Plan the management of a patient with uterine rupture

In one line

Uterine rupture is a full-thickness breach of the uterine wall threatening exsanguination of the mother and acute hypoxia of the fetus; survival is governed almost entirely by decision-to-delivery time, so the management plan is recognition → resuscitate → deliver immediately (laparotomy) → arrest haemorrhage → make a definitive repair-versus-hysterectomy decision in theatre.

This chapter assumes the mechanism, classification (complete vs dehiscence/window) and risk-factor groundwork from the Intermediate course — see uterine rupture basics and instrumental delivery — and concentrates on the consultant-level plan, the appraisal of who may labour, and the unresolved controversies.

Subtypes — why the distinction changes the plan

The word "rupture" hides four clinically distinct lesions, and the management diverges at the first branch point. The basic complete-vs-dehiscence split is covered in Intermediate; the consultant-level question is which one you are dealing with and what each one demands.

• Scar dehiscence (the "window"). A bloodless separation of the myometrium of a prior scar with the visceral peritoneum/serosa intact, the fetus and membranes still contained, and no significant haemorrhage. This is usually an incidental finding at repeat caesarean or a quiet ultrasound thinning — it is not an emergency, does not cause the rupture triad, and in an asymptomatic woman at elective caesarean needs only inspection and a clean two-layer closure. Conflating a window with a rupture is the commonest classification error and leads to over-treatment; the reverse error — dismissing pain in a labouring scarred woman as "just a window" — is the lethal one.
• Complete rupture of a scarred uterus (lower-segment). Full-thickness disruption usually along the prior transverse lower-segment scar, with communication into the peritoneal cavity. Because the lower segment is relatively avascular and the tear follows a predictable transverse line, haemorrhage is often more controllable and the tissue planes are cleaner — this is the subtype most amenable to primary repair. It is also the subtype where the herald is a subtle CTG change rather than collapse, because the scar gives way before the great vessels are reached.
• Complete rupture of an unscarred uterus. A different disease. The tear is unpredictable in site and shape — typically a vertical or stellate fundal/lower-segment tear driven by obstructed labour or uterotonic over-stimulation — frequently extends laterally into the broad ligament and uterine vessels, and presents later and more catastrophically (collapse, fetal extrusion, massive haemoperitoneum). Devitalised, ragged edges and vascular extension make this the subtype that most often forces hysterectomy. In SA district practice this is the high-parity, under-monitored, obstructed-labour patient — the rupture you must actively look for because there is no scar to "blame".
• Atypical sites — classical/vertical scar, posterior, and lateral/cervical extensions. A prior classical or inverted-T/J upper-segment scar ruptures higher, earlier, and often before labour through the contractile fundus, where bleeding is brisk and repair is harder; this is why a classical scar prohibits labour outright. Lateral and cervical/vaginal extensions threaten the uterine artery, ureter and bladder and convert a "simple" repair into vascular surgery. Identifying the subtype is what lets you anticipate the operative difficulty before you open.

The mechanism→consequence links are: a scarred lower-segment tear → cleaner plane, controllable bleed, repair feasible; an unscarred or lateral tear → vascular/ureteric jeopardy, devitalised tissue, hysterectomy more likely; a classical/posterior tear → early, pre-labour, brisk — surveillance and prohibition of labour, not detection in labour, is the only defence.

Assessment

Rupture is a clinical diagnosis confirmed at laparotomy; do not wait for imaging. The classic triad (pain, bleeding, non-reassuring fetal status) is unreliable, so weight the early, sensitive signs.

• Fetal heart rate is the most consistent herald. An abnormal CTG — typically prolonged or recurrent deceleration / bradycardia — precedes or accompanies most ruptures and is present in the majority of cases. New, atypical variable or late decelerations in a woman labouring with a scar should be read as rupture until disproved.
• Maternal signs: scar/abdominal pain breaking through effective regional analgesia, cessation of previously efficient contractions, vaginal bleeding, haematuria, loss of station / receding presenting part, palpable fetal parts abdominally, and signs of hypovolaemia (tachycardia, hypotension, restlessness). Shoulder-tip pain signals haemoperitoneum.
• In an unscarred uterus (multiparity, obstructed labour, injudicious oxytocin, prior perforation/myomectomy) rupture is often more catastrophic and later-recognised — a key SA reality in high-parity, under-monitored district labour.
• Investigations are resuscitative, not diagnostic: group-and-crossmatch (≥4 units), FBC, coagulation/fibrinogen, U&E — but never let a request for a scan or bloods delay laparotomy when the picture fits.

The advanced read — atypical presentations and the judgement calls

The basic triad is covered at Intermediate; the harder cases are the ones that do not present classically.

• The silent epidural dehiscence. Under a well-functioning epidural, a labouring scarred uterus can rupture with no maternal pain — the only sign is the CTG and a rising baseline maternal pulse. A "top-up that doesn't work" or breakthrough scar pain through a previously perfect block is a red flag, not an analgesia failure. The lesson: in a scarred labour, the CTG plus the maternal heart-rate trend outrank the pain history.
• The postpartum rupture. Rupture can declare after a successful VBAC delivery — persistent lower-abdominal pain, ongoing fresh bleeding with a contracted fundus, unexplained tachycardia, or a fall in haemoglobin not explained by the visible loss. Do not anchor on uterine atony; a contracted uterus that keeps bleeding, or a woman who is "shocked out of proportion" to the measured loss, needs the abdomen examined and imaged or explored.
• Loss of station as a hard sign. A presenting part that recedes on vaginal examination (the fetus retracting into the abdomen) is close to pathognomonic and trumps a "reassuring" cervix.
• Severity stratification at the bedside. The variables that predict death and hysterectomy — and therefore the urgency and the call for blood and a second surgeon — are complete (vs dehiscence) extent, fetal extrusion/placental separation, lateral/broad-ligament extension, unscarred uterus, and time elapsed since the FHR change. A woman with a receding presentation, abdominal fetal parts and a fetal bradycardia is at the catastrophic end and should be in theatre while you are still drawing blood; a quiet window found at elective section is at the benign end.
• Where investigations mislead. A bedside ultrasound may show free fluid or an empty uterus with the fetus in the abdomen, but a normal scan never excludes rupture and the time spent obtaining it is the time the baby does not have. CTG is sensitive but not specific — the same prolonged deceleration occurs in abruption and cord prolapse, which is why the response (immediate delivery) is identical and you do not need to discriminate them before acting. Haematuria points to bladder/anterior-segment involvement but its absence proves nothing.

Investigations

There is no diagnostic test to wait for. The investigations earn their place by driving resuscitation and the surgical plan, not by confirming the diagnosis — that is made with a knife.