(1)
Medical School, University of Porto, Porto, Portugal
2.1 Definition, Incidence and Main Risk Factors
Fetal hypoxia refers to the condition in which there is decreased oxygen concentration in fetal tissues, and this is insufficient to maintain normal cell energy production by way of aerobic metabolism. Oxygen is supplied to fetal tissues via a long pathway that involves the maternal respiratory system, maternal circulation, gas exchange at the placenta and finally the umbilical and fetal circulations (Fig. 2.1). Problems occurring at any of these levels may result in decreased oxygen concentration in the fetal circulation (hypoxaemia) and ultimately in fetal tissues (hypoxia).
Fig. 2.1
A representation of the pathway of oxygen supply to the fetus
Acute fetal hypoxia refers to the condition in which there is a rapid reduction in oxygen levels, i.e. occurring over the course of a few minutes. Its main causes are considered in Table 2.1.
Table 2.1
Main causes of acute fetal hypoxia/acidosis
Reversible causes |
Uterine hypercontractility |
Sudden maternal hypotension |
Maternal supine position with aorto-caval compression |
Irreversible causes |
Major placental abruption |
Uterine rupture |
Umbilical cord prolapse |
Maternal cardiorespiratory disorders |
Severe asthma, haemorrhagic shock, cardiorespiratory arrest, pulmonary thromboembolism, amniotic fluid embolism, generalised seizures, etc. |
Usually occult causes |
Occult cord compression (true cord knot, low-lying cord, nuchal cord with stretching) |
Major fetal haemorrhage (fetal-maternal haemorrhage, ruptured vasa praevia) |
Specific mechanical complications of labour |
Shoulder dystocia |
Retention of the after-coming head |
In the absence of oxygen, fetal cells may continue to produce the energy required for maintenance of basic homeostatic functions during a few more minutes, by resorting to anaerobic metabolism. However, the latter yields much less energy than aerobic metabolism and results in the production of lactic acid. The intra- and extracellular accumulation of hydrogen ions, due to increased lactic acid production, results in the development of metabolic acidosis (decreased pH caused by acids of intracellular origin) and, because these ions are taken away by the fetal circulation, metabolic acidaemia. The whole process of decreased oxygen concentration in tissues is therefore known as hypoxia/acidosis.
Some constituents of fetal blood are capable of neutralising (buffering) hydrogen ions. These are called bases, and they include bicarbonate, haemoglobin and plasma proteins. However, their availability is limited, and their depletion (base deficit) is directly related to the severity of metabolic acidosis. As there is no direct method of quantifying oxygen concentration within fetal tissues, the only objective way of diagnosing intrapartum fetal hypoxia/acidosis is to measure pH and base deficit in the umbilical cord blood at delivery or in the newborn circulation during the first minutes of life. Metabolic acidosis is defined as a pH below 7.00 and a base deficit in excess of 12 mmol/l (or alternatively a lactate value in excess of 10 mmol/l) in either of these circulations. The umbilical cord does not need to be clamped for sampling, but it is important to obtain blood from both artery and vein as soon as possible after birth, to guarantee the quality of results. Sampling of the wrong vessel may occur when the needle crosses the artery to pierce the vein, and this may also result in mixed sampling. After blood is drawn into two heparinised syringes, existing air bubbles are removed and the syringes capped and rolled between the fingers to mix blood with heparin; blood gas analysis should be performed within the next 30 min. When the difference in pH between the two samples is less than 0.02 and the difference in pCO2 is less than 5 mmHg (0.7 Kilopascal), samples are likely to be mixed or to have been obtained from the same vessel. When hypoxia/acidosis is of acute onset, there is usually also a large difference in pH between artery and vein.
Increasing concentrations of hydrogen ions that are no longer buffered because of base depletion affect energy production and cell homeostasis, leading to disrupted cell function and ultimately to a cascade of biochemical events that results in cell death. When hypoxia is sufficiently intense and prolonged to disrupt neurological, respiratory and cardiovascular control, this is reflected in reduced Apgar scores at birth. Apgar scores however are much less specific indicators of fetal hypoxia than umbilical blood gas values, as they can be affected by other factors such as prematurity, central nervous system depressors administered to the mother, birth trauma without hypoxia (i.e., subdural haematoma), infection, meconium aspiration, congenital anomalies, pre-existing lesions and early neonatal interventions such as vigorous endotracheal aspiration.
The overall incidence of fetal hypoxia/acidosis, as defined by the incidence of newborn metabolic acidosis, varies substantially between different European hospitals, depending on the risk characteristics of the population and on labour management strategies. Reported rates vary between 0.06 and 2.8 %.
The major risk factors for acute fetal hypoxia/acidosis are the ones responsible for its underlying causes: i.e. labour induction and augmentation with prostaglandins or oxytocin are major risk factors for uterine hypercontractility, regional analgesia is a major risk factor for sudden maternal hypotension, and early amniotomy is a risk factor for uterine hypercontractility and umbilical cord prolapse. A detailed description of the risk factors for all causes of acute fetal hypoxia/acidosis is beyond the aim of this book.
2.2 Consequences
Most newborns with metabolic acidosis and low Apgars recover quickly and do not develop short- or long-term functional impairments. However, when fetal hypoxia/acidosis is sufficiently intense and prolonged, changes in neurological function may become apparent in the first 48 h of life, manifested by hypotonia, seizures and/or coma, a situation that is termed hypoxic–ischaemic encephalopathy. In its mild forms (grade 1), a short period of hypotonia is documented, but very rarely it evolves into permanent handicap. When the newborn develops seizures (grade 2), the risk of mortality or long-term neurological sequelae is about 20–30 %. When a comatose state occurs (grade 3), perinatal death or long-term handicap is frequent.
Not all cases of neurological dysfunction occurring in the first 48 h of life (neonatal encephalopathy) are caused by fetal hypoxia/acidosis, so to establish the diagnosis of hypoxic-ischaemic encephalopathy, it is necessary to document metabolic acidosis in the umbilical cord or in the newborn circulation in the first minutes of life.
Cerebral palsy of the dyskinetic or spastic quadriplegic types is the long-term neurological sequela most strongly associated with fetal hypoxia/acidosis, although only 10–20 % of cases are caused by this entity. Perinatal infection, congenital diseases, metabolic diseases, coagulation disorders and the complications associated with birth trauma and prematurity constitute the majority of causal factors.
The speed of installation and intensity of acute fetal hypoxia/acidosis varies from case to case, so fetal risk is not uniform. In some cases, there may be a sudden and almost total reduction in oxygen supply, while in others, it may be less intense or of slower onset. The insults can also be transitory and repetitive in nature (uterine hypercontractility, occult cord compression). Finally, there is also some individual variation in the capacity to react to hypoxia/acidosis.
For all these reasons, it is difficult to establish how long a hypoxic insult may last before important injury occurs. However, some information can be extrapolated from cases of sudden maternal cardiorespiratory arrest. No long-term neurological sequelae were reported when the interval between arrest and birth was under 12 min, and perinatal death was common when more than 15 min had elapsed. This evidence is frequently used as an indicator of a 12-min margin of safety for the fetus, in situations where sudden and complete interruption of fetal oxygenation occurs. It is likely that this rule of thumb is only valid for normally grown fetuses at term, receiving adequate oxygenation before the insult occurred, and needs to be adapted in other situations.
2.3 Diagnosis
Acute fetal hypoxia/acidosis almost always manifests as a prolonged deceleration – a sudden and sustained decrease in the fetal heart rate (FHR), with an amplitude exceeding 15 bpm and lasting more than 3 min (Fig. 2.2). When the duration exceeds 10 min, it is called fetal bradycardia.
Fig. 2.2
Cardiotocographic (CTG) tracing with prolonged FHR deceleration and reduced variability within the deceleration (“paper speed” 1 cm/min)
Decreased oxygen concentration in fetal arterial blood triggers chemoreceptors located near the aortic arch to transmit neurological impulses to brain stem nuclei controlling the vagus nerve and causes a parasympathetically mediated drop in FHR. When fetal hypoxia/acidosis affects the central nervous system, the sympathetic-parasympathetic modulation of FHR is decreased, and this results in diminished signal oscillations, a phenomenon known as reduced variability (Fig. 2.2).
Other clinical symptoms and signs may appear in association with a prolonged deceleration, related to the underlying cause of fetal hypoxia/acidosis (see below).
2.3.1 Reversible Causes
The underlying cause of fetal hypoxia/acidosis is frequently reversible, as occurs with uterine hypercontractility, sudden maternal hypotension or aorto-caval compression by the pregnant uterus when the mother is in the supine position.
2.3.1.1 Uterine Hypercontractility
Uterine contractions compress the blood vessels running inside the myometrium, and this may cause a temporary reduction in placental perfusion. The umbilical cord may also be compressed between fetal bony parts or between the fetal head and the uterine wall, transitorily reducing umbilical blood flow. Usually these phenomena occur during the peak of uterine contractions, and the intervals between these events are sufficient to re-establish normal oxygenation. The frequency, duration and intensity of uterine contractions will determine the magnitude of the disturbances, and how much they affect fetal oxygenation.
Hypercontractility may be spontaneous or induced in nature and refers to an increased frequency, intensity and/or duration of contractions leading to reduced fetal oxygenation. Rather than exhibiting a single prolonged deceleration (Fig. 2.2), uterine hypercontractility usually manifests by repetitive decelerations that may merge to become a prolonged deceleration and ultimately exhibit loss of variability but with a tendency for FHR recovery between contractions (Fig. 2.3).
Fig. 2.3
CTG with uterine hypercontractility (tachysystole), prolonged decelerations with attempts to recover between contractions and reduced variability at the end (“paper speed” 1 cm/min)
Most cases of uterine hypercontractility are iatrogenic in nature, caused by oxytocin or prostaglandin administration. Local practices for labour induction and acceleration will therefore determine the incidence of this entity, and respecting established doses and intervals for drug administration limits its occurrence. Little is known about the incidence and risk factors of spontaneous uterine hypercontractility, but some cases have been described in association with myometrial infection and partial placental abruption.
Increased abdominal pain is usually referred, but in the context of epidural analgesia, the diagnosis will rely mainly on the detection of increased contraction frequency by cardiotocography (CTG) or on uterine fundus palpation. More than five contractions in 10 min on two successive 10-min periods or averaged in the last 30 min is the definition of tachysystole – increased frequency of uterine contractions. With external monitoring of uterine contractions, using a tocodynamometer or fundal palpation, only frequency of uterine contractions can be reliability assessed. Evaluation of their intensity and duration, as well as of basal uterine tone, requires the use of an intrauterine pressure sensor, a technique that is nowadays seldomly used. A sustained rise in uterine contraction baseline or the detection of a permanently contracted uterine fundus is very suggestive of increased basal tone (hypertonus), but intrauterine pressure measurement remains the gold standard for this diagnosis.
2.3.1.2 Sudden Maternal Hypotension
Sudden maternal hypotension is nearly always an iatrogenic complication associated with epidural or spinal analgesia, due to blocking of sympathetic nerves that regulate vessel tonus. It can manifest by nausea, dizziness, vomiting, blurred vision and loss of consciousness and is usually accompanied by a prolonged deceleration. The drop in blood pressure is usually moderate but sufficient to cause a decrease in placental perfusion and gas exchange.
When epidural analgesia began to be used in labour, maternal hypotension and the resulting CTG changes occurred in almost a third of cases. Prophylactic fluid administration before catheter placement reduced this incidence to about 2 %, and recent developments in the technique with lower doses of local anaesthetics have almost eliminated the need for prophylactic fluid administration.
2.3.1.3 Maternal Supine Position with Aorto-Caval Compression
Adoption of the maternal supine position can lead to important aorto-caval compression by the pregnant uterus, with a resulting reduction in placental perfusion and gas exchange. This position has also been associated with uterine hypercontractility due to sacral plexus stimulation. Asking the mother to adopt the upright, half-sitting or lateral recumbent position is usually followed by normalisation of the CTG pattern.
2.3.2 Irreversible Utero-Placental-Umbilical Disorders
These are rare events of an irreversible nature that pose great risk to fetal oxygenation. They include major placental abruption, uterine rupture and umbilical cord prolapse. All of them require rapid delivery to avoid adverse perinatal outcome, and the first two can also be associated with profuse maternal haemorrhage.
2.3.2.1 Major Placental Abruption
Major placental abruption can be defined as a separation between the chorion and decidua of sufficient area to condition fetal oxygenation and/or is associated with maternal haemorrhage of sufficient volume to produce the same effect (Fig. 2.4).
Fig. 2.4
Major placental abruption
Placental abruption affects about 1 % of all labours, but the vast majority of cases are insidious and of small dimension. Placental function needs to be reduced by about 50 % before fetal oxygenation is affected. Blood originating from vessels located behind the placenta may detach the fetal membranes and drain to the vagina, or it may accumulate to form a retroplacental haematoma. Occasionally, blood will infiltrate the myometrium and originate a Couvelaire uterus, a structure of petrous consistency that can be palpated through the abdomen when located anteriorly and/or fundally.
The main risk factors for placental abruption are a previous history of similar episodes, hypertensive diseases of pregnancy, abdominal trauma, maternal cocaine consumption, maternal smoking and fetal growth restriction.
Sudden abdominal pain, abdominal tenderness, vaginal bleeding and maternal haemodynamic changes may be present, but frequently the first manifestation is a prolonged deceleration. FHR sounds have been reported to be dulled when there is a large anterior placental haematoma, and in these cases it may be necessary to confirm heart movements on ultrasound. When the presenting part is fully engaged, blood may not exteriorise through the vagina and will accumulate inside the uterine cavity, draining after birth.
Stay updated, free articles. Join our Telegram channel
Full access? Get Clinical Tree
