14 Intrapartum Bleeding. Handbook CTG

 14

Intrapartum Bleeding

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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

Intrapartum vaginal bleeding may be benign – damage to maternal veins during

cervical dilatation, or rupture of membranes – or may indicate serious

underlying pathology.

Serious causes include rupture of fetal blood vessels traversing the membranes

below the presenting part (vasa previa), placental abruption, bleeding from a

low-lying placenta (placenta previa), uterine rupture or, rarely, bleeding from

local lesions such as polyps, tumours, or genital tract trauma.

Maternal causes of intrapartum bleeding often do not cause any change on the

CTG trace, unless it is very severe and is accompanied by maternal hypotension

(e.g. placenta previa). If this is a case, an acute prolonged deceleration will be

noted on the CTG trace.Figure 14.1

Key Pathophysiology behind Patterns Seen on

the CTG Trace

Bleeding from vasa previa or a sudden fetomaternal haemorrhage may result in

an ‘atypical sinusoidal pattern’ also called ‘Poole shark teeth pattern’ (Figure

14.1).

Premature separation of placenta may result in recurrent ‘late decelerations’

(Figure 14.2) in early stages but may result in an acute prolonged deceleration

culminating in a terminal bradycardia (see Chapter 2). A total loss of baseline

fetal heart rate (FHR) variability may also be noted (Figure 14.2).

Uterine rupture may present with recurrent variable or late decelerations or as

an acute prolonged deceleration (see Chapter 15).

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 (sympathetic and parasympathetic).

Recurrent ‘late decelerations’ (Figure 14.2) in early stages of abruption is

secondary to utero-placental insufficiency and metabolic acidosis resulting in the

stimulation of chemoreceptors. Acute prolonged deceleration culminating in a

terminal bradycardia is secondary to myocardial decompensation resulting fromFigure 14.2. Note the total loss of baseline fetal heart rate variability within the first 3

minutes of a prolonged deceleration

Figure 14.3 Note the presence of decelerations prior to the onset of the prolonged

deceleration.

hypoxia and acidosis due to a total disruption of the fetal oxygen supply (see

Chapter 2). A sudden reduction in fetal blood volume and resultant lack of

oxygen supply to the brain results in a total loss of baseline FHR variability

(Figure 14.2).

Recurrent variable decelerations may occur secondary to prolapsed umbilical

cord through the ruptured uterine scar, and late decelerations occur secondary to

progressive placental separation leading to progressive fetal hypoxia and

acidosis and resultant ‘chemoreceptor stimulation’ (Figure 14.3). An acute

prolonged deceleration may occur secondary to expulsion of the fetus into the

peritoneal cavity that results in a total separation of the placenta (see Chapter

15).Recommended Management

Key Tips to Optimize Outcome

In cases of fetomaternal haemorrhage or placental abruption presenting with

CTG changes suggestive of ongoing fetal hypoxia or hypotension, urgent delivery

should be accomplished by the quickest and safest approach. If the cervix is fully

dilated with presenting part at or below the ischial spines, an immediate

operative vaginal delivery is recommended. If this is not possible, then an

immediate (‘grade 1’) caesarean section should be performed.

The neonatal team should be informed as the neonate may be hypoxic and

hypotensive at birth requiring intensive neonatal resuscitation as well as

intravenous fluids and blood transfusion to correct ongoing hypovolaemia.

In cases of severe abruption with maternal hypotension and coagulopathy,

maternal resuscitation should take priority while making preparations for urgent

delivery. Maternal oxygen administration used in cases of maternal collapse may

also have a beneficial effect on the fetus.

Recognize atypical sinusoidal pattern and/or acute prolonged deceleration when

there is ongoing fetomaternal bleeding secondary to a vasa previa (Figure 14.3)

or a concealed abruption.

Remember that baseline FHR variability will be rapidly reduced within first 3

minutes of a prolonged deceleration due to ongoing fetal hypotension and

resultant sudden reduction in fetal cerebral blood flow.

Seek immediate senior obstetric and midwifery input and ensure effective

multidisciplinary communication and team working to accomplish immediate

delivery.Figure 14.4 Note the ruptured vasa praevia in a case with an atypical sinusoidal pattern

with a ‘jagged edge’ resembling ‘Poole Shark Teeth’.

Pitfalls

Consequences of Mismanagement

‘3, 6, 9, 12, 15’ rule for a prolonged deceleration is not applicable in this case.

Persists with traumatic operative vaginal delivery despite ongoing features on

the CTG suggestive of acute hypoxia.

Attempting additional tests of fetal well-being such as fetal ECG (STAN), fetal

scalp pH or lactate when there is clear evidence of hypoxia to the central organs

on the CTG trace.

Intrapartum fetal death

Early neonatal deathExercise

1. A 36-year-old primigravida presented with a history of painless vaginal bleeding

with reduced fetal movements at 40 weeks of gestation. On examination, the abdomen

was soft and nontender and FHR was 160 bpm. On speculum examination, fresh vaginal

bleeding was noted.

a. What is your differential diagnosis?

b. Is CTG monitoring indicated?

c. What abnormalities on the CTG would be expected based on your differential

diagnosis?

d. CTG was commenced and the following features were noted (Figure 14.5). What

is your diagnosis?

Figure 14.5

e. What is your management?

Further Reading

Severe hypoxic ischaemic encephalopathy (HIE)

Long-term fetal neurological sequelae secondary to delayed treatment of

hypotension1. Chandraharan E, Arulkumaran S. Prevention of birth asphyxia: responding appropriately to

cardiotocograph (CTG) traces. Best Pract Res Clin Obstet Gynaecol. 2007; 21(4): 609–24.

2. Gibb D, Arulkumaran S (Eds). Fetal monitoring in practice. Elsevier. 2008.

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

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

4. Jensen A, Hanson MA. Circulatory responses to acute asphyxia in intact and

chemodenervated fetal sheep near term. Reprod Fertil Dev. 1995; 7: 1351–9.

5. Graca LM, Cardoso CG, Calhaz-Jorge C. An approach to interpretation and classification

of sinusoidal fetal heart rate patterns. Eur J Obstet Gynecol Reprod Biol. 1988; 27: 203–12.