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Summary Table

Feature	Detail
Risk Factors	Prior classical (vertical) cesarean section, prior uterine surgery (myomectomy), grand multiparity, oxytocin or prostaglandin use during labor, trial of labor after cesarean (TOLAC), uterine overdistension (macrosomia, polyhydramnios, multiple gestation), prior uterine perforation
Etiology	Full-thickness disruption of the uterine wall, most commonly along a prior surgical scar that fails under the stress of labor contractions
Patient Presentation	Sudden, severe abdominal pain during active labor; loss of previously palpable contractions; vaginal bleeding; signs of hypovolemic shock
Classic Physical Exam	Sudden cessation of contractions, regression of the fetal presenting part (fetal station moves up), easily palpable fetal parts through the maternal abdomen, signs of peritoneal irritation, hemodynamic instability (tachycardia, hypotension)
Key Diagnostic Results	Non-reassuring fetal heart tracing (prolonged bradycardia is the most common and earliest sign on monitoring), clinical diagnosis confirmed at emergency laparotomy
Management	Immediate emergency laparotomy with delivery of the fetus; repair of the uterine defect if feasible, or hysterectomy if the rupture is extensive; aggressive fluid resuscitation and blood product transfusion
Keywords	"Prior cesarean," "sudden tearing pain," "loss of fetal station," "fetal bradycardia during TOLAC," "fetal parts palpable through abdomen," "contractions suddenly stopped"

1. Pathophysiology

The uterus during labor generates powerful, repetitive contractile forces that place considerable mechanical stress on the myometrium. In a previously scarred uterus, the scar tissue lacks the elasticity and tensile strength of normal myometrium. As labor progresses and intrauterine pressure rises, the weakest point of the wall (the scar) may give way, resulting in a full-thickness tear through the entire uterine wall, including the serosa. This is the defining distinction between true uterine rupture and the more benign entity known as uterine dehiscence, where the scar separates but the serosa remains intact.

Once the wall is breached, the fetus, placenta, or both may be partially or completely extruded into the peritoneal cavity. This explains why fetal parts become easily palpable on abdominal examination and why the presenting part appears to "retreat" on vaginal exam. The loss of uterine wall integrity means the uterus can no longer generate coordinated contractions, which is why contractions abruptly cease.

The torn uterine vessels and exposed placental bed result in rapid hemorrhage into the peritoneal cavity. Because bleeding is largely intra-abdominal, visible vaginal bleeding may be deceptively minimal. The hemorrhage leads to maternal hypovolemic shock (tachycardia, hypotension, altered sensorium). Simultaneously, placental separation or compression of the umbilical cord causes an acute interruption of fetal oxygen supply, producing prolonged fetal bradycardia, which is often the earliest detectable sign on the fetal heart rate monitor before the mother becomes overtly symptomatic.

The use of uterotonic agents (oxytocin, misoprostol, dinoprostone) increases the risk because they amplify the force and frequency of contractions against a vulnerable scar. Prostaglandin E1 (misoprostol) is particularly dangerous in a scarred uterus and is contraindicated for labor induction in patients with a prior cesarean scar because it causes sustained, poorly controllable uterine tachysystole.

2. Classification and Clinical Manifestation

Type	Definition	Clinical Features
Complete Rupture	Full-thickness disruption of the myometrium and overlying serosa; communication between uterine and peritoneal cavities	Sudden severe abdominal pain, loss of contractions, fetal bradycardia, hemodynamic instability, fetal parts palpable abdominally, possible extrusion of fetus into peritoneal cavity
Incomplete Rupture (Dehiscence)	Separation of the prior scar with intact serosa; no direct peritoneal communication	Often asymptomatic or discovered incidentally at repeat cesarean; may present with mild pain or a "window" in the lower segment; fetal heart tracing usually remains reassuring; hemodynamically stable

By Location

Classification	Description
Lower segment rupture	Most common; occurs along a prior low-transverse cesarean scar; bleeding may be more contained in the retroperitoneal or broad ligament space
Upper segment (fundal) rupture	Occurs along a prior classical cesarean scar or myomectomy scar; tends to be more catastrophic with rapid intraperitoneal hemorrhage and higher rates of fetal extrusion
Unscarred uterine rupture	Rare; associated with grand multiparity, uterine anomalies, invasive placentation, or trauma; often presents atypically and is diagnosed late

3. Diagnostic Workup

Test	Role	Key Findings
Continuous electronic fetal monitoring	Best initial indicator	Prolonged fetal bradycardia (heart rate < 110 bpm for > 2 minutes); variable or late decelerations preceding the bradycardia
Intrauterine pressure catheter (if in place)	Supportive clue	Sudden loss of adequate uterine tone; inability to register contractions
Clinical assessment	Primary diagnostic method	Sudden pain, loss of station, palpable fetal parts, vaginal bleeding, maternal tachycardia and hypotension
Emergency laparotomy	Confirmatory / Gold Standard	Direct visualization of the uterine defect; this is both diagnostic and therapeutic
Bedside ultrasound	Adjunctive only	May show free intraperitoneal fluid, abnormal fetal lie, or empty uterine cavity; should never delay surgical intervention

Uterine rupture is fundamentally a clinical diagnosis made in the operating room. There is no laboratory test or imaging study that should be awaited before proceeding to surgery when the clinical picture is suggestive. The best initial clue in an exam vignette is a sudden, prolonged fetal bradycardia in a patient undergoing trial of labor after cesarean. This finding, especially when combined with maternal pain and loss of contractions, should immediately prompt the decision for emergency laparotomy.

Laboratory studies such as a complete blood count and type-and-crossmatch are obtained simultaneously with surgical preparation but never as a prerequisite for intervention. A falling hemoglobin confirms hemorrhage retrospectively but plays no role in the acute diagnostic process.

Bedside ultrasound can be helpful in equivocal scenarios (e.g., the patient is not in labor and presents with abdominal pain after recent uterine instrumentation), but in the classic labor-ward presentation, it should not delay the decision to operate. The key teaching point: the diagnosis of uterine rupture is clinical and the confirmatory step is laparotomy, not imaging.

4. Management and Treatment

Phase	Intervention	Details
Immediate stabilization	Large-bore IV access, crystalloid and blood product resuscitation	Two large-bore (16- or 18-gauge) IVs; type-and-crossmatch; activate massive transfusion protocol if needed; target MAP > 65 mmHg
Stop uterotonics	Discontinue oxytocin and any prostaglandin agents immediately	Continued stimulation worsens the tear and hemorrhage
Emergency cesarean delivery	Laparotomy with delivery of the fetus	Goal: delivery within minutes of the diagnosis; neonatal resuscitation team should be present
Uterine repair vs. hysterectomy	Determined intraoperatively based on extent of the defect	Small, clean lower-segment tears can be repaired primarily; extensive tears, uncontrollable hemorrhage, or involvement of the uterine vessels warrant hysterectomy
Postoperative care	ICU monitoring, continued transfusion, antibiotics, thromboprophylaxis	Broad-spectrum antibiotics (e.g., ampicillin-sulbactam 3 g IV every 6 hours); monitor for disseminated intravascular coagulopathy; serial hemoglobin checks

The single most important concept for the exam is that the next best step when uterine rupture is suspected is emergency laparotomy. There is no role for observation, tocolysis, or further workup. Every minute of delay worsens both maternal and fetal outcomes.

Upon entering the abdomen, the surgeon assesses the rupture site. If the defect is limited, involves the lower uterine segment along the prior scar line, and bleeding is controllable, a primary two-layer repair of the myometrium can be performed. This preserves the uterus for future pregnancies, although the patient must be counseled that all subsequent deliveries require a scheduled cesarean well before the onset of labor.

If the rupture extends into the broad ligament, involves major uterine vessels, or if hemorrhage cannot be controlled despite repair, hysterectomy is the definitive and life-saving intervention. In an exam scenario, do not hesitate to choose hysterectomy when the vignette describes uncontrollable bleeding or extensive tissue destruction.

Contraindications to future TOLAC: Any patient who has experienced a complete uterine rupture should be delivered by scheduled cesarean in all future pregnancies, ideally at 36 to 37 weeks of gestation before the onset of spontaneous labor.

5. Differential Diagnosis and Distractors

Differential Diagnosis	Why It Looks Similar	Key Discriminator
Placental abruption	Painful vaginal bleeding, fetal distress, uterine tenderness, hemodynamic instability	Abruption presents with a rigid, "board-like" uterus with persistent hypertonicity and often dark, non-clotting vaginal blood; in rupture, the uterus loses tone and contractions disappear; fetal parts may be palpable outside the uterine contour in rupture
Uterine dehiscence	Prior cesarean scar, possible mild discomfort at the scar site	Dehiscence is usually asymptomatic or found incidentally; the serosa remains intact, there is no hemodynamic instability, and the fetal heart tracing remains reassuring
Vasa previa with rupture	Sudden fetal bradycardia, vaginal bleeding	Vasa previa causes fetal hemorrhage (not maternal), so the mother remains hemodynamically stable; the bleeding is fetal blood, and a positive Apt test (alkali denaturation test) confirms fetal origin
Cord prolapse	Sudden prolonged fetal bradycardia during labor	The cord is palpable or visible at the cervical os on vaginal examination; the mother has no abdominal pain and remains hemodynamically normal
Amniotic fluid embolism	Sudden cardiovascular collapse during labor	Presents with acute dyspnea, hypoxia, and disseminated intravascular coagulopathy rather than abdominal pain; the fetal heart tracing may show distress, but the primary maternal findings are cardiorespiratory, not abdominal

6. Traps and High-Yield Pearls

The most common way students miss uterine rupture questions is by confusing it with placental abruption. Both present with pain, bleeding, and fetal distress during labor. The discriminating detail is the behavior of the uterus: abruption makes the uterus hypertonic and rigid, while rupture causes the uterus to lose tone and contractions to vanish. If the vignette says "contractions ceased" or "loss of uterine tone," that points directly to rupture.

A second trap involves fetal bradycardia during TOLAC. When a vignette places a patient with a prior cesarean in active labor and the fetal monitor suddenly shows prolonged bradycardia, the expected answer is uterine rupture until proven otherwise. Students who pick "cord compression" or "placental insufficiency" are choosing generic causes of bradycardia without recognizing the contextual clue of the scarred uterus.

Another tested concept: misoprostol is contraindicated for cervical ripening or labor induction in patients with a prior uterine scar. A vignette may describe a well-meaning provider using misoprostol in a patient with a prior cesarean, followed by catastrophic rupture. The teaching point is pharmacologic risk stratification in the scarred uterus.

Finally, remember that the answer to "what is the next best step" in a suspected uterine rupture is always emergency laparotomy. No ultrasound, no CT, no waiting for lab results. The confirmatory test and the treatment are the same procedure. Any answer choice that delays surgery is incorrect.

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