• 1.
  

  a) F b) F c) T d) F e) F

The fetus requires oxygen and glucose to maintain cellular aerobic metabolism, its main source of energy production. While glucose can be stored and later mobilised, oxygen needs to be supplied continuously, as an interruption of only a few minutes is enough to place the fetus at risk. Oxygen is obtained via the maternal respiration and circulation, placental perfusion, placental gas exchange, umbilical cord, and fetal circulation. Complications occurring at any of these levels may result in decreased oxygen supply, with a subsequent reduction in fetal arterial oxygen concentration (hypoxemia), and ultimately oxygen supply to fetal tissues (hypoxia). In the absence of oxygen, energy production in fetal cells can still be maintained for a limited period of time, using the anaerobic metabolism pathway, but this yields 19 times less energy and results in the production of lactic acid. The consequent increase in hydrogen ion concentration inside the cell, in the extracellular fluid, and in the fetal circulation is called metabolic acidosis. Reduced energy production and increased hydrogen ion concentration will ultimately lead to cell death and to tissue injury.

• 2.
  

  a) F b) F c) T d) T e) T

The placenta acts as the fetus’ lungs, kidneys and gastrointestinal tract, allowing gas exchange, waste elimination and nutrient uptake via the mother’s blood supply. In the inter-villous space, oxygenated blood from the mother’s spiral arteries flows around the fetal chorionic villi, which contain deoxygenated blood. The two umbilical arteries transport deoxygenated blood and waste products from the fetus to the placenta, while the umbilical vein provides the fetus with oxygenated blood and nutrients from the mother. The neonatal acid–base status is therefore best reflected by the umbilical arterial blood, while the venous umbilical blood contents depend on the maternal acid–base status and placental function. Blood from the placenta passes via the umbilical vein almost unhindered through the ductus venosus across the right atrium, and through the foramen ovale to the left atrium and then the left ventricle, which pumps into the aortic arch and neck and head vessels.

• 3.
  

  a) T b) T c) T d) F e) T

The fetal cardiovascular system is designed such that the most highly oxygenated blood is delivered to the myocardium and brain. These circulatory adaptations are achieved in the fetus by both the preferential streaming of oxygenated blood and the presence of intra-cardiac and extra-cardiac shunts. Thus, the fetal circulation can be defined as a ‘shunt-dependent’ circulation. The heart is equipped with baro and volume receptors, which sense changes in the pressure and volume of blood in the heart. The aortic arch and carotid bodies, which contain chemoreceptors, are well positioned to sense any alteration in the oxygen content of the blood coming from the placenta via the umbilical vein. This enables the fetus to produce a cardiovascular response to hypoxia when necessary.

• 4.
  

  a) T b) T c) F d) F e) T

In the fetus, energy is produced mainly by glycolysis, ending with the formation of adenosine triphosphate (ATP) and pyruvate. In this pathway, glucose is first converted into pyruvate, and two ATP molecules are generated. Under aerobic conditions, pyruvate is usually converted to acetyl coenzyme A, and in the presence of oxaloacetate enters the citric acid cycle. Further on it is subjected to mitochondrial oxidation to CO ₂ as a waste product from these reactions, and water. The CO ₂ produced by the cells diffuses across the cell membrane into the surrounding blood, and enters the erythrocytes where it is rapidly converted by the enzyme carbonic anhydrase into carbonic acid (H ₂ CO ₃ ) and bicarbonate ion (HCO ₃ ⁻ ). Thus, the excess CO ₂ is removed by the bicarbonate buffering system, and this prevents large increases in acidity that H ⁺ would otherwise cause: CO ₂ + H ₂ O ↔ H ₂ CO ₃ ↔ H ⁺ + HCO ₃ ⁻ . This reaction occurs bi-directionally until the blood reaches the placenta, where the CO ₂ is eliminated. As in adults, buffers in the fetus play a central role in neutralizing H ⁺ production and maintaining constant blood and tissue pH values. Adequate buffering prevents significant changes in the fetal pH. The bicarbonate buffer, which is the main buffer system in plasma, accounts for 35% of the fetal buffering capacity in blood. Bicarbonate and the fixed acids cross the placenta much more slowly than does CO ₂ ; their equilibration takes hours rather than minutes. The rate at which CO ₂ crosses the placenta is limited by the blood flow, not the resistance to diffusion.

• 5.
  

  a) T b) T c) F d) F e) F

Fetal asphyxia almost always occurs as a result of a gradual insufficiency in the umbilical blood flow or insufficient uterine blood flow, and in most cases is attributable to a reduction in gas exchange for variable time periods. However, a sudden complete cessation of oxygen delivery to the fetus as a cause of asphyxia is clinically rare, but often catastrophic. Occlusion of one or more of the vessels in the umbilical cord can impede circulation to and from the fetus. During these events, the oxygen content of the fetal blood may decrease and the CO ₂ or H ₂ CO ₃ content may increase (producing hypercapnia). The excess CO ₂ is removed by the HCO ₃ ⁻ . Respiratory acidosis is defined as a decreased blood pH with an elevated blood p CO ₂ . Further decreases in the oxygen content of fetal blood, if repetitive and/or prolonged, can lead to hypoxia, which will in turn lead to an increase in lactate in the blood. The accumulation of lactic acid can deplete the buffer system, cause failure of the ATP-dependent sodium–potassium pump, and disrupt the exchange of ions across the cell membrane, initiating a cascade of reactions that lead to cell injury and death.

• 6.
  

  a) T b) F c) F d) T e) T

Uterine contractions may reduce placental bed perfusion by compressing the blood vessels running inside the myometrium. They may also reduce umbilical cord circulation by compressing the umbilical cord between fetal parts, or between the fetus and the uterine wall. Aorto-caval compression by the maternal supine position may decrease placental perfusion but does not usually cause sudden maternal hypotension. There are several different causes for maternal cardio-respiratory arrest, and this may or may not be reversible. The reversibility of the resulting fetal hypoxia/acidosis will therefore depend on the cause and duration of the arrest. Shoulder dystocia in association with nuchal cords will cause umbilical cord compression. It is believed that compression of fetal neck vessels also occurs during shoulder dystocia. Maternal pushing during second-stage contractions contributes to reduced placental perfusion and may aggravate fetal oxygenation. Asking the mother not to push, or pushing on alternate contractions, often results in an improvement in fetal heart rate characteristics.

• 7.
  

  a) T b) F c) F d) F e) F

Fetal hypoxia/acidosis can be documented in the umbilical cord immediately after birth or in the newborn circulation during the first minutes of life, by a pH value below 7.00 together with a base deficit (BD) in excess of 12 mmol/l, or alternatively a blood lactate concentration exceeding 10 mmol/l. With severe and prolonged hypoxia/acidosis, low Apgar scores will occur, but lesser degrees will usually not affect them, and values can be low due to other causes, such as prematurity, birth trauma, congenital anomalies, pre-existing lesions, medication administered to the mother, and vigorous endotracheal aspiration. Most newborns with metabolic acidosis, with or without decreased Apgar scores, recover quickly and do not develop relevant short or long-term complications. In only a few cases will hypoxia/acidosis be of sufficient intensity and duration to affect important organs and systems, and put the newborn at risk of death or long-term disability. Neonatal encephalopathy has many other causes besides intrapartum fetal hypoxia/acidosis. Hypoxic-ischemic encephalopathy (HIE) is the short-term neurological dysfunction caused by intrapartum hypoxia/acidosis, and the diagnosis requires the confirmation of metabolic acidosis and low Apgar scores. Only 10–20% of cerebral palsy cases are caused by intrapartum hypoxia/acidosis. Infection, congenital diseases, metabolic diseases, coagulation disorders, antepartum and post-natal hypoxia, birth trauma, and the complications of prematurity constitute the majority of causal situations.

• 8.
  

  a) F b) F c) F d) T e) F

The result shows a clear metabolic acidosis with low pH and high BDecf, however p CO2 is also elevated, which makes these acidoses combined. The pH is no longer compensated.

• 9.
  

  a) T b) F c) F d) F e) F

This term neonate, although acidotic and in need of a short period of resuscitation, does not show any signs of HIE.

• 10.
  

  a) F b) F c) T d) F e) T

Fetal electrodes can be placed both in cephalic and breech presentations. Internal FHR monitoring should not be attempted in patients with active genital herpes infection, but it is safe in those who are sero-positive to this agent. Ruptured membranes are required for the fetal electrode to be placed, and if amniotomy is inappropriate this constitutes a contra-indication to internal FHR monitoring. Fetal electrode placement should preferably be avoided before 32 weeks of gestation, but it can be used safely after that period. Because of an increased risk in vertical transmission of the disease, internal FHR monitoring should not be used in patients who are sero-positive to human immunodeficiency virus.

• 11.
  

  a) T b) F c) T d) F e) T

Incorrect placement of the tocodynamometer, reduced tension applied to the supporting elastic band, and increased abdominal adiposity may all result in failed or inadequate registration of UCs. External UC monitoring using a tocodynamometer may provide accurate information on the frequency of contractions, but not on their intensity and duration. Internal UC monitoring has been associated with few complications, but the intrauterine catheter is relatively expensive. Internal UC monitoring with IUP catheters has not been shown to be associated with improved outcomes in induced and augmented labour and so it is not recommended for routine clinical use in these situations. The location of the basal line on the UC graph is influenced by the location of the tocodynamometer, the tension applied to the elastic band, and maternal abdominal adiposity.

• 12.
  

  a) T b) F c) F d) F e) T

If the CTG prior to the deceleration is normal, the variability prior to or within the first 3 minutes of the deceleration is normal and acute intrapartum accidents are excluded, up to 90% are likely to recover to normal baseline in 6 minutes and up to 95% by 9 minutes. In the context of an acute hypoxia the pH drops at the rate of 0.01/minute. If one of the 3 major accidents is diagnosed (cord prolapse, abruption or uterine rupture), the appropriate management is immediate delivery by the quickest and safest mode (i.e. operative vaginal birth or an emergency caesarean section). In the presence of a concealed abruption and resultant loss of fetal blood volume, it is very likely that due to a sudden reduction of cerebral perfusion pressure during the deceleration, the baseline variability will be lost within the first 3 minutes of the deceleration. Therefore, the “3, 6, 9, 12, and 15 minute” rule cannot be applied in this case and urgent delivery should be undertaken. If there is evidence of uterine hyperstimulation, oxytocin should be immediately stopped and Terbutaline 250 mcg intravenously or subcutaneously should be administered to relax the myometrium so as to relieve umbilical compression.

• 13.
  

  a) F b) F c) T d) F e) F

The CTG features of chronic hypoxia include an increased baseline fetal heart rate secondary to release of catecholamines as a compensatory mechanism for stress, a reduced baseline fetal heart rate variability due to reduction of oxygenation to the autonomic nervous system, and the presence of repeated shallow decelerations. Immediate delivery is needed as ongoing uterine contractions can further increase the damage already caused by the chronic hypoxia by causing repeated umbilical cord compressions and reduction in utero-placental oxygenation. A ‘step ladder pattern’ to death may also be seen in terminal stages of a gradually evolving hypoxia and this reflects progressive myocardial hypoxia.

• 14.
  

  a) T b) F c) T d) T e) T

These decelerations reflect repeated umbilical cord compression or utero-placental insufficiency. If the baseline fetal rate is stable and there is good variability, there is good oxygenation of the central organs. The mechanism of the ‘overshoots’ is reduced vagal stimulation during the cord occlusion followed by myocardial beta-adrenergic stimulation once the occlusion ends. It is an abnormal feature as they reflect ongoing fetal hypotension that results in suppressed myocardial vagal tone and reflex sympathetic response (tachycardia). Regardless of the presence of decelerations, if there is a stable baseline with good variability, the fetus has enough time to oxygenate and perfuse its organs in between contractions. The first management when there are signs of hypoxia on the CTG trace is to improve the environment to improve oxygenation. Stopping the oxytocin infusion reduces the frequency and strength of the contractions allowing the fetus to perfuse its organs and recover from the hypoxia and this reflects on the CTG trace by showing shorter and less pronounced decelerations. If the hypoxic insult continues, the fetus shows the subsequent changes, once all the compensatory mechanisms are in place, the different organs will start to fail, first the ‘non-essential organs (peripheral tissues, gut, kidneys), followed by the brain (autonomic nervous system) showing loss of variability and finally the heart showing either a prolonged deceleration or a ‘step ladder pattern’ to death as the myocardium attempts to restore the heart rate back to normal baseline.

• 15.
  

  a) F b) F c) T d) F e) F

The sinusoidal pattern is classified into ‘typical’ or ‘atypical’. The typical sinusoidal is associated with fetal anaemia (Rhesus incompatibility, infection) and the atypical sinusoidal pattern is found in acute feto-maternal hemorrhage. The saltatory pattern reflects a ‘fight’ between the sympathetic and the parasympathetic systems to maintain a stable baseline rate, when this pattern is present in between atypical decelerations the intra-uterine environment needs to be improved (stop oxytocin infusion, increase intravenous fluids, positional changes) to allow fetal oxygenation. Failure to do so will lead to a prolonged deceleration or a ‘step ladder pattern’ to death. As previously mentioned, an ‘atypical’ sinusoidal pattern is related to acute feto-maternal hemorrhage. Immediate delivery is needed and the neonatologists should be informed to test fetal hemoglobin. ‘Cycling’ refers to the presence of periods of reduced variability (fetal sleep) with others of good variability, accelerations and stable baseline. This indicates that the CNS is well perfused. The saltatory pattern is defined as increased variability (>25 bpm) and, as previously mentioned, reflects a ‘fight’ between the sympathetic and the parasympathetic systems to maintain a stable baseline rate. This is an abnormal feature and needs further attention. There is a characteristic CTG pattern in the presence of thumb sucking, the features are a pseudo-sinusoidal pattern, similar in shape to the ‘typical’ sinusoidal pattern but there are accelerations present and generally it doesn’t persist more than 10 min. Ultrasound can be used to confirm that this is the case.

• 16.
  

  a) F b) T c) T d) T e) F

Maternal fever is not a formal contra-indication provided that the mother is under antibiotic treatment at the time of FBS. FBS may increase the risk of mother-to-child HIV infection. Fetal haemophilia is a rare contra-indication of FBS. When the mother is known to be a carrier of the disease, especially in case of a male fetus, FBS should be avoided. Active genital herpes is a contra-indication to vaginal birth. A previous history of genital herpes without any symptoms or clinical evidence of recurrence is not a contra-indication to FBS. FBS can be performed in cases of vaginal group B streptococcus colonisation, when the mother is properly treated by antibiotics during labour.

• 17.
  

  a) F b) T c) T d) F e) F

A fetal scalp pH < 7.25 is often quoted as “pre-acidosis”. This is an indication for repeated sampling after a short time interval. Intervention is recommended when fetal scalp pH is < 7.20. A scalp pH < 7.00 likely represents severe fetal academia and should lead to emergency intervention. A fetal scalp lactate measurement > 4.8 mmol/L was used as the cut-off for intervention in a large randomised controlled study comparing FBS for lactate analysis to FBS for pH analysis (Wiberg-Itzel et al. BMJ 2008). Base deficit is not usually calculated from scalp blood samples. There is no solid recommendation in favour of the use of base deficit in this indication. When blood analysis cannot be performed, an acceleration of fetal heart rate in response to nociceptive stimuli such as fetal scalp stimulation is reassuring and is indicative of a very low risk of fetal pH < 7.20, according to observation studies.

• 18.
  

  a) F b) F c) F d) T e) T

Inter- and intra-observer agreement on EFM interpretation has been studied extensively. The overwhelming majority of these studies have shown that levels of agreement for the elements of the FHR tracing as well as their overall classification have been no better than fair with a number of such elements being poor. These results do not appear to be related to experience, suggesting that visual assessment of FHR tracings is essentially a flawed process that is influenced by perception rather than knowledge base. Prediction of fetal compromise by visual interpretation of FHR patterns has long been shown to be both imprecise and often no better than random chance. Many FHR tracings contain abnormalities that are not related to fetal compromise but are perceived as abnormal by those who review such tracings. Fetal oximetry was a promising adjunctive method in the late 1990s and early 2000s to aid the prediction of fetal status when combined with standard assessment of FHR patterns. Later work has shown that this technology did not improve the delineation of compromised from normal fetus in the majority of cases. The three-tier classification scheme proposed by the American College of Obstetricians and Gynecologists has been available for more than five years. To date, no studies have been published to demonstrate a significant effect on intrapartum care or perinatal outcome. A number of computerized systems for FHR analysis have been developed and deployed for clinical care. While promising initial steps toward reducing the effects of inter- and intra-observer variation in classifying FHR patterns, data to demonstrate a significant impact on perinatal outcome is lacking.

• 19.
  

  a) T b) T c) F d) T e) F

Objective analysis of FHR patterns is the cornerstone of taking future intrapartum systems to the next level as it eliminates the “human” factor that is responsible for the vast majority of errors in FHR pattern interpretation. Most studies that have examined this factor have concluded that visual interpretation of FHR tracings remains the most problematic aspect of EFM. There is little if any doubt that the inherent risk factors of each pregnancy play a role in determining the risk of intrapartum fetal compromise. Modification of such risk requires the integration of individual patient data into any system designed to project perinatal outcome. Algorithmic approaches to fetal assessment, including scoring systems and nomograms have never been demonstrated to impact on clinical outcomes. The reasons that most of these approaches fail is that they cannot account for the number of variables and their rate of change that occur during labour. Hybrid systems employ the strengths of multivariate analysis and neural networks to deal with the chaotic environment of obstetric units. Given that the reduction of important clinical variables is required to develop workable prognostic systems, this is the new frontier of clinical decision support tools. Computerized FHR analysis has been shown to reduce the effect of inter-observer variation when tasked with interpretation of FHR tracings. However, beyond those observational studies, it has not been associated with improved perinatal outcomes.

• 20.
  

  a) T b) T c) F d) T e) T

Fetal pulse oximetry was FDA-approved for intrapartum use in 2000. In 2005, a large randomized trial, conducted by the NICHD’s Maternal-Fetal Medicine Network showed no difference in primary Caesarean rates or other secondary outcomes of interest whether or not fetal oximetry data were provided. Shortly thereafter, support for its use in the United States was withdrawn. Novel obstetric devices and systems are among the most difficult to introduce into practice for a number of reasons, including costs of research and development, obtaining FDA approval and being adopted by a significant portion of the obstetric community. With these considerations, few companies, at present, are even envisioning the development of new fetal surveillance systems. Most clinicians recognize that present monitoring systems are limited and, as the experience with fetal ECG analysis has demonstrated in Europe, would consider the adoption of improved monitoring systems should they show benefit. Sufficiently powered randomized controlled trials remain the gold standard for assessment of fetal surveillance systems. Such trials are large, expensive and time-consuming, as well as challenging to conduct properly. In the United States, product liability remains a concern for all licensed medical devices. Burdens are placed on both end-users and manufacturers to demonstrate that new devices and medical systems provide patient safety and are not associated with ill effects. Post-approval monitoring of new devices requires the reporting and archiving of adverse events associated with their use, and mandate that the manufacturers escrow significant sums of money in the event of litigation.

• 21.
  

  a) F b) F c) F d) F e) T

While there is an increasing risk of fetal acidosis with increasing severity of CTG pattern, even with severe (Category III) patterns the risk of acidosis is perhaps 50% or less. Decelerations with absent variability, for example, may represent fetal injury or anomaly, separate from significant fetal asphyxia. The use of CTG patterns for fetal surveillance during labour is currently predicated on the search for hypoxia and acidemia. Even severe fetal asphyxia at the time of birth is a poor predictor of subsequent neurological injury. It is expected that by detecting hypoxic/acidemic threats during labour and removing the fetus from its hostile environment neurological injury will be avoided. The majority of infants that die or suffer injury during labour, however, are not severely acidotic at the time of delivery. Preventing intrapartum injury appears to require closer attention to factors causing fetal cerebral ischemia. Because fetal death on the monitor is preceded by prolonged periods of abnormal tracing, including sustained bradycardia, it will not escape detection and “rescue” would likely effect delivery prior to death. Under these circumstances the baby may suffer neonatal death or long-term injury. Neurological injury, on the other hand, may occasionally develop so rapidly that even prompt intervention may not prevent injury.

• 22.
  

  a) T b) T c) F d) T e) T

Uterine contractions decrease uterine blood flow in direct proportion to the amplitude and duration of the contraction. The vessels supplying the maternal side of the placenta traverse the myometrium and are compressed during uterine contractions. When the intrauterine pressure exceeds about 50mmHg, the placenta is functionally isolated from the maternal circulation and placental function is temporarily impaired with limitation of oxygen availability to the fetus. Uterine contractions raise fetal intracranial pressure in direct proportion to their amplitude and duration. If the pressure within the head were not elevated during a contraction the pressure in the uterus would exceed the pressure in the head with potential compromise of fetal cerebral circulation and the ability to tolerate the forces on the head from both contractions and descent of the head through the pelvis. The diagnosis of excessive uterine activity should be predicated on such parameters as frequency, duration, the interval between contractions, baseline tone and the amount of rest time between consecutive contractions. Especially in early labour, the fetus may tolerate significant amounts of excessive uterine activity without apparent compromise or deterioration. Later in labour, however, as the head descends and moulds, especially if there is a malposition, excessive uterine activity may aggravate the ischaemic effects of contractions. Pushing and fundal pressure each increase the intracranial pressure above that of the contraction. The increases are significant with estimates of a 62% increase. This adds substantial pressure to the fetal head requiring further adaptation on the part of the fetus to prevent further decreases in cerebral blood flow. These features of the 2 ^nd stage of labour help to explain the increased frequency of deterioration or injury during this time.

• 23.
  

  a) T b) T c) F d) F e) F

CTG patterns permit more comprehensive assessment of the fetus than simply the presence or absence of hypoxia/acidemia. The features described including: a normal stable baseline FHT of 110-160 bpm with periods of accelerations with fetal movement and absent decelerations with contractions indicate rest/activity or sleep/wake cycles in the fetus and represent a high order of neurological integration. As such, the interpretation of the CTG tracing includes not only that the fetus shows no evidence of diminished oxygen availability but, in addition, it appears neurologically responsive and reasonably, uninjured. A baseline heart rate of 170 bpm with absent variability is not reflective of fetal hypoxia. Tachycardia reflects hypoxia only in association with decelerations. With absent decelerations, the more likely diagnosis is maternal fever, medication, fetal “anxiety” response (where the tachycardia will be limited in duration) or possibly neurological injury. This emphasizes the role of decelerations in the detection of head compression or other mechanical problems of labour. As described, the pattern does not reveal hypoxia. Indeed, it excludes this diagnosis. Proper management would call for an evaluation of the fetal head station, position, amount of moulding and descent, evaluations designed to better estimate the feasibility of safe vaginal delivery. This pattern, sometimes referred to as the “conversion pattern” likely represents an acute ischemic neurological injury in the fetus manifested as an apparent loss or diminution of vagal input to the control of the heart rate. Once present, even rapid intervention may not prevent an adverse outcome although the clinical presentation of the newborn varies widely.

• 24.
  

  a) T b) T c) F d) T e) F

Pushing should never begin prior to full dilatation. Full dilatation represents full retraction of the cervix around the fetal head, not the attainment of “10” centimeters of dilatation. Full retraction of the cervix around the fetal head is dependent upon descent of the presenting part. Pushing with contractions prior to full dilatation, for example, or manual dilatation of the cervix are often unsuccessful and expose the fetus to additional mechanical stresses and risk trauma to the cervix. There should be adequate rest time between the end of one contraction and the beginning of the next. This allows the fetus to recover, especially if there are decelerations in the CTG tracing. The contraction-free, pushing-free interval should be about 60 seconds or more. It may be necessary to have the patient refrain from pushing if any deceleration has not recovered to its previously normal baseline rate or if the normal baseline rate and variability cannot be clearly established. Pushing with every other or every third contraction will likely safeguard the wellbeing of the fetus. The presence of decelerations during the 2 ^nd stage of labour is more likely represent head compression rather than cord compression. It is important to give the fetus adequate time to recover and carefully evaluate various features of descent, position and moulding in the assessment of the feasibility of safe vaginal delivery. This is a fundamental principle of the safe conduct of the 2 ^nd stage of labour where the objective is not how quickly the fetus can be delivered, but how safely. This approach attempts to assure recovery from the augmented effects of pushing on the fetal head in that the resumption of pushing occurs only after the fetus has recovered from the previous deceleration as manifested by the return of the CTG pattern to the previously normal baseline rate and variability.

• 25.
  

  a) T b) F c) F d) T e) T

Metabolic acidosis is defined as the measurement in umbilical artery blood of a pH < 7.00 and a BD > 12 mmol/l, but lactate value ≥ 10 mmol/l can be used as an alternative. A vein lactate ≥ 10 mmol/l implies an even higher arterial value, so metabolic acidosis can still be diagnosed. Only HIE grade 2 and 3 are significantly associated with neonatal death and severe neurological disability. Neurological damage is rare in newborns with grade 1 HIE. Neuroimaging findings of unilateral arterial or venous infarction, as well as focal intra-parenchymal or intraventricular hamorrhage, are unlikely to be caused by intrapartum hypoxia/acidosis, and should therefore prompt screening for a genetic, coagulation and/or metabolic abnormality. CP of the “spastic quadriplegic” and “dyskinetic” types are the long-term neurological complications most strongly associated with hypoxia/acidosis occurring during labour. Exclusion of other identifiable aetiologies, such as birth trauma, coagulation disorders, infection and genetic disorders should be carried out in order to establish causation.

• 26.
  

  a) F b) F c) T d) T e) F

Grey matter lesions of the basal ganglia, thalamus, hippocampus, reticular formation and cerebellum typically affect full-term infants subjected to acute hypoxia, and are associated with the most severe motor and cognitive deficiencies. Multi-cystic encephalopathy is usually associated with fetal infection or metabolic disorders, and not with peri-partum hypoxia/acidosis. Para-sagittal brain injury to the periventricular and subcortical white matter (periventricular leukomalacia) occurs mainly in premature children exposed to intermittent reductions in fetal oxygenation over a period of at least one hour. Moderate and severe cases are associated with a high risk of “spastic quadriplegic” CP, as well as cognitive, psychomotor and neurosensory impairments. Watershed injury involving the para-sagittal white matter often with extension to the cortex is associated with cognitive and language performance in middle childhood, and usually no motor impairment. MRI between 24 and 96 hours of life is more sensitive in defining the timing of hypoxic injury, whereas MRI undertaken between 7 days and 21 days is more accurate in delineating the full extent of brain injury.

• 27.
  

  a) F b) T c) F d) T e) F

The development of computer analysis of fetal heart rate (FHR) and uterine contraction signals began in the 1980s in an attempt to overcome the well-demonstrated subjectivity of visual analysis. The first of these systems were only suitable for the analysis of antepartum cardiotocography (CTG), where reduced baseline instability, limited signal loss and artefacts, and smaller tracing length pose much lesser challenges for signal processing and algorithm development. Systems now incorporate real-time visual and sound alerts for healthcare professionals, based on the results of computer analysis, in order to raise attention to specific findings, thus promoting tracing and clinical re-evaluation and subsequent intervention, if considered necessary.

• 28.
  

  a) T b) F c) T d) T e) F

Visual analysis of intrapartum fetal monitoring signals has consistently been shown to be affected by limited intra- and inter-observer agreement, and computer systems are a way of overcoming this limitation. Digital recording and retrieval may overcome the problem of fading of paper records, but this does not necessarily imply the use of computer analysis of signals. Knowledge of an adverse neonatal outcome has been shown to influence the way healthcare professionals retrospectively interpret CTG tracings, and computer systems are a way of assuring that consistent analysis is always obtained. During intrapartum monitoring, healthcare professionals may indeed not always be looking at the CTG tracing, so computer analysis with visual and sound alerts may be a way of prompting them to re-evaluate the tracing, and to take action if necessary. While there is frequently uncertainty as to the cause of fetal hypoxia/acidosis, computer analysis does not currently contribute to the identification of the cause.

• 29.
  

  a) T b) T c) F d) T e) F

The National Institute of Child Health and Human Development guidelines were used for the development of the IntelliSpace Perinatal ^® and PeriCALM™ systems. All other systems provide computer analysis of cardiotocographic signals only. Both the PeriCALM™ and the INFANT ^® systems incorporate trained neural networks to evaluate cardiotocographic characteristics. Sound alerts that are produced when a colour-coded visual alert is not quickly acknowledged are a characteristic of the INFANT® system. The Trium CTG Online ^® system uses algorithms for analysis of basic cardiotocographic characteristics that are based on International Federation of Gynecology and Obstetrics guidelines of 1987.

• 30.
  

  a) T b) F c) F d) T e) T

All available computer systems have been evaluated by comparing their analysis with that of experts, generally yielding satisfactory results. There are no published randomised clinical trials evaluating these systems, but two such trials have recently been completed and their results are expected soon. A small number of studies have evaluated the accuracy of these systems in prediction of adverse neonatal outcome, but larger sample sizes are needed to confirm the results. Currently, there is no widely accepted gold standard of intrapartum hypoxia/acidosis with which to compare the results of computer analysis, and this is an important limitation for all research conducted in this area. Commercial issues have limited the conversion of CTG files between different systems, and this has made it difficult to conduct direct comparisons between them.