-analysis. Am J Obstet Gynecol 1995; 172: 1379-82. MEDLINE

Figures

Figure 1 On admission, the baseline FHR was in the 140s. An acceleration is noted on external FHR monitoring.

Figure 2 The initial appearance of a "W"-shaped variable deceleration. The baseline FHR and variability are normal.

Figure 3 "Wide V" and "W-shaped" variables are noted. Baseline FHR, variability essentially unchanged.

Figure 4 Several hours later, variable decelerations recur, this time associated with FHR baseline increase in the FHR. There is also a prolonged recovery phase see, as well as a suggestion of "overshoot" of the FHR on return to baseline.

Figure 5 Prolonged bradycardia resulted in an emergent cesarean delivery. The neonate was not asphyxiated at birth.

Tables

Table 1 Serial Ultrasonography Performed on Patient LA

Table 2 Patterns and Etiologies of Fetal Growth Restriction

October/November 2002, Volume 22, Number 7, Pages 588-591

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