The relationship between childbirth and anaesthesia has a rich history. In January 1847, just 3 months after the first public demonstration of ether anaesthesia by William Morton in Boston, James Young Simpson in Scotland used ether to provide pain relief during childbirth. Within a few years, inhalation analgesia with chloroform during labour became acceptable in the UK, not only providing pain relief but also facilitating surgical caesarean delivery during obstructed labour. Today, obstetric anaesthesia extends far beyond the provision of analgesia and anaesthesia during childbirth. In countries where anaesthesiology collaborates actively with obstetricians, it has evolved into a subspecialty which contributes to high qualitative obstetric care for both healthy and high-risk obstetric patients. Pain relief methods reduce the burden of delivery, obstetric intensive care optimizes treatment for severely ill pregnant patients, and advanced anaesthesia techniques facilitate interventions crucial for successful pregnancies and optimal outcomes for both mother and child.

Obstetric anaesthesiologists aim to minimally interfere with the natural course of childbirth. Contemporary techniques for labour analgesia, refined over the years, are based on optimized techniques, delivery methods and drugs. This has resulted in minimal effects on clinical progress. Recent studies show that the incidence of instrumental deliveries is no longer increased, and the duration of the first and second stage of labour is only minimally affected.^1,2 Providing effective labour analgesia that ensures patient comfort and security while optimizing clinical outcomes and patient satisfaction requires a delicate anaesthesiologic balancing act. In the era of social media, effective communication with patients, partners and professionals should include strategies to educate, manage patients’ expectations and combat misinformation. Potential side effects of the various analgesia options should be discussed and, where possible, prevented.

Despite advancements, several important issues in obstetric anaesthesia remain insufficiently understood.

1. Neuraxial analgesia interference with the natural course of labour. Epidural and combined spinal-epidural analgesia are regarded as the optimal methods for managing labour pain, offering superior pain relief with minimal adverse effects and leading to greater maternal comfort and satisfaction compared to alternative techniques. However, the impact of neuraxial analgesia on uterine activity (UA) and contraction frequency remains poorly understood and challenging to measure directly. Historically, epidural analgesia (EDA) was associated with increased rates of instrumental delivery, more frequent use of oxytocin for labour augmentation, and a longer duration of the first and second stage of labour. Contemporary neuraxial techniques, novel drug delivery regimens and the use of lower concentrations of local anaesthetics and opioids have largely mitigated these effects, though an increased need for oxytocin augmentation persists without a clear causal relationship established. Direct measurements of UA following EDA initiation have yielded inconsistent results, with recent studies reporting decreased, unchanged, or enhanced UA.^3–5 These conflicting findings may be attributed to variations in clinical settings, EDA drug compositions, and UA measurement methods. Current obstetric practice mostly relies on external tocodynamometry (TOCO) for UA monitoring, despite its limitations in accuracy and reliability, as the more precise but invasive intrauterine pressure catheters (IUPC) have associated risks which preclude routine use. A recently developed non-invasive monitoring technique which measures the myometrial electrical activity, electrohysterography (EHG), shows promise in providing more accurate and reliable UA measurements compared to TOCO.^{6 7} EHG may provide a new opportunity to enhance our understanding of the relationship between EDA and UA, potentially leading to improved monitoring and management of labour.

2. Maternal fever during epidural analgesia. The mechanisms causing maternal fever in some patients during epidural analgesia are still incompletely understood, which prevents the development of preventive measures. Maternal fever, defined as a temperature³ 38°C, occurs in approximately 20% of women receiving epidural labour analgesia, with an increased incidence with a longer exposure to EDA. Similarly to infectious fever, there is an underlying primary inflammatory mechanism, with increased risks possibly related to a preexisting inflammatory state. Epidural-associated maternal fever (EAMF) is associated with adverse maternal outcomes such as increased duration of labour, oxytocin augmentation and instrumental delivery, but causality has not been established and unknown confounding factors may be present. ^{8 9} It is accompanied by a higher rate of maternal antibiotic administration, contributes to peripartum anxiety and discomfort and neonates are at increased risk of neonatal sepsis evaluations and neonatal intensive care admission due to fetal tachycardia and hyperthermia. Hyperthermia and inflammation can be independently or synergistically deleterious to the term fetus and neonate and higher perinatal morbidity is reported, including seizures and cerebral palsy.^9,10 The aetiology of EAMF is still unknown, but various underlying mechanisms have been proposed, with increasing evidence for a non-infectious inflammatory process triggered by an anaesthetic drug-induced metabolic dysfunction.^{9 11} Distinguishing EAMF from infectious causes of fever such as chorioamnionitis, bacterial or viral infections is vital to initiate adequate treatment wherever possible. Fever associated with EDA presents challenges in the clinical care of parturients. Improve our understanding of the underlying mechanisms may contribute to prevention and management and enhance safety of mothers and newborns.

3. Postdural puncture headache (PDPH). The positional headache which often develops after accidental dural puncture during epidural labour initiation and occasionally after spinal anaesthesia is not always self-limiting nor benign. The current accepted pathophysiology considers PDPH the result from loss of CSF through a breach of the dura mater into the epidural space causing loss of CSF volume, which cannot be replaced by CSF production. The resulting CSF hypovolemia leads to a reduced cushioning and downward displacement of the intracranial brain tissue, causing traction on pain-sensitive structures and a secondary vasodilation.^12–14 But many questions remain unresolved: why do some patients develop severe PDPH after an uneventful spinal anaesthesia with a thin atraumatic needle, while other patients never experience any symptoms after severe spinal CSF loss? In anaesthesia, PDPH is a clinical diagnosis, which according to the international classification of headache Disorders (ICHD-3) is the result of low CSF pressure.¹⁵ It shares symptoms with other orthostatic headache syndromes attributed to low CSF pressure such as spontaneous intracranial hypotension or PDPH after lumbar punctures. And while diagnostic procedures are more often applied in these manifestations of low CSF pressure, there is limited evidence of reduced CSF pressure, nor is radiologic evidence of CSF leakage present in the majority of SIH cases.¹⁶ The development of various non-invasive MRI techniques which allow imaging of the dynamics of intracranial fluid components, recently improved insights in CSF homeostasis and the role of the glymphatic system in cerebrospinal fluid dynamics and increased understanding of cerebral blood flow regulation all raise new questions.^17–21Anaesthesiologists should actively collaborate with neuroscientists and physiologists in future multidisciplinary basic research projects in order to improve our understanding of PDPH, contribute to preventive measures and optimize treatment strategies.

Conclusion Most clinical research focuses on optimizing obstetric anaesthesia provision and studies the incidences and circumstances under which undesirable side effects occur. Contemporary basic research in this field, apart from studies into the origins of maternal fever during epidural analgesia, is less developed and many preclinical studies originate from last century. Since then, new tools have been developed and new insights emerged. Obstetricians and anaesthesiologists should collaborate more actively with basic scientists to improve our understanding of labour physiology and how various interventions affect it. Similarly, clarifying the mechanisms underlying epidural-related fever and PDPH will contribute to reduced complications and improved performance of obstetric anaesthesiology.

As we continue to advance the field of obstetric anaesthesia, we must never forget the adage: ‘Primum non nocere’ (First, do no harm). This requires a thorough understanding of our interventions and their potential consequences. By addressing these important issues through rigorous basic and clinical research and interdisciplinary collaboration, we can further enhance the safety and efficacy of obstetric anaesthesia, ultimately improving outcomes for mothers and newborns alike.

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