Fetal Asphyxia - Clinical Tree

‘Abnormal parturition, besides ending in death or recovery, not infrequently had a third termination in other diseases… a delay of only a few moments in the substitution of pulmonary for the ceased placental respiration would lead to the apprehension that even the want of a few breathings, if not fatal to the economy, may imprint a lasting injury upon it.’

William John Little

On the influence of abnormal parturition, difficult labours, premature birth, and asphyxia neonatorum, on the mental and physical condition of the child, especially in relation to deformities. Trans Obstet Soc London. 1861–62;3:293–344.

In 2016 the National Health Service Litigation Authority (NHSLA) in the UK published the status of claims for the years 2015 and 2016. Of all medical litigation cases, 10% of claims were related to obstetrics but accounted for 42% of the claims for pay out. The largest sums within this were paid out for neurological injury related to birth asphyxia. Detailed analysis of this subgroup revealed that inability to interpret cardiotocograph (CTG) traces, failure to incorporate the clinical situation, delay in taking action and poor communication and team work were the contributory factors. The very same factors were identified as causes for intrapartum stillbirths of babies over 1500 g in the 1997 Fourth Confidential Enquiry into Stillbirths and Deaths in Infancy (CESDI). The latter inquiry found that 50% of deaths were avoidable and another 25% were potentially avoidable by a different action. Although only a small percentage of all births are affected by long-term neurological handicap or stillbirth, they represent devastating outcomes for the parents and their family.

Although vast numbers of pathological CTGs are seen in labour, only a small percentage of cases are born with acidosis and low Apgar scores at birth and even fewer develop neonatal encephalopathy and subsequent cerebral palsy. Hence there is constant debate about whether an individual case is related to birth asphyxia. Animal experimentation studying different types of hypoxia-induced brain injury has revealed that hypoxia at different stages of gestation results in injury of the part of the brain with the highest metabolic activity and growth at that stage of gestation. What is seen in animal experiments is observed in the human fetus after birth asphyxia by performing magnetic resonance imaging (MRI). At term, prolonged partial hypoxia causes injury to the motor cortical area whilst acute profound hypoxia causes injury to the thalamic, hypothalamic and basal ganglia regions. The type of brain injury seen on MRI correlates with the type of cerebral palsy, i.e. motor cortical injury results in quadriplegic cerebral palsy, whilst thalamic, hypothalamic and basal ganglia injuries give rise to the athetoid or dyskinetic type of cerebral palsy. Based on such MRI observations, a study from Sweden suggests significantly more babies may have been affected with asphyxia in labor compared with figures based on epidemiological data. However, these figures are likely to vary somewhat in different labour units. It is important for each labour unit to audit the absolute numbers affected in relation to the total deliveries each year, review these figures on a case by case basis, and collectively over a period of time identify factors/practices that can be improved to reduce the number of babies affected by birth asphyxia. This chapter examines the CTG patterns associated with injuries due to birth asphyxia and how birth asphyxia-related litigation may be reduced by recognition of some specific fetal heart rate (FHR) patterns and timely delivery.

Hypoxaemia, Hypoxia and Asphyxia

In this chapter, the terms hypoxaemia, hypoxia and asphyxia are defined as follows: hypoxaemia refers to reduced oxygen in the blood and hypoxia refers to reduced oxygen in the tissues secondary to continuing hypoxaemia. Asphyxia is hypoxia and metabolic acidosis in the tissues. The fetus reacts to hypoxaemia by extracting more oxygen from the blood and this period is associated with reduced fetal movements and absence of FHR accelerations. With hypoxia there is a catecholamine surge causing vasoconstriction in nonessential organs (skin, muscle, bone, liver, intestines and kidneys), and an increase in cardiac output by raising the heart rate. This vascular redistribution mechanism maintains the oxygen requirements to the essential organs, i.e. brain, heart and the adrenals. If the hypoxia is sustained, there is further deprivation of oxygen and the cells undertake anaerobic metabolism, converting glucose into lactic acid rather than CO ₂ and water.

This state of hypoxia and metabolic acidosis results in asphyxia and is the final step before cellular and organ failure. The time needed to build up hypoxia and acidosis sufficient to cause asphyxia will vary from fetus to fetus depending on its ‘physiological reserve’ and on the extent to which the blood supply from the placenta is disrupted. The disruption of oxygen supply may be a complete acute cessation due to placental abruption, scar rupture or cord prolapse; or it may be intermittent in the form of cord compression in labour; or due to placental insufficiency as in intrauterine growth restriction (IUGR). In IUGR there is a lack of oxygen due to reduced placental perfusion, especially with uterine contractions. In these cases the cord can become compressed due to oligohydramnios. When these two mechanisms coexist, the fetal compromise may occur earlier compared with an appropriately grown fetus with adequate amniotic fluid.

The different mechanisms of hypoxia that lead to neurological injury have been studied by Myers and are described below:

Total (or acute profound) hypoxia causes damage to the brainstem and thalamus.
Prolonged partial hypoxia with acidosis causes brain swelling and cortical necrosis.
Prolonged partial hypoxia without acidosis causes white matter damage.
Total or acute profound hypoxia preceded by prolonged partial hypoxia with mixed acidosis causes damage to the cortex, thalamus and basal ganglia.

It is possible to correlate the FHR patterns that would lead to hypoxia and acidosis and to decide how urgently the baby should be delivered with a given CTG pattern to help avoid neurological injury. This may not be possible in all cases; however, it may be in most, and these CTG patterns are discussed below.

FHR Patterns Related to Hypoxia and Acidosis

The features of the CTG (baseline rate, baseline variability, accelerations and decelerations) described in Chapter 9 may occur in various combinations in each FHR trace. Beard et al showed that a fetus with FHR accelerations is unlikely to be acidotic. Fleischer et al found that 50% of the fetuses may become acidotic in 90 minutes with late decelerations; in 120 minutes with variable decelerations; and in 190 minutes with reduced baseline variability. By studying all four features of the FHR, certain patterns have been described that would suggest already existing hypoxia and neurological injury and others in which a rise in baseline rate and decelerations were prominent features before neurological injury occurred. The evolution of acidosis is not an exact science, as the rate at which acidosis develops depends on the type of FHR pattern and the ‘physiological reserve’ of the fetus. In the presence of similar pathological CTGs, those fetuses that are growth restricted, those with infection, or with scanty, thick meconium-stained fluid develop hypoxia and acidosis at a faster rate than a fetus that is appropriately grown with a normal amount of clear amniotic fluid.

The following patterns have been described with adverse birth outcomes, such as babies born in poor condition, babies with abnormal neurological outcome/cerebral palsy and stillbirths. Understanding the evolution of the CTG and possible outcome if not delivered in a timely manner would help to reduce babies born in poor condition. Timing and type of intervention should be based on the clinical situation.

Acute hypoxia usually presents with prolonged bradycardia <80 bpm.
Subacute hypoxia presents with steep decelerations reducing the FHR to <80 bpm lasting for longer than 90–120 seconds and spending less than 30–40 seconds at the baseline rate and during that time may show saltatory baseline variability.

The above two patterns usually present with acute clinical events such as placental abruption, cord prolapse or scar rupture, or in the late first or second stage of labour. At times the cause is not known and may be related to occult cord compression or tight nuchal cord.

Gradually developing hypoxia may be manifest with the appearance of decelerations, absent accelerations, increasing baseline rate and finally marked reduction in baseline variability.
Longstanding hypoxia may show a pattern with reduced baseline variability and shallow late decelerations in a nonreactive trace.

Acute Hypoxia

Prolonged bradycardia or deceleration <80 bpm leads to acute hypoxia and if it is associated with placental abruption, cord prolapse and uterine scar rupture it warrants immediate delivery. Uterine hyperstimulation causing bradycardia can be dealt with by acute tocolysis (see Chapter 11 ). Important considerations in other cases are the CTG prior to the bradycardia and potentially influencing associations such as scanty amount of thick meconium-stained amniotic fluid, IUGR, infection and antepartum haemorrhage – in which acidosis can develop rapidly.

An FHR <80 bpm for longer than 6 minutes, i.e. prolonged bradycardia/prolonged deceleration, can lead to rapid acute hypoxia and acidosis ( Fig. 10.1 ). A prolonged deceleration <3 minutes is considered suspicious and >3 minutes as pathological. Causes of transient bradycardia include hypotension (e.g. regional anaesthesia), dorsal position of the mother, uterine hyperstimulation, artificial rupture of the membranes and vaginal examination. In these cases, remedial actions should be undertaken, such as maternal repositioning, correction of hypotension, stopping oxytocin, and acute tocolysis for hyperstimulation with prostaglandins whilst awaiting recovery of the FHR. Pressure on the head at crowning with maternal bearing down in the second stage may also be associated with bradycardia, and if it does not recover within 6 minutes, delivery should be expedited. At times the cause for bradycardia is not known and the FHR may not recover despite the usual resuscitative measures, necessitating immediate delivery. The lower the FHR and longer the bradycardia, the greater is the chance for fetal acidosis. The pH is likely to decline more rapidly in high-risk clinical situations such as thick meconium, oligohydramnios, IUGR, intrauterine infection and in cases where the CTG was suspicious or pathological before the onset of bradycardia. In such cases, if the bradycardia does not recover by 6–7 minutes, delivery should be undertaken immediately.

FIG. 10.1, A cardiotocograph trace showing prolonged deceleration.

The placenta acts as the lungs for the fetus in utero. Carbon dioxide is eliminated and oxygen is absorbed through the placenta. For optimal gas exchange there should be adequate circulation on the maternal and fetal sides of the placenta. With the normal FHR of about 140 bpm for 10 minutes, there are 1400 circulations through the placenta that help transfer carbon dioxide out of the fetal circulation and absorb adequate oxygen for the fetus. When the FHR is 80 bpm, there will be only 800 circulations in 10 minutes and the fetus loses 600 circulations. The amount of carbon dioxide excreted becomes less and accumulates within the fetus, leading to the formation of carbonic acid with a decline in pH—respiratory acidosis. With increasing duration of bradycardia the oxygen transferred to the fetus is also reduced, leading to anaerobic metabolism and accumulation of metabolites giving rise to metabolic acidosis within the cell with the drop of the pH. This has an additive effect to the already existing respiratory acidosis. Acidosis causes malfunction of the intracellular metabolic process, e.g. the Na ⁺ /K ⁺ pump that maintains the cell wall integrity. This leads to influx of fluid and cell oedema that causes cell malfunction and finally death if the injury is not reversed in time.

If the FHR returns to normal within a short period of time, the number of circulations through the placenta will normalize, allowing the respiratory acidosis to be corrected by transferring the carbon dioxide to the maternal circulation. This is a quick process, whilst reversal of metabolic acidosis takes longer. If conservative measures fail and the FHR does not return to normal within 6–9 minutes, delivery of the fetus and establishing neonatal respiration will quickly reverse the respiratory acidosis and, with time, the metabolic acidosis. It is known that pH would drop by 0.01/minute with prolonged deceleration and it would be wise to deliver the baby within 15–30 minutes when there is no recovery of the FHR. In cases of scar rupture and prolonged deceleration, the neonatal condition gets progressively worse after 18 minutes and a delivery prior to this time is likely to result in a fetus in good condition.

Subacute Hypoxia

Prolonged decelerations with the FHR reducing to levels below 80 bpm for >90 to 120 seconds and less than 60 seconds at the baseline rate leads to subacute hypoxia, i.e. the development of hypoxia and acidosis, but less rapidly compared with acute and prolonged bradycardia/deceleration. When such FHR decelerations are frequent and profound, the evolution of hypoxia and acidosis can be rapid. It is difficult to quantify the duration for which the FHR should be below the baseline rate and the duration for which it should be at the correct baseline to prevent hypoxia and acidosis. It will depend on the ‘physiological reserve’ of each fetus. One could consider that the build-up of hypoxia and acidosis is likely to be greater if the duration of the FHR at the normal baseline rate is one-third or less of the duration of deceleration. Initially this will result in slow elimination of carbon dioxide, leading to respiratory acidosis, but as time passes, oxygen transfer will be critically reduced and metabolic acidosis will ensue with its consequences as explained above.

The series of traces in Figs. 10.2–10.6 show the subacute hypoxia pattern with atypical variable decelerations and the final outcome in a fetus with severe metabolic acidosis. The end of the trace was bradycardia for 10 minutes and the baby was delivered at that stage by forceps ( Fig. 10.6 ). Such CTG changes are not that uncommon in the second stage of labour and may be due to an occult cord occlusion or tight nuchal cord. Care givers give time to achieve vaginal delivery as they see the head advancing and get a false reassurance with the FHR recovering momentarily to the baseline without the understanding that with such traces pH can drop by 0.01 every 2 to 3 minutes and hence the need for delivery by 30–45 minutes.

FIG. 10.2, Decelerations start as shallow and then get steeper and wider lasting for 2 minutes and recovering to the baseline rate of 140 bpm for only 30 seconds.

FIG. 10.3, Prolonged decelerations with saltatory baseline variability during short period of recovery.

FIG. 10.4, The baseline rate drops from 150 bpm to <80 bpm with prolonged decelerations.

FIG. 10.5, Prolonged bradycardia following decelerations.

FIG. 10.6, Time of delivery is annotated and the strip shows a low pH and high base excess.

Gradually Developing Hypoxia

In gradually developing hypoxia, decelerations appear, followed by absence of accelerations, a rise in the baseline rate (with catecholamine surge) and finally a reduction in baseline variability. The deterioration of the fetal condition is also exhibited by progressive increase in the depth and duration of decelerations and decrease in interdeceleration intervals. As always, one should consider the clinical picture of parity, cervical dilatation, rate of progress of labour and high-risk factors, and institute conservative measures (e.g. stopping oxytocin, hydration, change of maternal position), or perform fetal blood sampling, or consider delivery.

Figs. 10.7–10.9 exhibit the pattern seen with gradually developing hypoxia: first the decelerations appear and accelerations disappear, then the depth and duration of the decelerations progressively become greater with shortening of the interdeceleration intervals, along with a rise in the baseline rate due to the catecholamine surge due to hypoxic stress, and finally a reduction of the baseline variability when hypoxia affects the autonomic nervous system. The decelerations seen are variable, suggestive of cord compression as the mechanism that causes the hypoxia.

FIG. 10.7, The trace shows a baseline rate of 140 bpm with simple variable decelerations, normal baseline variability and accelerations. It has been misinterpreted as early decelerations.

FIG. 10.8, Rise in baseline rate to 150 bpm, reduced baseline variability and no accelerations.

FIG. 10.9, Rise in baseline rate to 170 bpm with no baseline variability.

Longstanding Hypoxia

In cases with longstanding hypoxia there are no accelerations, the baseline variability is markedly reduced and there are shallow late decelerations, often <15 bpm. These characteristic features of hypoxia are seen even though the fetus may have a normal baseline rate. The absence of accelerations and ‘cycling’ suggests that the fetus may have already sustained asphyxial injury, or is hypoxic, or is affected by some other insult such as infection. Fig. 10.10 is an FHR trace with features suggestive of long-standing hypoxia. If the CTG trace observed is due to hypoxia, progressive contractions in labour would further aggravate the hypoxia leading to sudden bradycardia and collapse of the fetus without much change in the CTG. Hence there is an imperative to deliver these fetuses early if such a trace is identified. Many of these cases would have additional clinical features to suggest possible compromise, such as absent fetal movements, maternal pyrexia suggestive of infection, thick scanty meconium or bleeding.

FIG. 10.10, A cardiotocograph with the baseline rate in the normal range, with no accelerations, minimal baseline variability and shallow decelerations suggestive of pre-existing hypoxia.

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