Primary Arrest and Secondary Arrest in Labour

Definitions

In older classification (Friedman's curve), protraction = slow progress; arrest = complete cessation. Primary vs secondary arrest both fall under "arrest disorders."

ACOG Definition of Active Phase Arrest

Active phase arrest is defined as no progression in cervical dilation in patients who are ≥6 cm dilated with ruptured membranes despite:

• 4 hours of adequate uterine activity, OR
• 6 hours of inadequate uterine activity with oxytocin augmentation (Conditional Recommendation, Low-Quality Evidence)

The 3 P's — Causes (Etiology)

Distinguishing Primary vs Secondary Arrest

Diagnosis

1. Confirm active labour — cervix ≥6 cm with regular painful contractions
2. Confirm ruptured membranes (a prerequisite per ACOG criteria)
3. Assess uterine activity — via IUPC (intrauterine pressure catheter):
   • Adequate = ≥200 Montevideo units over 10 minutes
4. Evaluate the fetus — position, presentation, estimated fetal weight
5. Evaluate the pelvis — clinical pelvimetry, engagement

Management

Step 1: Identify and correct the cause

• Malposition → maternal repositioning, manual rotation, amnioinfusion if cord compression
• Hypotonic contractions → oxytocin augmentation (titrate to adequate uterine activity)
• Epidural-related → ensure adequate hydration, consider dose adjustment

Step 2: Wait (if safe)

• Allow adequate trial before declaring arrest (4–6 hours per ACOG, as above)
• Continuous fetal heart rate monitoring is mandatory

Step 3: Operative intervention

• Category 1 or 2 CTG abnormality → expedite delivery immediately
• Persistent arrest with adequate contractions → caesarean section
• If fully dilated with arrest of descent → consider instrumental delivery (ventouse/forceps) if criteria met

Key Points for Exams

• Primary arrest: active phase entered, never progresses → think structural/mechanical cause (CPD)
• Secondary arrest: was progressing, then stops → think power failure or positional issue
• ACOG 2014 redefined active phase start as 6 cm (not 4 cm per Friedman's original curve) — this has reduced the caesarean rate for "failure to progress"
• Do not diagnose arrest before adequate duration and adequate uterine activity have been ensured
• Arrest in the second stage (descent) is a separate entity — defined as no descent after 2–4 hours (depending on parity and epidural use)

Latent and Active Phase of Labour

First Stage — Overview

Latent Phase

• Begins with the onset of regular uterine contractions (as perceived by the mother)
• Ends when rapid cervical change begins
• Characterised by gradual, relatively slow cervical dilatation
• Cervix undergoes effacement (thinning) and softening alongside slow dilatation
• Clinically corresponds to approximately 0–6 cm dilatation (ACOG now places the latent/active transition at ~6 cm)

• Nulliparous: up to ~20 hours
• Multiparous: up to ~14 hours

Active Phase

• Begins when rapid cervical change initiates (≥6 cm by ACOG 2014 criteria)
• Ends at complete cervical dilatation (10 cm)
• Characterised by faster, progressive dilatation
• Minimum expected rate: ≥1 cm/hour (though this varies by parity and individual)

Comparison Table

Key Clinical Points

• The latent phase can be difficult to time precisely — onset of regular contractions is subjective
• Prolonged latent phase → options include therapeutic rest (morphine), oxytocin augmentation, or expectant management
• Active phase arrest (not the latent phase) is the primary indication for caesarean for failure to progress
• The Friedman curve (1950s) described an S-shaped cervicograph — the transition between phases was originally placed at 4 cm, but this has been revised upward to 6 cm by modern evidence

Hemoglobin Levels in Pregnancy

Physiological Basis

Normal & Threshold Hemoglobin Values by Trimester

The 2nd trimester has the lowest threshold (10.5 g/dL) because this is the nadir of haemodilution — plasma volume expansion peaks around 28–34 weeks.

Why Hb Dips in the 2nd Trimester?

• Plasma volume expansion begins early in the 1st trimester and peaks at 28–34 weeks
• Red cell mass expansion lags behind plasma expansion
• This mismatch is greatest in the 2nd trimester, explaining the lower Hb threshold
• By the 3rd trimester, RBC mass has caught up partially, so the threshold rises back to 11.0 g/dL

Rescreening Recommendation

• All pregnant patients should be rescreened for anaemia at 24–28 weeks (2nd trimester), regardless of 1st trimester results (Management of Pregnancy, p. 89)
• Initial screen is done at the first antenatal visit

WHO Classification of Anaemia in Pregnancy

Key Clinical Points

• Most common cause of anaemia in pregnancy: iron deficiency (microcytic, hypochromic)
• Second most common: folate deficiency (megaloblastic)
• Low Hb in 2nd/3rd trimester → check serum ferritin, peripheral smear, MCV
• Iron supplementation is recommended routinely in pregnancy in many guidelines (especially in regions with high prevalence)
• Severe anaemia (Hb <7 g/dL) in pregnancy is associated with preterm labour, low birth weight, maternal cardiac failure, and increased peripartum mortality

Cord Prolapse

Definition

Classification

Incidence

• Approximately 1 in 300–600 deliveries
• Higher in multiparous women and in the presence of predisposing factors

Risk Factors

• Malpresentation — footling breech (highest risk, ~5%), transverse/oblique lie, unstable lie
• Prematurity (small presenting part, poor fit)
• Polyhydramnios (cord floats freely)
• Multiple pregnancy (especially 2nd twin after delivery of 1st)
• Low birth weight / small for gestational age

• Artificial rupture of membranes (ARM) — especially when presenting part is high/unengaged
• External cephalic version (ECV)
• Insertion of intrauterine pressure catheter or fetal scalp electrode
• Manual rotation of fetal head
• Disimpaction of an engaged head

• Low-lying placenta
• Long umbilical cord

Pathophysiology

1. It is compressed between the presenting part and the bony pelvis
2. Umbilical blood flow is obstructed → acute fetal hypoxia
3. Vasospasm of cord vessels may occur on exposure to cold/air, worsening ischaemia
4. Without prompt delivery, this leads to fetal acidosis, brain damage, and death

Diagnosis

• Sudden severe variable or prolonged decelerations on CTG, especially after membrane rupture
• CTG shows bradycardia following ARM or spontaneous ROM

• Vaginal examination (VE) — cord felt as a pulsating structure in the vagina or at the cervix
• Cord may be visible at the introitus in overt cases

Immediate Management

Step 1 — Relieve cord compression immediately

• Manual elevation of presenting part: examiner's hand in vagina, lifts presenting part off the cord — must be maintained until delivery
• Maternal positioning:
  • Knee-chest (all-fours) position — most effective
  • Left lateral (Sims) position
  • Trendelenburg (head-down tilt)
• Bladder filling: instil 500–750 mL saline into the bladder via catheter to elevate presenting part — useful if transferring patient

Step 2 — Call for help

• Obstetrician, midwife, anaesthetist, neonatologist — full emergency team
• Activate emergency protocols / crash call

Step 3 — Oxygen

• High-flow oxygen to mother (though benefit is debated, commonly given)
• Stop oxytocin if running

Step 4 — Tocolysis (if time permits)

• Terbutaline 0.25 mg SC or salbutamol IV — to reduce contractions and relieve intermittent compression

Step 5 — Deliver the baby

Do NOT:

• Push the cord back (increases vasospasm and risk of further prolapse)
• Allow cord to dry out — keep it warm and moist if outside the vagina
• Remove the hand from the vagina until the baby is delivered

Fetal Monitoring During Management

• Continuous CTG or intermittent auscultation
• Cord pulsation can be checked manually to assess viability

Prognosis

Key Summary Points

• Cord prolapse = obstetric emergency, cord compressed → fetal hypoxia
• Most common predisposing factor = malpresentation (especially footling breech)
• Biggest iatrogenic risk = ARM with unengaged head
• First response = elevate presenting part manually + knee-chest position
• Definitive treatment = emergency caesarean (if not fully dilated)
• Never remove the hand from the vagina until delivery is complete

Why Polyhydramnios and Oligohydramnios Occur in TTTS

Background

The Core Mechanism

Step-by-Step Pathophysiology of Amniotic Fluid Imbalance

Donor Twin → Oligohydramnios

1. Net blood flows away from donor → chronic hypovolaemia
2. Hypovolaemia → low renal perfusion pressure
3. Activation of renin-angiotensin-aldosterone system (RAAS) → vasoconstriction, sodium & water retention
4. Despite RAAS activation, renal blood flow remains poor → reduced GFR
5. Urine output drops → less fluid entering the amniotic sac
6. Result: oligohydramnios (deepest vertical pocket <2 cm)
7. Severe oligohydramnios → fetus becomes "stuck twin" — plastered against the uterine wall with no room to move

Recipient Twin → Polyhydramnios

1. Net blood flows into recipient → chronic hypervolaemia
2. High cardiac preload → increased renal perfusion
3. High renal blood flow → increased GFR and urine output
4. Additionally, recipient produces excess atrial natriuretic peptide (ANP) due to cardiac volume overload → further promotes diuresis
5. Urine output markedly increases → excess fluid in amniotic sac
6. Result: polyhydramnios (deepest vertical pocket >8 cm)
7. Progressive polyhydramnios → uterine overdistension → risk of preterm labour

The "Stuck Twin" Phenomenon

• The membrane wraps tightly around it
• On ultrasound, it appears "stuck" to the uterine wall
• The recipient's sac is grossly enlarged by polyhydramnios

Summary Diagram (Conceptual)

Placental AV anastomosis (unbalanced)
         ↓
Blood flows: DONOR → RECIPIENT
         ↓                    ↓
  Hypovolaemia          Hypervolaemia
         ↓                    ↓
  ↓ Renal flow           ↑ Renal flow
         ↓                    ↓
  ↓ Urine output         ↑ Urine output
         ↓                    ↓
  OLIGOHYDRAMNIOS       POLYHYDRAMNIOS
  ("Stuck twin")        (Uterine overdistension)

Quintero Staging (Based on Amniotic Fluid)

Key Points

• Oligohydramnios in donor = reduced urine output from hypovolaemia and poor renal perfusion
• Polyhydramnios in recipient = increased urine output from hypervolaemia and high renal perfusion + ANP-driven diuresis
• The amniotic fluid discordance is the diagnostic hallmark of TTTS on ultrasound
• Treatment: selective laser photocoagulation of communicating placental vessels (SLPCV) — ablates the anastomoses and equalises flow (Targeted Neonatal Echocardiography, p. 24)
• Untreated TTTS carries mortality approaching 100% in one or both fetuses