Fetal Monitoring

A Cochrane Database Review of cardiotocography (changes in the fetal heart rate and their temporal relationship to uterine contractions) found twelve randomised or quasi-randomised controlled trials including over 37,000 women, only two of which were high quality – compared to intermittent auscultation, continuous cardiotocography showed no significant difference in overall perinatal death rate (relative risk (RR) 0.85, 95% confidence interval (CI) 0.59 to 1.23, n = 33,513, 11 trials), but was associated with a halving of neonatal seizures (RR 0.50, 95% CI 0.31 to 0.80, n = 32,386, nine trials) although no significant difference was detected in cerebral palsy (RR 1.74, 95% CI 0.97 to 3.11, n = 13,252, two trials). There was a significant increase in caesarean sections associated with continuous cardiotocography (RR 1.66, 95% CI 1.30 to 2.13, n =18,761, 10 trials). Women were also more likely to have an instrumental vaginal birth (RR 1.16, 95% CI 1.01 to 1.32, n = 18,151, nine trials) [Alfirevic Z et al. Cochrane Database Syst Rev 3: CD006066, 2006]

Biophysical Monitoring

Can be measured both directly and indirectly. Direct measurements require a fetal presenting part (for EKG), and rupture of membranes and 1.5 cm of cervical dilation (to place a hydraulic catheter into the uterus). Indirect measurements can be made with a simple transducer applied to the maternal abdomen. Variables of interest include fetal heart rate (120-160 bpm), variability, and uterine activity

Fetal Heart Rate

Normally 120-160. Should increase due to vaginal examinations, fetal blood sampling, etc. Tachycardia may be due to distress, fever, or drugs such as ephedrine or atropine. Bradycardia may be due to hypoxia, acidosis, or congenital heart disease

Heart Rate Variability

Normal response to interplay between SNS and PNS, fetal heart rate should very by 5-25 bpm. Can be reduced by anesthetic or analgesic agents, atropine, or fetal “sleeping,” and can be increased by ephedrine

Uterine Contractions

Early decelerations follow uterine contractions, and rarely drop below 100 bpm. They are a normal, vagal response to increased intracranial pressure. Late decelerations don’t begin until 20-30 seconds after uterine contractions begin, and bottom out long after contractions have peaked – these are believed to be caused by myocardial ischemia secondary to uteroplacental insufficiency. Treatment should be with oxygenation, change of positioning, and fluid administration. If prolonged, the fetus may be at risk, attempts at monitoring the fetal acid-base status should be made, and urgent delivery should be considered. Variable decelerations are the most common form, and occur subsequent to umbilical cord compression. Their shape and onset are both highly variable, and heart rate may decrease to < 100 bpm. If frequent, or prolonged (2-10 minutes), variable decelerations can be a sign of danger.

Contractions should occur every 2-3 minutes in the active phase of labor, lasting ~ 1 min at a time and reaching up to 80 mm Hg of pressure (baseline uterine pressure is 5-20 mm Hg). Excessive uterine activity may be a sign of a problem such as abruption placentae or oxytocin overdose. Weak uterine pressure may be a sign of multiple gestation, polyhydramios, or uteroplacental insufficiency

Biochemical Monitoring

The chain of events leading to fetal demise usually begins with a respiratory acidosis (CO2 accumulation due to short-term placental insufficiency), followed by a metabolic acidosis (due to anaerobic metabolism). Thus, a fetal ABG can give the practitioner a sense of how long a fetus has been threatened. Fetal scalp ABGs have been validated in primate models (in which they closely correlate with carotid artery ABGs). Fetal blood sampling has also been shown to correlate with APGAR scores [Beard RW. Br J Hosp Med 3: 523, 1970; Bowe T et al. Am J Obstet Gynecol 107: 279, 1970] – based on Bowe’s data, 92% of infants with a pH > 7.25 will have APGARs 7 or higher at 1-2 minutes, whereas 80% of infants with pH < 7.16 will have APGARS 6 or less. Based on these data, pH < 7.20 is considered acidotic, with 7.20-7.25 “pre-acidotic.” There are, of course, instances of false negatives (10.4%) and false positives (7.6%). False tests are sometimes associated with maternal acidosis, thus a simultaneous maternal ABG may be helpful (if fetal/maternal gases are similar, the fetus is less likely to have low APGAR scores for a given level of acidosis)

Fetal Pulse Oximetry

FHO is a new technology that is placed between the fetal cheek and uterine wall, usually only during cases on non-reassuring or unreliable biophysical monitoring. Normal saturations are 30-70%, if SpO2 drops below 30% for 10 or more minutes, acidosis should be suspected. ACOG has not, to date, endorsed FHO as a routine monitor, stating that it “cannot endorse the adoption of this device in clinical practice at this time because of concerns that its introduction could further escalate the cost of medical care without necessarily improving clinical outcome.” A recent economic analysis of the Australian intrapartum fetal pulse oximetry (FPO) multicentre randomised controlled trial (the FOREMOST trial) showed that “The addition of FPO to CTG monitoring represented a less costly and more effective use of resources to reduce operative delivery rates for non-reassuring fetal status than the use of conventional CTG monitoring alone” [East CE et al. BJOG 113: 1080, 2006]. A Cochrane Database Review of randomised controlled trials comparing maternal and fetal outcomes when fetal pulse oximetry was used in conjuction with cardiotocography, compared with using cardiotocography (CTG) alone, found five published trials including 7424 pregnancies, and determined that there was a statistically significant decrease in caesarean section for nonreassuring fetal status with fetal pulse oximetry in post-36 week gestations wihtout a fetal blood sample requirement, or in all comers in whom fetal blood sampling was required prior to study entry, but there was no statistically significant difference in caesarean section for dystocia when fetal pulse oximetry (fetal pulse oximetry) was added to CTG monitoring [East CE et al. Cochrane Database Syst Rev (2): CD004075, 2007]

Fetal Lung Maturity

Lecithin and sphingomyelin are the primary phospholipids which make up surfactant. In early pregnancy, the concentration of lecithin is very small, while that of sphingomylin is much greater. Lecithin begins to be secreted into amniotic fluid by the developing fetal lung between 24 and 26 weeks gestation. At 32 to 33 weeks gestation, lecithin and sphingomyelin concentrations are about equal. Subsequently, lecithin begins to increase, with an abrupt rise around 35 weeks. In the mature lung, lecithin comprises 50-80% of the total surfactant lipid. Fetal lung maturity is present when the L/S ratio increases to 2.0 or more (or 3.5 or more for diabetic mothers).

Other options for assessment of fetal lung maturing include saturated phosphotidylglycerol (should be > 500 mg/dL in normal pregnancies, > 1000 mg/dL in diabetic women), and the simpler, faster, TDx-FLM. TDx-FLM is a fluorescent test accomplished by mixing a specific probe with amniotic fluid. It can be used quickly, including near immediate use in women with ruptured membranes. It is consistent across laboratories (< 40 mg/g indicates immaturity, > 55 mg/g predicts maturity) and does not need to be adjusted for diabetic women

Tests of Fetal Lung Maturity: Summary

  • L/S Ratio: 2 or higher in normal pregnancies, 3.5 or higher in diabetic women
  • Saturated phosphotidylglycerol > 500 mg/dL in normal pregnancies, > 1000 mg/dL in diabetic women
  • TDx-FLM < 40 mg/g indicates immaturity, > 55 mg/g predicts maturity, no adjustment for diabetics