‘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.
Since only a small percentage of cases of cerebral palsy are thought to be due to birth asphyxia whilst there are vast numbers of pathological CTGs which do not give rise to poor outcome, there is constant debate about whether an individual case is related to birth asphyxia. The advent of magnetic resonance imaging (MRI) and animal experimentation studying different types of hypoxia and induced brain injury have 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. 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 observations, a study from Sweden suggests that up to 28% rather than the conventional 10% of cases of cerebral palsy may be related to intrapartum asphyxia. In light of this information, this chapter examines the CTG patterns associated with injuries due to birth asphyxia and how birth asphyxia-related litigation may be reduced.
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 fetal heart rate accelerations. With hypoxia there is a catecholamine surge causing vasoconstriction in non-essential 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 also on the extent to which the blood supply to and from the placenta is disrupted. The disruption of oxygen supply may be a complete acute cessation due to placental abruption, or it may be intermittent in the form of cord compression in labour, or due to placental insufficiency. Lack of oxygen due to reduced placental perfusion associated with intrauterine growth restriction leads to hypoxaemic hypoxia, whilst that due to cord compression leads to ischaemic hypoxia, and these two mechanisms can co-exist. The different mechanisms of hypoxia that lead to acidosis and neurological injury have been studied by Myers and are described below;
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Total asphyxia causes damage to the brainstem and thalamus
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Prolonged hypoxia with acidosis causes brain swelling and cortical necrosis
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Prolonged hypoxia without acidosis causes white matter damage
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Total asphyxia preceded by prolonged hypoxia with mixed acidosis causes damage to the cortex, thalamus and basal ganglia.
Based on the above, one should be able to identify the fetal heart rate (FHR) patterns associated with hypoxia and acidosis that may lead to neurological injury and these 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 6 may occur in various combinations in a given 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 get 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 are described with adverse birth such as stillbirth or abnormal neurological outcome/cerebral palsy and may prove clinically useful in deciding the timing of intervention when taken in consideration with the clinical picture.
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Acute hypoxia usually presents with prolonged bradycardia < 80 bpm.
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Subacute hypoxia presents with steep decelerations reducing the FHR to < 80 bpm and which last longer during the deceleration than the time the FHR is at the normal baseline rate.
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.
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Gradually developing hypoxia may be manifest with the appearance of decelerations, absent accelerations, increasing tachycardia and finally marked reduction in baseline variability.
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Longstanding hypoxia may show a pattern with reduced baseline variability and shallow late decelerations in a non-reactive 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 warrants immediate delivery. Uterine hyperstimulation causing bradycardia can be dealt with by acute tocolysis (see Chapter 28 ). Important considerations in other cases are the CTG prior to the bradycardia and potentially influencing associations such as thick meconium-stained amniotic fluid, intrauterine growth restriction (IUGR), infection and antepartum haemorrhage – in which acidosis can develop rapidly.
A FHR < 80 bpm for longer than 6 minutes, i.e. prolonged bradycardia/prolonged deceleration, can lead to rapid acute hypoxia and acidosis. A prolonged deceleration < 3 minutes is considered suspicious and > 3 minutes as abnormal. 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 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 to 7 minutes, delivery should be undertaken immediately.
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 will miss 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.
Subacute Hypoxia
Prolonged decelerations with the FHR below the baseline for a longer time than at the normal baseline rate lead 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 Figures 7-1–7-5 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 7-5 ).
Gradually Developing Hypoxia
In gradually developing hypoxia decelerations appear, followed by absence of accelerations, a rise in the baseline rate (with catecholamine surge) and a reduction in baseline variability. As always, one should consider the clinical picture of parity, cervical dilatation, rate of progress and high-risk factors and institute conservative measures (e.g. stopping oxytocin, hydration, change of maternal position), or perform fetal blood sampling (FBS), or consider delivery.
Figures 7-6–7-8 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, 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.
