The labour ward

Published on 06/02/2015 by admin

Filed under Anesthesiology

Last modified 22/04/2025

Print this page

rate 1 star rate 2 star rate 3 star rate 4 star rate 5 star
Your rating: none, Average: 0 (0 votes)

This article have been viewed 2796 times

TOPIC 8 The labour ward

Topic Contents

Fetal well-being: Antenatal investigations 153

Test: Cardiotocograph (CTG) 153
Test: Fetal scalp blood sampling 158
Test: Fetal lactate 159
Test: Fetal electrocardiogram (ECG) analysis 160
Fetal well-being: Postnatal investigations 160

Test: Cord blood sampling 160
Test: APGAR scoring 161
Maternal well-being 162

Test: Electrocardiogram 162
Test: Antenatal tests in the UK 162
Test: Blood tests during pregnancy 163

Fetal well-being: Antenatal investigations

The main aim of fetal monitoring is to identify the fetus at risk in order to allow sufficient time to intervene thereby preventing permanent injury or death from occurring. Currently the optimal method for assessing fetal well-being during labour and delivery has not been determined.

Test: Cardiotocograph (CTG)

Indications

For factors in high-risk pregnancies see Table 8.1.

Table 8.1 Factors involved in high-risk pregnancies

Maternal factors Fetal factors
Pre-eclampsia/hypertension
Diabetes
Other significant maternal medical conditions
Maternal pyrexia
Previous caesarean section
Post-term pregnancy (>42 weeks)
Prolonged membrane rupture (>24 hours)
Induced/augmented labour
Antepartum haemorrhage
Epidural analgesia

Fetal growth restriction
Prematurity
Oligohydramnios
Abnormal Doppler artery velocimetry
Multiple pregnancies
Meconium-stained liquor
Breech presentation

How it is done

A cardiotocograph simultaneously records both the fetal heart rate (FHR) and uterine contractions.

External monitoring

The FHR is derived from a Doppler ultrasound transducer that detects fetal heart movements and a pressure transducer that records the frequency and duration (but not strength) of uterine contractions. Both transducers are applied externally to the maternal abdominal wall.

Internal monitoring

The FHR is monitored via an electrode that is inserted transcervically to penetrate the fetal scalp and the frequency, duration and strength of uterine contractions are recorded via a fine intrauterine pressure catheter. Internal monitoring requires cervical dilatation and rupture of the membranes. Internal FHR monitoring provides a more accurate measurement of beat to beat and baseline variability than external monitoring.

A hybrid of internal measurement of fetal heart rate with external monitoring of contractions may be performed.

Data presented as

The CTG trace (Fig. 8.1) shows two lines:

• The upper line is a record of the fetal heart rate in beats per minute
• The lower line is a recording of uterine contractions
image

Fig. 8.1 Normal CTG.

Interpretation

Physiological principles

• An electronic method of determining fetal heart rate, presence and duration of uterine contractions in addition to the reaction of the fetus to contractions.
• Assessments are made of fetal heart rate, variability of heart rate, presence or absence of accelerations and decelerations.

The fetus requires an adequate supply of oxygen via the placenta and umbilical vein. Interruption of this blood supply may compromise a fetus without adequate reserve. Uterine contractions or cord compression may interrupt this blood supply. Fetal hypoxaemia may present itself as changes to the CTG tracing as discussed below.

Definitions

Baseline FHR

The average FHR, excluding accelerations and decelerations, determined over a 5–10-minute period. Normal valves are 110–160 beats per minute (bpm).

Bradycardia

A baseline heart rate of less than 110 bpm (Fig. 8.2). A profound and sustained decrease in FHR is indicative of fetal distress.

image

Fig. 8.2 CTG of fetal bradycardia.

Tachycardia

A suspicious tachycardia is defined as being between 160 and 180 bpm, whereas a pathological recording is above 180 bpm. Fetal tachycardias may be associated with fetal distress, maternal pyrexia and/or intrauterine infection.

Baseline variability

This is the minor fluctuation in baseline fetal heart rate. It is measured by estimating the difference in beats per minute between the highest peak and lowest trough of fluctuation in a 1-minute segment of the trace. The normal baseline variability is >5 bpm between contractions. Decreased or absent variability (Fig. 8.3) reflects decreased fetal central nervous system activity (associated with fetal sleep cycles or maternal drug administration, e.g. opioid, magnesium, benzodiazepines). However sustained reduction in variability may indicate fetal hypoxaemia/acidosis.

image

Fig. 8.3 CTG of loss of variability.

Accelerations

This is defined as a transient increase in heart rate >15 bpm for at least 15 seconds. Accelerations are normal indicating fetal responsiveness. Two accelerations in 20 minutes is considered a reactive trace. The absence of accelerations with an otherwise normal CTG is of uncertain significance.

Decelerations

These may either be normal or pathological:

• Early decelerations (Fig. 8.4A) occur at the same time as uterine contractions and are thought to result from fetal head compression, transient elevation of intracranial pressure and reflex increased vagal tone. They are considered benign.
• Late decelerations (Fig. 8.4B) start during the mid–end period of the contraction and end after the completion of the contraction. Their presence suggests fetal hypoxaemia/acidosis.
• Variable decelerations (Fig. 8.4C) have a variable temporal relationship to uterine contractions or occur in isolation. They are thought to result from umbilical cord compression.
image

Fig. 8.4 CTGs of (A) early decelerations, (B) late decelerations and (C) variable decelerations.

Normal values, abnormalities and management principles

See Table 8.2 and Table 8.3.

Table 8.2 Categorization of fetal heart traces

Category Definition
Normal A CTG where all four features fall into the reassuring category
Suspicious A CTG whose features fall into one of the nonreassuring categories and the remainder of the features are reassuring
Pathological A CTG whose features fall into two or more nonreassuring categories or one or more abnormal categories

From Royal College of Obstetricians and Gynaecologists (2001) The use of electronic fetal monitoring: the use and interpretation of cardiotocography in intrapartum fetal surveillance. http://www.rcog.org.uk

Table 8.3 Categorization of fetal heart rate (FHR) features (Table 2.3 RCOG guidelines)

image

Management principles

RCOG guidelines recommend:

• Those falling into the suspicious category should follow the conservative approach
• Conservative measures include:

– Maternal supplemental oxygen
– Maternal repositioning (thereby reducing aorto-caval compression or dislodgement of occult cord prolapse)
– Administration of intravenous fluid bolus (non-glucose crystalloid 500 mL) unless concern about possible intravascular fluid overload (e.g. pre-eclampsia)
– Stopping/reducing oxytocin augmentation as blood flow to the placenta is reduced during contractions
– Consideration of tocolysis (e.g. terbutaline 0.25 mg subcutaneously).

• Those patients in the pathological category should undergo further assessment with fetal blood sampling with a view to urgent delivery if necessary.
• However if fetal compromise is present, this should not delay immediate delivery, ideally within the accepted standard of 30 minutes.

Note that all CTG tracings should be kept as part of the birth record for a minimum of 25 years for medicolegal reasons.

Limitations and complications

• FHR monitoring is accurate at confirming a healthy non-acidotic fetus, however it is poor at predicting a hypoxaemic acidotic fetus. This is due to the low prevalence of asphyxia in labour and the fact that the positive predictive valve of any test is directly proportional to the prevalence of the disease it is predicting.
• Although continuous intrapartum FHR monitoring was introduced in order to reduce perinatal mortality and cerebral palsy, it has failed to achieve this aim. The likely explanation is that only 10% of cases of cerebral palsy are thought to have intrapartum causes. Its use, however, does appear to have reduced the incidence of neonatal seizures.
• There is considerable intra- and inter-observer variation in interpretation of the CTG even amongst experts, increasing likelihood of both false-positive and false-negative results.
• Maternal drugs affect FHR monitoring (e.g. beta-blockade and spinal opioids associated with fetal bradycardia).
• The mother is confined to bed (with application of monitor belts or fetal scalp electrode) unless telemetry available.
• The use of intrapartum CTG monitoring has been associated with an increase in interventional/operative delivery, without necessarily being justified.
• Early rupture of membranes may be required for internal monitoring via a fetal scalp electrode and this may cause fetal distress (the procedure can cause increased direct pressure of the fetal head on the cervix causing intense and prolonged contractions).
• Fetal scalp electrode application carries an infective risk.

Further investigations

• Fetal blood sampling.
• Fetal scalp lactate measurement.
• Fetal electrocardiogram analysis.

Test: Fetal scalp blood sampling

Indications

• Assessment of fetal acid-base balance and adequacy of oxygenation.
• Usually other markers of fetal hypoxia are present such as CTG abnormality.
• The evidence supports that with pathological fetal heart rate the use of fetal scalp blood sampling as an additional surveillance is associated with less vaginal operative deliveries, and improved short-term neonatal outcome.

How it is done

• Requires ruptured membranes, cervical dilatation >3 cm.
• Left lateral or occasionally lithotomy position.
• Small cut made in fetal scalp skin and 30–40 μL of blood collected.

Interpretation

Physiological principles

• Impaired fetal oxygen supply causes anaerobic metabolism of glucose.
• This in turn causes a metabolic acidaemia via pyruvate and lactate.

Abnormalities and management principles

• Normal scalp blood pH 7.25–7.35.
• Scalp pH >7.25 and fetal heart trace remains non-reassuring:

– Continue to observe labour
– Repeat scalp sampling every 2–3 hours.

• Scalp pH 7.21–7.24 and fetal heart trace remains non-reassuring:

– Repeat scalp sample in 15–30 minutes or consider rapid delivery if rapid decrease in pH since last sample.

• Scalp pH <7.20:

– Immediate delivery indicated.

• Assessment of fetal pH should be in context of clinical scenario.

Limitations and complications

• Breech presentations (debatable relationship between buttock and scalp pH).
• Avoid in parturient with HIV, hepatitis B, herpes simplex.
• Avoid in fetal bleeding disorders and prematurity (<34 weeks’ gestation).
• Often contaminated causing rejection of sample (amniotic fluid, etc).
• Uncomfortable for patient.

Test: Fetal lactate

Indications

• Assessment of fetal well-being.
• Adjunct to CTG monitoring.

How it is done

• See fetal blood sampling above.
• Less blood needed – 5 μL versus 30–40 μL.
• Lower failure rate than fetal blood sampling.
• Hand-held devices available.

Interpretation

Physiological principles

• Lactate is produced as glucose is metabolized anaerobically in absence of oxygen.
• Good correlation between fetal pH and lactate levels.
• Lactate may be better at predicting poor outcomes than pH.

Abnormalities and management principles

• High lactate levels are more predictive of subsequent neurological disability than a low pH.
• Levels >4.2 mmol/L have been suggested as a trigger for delivery.

Management principles

• Early delivery of the fetus to avoid hypoxic injury when lactate levels exceed 4.2 mmol/L.

Limitations and complications

• Further work needed to ascertain validity of trigger values.
• May be nonhypoxic reasons for high lactate.

Test: Fetal electrocardiogram (ECG) analysis

Assessment of fetal well-being using electrodes attached to the fetal scalp once membranes ruptured. ECG analysis by computer specifically looking at ST changes, which may reflect hypoxia. The use of ST waveform analysis has been associated with neonates with severe metabolic acidosis at birth, fetal scalp blood sampling and operative deliveries.

Fetal well-being: Postnatal investigations

Test: Cord blood sampling

Indications

• Postpartum – assessment of hypoxia, acid-base balance or for research purposes.
• All caesarean sections, instrumental deliveries, meconium staining, deliveries where fetal scalp blood testing has been performed or if the neonatal condition is poor.
• Useful medicolegal tool.
• In pregnancy – investigation and diagnosis of fetal abnormality (as with fetal blood sampling and amniocentesis in utero).

How it is done

• A 10–20-cm segment of cord should be double clamped immediately after delivery to reduce erroneous alterations of pH and gas values resulting from continuing metabolism and gaseous diffusion.
• Postpartum samples must be taken from both umbilical artery and vein and promptly tested for pH, PO2, PCO2 and base excess.

Interpretation

Physiological principles

See arterial blood gas in Chapter 2, and Table 8.4.

Table 8.4 Normal ranges in fetal cord sampling

  Venous Arterial
pH 7.20–7.41 7.15–7.38
PO2 (kPa) 3.7–4.2 2.1–2.6
PCO2 (kPa) 3.5–7.9 4.9–10.7
Base excess 0–5 0–10

Management principles

• Umbilical arterial (rather than venous) blood pH and gas values provide the best information on fetal acidosis.
• In association with APGAR scoring (see later) may be indicative of further hypoxia-related problems and may guide need for postnatal care.
• Can be used to distinguish hypoxia-induced low APGAR scores from non-hypoxia causes.
• Metabolic acidaemia is one of the essential criteria for establishing an intrapartum cause for cerebral palsy.
• Severe metabolic acidosis (pH <7.0–7.04) has been shown to correlate with neurological dysfunction and death. However the majority of neonates with pH <7.0 will be functionally normal.
• Cord PO2 is not particularly useful as many newborns are initially hypoxaemic until normal extrauterine respiration is established.
• Respiratory acidosis alone is not predictive of long-term injury.
• Normal postpartum cord gases virtually exclude intrapartum cause for hypoxia-related problems.
• A difference of PCO2 of >3.3 kPa indicates an acute rather than a chronic (prelabour) acidosis.
• Note that records need to be kept for 25 years for medicolegal purposes.

Limitations and complications

• An end-point that does not aid avoidance of hypoxia but only helps diagnosis.

Test: APGAR scoring

Indications

• All newborn babies.

How it is done

• Performed at 1 minute and 5 minutes after birth and assessing the newborn’s status through muscle tone, heart rate, reflex response, colour and breathing. Scored 0–2 for each variable (Table 8.5).

Table 8.5 APGAR data presented as

image

Interpretation

Normal range

A score of 7 or above at 1 minute suggests good health.

Abnormalities and management principles

• Scores of 4–6 mean conservative measures such as suctioning or oxygen might be needed.
• 3 or below at 1 minute suggest problems. Call a paediatrician – interventions may be required such as tracheal intubation and/or resuscitation.
• Look for an improvement in scores to above 7 at 5 minutes.

Management principles

• Simple and repeatable bedside test.
• Nonspecific test for fetal depression (e.g. due to maternal drug effects, fetal anomalies, prematurity).
• Commonly low in premature infants, emergency caesarean sections.
• A low 1-minute score is not indicative of future problems.
• An APGAR of 0–3 at 5 minutes correlates with neonatal mortality but is not predictive of future neurological status.

Limitations and complications

• Poor predictive value for long-term outcome.
• Not useful in preterm infants.
• 75% of children with subsequent cerebral palsy had normal APGAR scores at 5 minutes.

Further investigations

• Cord blood sampling ascertains a hypoxic cause for low APGAR score.

Maternal well-being

Test: Electrocardiogram

Changes in the electrocardiogram (ECG) in pregnancy are due to alterations in ventricular mass and the position of the heart. The enlarging uterus causes upward movement of the diaphragm causing the heart to shift to the left and anteriorly. These changes result in left axis deviation and nonspecific ST segment changes. Flow murmurs are also common.

Test: Antenatal tests in the UK

• Blood group and antibody screen. It is recommended that routine antenatal anti-D prophylaxis be offered to all nonsensitized pregnant women who are RhD negative. Women should be screened for atypical red cell alloantibodies in early pregnancy and again at 28 weeks regardless of their RhD status. Haemoglobin levels outside the normal UK range for pregnancy (11 g/dL at first contact and 10.5 g/dL at 28 weeks) should be investigated and iron supplementation considered if indicated.
• Routine blood test include full blood count, urea and electrolytes, liver function tests and random glucose.
• Serological tests include rubella antibody status, syphilis, HIV and hepatitis B serology.
• Midstream urine.
• Screening for haemoglobinopathies.
• Obstetric ultrasound scan. Pregnant women should be offered an ultrasound scan to screen for structural anomalies and placental localization, ideally between 18 and 20 weeks’ gestation.

Test: Blood tests during pregnancy

Renal function tests

Interpretation

• During pregnancy the serum sodium is about 3–5 mmol/L lower than normal because of an increase in intravascular volume.
• Cardiac output and renal blood flows are also increased.
• Glomerular filtration rate (GFR) is increased with resultant decrease in concentrations of serum urea, creatinine and uric acid.

Table 8.6 shows renal function values in pregnant and non-pregnant women.

Table 8.6 Renal function values in pregnant and nonpregnant women

image

Liver function tests

Interpretation

Physiological principles

• Serum albumin, transaminases (aspartate aminotransferase (AST) and alanine aminotransferase (ALT)) and total bilirubin are low compared with the non-pregnant state due to the expansion of extracellular fluid (Table 8.7).
• Serum alkaline phosphatase (ALP) is elevated as it is secreted by the placenta.

Table 8.7 Comparison of liver enzymes between pregnant and nonpregnant

image

Platelet count

Platelet count may be reduced by:

• Pregnancy-induced causes (e.g. pre-eclampsia, gestational thrombocytopaenia, haemolysis elevated liver enzymes low platelet (HELLP) syndrome)
• Non-pregnancy-related causes (e.g. infection, immune thrombocytopaenic purpura, leukaemia, etc.).

In a normal pregnancy platelet count may be reduced, whilst in pre-eclampsia there may be a reduction in platelet function as well as number. There is limited data to suggest a safe lower limit for regional blockade. In our institution, an isolated platelet count of >80 × 109/L is acceptable for siting a regional block. An isolated platelet count between 50 and 80 × 109/L should be discussed with a haematologist and an obstetric anaesthetist. Consider the use of the TEG (thromboelastography) or PFA-100 (platelet function analyzer). A platelet count of <50 × 109/L is an absolute contraindication to a regional block.

Share this:

Related posts:

The airway Peripheral nervous system Haematology and coagulation Central nervous system Cardiovascular system Respiratory system