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Tags: Obstetrics

Intrauterine fetal resuscitation

Intrauterine resuscitation (IUR) involves measures to improve oxygen delivery to the placenta and subsequent transfer to the distressed fetus in an attempt to reverse hypoxia and normalise the fetal pH.

These interventions may improve the fetal condition and allow for normal delivery or improve fetal well-being before an emergency operative delivery, giving time for an epidural top-up or spinal anaesthetic to become effective, thereby avoiding the need for general anaesthesia

Fetal distress

Mechanism of fetal hypoxia:

‘Fetal distress' refers to a suspicious fetal heart trace with or without evidence of acidosis from a fetal blood sample

Persistent fetal distress can lead to a ‘progressive fetal asphyxia state’.

When fetal heart rate (FHR) patterns are abnormal or variable, EFM has a high sensitivity (the ability to detect a healthy fetus when a fetus is truly healthy), but a low specificity (the ability to detect a compromised fetus while excluding healthy pregnancies from the criteria).

Acute deterioration in FHR pattern can be produced by reversible factors (e.g. increased uterine activity or poor maternal positioning) as well as irreversible factors (e.g. placental abruption, maternal haemorrhage, cord prolapse or uterine rupture).

Ultimately fetal wellbeing is dependent on maternal, placental, and fetal factors.

Maternal factors

In addition to uterine perfusion pressure (arterial pressure − venous pressure), placental blood flow is affected by resistance to blood flow. Uterine perfusion pressure is affected in pregnancy as aortocaval compression is significant during the third trimester
During late pregnancy, uterine spiral arteries are maximally relaxed and placental oxygen delivery is close to maximum.

Active contractions during labour raise intrauterine pressure to 50 mmHg, compressing the veins at first and increasing the volume of intervillous blood until intrauterine pressure is high enough to block blood flow to the uterus

There is a subsequent fall in fetal oxygen saturation by about 7% at about 90–120 seconds following a peak contraction, indicating a decline in blood oxygenation in the intervillous space. After contractions, oxygenation recovers at a similar pace. When oxygenation is impaired there may be a significant reduction in oxygen saturations causing fetal bradycardia. Oxygenation is unlikely to recover between contractions if it has been severely compromised.

To allow sufficient oxygen diffusion through maternal–fetal membranes in the intervillous gap, the maternal haemoglobin level must be above 10 g/dL and the oxygen saturation should be sustained above 95%.

Hypovolaemia or hypotension can cause blood volume to be shunted away from the gravid uterus, reducing fetal oxygen supply. Lack of autoregulation will lead to a linear decrease in uterine blood flow with maternal blood pressure.

Aortocaval compression

Aortocaval compression (ACC) is usually asymptomatic due to sympathetic compensation such as peripheral vasoconstriction which promotes the development of collaterals for venous return
(normal compensation disrupted by Neuraxial block)

10% of parturients may be unable to compensate and suffer from the ‘supine hypotension syndrome’

During IUR the mother should be placed in the full lateral position to maximise blood pressure and uteroplacental blood flow

Placental factor

It is a passive process transferring oxygen (from placenta to fetus) along a gradient from a high maternal PO2 of 100 mmHg to a low fetal PO2 of 35 mmHg. Since fetal haematocrit is higher and fetal haemoglobin has a stronger affinity for oxygen, the increase in fetal oxygen concentration and FSpO2 during maternal oxygen treatment is steeper

Fetal factors

Umbilical venous oxygen saturation levels are 30–35 mmHg at term, while the fetal haemoglobin saturation is 75–80% due to several factors including a high fetal haematocrit (17–19 g/dL), a high fetal cardiac index (350 mL/m2/min) as well as the presence of haemoglobin F which helps to warrant adequate fetal oxygen content.

If the cord is caught by the presenting part or wrapped around the fetal head or shoulder during labour, it might be compressed intermittently. Variable decelerations on the FHR may result

In cases of complete cord occlusion, oxygenated blood cannot be delivered to the fetus via the umbilical vein, necessitating immediate operative delivery. To restore blood flow through the cord, the compression can be relieved directly (by manually elevating the presenting part) or indirectly (by filling the bladder with saline or by assuming a modified Trendelenburg or knee-chest position).

The FHR is the key component in predicting cardiac output as stroke volume is relatively constant.

Technique of intra-uterine resus

Intervention Comment
Call for help Ensure senior anaesthetic and obstetric help is present
Position Full left lateral position in an attempt to relieve aortocaval compression. If there is no improvement in the FHR, attempt other positions such as right lateral or knee-chest position
Tocolysis Stop oxytocin or remove prostaglandin intravaginal pessaries immediately

Active tocolysis is often recommended to decrease uterine contraction frequency and general uterine tone Terbutaline **250 mcg by subcutaneous injection** is the recommended drug of choice. Note that beta stimulants may result in maternal and fetal tachycardia. They may also result in poor uterine tone after caesarean delivery, which should be actively managed using uterotonics

Glyceryl trinitrate (GTN) is an alternative, which is given at a dose of 800 mcg (2 metered puffs) by sublingual spray (unlicensed use). This can be repeated every minute to a maximum of 3 doses. Monitor blood pressure closely and avoid GTN if the patient is hypotensive
Intravenous Fluids Rapid administration of 1000 mL of a balanced crystalloid solution

If the patient is fluid restricted or fluid overloaded, has cardiac disease or pre-eclampsia, more judicious 250 mL fluid boluses are recommended
Treat hypotension Treat hypotension with an intravenous vasopressor such as phenylephrine 50 mcg or ephedrine 3–6 mg IV boluses titrated to BP to maintain uteroplacental flow while awaiting intravenous fluid volume expansion
Exclude an acute event Placental abruption, cord prolapse, sepsis and haemorrhage should be excluded and/or treated accordingly
Oxygen Maternal oxygen administration is not routinely recommended for IUR because of its unproven benefit and possible risk of hyperoxia to the fetus. Maternal oxygen is therefore only advised if it is for maternal indications such as maternal hypoxia or as part as preoxygenation before general anaesthesia
also stop EA

Increasing maternal intravascular volume with fluid boluses can increase uterine blood flow and placental perfusion by augmenting cardiac output, reducing blood viscosity and having a short-term tocolytic impact

Fluid infusion improves the fetal condition even when there are no symptoms of maternal hypotension. It is recommended that rapid IV crystalloid infusions with lactated Ringer's solution be given when a fetus is in distress; 1000 mL has been shown to improve outcomes more than 500 mL, and the effects last well after infusion

In contrary to phenylephrine, ephedrine crosses the placenta, increases FHR, and directly affects the fetal metabolic status (evidenced by the reduced umbilical arterial pH). The advantages of increasing FHR are expected to exceed the unfavourable metabolic effects of ephedrine in the event of fetal bradycardia because fetal cardiac output relies on FHR.

References

Quick hits chapter

Intrauterine Fetal Resuscitation - A&ICM