Obstetric Emergencies

1. Cord Prolapse (Umbilical Cord Prolapse)

Definition

Causes / Predisposing Factors

• Malpresentations - breech (especially incomplete/footling), transverse lie, shoulder, compound presentations; these account for ~50% of all cord prolapse cases
• High presenting part that fails to fill the birth canal (polyhydramnios, prematurity, small fetus)
• Artificial rupture of membranes before the presenting part is engaged
• Multiparity - lax lower uterine segment
• Long cord or low-lying cord insertion
• Interventions - manual rotation, internal version, application of forceps or scalp electrode

Clinical Features

• Cord visible at the introitus or palpable on vaginal examination as a soft, pulsating structure
• Sudden fetal bradycardia or prolonged decelerations on CTG - the hallmark sign
• Fetal heart rate changes are often the first clue
• Diagnosis also possible by Doppler ultrasonography

Complications

• Fetal asphyxia / hypoxia from cord compression - the primary danger
• Fetal death - perinatal mortality estimated at just under 10%
• Mortality is higher for out-of-hospital cord prolapse vs. monitored hospital setting
• Risk of permanent neurological injury from prolonged hypoxia

Management Principles

• Place mother in knee-chest or Trendelenburg position
• Manually elevate the presenting part off the cord - keep hand in vagina during transport
• Do NOT attempt to replace the cord (avoid vasospasm from handling)
• Emergency cesarean section is the delivery of choice for a viable fetus
• The 30-minute window from diagnosis to delivery is critical for outcome

2. Uterine Inversion

Definition

Causes / Predisposing Factors

• Excessive fundal pressure during the third stage of labor (Credé maneuver done incorrectly)
• Forceful cord traction before placental separation, especially with a fundally-attached placenta
• Placenta accreta (abnormal placentation preventing normal separation)
• Connective tissue disorders - uterine structural weakness
• Uterine abnormalities (bicornuate uterus, septate uterus)
• Magnesium sulfate use in the antepartum period (uterine relaxation)
• Primiparity - less experienced uterine musculature

Clinical Features

• Sudden, severe lower abdominal pain following delivery of the placenta
• Profuse postpartum hemorrhage - can be massive and immediately life-threatening
• Hemodynamic instability - hypotension, tachycardia, shock disproportionate to visible blood loss (due to neurogenic component from traction on uterine ligaments)
• Abdominal examination: absence of the uterine corpus where it would normally be palpated
• The inverted fundus may be visualized at the cervical os or bulging from the introitus as a bluish-red mass
• Ultrasound may assist if diagnosis is unclear

Complications

• Hemorrhagic shock - maternal mortality up to 15% if untreated
• Neurogenic shock - stimulation of peritoneal nerve endings
• DIC from massive hemorrhage
• Uterine perforation during manual repositioning
• Recurrence in subsequent pregnancies

Management Principles

• Withhold all uterotonic agents immediately (oxytocin, ergometrine, prostaglandins - prevent cervical ring formation)
• Aggressive fluid resuscitation and blood transfusion
• Manual replacement (Johnson's maneuver) - push fundus back through the introitus with a closed fist; do NOT remove the placenta until after repositioning
• If cervical ring prevents repositioning: tocolytics - terbutaline (0.25 mg IV/SC) or magnesium sulfate (4-6 g IV over 15-20 min)
• Rüsch balloon catheter can be used post-repositioning to maintain position
• If all medical measures fail: surgical repair under halogenated anesthesia

3. Amniotic Fluid Embolism (AFE)

Definition

Causes / Pathophysiology

• Breach of the feto-maternal barrier allowing amniotic fluid entry into uterine venous sinuses, most commonly during labor, delivery, or uterine manipulation
• 78% of cases had ruptured membranes; many occurred after intrauterine procedures
• The exact mechanism remains debated - it is not purely embolic but resembles an anaphylactoid/complement activation cascade
• Mediators involved: leukotrienes, arachidonic acid metabolites (especially prostaglandin F2α), complement system (C1-esterase inhibitor levels depressed)
• Hemodynamic response is biphasic: initial pulmonary hypertension → then left ventricular failure
• Also termed "anaphylactoid syndrome of pregnancy" by Clark et al.

Clinical Features

1. Hemodynamic collapse - sudden hypotension, cardiac arrest
2. Acute hypoxia - respiratory distress, cyanosis, pulmonary edema
3. DIC / coagulopathy - uncontrolled hemorrhage

• Occurs during labor, delivery, or within 48 hours postpartum
• Seizures (may mimic eclampsia)
• Fetal compromise / fetal distress
• CXR/CT: bilateral parenchymal opacities (ARDS pattern)
• Pathology: fetal squamous cells visible in maternal pulmonary capillaries at autopsy

Complications

• Maternal mortality historically up to 86%; more recent data suggest 11-43%; accounts for ~4.9% of all maternal deaths
• Fetal demise in ~40% of cases
• ARDS and multi-organ failure
• Neurological damage from hypoxic arrest
• Major organ thrombosis (risk with recombinant factor VIIa)
• Sheehan syndrome (pituitary infarction from hypovolemic shock)

Management Principles

• Supportive treatment - early intubation, 100% O2, PEEP
• High-quality CPR for cardiac arrest
• If before delivery: emergency cesarean section to facilitate maternal resuscitation
• Vasopressors, inotropes, pulmonary vasodilators
• Massive transfusion: packed RBCs, FFP, platelets in 1:1:1 ratio
• TEG/ROTEM guided coagulation management
• Consider ECMO for refractory arrest or severe ventricular dysfunction
• Avoid recombinant factor VIIa (associated with worse outcomes)

4. Obstetric Shock

Definition

Causes / Types

Clinical Features

• Hemorrhagic shock (most common): tachycardia, hypotension, pallor, cold clammy extremities, decreased urine output, altered consciousness; blood loss >1,500 mL typically required to see hypotension due to physiological compensation of pregnancy
• Septic shock: fever/hypothermia, warm peripheries initially, then circulatory collapse, signs of infection
• Neurogenic shock (uterine inversion): hypotension and bradycardia disproportionate to apparent blood loss
• AFE-related shock: sudden cardiovascular collapse with coagulopathy

Complications

• Acute kidney injury (from prolonged hypoperfusion)
• DIC - consumption of clotting factors from massive hemorrhage or AFE
• ARDS
• Sheehan syndrome - pituitary necrosis from sustained hypovolemic shock
• Multi-organ failure
• Fetal compromise and death
• Maternal death - hemorrhage is the leading direct cause of maternal mortality worldwide

Management Principles

• Identify and treat the underlying cause simultaneously with resuscitation
• Two large-bore IV lines, aggressive crystalloid + blood product resuscitation (massive transfusion protocol 1:1:1)
• Control hemorrhage: uterotonic agents (oxytocin), surgical interventions (B-Lynch suture, uterine artery ligation, hysterectomy)
• Vasopressors for septic/neurogenic shock after adequate volume resuscitation
• Fetal monitoring and delivery when appropriate

5. Uterine Rupture

Definition

Causes / Predisposing Factors

• Previous cesarean section - the most important risk factor; occurs in ~1% of VBAC (vaginal birth after cesarean) attempts; risk increases with multiple prior cesarean sections
• Single-layer uterine closure at previous C-section (higher risk than double-layer)
• Labor augmentation/induction - oxytocin and prostaglandins increase risk in a scarred uterus
• Grand multiparity - weakened uterine musculature
• Uterine anomalies - bicornuate uterus
• Connective tissue disorders
• Fetal macrosomia (>3,500 g increases risk during VBAC)
• Trauma - motor vehicle accidents, blunt abdominal trauma
• Abnormal placentation (placenta accreta)
• Obstructed labor - especially in neglected labor in resource-limited settings

Clinical Features

• Abrupt, severe abdominal pain - often described as a "tearing" sensation, or conversely, sudden relief of contractions (as uterus decompresses)
• Cessation of uterine contractions
• Fetal heart rate abnormalities - prolonged deceleration or bradycardia (most reliable sign of fetal extrusion); fetal distress on CTG
• Vaginal bleeding (may be minimal if blood pools intraperitoneal)
• Loss of fetal station - the presenting part rises back up in the pelvis or becomes non-palpable
• Palpable uterine defect on abdominal examination
• Signs of hemorrhagic shock in severe cases
• May be occult - some ruptures are painless, found only at repeat cesarean

Complications

• Maternal hemorrhagic shock - significant hemorrhage in ~1/3 of cases
• Maternal death - rare but possible
• Perinatal mortality - <1% with minimal fetal extrusion, 10-20% with complete extrusion
• Bladder/urinary tract injury from extension of rupture
• Hysterectomy may be necessary (loss of future fertility)
• DIC

Management Principles

• Immediate emergency cesarean section - ACOG identifies a 30-minute window to maximize fetal outcome
• Do NOT administer uterotonic agents (contraindicated - may extend rupture)
• Surgical repair vs. hysterectomy depending on extent and fertility wishes
• Blood transfusion and management of hemorrhagic shock

Summary Comparison Table

• Rosen's Emergency Medicine: Concepts and Clinical Practice (9e), pp. 3419-3094
• Tintinalli's Emergency Medicine: A Comprehensive Study Guide, pp. 2064-2153
• Murray & Nadel's Textbook of Respiratory Medicine (2-vol), pp. 2255-2290
• Creasy & Resnik's Maternal-Fetal Medicine: Principles and Practice, pp. 6137-6146