This case presents a clinical vignette of a nine-month-old female who ingested a foreign object, likely a wedding ring. The learner is provided an opportunity to formulate a differential, presentation, and note before comparing against an ideal standard. Key clinical points include the recognition of esophageal foreign body symptoms—such as drooling and fussiness—and the need for prompt radiographic evaluation and consultation for endoscopic removal. Early identification and intervention are essential to prevent complications such as aspiration, perforation, or complete obstruction.

This case presents a clinical vignette of a 21-year-old male college student who experiences a syncopal episode in class. The learner is given the opportunity to formulate their own patient presentation and clinical note before reviewing an ideal version. The case emphasizes the importance of distinguishing benign from life-threatening causes of syncope. Key discussion points include the evaluation of vasovagal versus cardiogenic etiologies, the use of tools like ECG and family history to risk-stratify patients, and the identification of red flags such as exertional syncope or sudden death in relatives. A systematic review of dangerous ECG findings (e.g., Brugada, WPW, HOCM) is highlighted, along with appropriate disposition planning for outpatient versus inpatient workup.

Repetitive, intense or sustained uterine contractions constitute the predominant cause of hypoxic stress to human fetuses during labour. This is because contraction of the myometrial fibres compresses the branches of the uterine arteries and the spiral arterioles supplying the placental bed, which results in a transient cessation of oxygen delivery to the placenta. Compression of the umbilical cord loops between the uterine wall and the fetal body parts during uterine contractions may lead to the occlusion of blood vessels within the umbilical cord. This may lead to impaired transfer of oxygen and nutrients to the fetus and removal of carbon dioxide and metabolic by-products from the fetus. Excessive frequency of uterine contractions (uterine tachysystole), increased intensity of the uterine contractions (hypertonus), and increased duration (tocospanus) can independently contribute to fetal hypoxic stress, increasing the likelihood of hypoxic–ischaemic encephalopathy (HIE) and its long-term sequalae, and perinatal deaths. Therefore, a combination of uterine tachysystole, hypertonus and tocospanus may have disastrous consequences for the fetus, as well as the mother.

Uterine scar dehiscence refers to disruption on the myometrium but with an intact serosa. Uterine rupture refers to the complete disruption of the uterine wall, including the serosa. The risk of uterine scar rupture is approximately 0.5% with spontaneous onset of labour and 0.8% when the labour is augmented with oxytocin. A high index of clinical suspicion is necessary when managing women attempting VBAC because most of the studies were carried out using CTG guidelines based on ‘pattern recognition’ with classification systems that group random features into different ‘categories’ with arbitrary time limits, leading to an ‘overall’ classification of CTG into ‘normal, suspicious and pathological’. Therefore, It is not surprising that this approach that disregards the features of fetal responses to hypoxic stress failed to demonstrate any predictive or diagnostic value of CTG for scar dehiecence or rupture. Recurrent ‘quicklie’ decelerations and/or ‘tardy’ decelerations with reduced variability and/or the ZigZag pattern, Poole shark teeth pattern and myometrial irritability may be noted prior to the onset of terminal prolonged deceleration.

Obstetrics claims accounted for 62% of all clinical claims by value received in the year, highlighting the underlying impact of the financial costs of maternity indemnity payments, alongside the impact of harm on patients, families and healthcare staff. CTG misinterpretation contributes substantially to claims pertaining to mismanagement of labour and cerebral palsy. Medical negligence involves establishing causation and liability. Presence of abnormal CTG, low Apgar score, low cord arterial pH, assisted ventilation, admission to neonatal intensive care, moderate or severe neonatal encephalopathy and subsequent neurological damage point to asphyxia as a possible cause. However, several intrinsic fetal disorders cause neurological disability and an abnormal CTG may have been coincidental. Causation is best determined by neuroradiologist and paediatric neurologist based on the areas of scarring within the brain on MRI. The thalamus, basal ganglia injury show scarring, reflecting acute profound hypoxia while prolonged partial hypoxia results in bilateral cortical atrophy. Expert opinion is requested to judge whether the care provided fell short of what was expected (Bolam principle).

This clinical vignette explores the complex decision-making involved in terminating resuscitation after prolonged, unsuccessful advanced cardiac life support (ACLS) for a 72-year-old female in unwitnessed cardiac arrest. Despite high-quality CPR, PEA persisted without return of spontaneous circulation (ROSC), and serial assessments showed a non-perfusing rhythm, absent cardiac motion on ultrasound, and persistently low end-tidal CO₂. Reversible causes were systematically ruled out using the Hs and Ts framework. After 20 minutes of resuscitation and no signs of ROSC, the code team, led by the resident, called time of death. This case emphasizes the use of ETCO₂, point-of-care ultrasound, and AHA termination of resuscitation (TOR) criteria, while modeling collaborative leadership and thoughtful clinical judgment in high-stakes decision-making.

Computerized CTG (cCTG) was designed to overcome human errors with visual assessment and pattern recognition that contribute to CTG misinterpretation; visual assessment is associated with poor accuracy and high inter-/intra-observer variability, leading to variation in recognition of abnormal patterns and in clinical outcomes. It has been introduced for the evaluation of features such as the baseline fetal heart rate, short-term variability, accelerations, decelerations, sinusoidal patterns and electronic quality. This approach began in the 1980s, evolved rapidly, and many systems are now in use. Two large randomized controlled trials on cCTG concluded that compared to visual analysis, computerized analysis did not significantly reduce the rate of neonatal metabolic acidosis or operative interventions. The most important drawback of these systems is the use of pattern recognition guidelines, which classify traces without considering fetal response to stress. These systems also did not account for other important labour-related information (e.g. duration and rate of progress of labour and presence of meconium staining of amniotic fluid) required to make informed clinical decisions.

The ‘pattern recognition’ model of interpretation of the CTG that groups features into different categories and applied the same parameters to all human fetuses (growth-restricted, premature, term, post-term, presence of meconium, etc.) failed to appreciate their specific requirements and reserves/compensatory mechanisms. Recently, four consecutive ‘Each Baby Counts’ reports (2015–2019) published by the Royal College of Obstetricians and Gynaecologists, where the illogical and unscientific NICE CTG guidelines with arbitrary time limits based on personal opinions were almost universally used until recently, have concluded that in approximately 70% of cases of intrapartum hypoxia-relared perinatal deaths and severe hypoxic brain injuries, different care would have resulted in a different outcome. Moreover, errors with CTG interpretation and the use of FBS had contributed to >50% of these poor outcomes. Physiological CTG interpretation was developed in the UK in 2006 to reduce the rates of HIE and intrapartum emergency caesareans and the use of AI such as the Tweris app based on physiological CTG interpretation may aid clinicians in the future.

It is very much hoped that this book, which has moved away from the illogical, unscientific and potentially dangerous ‘nNormal, suspicious, pathological’ classification from its first publication in 2017, and is based on the principles of physiological interpretation of CTG, in line with the International Expert Consensus Statement published by more than 50 CTG experts from over 20 countries in 2024, will continue our journey to reduce avoidable harm to women, birthing people, their babies and the families. We owe this to women, birthing people, their babies and families who have placed in their trust in us to provide evidence-based clinical care, which is based on scientific foundations and the application of the knowledge of fetal pathophysiology.

CTG is considered a screening test for intrapartum fetal hypoxia so that features suggestive of ongoing hypoxic stress may be recognized and timely and appropriate action taken to avoid hypoxic–ischaemic brain injury. Several non-hypoxic causes may also give abnormal changes on the trace. In the absence of a coexisting or superimposed hypoxic stress, deep and repetitive decelerations may be absent on the CTG. Traditional guidelines may miss these abnormalities. Understanding features likely to be seen on the trace in non-hypoxic causes is essential to ensure timely and appropriate action and may help clinicians counsel the patient regarding recommended mode of intrapartum fetal heart rate monitoring and optimal mode of birth. Tests such as fetal ECG are contraindicated in cases of fetal cardiac malformations and conduction defects. Fetal scalp blood sampling is also not appropriate in non-hypoxic causes of non-reassuring features on the CTG trace. Chorioamnionitis and fetal inflammation are also important non-hypoxic pathways of fetal neurological damage and death. Physiological interpretation of CTG is essential to recognize features of non-hypoxic pathways of fetal compromise.

This vignette explores a communication challenge that arises during the care of a critically ill neonate requiring a lumbar puncture. The learner is provided with an opportunity to observe and reflect on interprofessional conflict and the skills needed to navigate it. They are then presented with a model response to guide future encounters. The case emphasizes the importance of validating team members’ concerns, maintaining professionalism, and redirecting focus toward shared goals. Learners will also gain strategies to de-escalate emotionally charged situations and preserve teamwork in high-stakes environments. Ultimately, this scenario highlights that delivering high-quality emergency care requires more than clinical knowledge—it also demands emotional intelligence and leadership under pressure.

This clinical vignette explores the challenges of interprofessional communication in high-stakes cardiology cases. A 58-year-old male presents with exertional chest pain and an ECG showing hyperacute T waves—findings that suggest early occlusion myocardial infarction (OMI), despite not meeting traditional STEMI criteria. The ED physician appropriately escalates the case, calling cardiology and advocating for cath lab evaluation. When the cardiology fellow dismisses the concern, the emergency physician responds with professionalism and persistence, escalating the case to a senior fellow. A repeat ECG shows evolving ST-segment elevations, confirming the diagnosis and prompting urgent cath lab activation. This case underscores the critical balance between diplomacy and decisiveness, and highlights how preparation, calm communication, and firm advocacy can ensure optimal outcomes, even when facing resistance. Learners will practice communicating clinical judgment, interpreting early ischemic patterns, and navigating hierarchies in complex multidisciplinary environments.

Any bleeding from the genital tract that is heavier than the usually expected blood-stained mucus discharge (‘show’) during labour should be considered as ‘significant’ intrapartum bleeding. Vaginal bleeding during labour may indicate a pathological cause such as a sudden onset of fetomaternal haemorrhage (e.g. rupture of vasa praevia), placental abruption or rupture of the uterus. In most cases, intrapartum bleeding may occur due to benign conditions such as secondary to damage to maternal veins during cervical dilatation or rupture of membranes. It is important to differentiate the pathological causes from bleeding secondary to a benign condition usually associated with cervical dilatation during labour. Specific CTG patterns include the Poole shark teeth pattern (atypical sinusoidal pattern) due to a sudden fetal hypovolaemia and hypotension in vasa praevia), recurrent late decelerations (gradual placental separation in uterine rupture prior to the onset of terminal bradycardia) or a sudden and prolonged deceleration (placental abruption or uterine rupture). These require an urgent birth.

This clinical vignette presents a decompensating 59-year-old woman with fatigue, melena, altered mental status, and subsequent hematemesis. Learners must rapidly identify upper-GI bleeding, recognize signs of hepatic encephalopathy, and manage suspected variceal hemorrhage in the context of alcohol-related cirrhosis. With findings including asterixis, hepatomegaly, jaundice, anemia, thrombocytopenia, elevated INR, and hyperammonemia, the case emphasizes early airway protection, massive transfusion, and the administration of octreotide and ceftriaxone. Trainees are challenged to prioritize interventions, anticipate deterioration, and coordinate care with gastroenterology for endoscopic hemostasis. The vignette also highlights when and how to use AIMS65, MELD, and GBS scores to predict mortality and triage care appropriately. Core emergency medicine principles (resuscitate before you intubate, manage coagulopathy, and protect the airway) are stressed throughout. This case reinforces critical thinking, leadership under pressure, and a systematic approach to shock in the setting of GI bleeding and liver failure.

Peripheral tests of fetal well-being are aimed at testing a blood sample from the fetal scalp to determine fetal acidosis or to assess oxygenation saturation from fetal skin (fetal pulse oximetry, FPO) to be used as an adjunct to the CTG. They were introduced following the routine use of CTG without any prior randomized controlled trials (RCTs) or scientific research to confirm their effectiveness. Ignorance of basic fetal physiology resulted in the random grouping of features into categories without any scientific basis and an exponential increase in intrapartum c-sections. Swedish evidence has concluded that repetitive fetal blood sampling (FBS) doubled the emergency c-section rate and a UK multicentre study concluded that FBS increased the emergency c-section rate by ~60% without improving perinatal outcomes. The only RCT comparing FBS + CTG with CTG only failed to show any benefit. Systematic reviews on FPO, fetal ECG and fetal scalp stimulation also concluded these were ineffective. Clinicians must understand fetal physiology and the underlying pathophysiology behind observed features on the CTG trace, which make peripheral tests redundant.