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OG14.2 | Rupture Uterus — SDL Guide

Learning Objectives

• Classify uterine rupture as complete or incomplete, and by cause (scarred vs unscarred uterus)
• Describe the clinical features that distinguish impending rupture from established rupture
• Outline the immediate management including resuscitation and surgical options
• Discuss prevention strategies including VBAC counselling and antenatal risk stratification

INSTRUCTIONS

Uterine rupture is one of the most catastrophic obstetric emergencies — it carries a maternal mortality risk of up to 10% and a perinatal mortality of up to 80% in many settings if not managed within minutes. As obstetric practice increasingly involves women with previous caesarean section scars, understanding scar rupture — its subtle presentation, risk factors, and the evidence on trial of labour after CS — is a core clinical competency for every graduating doctor.

References

• DC Dutta's Textbook of Obstetrics, 9th edition, Chapter 36 — Rupture of the Uterus (textbook)
• Williams Obstetrics, 25th edition, Chapter 27 — Uterine Rupture (textbook)
• RCOG Green-top Guideline No. 45 — Birth After Previous Caesarean Birth (guideline)

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Version 2.0 | NMC CBUC 2024

Clinical Presentation of Uterine Rupture

Uterine rupture is the tearing of the uterine wall, partial or complete, occurring before or during labour. Its presentation depends on whether the rupture is complete (all layers, including visceral peritoneum) or incomplete (myometrium torn but serosa intact — also called dehiscence), and on whether it occurs on a scarred or unscarred uterus.

The classical presentation of complete rupture of an unscarred uterus — most often following neglected obstructed labour — is dramatic and unmistakable. There is sudden, acute, tearing abdominal pain at the height of a contraction, followed by an abrupt cessation of contractions as the uterine pressure is lost. The woman's condition rapidly deteriorates: she becomes pale, sweaty, tachycardic, and hypotensive as blood fills the peritoneal cavity. On abdominal examination, the uterine contour is lost — the fetus is no longer confined within a tense uterine globe but seems to lie freely under the abdominal wall. Fetal parts may be more superficially palpable than before. The fetal heart is absent in most complete ruptures because fetal exsanguination or placental separation is rapid. The previously noted Bandl's ring may have disappeared as the uterus relaxes after tearing.

By contrast, scar dehiscence of a lower-segment CS scar is frequently silent. The scar separates gradually and may only be discovered at the time of repeat CS as a window or thinned area. There is little or no haemorrhage (the visceral peritoneum contains the bleed), the fetal heart remains reassuring, and the clinical picture is much less dramatic. Between these extremes, incomplete scar rupture may present with scar tenderness (pain localised to the lower uterine segment just above the pubic symphysis), non-reassuring CTG patterns (variable or late decelerations), and haematuria from bladder involvement.

Clinical Signs of Uterine Rupture

Haematuria is a particularly important clinical sign: the urinary bladder lies immediately anterior to the lower uterine segment and is frequently injured during rupture of an anterior LUS scar, producing blood in the catheter bag. In any woman in labour with haematuria, scar tenderness, and a non-reassuring CTG, scar rupture must be the primary diagnosis until proven otherwise.

Pathophysiology and Causes

The pathophysiology of uterine rupture centres on the relationship between myometrial tensile strength and the forces acting upon it during labour. When the force exceeds the strength — whether because the wall is weakened by a scar, the force is pathologically elevated by obstruction or injudicious oxytocin, or the uterus is abnormally thin from grand multiparity — the wall tears.

In scarred-uterus rupture, the scar tissue that replaces normal myometrium after a previous CS lacks the elasticity of intact muscle. Under the mechanical stress of uterine contractions in labour, particularly at the transition from latent to active phase when intrauterine pressure rises sharply, the scar may separate. The lower-segment transverse scar generally gives way gradually and bleeds relatively slowly (the LUS is poorly vascularised); the classical vertical scar involves the vascular upper segment and bleeds rapidly. A previous myomectomy scar, especially if the uterine cavity was entered, carries a rupture risk comparable to a classical CS.

Unscarred-uterus rupture is almost invariably caused by neglected obstructed labour. The pathophysiology mirrors what was described in the obstructed labour module: the LUS is progressively stretched thinner until it tears, often at a point already weakened by ischaemia from prolonged head pressure. Grand multiparity contributes by causing myometrial thinning from repeated stretching. Injudicious use of oxytocin — particularly high-dose infusions in a multipara or in the presence of malpresentation or CPD — can drive the uterus to rupture by generating intrauterine pressures beyond what the myometrium can bear. Traumatic rupture (road traffic accidents, external version, difficult instrumental delivery) is less common.

Provided image

Type	Key cause	Typical timing	Completeness	Haemorrhage
LUS scar (previous LSCS)	Scar weakness under labour	Intrapartum, active phase	Often incomplete (dehiscence)	Variable — can be contained
Classical/vertical scar	Upper segment scar weakness	May rupture before labour	Usually complete	Severe — upper segment is vascular
Unscarred uterus	Neglected obstructed labour	Late intrapartum	Usually complete	Catastrophic
Injudicious oxytocin	Excessive uterine force	Intrapartum	Complete	Severe
Traumatic	External force / operative	Any time	Variable	Variable

Diagnosis

Uterine rupture is a clinical diagnosis — in the acute setting, there is neither time nor need for imaging. The diagnosis must be made on the history and examination within seconds to minutes, because the window for saving the mother and fetus is extremely narrow. Every clinician who manages labour must carry a mental checklist of the diagnostic features of rupture and run through it instantaneously whenever a woman in labour deteriorates acutely.

The diagnostic criteria that together establish the diagnosis are: (1) acute onset of abdominal pain that differs from contractions in character and persistence; (2) sudden cessation of contractions (the uterus can no longer generate pressure once its wall is breached); (3) maternal haemodynamic deterioration (tachycardia, hypotension, pallor) disproportionate to any visible bleeding — most haemorrhage is intraperitoneal; (4) change in uterine contour or palpation of fetal parts outside the expected uterine outline; (5) fetal heart rate changes (sudden severe bradycardia, absent FHR) as fetal compromise follows rupture rapidly; (6) haematuria, particularly in LUS scar rupture.

The most important differential is placental abruption — also causing sudden abdominal pain and fetal distress. Distinguishing features: in abruption, the uterus is typically woody-hard and contracted (haemorrhage is concealed within the uterus or decidua), not soft and relaxed as in rupture; contractions continue in abruption; the fetal outline remains within the uterine contour; and haemodynamic shock in abruption may be accompanied by vaginal bleeding. However, in practice the two emergencies can coexist, and laparotomy may be needed to determine the diagnosis definitively.

For scar surveillance in VBAC labour, the early warning signs are more subtle: uterine scar tenderness (pain on palpation over the LUS scar site, between contractions), non-reassuring CTG patterns — particularly variable decelerations or a prolonged bradycardia — and haematuria. Any one of these in a VBAC labour should prompt urgent clinical review and a low threshold to proceed to emergency CS.