5.3 Third Stage Management: Active vs Physiological & Examination of Placenta/Membranes
Key Takeaways
The third stage of labour encompasses the interval from the birth of the baby to the complete expulsion of the placenta and fetal membranes, achieved through myometrial retraction and physiological living ligatures.
NICE NG235 active management uses oxytocin 10 IU IM, cord clamping no earlier than 1 minute and before 5 minutes, and controlled cord traction after separation.
Physiological management relies on endogenous oxytocin surges, skin-to-skin contact, gravity, and maternal effort without prophylactic uterotonics, completing within 60 minutes.
Clinical separation signs include lengthening of the cord, a sudden gush of blood, and a rising, firm, globular fundus; excessive bleeding (>500 mL) or 60-minute retention mandates conversion to active management.
Systematic placental and membrane examination safeguards against retained cotyledons, missing succenturiate lobes, and umbilical vessel abnormalities (confirming two arteries and one vein).
Third Stage Management: Active vs Physiological & Examination of Placenta/Membranes
The third stage of labour is the critical transitional interval from the complete birth of the baby to the complete expulsion of the placenta, fetal membranes, and blood clot. Although physiologically natural, the third stage presents the highest acute risk of maternal morbidity and mortality in the intrapartum period, primarily due to primary postpartum haemorrhage (PPH). Registered midwives must possess mastery of both physiological and active management pathways, recognize early signs of separation and haemorrhage, and perform meticulous anatomical examination of the secundines.
Physiological Mechanisms of the Third Stage of Labour
During pregnancy, maternal blood flows through the low-resistance placental bed at a rate of 600 to 800 mL per minute via 100 to 150 terminal spiral arterioles. With the birth of the neonate, the uterine cavity empties dramatically, triggering intense physiological mechanisms to arrest this substantial blood flow.
1. Myometrial Contraction, Retraction, and "Living Ligatures"
Immediately following the birth of the baby, the myometrium undergoes powerful contraction and profound retraction (brachystasis). Unlike skeletal muscle, myometrial smooth muscle fibres shorten permanently during contractions without relaxing back to their baseline length:
- The middle layer of the myometrium consists of a dense, interlacing figure-of-eight network of smooth muscle bundles.
- As these muscle fibres retract, they physically constrict, kink, and occlude the tortuous maternal spiral arterioles traversing them.
- These anatomical muscle bundles function as "living ligatures" (pinces anatomiques), providing the primary mechanism of physiological haemostasis. Secondary haemostasis follows via platelet aggregation and local fibrin clot formation.
2. Shearing of the Decidual Cleavage Plane
The surface area of the uterine cavity shrinks to approximately one-quarter of its pre-delivery size, reducing the placental implantation site from an area of roughly 20 cm in diameter to less than 10 cm. However, the placenta is a spongy, non-muscular organ lacking contractile elements:
- The placenta cannot reduce its surface area to match the contracting placental site.
- The placenta buckles, detaches, and shears away along the weakest anatomical layer: the spongy layer (stratum spongiosum) of the decidua basalis.
- The deep basal layer of the decidua remains attached to the myometrium to regenerate the endometrium postpartum, while the superficial compact and spongy layers are cast off with the placenta.
Modes of Placental Separation and Extrusion
MODES OF PLACENTAL SEPARATION
┌─────────────────────────────────┬─────────────────────────────────┐
│ SCHULTZE MECHANISM (~80%) │ MATTHEWS DUNCAN MECHANISM │
│ │ (~20%) │
├─────────────────────────────────┼─────────────────────────────────┤
│ • Separation begins centrally │ • Separation begins at margins │
│ • Retroplacental haematoma forms│ • Blood escapes continuously │
│ behind placenta, inverted sac │ • Placenta slides out sideways │
│ • Fetal surface emerges first │ • Maternal surface emerges first│
│ • Minimal blood loss visible │ • Higher visible blood loss │
│ until placenta delivered │ throughout separation │
└─────────────────────────────────┴─────────────────────────────────┘
- Schultze Mechanism (approx. 80%): Separation initiates centrally. Bleeding from sheared spiral arterioles accumulates behind the detached central zone, forming a retroplacental haematoma. The weight of this haematoma exerts downward traction, peeling the remainder of the placenta away from the myometrium. The placenta inverts into the amniotic sac and delivers with its glistening fetal surface presenting first, trailing the membranes behind it like an inverted umbrella. Blood loss is contained within the sac until final delivery.
- Matthews Duncan Mechanism (approx. 20%): Separation initiates at the inferior or lateral margin of the placenta. Because the margin is unsealed, maternal blood escapes immediately, presenting as a continuous dark trickle or gush throughout the third stage. The placenta slides down sideways through the birth canal and delivers with its rough maternal surface presenting first. This mechanism is often associated with slower separation and higher total blood loss.
Active Management of the Third Stage
Active management of the third stage of labour involves proactive clinical interventions designed to accelerate placental separation, ensure vigorous myometrial contraction, and minimize blood loss. NICE NG235 estimates that, compared with physiological management, active management results in about 120 fewer women per 1,000 having blood loss of 500 mL or more, and about 16 fewer per 1,000 having blood loss of 1 litre or more, although nausea and vomiting are more common.
Under NICE guideline NG235, active management is advised for all women, especially those with risk factors for PPH, and women at low risk who choose physiological management are supported in that choice after an informed discussion.
The Three Core Components of Active Management
1. Routine Prophylactic Uterotonic Administration
- First-Line Drug: Intramuscular injection of 10 IU oxytocin (Syntocinon) administered into the vastus lateralis of the maternal thigh.
- Timing: Administered with the delivery of the anterior shoulder or immediately following the complete birth of the baby (and prior to cord clamping).
- Alternative Agents: Intramuscular Syntometrine (combination of 5 IU oxytocin and 500 mcg ergometrine) is a potent uterotonic option, but causes significant maternal side effects including nausea, vomiting, and acute vasoconstriction. Syntometrine is strictly contraindicated in women with hypertension, pre-eclampsia, or cardiac disease due to the risk of hypertensive crisis and cerebrovascular accident.
2. Delayed Cord Clamping (DCC)
- Timing: NICE NG235 advises not clamping the cord earlier than 1 minute after birth, and clamping before 5 minutes in active management (a woman may request a longer delay).
- Physiological Benefits: DCC facilitates placental transfusion, transferring approximately 80 to 100 mL of autologous, oxygenated blood (equivalent to 20-30% of total fetal-placental blood volume) from the placenta into the neonate. This increases neonatal blood volume, prevents hypotension, improves neonatal ferritin stores and iron reserves up to 6 months of age, and may improve neurodevelopmental outcomes, without increasing maternal haemorrhage risk. A small increase in jaundice needing phototherapy has been reported in term babies, so jaundice is monitored.
- Exception: The cord is clamped earlier if there are concerns about cord integrity, or if the baby's heart rate is below 60 beats per minute and not getting faster, and resuscitation with an intact cord is not possible.
3. Controlled Cord Traction (CCT) via Brandt-Andrews Technique
- Following cord clamping and after confirming strong uterine contraction (induced by the administered oxytocin):
- The midwife applies a pair of artery forceps or cord clamp close to the maternal vulva.
- Suprapubic Counter-Traction: The midwife places the palmar surface of their non-dominant hand suprapubically above the symphysis pubis, pushing the uterine body upward and backward towards the maternal umbilicus.
- Cord Traction: Simultaneously, the dominant hand applies steady, gentle, continuous traction on the umbilical cord in a downward and backward direction following the anatomical axis of the pelvic inlet.
- As the placenta enters the vagina, traction is redirected upwards following the curve of Carus.
- As the placenta emerges from the introitus, the midwife holds it in cupped hands and twists it gently to form the trailing membranes into a rope-like strand, preventing membrane tearing.
- Expected Completion Time: Completed within 30 minutes.
Important
Counter-traction using the Brandt-Andrews technique is mandatory whenever applying cord traction. Pulling on the cord without suprapubic counter-traction against a relaxed or poorly contracted uterus can cause acute uterine inversion, an immediate life-threatening obstetric emergency resulting in profound neurogenic and hypovolaemic shock.
Physiological Management of the Third Stage
Physiological (expectant) management of the third stage supports natural maternal biological processes without pharmacological or manual intervention. It is an appropriate option for low-risk women who have experienced an uncomplicated pregnancy and physiological labour, and who make an informed choice after discussing the comparative risks and benefits.
Clinical Principles and Protocol
- No Prophylactic Uterotonics: No synthetic oxytocin or ergot alkaloids are administered.
- Deferred Cord Clamping: The umbilical cord is not clamped or cut until cord pulsations have completely ceased or until after the placenta has delivered.
- Endogenous Oxytocin Promotion: Immediate, uninterrupted skin-to-skin contact between mother and baby is maintained. Early breastfeeding or suckling at the breast is encouraged, which stimulates neurosensory pathways triggering endogenous hypothalamic oxytocin release.
- Maternal Effort and Upright Posture: The woman assumes an upright, squatting, or forward-leaning sitting posture, utilizing gravity to facilitate descent. The placenta is delivered entirely by maternal voluntary expulsive effort once clinical signs of separation appear.
- Expected Completion Time: Completed within 60 minutes.
Clinical Signs of Placental Separation
Before encouraging maternal expulsive efforts in physiological management—or before commencing controlled cord traction in active management—the midwife must verify that the placenta has physically separated from the uterine wall. Applying traction to an unseparated placenta leads to cord avulsion, severe haemorrhage, and uterine inversion.
| Sign of Separation | Clinical Finding | Underlying Biomechanical Cause |
|---|---|---|
| 1. Cord Lengthening | The umbilical cord visible at the vulva advances outward by 5 to 10 cm and does not retract when the uterus is elevated. | The placenta has detached from the fundal myometrium and dropped into the lower uterine segment and vaginal vault. |
| 2. Sudden Gush of Blood | A sudden trickle or gush of dark maternal blood (typically 30 to 60 mL) escapes from the introitus. | The retroplacental haematoma formed during central cleavage is released as the detached placenta passes through the cervix. |
| 3. Fundal Elevation and Globular Shape | The uterine fundus rises up in the maternal abdomen (often displaced to the right) and becomes small, firm, hard, and globular. | The empty upper uterine segment contracts and retracts tightly, perched atop the bulky placenta now occupying the lower segment. |
| 4. Negative Cord Retraction Test | The midwife places a hand suprapubically and gently lifts the uterine fundus upward; the umbilical cord does not move or retract inward. | If the placenta were still adherent to the fundus, lifting the uterus would pull the cord upward; lack of movement confirms complete detachment. |
Conversion from Physiological to Active Management
Midwives must maintain continuous clinical vigilance during physiological management. A low-risk woman undergoing physiological management must be immediately converted to active management if any of the following conversion triggers occur:
- Excessive Blood Loss: Any acute blood loss exceeding 500 mL, or any bleeding causing clinical concern, pallor, tachycardia, or maternal hemodynamic compromise.
- Prolonged Third Stage: Failure to deliver the placenta and membranes within 60 minutes of the baby's birth (diagnosing a retained placenta).
- Incomplete Separation: Persistent, continuous trickling of blood with failure of separation signs to manifest.
- Maternal Request: Maternal distress, fatigue, or request to expedite the completion of labour.
Conversion Action Steps
- Explain the clinical findings clearly to the woman and gain her informed consent.
- Administer an intramuscular injection of 10 IU oxytocin (Syntocinon) into the vastus lateralis.
- Palpate the abdomen to confirm myometrial contraction.
- Apply controlled cord traction with suprapubic counter-traction (Brandt-Andrews technique).
- Ensure maternal bladder emptying (intermittent catheterisation if a full bladder is obstructing descent).
- If the placenta remains undelivered despite active uterotonic administration and gentle traction, alert the obstetric multidisciplinary team and prepare for transfer to theatre for manual removal of placenta (MROP) under regional or general anaesthesia.
Examination of Placenta, Membranes, and Cord
A systematic, methodical examination of the placenta, fetal membranes, and umbilical cord must be conducted following every birth. This anatomical inspection is a core professional midwifery responsibility that verifies completeness and detects retained tissue, which represents the leading cause of secondary postpartum haemorrhage and puerperal endometritis.
SYSTEMATIC SECUNDINES EXAMINATION PROTOCOL
1. Maternal Surface (Basal Plate)
├── Wipe away blood clots and approximate all 15-20 cotyledons
├── Check for missing lobes, deep fissures, or ragged tissue loss
└── Note extensive infarction, calcification, or retroplacental clots
│
▼
2. Fetal Surface (Chorionic Plate)
├── Inspect glistening amnion and subamniotic vessel branching
└── TRACE ALL VESSELS TO THE MARGIN:
• Do vessels end abruptly at membrane edge? → SUSPECT SUCCENTURIATE LOBE
│
▼
3. Fetal Membranes (Amnion & Chorion)
├── Reconstruct amniotic sac by holding placenta by cord
├── Verify single circular exit hole through which baby passed
└── Ensure both layers (inner tough amnion, outer friable chorion) are complete
│
▼
4. Umbilical Cord Examination
├── Inspect cross-section for 3 VESSELS: 2 thick-walled arteries + 1 vein
├── Check insertion site: Central, Eccentric, Battledore, or Velamentous
└── Assess length, presence of true knots, and Wharton's jelly distribution
1. Maternal Surface (Basal Plate)
- Place the placenta flat on a clean, firm surface with the maternal surface facing upward.
- Gently wipe away adherent blood clots to expose the parenchyma.
- Inspect the 15 to 20 cotyledons (lobes) separated by shallow grooves (sulci).
- Carefully approximate (fit together) the cotyledons by curving the placenta in both hands. Verify that the lobes form a complete, continuous cobblestone surface without ragged gaps, missing fragments, or raw bleeding depressions.
- Note areas of calcification (normal gritty white plaques resulting from placental senescence at term) or infarction (firm, grey-white fibrotic patches).
2. Fetal Surface (Chorionic Plate)
- Invert the placenta so the fetal surface faces upward.
- Inspect the amnion, a smooth, glistening, translucent membrane covering the chorionic plate.
- Trace the chorionic blood vessels radiating outward from the cord insertion across the surface.
- Crucial Diagnostic Check for Succenturiate Lobe: Follow every fetal blood vessel to its terminal margin. Normal chorionic vessels branch into capillaries before reaching the placental rim. If a blood vessel crosses the placental margin into the membranes and terminates abruptly at a torn membrane edge, this confirms that an accessory or succenturiate placental lobe was attached in utero and has been torn away and retained within the uterine cavity. Immediate obstetric escalation is mandatory.
3. Fetal Membranes
- Hold the placenta suspended by the umbilical cord to reconstruct the fluid-filled gestational sac.
- Identify the inner amnion (smooth, tough, elastic; can be stripped back to the cord root) and the outer chorion (thick, friable, opaque; continuous with the placental margin).
- Examine the circular hole through which the infant emerged. Verify that both amnion and chorion are intact and that no substantial membrane fragments are missing.
4. Umbilical Cord Examination
- Vessel Count: Cut a clean cross-section of the umbilical cord approximately 2-3 cm from its placental insertion. Inspect the cut surface under direct light:
- Normal anatomy consists of three vessels: two small, thick-walled, muscular umbilical arteries (carrying deoxygenated blood from fetus to placenta) and one larger, thin-walled, compliant umbilical vein (carrying oxygenated, nutrient-rich blood from placenta to fetus), embedded in gelatinous Wharton's jelly.
- The presence of a single umbilical artery (two-vessel cord) occurs in approximately 0.5-1% of births and is associated with congenital renal, cardiovascular, and chromosomal abnormalities, warranting formal paediatric referral and neonatal clinical review.
- Cord Insertion: Document the anatomical insertion site:
- Central: Cord inserts directly into the middle of the chorionic plate.
- Eccentric: Inserts off-centre towards the margin.
- Battledore (Marginal): Cord inserts directly into the edge or margin of the placenta.
- Velamentous: Cord vessels insert into the fetal membranes away from the placental disc, traveling unprotected between amnion and chorion before reaching the placenta. Velamentous insertion carries a catastrophic risk of vasa praevia, where fetal vessels overlie the internal os and can rupture with membrane rupture, causing rapid fetal exsanguination.
- Cord Length & Pathology: Measure length (normal range 50 to 60 cm); inspect for true knots (differentiated from false knots caused by localized vascular varicosities), constriction, or haematomas.
What are the three essential components of active management of the third stage of labour according to national and international evidence-based standards?
Administration of 500 mL IV syntometrine bolus, immediate cord clamping within 10 seconds, and manual extraction of the placenta.
Withholding all uterotonics, waiting 60 minutes for spontaneous expulsion, and encouraging maternal pushing on all-fours.
Routine administration of 10 IU IM oxytocin, deferred cord clamping (no earlier than 1 minute and before 5 minutes), and controlled cord traction with suprapubic counter-traction.
Fundal massage commenced immediately prior to birth, cord clamping at 5 minutes, and manual removal under spinal anaesthesia.
A low-risk woman chose physiological management of the third stage. Sixty minutes have elapsed since the birth of the baby, no placental separation signs have occurred, and maternal blood loss has just reached 550 mL with ongoing active bleeding. What is the immediate, mandatory midwifery action?
Wait a further 30 minutes in an upright position and offer a warm herbal beverage.
Apply vigorous downward cord traction immediately without administering any uterotonic medication.
Perform an immediate episiotomy and apply fundal pressure to express the placenta.
Explain the findings, gain consent, convert to active management by administering 10 IU IM oxytocin, and escalate for obstetric support.
While performing a systematic examination of a newly delivered placenta, the midwife notes that several fetal blood vessels branch out across the chorionic plate and terminate abruptly at the torn edge of the membranes. What clinical complication does this finding strongly suggest?
Retained succenturiate (accessory) placental lobe in utero, requiring urgent obstetric exploration.
Normal anatomical variation known as battledore insertion with no clinical consequence.
Presence of a single umbilical artery associated with congenital fetal anomalies.
Amniotic band syndrome that caused premature rupture of the membranes.
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