19 Unusual Fetal Heart Rate Patterns. Handbook CTG

 19

Unusual Fetal Heart Rate Patterns

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Sinusoidal and Saltatory Patterns

Madhusree Ghosh and Edwin Chandraharan

Handbook of CTG Interpretation: From Patterns to Physiology, ed. Edwin Chandraharan.

Published by Cambridge University Press. © Cambridge University Press 2017.

Key Facts

Key Features on the CTG Trace

Features of sinusoidal heart rate are:

A sinusoidal (typical) fetal heart rate (FHR) pattern may be due to physiological

causes like fetal thumb sucking or administration of narcotic analgesics like

alphaprodine2,3 and butorphanol.4,5

The most common pathological cause of sinusoidal FHR is fetal anaemia due to

rhesus isoimmunization (typical sinusoidal pattern) with fetal hypoxia and

acidosis and sudden loss of fetal blood volume due to acute fetomaternal

haemorrhage (atypical sinusoidal pattern).

Saltatory FHR patterns6 can be due to uterine hyperstimulation, ephedrine

administration and repeated intensive hypoxic stress such as active maternal

pushing in active second stage of labour.The features of saltatory pattern are (see Figure 19.2):

Sinusoidal FHR can be further classified as7:

Figure 19.1 Atypical sinusoidal pattern: ‘Poole shark teeth pattern’.

Stable baseline FHR of 120 to 160 beats per minute with regular sine-wave

oscillations

Amplitude of 5 to 15 beats per minute

Frequency of 2 to 5 cycles per minute

Reduced or absent baseline variability

Absence of accelerations

Fetal heart rate baseline amplitude changes greater than 25 beats per minute

Oscillatory frequency of greater than 6 per minute

Minimum duration of 1 minute

Smooth or typical – rounded, symmetric in shape

Jagged or atypical – jagged, saw-toothed form, also termed as ‘Poole shark teeth

pattern’ (Figure 19.1)

Pseudo-sinusoidal – undulatory waveforms or regular FHR baseline oscillations

of constant amplitude, alternating with episodes of normal baseline variability

and reactivityFigure 19.2 Pseudo-sinusoidal pattern. Note the presence of normal variability prior to

sinusoidal pattern.

Key Pathophysiology of Sinusoidal and

Saltatory FHR Patterns

Exact pathophysiology not well understood due to its rare occurrence.

Sinusoidal FHR is either due to central nervous system involvement or an

umbilical cord–related aetiology such as acute and repeated umbilical cord

compression leading to alternative episodes of fetal hypovolemia and

hypertension.

Derangement or loss of central nervous system control over the FHR is believed

to be the common pathway of sinusoidal FHR patterns. This may explain the

occurrence of this pattern after administration of certain drugs that act on the

central nervous system and fetal hypoxia and acidosis.

Sinusoidal FHR pattern may occur due to a massive fetomaternal transfusion and

maternal anaemia. Severe anaemia may lead to local relative hypoxia of

specialized tissues such as the central nervous system cardiac centre leading to

sinusoidal pattern.

Sinusoidal FHR is also seen in the presence of chorioamnionitis. The fetuses

may not be hypoxic but show a sinusoidal FHR pattern due to maternal pyrexia.

This is because elevated maternal temperature may adversely affect fetal brain

function, thereby inactivating central nervous system control over FHR.Recommended Management

Atypical sinusoidal pattern is believed to occur secondary to acute fetal

hypotension and resultant acute hypoxia to the central nervous system that causes

instability of the autonomic nervous system.

Pseudo-sinusoidal FHR is not typically associated with fetal compromise.

Saltatory FHR is probably a result of instability between sympathetic and

parasympathetic nervous systems resulting in rapidly evolving hypoxia to the

central nervous system.

Exclude predisposing causes for sinusoidal and saltatory patterns.

Sinusoidal traces secondary to administration of drugs can be managed

expectantly.

Due to a lack of correlation between sinusoidal traces and documented fetal

hypoxia, one needs to consider the underlying clinical picture, for example,

reduced fetal movement, presence of meconium, intrapartum bleeding prior to

embarking on operative delivery.

An ultrasound scan may be performed to confirm fetal thumb sucking.

In cases of typical or atypical sinusoidal traces for >10 minutes in the presence

of risk factors (Rhesus-negative status, sudden fetomaternal bleeding), urgent

delivery is indicated by the quickest and safest mode of birth.

In cases of saltatory patterns, oxytocin infusion should be reduced or stopped

and the woman should be advised to stop pushing in the second stage of labour

to improve utero-placental circulation and re-establish oxygenation of the brain.

If improvement in the features of CTG trace are observed, labour may be

allowed to continue. If saltatory pattern persists despite conservative measures

and immediate delivery is not imminent, tocolysis should be continued. Delivery

should be accomplished if there is no improvement despite intrauterine

resuscitation.Key Tips to Optimize Outcome

Pitfalls

The neonatal team should be notified as the neonate may be hypoxic or

hypotensive at birth requiring advanced neonatal resuscitation and blood

transfusion.

Unusual FHR patterns may be physiological; however, pathological causes need

to be excluded.

Exclude predisposing factors such as chronic fetal anaemia, chorioamnionitis

and administration of drugs to the mother.

Prompt recognition of sinusoidal pattern where there is an ongoing fetomaternal

haemorrhage is essential.

Clear communication with multidisciplinary team is mandatory.

Escalate and seek immediate senior obstetric help when unsure about unusual

patterns.

Continuous training of obstetric doctors and midwives on unusual FHR patterns,

their significance and management is recommended.

Failure to differentiate between physiological and persisting sinusoidal patterns

due to ongoing fetomaternal haemorrhage.

Failure to recognize concealed placental abruption and ongoing atypical

sinusoidal pattern.

Failure to inform the neonatal team regarding the possibility of severe fetal

anaemia and/or hypotension, which may require an urgent neonatal blood

transfusion after birth.Consequences of Mismanagement

Exercise

1. A 35-year-old primigravida presents at 38 weeks of gestation with abdominal pain

for 3 hours and reduced fetal movements with no vaginal bleeding. On examination,

uterine contractions were palpated and the cervix was fully effaced, 2 cm dilated.

a. What is your differential diagnosis?

b. Is a CTG indicated?

c. She was re-examined in 4 hours and established to be in labour. She was later

commenced on oxytocin for confirmed delay in the first stage of labour. Vaginal

examination after 4 hours of oxytocin demonstrated that she was 8 cm dilated. Describe

the CTG at this stage (Figure 19.3). Do you have any concerns?

d. She opted for an epidural anesthesia and is now fully dilated and has had a 2-hour

passive descent. A repeat vaginal examination suggests that she is fully dilated with the

fetal head in occipito-anterior position, at station +1. A decision has been made to start

active pushing. She has been actively pushing for 20 minutes and CTG is given below

(Figure 19.4). How would you describe the CTG?

e. What is your management plan based on the features observed on the CTG (Figure

19.4)?

Intrapartum fetal death and early neonatal death.

Severe hypoxic-ischaemic encephalopathy (HIE).

Unnecessary operative intervention due to lack of recognition and treatment of a

sinusoidal pattern secondary to a physiological cause.

Maternal hypotension and disseminated intravascular coagulopathy (DIC) due to

a failure of recognition of an atypical sinusoidal pattern secondary to a

concealed abruption.Figure 19.3

Figure 19.4

References

1. The Use of Electronic Fetal Monitoring. London: National Institute for Clinical

Excellence; 2001.

2. Gray JH, Cudmore DW, Luther ER, Martin TR, Gardner AJ. Sinusoidal fetal heart rate

pattern associated with alphaprodine administration. Obstet Gynecol 1978;52:678–81.

3. Veren D, Boehm FH, Killam AP. The clinical significance of sinusoidal fetal heart rate

pattern associated with alphaprodine administration. J Reprod Med 1982;27:411–4.

4. Angel JL, Knuppel RA, Lake M. Sinusoidal fetal heart rate pattern associated with

intr

avenous butorphanol administration: a case report. Am J Obstet Gynecol 1984;149:465–7.

5. Hatjis CG, Meis PJ. Sinusoidal fetal heart rate pattern associated with butorphanol

administration. Obstet Gynecol 1986;67:377–80.

6. Yanamandra N, Chandraharan E. Saltatory and sinusoidal fetal heart rate patterns and

significance of FHR ‘overshoots’. Curr Women’s Health Rev. 2013;9:175–82.

7. Graca LM, Cardoso CG, Calhaz-jorge C. An approach to interpretation and classificationof sinusoidal fetal heart rate patterns. Eur J Obstet Gynecol Reprod Biol 1988;27:203–12.