Uterine inversion, uterine rupture and Sheehan syndrome

• Uterine inversion is a rare, sudden event in which the uterus turns inside out after delivery, the fundus (the dome of the womb) descending through or beyond the cervix. It causes concealed and revealed bleeding, a soft empty pelvis on abdominal palpation, and shock that is far out of proportion to the visible loss.
• Its immediate management is to replace the uterus, not to pull on the placenta: call senior help, resuscitate, leave an attached placenta in place, replace the uterus by hand (and, if that fails, by hydrostatic pressure or at laparotomy), then give uterotonics and check for trauma.
• Uterine rupture is a tear through the wall of the uterus, most often through a previous scar, that threatens both mother and baby. The warning pattern is sudden severe pain or a cessation of contractions, loss of the baby's heart rate pattern with severe fetal bradycardia, vaginal bleeding and maternal shock; the management is immediate laparotomy, delivery and repair or hysterectomy.
• Both are causes of the "Trauma" T of postpartum haemorrhage, and both are indications for delivery in a consultant-led unit.
• Sheehan syndrome is postpartum pituitary necrosis after severe hypotension or shock around delivery. It presents acutely with headache, confusion or coma, hypoglycaemia, hyponatraemia and failure to lactate, or, more often years later, with amenorrhoea, inability to breastfeed, cold intolerance and sparse body hair.
• Sheehan syndrome is treated by replacing the missing hormones; the order matters: treat adrenal failure first with glucocorticoids, then thyroid hormone, then gonadal steroids and, where available, growth hormone.
• Febrile illness after birth is usually a puerperal infection (most often endometritis, wound infection or urinary tract infection) and needs the source found and treated, alongside the recognition that endometritis after a delivery complicated by inversion or rupture carries a higher risk than after an uncomplicated birth.

By the end of this page you should be able to:

1. Recognise uterine inversion and uterine rupture at the bedside and distinguish them from uterine atony and retained placenta.
2. Give the immediate, step-by-step management of uterine inversion and of suspected uterine rupture.
3. Explain why a bleeding uterine inversion must be replaced before anything else, and why an attached placenta is not removed first.
4. State the diagnostic criteria, acute presentation and hormone replacement sequence for Sheehan syndrome.
5. Interpret the investigations used in Sheehan syndrome, including the cortisol cut-off and the imaging.
6. Place inversion, rupture and Sheehan syndrome inside the prevention and management pathways of RCOG, ACOG, NICE and WHO postpartum haemorrhage guidance.
7. Compare postpartum collapse from inversion, rupture, atony and coagulopathy using a feature-by-feature table.
8. Outline the long-term follow-up of Sheehan syndrome and the comorbidities that persist despite replacement.

• Uterine inversion and uterine rupture are both causes of the "Trauma" T of postpartum haemorrhage, alongside genital tract tears and perineal haematomas. ^{[1] [5]}
• Sheehan syndrome is listed by ACOG among the serious downstream sequelae of haemorrhagic shock, alongside disseminated intravascular coagulation, renal failure and loss of fertility. ^[2]
• NICE flags both a previous uterine rupture and a previous postpartum haemorrhage requiring additional treatment or blood transfusion as risk factors that warrant delivery in an obstetric unit. ^[3]

Uterine inversion is rare and most series describe it as an intrapartum or immediate postpartum emergency. Risk factors described in major haemorrhage guidance and reviews include uterine atony, fundal placental implantation, a short umbilical cord, excessive traction on the cord before the placenta separates, prolonged third stage of labour, sudden increases in intra-abdominal pressure, grand multiparity, and previous uterine inversion. ^{[1] [5]}

Uterine rupture is most strongly associated with a previous uterine scar. RCOG guidance, NICE intrapartum care and ACOG all treat a planned vaginal birth after a single previous lower segment caesarean delivery as a clinically safe option for most women, provided that induction or augmentation is undertaken with caution and that the woman is counselled about the small risk of rupture and monitored in labour. ^{[3] [7]} Other risk factors are a classical or vertical uterine scar, previous rupture, high parity, obstructed labour, transverse lie, malpresentation, multiple pregnancy, placenta accreta spectrum, instrumental delivery, and injudicious use of oxytocin. ^{[1] [3] [5]}

There is a consensus among NICE, RCOG and ACOG that planned vaginal birth after one previous lower segment caesarean delivery is safe for most women, but the scar must be respected. ^{[3] [7]}

Sheehan syndrome still occurs, particularly where severe postpartum haemorrhage is not prevented or treated quickly; ACOG still lists pituitary necrosis as a recognised sequela of haemorrhage. ^[2] In the modern series reviewed by Karaca and Kelestimur, diagnosis is commonly delayed by years because the early features (failure to lactate, amenorrhoea, tiredness) are attributed to other causes. ^[6]

• The underlying risk is vascular: the pituitary gland is markedly enlarged in the third trimester and relies on blood flow that is easily compromised when blood pressure falls. ^[6]
• Other contributing factors include a small sella turcica, vasospasm, thrombosis, coagulation disorders, and the consumptive coagulopathy of severe haemorrhage. ^[6]
• Autoimmunity appears to play a part in the later deterioration of pituitary function. ^[6]

The acute event starts when part of the fundus, often where the placenta is attached, invaginates into the uterine cavity and is forced downwards. The placenta then remains attached and its vessels stay open, so bleeding continues into the cavity and around the inverted mass. The ligaments that normally support the uterus are pulled taut and then invert, the myometrium atrophies and cannot contract, and the sudden pull on the pelvic autonomic nerves and the abrupt shift of blood into the uterine vasculature produce a shock that is disproportionate to the visible loss. Hypovolaemia comes both from blood loss and from the sequestration of blood in the dilated uterine vessels. ^{[1] [5]}

Rupture occurs when intrauterine pressure exceeds the tensile strength of the myometrium at its weakest point, which is very often a previous scar. In obstructed labour the pressure can rise enough to tear even an unscarred uterus. Once the tear extends, placental separation and fetal extrusion occur, bleeding is uncontrolled because the uterine contraction that would compress the vessels is lost at the tear, and the peritoneal or pelvic vessels may be involved. The baby deteriorates rapidly because oxygen transfer across the separated placenta stops. ^{[1] [3] [5]}

During pregnancy, the anterior pituitary enlarges as lactotrophs proliferate under high oestrogen stimulation, and its blood supply becomes vulnerable. Severe hypotension or shock reduces perfusion, especially when the gland is compressed in a small sella turcica; vasospasm, thrombosis and coagulation disorders add to the insult. Necrosis most often involves the whole gland, beginning with growth hormone, prolactin and the gonadotrophins; adrenocorticotrophic hormone and thyroid-stimulating hormone may also fail. A fibrous scar eventually replaces the necrotic tissue, leaving an empty sella on imaging. Autoimmune attack appears later and may worsen the deficiency over the years. ^[6]

• Sudden, heavy bleeding after delivery with clots or a mass at the perineum.
• Severe lower abdominal or sacral pain.
• The woman looks shocked (pale, tachycardic, hypotensive, agitated) far out of proportion to the measured or visible loss.
• Vaginal examination: the placenta or a fleshy mass is felt at or beyond the cervix, and the umbilical cord is pulled down with it.
• Abdominal examination: there is no firm uterine fundus; instead the cupped lower segment is felt and the abdomen feels empty at the top.
• A sudden collapse after a seemingly normal delivery should raise the possibility immediately.

• Sudden, severe, tearing abdominal pain, often between contractions.
• A contraction pattern that suddenly stops or becomes weak and irregular.
• Vaginal bleeding, sometimes massive and concealed, with haematuria.
• Loss of the fetal heart rate pattern: sudden fetal bradycardia, prolonged deceleration or absent fetal heart sounds.
• Loss of fetal station on vaginal examination (the presenting part is no longer felt).
• Maternal tachycardia and hypotension, progressing to collapse.
• Referred shoulder pain if bleeding tracks under the diaphragm.
• The scar itself can dehisce silently in a woman with epidural analgesia, so continuous monitoring matters.

Acute presentation (within hours or days of delivery):

• Severe headache and postpartum amenorrhoea beyond the expected period.
• Failure to lactate (agalactia), which is often the earliest clue.
• Symptoms of acute adrenal failure: hypotension, hypoglycaemia, nausea and vomiting.
• Confusion, coma, hyponatraemia and hypothermia.
• Flaccid or altered behaviour that may be misdiagnosed as eclampsia or sepsis.

Chronic presentation (months to many years later):

• Amenorrhoea, oligomenorrhoea or irregular cycles, and loss of libido.
• Inability to breastfeed, or short, scanty lactation in a previous pregnancy.
• Cold intolerance, lethargy, constipation and dry, coarse skin.
• Pallor and weakness, often more marked than the anaemia explains.
• Sparse axillary and pubic hair and breast atrophy.
• Fine wrinkling around the eyes and mouth, and hypopigmented skin.
• Hypotension and hypoglycaemia, and easy bruising.

Panhypopituitarism is the most common pattern, with growth hormone and prolactin most frequently and most severely deficient; adrenocorticotrophic hormone and thyroid-stimulating hormone deficiency are seen in 56 to 100% and 73 to 100% of cases in the reviewed series. ^[6]

• General and vital signs: tachycardia out of proportion to visible bleeding, hypotension, cold peripheries.
• Abdominal: for inversion, look for the absent fundus; for rupture, look for a tender uterus and loss of fetal parts at the top.
• Vaginal: note bleeding; in inversion, a mass and cord are present at the cervix; in rupture, the presenting part has withdrawn.
• Fetal heart rate: rupture carries an acute fetal emergency.

• Blood pressure and pulse lying and standing (postural drop).
• Skin: pallor, dryness, loss of axillary and pubic hair, fine perioral wrinkling.
• Breasts: atrophy; inability to squeeze colostrum.
• Reflexes: delayed relaxation of the ankle jerks in hypothyroidism.
• Mental state: confusion, apathy or delayed responses.

Adrenocorticotrophic hormone deficiency can cause hyponatraemia, muscle enzyme elevation and salt-wasting; thyroid-stimulating hormone deficiency lowers free thyroxine. ^[6]

Management of inversion and rupture is not outpatient medicine: both are emergencies. Summon senior midwives, an obstetrician, an anaesthetist and, for massive bleeding, the haematology and surgical teams early, and move the woman to an obstetric theatre. ^{[1] [3] [4]}

1. Call for senior help and declare a major haemorrhage if bleeding is significant.
2. Resuscitate (airway, breathing, circulation), give high-flow oxygen, keep warm, set up large-bore intravenous access, and cross-match blood.
3. Do not pull on the cord and do not manually remove the placenta if it is attached; doing so worsens the inversion and the bleeding.
4. Attempt manual replacement without delay: place a hand in the vagina, push the fundus back through the cervix with the palm and fingers (the classic manoeuvre), and keep the uterus from re-inverting by holding it in place.
5. If the uterus will not pass through the cervix, a tocolytic (for example terbutaline, or a glyceryl trinitrate spray if available locally) can relax the cervix and lower segment so replacement succeeds; this is given under senior guidance.
6. If manual replacement fails, use hydrostatic pressure (warm saline run under pressure into the vagina behind a cup or condom) while the constriction ring is relaxed.
7. If these measures fail, or if the inversion is chronic, proceed to laparotomy, reposition the uterus abdominally and close any tear.
8. Only once the uterus is restored to its normal position, give uterotonics (oxytocin, plus ergometrine, misoprostol or carboprost as locally available) to keep it contracted, remove the placenta by controlled traction if still attached, and inspect the cervix and vagina for tears.
9. Given its trauma origin, avoid delaying surgery while giving uterotonics alone.

1. Recognise the pattern: sudden fetal bradycardia, loss of station, severe pain or cessation of contractions, maternal collapse.
2. Make a major haemorrhage call; prepare for immediate theatre, with the anaesthetist and paediatric team on hand.
3. Resuscitate mother and baby in parallel (oxygen, intravenous access, blood products as needed), and monitor the fetal heart continuously if the baby is in utero.
4. Deliver the baby by the fastest safe route; if the fetus has already extruded, laparotomy is mandatory.
5. Repair the rent if bleeding can be controlled and fertility is desired; consider hysterectomy for an extensive tear or ongoing shock.
6. Check the bladder and the ureters, and replace clotting factors if there has been massive haemorrhage.
7. Women with a previous scar need consultant-led intrapartum care; induced labour, especially with prostaglandins, carries a higher rupture risk and should follow local policy. ^{[3] [7]}

Acute management:

• Suspect it in a woman who collapses or remains confused after a severe postpartum haemorrhage, when hypoglycaemia, hyponatraemia or hypothermia are present and lactation has not started.
• Check cortisol, glucose, sodium and thyroid function; a basal cortisol below 3 micrograms per dL is diagnostic of adrenal failure.
• Start intravenous hydrocortisone immediately, after drawing blood for cortisol, in acute adrenal failure; replace glucose and correct sodium; warm the patient.
• Add levothyroxine only after the adrenal problem is covered; never start thyroid hormone first in an acutely unwell patient.
• Consider vasopressin (diabetes insipidus) treatment when sodium and osmolality suggest it; it is rare but does occur.

Chronic replacement:

• Glucocorticoid (usually hydrocortisone) first, at the lowest effective daily dose, with instructions on stress-dose increases.
• Levothyroxine second, titrated against free thyroxine, not against thyroid-stimulating hormone, which is unreliable in central disease; start low and go slowly in older patients and in those with cardiac disease.
• Gonadal hormone (oestrogen with or without progesterone) for premenopausal women, unless contraindicated by thrombosis, severe liver disease or uncontrolled hypertension, continuing until the average age of menopause in that population; oral oestrogen can lower IGF-1 in patients on growth hormone.
• Growth hormone, where available and indicated, after the other replacements; dose by clinical response and IGF-1, since deficiency is severe in most patients with Sheehan syndrome.
• Adrenal androgen (dehydroepiandrosterone) has been studied but has no general recommendation.

Counselling points:

• Delay in diagnosis is common and can stretch to over a decade, so take a postpartum history of bleeding, failure to lactate and amenorrhoea in every woman with unexplained hypopituitarism. ^[6]
• Hyponatraemia is a common presenting clue (reported in 21 to 59% of patients), with reported median serum sodium around 119 mmol per L in the series cited. ^[6]
• Empty sella on MRI is a classic late finding; before imaging, question the obstetric history carefully.
• Cardiovascular, metabolic and bone consequences persist despite replacement, so screen for diabetes, dyslipidaemia, cardiovascular disease and low bone density at follow-up. ^[6]

Because the book page also covers postpartum infection, a few principles belong here. Postpartum fever is best evaluated by source, in this order: endometritis (the commonest cause after caesarean birth, presenting in the early puerperium with fever, uterine tenderness and offensive lochia), wound infection, urinary tract infection or pyelonephritis, mastitis or breast abscess, respiratory infection, venous thrombophlebitis (including pelvic thrombophlebitis), and less common intra-abdominal collections. ^{[1] [2]}

• Take blood and wound or urine cultures, start broad-spectrum therapy in accordance with local policy (an intravenous cephalosporin plus metronidazole or clindamycin is one common regimen) and narrow once results return.
• Re-review promptly if there is no improvement; failure to improve should prompt imaging for retained tissue, haematoma or abscess.
• Low-grade fever that settles rapidly is often physiological; fever that persists beyond the early puerperium, or that is accompanied by uterine, wound, breast or urinary symptoms, should be investigated as a real infection rather than attributed to normal involution. ^{[1] [2]}
• Prevention rests on aseptic technique, removal of retained tissue at delivery, and prophylactic antibiotics at caesarean section in accordance with local policy. ^[4]

• Preventing severe postpartum haemorrhage is the prevention of Sheehan syndrome. Active management of the third stage with a prophylactic uterotonic, monitoring of uterine tone, and treatment of anaemia are the basis, with the WHO and FIGO recommendations for all deliveries. ^{[3] [4] [5]}
• NICE advises antenatal risk assessment for postpartum haemorrhage and delivery in an obstetric unit for women with risk factors, including previous postpartum haemorrhage over 1000 mL or needing transfusion, and previous uterine rupture. ^[3]
• Postpartum collapse should be assessed for pituitary failure when there is a history of severe blood loss, transfusion or hypovolaemic shock, rather than waiting for late endocrine failure. ^[6]
• After inversion or rupture, a written plan for the next pregnancy (place of delivery, scar review, avoidance of induction unless indicated) should be provided before discharge.

• Inversion and rupture: haemorrhagic shock, disseminated intravascular coagulation, acute renal failure, transfusion reactions, infection, loss of fertility after hysterectomy, and maternal death if not controlled. ^{[1] [2] [5]}
• Uterine rupture: fetal hypoxia or death, uterine or urinary bladder fistula, and a higher chance of recurrence in a future pregnancy.
• Sheehan syndrome: acute adrenal crisis, myxoedema coma, circulatory collapse and death in the acute phase; and in the chronic phase low blood pressure, dyslipidaemia, metabolic syndrome, osteoporosis or osteopenia and cognitive impairment. ^[6]
• Long-term fracture risk, dental changes and cardiovascular morbidity persist despite adequate replacement. ^[6]

Most inversions are corrected and the woman recovers fully when replacement is performed before deep shock; the main determinant is the interval to recognition. After uterine rupture, maternal outcomes depend on the speed of laparotomy and resuscitation, and future fertility and pregnancy planning become the focus. With Sheehan syndrome, prognosis depends on whether the woman escapes acute adrenal or thyroid crisis; once on replacement, life expectancy is good, but quality of life and bone and metabolic health need lifelong attention. ^[6]

• Pregnancy and intrapartum: previous uterine rupture is a contraindication to planned vaginal birth; a prior inversion does not automatically preclude vaginal birth but warrants consultant-led care. Both warrant delivery in an obstetric unit. ^{[3] [7]}
• Women with bleeding disorders or on anticoagulants: their haemorrhage risk is higher and managed with haematology input; intramuscular uterotonics may need to be avoided. ^[1]
• Older women: delayed presentation of Sheehan syndrome in women who had a difficult birth decades earlier is common and is misdiagnosed as anaemia or depression. ^[6]
• Children and infants: not applicable to these conditions directly, but infants born after a ruptured uterus need immediate neonatal resuscitation and assessment.
• Women with a classical uterine scar: rupture risk is higher than after a lower segment scar, so elective caesarean birth is commonly advised. ^[7]

A major haemorrhage or a ruptured uterus is a traumatic experience, and care does not stop when the bleeding does. Detailed documentation of the sequence of events, the measured blood loss, the drugs and blood products given, the decision times and the lessons learned supports both clinical handover and medico-legal review. Women benefit from a structured debrief before discharge, with honest explanation of what happened, the implications for future pregnancies and a written summary they can carry; a referral to counselling should be offered where memory of the event is intrusive. ^{[1] [3]}

For Sheehan syndrome in particular, follow-up should be planned before discharge: an endocrinology referral, a clear letter explaining the diagnosis to future caregivers, instructions on stress-dose glucocorticoids, and arrangements for monitoring blood pressure, glucose and lipids. Sons and daughters of affected women are not themselves at risk of Sheehan syndrome, but family planning should be discussed. ^[6]

Cardiovascular, metabolic and bone health need lifelong attention in Sheehan syndrome, and the transition from postpartum care to long-term endocrine review should be explicit rather than left to emerge later. ^[6]

Postpartum haemorrhage; postpartum pyrexia and infection; uterine atony and the four Ts; disseminated intravascular coagulation; hypopituitarism and pituitary disease; vaginal birth after caesarean delivery; preeclampsia, HELLP syndrome and eclampsia.