Human Reproduction, Development & Ageing: Labour & Parturition

Topic = Labour & Parturition

Introduction to Labour & Parturition

• Labour: Refers to the 'work' done to deliver the fetus at the end of pregnancy.

• Parturition: An overarching term encompassing both the process of labour and the delivery of the fetus(es) and placenta(e).

• Stages of Labour: The entire process is divided into three distinct stages:

  1. Dilation Stage

  2. Expulsion Stage

  3. Placental Stage

Anatomy of the Uterus

• Uterus: The muscular organ where the fetus develops.

  • Fundus: The topmost, rounded part of the uterus.

  • Body (Corpus): The main part of the uterus.

  • Cervix: The lower, narrow part of the uterus that opens into the vagina.

    • Uterine cavity: The internal space within the body of the uterus.

    • Cervical canal: The channel through the cervix.

    • External os: The opening of the cervical canal into the vagina.

    • Internal os: The opening of the cervical canal into the uterine cavity.

Onset of Labour: The Underlying Causes

• The uterus is capable of expelling its contents before full term (e.g., miscarriage, premature labour), yet it usually remains quiescent during pregnancy and begins to contract at term.

• The precise reasons for the initiation of labour are not fully understood, but two major categories of effects are believed to lead to contractions for birth:

(i) Progressive Hormonal Changes

• Progesterone and Oestrogen: Both hormones progressively increase during pregnancy.

  • Around the $7^{th}$ month, oestrogen secretion continues to rise, while progesterone levels remain constant or may slightly decrease.

  • Progesterone inhibits uterine contractions, maintaining uterine quiescence to prevent premature expulsion of the fetus.

  • Oestrogen stimulates uterine contractions and its rising levels toward term contribute to uterine excitability.

• Oestrogen to Progesterone Ratio Hypothesis: It is hypothesised that an increase in this ratio towards the end of pregnancy contributes significantly to increased uterine contractility.

• Gap Junctions (Nexuses): Oestrogens are known to increase the number of gap junctions between smooth muscle cells in the myometrium (the muscular layer of the uterus). These junctions facilitate coordinated electrical activity and contraction among uterine muscle cells.

• Fetal Hormones and the Fetoplacental Endocrine System: Fetal hormones play a crucial role in orchestrating development and preparations for birth.

  • The fetoplacental endocrine system significantly influences maternal physiology.

  • Stress Hormones (Glucocorticoids): During pregnancy, maternal stress is associated with deleterious effects, potentially linked to glucocorticoids.

    • 11eta Hydroxysteroid Dehydrogenase (11eta-HSD-2): This enzyme, primarily in the placenta, converts active cortisol into inactive cortisone, thereby blocking the transport of active glucocorticoids from mother to fetus and limiting fetal exposure.

    • Despite potential negative effects of excessive antenatal stress, glucocorticoids are crucial for fetal development.

    • Functions of Fetal Adrenal Cortex Glucocorticosteroids (towards term):

      • Circulatory system: Increase in fetal cardiac output, peripheral resistance, and blood pressure.

      • Lung maturation: Induction of enzymes for surfactant synthesis, stimulation of alveolar water resorption, and central/local respiratory mechanisms.

      • Haematopoiesis: Promotes a 'switch' from fetal to adult haemoglobin production and shifts haematopoiesis to bone marrow and spleen.

      • Glucose storage and gluconeogenesis: Induction of enzyme systems in the liver and myocardium.

      • Insulin secretion: Regulates maturation of fetal pancreatic islets.

      • Synthesis of adrenaline: Induction of phenylethanolamine-N-methyl transferase in the adrenal medulla.

      • Production of thyroxine: May promote the conversion of T4 to T3

      • Maturation of salt:water ratio control: Activation of atrial natriuretic factor, stimulation of glomerular filtration rate, and regulation of $Na^+$ reabsorption; also involves DHEA.

      • Lactogenesis: Ductular-lobular-alveolar growth in pregnancy.

      • Parturition: Induction of placental oestrogen-synthesising enzymes and an increase in oestradiol precursor (dihydroepiandrosterone) concentrations (a function of the fetal zone).

• Oxytocin: Implicated as a key hormone in initiating and progressing labour.

  • As pregnancy nears full term, the maternal posterior pituitary releases more oxytocin, and uterine tissue produces more oxytocin receptors.

  • Mechanisms of Oxytocin's Action:

    1. Direct Stimulation: Directly stimulates the smooth muscle cells of the myometrium.

    2. Prostaglandin Production: Stimulates fetal membranes to produce prostaglandins, which act as synergists to oxytocin in promoting uterine contractions.

  • Evidence for Oxytocin's Role:

    1. Increased oxytocin secretion from the neurohypophysis during labour.

    2. The uterus becomes increasingly responsive to the same dose of oxytocin in later stages of pregnancy.

    3. Women who have had their pituitary gland removed can still deliver a fetus, but labour is often prolonged, suggesting other factors also play a role.

    4. In both animals and humans, stretching of the cervix causes the neurohypophysis to secrete greater amounts of oxytocin.

• Fetal Oxytocin and Cortisol: The fetal pituitary gland also secretes increasing amounts of oxytocin, which can stimulate uterine contractions. Additionally, fetal adrenal glands secrete large amounts of cortisol, which may also facilitate uterine contractions.

  • Clinical Observation: In an anencephalic fetus (a congenital condition involving defective brain development) with a defective adrenal cortex, pregnancy is often prolonged, and labour typically requires artificial induction.

• Prostaglandins: In addition to their synergistic role with oxytocin, prostaglandins may independently cause the onset of labour and increase uterine contractility.

  • Stimulating the cervix and separation of fetal membranes causes localised secretion of prostaglandins.

  • Prostaglandins are also found in the decidua (the modified endometrium of pregnancy) in late pregnancy.

(ii) Progressive Mechanical (Anatomical) Changes

• Uterine Stretching: Stretching of smooth muscle (myometrium) generally causes greater contractility.

  • Intermittent Stretch: The intermittent movements of the fetus within the uterus also contribute to muscle contractions.

  • Multiple Pregnancies: This mechanical stretching is a reason why twins and other multiple births are often born earlier than singletons, due to the greater distension of the uterus.

• Cervical Stretching and Membrane Rupture: Stretching of the cervix and the rupturing of the amniotic membranes (bag of waters) are known to often trigger the onset of labour.

The Positive Feedback Loop of Labour

• The onset and progression of labour, particularly the interplay of cervical stretching, oxytocin release, and uterine contractions, is considered a classic example of positive feedback.

  • Cervical stretching leads to increased oxytocin secretion from the neurohypophysis (posterior pituitary gland).

  • Oxytocin then further increases uterine contractions.

  • These stronger contractions push the baby further into the cervix, stretching it more, which in turn causes even stronger contractions and more oxytocin release. This cycle continues until the baby is delivered.

Inducing Labour

• Knowledge of hormonal and mechanical factors allows for labour induction in certain circumstances:

  • Reasons for Induction:

    • Pregnancy extending beyond the normal $40$ weeks ($ext{post-term}$ pregnancy, usually gestation).

    • Medical reasons where the mother or fetus is at risk (e.g., preeclampsia, placental abruption, fetal growth restriction).

    • Oligohydramnios (low amniotic fluid volume).

  • Note on Induction: Inducing labour essentially 'bypasses' the normal physiological processes (changes in progesterone/oestrogen levels, Braxton-Hicks contractions, spontaneous oxytocin release from mother and baby).

    • It is generally not recommended unless medically necessary due to the ongoing growth and maturation of fetal lungs, brain, and other organs.

  • Methods of Induction:

    • Amniotomy: Artificial rupture of the membranes (AROM).

    • Oxytocin Intravenous (IV) Drip: Administration of exogenous oxytocin to stimulate uterine contractions.

    • Prostaglandin Pessary/Gel: Insertion of a prostaglandin-containing pessary or gel into the vagina, near the cervix, to ripen the cervix and stimulate contractions.

    • Combination of Methods: Often a combination of these techniques is used.

  • Natural Methods for Stimulating Labour (Limited Evidence for Induction):

    • Nipple and Breast Stimulation: Can cause the production and release of oxytocin.

    • Sexual Intercourse: Prostaglandins found in semen can potentially help ripen the cervix.

    • Female Orgasm: Can cause uterine contractions and may stimulate labour.

Cephalopelvic Disproportion (CPD)

• Definition: A condition where the baby's head is too large to fit through the mother's pelvis.

• Evolutionary Context: The human pelvis, adapted for bipedal locomotion, has a relatively narrow outlet compared to primates like chimpanzees, creating a tighter fit for the larger human fetal head. This is a significant factor contributing to the pain and complexity of human birth.

Maternal Mortality

• Global Trends: Maternal mortality rates have significantly decreased over time globally, although some recent increases are debated.

• Regional Disparities: One region of the world (sub-Saharan Africa) still has stubbornly high maternal mortality rates. In 2020, mortality rates could be $980$ deaths per $100,000$ live births in some areas.

• Historical Context (England and Wales, $1850-1970$):

  • A significant drop in maternal mortality occurred from the $1930s$ onwards.

  • This decline is attributed to the widespread use of antibiotics (like penicillin and sulphonamides) for infection control and improved obstetric care, enhanced by national health services.

  • Currently, in less-developed regions, nearly 80 ext{%} of maternal deaths are due to direct obstetric causes reminiscent of the $19^{th}$ and early $20^{th}$ centuries in the UK, including haemorrhage, infection, complications from unsafe abortion, eclamptic convulsions, and obstructed labour.

• Maternal Mortality in the U.S.:

  • The U.S. maternal mortality rate (MMR) is inconsistent and widely considered an underestimate due to differing definitions and inconsistent data collection across states.

  • The World Health Organization (WHO) defines maternal deaths as occurring while pregnant or within $42$ days of pregnancy termination.

  • The Centers for Disease Control and Prevention (CDC) defines it as death while pregnant or within $1$ year of pregnancy termination.

  • Since $1987$, the MMR in the U.S. has doubled, with approximately $800$ maternal deaths annually.

  • Racial Disparities: Black women in the U.S. are $3$ to $4$ times more likely to die from pregnancy-related conditions (e.g., cardiac issues, haemorrhage) and experience serious complications, regardless of income, education, or geographical location. This suggests structural racism plays a role.

  • Causes of Death (U.S.): Leading causes include cardiovascular conditions (20-25 ext{%}), non-cardiovascular conditions, haemorrhage (10-15 ext{%}), hypertensive disorders (10-15 ext{%}), infection (5-10 ext{%}), and thrombotic pulmonary embolism (5-10 ext{%}).

  • Preventability: A significant portion of maternal deaths (e.g., $63$ overall, $70$ for haemorrhage, $68$ for cardiovascular/coronary conditions) are considered preventable through better understanding of contributing factors, educating patients, improving healthcare provider practices, and better communication among healthcare teams.

  • Contributing Factors: Poverty, lack of insurance, insufficient access to care, racism, discrimination, and excessive use of unnecessary interventions (episiotomy, C-sections) are associated with poor health outcomes.

Braxton-Hicks Contractions

• Nature: Throughout pregnancy, the uterus undergoes periodic weak, slow, rhythmic contractions known as Braxton-Hicks contractions.

• Timing: They begin early in pregnancy and strengthen late in pregnancy, often referred to as 'false labour'.

• Transition: These contractions can suddenly transform into the more powerful and organised contractions of true labour.

The Fetus's Role in Birth

• Fetal Position: In the $7^{th}$ month, the fetus typically turns into a head-down (vertex) position, which is the most common presentation for birth.

  • The head, acting as a wedge, helps to widen the cervix, vagina, and vulva during birth.

• Active vs. Passive Role: The fetus is often considered a 'passive player' whose expulsion is primarily achieved by the mother's uterine and abdominal muscle contractions.

  • However, the fetus is also thought to play a chemical role by sending chemical messages that signal when it is sufficiently developed and ready to be born, stimulating labour contractions.

First Stage of Labour: Dilation

• Definition: This stage begins with the onset of true labour contractions and ends when the cervix is fully dilated ($10$ cm).

• Signs & Symptoms of Onset:

  • Painful Contractions of the Uterus: Transition from Braxton-Hicks to regular, painful contractions. The uterus can be felt to 'harden' during each contraction, lasting about $45$ seconds. Intervals between initial contractions can range from $5$ to $20$ minutes.

  • Cervical Mucus (The 'Show'): Part of the mucous plug, which has sealed the fetus in the uterus, is expelled as the internal os pulls open. This discharge often contains some blood.

  • Shortening & Dilation of the Cervix: The cervix effaces (shortens) and dilates (opens).

  • Rupture of Membranes (for some): The 'water breaking' can occur at any point in labour but typically happens towards the end of the first stage.

• Contraction Progression:

  • Contractions increase in frequency and duration, becoming more painful.

  • By the end of the first stage, contractions may occur every $2-3$ minutes and last up to one minute.

• Uterine Circulation during Contractions: Blood circulation through the uterine wall is temporarily impeded during contractions. It is crucial that contractions are not continuous, as intervals allow placental circulation to be re-established, providing oxygen to the fetus and allowing the mother to recover.

• Neuroendocrine Reflex: Cervical stretching induces a neuroendocrine reflex through the spinal cord, hypothalamus, and neurohypophysis (posterior pituitary gland).

  • The neurohypophysis releases oxytocin, which is carried by the bloodstream to stimulate uterine muscles, both directly and through the action of prostaglandins.

  • This forms a positive feedback loop: cervical stretching, oxytocin secretion, uterine contraction, cervical stretching.