Physiological haemodilution must be distinguished from true anaemia.

Definition

According to the WHO, anaemia in pregnancy exists when the haemoglobin concentration in peripheral blood is 11 g/dL or less. Because plasma volume expands maximally around 32 weeks and dilutes the haemoglobin, a level below 10 g/dL at any time in pregnancy is taken as anaemia; Hb ≤ 9 g/dL demands full investigation and treatment, and Hb < 7 g/dL is severe anaemia. Anaemia is the commonest haematological disorder of pregnancy and contributes to about 20% of maternal deaths in developing countries.

Classification of Anaemia in Pregnancy

Physiological ("apparent") Anaemia of Pregnancy

Maternal plasma volume rises by 40–50% while red-cell mass rises by only 20–30%; this haemodilution, together with the heavy fetal demand for iron, produces a fall in haemoglobin and haematocrit in the second half of pregnancy. The lower limits of physiological anaemia are Hb 10 g%, RBC 3.2 million/mm³, PCV 32%, with a normocytic–normochromic film. Values below these are pathological.

Classification (D.C. Dutta)

• Physiological anaemia of pregnancy.
• Pathological —

– Deficiency anaemia (isolated or combined): iron, folic acid, vitamin B12, protein.

– Haemorrhagic: acute (early-pregnancy bleeding or APH) and chronic (hookworm, bleeding piles).

– Hereditary: thalassaemias, sickle-cell and other haemoglobinopathies, membrane defects.

– Bone-marrow insufficiency (hypoplasia/aplasia — radiation, drugs).

– Anaemia of infection (malaria, tuberculosis, kala-azar), chronic renal disease and malignancy.

By severity (Hb level): mild 10–8 g%, moderate < 8–7 g%, severe < 7 g%. The two types of obstetric importance are iron-deficiency and megaloblastic (folate/B12) anaemia, of which iron deficiency accounts for the large majority (≈ 95%) in India.

Aetiology of Iron-deficiency Anaemia in Pregnancy

• Increased demand: the total iron requirement of pregnancy is about 1000 mg (fetus and placenta ≈ 300 mg, expansion of maternal red-cell mass ≈ 500 mg, basal/blood loss ≈ 200 mg) — far beyond ordinary dietary intake.
• Deficient intake: poverty, vegetarian diet poor in bioavailable iron, anorexia and nausea of pregnancy.
• Defective absorption: achlorhydria, intestinal disease, diarrhoea, antacids.
• Chronic blood loss: hookworm infestation, bleeding piles, peptic ulcer, menorrhagia before conception.
• Pre-pregnancy depletion: closely-spaced pregnancies, multiparity, previous heavy menstrual loss and lactation leave the stores already empty ("latent" iron deficiency) before pregnancy begins.

Effects of Anaemia on Pregnancy

Maternal — increased susceptibility to infection, pre-eclampsia, preterm labour, poor tolerance of even minor blood loss, postpartum haemorrhage, cardiac failure (especially with Hb < 5 g/dL around the dangerous periods of 30–32 weeks, during labour and immediately postpartum), puerperal sepsis, failing lactation and venous thrombosis. Fetal — intra-uterine growth restriction, prematurity, intra-uterine death and reduced neonatal iron stores predisposing to infantile anaemia.

Investigations

• Haemoglobin estimation and complete blood count with red-cell indices (microcytic, hypochromic; low MCV, MCH, MCHC in iron deficiency; macrocytic in megaloblastic anaemia).
• Peripheral blood film — microcytic hypochromic cells with anisopoikilocytosis.
• Iron studies — low serum ferritin (most sensitive marker of stores, < 15 µg/L), low serum iron, raised total iron-binding capacity, transferrin saturation < 16%.
• Reticulocyte count, stool examination for ova/occult blood, urine for protein and bacteriuria.
• Haemoglobin electrophoresis when a haemoglobinopathy is suspected (family history, refractory anaemia).

Prophylaxis

Dietary advice (green leafy vegetables, jaggery, pulses, vitamin-C–rich foods to aid absorption), deworming, treatment of any chronic infection, and routine iron–folic-acid supplementation — under the national programme, 60 mg elemental iron with 500 µg folic acid daily for at least 100 days from the second trimester, continued through lactation.

Management

Oral iron therapy

First line in mild-to-moderate anaemia diagnosed early. The therapeutic dose is 180–200 mg of elemental iron per day (e.g. Ferrous sulphate 200 mg tablet ≈ 60 mg elemental iron, thrice daily), best taken on an empty stomach with vitamin C and continued for 3 months after the haemoglobin is restored to replenish stores. A reticulocyte rise in 5–10 days and a haemoglobin rise of ≈ 0.8 g/dL per week confirm response.

Parenteral iron therapy

Indicated when oral iron is not tolerated or is contraindicated, the patient is non-compliant, or the woman presents late (after 30 weeks) with moderate–severe anaemia. The iron deficit is calculated and given as iron sucrose 100–200 mg per sitting (IV) on alternate days, or as a total-dose infusion. Expected haemoglobin response is 0.7–1 g/dL per week. Iron sucrose is safe and well-tolerated; a previous reaction to parenteral iron is a contraindication.

Blood transfusion

Reserved for severe anaemia near term/in labour, decompensated anaemia with cardiac failure, refractory anaemia, or coexisting haemorrhage. Packed cells are preferred to whole blood to avoid volume overload; in cardiac failure, transfuse slowly with a diuretic, or use exchange transfusion when delivery is imminent.

• Clinical pearl — Management of severe anaemia at 32–36 weeks (e.g. G3P2 multigravida).
• Admit and investigate the type and cause.
• If ≥ 4 weeks remain before delivery and there is no cardiac failure, correct with parenteral iron (iron sucrose / TDI).
• If delivery is imminent, anaemia is decompensated, or Hb < 5 g/dL, give packed-cell transfusion (slow, with frusemide) or exchange transfusion.
• Treat the underlying cause (deworming, antimalarials), continue folic acid, plan delivery in a unit with blood available, keep the third stage actively managed to prevent PPH, and ensure strict asepsis to prevent puerperal sepsis.

Definition

Gestational hypertension — blood pressure ≥ 140/90 mmHg on two occasions ≥ 4 hours apart, arising after 20 weeks in a previously normotensive woman, without proteinuria.

Pre-eclampsia — gestational hypertension plus proteinuria (≥ 300 mg/24 h, or spot protein:creatinine ≥ 0.3, or dipstick ≥ 1+) or, in its absence, new-onset end-organ dysfunction (thrombocytopenia, raised liver enzymes, renal insufficiency, pulmonary oedema, or cerebral/visual symptoms) after 20 weeks.

Eclampsia — occurrence of generalised tonic–clonic convulsions and/or coma in a woman with pre-eclampsia, not attributable to any other cause (e.g. Epilepsy).

Classification of Hypertensive Disorders of Pregnancy

Classification

Pre-eclampsia is graded as without severe features (mild) or with severe features. Features of severe pre-eclampsia include BP ≥ 160/110 mmHg, platelets < 100,000/mm³, serum creatinine > 1.1 mg/dL, liver enzymes ≥ twice normal with epigastric/right-upper-quadrant pain, pulmonary oedema, and persistent headache or visual disturbance. The wider spectrum of hypertensive disorders comprises gestational hypertension, pre-eclampsia–eclampsia, chronic hypertension, and chronic hypertension with superimposed pre-eclampsia.

Risk Factors

Nulliparity, extremes of maternal age, previous or family history of pre-eclampsia, chronic hypertension or renal disease, diabetes, obesity, multiple pregnancy, hydatidiform mole, and antiphospholipid syndrome.

Pathophysiology (brief)

The primary defect is defective trophoblastic invasion with failure of the spiral arteries to undergo physiological remodelling, producing placental ischaemia. Release of anti-angiogenic factors causes widespread endothelial dysfunction, generalised vasospasm, increased vascular permeability and activation of coagulation — explaining the hypertension, proteinuria, oedema and multi-organ involvement.

Clinical Features and Danger (imminent Eclampsia) Signs

Rising blood pressure and proteinuria, rapidly increasing oedema and weight gain; the premonitory signs of imminent eclampsia are severe headache, drowsiness, blurring of vision or flashes of light, epigastric pain, nausea/vomiting, oliguria and exaggerated reflexes.

Complications

Maternal — eclampsia, HELLP syndrome, abruptio placentae, DIC, acute renal failure, pulmonary oedema, cerebral haemorrhage (the leading cause of death), and aspiration. Fetal — intra-uterine growth restriction, prematurity, oligohydramnios and intra-uterine death.

Management of Eclampsia

Eclampsia is an obstetric emergency managed on the principles of controlling fits, controlling blood pressure, and effecting delivery once the mother is stabilised.

1. Immediate / general measures

• Summon help; place the patient in the left-lateral position, maintain a clear airway, give oxygen, and protect from injury and aspiration; insert a padded mouth gag and suck out secretions.
• Establish IV access, catheterise the bladder to monitor urine output, and record BP, pulse, respiratory rate, reflexes and fetal heart at fixed intervals. Nurse in a quiet, dimly-lit room.

2. Control of convulsions — Magnesium sulphate (drug of choice)

Pritchard (intramuscular) regimen: loading dose 4 g of 20% MgSO₄ IV over 3–5 minutes followed immediately by 10 g of 50% MgSO₄ deep IM (5 g into each buttock); maintenance 5 g of 50% IM 4-hourly in alternate buttocks. The Zuspan (IV) regimen uses 4–6 g IV loading over 15–20 minutes then 1–2 g/hour by infusion. A recurrent fit is treated with a further 2 g IV bolus.

• the knee-jerk is present, urine output exceeds 30 mL/hour, and the respiratory rate is more than 12/minute.
• The therapeutic serum level is 4–7 mEq/L.
• The antidote for magnesium toxicity is calcium gluconate 1 g (10 mL of 10%) IV.
• MgSO₄ is continued for 24 hours after the last fit or after delivery, whichever is later.

3. Control of blood pressure

Antihypertensives are started when BP is ≥ 160/110 mmHg, aiming for 140–150 / 90–100 mmHg (avoiding a sudden drop that compromises placental perfusion). Options: labetalol IV, hydralazine 5–10 mg IV repeated, or oral nifedipine 10 mg; methyldopa or labetalol for maintenance.

4. Delivery

Delivery is the only definitive cure and is undertaken once convulsions are controlled and the mother is stabilised, irrespective of gestation. The mode depends on the cervix and fetal condition — induction/ vaginal delivery if the cervix is favourable and labour is likely to be quick, otherwise caesarean section for an unfavourable cervix, fetal distress or other obstetric indications. Ergometrine is avoided in the third stage (it raises blood pressure); oxytocin is preferred.

5. Postpartum care

Most fits occur within 48 hours of delivery, so MgSO₄, antihypertensives and close monitoring of BP, urine output and reflexes are continued. Watch for pulmonary oedema, renal failure and HELLP; arrange contraception and follow-up of blood pressure.

Hypertensive disorders form a spectrum from gestational hypertension through pre-eclampsia and severe pre-eclampsia to eclampsia (the addition of seizures). Magnesium sulphate, given by the Pritchard regimen, is the drug of choice to prevent and treat eclamptic fits, monitored before each dose by the knee jerk, respiratory rate and urine output, with calcium gluconate as the antidote. Delivery is the only definitive cure.

WHY Delivery Is the Only Cure

The central principle in pre-eclampsia is why delivery — and only delivery — cures the disease. The disorder originates in the placenta: defective trophoblastic invasion leaves the spiral arteries narrow and high-resistance, so the placenta is under-perfused and releases anti-angiogenic factors (sFlt-1, soluble endoglin) into the maternal circulation. These produce the widespread endothelial dysfunction that underlies every feature of the disease — vasospasm (hypertension), glomerular endotheliosis (proteinuria), increased capillary permeability (oedema, pulmonary oedema), platelet consumption and hepatic involvement (HELLP), and cerebral vasospasm and oedema (fits). Because the placenta is the source, no drug can cure it: antihypertensives lower the blood pressure and protect the mother from stroke, and magnesium sulphate prevents fits, but neither halts the underlying process, which continues to worsen while the placenta remains in situ. Removing the placenta removes the cause, and the disease resolves over the following days. This is why management is a constant balance — delaying delivery to gain fetal maturity while the mother deteriorates, versus delivering early with the risks of prematurity — and why, once the disease is severe or the pregnancy at term, delivery proceeds without hesitation, after stabilising the mother.

WHY Mgso4 — Not a Conventional Anticonvulsant — Is the Drug of Choice

A frequently misunderstood point is why magnesium sulphate is superior to diazepam or phenytoin for preventing and treating eclamptic fits. Eclamptic seizures are not epileptic: they arise from cerebral vasospasm, hypertensive encephalopathy and oedema, and magnesium acts on precisely this mechanism — it is a cerebral vasodilator (relieving vasospasm and improving cerebral perfusion), blocks NMDA receptors and stabilises the neuronal membrane. Large randomised trials (Magpie and the Collaborative Eclampsia Trial) showed it halves the risk of eclampsia and is clearly better than diazepam or phenytoin at preventing recurrent fits, with fewer maternal and neonatal complications. Crucially, unlike diazepam, it does not depress maternal consciousness or the fetal respiratory centre. Its safety rests on simple bedside monitoring, because toxicity develops in a predictable order: the knee jerk disappears first, then respiration is depressed, and only then the heart — so checking the patellar reflex, a respiratory rate above 12/min and a urine output above 30 mL/h before each dose detects toxicity long before it becomes dangerous, with calcium gluconate as the antidote.

• Pre-eclampsia is a placental disease causing widespread endothelial dysfunction — hypertension, proteinuria and multi-organ involvement.
• Severe features: BP ≥160/110, headache, visual disturbance, epigastric pain, oliguria, HELLP, eclampsia.
• Magnesium sulphate is the drug of choice to prevent and treat eclamptic fits (superior to diazepam/phenytoin); calcium gluconate is the antidote.
• Antihypertensives (labetalol, nifedipine, hydralazine) protect the mother from stroke but do not cure the disease.
• Delivery is the only definitive cure — stabilise the mother first, then deliver.

Head sparing reflects preferential brain perfusion in placental insufficiency.

Definition

Intra-uterine growth restriction (IUGR) is a condition in which the estimated fetal weight is below the 10th percentile for gestational age, i.e. The fetus fails to achieve its genetically-determined growth potential. It must be distinguished from the constitutionally small-for-gestational-age (SGA) but otherwise healthy fetus.

Types of Fetal Growth Restriction

Types

Causes

• Maternal — pre-eclampsia and chronic hypertension, chronic renal disease, anaemia, malnutrition, smoking, alcohol and drug use, cyanotic heart disease, and small maternal stature.
• Placental — uteroplacental insufficiency, infarction, abruption, circumvallate placenta and abnormal cord insertion.
• Fetal — chromosomal abnormalities (trisomies), structural malformations, congenital (torch) infections and multiple pregnancy.

Diagnosis

• Clinical — a symphysio-fundal height lagging ≥ 4 cm behind the period of gestation, poor maternal weight gain, and reduced abdominal girth.
• Ultrasound biometry — serial measurement of biparietal diameter, head circumference, abdominal circumference (the most sensitive single parameter) and femur length, with estimation of fetal weight and of the HC:AC ratio; oligohydramnios (reduced amniotic fluid index) supports the diagnosis.
• Doppler velocimetry — umbilical artery Doppler is the key surveillance tool; increasing resistance with absent or reversed end-diastolic flow indicates serious compromise. Middle-cerebral-artery and ductus-venosus Doppler help to time delivery.
• Fetal surveillance — non-stress test and biophysical profile.

Management

• Treat the cause where possible — control hypertension, stop smoking/alcohol, improve nutrition, and advise rest in the left-lateral position.
• Surveillance — serial growth scans (every 2–3 weeks), liquor volume, and Doppler/biophysical monitoring to detect deterioration.
• Corticosteroids for lung maturity if delivery before 34 weeks is anticipated.
• Timing of delivery — balance the risks of prematurity against continued intra-uterine hypoxia. Deliver when the fetus is mature, or earlier for absent/reversed end-diastolic flow, an abnormal biophysical profile, severe oligohydramnios or arrest of growth.
• Mode of delivery — vaginal delivery with continuous fetal monitoring if the fetus tolerates labour; caesarean section for fetal distress, severe IUGR with abnormal Doppler, or an unfavourable cervix. Anticipate birth asphyxia, hypoglycaemia, hypothermia and polycythaemia in the neonate, and arrange skilled neonatal care.

WHY Symmetrical and Asymmetrical IUGR Matter

A key distinction is why growth restriction is divided into symmetrical and asymmetrical types, and what each implies. In asymmetrical IUGR (the commoner type), the insult is late and utero-placental — pre-eclampsia, hypertension, placental insufficiency — so the fetus, already largely formed, responds by 'brain-sparing': blood is redistributed to the brain, heart and adrenals at the expense of the liver, gut, kidneys and subcutaneous fat. The result is a baby with a relatively normal head but a small abdomen (a raised head-to-abdomen circumference ratio), thin and wasted, with reduced liquor. Because organogenesis was normal, the prognosis is comparatively good if delivery is timed well. In symmetrical IUGR, the insult acts early — chromosomal abnormality, congenital (torch) infection, or drugs and alcohol — impairing cell division itself, so head, abdomen and limbs are all proportionately small; the prognosis is poor, because the problem is intrinsic to the fetus and cannot be corrected by delivery. Understanding this explains why asymmetry prompts a search for maternal placental disease and a plan for timely delivery, whereas symmetry prompts a search for infection and a karyotype.

WHY Doppler Guides the Timing of Delivery

Understanding why umbilical artery Doppler is the key investigation in IUGR explains the whole logic of surveillance. The dilemma is one of timing: the fetus is being starved in utero, but delivering it prematurely exposes it to the hazards of prematurity — so one must know when the womb has become more dangerous than the nursery. Doppler answers this by measuring resistance in the placental circulation. As placental insufficiency worsens, umbilical artery diastolic flow falls, then becomes absent, and finally reverses — absent or reversed end-diastolic flow signals critical placental failure and impending fetal death. Middle cerebral artery Doppler shows brain-sparing (reduced cerebral resistance), and ductus venosus changes appear late, indicating cardiac decompensation. This provides a graded warning system, allowing delivery to be timed before decompensation but after maximal maturity, with corticosteroids for lung maturity if preterm. Recognising that Doppler tracks both the deterioration of the placenta and the fetal response explains why it, rather than growth scans alone, dictates the timing of delivery.

• IUGR = failure of the fetus to achieve its genetic growth potential (estimated fetal weight <10th centile with evidence of compromise).
• Asymmetrical (commoner): late, placental insufficiency; brain-sparing → small abdomen, raised HC/AC ratio, oligohydramnios; better prognosis.
• Symmetrical: early insult (chromosomal, torch infection, drugs/alcohol) → all parameters small; poor prognosis.
• Surveillance: serial growth scans, amniotic fluid, NST/BPP and — above all — umbilical artery Doppler.
• Absent or reversed end-diastolic flow signals critical placental failure → deliver (with corticosteroids if preterm).

The first 24 hours postpartum carry the greatest risk of failure.

Definition

Heart disease complicates about 1% of pregnancies and is an important cause of indirect maternal death. Rheumatic heart disease (chiefly mitral stenosis) remains the commonest type in developing countries, while congenital heart disease predominates in the West. Severity is graded by the New York Heart Association (NYHA) functional classification.

Nyha Grading & Management Timeline

Nyha Functional Classification

• Class I — no limitation of physical activity; ordinary activity causes no symptoms.
• Class II — slight limitation; comfortable at rest, but ordinary activity causes fatigue, palpitation or dyspnoea.
• Class III — marked limitation; symptoms on less-than-ordinary activity.
• Class IV — symptoms at rest; any activity causes discomfort.

Classes I–II generally tolerate pregnancy well; Classes III–IV carry a high risk of maternal mortality.

Effects of Pregnancy on the Heart

The physiological changes of pregnancy stress a diseased heart: blood volume and cardiac output rise by 30–50% (output peaks at 28–32 weeks), heart rate rises, and there are sudden additional loads during labour (each contraction shifts 300–500 mL into the circulation) and especially immediately after delivery, when relief of caval compression and uterine retraction abruptly increase venous return. The critical periods for cardiac failure are therefore 28–32 weeks, during labour, and the immediate puerperium.

Effects of Heart Disease on Pregnancy

Cardiac failure and pulmonary oedema, arrhythmias, infective endocarditis, thromboembolism, increased abortion/preterm labour, intra-uterine growth restriction, fetal hypoxia and increased perinatal loss.

Diagnosis

History of rheumatic fever or known cardiac lesion; symptoms of dyspnoea, orthopnoea or haemoptysis; signs including a diastolic murmur, loud or persistently split heart sounds, or cardiomegaly. Echocardiography confirms the lesion and assesses severity; ECG and chest radiograph (with shielding) assist.

Management

Pre-pregnancy counselling

Assess the lesion and functional class, optimise/correct it before conception (e.g. Valvotomy), and advise on the risks. Class III–IV disease may warrant advice against pregnancy or its termination.

Antenatal

• Shared (obstetrician–cardiologist) care with frequent visits; adequate rest, treatment of anaemia and infection, and avoidance of excess weight gain and salt.
• Prevent and promptly treat heart failure — recognise early signs (basal crepitations, persistent tachycardia, worsening dyspnoea); treat with rest, diuretics, digoxin and oxygen.
• Continue anticoagulation where indicated (e.g. Prosthetic valves), and give thromboprophylaxis.
• Hospitalise around the critical 28–32-week period and well before term in significant disease.

Intrapartum (labour)

• Aim for vaginal delivery in most cases; caesarean section is reserved for obstetric indications.
• Nurse in the propped-up left-lateral position; give oxygen and effective epidural analgesia to minimise the cardiovascular stress of pain.
• Shorten and assist the second stage (forceps/ventouse) to avoid prolonged bearing-down.
• Antibiotic prophylaxis against infective endocarditis for high-risk lesions.
• In the third stage, avoid ergometrine (sudden venous return and rise in pressure); manage with oxytocin, and avoid rapid IV fluids.

Postpartum

The first hour and first few days are the most dangerous — observe closely for pulmonary oedema and failure. Continue antibiotics if indicated, allow graded ambulation with thromboprophylaxis, advise effective contraception (sterilisation may be appropriate after a completed family), and support breastfeeding in stable women.

WHY the Three Critical Periods Determine Management

Understanding why cardiac disease in pregnancy is dangerous at three specific moments converts a list of complications into a plan. Pregnancy imposes a haemodynamic load: blood volume and cardiac output rise by 40–50%, and a diseased heart with limited reserve fails where that load peaks. The first peak is at 28–32 weeks, when plasma volume and cardiac output reach their maximum — the commonest time for heart failure to appear. The second is labour, especially the second stage, when each contraction squeezes 300–500 mL of blood into the circulation and bearing down (Valsalva) causes wide swings in venous return — which is why the second stage is cut short by forceps or ventouse and the mother told not to push. The third, and most dangerous, is the immediate puerperium: as the uterus contracts after delivery of the placenta it autotransfuses some 500 mL into the circulation, while caval compression is relieved — a sudden preload surge that can precipitate acute pulmonary oedema in the first hours after birth. Recognising these three peaks explains why such women are admitted early, delivered under epidural with an assisted second stage, and monitored intensively for 24–48 hours afterwards.

WHY Vaginal Delivery Is Usually Preferred

A point that often surprises students is why a woman with serious heart disease is usually delivered vaginally rather than by elective caesarean. Intuitively, a planned operation seems safer. In fact, caesarean imposes the greater cardiovascular stress: major surgery, greater blood loss, larger fluid shifts, the haemodynamic effects of anaesthesia, and higher risks of infection and thromboembolism — and it does not avoid the autotransfusion of the puerperium. A well-conducted vaginal delivery, by contrast, can be made remarkably gentle: epidural analgesia abolishes the pain-driven surges of catecholamines and cardiac output; the mother is nursed propped up in the left lateral position with oxygen and careful fluid balance; and the second stage is shortened by forceps or ventouse so that she never bears down. Caesarean is therefore reserved for obstetric indications or specific severe lesions. Ergometrine is avoided (it causes an abrupt rise in venous return and blood pressure), and oxytocin is given cautiously by slow infusion. Understanding that the aim is to avoid surges in cardiac output — which surgery causes and a well-managed labour avoids — explains this counter-intuitive preference.

• Pregnancy raises blood volume and cardiac output by 40–50%; a diseased heart may fail at the three critical periods.
• Critical periods: 28–32 weeks (peak cardiac output), labour (second stage) and the immediate puerperium (autotransfusion).
• Rheumatic mitral stenosis is the commonest lesion in India; NYHA class predicts outcome (III/IV = high risk).
• Vaginal delivery under epidural with a shortened second stage (forceps/ventouse) is usually preferred; avoid ergometrine.
• Nurse propped up, restrict fluids, give oxygen and antibiotic prophylaxis where indicated; monitor closely for 24–48 h after delivery.

Screening by OGTT is done at 24–28 weeks.

Definition

Gestational diabetes mellitus (GDM) is carbohydrate intolerance of variable severity with its onset or first recognition during the present pregnancy, irrespective of whether insulin is used or whether it persists after delivery. It must be distinguished from pre-gestational (overt) diabetes, which exists before conception.

Screening & Diagnosis of GDM

Classification (white's)

White's classification grades diabetes in pregnancy by onset, duration and vascular complications. Class A is gestational diabetes — A1 (controlled by diet) and A2 (requiring insulin). Pre-gestational diabetes is graded B–T (Class B onset > 20 years/duration < 10 years, through to classes with retinopathy, nephropathy and transplantation).

Screening and Diagnosis

Universal screening is recommended in high-prevalence populations such as India.

• DIPSI (Diabetes in Pregnancy Study Group of India) — a single-step test: 75 g oral glucose irrespective of the last meal, with a venous plasma glucose at 2 hours of > 140 mg/dL diagnosing GDM.
• IADPSG / WHO (fasting 75 g OGTT) — GDM if any value is met or exceeded: fasting ≥ 92 mg/dL, 1 hour ≥ 180 mg/dL, 2 hours ≥ 153 mg/dL.
• Overt diabetes is diagnosed by fasting ≥ 126 mg/dL, random/2-hour ≥ 200 mg/dL or HbA1c ≥ 6.5%.

Effects on Pregnancy

Maternal — increased pre-eclampsia, polyhydramnios, recurrent infections (urinary, vaginal), preterm labour, increased operative and instrumental delivery, recurrence in later pregnancies and a high lifetime risk of type-2 diabetes. Fetal/neonatal — macrosomia with shoulder dystocia and birth trauma, sudden unexplained intra-uterine death, congenital malformations (mainly with pre-gestational diabetes, not GDM), and neonatal hypoglycaemia, respiratory distress syndrome, hypocalcaemia, polycythaemia and hyperbilirubinaemia.

Management

Medical nutrition therapy and exercise

The mainstay is a diabetic diet (≈ 30–35 kcal/kg with controlled carbohydrate, split into three meals and snacks) and regular moderate exercise. Most A1 cases are controlled by these measures alone.

Glucose monitoring and targets

Self-monitoring of blood glucose with targets of fasting < 95 mg/dL, 1-hour post-prandial < 140 mg/dL and 2-hour < 120 mg/dL.

Drug therapy

Insulin is the drug of choice when diet fails to achieve targets (it does not cross the placenta); metformin is an accepted alternative in selected women. Doses are titrated to the glucose profile.

Fetal surveillance and timing of delivery

Serial growth scans, amniotic-fluid assessment and antenatal fetal monitoring (NST/biophysical profile) in the third trimester. Well-controlled GDM is usually delivered at term (around 38–39 weeks); earlier delivery for poor control or complications. Caesarean section is considered for an estimated fetal weight suggesting macrosomia (≥ 4–4.5 kg) or for the usual obstetric indications.

Intrapartum and postpartum

Maintain maternal blood glucose with an insulin–dextrose infusion during labour. Anticipate and treat neonatal hypoglycaemia. Insulin requirement falls sharply after delivery; perform a 75 g OGTT at 6 weeks postpartum to detect persisting diabetes, counsel on lifestyle and future risk, and advise contraception.

WHY GDM Harms the Fetus — One Mechanism Explains Everything

Understanding why maternal hyperglycaemia harms the fetus makes every complication of gestational diabetes coherent. Glucose crosses the placenta freely, but maternal insulin does not. The fetus is therefore exposed to the mother's high glucose and responds by producing its own insulin — becoming hyperinsulinaemic (the Pedersen hypothesis). Since insulin is the principal fetal growth hormone, this drives macrosomia — but of a particular kind: fat is deposited on the shoulders and trunk while the head grows normally, which is precisely why these babies suffer shoulder dystocia (and brachial plexus injury) even when the head delivers easily. Fetal hyperinsulinaemia also delays surfactant production (so respiratory distress may occur even near term) and, at birth — when the maternal glucose supply is abruptly cut off while the baby's high insulin persists — produces profound neonatal hypoglycaemia within hours, along with polycythaemia, hypocalcaemia and jaundice; fetal polyuria causes polyhydramnios. Recognising that a single mechanism — fetal hyperinsulinaemia driven by maternal glucose — explains macrosomia, shoulder dystocia, RDS and neonatal hypoglycaemia makes the whole subject intelligible, and explains why tight glycaemic control is the goal.

WHY Screening and Postpartum Follow-up Both Matter

A useful concept is why GDM is screened for universally in India, and why the story does not end at delivery. GDM is usually asymptomatic — the mother feels perfectly well — so it is missed unless actively sought; yet its complications are largely preventable by treatment, beginning with diet and exercise and, if targets are not met, insulin (or metformin). This is why India uses a simple, single-step, non-fasting 75 g oral glucose test (DIPSI: a 2-hour value ≥140 mg/dL is diagnostic), applicable at any time of day — designed for practicality in a population that cannot easily attend fasting. Equally important is what follows: GDM is a window into the woman's future, revealing a beta-cell reserve that failed under stress — and around half of such women develop type 2 diabetes within a decade. She must therefore be re-tested at about 6 weeks postpartum, screened regularly thereafter, and counselled about weight, diet and exercise; her child, too, carries a raised lifetime risk of obesity and diabetes. Understanding that GDM is both an immediate obstetric risk and a lifelong metabolic warning explains why screening and long-term follow-up are equally essential.

• GDM = carbohydrate intolerance first recognised in pregnancy, caused by the insulin resistance of placental hormones (hPL, cortisol).
• India screens universally with the DIPSI test: 75 g oral glucose (non-fasting); a 2-hour value ≥140 mg/dL diagnoses GDM.
• Fetal effects follow fetal hyperinsulinaemia: macrosomia → shoulder dystocia, polyhydramnios, RDS, and neonatal hypoglycaemia.
• Treatment: medical nutrition therapy and exercise first; insulin (or metformin) if targets are not achieved.
• Re-test at 6 weeks postpartum — about half develop type 2 diabetes within 10 years.

Chorionicity, not zygosity, determines the risk.

Definition

Multiple pregnancy is the simultaneous development of more than one fetus in the uterus; twins (two fetuses) is the commonest form. Its incidence is rising with assisted reproduction and increasing maternal age.

Zygosity & Chorionicity in Twins

Types and Chorionicity

• Dizygotic (fraternal) twins (≈ two-thirds) — from fertilisation of two ova by two sperm; always dichorionic–diamniotic, the fetuses may be of different sex and are genetically like siblings.
• Monozygotic (identical) twins (≈ one-third) — from a single fertilised ovum that divides; chorionicity depends on the timing of division — dichorionic–diamniotic (< 72 h), monochorionic– diamniotic (4–8 days), monochorionic–monoamniotic (8–13 days) or conjoined twins (> 13 days).

Chorionicity (best assessed by early ultrasound — the "lambda/twin-peak" sign in dichorionic and the "T" sign in monochorionic) is the single most important determinant of risk.

Diagnosis

Suggested clinically by a uterus larger than the period of gestation, more than two fetal poles, multiple fetal heart sounds and exaggerated pregnancy symptoms. Ultrasound is confirmatory, establishing the number of fetuses, chorionicity and growth.

Complications

Maternal — hyperemesis, anaemia, pre-eclampsia, polyhydramnios, antepartum haemorrhage, malpresentation, preterm labour, increased operative delivery and postpartum haemorrhage. Fetal — abortion, prematurity (the chief cause of perinatal loss), growth restriction and discordant growth, congenital malformations, twin-to-twin transfusion syndrome, cord entanglement (monoamniotic), locked/interlocking twins and the vanishing-twin phenomenon.

Management

Antenatal

• Increased rest, a high-calorie diet with iron and folic-acid supplementation, and more frequent visits.
• Serial ultrasound surveillance of growth and liquor (more often, e.g. 2-weekly, in monochorionic pregnancies to detect TTTS); screen for and treat anaemia and pre-eclampsia.
• Corticosteroids for lung maturity if preterm delivery is likely; consider hospitalisation near term.

Intrapartum

• Conduct in a well-equipped unit with facilities for caesarean section and neonatal resuscitation; secure IV access and keep blood available.
• The presentation of the first (leading) twin guides the mode: vaginal delivery is appropriate when the first twin is cephalic; caesarean section for a non-cephalic first twin, monoamniotic twins, conjoined twins or other obstetric indications.
• After delivery of the first twin, check the lie of the second by examination/ultrasound, deliver it without undue delay, and be prepared for internal podalic version or assisted breech delivery.
• Active management of the third stage is essential to prevent the high risk of PPH from the over-distended uterus.

WHY Monochorionic Twins Are the Dangerous Ones

The most important fact in twin pregnancy is why chorionicity — not zygosity — determines the risk, and why it must be established in the first trimester. All twins share the risks of preterm labour, growth restriction, anaemia, pre-eclampsia, malpresentation and PPH. But monochorionic twins share a single placenta, and their circulations are joined by vascular anastomoses — creating dangers unique to them. Unbalanced flow through these anastomoses causes twin-to-twin transfusion syndrome: the donor becomes anaemic, growth-restricted and oliguric with oligohydramnios (the 'stuck twin'), while the recipient becomes plethoric, polyuric and polyhydramniotic and may go into cardiac failure — an untreated severe case carries a very high mortality. They also risk selective growth restriction and, if one twin dies, acute exsanguination or neurological injury in the survivor through the shared circulation. This is why chorionicity must be determined by ultrasound before 14 weeks (the lambda or 'twin-peak' sign of dichorionic versus the 'T sign' of monochorionic), and why monochorionic pregnancies are scanned fortnightly from 16 weeks, so that TTTS can be detected and treated by fetoscopic laser ablation of the anastomoses.

WHY the Delivery of Twins Needs Special Planning

Understanding why the second twin is the more vulnerable explains the intrapartum management. Mode of delivery depends chiefly on the presentation of the first twin: if cephalic, vaginal delivery may be attempted; if non-cephalic (breech or transverse), caesarean is generally advised. The peculiar danger arises after the first twin is born: the uterus suddenly shrinks, which may precipitate placental separation, and the second twin — now in a roomy, partly-emptied uterus — may adopt a transverse lie or suffer cord prolapse, while its cord may be compressed and its placental perfusion falls. Its risk of asphyxia therefore rises with the interval between deliveries. Hence twins must be delivered where ultrasound, an experienced obstetrician, an anaesthetist and a paediatrician for each baby are immediately available; the lie of the second twin is checked at once after the first is born, and it is delivered promptly — by internal podalic version and breech extraction, or by caesarean if necessary. Finally, the overdistended uterus is prone to atonic PPH, so active management of the third stage is essential.

• Determine chorionicity by ultrasound before 14 weeks (lambda/twin-peak sign = dichorionic; T sign = monochorionic) — it determines the risk.
• Monochorionic twins share a placenta with vascular anastomoses → twin-to-twin transfusion, selective growth restriction, co-twin death.
• TTTS: donor anaemic, growth-restricted, oligohydramnios ('stuck twin'); recipient plethoric, polyhydramnios, cardiac failure — treat by fetoscopic laser.
• Common complications: preterm labour (the main cause of perinatal loss), anaemia, pre-eclampsia, malpresentation and PPH.
• Delivery: mode depends on the first twin's presentation; the second twin is the more vulnerable; PPH prophylaxis is essential.

Definition

Labour is the series of events by which the products of conception are expelled from the uterus after the period of viability. Normal labour (eutocia) is one that begins spontaneously at term (37–42 weeks) with the fetus presenting by the vertex, is completed vaginally without undue prolongation or complications and leaves the mother and baby in good condition.

Stages of Normal Labour

Stages of Labour

• First stage — from the onset of true labour pains to full dilatation of the cervix (10 cm); it has a latent phase (up to ~4 cm, slow) and an active phase (rapid dilatation). It lasts about 12 hours in a primigravida and 6 hours in a multigravida.
• Second stage — from full dilatation to the delivery of the baby (≈ 1–2 hours in a primi, ½ hour in a multi); it has a propulsive and an expulsive (bearing-down) phase.
• Third stage — from delivery of the baby to expulsion of the placenta and membranes (≈ 5–15 min).
• Fourth stage — the first hour after delivery of the placenta, during which the mother is observed for haemorrhage.

Mechanism of Labour (in Left Occipito-anterior Position)

The series of passive movements undergone by the head and trunk to negotiate the birth canal — the cardinal movements:

• Engagement — the biparietal diameter passes the pelvic inlet.
• Descent — continuous, brought about by uterine contractions and maternal effort.
• Flexion — the chin approaches the chest, presenting the smallest (suboccipito-bregmatic) diameter.
• Internal rotation — the occiput rotates 1/8 of a circle forwards to lie behind the symphysis pubis.
• Crowning and extension — the head, born by extension, distends the vulva (the occiput pivots under the symphysis).
• Restitution — the head untwists to correct the neck torsion (occiput turns to its original side).
• External rotation — accompanies internal rotation of the shoulders to the antero-posterior diameter.
• Expulsion — the anterior shoulder slips under the pubis, then the posterior shoulder and the rest of the body are delivered.

Management of Labour

First stage

• Reassurance, light diet/fluids, and ambulation in early labour; record observations on a partogram.
• Monitor the fetal heart (every 30 min, after a contraction), maternal pulse/BP/temperature, and contractions; assess cervical dilatation and descent by periodic examination.
• Keep the bladder empty; avoid routine early amniotomy. Provide analgesia as required (epidural).

Second stage

• Encourage bearing-down only with full dilatation; conduct delivery with strict asepsis.
• Support the perineum and control the delivery of the head to prevent tears; perform an episiotomy only if indicated; check for a cord round the neck.
• Deliver the shoulders and body, note the time of birth, and place the baby for immediate care and delayed cord clamping.

Third stage

• Active management — prophylactic oxytocin 10 IU IM with delivery of the anterior shoulder, controlled cord traction with suprapubic counter-traction, and uterine massage after the placenta delivers.
• Examine the placenta and membranes for completeness, inspect the genital tract for tears and repair them, and estimate blood loss.

Fourth stage

Observe the pulse, blood pressure, uterine tone and vaginal bleeding for at least one hour to detect early postpartum haemorrhage; encourage early breastfeeding and skin-to-skin contact.

The partogram plots cervical dilatation against time. The alert line represents the expected rate of progress in the active phase (about 1 cm per hour), and the action line lies four hours to its right. If the patient's progress crosses the alert line, labour is progressing poorly and she should be reassessed and, if necessary, transferred to a unit with emergency obstetric care; crossing the action line demands intervention — which is how the partogram prevents obstructed labour and uterine rupture.

WHY Labour Is Divided Into Stages and Plotted on a Partogram

Understanding why labour is divided into stages, and why progress is plotted rather than merely observed, explains the whole of intrapartum care. The stages mark physiologically distinct processes with different risks: the first stage (onset to full dilatation) is about effacement and dilatation of the cervix; the second (full dilatation to delivery) is about descent and expulsion, and is when fetal hypoxia is most likely; the third (delivery of the placenta) is when the mother is at greatest risk of haemorrhage. The partogram then turns monitoring into a decision tool. By plotting cervical dilatation against time, with an alert line (the expected 1 cm per hour of the active phase) and an action line four hours to its right, it makes the abstract idea of 'poor progress' visible at a glance. Crossing the alert line warns that progress is slow — prompting reassessment and, in a peripheral unit, transfer to a facility with emergency obstetric care; crossing the action line demands intervention (augmentation or caesarean). Its great achievement is the prevention of obstructed labour and its terrible sequelae — uterine rupture, obstetric fistula and fetal death.

WHY the Mechanism of Labour Is a Sequence of Adaptations

A concept that makes normal labour intelligible is why the fetus must perform a precise series of movements to be born. The problem is geometric: the fetal head is not round, and the maternal pelvis is not a straight tube — its inlet is widest transversely, while its outlet is widest antero-posteriorly. The head must therefore continually adjust its orientation, presenting its smallest diameters to each successive plane. Hence the classical sequence: engagement and descent; flexion (chin to chest, converting the presenting diameter from the large occipito-frontal, 11.5 cm, to the small suboccipito-bregmatic, 9.5 cm — the single most important movement); internal rotation (the occiput turns anteriorly to fit the AP outlet); extension (the head pivots under the pubic symphysis and is born); restitution and external rotation (the head untwists as the shoulders rotate); and finally expulsion of the shoulders and body. Understanding that each movement solves a specific mismatch between head and pelvis explains why the mechanism is invariable, why deflexion (as in the occipito-posterior position) presents a larger diameter and prolongs labour, and why the mechanism is the key to every malposition.

• Labour: stage 1 (onset to full dilatation), stage 2 (full dilatation to delivery), stage 3 (delivery of the placenta), stage 4 (first hour — watch for PPH).
• Mechanism: engagement/descent → flexion → internal rotation → extension → restitution/external rotation → expulsion.
• Flexion is crucial — it converts the presenting diameter to the smallest (suboccipito-bregmatic, 9.5 cm).
• The partogram plots dilatation against time with alert and action lines — crossing them prompts reassessment and intervention.
• It prevents obstructed labour, uterine rupture, fistula and fetal death — recommended by the WHO for every labour.

Bishop score predicts the likelihood of successful induction.

Definition

Induction of labour is the artificial initiation of uterine contractions, after the period of viability, before their spontaneous onset, with the aim of achieving vaginal delivery. (Augmentation is the enhancement of contractions that have already begun.)

Induction of Labour - Method BY Bishop Score

Indications

Conditions in which continuing the pregnancy is more hazardous than delivery — post-term pregnancy, pre-eclampsia, intra-uterine growth restriction, premature rupture of membranes at term, diabetes, Rh isoimmunisation, intra-uterine fetal death, chorioamnionitis and certain medical disorders.

Contraindications

Cephalopelvic disproportion, malpresentation (transverse lie), placenta praevia and vasa praevia, a previous classical caesarean or major uterine surgery, cord prolapse, active genital herpes, and established fetal distress (which needs immediate delivery, usually caesarean).

Assessment — the Bishop Score

The favourability of the cervix is graded by the modified Bishop's pre-induction scoring system, scoring cervical dilatation, effacement, consistency, position and the station of the head. A score ≥ 6 is favourable (induction likely to succeed); a low score calls for cervical ripening first.

Pre-requisites Before Induction

Before inducing, confirm a valid indication, a cephalic presentation with the head engaging and no disproportion, a reassuring fetal heart, and an assessed (and if necessary ripened) cervix. Confirm the gestational age, obtain informed consent, and ensure facilities for continuous monitoring and for emergency caesarean section.

Methods

Cervical ripening (for an unfavourable cervix)

• Prostaglandins — PGE₂ (dinoprostone) gel/pessary or PGE₁ (misoprostol).
• Mechanical — transcervical Foley/balloon catheter or hygroscopic dilators (laminaria).
• Membrane sweeping (stripping) — digital separation of the membranes from the lower segment releases local prostaglandins and may initiate labour; useful as a simple outpatient measure near term.

Medical

• Oxytocin infusion — titrated, with continuous fetal-heart and contraction monitoring (most effective once the cervix is favourable and the membranes are ruptured).

Surgical

• Amniotomy (artificial rupture of membranes, arm) — releases prostaglandins and is usually combined with oxytocin.

Conduct of Induction and Failed Induction

During induction, monitor the fetal heart and uterine contractions continuously, watch for hyperstimulation (more than five contractions in 10 minutes or sustained contractions, with fetal-heart changes — stop oxytocin, give a tocolytic, reposition and oxygenate), and chart progress on a partogram. Failed induction — failure to achieve active labour despite an adequate attempt — is an indication for caesarean section; the chance of failure is higher with a low Bishop score.

Complications

Failed induction (ending in caesarean section), uterine hyperstimulation with fetal distress, uterine rupture (especially in a scarred uterus), cord prolapse (after arm with a high head), intra-uterine infection, iatrogenic prematurity and an increased risk of postpartum haemorrhage.

WHY the Bishop Score Decides the Method

Understanding why the Bishop score is assessed before every induction explains why some inductions succeed easily and others end in caesarean section. Induction attempts to start labour artificially; whether it will succeed depends on whether the cervix is 'ripe' — soft, effaced, dilated, anterior, with the head well applied. The Bishop score quantifies precisely this (dilatation, effacement, station, consistency, position). If the score is favourable (≥6), the cervix is already primed, and simple amniotomy with an oxytocin infusion will usually establish labour. If it is unfavourable (<6), driving the uterus with oxytocin against an unripe cervix produces painful, prolonged, ineffective labour, fetal distress and a failed induction ending in caesarean section. Such a cervix must first be ripened — with prostaglandins (PGE2 gel or misoprostol), which soften and efface the cervix by dissolving its collagen, or mechanically with a Foley catheter balloon. Understanding that the state of the cervix, not the strength of the contractions, determines the success of induction explains why the Bishop score is the first step and why ripening must precede oxytocin in an unfavourable cervix.

WHY Hyperstimulation and Rupture Are the Key Dangers

A crucial safety concept is why induced and augmented labour must be monitored so closely. Both oxytocin and prostaglandins can cause uterine hyperstimulation — contractions that are too frequent (more than five in ten minutes), too long, or with inadequate relaxation between them. This matters because the placenta is perfused only between contractions: during a contraction the intramural vessels are compressed and blood flow largely ceases. If the uterus does not relax properly, the fetus is progressively deprived of oxygen, producing fetal distress — which is why continuous fetal heart monitoring is mandatory during induction. In the extreme, or in a uterus already scarred by a previous caesarean, sustained hyperstimulation can cause uterine rupture — catastrophic for mother and fetus (hence prostaglandins are used with great caution, and misoprostol avoided, in a woman with a scar). Hyperstimulation is managed by stopping the oxytocin (or removing the prostaglandin), turning the woman into the left lateral position, giving oxygen and fluids, and considering a tocolytic. Recognising that the danger lies in losing the relaxation phase explains the entire safety framework of induction.

• Induction = artificially starting labour when continuing the pregnancy is more dangerous than delivering (post-dates, pre-eclampsia, PROM, IUGR, IUFD, diabetes).
• Assess the cervix with the BISHOP score: favourable (≥6) → arm + oxytocin; unfavourable (<6) → ripen first (PGE2/misoprostol or Foley balloon).
• Contraindications: placenta praevia, transverse lie, cephalopelvic disproportion, active herpes, classical caesarean scar, fetal distress.
• Complications: hyperstimulation with fetal distress, failed induction, uterine rupture (especially with a scar), cord prolapse after arm, PPH.
• Continuous fetal monitoring is mandatory; for hyperstimulation — stop oxytocin, left lateral position, oxygen, tocolytic.

Definition

Breech presentation is a longitudinal lie in which the podalic pole (buttocks/lower limbs) occupies the lower pole of the uterus and presents at the pelvic brim, the head lying at the fundus. It is the commonest malpresentation, occurring in about 3–4% of term pregnancies.

Types of Breech Presentation

Types

• Frank (extended) breech — thighs flexed, legs extended over the abdomen; the commonest at term, especially in primigravidae.
• Complete (flexed) breech — thighs and legs both flexed; the fetus "sits" with buttocks and feet presenting.
• Footling / incomplete breech — one or both feet (or a knee) present below the buttocks; carries the highest risk of cord prolapse.

Causes

Factors favouring breech include prematurity, multiple pregnancy, polyhydramnios, placenta praevia, uterine anomalies (septate/bicornuate) and fibroids, fetal anomalies (hydrocephalus, anencephaly), contracted pelvis, a short cord and intra-uterine fetal death.

Diagnosis

Clinical — a hard, round, ballotable head felt at the fundus, the softer breech in the lower pole, and the fetal heart heard at or above the umbilicus. Ultrasound confirms the presentation and type, locates the placenta, estimates fetal weight and excludes anomalies.

Complications

Fetal — cord prolapse (especially footling), entrapment of the after-coming head, birth asphyxia, intracranial haemorrhage, and birth injuries (fractures of the humerus/ clavicle, brachial-plexus/Erb's palsy, visceral injury). Maternal — increased operative delivery, genital-tract trauma and infection.

Management

Antenatal — external cephalic version (ECV)

In a suitable case, ECV at 36–37 weeks converts the breech to cephalic and reduces the need for caesarean section.

Choice of delivery

The mode is individualised. Planned caesarean section is preferred for most term breeches — primigravida, estimated fetal weight > 3.5 kg or < 2 kg, footling presentation, hyperextended head, contracted pelvis, placenta praevia or a previous scar. Assisted vaginal breech delivery may be offered in carefully selected cases (flexed/frank breech, adequate pelvis, average-sized baby, flexed head, skilled attendant).

Assisted breech delivery (principles)

• Allow the breech to descend and deliver spontaneously up to the umbilicus ("hands-off"), avoiding traction.
• Deliver extended legs (Pinard manoeuvre) and the arms by Løvset's manoeuvre (rotation of the trunk).
• Deliver the after-coming head by the Mauriceau–Smellie–Veit manoeuvre (jaw flexion and shoulder traction) or with Burns–Marshall technique / forceps to the after-coming head; keep the head flexed and the delivery controlled.

There are three types of breech. In the frank (extended) breech — the commonest and the most favourable for vaginal delivery — the hips are flexed and the knees extended. In the complete (flexed) breech both hips and knees are flexed. In the footling breech a foot presents first, carrying the highest risk of cord prolapse and therefore requiring caesarean section. At term the options are external cephalic version, elective caesarean (usual) or, in selected cases, assisted breech delivery.

WHY the After-coming Head Is the Danger

The whole of breech management turns on a single fact: the danger is the after-coming head. In a cephalic delivery the head — the largest, least compressible part — comes first, moulding slowly over hours; once it is born, the rest of the body follows easily. In a breech the sequence is reversed: the soft, compressible buttocks and body deliver first — and they may pass through a pelvis that the head cannot. The head must then negotiate that pelvis rapidly, with no time to mould, and — critically — with the umbilical cord compressed between the head and the pelvic brim, so the fetus is being asphyxiated while the head is being delivered. There is thus a strict time limit, and any obstruction (or an unrecognised hydrocephalus, or an extended, deflexed head) may cause the head to become entrapped — an obstetric catastrophe. This is why breech delivery demands controlled, unhurried descent with 'hands off the breech' until the scapulae appear, and then a specific manoeuvre to deliver the head in flexion (Mauriceau-Smellie-Veit, or forceps applied to the after-coming head), and why the cord must never be pulled upon. Recognising that the head arrives last, quickly, and with the cord compressed explains every rule of breech delivery.

WHY Elective Caesarean Became the Norm — and WHY Ecv Is Offered First

Understanding why most breeches at term are delivered by caesarean, and why external cephalic version is nevertheless offered first, explains modern practice. The Term Breech Trial showed that planned caesarean significantly reduced perinatal mortality and serious neonatal morbidity compared with planned vaginal breech delivery, and — combined with the steady loss of the skills needed for assisted breech delivery — this made elective caesarean the standard of care at term. But caesarean carries its own costs: maternal morbidity, and a scarred uterus that jeopardises every subsequent pregnancy (rupture, placenta praevia and accreta). Hence the logic of external cephalic version: turning the fetus to cephalic at or after 36–37 weeks, under tocolysis and ultrasound guidance with CTG monitoring, succeeds in roughly half of cases — and each success converts a planned caesarean into a normal vaginal delivery. It is contraindicated wherever the uterus must not be manipulated or the fetus not left in utero (APH, ruptured membranes, multiple pregnancy, fetal compromise, a scarred uterus, oligohydramnios). Understanding that ECV is the one intervention that can avoid the caesarean altogether explains why it should be offered to every suitable woman with a breech at term.

• Breech types: frank/extended (commonest, ~65%; best for vaginal delivery), complete/flexed, and footling (highest risk of cord prolapse → caesarean).
• The danger is the after-coming head — it delivers last, rapidly, with the cord compressed, risking asphyxia and head entrapment.
• Offer external cephalic version at 36–37 weeks (success ~50%) unless contraindicated — it can avoid caesarean altogether.
• Planned caesarean is the usual mode at term (Term Breech Trial); assisted breech delivery only in selected cases.
• Assisted breech delivery: 'hands off the breech' until the scapulae appear; deliver the head in flexion (Mauriceau-Smellie-Veit or forceps); never pull on the cord.

The partogram detects obstruction before these complications occur.

Definition

Obstructed labour is one in which, despite good uterine contractions, there is no advance of the presenting part owing to a mechanical obstruction to descent. Unrelieved, it leads to serious maternal and fetal morbidity and mortality.

Obstructed Labour - Causes & Signs

Causes

• Fault in the passage — contracted pelvis / cephalopelvic disproportion, pelvic tumours (fibroid, ovarian), a high assimilation pelvis, and soft-tissue obstruction (stenosis, full bladder/rectum).
• Fault in the passenger — malpresentations and malpositions (shoulder/transverse lie, brow, persistent occipito-posterior, face mento-posterior), a big baby, hydrocephalus, locked twins and fetal tumours.

Clinical Features

• General/maternal — exhaustion and maternal distress — dehydration, ketoacidosis, rising pulse and temperature, and scanty, concentrated urine.
• Abdominal — the uterus is tonically contracted and tender
• a Bandl's (pathological retraction) ring rises towards the umbilicus, separating the upper from the over-stretched lower segment
• fetal parts are difficult to feel and the fetal heart is often absent.
• Vaginal — a dry, hot vagina, an oedematous cervix and vulva, a large caput and excessive moulding, the presenting part jammed and not advancing, and sometimes a foul discharge.

Investigations

Mainly clinical, supported by haemoglobin and electrolytes (dehydration), blood grouping and cross-match, urine for ketones, and ultrasound to confirm the presentation and fetal viability. Continuous watch is kept for the warning signs of impending rupture — a rising Bandl's ring, severe lower-segment tenderness, haematuria and maternal restlessness.

Complications

Maternal — rupture of the uterus, obstructed-labour sepsis, postpartum haemorrhage (atony), genital fistulae (vesico-vaginal/recto-vaginal) from pressure necrosis, obstetric (foot-drop) palsy, and death. Fetal — asphyxia, intra-uterine death, and birth injury.

Management

Prevention

The condition is largely preventable — antenatal detection of disproportion/malpresentation, and use of the partograph to detect arrest early and refer in time.

Treatment of established obstruction

• Resuscitate — large-bore IV fluids to correct dehydration and electrolytes, broad-spectrum antibiotics, bladder catheterisation, and blood arranged.
• Relieve the obstruction by delivery — if the fetus is alive (or dead but undeliverable vaginally), caesarean section. If the fetus is dead and conditions are suitable, a destructive operation (craniotomy) may be done by the experienced; caesarean is safer when in doubt.
• Manage complications — repair uterine rupture (or hysterectomy), treat sepsis, watch for and manage postpartum haemorrhage, and arrange later fistula repair.

WHY Obstructed Labour Is a Preventable Catastrophe

The tragedy of obstructed labour is that it happens at all, when it is so easily prevented. It is not a sudden event but the end point of a labour that has been failing for hours — the presenting part cannot descend despite good contractions, because of cephalopelvic disproportion, malpresentation, a malposition or a pelvic tumour. Every hour of obstruction inflicts damage: the upper segment retracts and thickens while the lower segment stretches and thins, producing the pathological retraction (Bandl's) ring — the visible warning that the uterus is about to rupture; and the soft tissues of the bladder, vagina and rectum are crushed between the fetal head and the pelvic bones, becoming ischaemic and sloughing to produce an obstetric fistula — a lifelong, socially devastating injury. Meanwhile the fetus dies of asphyxia, and the mother of rupture, sepsis or haemorrhage. Yet all of this unfolds slowly and visibly, and can be prevented entirely by the simple act of plotting the labour on a partogram and acting when the action line is crossed. Recognising that obstructed labour is the price of unmonitored labour explains why the partogram, and access to emergency caesarean section, are the true remedies.

WHY the Management Is Never 'push Harder'

A crucial rule is why oxytocin must never be given to augment an obstructed labour — an error that kills. Faced with a labour that is not progressing, the instinct is to strengthen the contractions. But if the cause is true obstruction (a head that cannot pass the pelvis), stimulating the uterus does not overcome the obstruction — it merely drives the already-retracting upper segment harder against an immovable object, thinning the lower segment further until the uterus ruptures, killing the fetus and often the mother. This is why obstructed labour is an absolute contraindication to oxytocin, and why the signs of impending rupture — a rising, tender Bandl's ring, an exhausted and distressed mother, haematuria, fetal distress or death — must be recognised as an emergency. The correct management is immediate resuscitation (intravenous fluids, blood, antibiotics, catheterisation) and delivery by caesarean section, whatever the state of the fetus — because the operation is being performed to save the mother. Understanding that the uterus must be relieved rather than driven explains why the treatment of obstructed labour is always delivery, never augmentation.

• Obstructed labour: the presenting part fails to descend despite good contractions — from CPD, malpresentation, malposition or a pelvic tumour.
• Signs: prolonged labour, an exhausted dehydrated mother, tachycardia, ketosis, oliguria/haematuria, oedematous vulva, excessive caput and moulding, fetal distress.
• The pathological retraction (BANDL'S) ring signals impending uterine rupture — an emergency.
• Never give oxytocin to an obstructed labour — it causes uterine rupture; resuscitate and deliver by caesarean section.
• Sequelae: uterine rupture, sepsis, PPH, obstetric (vesicovaginal) fistula and fetal death — all preventable with the partogram.

Pelvic assessment matters only in the context of labour progress.

Definition

A contracted pelvis is one in which one or more diameters are sufficiently reduced to interfere with the normal mechanism of labour. Cephalopelvic disproportion (CPD) is a disparity between the size of the fetal head and the maternal pelvis such that the head cannot safely negotiate the pelvis.

Contracted Pelvis & CPD - Assessment

Pelvic Diameters of the Inlet

• True (anatomical) conjugate — sacral promontory to the inner upper border of the symphysis ≈ 11 cm.
• Obstetric conjugate — sacral promontory to the nearest (prominent) point of the symphysis ≈ 10 cm; the shortest antero-posterior diameter and the one of obstetric importance.
• Diagonal conjugate — lower border of the symphysis to the sacral promontory ≈ 12 cm; the only one measurable clinically (obstetric conjugate = diagonal conjugate − 1.5–2 cm).

Grading (BY the Obstetric Conjugate)

Borderline 9.5–10 cm; moderate 8–9.5 cm; severe < 8 cm. The degree determines whether a trial of labour is safe.

Causes of a Contracted Pelvis

Nutritional/metabolic — rickets and osteomalacia; congenital — Naegele and Robert pelvis, high-assimilation pelvis; and traumatic or disease of the pelvis and spine (fractures, kyphosis, scoliosis, tuberculosis).

Levels of Pelvic Contraction

• Inlet contraction — obstetric conjugate < 10 cm; the head fails to engage, predisposing to malpresentation, non-engagement and cord prolapse.
• Mid-cavity contraction — converging side walls and prominent ischial spines (interspinous < 9.5 cm); causes deep transverse arrest.
• Outlet contraction — a narrow sub-pubic angle and reduced inter-tuberous diameter, often associated with mid-cavity contraction.

Effects on Pregnancy and Labour

During pregnancy — non-engagement of the head, malpresentations (breech, transverse) and a pendulous abdomen. During labour — prolonged labour, early rupture of the membranes and cord prolapse, prolonged/obstructed labour with the risk of uterine rupture and fistula, and fetal asphyxia or birth injury.

Diagnosis

• History — short stature, limp or rickets, and a previous difficult/operative delivery or stillbirth.
• Abdominal examination — a non-engaged head in a primigravida at term, a pendulous abdomen, and malpresentation.
• Pelvic assessment — measurement of the diagonal conjugate and assessment of the sacrum, ischial spines and sub-pubic angle.
• Head-fitting test (Müller–Munro Kerr) — assessing whether the head can be pushed into the brim — and, where indicated, imaging pelvimetry/ultrasound.

Management

• Borderline/mild disproportion — a closely-monitored trial of labour with a partograph, ready to proceed to caesarean section if progress arrests.
• Moderate-to-severe contraction or absolute CPD — elective caesarean section.
• Anticipate and prevent obstructed labour; never persist with augmentation against an unyielding pelvis.

WHY a 'trial of Labour' Is the Only Real Test

A subtle but vital concept is why the adequacy of a pelvis can rarely be decided in advance, and why the trial of labour is the true test. Clinical pelvimetry gives useful information (the diagonal conjugate, the sacral promontory, the ischial spines, the sub-pubic angle), and X-ray pelvimetry can measure the bones — yet neither predicts delivery reliably, because the outcome depends not on the pelvis alone but on the dynamic interaction of the three Ps: the passage (pelvis and soft tissues), the passenger (the size of the fetal head and, crucially, its ability to flex and mould) and the powers (the efficiency of the contractions). A pelvis inadequate for a large, deflexed, poorly-moulding head may be perfectly adequate for a smaller, well-flexed one. Hence, in borderline disproportion with a cephalic presentation and no other contraindication, the pelvis is 'tested' by allowing carefully-monitored labour — a trial of labour — with progress plotted on the partogram, watching descent, dilatation, caput and moulding; if progress is good, delivery follows, and if not, caesarean is performed before obstruction develops. Understanding that only labour itself can test the fit explains why a trial of labour is safe when supervised, and dangerous when it is not.

WHY Disproportion Matters Beyond This Delivery

Understanding why contracted pelvis is a public-health problem, not merely an obstetric one, gives the topic its proper weight in India. A contracted pelvis is largely a consequence of poverty and childhood undernutrition: rickets and osteomalacia (vitamin D deficiency), and stunting from chronic malnutrition, deform or simply shrink the pelvis — so it is commonest in exactly those women with the least access to skilled obstetric care. The consequences ripple outwards. In pregnancy it causes non-engagement of the head, malpresentation and an unstable lie; in labour, prolonged and obstructed labour, early rupture of the membranes with cord prolapse, uterine rupture and — in the survivors — obstetric fistula; and for the fetus, asphyxia, birth injury and death. Its prevention lies less in the labour room than in childhood nutrition and vitamin D, and in preventing early marriage and adolescent pregnancy (since a girl's pelvis is not fully grown until several years after menarche). Recognising that a contracted pelvis links a woman's childhood nutrition to her risk of dying in labour explains why it is as much a matter for public health as for the obstetrician.

• Cephalopelvic disproportion: the fetal head is too large, or the pelvis too small, for safe vaginal delivery.
• Causes of contracted pelvis: rickets/osteomalacia, malnutrition and stunting, trauma and congenital abnormality — largely diseases of poverty.
• Assess by clinical pelvimetry (diagonal conjugate, promontory, ischial spines, sub-pubic angle) and abdominally (head not engaged in a primigravida at term — Muller-Munro Kerr method).
• In borderline disproportion, a supervised trial OF labour on the partogram is the definitive test; abandon it for caesarean if progress fails.
• Absolute disproportion, or disproportion with a previous scar → elective caesarean section.

About 90% rotate spontaneously to occipito-anterior.

Definition

Occipito-posterior (OP) position is a vertex presentation in which the occiput is directed towards one of the sacro-iliac joints (right or left) — i.e. Lies in the posterior segment of the pelvis. It is the commonest malposition of the vertex.

Occipito-posterior Position - Outcomes

Causes

An android or anthropoid pelvis (favouring the occiput to occupy the roomy hind-pelvis), a deflexed head, a high (non-engaged) head, an anterior placenta, and a flat sacrum.

Diagnosis

• Abdominal — a flattening or "saucer-shaped" depression below the umbilicus (the hollow over the limbs), the fetal back felt in the flank, and the fetal heart heard in the flank; the head feels large and non-engaged.
• Vaginal — the anterior fontanelle is felt centrally/anteriorly (deflexion), with the sagittal suture in an oblique diameter; the posterior fontanelle is in the hollow of the sacrum.

Course and Mechanism of Labour

• Long anterior rotation (≈ 90%) — with good flexion and contractions, the occiput rotates 3/8 of a circle anteriorly to deliver as a normal occipito-anterior — the most favourable outcome.
• Short posterior rotation — the occiput rotates backwards and the head is born face-to-pubis (persistent OP), with a difficult, prolonged second stage.
• Non-rotation / deep transverse arrest — rotation is incomplete and the head arrests in the transverse diameter at the level of the ischial spines.

Effects on Labour

Because the deflexed head presents larger diameters, OP position is associated with a longer first and second stage, early rupture of the membranes, secondary uterine inertia, increased instrumental and caesarean delivery, a higher risk of deep transverse arrest and obstructed labour, and — in face-to-pubis delivery — extensive perineal trauma. The fetus faces a greater risk of asphyxia.

Management

• Expectant (first stage) — most cases rotate spontaneously; encourage adequate hydration, analgesia, and good contractions; avoid early pushing.
• Second stage — if there is delay or arrest with the criteria met, deliver by manual rotation and forceps, rotational forceps (Kielland's) or ventouse, or by caesarean section for disproportion, deep transverse arrest or fetal distress.
• A generous episiotomy protects the perineum, which is at high risk of extended tears in face-to-pubis delivery.

WHY the Op Position Prolongs Labour

Understanding why an occipito-posterior position makes labour long and painful follows directly from the mechanism of labour. In the normal (occipito-anterior) position the head is well flexed, presenting its smallest diameter, and the occiput meets the pelvic floor first, so that the floor's gutter-shaped slope rotates the occiput forwards. In the OP position the occiput lies posteriorly, and the head tends to be deflexed — so it presents a larger diameter (occipito-frontal, ~11.5 cm, instead of suboccipito-bregmatic, 9.5 cm). The consequences follow: engagement and descent are delayed, the head fits the pelvis poorly, the contractions are less efficient, and labour is prolonged — with the head pressing on the sacrum causing the characteristic severe backache ('back labour'), and an early, ineffective urge to bear down as the occiput presses on the rectum. Because the presenting part fits poorly, there is also early rupture of the membranes and a greater risk of cord prolapse. Recognising that the whole clinical picture flows from a deflexed head presenting a larger diameter explains both the symptoms and the delays of the OP position.

WHY Most Op Positions Still Deliver Normally

A reassuring and important point is why the great majority of occipito-posterior positions end in a normal delivery, despite the prolonged labour. Given time and good contractions, the head flexes further as it descends, and when the occiput reaches the pelvic floor it undergoes a long anterior rotation of three-eighths of a circle (135°), bringing the occiput anteriorly so that delivery proceeds normally — this occurs in about 90% of cases. The obstetrician's role is therefore largely patience and support: adequate analgesia (an epidural greatly relieves the backache), hydration, and oxytocin augmentation if the contractions are inadequate, allowing the natural mechanism to complete itself. Only when rotation fails do the abnormal outcomes appear: deep transverse arrest (the head arrested transversely at the ischial spines), persistent occipito-posterior (delivering 'face to pubis' — possible, but with a large perineal tear), or true obstruction. These are managed by rotational forceps or ventouse, or by caesarean section. Understanding that the OP position is usually a delay rather than an obstruction explains why patient, well-supported management — rather than immediate intervention — is the rule.

• Occipito-posterior: the occiput lies in the posterior half of the pelvis — the commonest malposition (associated with an android or anthropoid pelvis).
• The head tends to be deflexed, presenting the larger occipito-frontal diameter (11.5 cm) → delayed engagement, prolonged labour, severe backache.
• About 90% undergo long anterior rotation (3/8 of a circle) and deliver normally — manage with patience, analgesia, hydration and oxytocin if needed.
• Abnormal outcomes: deep transverse arrest, persistent OP ('face-to-pubis' delivery with a big perineal tear), or obstruction.
• Failed rotation → rotational forceps/ventouse or caesarean section; give a generous episiotomy if delivering face-to-pubis.

Definition

Antepartum haemorrhage (APH) is bleeding from or into the genital tract after the 28th week of pregnancy (period of viability) and before the birth of the baby. It complicates 3–5% of pregnancies and remains an important cause of maternal and perinatal morbidity and mortality.

Causes of Antepartum Haemorrhage

Causes

• Placental bleeding (the major group) — placenta praevia and abruptio placentae (accidental haemorrhage).
• Unexplained / indeterminate haemorrhage — including marginal sinus bleeding.
• Extra-placental (local) causes — cervical ectropion, polyp or carcinoma, vaginal/cervical trauma or infection, and vasa praevia (fetal vessels crossing the os, with fetal blood loss).

A. Placenta Praevia

Definition

Placenta praevia is implantation of the placenta, wholly or partially, over the lower uterine segment (over or close to the internal os).

Types/degrees (Dutta) — Type I (low-lying):

• lower margin in the lower segment but not reaching the os
• Type II (marginal): reaches the margin of the internal os but does not cover it
• Type III (incomplete/partial central): covers the os partially
• Type IV (complete/central): covers the internal os completely even when dilated.
• Type II posterior is termed the dangerous placenta praevia. Risk factors include multiparity, advanced maternal age, previous caesarean/uterine scar, multiple pregnancy, and prior curettage.

Clinical features — painless, causeless, recurrent, apparently external bleeding (bright red); a soft, relaxed, non-tender uterus; a high or floating presenting part with frequent malpresentations; and a fetal condition usually proportionate to visible blood loss.

Diagnosis — by transabdominal/transvaginal ultrasound for placental localisation. A vaginal examination is contraindicated outside a fully-equipped theatre ("double set-up").

Management — depends on bleeding, maturity and fetal state.

• Expectant (McAfee–Johnson) when bleeding is slight, mother and fetus are stable and the fetus is preterm: admission and bed rest, correction of anaemia, anti-D if Rh-negative, corticosteroids for lung maturity if < 34 weeks, and close surveillance until ≥ 37 weeks or until bleeding forces delivery.
• Active management for heavy/continued bleeding, term pregnancy or fetal distress: resuscitation and delivery — caesarean section for major degrees (Types III–IV, and Type II posterior), with vaginal delivery considered only in minor degrees with a cephalic presentation and minimal bleeding.

B. Abruptio Placentae (accidental Haemorrhage)

Definition

Abruptio placentae is premature separation of a normally situated placenta after 28 weeks and before delivery.

Types — revealed (blood escapes through the cervix), concealed (blood collects behind the placenta, no external loss) and mixed. Grades (Sher) — Grade 0 (diagnosed retrospectively), Grade 1 (mild, < ¼ separated), Grade 2 (moderate, ¼–⅔, fetus alive), Grade 3 (severe, > ⅔, fetal death ± coagulopathy). Predisposing factors include pre-eclampsia/hypertension, trauma, sudden uterine decompression, short cord, folate deficiency, smoking and a previous abruption.

Clinical features — painful vaginal bleeding (often dark), a tense, tender, "woody-hard" uterus with poorly-felt fetal parts, signs of shock out of proportion to visible loss (in concealed type), and frequently fetal distress or death.

Complications — haemorrhagic shock, Couvelaire uterus (uteroplacental apoplexy), DIC, acute renal failure (acute tubular/cortical necrosis), postpartum haemorrhage and fetal death.

Management — this is an emergency.

• Resuscitate — large-bore IV access, restore blood volume with crystalloids and blood/blood products, monitor vitals, urine output and central venous pressure; correct coagulopathy (fresh frozen plasma, cryoprecipitate, platelets) guided by clotting studies.
• Deliver — if the fetus is alive and delivery is not imminent, caesarean section; if the cervix is favourable and labour is rapid, amniotomy with oxytocin and vaginal delivery. If the fetus is dead, vaginal delivery is preferred after stabilisation provided maternal condition allows.
• Watch for postpartum haemorrhage (active third-stage management) and renal failure in the puerperium.

Differentiating Placenta Praevia from Abruptio Placentae

In placenta praevia the placenta is implanted in the lower uterine segment, over or near the internal os, causing painless, causeless, recurrent bleeding with a soft, relaxed uterus. In abruptio placentae a normally-sited placenta separates prematurely, forming a retroplacental clot: bleeding is painful and may be concealed, the uterus is tense, tender and 'woody', and the fetus is often distressed or dead, with a serious risk of DIC.

WHY a Vaginal Examination Is Forbidden in APH

The first rule of antepartum haemorrhage is why a digital vaginal examination must never be performed until placenta praevia has been excluded by ultrasound. If the placenta lies over or near the internal os, an examining finger passing through the cervix can separate it from the lower segment and tear the large dilated sinuses there, converting a modest 'warning' bleed into torrential, uncontrollable haemorrhage that can exsanguinate the mother within minutes — and it may do so far from an operating theatre or blood bank. The lower segment is poorly contractile, so it cannot arrest such bleeding by retraction as the upper segment does. The safe sequence is therefore: resuscitate, confirm the placental site by ultrasound (quick, safe and definitive), and only then — if the placenta is normally sited — examine. If examination is unavoidable in a bleeding woman of unknown placental site, it is performed as a 'double set-up' examination in theatre, fully prepared to proceed immediately to caesarean section. Understanding that the lower segment cannot control bleeding explains why this single prohibition is the first thing taught about APH.

WHY Abruption Causes Shock Out of Proportion and DIC

A crucial concept is why abruptio placentae endangers the mother far more than the visible blood loss suggests. Two mechanisms explain it. First, the bleeding may be concealed: blood collects behind the placenta and within the myometrium rather than escaping through the cervix, so a woman may be in profound hypovolaemic shock with little or no external bleeding — the tense, tender, 'woody' uterus and the degree of shock, not the visible loss, are the guide. Second, the retroplacental clot and damaged decidua release large amounts of thromboplastin into the maternal circulation, triggering disseminated intravascular coagulation — the clotting cascade is consumed, fibrinogen falls, and the blood ceases to clot, so that the woman then bleeds from the uterus, from venepuncture sites and from any incision. This is compounded by Couvelaire uterus (blood extravasating into the myometrium, impairing contraction and predisposing to atonic PPH) and by acute renal failure. Recognising that abruption threatens through concealed loss, DIC and postpartum atony — not merely through what is seen — explains why management is aggressive resuscitation with blood and clotting products, and prompt delivery.

• APH = bleeding from the genital tract after 28 weeks; the two major causes are placenta praevia and abruptio placentae.
• Praevia: painless, causeless, recurrent bleeding with a soft, relaxed uterus and a usually live fetus.
• Abruption: painful, continuous bleeding (often concealed), a tense, tender uterus, fetal distress, and shock out of proportion to visible loss.
• Never perform a digital vaginal examination until ultrasound has excluded placenta praevia.
• Abruption risks DIC, Couvelaire uterus, PPH and renal failure — resuscitate and deliver.

Definition

Postpartum haemorrhage (PPH) is blood loss of 500 mL or more from the genital tract after a vaginal birth (or ≥ 1000 mL after caesarean section), or any amount of blood loss that adversely affects the mother's haemodynamic state. It is a leading cause of maternal death worldwide.

Causes of PPH - the 4 T'S

Types

• Primary PPH — occurs within the first 24 hours of delivery. It includes third-stage haemorrhage (before expulsion of the placenta) and true PPH (after expulsion).
• Secondary PPH — abnormal bleeding between 24 hours and 6 weeks postpartum, usually from retained products or endometritis.

Causes — the "four T'S"

• Tone — atonic uterus (≈ 80%): failure of the uterus to contract. Causes include over-distension (twins, polyhydramnios, big baby), prolonged or precipitate labour, grand multiparity, antepartum haemorrhage, prolonged oxytocin use, general anaesthesia, retained placenta and a full bladder.
• Trauma: lacerations of the cervix, vagina or perineum, episiotomy, uterine rupture or inversion.
• Tissue: retained placenta, placental fragments or a morbidly adherent placenta (accreta).
• Thrombin: coagulation disorders — DIC (abruption, sepsis, amniotic-fluid embolism), HELLP, or inherited bleeding disorders.

Management of Atonic PPH

Atonic PPH is managed by simultaneous resuscitation and arrest of bleeding, calling for senior help early ("call for help").

1. Resuscitation

• Two large-bore IV cannulae; send blood for grouping/cross-match and clotting; start rapid crystalloids and blood transfusion; give oxygen, keep the patient warm, catheterise the bladder and monitor vitals and urine output.

2. Mechanical measures

• Rub up a contraction by firm uterine massage; ensure the bladder is empty.
• Bimanual compression of the uterus while drugs take effect.

3. Uterotonic drugs

• Oxytocin — 10 IU IM or 20 IU in 500 mL infusion (first line).
• Ergometrine / methylergometrine 0.2 mg IM/slow IV — contraindicated in hypertension and cardiac disease.
• Carboprost (15-methyl PGF₂α) 250 µg IM, repeated every 15 minutes (max 8 doses) — avoid in asthma.
• Misoprostol 800 µg per rectum/sublingual.
• Tranexamic acid 1 g IV (give early) reduces death from bleeding.

4. If bleeding continues

• Uterine tamponade — intrauterine balloon (e.g. Bakri/condom catheter) or uterine packing.
• Examine for and repair genital-tract trauma; explore the uterus and remove retained tissue.
• Non-pneumatic anti-shock garment as a temporising measure during transfer.

5. Surgical measures (if conservative measures fail)

• B-Lynch (brace) suture.
• Stepwise uterine devascularisation — bilateral uterine and ovarian artery ligation, then internal iliac (hypogastric) artery ligation.
• Uterine artery embolisation where available and the patient is stable.
• Peripartum hysterectomy — the life-saving last resort.

Postpartum haemorrhage is caused by one of the '4 Ts': Tone (uterine atony — by far the commonest, giving a soft, boggy uterus), Trauma (genital tract tears — bleeding despite a firm uterus), Tissue (retained placenta) and Thrombin (coagulopathy). Management resuscitates and treats the cause simultaneously, escalating from uterotonics through tamponade and compression sutures to hysterectomy; active management of the third stage prevents about 60% of cases.

WHY the '4 TS' Are the Key to Managing PPH

The value of the '4 Ts' — Tone, Trauma, Tissue, Thrombin — is that they convert a terrifying emergency into a systematic drill. In a woman bleeding torrentially, the temptation is to give one uterotonic after another; but if the cause is a cervical tear or a retained placenta, no amount of oxytocin will stop the bleeding, and the delay is fatal. The 4 Ts force the accoucheur to identify the cause while resuscitating. The single most useful bedside sign is the state of the uterus: if it is soft and boggy, the cause is atony (Tone — by far the commonest, ~70%), and massage and uterotonics are the answer; if the uterus is firmly contracted yet the woman is still bleeding, the cause cannot be atony — it must be Trauma (a tear of the cervix, vagina or perineum, or uterine rupture), and the genital tract must be inspected and repaired. If the placenta was incomplete, suspect Tissue; if the blood simply will not clot anywhere, suspect Thrombin (DIC). Understanding that a contracted-or-boggy uterus immediately separates the two commonest causes explains why the 4 Ts are the framework of every PPH protocol.

WHY Prevention Beats Treatment

Understanding why active management of the third stage is the most valuable single intervention in obstetrics for maternal survival explains its universal adoption. PPH is the leading direct cause of maternal death worldwide, and it kills quickly — a woman with an atonic uterus can lose her entire blood volume within minutes, often where blood and surgery are not immediately available. Treating established PPH therefore depends on resources many women do not have. Prevention, by contrast, is cheap, simple and applicable to every delivery: a prophylactic uterotonic (oxytocin 10 IU IM) with delivery of the anterior shoulder, controlled cord traction, and uterine massage — together reducing the incidence of PPH by around 60%. The physiology is straightforward: the placental bed bleeds until the interlacing 'living ligature' fibres of the myometrium contract and occlude the spiral arteries; giving a uterotonic ensures this happens promptly and completely rather than leaving it to chance. Recognising that PPH is best defeated before it starts explains why AMTSL is recommended for every birth, and why oxytocin is the essential drug of every labour room.

• PPH = blood loss >500 mL (vaginal) or >1000 mL (caesarean), or any loss causing haemodynamic compromise; primary (<24 h) or secondary (24 h–12 wk).
• Causes — the 4 Ts: Tone (atony, ~70%), Trauma (tears/rupture), Tissue (retained products), Thrombin (coagulopathy).
• A soft, boggy uterus = atony; bleeding despite a firm uterus = trauma → inspect the genital tract.
• Stepwise: massage/bimanual compression → oxytocin → ergometrine → carboprost → misoprostol → tranexamic acid → balloon tamponade → B-Lynch/devascularisation → hysterectomy.
• Prevention: active management of the third stage (oxytocin 10 IU IM) reduces PPH by ~60%.

Antenatal corticosteroids reduce neonatal mortality most effectively.

Definition

Preterm labour is the onset of regular uterine contractions with progressive cervical change occurring after viability and before 37 completed weeks. Premature rupture of membranes (PROM) is spontaneous rupture of the membranes before the onset of labour; when this happens before 37 weeks it is preterm PROM (PPROM).

Preterm Labour - Management Pathway

Causes and Risk Factors

Previous preterm birth, infection (urinary, genital, chorioamnionitis), polyhydramnios and multiple pregnancy (over-distension), cervical incompetence, antepartum haemorrhage, pre-eclampsia, uterine anomalies and fibroids, low socio-economic status, smoking and a short inter-pregnancy interval. Many cases are idiopathic.

Diagnosis

• Preterm labour — documented uterine contractions with cervical dilatation/ effacement
• a short cervix on transvaginal ultrasound and a positive fetal fibronectin test support the diagnosis and predict risk.
• PROM — a history of sudden gush of fluid, with pooling of liquor in the posterior fornix on sterile speculum examination
• supported by a positive nitrazine test (alkaline pH) and ferning on microscopy, and by oligohydramnios on ultrasound.
• Digital examination is avoided in PROM to reduce infection.

Management of Preterm Labour

• Confirm the diagnosis, assess gestation and fetal wellbeing, and exclude contraindications to continuing the pregnancy (chorioamnionitis, abruption, fetal distress, lethal anomaly).
• Tocolysis to gain 48 hours for steroid action and in-utero transfer — nifedipine (calcium-channel blocker), atosiban (oxytocin antagonist) or isoxsuprine; contraindicated when prolonging pregnancy is unsafe.
• Antenatal corticosteroids — betamethasone (12 mg IM, two doses 24 h apart) or dexamethasone — to accelerate fetal lung maturity and reduce RDS, intraventricular haemorrhage and necrotising enterocolitis.
• Magnesium sulphate for fetal neuroprotection when birth before 32 weeks is imminent.
• Group-B-streptococcus prophylaxis (intrapartum penicillin) as indicated, and in-utero transfer to a unit with neonatal intensive care.

Management of Prom / Pprom

• Confirm rupture and gestation; assess for chorioamnionitis (maternal fever, tachycardia, uterine tenderness, offensive liquor, fetal tachycardia, raised white-cell count/CRP).
• At term, if labour does not start spontaneously, induce (risk of infection rises with the latent period).
• In PPROM without infection, manage expectantly with monitoring, latency antibiotics (e.g. Erythromycin) to prolong pregnancy and reduce infection, and corticosteroids ± magnesium; deliver if chorioamnionitis, fetal distress or abruption supervene, or once a safe gestation is reached.

WHY Tocolysis Buys Time Rather Than Stops Labour

A concept that clarifies the whole management of preterm labour is why tocolytics are given at all, when they rarely prevent preterm birth. Tocolysis does not cure the underlying cause (infection, overdistension, cervical weakness), and by itself does not significantly improve perinatal outcome. Its value lies entirely in the 48 hours it buys — and those hours are golden, because they permit the two interventions that genuinely save babies: a course of antenatal corticosteroids (betamethasone or dexamethasone), which take about 24–48 hours to act and reduce respiratory distress syndrome, intraventricular haemorrhage, necrotising enterocolitis and neonatal death; and in-utero transfer to a centre with neonatal intensive care — the fetus being the safest incubator for transport. Magnesium sulphate may also be given for fetal neuroprotection before 32 weeks. Understanding that tocolysis is a means to an end — a window for steroids and transfer — rather than an end in itself explains why it is used only for a strictly limited period, why it is pointless once these have been achieved, and why it is withheld when prolonging the pregnancy would be dangerous (chorioamnionitis, severe pre-eclampsia, fetal distress).

WHY Pprom Is a Balance Between Infection and Prematurity

The management of preterm prelabour rupture of membranes turns on one dilemma: the risk of infection weighed against the risk of prematurity. Once the membranes rupture, the protective barrier is gone and ascending infection becomes progressively more likely with time — chorioamnionitis threatens the mother with sepsis and the fetus with pneumonia, sepsis and neurological injury; oligohydramnios adds cord compression and, if very early and prolonged, pulmonary hypoplasia. Yet delivering immediately at, say, 30 weeks exposes the baby to every hazard of prematurity. The resolution is a balance based on gestation: before 34 weeks, if there is no infection and the fetus is well, manage expectantly — with corticosteroids, prophylactic antibiotics (erythromycin, which prolongs latency and reduces infection) and close surveillance for chorioamnionitis (maternal fever, tachycardia, uterine tenderness, offensive discharge, fetal tachycardia, rising leucocyte count and CRP); after 34 weeks, or at any gestation once infection or fetal compromise appears, deliver. Recognising that time is both friend (maturity) and enemy (infection) explains why digital examination is avoided (a sterile speculum is used instead) and why vigilance for infection must be constant.

• Preterm labour = labour before 37 completed weeks — the leading cause of perinatal mortality and morbidity.
• Tocolytics (nifedipine, atosiban) buy ~48 hours; their value is to allow corticosteroids to act and to permit in-utero transfer.
• Antenatal corticosteroids reduce RDS, IVH, NEC and neonatal death; MgSO4 gives fetal neuroprotection before 32 weeks.
• PPROM: manage expectantly before 34 weeks with steroids and erythromycin, watching closely for chorioamnionitis; deliver if infection or compromise appears.
• Avoid digital vaginal examination in PPROM (it introduces infection) — use a sterile speculum.

Retained dead fetus beyond 4 weeks risks consumptive coagulopathy.

Definition

Intra-uterine fetal death (IUFD) is death of the fetus in utero after 28 weeks of gestation (period of viability) and before the onset of labour. (Death before viability is an early fetal/missed loss.)

Intra-uterine Fetal Death - Approach

Causes

• Maternal — pre-eclampsia/eclampsia and chronic hypertension, diabetes, antepartum haemorrhage, severe anaemia, infections, Rh isoimmunisation, antiphospholipid syndrome and post-term pregnancy.
• Fetal — congenital malformations and chromosomal abnormalities, cord accidents (true knot, prolapse, entanglement), and severe growth restriction.
• Placental — abruption, placental insufficiency and infarction.
• A proportion remain unexplained.

Diagnosis

• Symptoms/signs — cessation of fetal movements, retrogression of breast changes, a uterus smaller than dates and not enlarging, and absent fetal heart sounds.
• Ultrasound (confirmatory) — absent cardiac activity and fetal movements; later, overlapping skull bones and collapse of the fetal pole.
• Radiological signs (after several days) — Spalding's sign (overlapping of skull bones), Robert's sign (gas in the great vessels/heart), the "ball" sign (hyperflexion of the spine) and crowding of the rib shadows.

Complications

• Psychological distress to the mother and family.
• Disseminated intravascular coagulation (DIC) — release of thromboplastin from the retained dead fetus causes hypofibrinogenaemia, with a significant bleeding risk if the fetus is retained beyond 4 weeks.
• Infection of the uterine contents and, rarely, sepsis.

Management

• Confirm the diagnosis by ultrasound and break the news with empathy and support.
• Investigate the cause — blood pressure, urine protein, blood sugar, blood group and antibodies, infection screen, and a coagulation profile (fibrinogen, platelets) which is repeated while awaiting delivery.
• Induction of labour — most women prefer prompt delivery. With an unfavourable cervix, use mifepristone followed by misoprostol, or vaginal prostaglandins; oxytocin and amniotomy when the cervix is favourable. Vaginal delivery is the aim; caesarean section is reserved for obstetric indications.
• Manage coagulopathy — correct with fresh frozen plasma/cryoprecipitate if DIC develops; give anti-D to Rh-negative women.
• After delivery — examine the baby and placenta, offer autopsy and karyotyping to establish the cause, suppress lactation, provide grief support and counsel about future pregnancies.

WHY a Retained Dead Fetus Threatens the Mother's Coagulation

Understanding why a dead fetus retained in the uterus endangers the mother explains the urgency of an apparently 'non-urgent' situation — the baby, after all, is already dead. The danger is disseminated intravascular coagulation. The macerating fetus and degenerating placenta slowly release thromboplastin into the maternal circulation, activating the coagulation cascade; over weeks this consumes fibrinogen, platelets and clotting factors, producing a consumptive coagulopathy. The risk becomes significant if the fetus is retained beyond about four weeks (occurring in roughly a quarter of such women), and may declare itself catastrophically as torrential haemorrhage at delivery, when the blood simply will not clot. This is why a retained dead fetus is never left indefinitely 'to come away on its own', why fibrinogen and the coagulation profile are monitored serially if spontaneous labour is awaited, and why delivery is expedited (usually induced with mifepristone and misoprostol) rather than delayed, with blood and clotting products available. Recognising that the dead fetus acts as a slow-release source of thromboplastin explains this entire approach.

WHY the Cause Must Be Sought — and WHY Grief Matters

Two aspects of intrauterine fetal death are easily neglected yet central to good care. The first is why a systematic search for the cause is essential, even though it cannot help this baby — it can help the next one. A cause is found in many cases: hypertensive disease, abruption, diabetes, infection, congenital or chromosomal abnormality, cord accident, Rh isoimmunisation, antiphospholipid syndrome or thrombophilia — and identifying it permits specific treatment and surveillance in the next pregnancy (for instance aspirin and heparin in antiphospholipid syndrome), transforming the recurrence risk. Hence the recommended workup: maternal glucose and HbA1c, blood pressure and urine, a Kleihauer test, antiphospholipid antibodies, an infection screen, karyotype and — most informative of all — placental histology and, where accepted, post-mortem examination. The second is that this is a bereavement: the parents have lost a child, and their care must include sensitive communication, the opportunity to see and hold the baby, an explanation of the findings, suppression of lactation, contraceptive advice and follow-up counselling. Recognising that good management is both a search for answers and a response to grief explains why IUFD tests the whole clinician.

• IUFD = death of the fetus after 20 weeks (or ≥500 g) before delivery; diagnosed by absent fetal cardiac activity on ultrasound.
• The main maternal risk is DIC — thromboplastin from the dead fetus consumes clotting factors, especially after ~4 weeks' retention.
• Monitor fibrinogen and the coagulation profile; expedite delivery (mifepristone + misoprostol) rather than waiting indefinitely.
• Search for the cause: hypertension, diabetes, abruption, infection, anomaly, Rh disease, antiphospholipid syndrome — placental histology is the most informative test.
• Provide bereavement care: sensitive communication, seeing the baby, lactation suppression, contraception and follow-up counselling.

Give thiamine before dextrose to prevent Wernicke encephalopathy.

Definition

Hyperemesis gravidarum is severe, persistent vomiting in early pregnancy, severe enough to cause dehydration, ketosis, electrolyte imbalance and weight loss (> 5% of body weight), and to interfere with daily life — in contrast to the mild "morning sickness" of normal pregnancy.

Hyperemesis Gravidarum - Stepwise Care

Aetiology

The cause is uncertain but is linked to high human chorionic gonadotrophin (hCG) and oestrogen levels — hence its association with multiple pregnancy and hydatidiform mole — together with altered gastric motility, Helicobacter pylori infection and psychological factors.

Clinical Features

Intractable vomiting, inability to retain food or fluids, weight loss, and signs of dehydration (dry tongue, sunken eyes, tachycardia, hypotension, reduced urine output) and ketosis (acetone breath, ketonuria).

Investigations

• Urine — ketones, specific gravity (and to exclude infection).
• Serum electrolytes (hypokalaemia, hyponatraemia, hypochloraemic alkalosis), urea/creatinine.
• Liver and thyroid function tests (transient abnormalities are common).
• Ultrasound — to confirm viability and exclude multiple pregnancy and molar pregnancy.

Grading / Assessment of Severity

Severity is judged by the degree of dehydration and ketonuria, the percentage of weight loss and the electrolyte derangement; the PUQE score (Pregnancy-Unique Quantification of Emesis) grades it as mild, moderate or severe from the number of vomiting and retching episodes. Worsening ketosis, jaundice, neurological signs or a falling weight indicate severe disease.

Differential Diagnosis

Gastroenteritis, urinary-tract infection and pyelonephritis, viral hepatitis, peptic ulcer, thyrotoxicosis (hCG-mediated), and surgical causes of vomiting (appendicitis, intestinal obstruction) must be excluded, along with molar and multiple pregnancy.

Complications

Tears and

Oesophageal rupture (Boerhaave)

From forceful vomiting, hepatic and renal dysfunction, hyponatraemic encephalopathy (central pontine myelinolysis with over-rapid correction) and venous thromboembolism.

Management

• Admit the patient; keep nil by mouth initially, then reintroduce small, frequent, bland meals.
• Intravenous fluids — correct dehydration and electrolytes with normal saline ± potassium, guided by serum levels; avoid dextrose until thiamine is given.
• Thiamine (vitamin B1) supplementation to prevent Wernicke's encephalopathy.
• Antiemetics — doxylamine–pyridoxine (B6) as first line, with metoclopramide, promethazine or ondansetron as required; a short course of corticosteroids in refractory cases.
• Supportive care — thromboprophylaxis, nutritional support (enteral/parenteral if severe), correction of anaemia, and reassurance; the condition usually settles by 14–16 weeks.

WHY Hyperemesis Is Not Just 'bad Morning Sickness'

The essential point is why hyperemesis gravidarum is a serious medical condition and not merely severe nausea. Ordinary morning sickness, however unpleasant, does not disturb the woman's physiology. Hyperemesis is defined by its consequences: persistent vomiting causing dehydration, ketosis, electrolyte disturbance and weight loss of more than 5% of body weight. The losses are specific and dangerous: vomiting loses hydrogen and chloride ions, producing a hypochloraemic, hypokalaemic metabolic alkalosis; starvation drives fat breakdown and ketosis; and dehydration concentrates the blood, predisposing to thromboembolism. Most feared is thiamine deficiency, which in a woman vomiting for weeks can precipitate Wernicke's encephalopathy — confusion, ophthalmoplegia and ataxia — and which can be triggered by giving intravenous dextrose without thiamine, an error that may leave permanent amnesia (Korsakoff's psychosis). This is why management is admission, intravenous rehydration with normal saline (not dextrose alone), potassium replacement, parenteral thiamine, antiemetics and thromboprophylaxis. Recognising that the danger lies in dehydration, electrolyte loss and vitamin deficiency — not in the vomiting itself — explains this whole approach.

WHY the Cause Must Always Be Sought

A useful concept is why hyperemesis is a diagnosis of exclusion, and what must be excluded. Although the condition is driven by the high hCG and oestrogen of early pregnancy (which is why it peaks at 8–12 weeks, when hCG peaks, and is worse when hCG is unusually high), that very association is a clue that must be pursued. Markedly excessive hCG occurs in multiple pregnancy and, importantly, in molar (hydatidiform) pregnancy — so ultrasound is mandatory in every case, both to confirm a viable intrauterine pregnancy and to exclude twins and a mole. Other conditions must also be excluded, because vomiting in pregnancy is not always due to pregnancy: urinary tract infection, gastroenteritis, hepatitis, pancreatitis, raised intracranial pressure and — particularly — thyrotoxicosis, since hCG cross-stimulates the TSH receptor and can produce a biochemical hyperthyroidism. Vomiting that begins or persists after 16 weeks, or is accompanied by abdominal pain or fever, should raise particular suspicion of another cause. Understanding that hyperemesis is both a consequence of high hCG and a signal not to be accepted uncritically explains why ultrasound and a careful search for other causes are part of its management.

• Hyperemesis gravidarum = intractable vomiting of pregnancy causing dehydration, ketosis, electrolyte imbalance and >5% weight loss.
• Metabolic picture: hypochloraemic, hypokalaemic metabolic alkalosis with ketonuria; peaks at 8–12 weeks (with hCG).
• Always ultrasound to exclude multiple and molar pregnancy; exclude UTI, hepatitis, thyrotoxicosis and other causes.
• Treat with IV normal saline, potassium and parenteral thiamine (before any dextrose — to prevent Wernicke's), plus antiemetics and thromboprophylaxis.
• Complications: Wernicke's encephalopathy, Mallory-Weiss tear, hyponatraemia, thromboembolism, and fetal growth restriction if prolonged.

Painless dilatation without contractions is the hallmark.

Definition

Cervical incompetence (insufficiency) is the inability of the internal cervical os to retain the products of conception, causing painless progressive dilatation of the cervix in the mid-trimester and leading to recurrent second-trimester abortion or early preterm birth, owing to a functional or anatomical weakness of the internal os.

Cervical Incompetence - Approach

Causes

• Congenital — a constitutional weakness of the cervix, uterine anomalies, and prior diethylstilbestrol exposure.
• Acquired (traumatic) — the commonest: previous mechanical dilatation (dilatation and curettage, MTP), cervical amputation, conisation or extensive cautery, and obstetric cervical lacerations (precipitate labour, difficult instrumental delivery).

Diagnosis

• History (the cornerstone) — recurrent painless mid-trimester losses with a short, relatively painless labour and delivery of a live but pre-viable/immature fetus, often preceded by sudden rupture of the membranes.
• In the non-pregnant state — painless passage of a No. 8 Hegar dilator through the internal os, or a funnel-shaped internal os on hysterosalpingography.
• In pregnancy — transvaginal ultrasound showing a cervical length < 25 mm and/or funnelling of the internal os, with dilatation but without contractions.

Management

Cervical cerclage (encirclage)

A purse-string suture is placed around the cervix to reinforce the internal os.

• McDonald (simple purse-string at the cervico-vaginal junction) and Shirodkar (submucosal) are the common transvaginal techniques.
• Timing — an elective ("history/ultrasound-indicated") cerclage is placed at 12–14 weeks; a rescue (emergency) cerclage may be attempted with a dilating cervix and bulging membranes in the absence of infection/labour.
• Transabdominal cerclage is reserved for failed vaginal cerclage or an absent/scarred cervix.
• The suture is removed at about 37 weeks or earlier if labour starts, the membranes rupture, or infection supervenes (to avoid cervical tearing).

Adjuncts

Restriction of activity, vaginal progesterone (especially with a short cervix), a cervical pessary in selected cases, and treatment of any vaginal infection. Serial transvaginal ultrasound surveillance of cervical length (every 1–2 weeks in the mid-trimester) helps select women for an ultrasound-indicated cerclage and detects progressive shortening early.

Distinction from Preterm Labour

Cervical incompetence causes painless dilatation without uterine contractions, whereas preterm labour is accompanied by regular painful contractions with cervical change — a distinction that determines whether cerclage (rather than tocolysis and corticosteroids) is the appropriate treatment.

WHY the Cervix Fails Painlessly — and WHY That Is the Clue

The characteristic feature of cervical incompetence — and the key to diagnosing it — is why the pregnancy is lost without pain. In an ordinary miscarriage or preterm labour, the uterus contracts to expel the fetus, so the woman has painful contractions before anything is lost. In cervical incompetence the fault lies not in the uterus but in the cervix itself, whose fibromuscular ring is structurally weak — from previous obstetric or surgical injury (dilatation and curettage, cone biopsy, obstetric laceration) or a congenital collagen deficiency. As the pregnancy grows, the cervix is simply unable to bear the weight: it dilates and effaces silently under the load, the membranes bulge into the vagina, rupture, and the fetus is expelled — painlessly, rapidly, and typically as a live, normally-formed fetus in the mid-trimester (14–28 weeks). This gives the classic history: recurrent, painless mid-trimester losses, each at a similar or earlier gestation, with a live fetus. Recognising that painlessness and mid-trimester timing distinguish this from every other cause of pregnancy loss explains why the diagnosis rests chiefly on the history — and why it matters so much, since, uniquely among the causes of recurrent loss, it is mechanically correctable.

WHY Cerclage Works — and its Limits

Understanding why a stitch around the cervix can save a pregnancy, and when it must not be used, explains the treatment. Cerclage (the McDonald purse-string suture, simple and easily removed; or the Shirodkar suture, placed higher after dissecting the bladder) works by mechanically reinforcing the weak internal os, restoring its ability to bear the load. Its success depends on timing and selection. It is placed electively at 12–14 weeks — after the period of spontaneous first-trimester miscarriage (so that a doomed pregnancy is not stitched) but before the cervix begins to yield, and removed at about 37 weeks, or earlier if labour begins (leaving it in during labour would tear the cervix). It is contraindicated where there is infection or chorioamnionitis, active bleeding, ruptured membranes, a fetal anomaly or established labour — in these situations a stitch would trap infection or simply fail. An 'emergency' or rescue cerclage on an already-dilated cervix with bulging membranes has a much poorer prognosis. Understanding that cerclage is a mechanical solution to a mechanical problem — and useless where the problem is infection or contractions — explains both its impressive success in the right patient and its failure in the wrong one.

• Cervical incompetence: painless, progressive cervical dilatation causing recurrent mid-trimester (14–28 wk) loss of a live fetus.
• Causes: previous cervical trauma (D&C, cone biopsy, obstetric laceration) or congenital weakness; the history is the key to diagnosis.
• Diagnosis: classic history plus a short cervix (<25 mm) or funnelling on transvaginal ultrasound.
• Treatment: cervical cerclage (McDonald or Shirodkar) at 12–14 weeks; remove at 37 weeks or at the onset of labour.
• Contraindicated with infection, bleeding, ruptured membranes, fetal anomaly or established labour; vaginal progesterone is an alternative for a short cervix.

Definition

Carcinoma of the cervix is a malignant tumour of the uterine cervix, the great majority being squamous-cell carcinomas arising at the squamo-columnar junction (transformation zone); the rest are adenocarcinomas. It is one of the commonest genital cancers in women in developing countries.

Natural History & Figo Stages of Carcinoma Cervix

Aetiology and Risk Factors

The central cause is persistent infection with high-risk human papilloma virus (HPV types 16 and 18). Co-factors are early age at marriage/first coitus, multiple sexual partners, high parity, smoking, poor genital hygiene, immunosuppression (HIV), and long-term oral-contraceptive use.

Premalignant Lesion — Cervical Intraepithelial Neoplasia (cin)

Invasive cancer is preceded by a long premalignant phase — CIN (dysplasia → carcinoma in situ) — over 10–15 years, which is the basis of screening and prevention.

Spread

Direct — into the vagina, body of the uterus and parametrium (towards the pelvic wall, ureters, bladder and rectum); lymphatic — to the pelvic (and later para-aortic) nodes; and late blood-borne spread to liver, lung and bone.

Clinical Features

Early disease is often asymptomatic (detected on screening). The classic symptoms are post-coital bleeding, irregular intermenstrual or post-menopausal bleeding, and an offensive blood-stained vaginal discharge. Advanced disease causes pelvic/back pain, leg oedema, urinary or rectal symptoms and uraemia from ureteric obstruction.

Figo Staging (clinical)

• Stage I — carcinoma strictly confined to the cervix. IA microinvasive (diagnosed only on microscopy, depth ≤ 5 mm); IB clinically visible lesion confined to the cervix.
• Stage II — extends beyond the uterus but not to the pelvic wall or the lower third of the vagina. IIA without parametrial involvement; IIB with parametrial involvement.
• Stage III — extends to the pelvic wall and/or the lower third of the vagina, and/or causes hydronephrosis/non-functioning kidney (IIIA lower vagina, IIIB pelvic wall/hydronephrosis).
• Stage IV — spread beyond the true pelvis or into the bladder/rectal mucosa (IVA), or distant metastasis (IVB).

Investigations

Pap smear and colposcopy with directed biopsy for diagnosis; examination under anaesthesia for clinical staging; cystoscopy and proctoscopy, intravenous urography, and cross-sectional imaging (MRI/CT, or pet) to assess spread.

Treatment

• CIN / Stage IA1 — conisation (to preserve fertility) or simple (extrafascial) hysterectomy.
• Stage IA2–IIA (early invasive) — radical hysterectomy (Wertheim's) with pelvic lymphadenectomy, or radical radiotherapy — both give comparable cure; chemoradiation if high-risk features are present.
• Stage IIB–IVA (advanced) — concurrent chemoradiation (external-beam radiotherapy + brachytherapy + cisplatin).
• Stage IVB / recurrence — palliative chemotherapy and supportive/palliative care.

Cervical cancer develops from persistent infection with high-risk HPV (types 16 and 18) through a long precancerous sequence — CIN 1, CIN 2–3, carcinoma in situ — lasting some 10 to 15 years before invasion. This long window is precisely why screening is so effective. Prevention operates at two levels: HPV vaccination of girls before exposure (primary) and screening with treatment of CIN (secondary). Staging is clinical (FIGO), and treatment depends on stage.

WHY Cervical Cancer Is Almost Entirely Preventable

The central fact about carcinoma cervix is why it is one of the few cancers that we could, in principle, abolish altogether. Three features make this possible. First, it has a single necessary cause: persistent infection with high-risk human papillomavirus (chiefly types 16 and 18) — essentially no HPV, no cervical cancer. Second, that cause is vaccine-preventable: immunising girls at 9–14 years, before sexual exposure, prevents infection with the oncogenic types (primary prevention). Third, and most importantly for women already exposed, invasive cancer does not arise suddenly — it is preceded by a long, silent, precancerous phase (CIN 1 → CIN 2–3 → carcinoma in situ) lasting some 10–15 years, during which the lesion is confined to the epithelium, is completely curable by simple outpatient treatment (cryotherapy, LEEP), and — crucially — is detectable on a screening test of an accessible organ. This unusually long window is what makes screening so effective. It is therefore a tragedy of access, not of biology, that cervical cancer remains a leading cancer of Indian women: the disease persists chiefly where women are never screened. Understanding that a known virus, a vaccine and a decade-long precancerous phase together make this cancer preventable explains the whole strategy against it.

WHY It Is Staged Clinically — and WHY Stage Dictates Treatment

A distinctive feature worth understanding is why carcinoma cervix is one of the few cancers still staged clinically rather than surgically. The reason is practical and global: it is predominantly a disease of poor women in low-resource settings, where sophisticated imaging and surgical staging are unavailable — so FIGO deliberately based the staging on what can be determined by clinical examination (an examination under anaesthesia, with cystoscopy and proctoscopy as needed), ensuring that a stage assigned in a district hospital means the same as one assigned in a teaching centre, and that treatment and outcomes can be compared worldwide. Stage then determines treatment absolutely: early disease (confined to the cervix, roughly stage IA–IIA) is treated surgically — by radical (Wertheim's) hysterectomy with pelvic lymphadenectomy — which preserves ovarian function and vaginal length; while more advanced disease that has spread to the parametrium or beyond (IIB and above) is beyond surgical clearance and is treated by concurrent chemoradiation (external beam radiotherapy plus brachytherapy, with cisplatin). Recognising that the key clinical question is whether the parametrium is involved — which is assessed by the examining finger — explains why the bimanual and rectal examination remains decisive.

• Cervical cancer is caused by persistent high-risk HPV infection (types 16, 18) — the leading cancer in Indian women, and almost entirely preventable.
• It has a long precancerous phase (CIN 1 → CIN 2/3 → cis, over 10–15 years) — which is why screening works so well.
• Prevention: HPV vaccine at 9–14 years (primary) + screening by Pap smear/VIA/HPV testing and treatment of CIN (secondary).
• Presents with postcoital or irregular bleeding and offensive discharge; staged clinically (FIGO) — the parametrium is the key.
• Treatment: early stage → radical (Wertheim's) hysterectomy; stage IIB and beyond → concurrent chemoradiation.

Epithelial tumours present late — hence poor prognosis.

Definition

Ovarian tumours are neoplasms arising from the ovary; they may be benign or malignant and arise from any of its tissue components. Ovarian cancer is notorious for presenting late ("the silent killer").

Classification of Ovarian Tumours (WHO)

Classification (WHO, BY Tissue of Origin)

• Surface epithelial tumours (~65%) — serous, mucinous, endometrioid, clear-cell and Brenner tumours (the commonest malignant group).
• Germ-cell tumours — benign cystic teratoma (dermoid cyst), dysgerminoma, yolk-sac tumour, choriocarcinoma (common in young women).
• Sex-cord stromal tumours — granulosa-cell, theca-cell, Sertoli–Leydig (often hormone-producing).
• Metastatic tumours — e.g. Krukenberg tumour from the gastrointestinal tract.

Clinical Features

Often silent until large or malignant. Symptoms include abdominal swelling/mass, vague discomfort, pressure effects (urinary, bowel), and — in functioning tumours — hormonal effects (precocious puberty, menstrual disturbance, virilisation). Malignancy is suggested by ascites, rapid growth, fixity, nodularity and weight loss.

Complications

Torsion (axial rotation) causing acute pain, rupture, intracystic/intraperitoneal haemorrhage, infection, pseudomyxoma peritonei (mucinous), and malignant change.

Investigations

Ultrasound (with the morphology/risk index) and Doppler; tumour markers — CA-125 (epithelial), AFP and β-hCG (germ-cell), LDH (dysgerminoma) and inhibin (granulosa); and CT/MRI for staging.

Figo Staging of Ovarian Cancer

• Stage I — confined to the ovaries (IA one ovary, capsule intact; IB both ovaries; IC capsule breached/surface tumour/malignant washings).
• Stage II — one or both ovaries with pelvic extension.
• Stage III — spread to the peritoneum outside the pelvis and/or retroperitoneal (para-aortic) nodes.
• Stage IV — distant metastasis (liver parenchyma, pleural effusion, etc.).

Management

• Benign tumours — cystectomy (preserving the ovary in young women) or oophorectomy.
• Malignant tumours — staging laparotomy with cytoreductive (debulking) surgery — total hysterectomy, bilateral salpingo-oophorectomy, omentectomy and node sampling — followed by platinum-based chemotherapy (carboplatin + paclitaxel).
• Fertility-sparing surgery for early germ-cell tumours in young women.

WHY Ovarian Cancer Is the 'silent Killer'

The dominant fact about malignant ovarian tumours is why they are usually diagnosed late, and why this makes them so lethal. Unlike the cervix, which can be seen and scraped, and unlike the endometrium, which announces itself early by abnormal bleeding, the ovary lies free within the peritoneal cavity, where a tumour can grow to a considerable size without pressing on anything or producing any specific symptom. Its early symptoms — bloating, vague abdominal discomfort, early satiety, urinary frequency — are so non-specific that they are attributed to indigestion or irritable bowel and dismissed by both patient and doctor. Worse, the peritoneal cavity provides a ready route for transcoelomic spread: malignant cells shed from the ovarian surface seed the peritoneum, omentum and diaphragm, so the disease is widely disseminated (with ascites) by the time it is felt. Consequently, about 70% present in stage III or IV, when cure is rarely possible — and no screening test (neither CA-125 nor ultrasound) has been shown to reduce mortality in the general population. Understanding that anatomy, non-specific symptoms and early transcoelomic spread together conspire to delay diagnosis explains both the grim prognosis and why any persistent, unexplained abdominal symptom in an older woman deserves a pelvic examination and an ultrasound.

WHY the Histological Origin Explains the Classification

Understanding why ovarian tumours are classified by their cell of origin turns an intimidating list into a logical scheme. The ovary contains three tissue types, and each gives rise to its own family of tumours, with characteristic ages and behaviour. Surface epithelial tumours (about 65–70%, and the great majority of malignancies) arise from the coelomic epithelium and mimic the other Mullerian epithelia — serous (commonest; mimicking tube), mucinous (mimicking endocervix; may give pseudomyxoma peritonei), endometrioid and clear-cell; they occur chiefly in older, peri- and postmenopausal women. Germ cell tumours (about 15–20%) arise from the totipotent germ cells and therefore may contain any tissue — the benign mature cystic teratoma (dermoid) is the commonest ovarian tumour in young women, and the malignant forms (dysgerminoma, yolk sac, choriocarcinoma) occur in children and young adults and produce tumour markers (AFP, hCG, LDH). Sex cord-stromal tumours (5–10%) arise from the hormone-producing cells, so they are functional — granulosa cell tumours secrete oestrogen (precocious puberty, postmenopausal bleeding, endometrial hyperplasia), and Sertoli-Leydig tumours secrete androgens (virilisation). Recognising that origin predicts age, hormone production and marker explains the entire classification.

• Ovarian tumours are classified by origin: surface epithelial (65–70%, most malignancies), germ cell (15–20%), and sex cord-stromal (5–10%).
• Epithelial: serous (commonest), mucinous, endometrioid, clear cell — in older women; germ cell: mature cystic teratoma (dermoid — commonest in young women), dysgerminoma, yolk sac.
• Sex cord-stromal tumours are functional: granulosa cell (oestrogen → postmenopausal bleeding), Sertoli-Leydig (androgen → virilisation).
• Ovarian cancer is the 'silent killer' — vague symptoms and early transcoelomic spread mean ~70% present in stage III/IV.
• Investigate with ultrasound, CA-125 (epithelial), AFP/hCG/LDH (germ cell); treat by staging laparotomy with cytoreductive surgery + platinum-based chemotherapy.

Postmenopausal bleeding is endometrial cancer until excluded.

Definition

Carcinoma of the endometrium is a malignant tumour of the endometrial lining of the uterus, the majority being adenocarcinomas. It is predominantly a cancer of post-menopausal women and is the commonest pelvic genital malignancy in many developed countries.

Types of Endometrial Carcinoma

Types

• Type I (≈ 80%, endometrioid) — oestrogen-dependent, arises from endometrial hyperplasia, occurs in younger/peri-menopausal obese women, is well-differentiated and carries a good prognosis.
• Type II (serous, clear-cell) — non-oestrogen-dependent, occurs in older women on an atrophic endometrium, is poorly-differentiated and aggressive.

Risk Factors

Conditions of unopposed oestrogen — obesity, nulliparity, late menopause, anovulation/PCOS, oestrogen-only HRT, oestrogen-secreting tumours (granulosa cell) and tamoxifen — together with diabetes, hypertension and Lynch syndrome (HNPCC). The precursor is atypical endometrial hyperplasia.

Clinical Features

Post-menopausal bleeding is the cardinal symptom (and any post-menopausal bleeding is endometrial cancer until proven otherwise); peri-menopausal women present with irregular/intermenstrual bleeding, and there may be a blood-stained or watery discharge. Pain and a mass occur late.

Investigations

• Transvaginal ultrasound — an endometrial thickness > 4 mm in a post-menopausal woman with bleeding warrants sampling.
• Endometrial biopsy/aspiration (e.g. Pipelle) or hysteroscopy with dilatation and curettage — the definitive diagnosis.
• MRI/CT for myometrial invasion and spread, and chest imaging.

Figo Staging (surgical)

• Stage I — confined to the corpus uteri (IA < ½ myometrial invasion, IB ≥ ½).
• Stage II — invades the cervical stroma but not beyond the uterus.
• Stage III — local/regional spread to serosa/adnexa, vagina/parametrium, or pelvic/para-aortic nodes.
• Stage IV — invasion of bladder/bowel mucosa (IVA) or distant metastasis (IVB).

Management

• Surgery (mainstay) — total hysterectomy with bilateral salpingo-oophorectomy, peritoneal washings and pelvic ± para-aortic lymphadenectomy (surgical staging).
• Adjuvant radiotherapy (vault brachytherapy/pelvic) for intermediate/high-risk disease, and chemotherapy for advanced or high-grade (serous) tumours.
• Progestins — for fertility preservation in selected young women with early well-differentiated tumours, and for advanced/recurrent hormone-responsive disease.

WHY Unopposed Oestrogen Is the Common Thread

The single concept that explains nearly every risk factor for endometrial carcinoma is unopposed oestrogen. Oestrogen stimulates the endometrium to proliferate; progesterone opposes this, converting it to a stable secretory endometrium and limiting its growth. Whenever the endometrium is exposed to oestrogen without adequate progesterone — that is, in the absence of ovulation, since it is the corpus luteum that produces progesterone — it proliferates unchecked, passing through hyperplasia (which, once atypical, is frankly premalignant) to carcinoma. Every classical risk factor is an instance of this: obesity (adipose tissue converts androgens to oestrogen by aromatase, and this oestrogen is unopposed after the menopause); nulliparity and late menopause (more ovulatory-free or oestrogen-exposed years); PCOS (chronic anovulation → chronic unopposed oestrogen — which is why young women with PCOS need progestogen protection); oestrogen-only HRT; tamoxifen (an anti-oestrogen in the breast but an oestrogen agonist in the uterus); and oestrogen-secreting granulosa cell tumours. Diabetes and hypertension travel with obesity. Understanding this single mechanism explains why the pill (which supplies progestogen) is protective, and why the treatment of hyperplasia is progestogen.

WHY It Presents Early — and WHY That Is Fortunate

A striking contrast with ovarian cancer is why endometrial carcinoma generally has a good prognosis. It is not because the tumour is less aggressive but because it announces itself early: any growth of the endometrium bleeds, and since the disease occurs chiefly after the menopause, that bleeding is immediately abnormal and alarming. Hence about 90% of women present with postmenopausal bleeding, and most are diagnosed in stage I, when the disease is confined to the uterus and is curable by surgery alone. This gives the cardinal rule of gynaecology: postmenopausal bleeding is endometrial carcinoma until proved otherwise, and must always be investigated — by transvaginal ultrasound (an endometrial thickness above 4–5 mm demands sampling) and by endometrial biopsy or hysteroscopy with curettage, which gives the histological diagnosis. The contrast with the ovary is instructive: the same woman's ovarian cancer would have grown silently to stage III, while her endometrial cancer bled at stage I. Understanding that the symptom appears at the earliest stage of the disease explains both the favourable prognosis and why no woman with postmenopausal bleeding may ever be reassured without investigation.

• Endometrial carcinoma arises from unopposed oestrogen → hyperplasia (atypical = premalignant) → carcinoma; usually postmenopausal.
• Risk factors (all reflect unopposed oestrogen): obesity, nulliparity, late menopause, PCOS/anovulation, oestrogen-only HRT, tamoxifen, diabetes, hypertension.
• ~90% present with postmenopausal bleeding — which is endometrial cancer until proved otherwise; most are therefore diagnosed in stage I.
• Investigate with transvaginal ultrasound (endometrial thickness >4–5 mm) and endometrial biopsy/hysteroscopy + curettage.
• Treatment: total hysterectomy with bilateral salpingo-oophorectomy ± lymphadenectomy; adjuvant radiotherapy in higher-risk disease. Prognosis is good.

Groin node status is the key prognostic factor.

Definition

Carcinoma of the vulva is a malignant tumour of the vulva, the great majority being squamous-cell carcinomas. It is predominantly a disease of elderly post-menopausal women and most often arises on the labium majus.

Carcinoma Vulva - Spread

Risk Factors

Vulval intraepithelial neoplasia (vin) and HPV infection (in younger women), lichen sclerosus and chronic vulval dystrophy (in older women), smoking, immunosuppression, chronic irritation, and a history of cervical neoplasia.

Premalignant Lesion

Vulval intraepithelial neoplasia (vin) — atypical cells confined to the epithelium — is the precursor, analogous to CIN of the cervix.

Clinical Features

Long-standing vulval pruritus, a lump, ulcer or warty growth, bleeding, discharge, pain and occasionally a groin swelling (nodal disease). The lesion is often neglected, so women present late.

Spread

Direct — to the adjacent vagina, urethra and anus; lymphatic (the main route) — to the inguinal, then femoral, and finally pelvic nodes; blood-borne spread is late.

Investigations

Diagnosis is confirmed by a wedge biopsy of the lesion (with vulvoscopy of the remaining vulva). Spread is assessed by palpation of the groin nodes, cystoscopy/proctoscopy for local extension, and cross-sectional imaging (CT/MRI/pet) of the groin and pelvis; a cervical smear is taken in view of the HPV field association.

Figo Staging

• Stage I — tumour confined to the vulva/perineum (IA ≤ 2 cm with stromal invasion ≤ 1 mm).
• Stage II — extension to adjacent structures (lower urethra, vagina, anus) with negative nodes.
• Stage III — spread to the inguino-femoral lymph nodes.
• Stage IV — invasion of upper urethra/bladder/rectum/bone or distant metastasis.

Management

• Early disease — wide local excision with assessment of the groin nodes (sentinel-node biopsy or inguino-femoral lymphadenectomy).
• Operable invasive disease — radical vulvectomy with bilateral inguino-femoral lymphadenectomy.
• Advanced/inoperable disease — radiotherapy or chemoradiation, with surgery where feasible.
• Treat vin to prevent progression, and counsel on smoking cessation and follow-up.

WHY Vulval Cancer Is Often Diagnosed Late, Despite Being Visible

A striking paradox worth understanding is why carcinoma of the vulva — a cancer on the body's surface, which the woman can see and feel — is so often advanced at diagnosis. The tumour is not hidden; the delay is human. It occurs typically in elderly women, who may be embarrassed to seek help for a genital complaint, may attribute the symptoms to 'old age', or may have limited access to care. Its principal symptom, long-standing pruritus vulvae, is extremely common and is very frequently treated — by the woman herself, by pharmacists, and by doctors — with topical steroids or antifungals for months or years without anyone ever looking properly, or taking a biopsy. Meanwhile the underlying lesion (often arising in a background of lichen sclerosus or vin) progresses to an ulcer or a growth. Hence the cardinal rule: any persistent vulval itching, ulcer, lump or white patch in an older woman must be biopsied, not treated blindly — no vulval lesion should be treated for more than a few weeks without a histological diagnosis. Understanding that the disease is missed not because it is invisible but because it is not looked at explains why the biopsy is the whole key.

WHY the Groin Nodes Dominate the Treatment

Understanding why the surgical treatment of vulval cancer is so extensive, and centred on the groins, follows from its pattern of spread. The vulva has a rich, predictable lymphatic drainage, which passes first to the superficial inguinal nodes, then to the deep inguinal (including Cloquet's node) and thence to the pelvic nodes — and, importantly, the lymphatics of the midline structures (clitoris, perineum) cross, so drainage may be bilateral. Because lymph-node status is by far the most important prognostic factor — survival falls dramatically once the groin nodes are involved — the operation must address them. This is why the classical treatment is a radical vulvectomy with bilateral inguinofemoral lymphadenectomy, and why leaving the nodes untreated is unacceptable except in the earliest lesions. But this surgery is mutilating and carries heavy morbidity — wound breakdown, infection, and lifelong lymphoedema of the legs. Hence the modern trend towards individualisation: a wide local excision with ipsilateral (or sentinel) node assessment for small, unilateral, early tumours, sparing many women the full operation. Understanding that the groin nodes determine both prognosis and the extent of surgery explains the whole surgical strategy.

• Carcinoma vulva: usually squamous cell carcinoma in elderly women; arises from vin or lichen sclerosus (and HPV in younger women).
• Presents with long-standing pruritus vulvae, then an ulcer, lump or bleeding — often treated blindly for months, hence late diagnosis.
• Golden rule: biopsy any persistent vulval ulcer, lump, white patch or itch in an older woman — never treat blindly.
• Spreads to the inguinal nodes (superficial → deep → pelvic; midline lesions drain bilaterally) — node status is the key prognostic factor.
• Treatment: radical vulvectomy with bilateral inguinofemoral lymphadenectomy; wide local excision with sentinel-node biopsy for early unilateral lesions; radiotherapy for advanced disease.

Highly chemosensitive — curable even with metastases.

Definition

Gestational trophoblastic neoplasia (GTN) is the malignant form of gestational trophoblastic disease, comprising invasive mole, choriocarcinoma and placental-site trophoblastic tumour. Choriocarcinoma is a highly malignant tumour of the trophoblast that invades and metastasises early via the blood-stream.

Gestational Trophoblastic Disease Spectrum

Antecedent Pregnancy

GTN follows a hydatidiform mole in ~50% of cases, an abortion/ectopic in ~25%, and a normal term pregnancy in ~25%. Post-molar GTN is diagnosed when the β-hCG plateaus or rises over consecutive weeks after evacuation.

Pathology

Choriocarcinoma is a soft, purple, haemorrhagic and necrotic tumour composed of sheets of malignant cyto- and syncytio-trophoblast with no chorionic villi; it invades the myometrium and blood vessels early, which explains its rapid haematogenous spread. An invasive mole, by contrast, retains hydropic villi that penetrate the myometrium. Bilateral theca-lutein cysts may persist owing to the high β-hCG.

Clinical Features

Persistent or irregular vaginal bleeding after a molar pregnancy, abortion or delivery, with subinvolution of the uterus and a rising/plateauing β-hCG. Because spread is haematogenous, women may present with features of metastases — lung (commonest — haemoptysis, dyspnoea), vagina (a bluish nodule that bleeds), brain (neurological deficit) and liver.

Investigations

• Serial β-hCG — the tumour marker for diagnosis, monitoring and follow-up.
• Ultrasound of the uterus/pelvis (Doppler shows vascular invasion).
• Metastatic work-up — chest radiograph/CT, CT/MRI brain, and liver imaging.

Staging and Risk Scoring

Staged by the FIGO anatomical stages I–IV and risk-stratified by the WHO/FIGO prognostic scoring system (age, antecedent pregnancy, interval, hCG level, tumour size, site and number of metastases, and prior chemotherapy): a score of ≤ 6 is low-risk and ≥ 7 is high-risk, which determines therapy.

Management

• GTN is highly chemosensitive and chemotherapy is the mainstay.
• Low-risk disease — single-agent chemotherapy (methotrexate with folinic-acid rescue, or actinomycin-D).
• High-risk disease — multi-agent chemotherapy (EMA-CO regimen), with surgery/radiotherapy for selected sites (e.g. Brain metastases).
• Follow-up with serial β-hCG until normal for a defined period, and reliable contraception during treatment and follow-up.

WHY Β-HCG Makes GTN a Uniquely Manageable Cancer

The extraordinary feature of gestational trophoblastic neoplasia is why it is one of the most curable of all malignancies — even when widely metastatic. Two properties account for this. First, it possesses a near-perfect tumour marker: the trophoblast secretes β-hCG in direct proportion to the number of viable tumour cells, and this can be measured in the blood with great sensitivity. This means the disease can be diagnosed early (by a plateauing or rising β-hCG during follow-up after a molar pregnancy), its response to treatment monitored precisely (a falling titre proves the chemotherapy is working), its complete eradication confirmed (a normal titre), and its recurrence detected before any clinical sign — a degree of biological surveillance available in almost no other cancer, and the reason that the follow-up of every hydatidiform mole is by serial β-hCG. Second, the tumour is exquisitely sensitive to chemotherapy (methotrexate in low-risk disease; multi-agent EMA-CO in high-risk). Together these give cure rates approaching 100% in low-risk and above 90% in high-risk disease, with fertility usually preserved. Understanding that a measurable marker plus a chemosensitive tumour equals cure explains the whole approach to this disease.

WHY Every Mole Must Be Followed Up — and Contraception Is Mandatory

A rule of absolute importance is why a woman whose hydatidiform mole has been evacuated is not discharged, but followed with serial β-hCG — and why she must not conceive during that period. After evacuation, a proportion of moles (about 15–20% of complete moles) do not resolve but persist as invasive mole or progress to choriocarcinoma — and this can only be detected by watching the β-hCG: it should fall progressively to normal; a plateau or a rise signals persistent trophoblastic disease and the need for chemotherapy. This surveillance is the whole reason such women survive. But it depends entirely on the β-hCG being interpretable — and a new pregnancy also produces β-hCG, which would completely obscure the signal, making it impossible to tell a normal pregnancy from a growing malignancy. This is why effective contraception is mandatory throughout the follow-up period (the combined oral pill is suitable; an IUCD is avoided until the β-hCG is normal, because of the risk of uterine perforation). Understanding that follow-up is a chemical watch that pregnancy would blind explains why contraception is not advice but a requirement.

• GTN includes invasive mole, choriocarcinoma, placental-site trophoblastic tumour and epithelioid trophoblastic tumour; it follows a molar pregnancy (~50%), abortion or a normal pregnancy.
• Choriocarcinoma spreads early and haematogenously — the lungs are the commonest site (also vagina, brain, liver).
• β-hCG is a near-perfect tumour marker — used for diagnosis, monitoring response, confirming cure and detecting recurrence.
• Treatment: single-agent methotrexate (low-risk, WHO score ≤6) or multi-agent EMA-CO (high-risk) — cure rates approach 100% (low-risk) and >90% (high-risk), with fertility preserved.
• Every mole needs serial β-hCG follow-up with mandatory contraception (a new pregnancy would obscure the marker).

Definition

A fibroid (leiomyoma/myoma) is a benign tumour arising from the smooth muscle of the uterus. It is the commonest benign tumour of the uterus and of the female pelvis, and is oestrogen-dependent (grows in the reproductive years, regresses after menopause).

Classification of Uterine Fibroids BY Site

Classification (BY Location)

• Intramural (interstitial) — within the myometrium (commonest).
• Submucous — projecting into the cavity (may become a fibroid polyp); causes the most bleeding.
• Subserous — projecting outward beneath the serosa (may be pedunculated or "wandering").
• Cervical and broad-ligament (intraligamentary) fibroids.

Pathology

A firm, well-circumscribed, whorled tumour with a false capsule (pseudocapsule) of compressed myometrium that allows easy enucleation; histology shows interlacing bundles of smooth muscle and fibrous tissue.

Degenerations

• Hyaline (≈ 65%, commonest) — homogeneous, soft, with loss of the whorled pattern.
• Cystic — liquefaction of hyaline areas (may mimic an ovarian cyst).
• Fatty — at/after menopause.
• Calcific (≈ 10%) — in subserous/post-menopausal fibroids ("womb-stone").
• Red (carneous) degeneration — aseptic necrobiosis, typically in the second half of pregnancy/ puerperium, giving a "raw-beef" appearance with a fishy odour (see short note).
• Atrophy after menopause, and rare sarcomatous change (≈ 0.1%).

Clinical Features

Often asymptomatic. When symptomatic — menorrhagia/heavy menstrual bleeding (especially submucous), a lower-abdominal mass, pressure effects (urinary frequency, retention, constipation), dysmenorrhoea/pelvic pain, and subfertility or recurrent miscarriage.

Complications

Degenerations, torsion of a pedunculated fibroid, infection, capsular haemorrhage, rare malignant change, and pregnancy-related problems (miscarriage, malpresentation, obstructed labour, PPH).

Investigations

Ultrasound (transvaginal/abdominal) is the main investigation — it confirms the number, size and location of fibroids and distinguishes them from an ovarian mass; saline sonohysterography or hysteroscopy defines submucous fibroids, and MRI helps when the anatomy is complex or before uterine-artery embolisation. Haemoglobin is checked for anaemia from menorrhagia.

Fibroid in Pregnancy

Fibroids may enlarge and undergo red degeneration; they predispose to miscarriage, malpresentation, obstructed labour and postpartum haemorrhage. They are managed conservatively in pregnancy (myomectomy is avoided owing to the risk of severe haemorrhage).

Management

• Expectant — small, asymptomatic fibroids with periodic review.
• Medical — for symptom control/pre-operative shrinkage: tranexamic acid and NSAIDs for bleeding, progestins/LNG-IUS, and GnRH analogues or ulipristal to shrink the tumour temporarily.
• Surgical — myomectomy (to preserve fertility) or hysterectomy (completed family); uterine artery embolisation and hysteroscopic resection of submucous fibroids are alternatives.

Fibroids are classified by their location, which determines the symptoms. A submucous fibroid projects into the uterine cavity and causes heavy menstrual bleeding, infertility and miscarriage even when small. An intramural fibroid (the commonest) lies within the myometrial wall, causing menorrhagia and bulk symptoms. A subserous fibroid projects outward, causing pressure symptoms rather than bleeding, and may become pedunculated and undergo torsion.

WHY the Symptoms Depend Entirely on the Location

The key to understanding fibroids is why two women with fibroids of identical size may have utterly different symptoms — or none at all. The answer is location, not size. A submucous fibroid, though it may be tiny, projects into the uterine cavity, distorting and increasing the endometrial surface and interfering with uterine contraction and with the vascular architecture — so it causes heavy, prolonged menstrual bleeding (menorrhagia) out of all proportion to its size, and, by distorting the cavity, may cause infertility and recurrent miscarriage. An intramural fibroid (the commonest) sits within the myometrial wall and causes menorrhagia and bulk symptoms as it enlarges. A subserous fibroid projects outward from the uterus into the peritoneal cavity, and therefore does not affect the cavity or menstruation at all: it may grow very large and remain silent, or cause pressure symptoms on the bladder (frequency) or rectum, and if it becomes pedunculated it may undergo torsion. Understanding that it is the relationship to the endometrial cavity that determines the bleeding, and the relationship to the peritoneal cavity that determines the pressure symptoms, explains why the clinical picture, the need for treatment and the choice of operation all follow from location.

WHY Fibroids Are Oestrogen-dependent — and What Follows

A concept that explains much of the natural history and treatment of fibroids is that they are oestrogen (and progesterone) dependent tumours. Several clinical observations follow directly from this. They arise only during the reproductive years, are commoner in nulliparous women and in conditions of unopposed oestrogen, and — crucially — they regress after the menopause, when oestrogen falls: a fibroid that grows after the menopause must therefore be regarded with suspicion (raising the question of the rare leiomyosarcoma). Conversely, they frequently enlarge in pregnancy (under the influence of high oestrogen and increased vascularity), which is when a large fibroid may outgrow its blood supply and undergo red (carneous) degeneration — causing acute pain, tenderness, low-grade fever and vomiting in the second trimester. Hormone dependence also underlies treatment: GnRH agonists induce a temporary, reversible pseudo-menopause that shrinks fibroids — useful pre-operatively to reduce size and correct anaemia, but not a definitive cure, since the fibroids regrow when the drug is stopped. Recognising the hormonal dependence of fibroids explains their timing, their behaviour in pregnancy and after menopause, and the logic behind their medical treatment.

• Fibroid (leiomyoma) = benign smooth-muscle tumour of the uterus; the commonest pelvic tumour in women; oestrogen-dependent (regresses after the menopause).
• Symptoms depend on location: submucous → menorrhagia, infertility, miscarriage (even when small); intramural (commonest) → menorrhagia, bulk; subserous → pressure symptoms, torsion if pedunculated.
• Degenerations: hyaline (commonest), cystic, red/carneous (in pregnancy — acute pain), calcification; malignant change (leiomyosarcoma) is rare (<0.5%).
• Diagnosis: bimanual examination (firm, irregular, mobile mass moving with the cervix) + ultrasound (and hysteroscopy for submucous).
• Treatment: observation if asymptomatic; medical (tranexamic acid, LNG-IUS, GnRH agonist pre-op); surgical — myomectomy (fertility desired) or hysterectomy.

Male factor accounts for about 30–40% — test him first, it is simplest.

Definition

Infertility is the failure of a couple to conceive after one year of regular, unprotected sexual intercourse. It is primary when conception has never occurred, and secondary when it follows a previous conception. About 10–15% of couples are affected.

Infertility - Evaluation Pathway

Causes

• Female factors — ovulatory/endocrine (PCOS, hyperprolactinaemia, thyroid disorders, premature ovarian failure), tubal (pelvic inflammatory disease, tuberculosis, endometriosis, previous surgery), uterine (fibroid, synechiae, anomalies) and cervical factors.
• Male factors — defective spermatogenesis (oligo-/astheno-/azoospermia), varicocele, obstruction, infection, endocrine and sexual/ejaculatory dysfunction.
• Combined and unexplained infertility (normal basic tests in ~10–15%).

Investigation of the Infertile Couple

Both partners are investigated together.

General

History (duration, coital frequency, menstrual and medical/surgical history) and examination of both partners.

Male

Semen analysis (after 2–3 days' abstinence) is the single most important male test — volume, sperm count, motility and morphology; repeated and supplemented by hormones/imaging if abnormal.

Female

• Tests of ovulation — mid-luteal (day-21) serum progesterone, basal body temperature, ultrasound folliculometry, and LH-surge detection.
• Tests of tubal patency — hysterosalpingography (HSG), laparoscopy and dye (chromopertubation, the gold standard), or sono-salpingography.
• Uterine cavity — ultrasound and hysteroscopy for fibroids, polyps, synechiae and anomalies.
• Ovarian reserve — anti-Müllerian hormone (AMH) and antral follicle count.

Management

• General — correct lifestyle factors (weight, smoking, alcohol), optimise coital timing, and treat infection.
• Ovulatory disorders — ovulation induction with clomiphene citrate or letrozole, and gonadotrophins in resistant cases; dopamine agonists for hyperprolactinaemia.
• Tubal disease — tubal microsurgery in selected cases, otherwise in-vitro fertilisation (IVF).
• Male factor — treat the cause (varicocele ligation, infection); intra-uterine insemination (IUI) for mild defects and ICSI for severe oligospermia/azoospermia.
• Assisted reproduction — IUI, IVF and ICSI for unexplained or refractory infertility; donor gametes and surrogacy where appropriate.

WHY Both Partners Must Be Investigated from the Start

A principle that shapes the whole management of infertility is why the couple, not the woman, is the unit of investigation. Cultural assumption — particularly in India — tends to place the 'fault' with the wife, and she may undergo months of investigation before her husband is tested at all. This is both unjust and clinically irrational, because a male factor is responsible in about 30–40% of cases (alone or in combination), and it is identified by a test that is simple, cheap, non-invasive and immediate — a semen analysis. It would be absurd to subject a woman to hysterosalpingography or laparoscopy while the husband's semen has never been examined. Hence the rule: investigate both partners simultaneously, starting with the simplest tests — semen analysis for him; confirmation of ovulation (cycle history, mid-luteal progesterone) for her; and tubal patency (HSG) once these are known. This ordering also reflects the three questions that between them explain almost all infertility: is there sperm? Is there an egg? Can they meet? Understanding that infertility is a couple's problem — and that the cheapest, easiest test belongs to the man — explains the logic and the sequence of investigation.

WHY the Causes Map Onto a Simple Anatomical Sequence

Understanding why the causes of infertility can be organised as a physiological sequence converts a long list into a system. Conception requires, in order: a sperm produced and delivered; an egg released; a patent tube for them to meet in; and a receptive uterus for implantation. Each step yields its own causes and its own test. Male factor (30–40%): defective spermatogenesis (varicocele, infection, heat, drugs, undescended testis), obstruction, or sexual/ejaculatory dysfunction — tested by semen analysis. Ovulatory factor (~30%): PCOS (much the commonest), hypothalamic-pituitary dysfunction (stress, weight loss, exercise), hyperprolactinaemia, thyroid disease, premature ovarian insufficiency — confirmed by a mid-luteal serum progesterone. Tubal and peritoneal factor (~25%, and especially important in India): blockage from pelvic inflammatory disease or genital tuberculosis, and endometriosis — assessed by HSG and, definitively, laparoscopy with chromopertubation. Uterine and cervical factors: fibroids, adhesions (Asherman's), anomalies. And a proportion remains unexplained. Recognising that each cause corresponds to a step in the journey of sperm and egg explains why the investigations are what they are.

• Infertility = failure to conceive after one year of regular unprotected intercourse; primary (never conceived) or secondary.
• Always investigate both partners together — male factor accounts for 30–40% and semen analysis is the cheapest, easiest test.
• Causes: male factor (30–40%), ovulatory (~30%, PCOS commonest), tubal/peritoneal (~25% — PID and genital TB are important in India), uterine/cervical; some unexplained.
• Basic tests: semen analysis; mid-luteal progesterone (confirms ovulation); HSG for tubal patency; ultrasound; laparoscopy with chromopertubation if needed.
• Treatment: correct the cause — ovulation induction (letrozole/clomiphene), tubal surgery, IUI, and IVF/ICSI for tubal block or severe male factor.

palm-COEIN gives a systematic framework for every case.

Definition

Abnormal uterine bleeding (AUB) is any uterine bleeding that is abnormal in frequency, regularity, duration or volume in a non-pregnant woman of reproductive age. Dysfunctional uterine bleeding (DUB) is AUB in the absence of any organic (structural), systemic or pregnancy-related cause — a diagnosis of exclusion resulting from a disturbance of the hypothalamo-pituitary-ovarian axis.

Aub - Palm-coein Classification

Classification of Aub — Palm-coein (figo)

• Structural (palm) — Polyp, Adenomyosis, Leiomyoma, Malignancy/hyperplasia.
• Non-structural (COEIN) — Coagulopathy, Ovulatory dysfunction, Endometrial, Iatrogenic, Not otherwise classified.

DUB corresponds mainly to the ovulatory and endometrial categories.

Types of Dub

• Anovulatory (≈ 90%) — at the extremes of reproductive life (adolescence and peri-menopause); unopposed oestrogen causes irregular, heavy and prolonged bleeding.
• Ovulatory — regular but heavy menstrual loss, often due to a luteal-phase or endometrial defect.

Pathophysiology of Anovulatory Dub

In the absence of ovulation no corpus luteum forms, so there is no progesterone to oppose oestrogen. The endometrium proliferates under continuous unopposed oestrogen until it outgrows its blood supply and breaks down irregularly and incompletely — producing the characteristic irregular, heavy and prolonged bleeding.

Evaluation

A careful menstrual and drug history, examination, and a pregnancy test; pelvic examination and investigations to exclude structural and systemic causes before labelling bleeding as DUB.

Investigations

• Haemoglobin (anaemia), thyroid function and a coagulation screen (especially in adolescents).
• Transvaginal ultrasound for fibroids, polyps and endometrial thickness.
• Endometrial biopsy/hysteroscopy in women > 40 years or with risk factors, to exclude hyperplasia/malignancy.

Management

• Medical (first line) — tranexamic acid and NSAIDs (mefenamic acid) for ovulatory heavy bleeding; combined oral pills or cyclical/continuous progestins; the levonorgestrel-IUS (Mirena) is highly effective; GnRH analogues for short-term control.
• Surgical — endometrial ablation for those who have completed their family and failed medical treatment, and hysterectomy as definitive treatment.

Age-related Approach

In adolescents, anovulatory DUB usually settles with reassurance and hormonal regulation (and a coagulation screen). In the reproductive years, exclude structural causes and use medical therapy/LNG-IUS. In the peri-menopausal woman, the endometrium must be sampled to exclude hyperplasia/malignancy before treatment.

WHY Anovulation Explains Most Dysfunctional Bleeding

The key to abnormal uterine bleeding of the non-structural kind is why failure to ovulate causes irregular, heavy bleeding. In a normal ovulatory cycle, the corpus luteum produces progesterone, which stabilises the proliferative endometrium, converts it to a secretory endometrium and — when it withdraws in a coordinated fashion — produces a predictable, self-limiting bleed of normal volume. In an anovulatory cycle, no corpus luteum forms, so there is no progesterone: the endometrium is exposed to unopposed oestrogen and simply goes on proliferating, becoming thick, fragile and structurally disorganised, with no coordinated withdrawal. It then breaks down erratically and incompletely, shedding from different areas at different times — which is precisely why the bleeding is irregular in timing, unpredictable in duration and often heavy and prolonged. This is why anovulatory bleeding clusters at the extremes of reproductive life (adolescence, when the axis is immature, and the perimenopause, when it is failing) and in PCOS — the three situations in which ovulation is unreliable. And it explains the treatment: giving progestogen (or a combined pill, or an LNG-IUS) supplies what is missing, stabilising the endometrium and restoring a controlled withdrawal bleed.

WHY Structural Causes Must Be Excluded First — Palm-coein

A vital clinical discipline is why 'dysfunctional' bleeding is a diagnosis of exclusion, and why the palm-COEIN system is used. It is dangerous to label abnormal bleeding as hormonal without first excluding a lesion — above all a malignancy. FIGO's palm-COEIN classification separates the causes into structural (palm: Polyp, Adenomyosis, Leiomyoma, Malignancy and hyperplasia — all of which can be seen or biopsied) and non-structural (COEIN: Coagulopathy, Ovulatory dysfunction, Endometrial, Iatrogenic, Not otherwise classified). The value of this discipline is that it enforces the right investigations: ultrasound and hysteroscopy to look for polyps, fibroids and adenomyosis; and — crucially — endometrial sampling in any woman over 40, or with risk factors for hyperplasia (obesity, PCOS, tamoxifen), or with persistent bleeding, to exclude hyperplasia and carcinoma. It also reminds one to look for the systemic causes that are easily missed: a coagulopathy (von Willebrand's disease, present in a significant minority of adolescents with severe menorrhagia), hypothyroidism, and iatrogenic causes (anticoagulants, hormonal contraception). Understanding that a hormonal diagnosis may only be made once a structural one has been excluded explains the entire investigative sequence.

• Abnormal uterine bleeding is classified by FIGO as palm (structural: Polyp, Adenomyosis, Leiomyoma, Malignancy/hyperplasia) and COEIN (non-structural: Coagulopathy, Ovulatory dysfunction, Endometrial, Iatrogenic, Not classified).
• Most 'dysfunctional' bleeding is anovulatory: no corpus luteum → no progesterone → unopposed oestrogen → a thick, fragile endometrium shedding erratically.
• It clusters at the extremes of reproductive life (adolescence, perimenopause) and in PCOS.
• Always exclude structural causes and malignancy: ultrasound ± hysteroscopy, and endometrial sampling in women over 40, or with risk factors or persistent bleeding.
• Treatment: medical first — tranexamic acid, NSAIDs, progestogens, combined pill, LNG-IUS (first-line for menorrhagia); surgery (ablation, hysterectomy) if medical treatment fails.

Severity of disease correlates poorly with severity of pain.

Definition

Endometriosis is the presence of functioning endometrial tissue (glands and stroma) outside the uterine cavity. Being hormonally responsive, it bleeds cyclically at the ectopic sites, producing inflammation, adhesions and pain.

Endometriosis - Sites & Theory

Sites

Most often within the pelvis — the ovary (forming a "chocolate cyst"/endometrioma), the pouch of Douglas, the uterosacral ligaments, the pelvic peritoneum, the recto-vaginal septum and the bladder; rarely at distant sites (umbilicus, scars, lung).

Theories of Origin

Sampson's retrograde menstruation theory (the most accepted), coelomic metaplasia, and lymphatic/ vascular dissemination, with a contribution from genetic and immunological factors.

Pathology

The ectopic deposits bleed cyclically, producing small "powder-burn"/blue-black lesions on the peritoneum and chocolate cysts (endometriomas) in the ovary (altered, tarry, retained blood), with surrounding fibrosis and dense adhesions. Microscopy shows endometrial glands and stroma with haemosiderin-laden macrophages.

Clinical Features

The classic triad is secondary dysmenorrhoea, deep dyspareunia and infertility, with chronic cyclical pelvic pain; there may be cyclical bowel/bladder symptoms. The severity of symptoms correlates poorly with the extent of disease.

Examination

A fixed retroverted uterus, tender nodularity of the uterosacral ligaments and pouch of Douglas, and a tender adnexal (ovarian) mass.

Investigations

• Ultrasound for an endometrioma; MRI for deep/extensive disease.
• Serum CA-125 may be mildly raised (non-specific).
• Laparoscopy is the gold standard for diagnosis (powder-burn deposits, endometriomas, adhesions) and allows staging (revised ASRM) and biopsy.

Complications

Infertility (the major concern — from adhesions and distorted tubo-ovarian anatomy), chronic pelvic pain, rupture or torsion of an endometrioma, dense pelvic adhesions with bowel/ureteric involvement, and rare malignant change in an endometrioma.

Management

• Medical (to suppress cyclical activity) — NSAIDs for pain; combined oral pills, progestins, the levonorgestrel-IUS, GnRH analogues (with add-back) and danazol.
• Surgical — laparoscopic ablation/excision of deposits, cystectomy of endometriomas and adhesiolysis; definitive surgery (hysterectomy with bilateral salpingo-oophorectomy) for severe disease in women who have completed their family.
• Infertility — surgery improves fertility in mild disease; assisted reproduction (IVF) for those who do not conceive.

WHY Endometriosis Causes Pain That Is Cyclical and Progressive

Understanding why the symptoms of endometriosis take the form they do follows directly from what the disease is: functioning endometrial tissue in an abnormal site. Because this ectopic tissue responds to the same hormonal cycle as the endometrium, it proliferates under oestrogen and bleeds at menstruation — but the blood has nowhere to escape. It therefore collects locally, causing inflammation, and — as this is repeated month after month — fibrosis, scarring and dense adhesions. Every symptom follows. The pain is cyclical, beginning a day or two before the period and worst during it (secondary dysmenorrhoea), and it is progressive, worsening year by year as the adhesions build up. Deposits in the pouch of Douglas and on the uterosacral ligaments cause deep dyspareunia and dyschezia; adhesions distort the tubes and ovaries and impair oocyte release and transport, causing infertility (present in up to 30–50% of women with the disease); and repeated bleeding into the ovary forms a 'chocolate' cyst (endometrioma). Note the classic paradox: the extent of the disease correlates poorly with the severity of the pain. Understanding that this is normal tissue behaving normally in the wrong place explains the whole clinical picture.

WHY Treatment Aims to Suppress Oestrogen — and its Limits

A useful concept is why the medical treatment of endometriosis is essentially the induction of a hormonal state in which the disease cannot thrive. Since the ectopic tissue is oestrogen-dependent, all medical treatments work by removing the cyclical oestrogen stimulus — either by producing a steady, progestogen-dominant state (the continuous combined pill, progestogens, the LNG-IUS) or by inducing a temporary, reversible pseudo-menopause (GnRH agonists). This suppresses the tissue, prevents its cyclical bleeding, and relieves the pain — which is why the disease also regresses naturally in pregnancy and after the menopause. But this approach has two important limits. First, the treatments are contraceptive — so they cannot be used by a woman who is trying to conceive, which is precisely the group in whom endometriosis-related infertility matters most; for her, the treatment is surgical (laparoscopic ablation/excision of deposits and adhesiolysis) or assisted reproduction. Second, medical treatment suppresses but does not cure: symptoms typically recur when it is stopped. Understanding that the disease is oestrogen-driven — and that suppressing oestrogen also suppresses fertility — explains both the logic and the frustration of treating endometriosis.

• Endometriosis = functioning endometrial tissue outside the uterus (commonest sites: ovary — chocolate cyst; pouch of Douglas; uterosacral ligaments).
• It bleeds cyclically with no escape → inflammation, fibrosis and adhesions — hence progressive, cyclical pain.
• Classic symptoms: secondary dysmenorrhoea, deep dyspareunia, chronic pelvic pain, dyschezia and infertility; the extent of disease correlates poorly with the pain.
• Diagnosis: laparoscopy is the gold standard (powder-burn deposits, chocolate cysts, adhesions); ultrasound shows endometriomas.
• Treatment: suppress oestrogen (continuous COC, progestogens, LNG-IUS, GnRH agonists) for pain; surgery (laparoscopic ablation/excision) if fertility is desired or medical treatment fails.

Definition

Polycystic ovary syndrome (PCOS) is a heterogeneous endocrine disorder of reproductive-age women characterised by hyperandrogenism, ovulatory dysfunction and polycystic ovaries. It is the commonest cause of anovulatory infertility.

Pcos - Rotterdam Criteria (2 of 3)

Diagnostic Criteria (rotterdam — Eshre/asrm)

Diagnosis requires any two of the following three (after excluding other causes):

• Oligo- or anovulation (oligomenorrhoea/amenorrhoea).
• Clinical and/or biochemical hyperandrogenism (hirsutism, acne; raised serum testosterone).
• Polycystic ovaries on ultrasound (≥ 12 small follicles per ovary and/or ovarian volume > 10 mL).

Pathophysiology

Central features are insulin resistance with compensatory hyperinsulinaemia, an increased LH:FSH ratio, and ovarian/adrenal hyperandrogenism, which together disturb folliculogenesis and ovulation.

Clinical Features

Menstrual irregularity (oligo-/amenorrhoea), hirsutism, acne and male-pattern hair loss, obesity (central), infertility, and acanthosis nigricans (a marker of insulin resistance).

Investigations

Serum testosterone, LH and FSH, prolactin and TSH (to exclude mimics); fasting glucose/insulin and an oral glucose-tolerance test, and a lipid profile; transvaginal ultrasound of the ovaries.

Differential Diagnosis

Other causes of hyperandrogenism/anovulation must be excluded — thyroid dysfunction, hyperprolactinaemia, congenital adrenal hyperplasia (late-onset), Cushing's syndrome and an androgen-secreting tumour (suggested by rapidly progressive virilisation).

Complications

Anovulatory infertility, type-2 diabetes and metabolic syndrome, dyslipidaemia, obstructive sleep apnoea, and — from chronic unopposed oestrogen — endometrial hyperplasia and carcinoma.

Management

• Lifestyle and weight reduction — the first-line measure; even modest weight loss restores ovulation and improves the metabolic profile.
• Menstrual regulation / endometrial protection — combined oral pills or cyclical progestins.
• Hirsutism — combined pills with anti-androgens (cyproterone, spironolactone), and cosmetic measures.
• Infertility — ovulation induction with letrozole (first line) or clomiphene, adding metformin, then gonadotrophins or laparoscopic ovarian drilling; IVF if these fail.
• Metabolic — metformin for insulin resistance and management of the cardiometabolic risk.

PCOS is diagnosed by the Rotterdam criteria — any two of three: oligo- or anovulation, clinical or biochemical hyperandrogenism, and polycystic ovaries on ultrasound. Underlying it is insulin resistance: the resulting hyperinsulinaemia raises ovarian androgen production and lowers sex-hormone-binding globulin, causing hirsutism, follicular arrest and anovulation. The long-term consequences are metabolic (type 2 diabetes, metabolic syndrome) and endometrial (hyperplasia and carcinoma from unopposed oestrogen).

WHY Insulin Resistance Is the Engine of Pcos

The concept that unifies the whole syndrome is why insulin resistance drives the reproductive features of PCOS. The primary abnormality in most women is insulin resistance, so the pancreas compensates by secreting more insulin (hyperinsulinaemia). That excess insulin then acts on the ovary and liver in two ways. It directly stimulates the ovarian theca cells (acting with LH) to produce more androgens; and it suppresses hepatic production of sex-hormone-binding globulin, so a greater fraction of the circulating testosterone is free and biologically active. The result is hyperandrogenism — clinically, hirsutism and acne. The high intraovarian androgen also disrupts follicular development, so follicles are recruited but arrest before maturity, accumulating as the multiple small subcapsular follicles that give the ovary its polycystic appearance — and, since no dominant follicle emerges, ovulation fails: hence oligomenorrhoea and infertility. This single chain explains all three Rotterdam criteria at once. It also explains why weight loss is the single most effective treatment — by reducing insulin resistance it can restore ovulation, regularise cycles and lower androgens, and why metformin has a role.

WHY Pcos Is a Lifelong Metabolic Disorder, Not Just a Gynaecological One

A crucial point often missed is why the young woman treated for irregular periods or hirsutism must be followed for the rest of her life. PCOS is not merely an ovarian problem; the underlying insulin resistance carries major long-term metabolic consequences: impaired glucose tolerance and type 2 diabetes, dyslipidaemia, hypertension, metabolic syndrome, non-alcoholic fatty liver disease and an increased cardiovascular risk. Separately, the chronic anovulation means the endometrium is exposed to years of unopposed oestrogen with no progesterone — producing endometrial hyperplasia and a significantly increased risk of endometrial carcinoma, even in young women. Both consequences are preventable. Hence the management of PCOS must always include: screening for diabetes and lipids, blood-pressure monitoring, and vigorous encouragement of weight loss and exercise (the treatment that addresses the root cause); and endometrial protection — ensuring that a woman not on a combined pill has at least a withdrawal bleed every three months, with cyclical progestogen or an LNG-IUS. Understanding that PCOS is a metabolic disease with gynaecological manifestations — not the reverse — explains why its management extends far beyond restoring periods or fertility.

• PCOS: diagnosed by any 2 of 3 Rotterdam criteria — oligo/anovulation, clinical or biochemical hyperandrogenism, polycystic ovaries on ultrasound.
• The engine is insulin resistance → hyperinsulinaemia → ↑ovarian androgens + ↓SHBG → hirsutism, acne, follicular arrest and anovulation.
• Long-term risks: type 2 diabetes, metabolic syndrome, dyslipidaemia, cardiovascular disease — and endometrial hyperplasia/carcinoma from unopposed oestrogen.
• Weight loss is the single most effective treatment — it can restore ovulation and regularise cycles.
• Treat by need: cycle control/endometrial protection (COC or cyclical progestogen); hirsutism (COC + anti-androgen); fertility (letrozole — first line — or clomiphene, ± metformin).

Primary begins with ovulatory cycles soon after menarche.

Definition

Dysmenorrhoea is painful menstruation severe enough to interfere with normal daily activity and to require treatment. It is classified as primary (spasmodic) — without demonstrable pelvic pathology — and secondary (congestive) — due to identifiable pelvic disease.

Types of Dysmenorrhoea

Primary Dysmenorrhoea

Occurs in young women, usually beginning 6–12 months after menarche once cycles become ovulatory. The pain is cramping/spasmodic, lower-abdominal, radiating to the back and thighs, starting just before or with the flow and lasting 1–2 days. The cause is excess endometrial prostaglandins (PGF₂α) producing uterine hypercontractility and ischaemia; there is no pelvic pathology.

Secondary Dysmenorrhoea

Appears years after menarche in older women, the pain often congestive, dull, beginning days before the period and relieved by the flow. It is due to underlying pelvic pathology — endometriosis, adenomyosis, fibroids, pelvic inflammatory disease, an IUCD, cervical stenosis or a uterine/ovarian lesion — and is usually accompanied by other symptoms (menorrhagia, dyspareunia, infertility).

Clinical Evaluation

History distinguishes the two (age of onset, nature and timing of pain, associated symptoms). In suspected secondary dysmenorrhoea, pelvic examination, ultrasound and, where indicated, laparoscopy are done to find the cause.

Management

Primary dysmenorrhoea

• NSAIDs (the first line) — mefenamic acid/ibuprofen, which inhibit prostaglandin synthesis.
• Combined oral contraceptive pills — suppress ovulation and reduce menstrual prostaglandins (good when contraception is also desired).
• General measures — reassurance, local heat, exercise, and the levonorgestrel-IUS in resistant cases.

Secondary dysmenorrhoea

• Treat the underlying cause (e.g. Endometriosis, fibroid, PID, removal of an IUCD), medically or surgically as appropriate.

WHY Primary Dysmenorrhoea Is a Prostaglandin Disease

Understanding why primary dysmenorrhoea occurs, and why it responds so well to NSAIDs, is a satisfying piece of applied physiology. When progesterone withdraws at the end of an ovulatory cycle, the disintegrating endometrium releases prostaglandins (chiefly PGF2α). These cause intense, dysrhythmic myometrial contractions with raised resting tone, which compress the uterine vessels and produce ischaemia of the uterine muscle — and it is this ischaemia (an angina of the uterus) that is felt as cramping suprapubic pain. Prostaglandins entering the circulation also explain the associated nausea, vomiting, diarrhoea and headache. Every clinical feature follows from this. The pain begins with, or just before, the flow and lasts a day or two — because that is when the prostaglandins are released. It occurs only in ovulatory cycles — which is why it typically starts 6–12 months after the menarche, once ovulation is established, and not with the first periods. And the treatment follows directly: NSAIDs (prostaglandin synthetase inhibitors), which block the very mechanism, are first-line and highly effective, especially if started before the pain builds; and the combined pill, which suppresses ovulation altogether, abolishes it.

WHY Secondary Dysmenorrhoea Is a Warning

The most important clinical task is distinguishing primary dysmenorrhoea (a benign physiological phenomenon) from secondary dysmenorrhoea (a symptom of underlying pelvic disease) — because the second demands investigation. The distinction rests on the pattern. Primary dysmenorrhoea begins in adolescence, soon after ovulatory cycles are established, is confined to the first day or two of the flow, occurs with an otherwise normal pelvis, and tends to improve with age and after childbirth. Secondary dysmenorrhoea appears later (typically after the age of 25–30) in a woman whose periods were previously painless; the pain characteristically begins several days before the flow and may persist after it; and it is accompanied by other symptoms — deep dyspareunia, menorrhagia, chronic pelvic pain, infertility — and by abnormal pelvic findings. Its causes are precisely the important gynaecological diseases: endometriosis and adenomyosis (the commonest), pelvic inflammatory disease, fibroids (especially submucous), an IUCD, and cervical stenosis. Understanding that a change in the character of period pain, or its onset in an older woman, is a red flag explains why such a woman needs examination, ultrasound and often laparoscopy — while the adolescent with classic primary dysmenorrhoea needs only reassurance and an NSAID.

• Primary dysmenorrhoea: painful periods with no pelvic pathology — caused by prostaglandins (PGF2α) → dysrhythmic uterine contractions → myometrial ischaemia.
• It occurs only in ovulatory cycles — hence it begins 6–12 months after menarche, with pain starting with the flow and lasting 1–2 days.
• Treatment: NSAIDs (first-line — they block the mechanism; start early) and the combined pill (suppresses ovulation); plus heat, exercise and reassurance.
• Secondary dysmenorrhoea: due to pelvic pathology — begins later in life, pain starts days before the flow, and is associated with dyspareunia, menorrhagia and infertility.
• Causes of secondary dysmenorrhoea: endometriosis, adenomyosis, PID, fibroids, IUCD, cervical stenosis — investigate with examination, ultrasound and laparoscopy.

A common cause of infertility in India, often silent.

Definition

Genital tuberculosis is tuberculous infection of the female genital tract, caused by *Mycobacterium tuberculosis*. It is almost always secondary to a focus elsewhere (lungs, lymph nodes, gut, urinary tract or bones), reaching the genital tract by haematogenous (mainly), lymphatic or direct spread. It is an important and rising cause of infertility in developing countries.

Genital TB - Spread & Sites

Sites of Involvement

• Fallopian tubes (≈ 90–100%) — the primary and almost constant site.
• Endometrium (≈ 50%) — by downward spread from the tubes.
• Ovaries (≈ 20–30%), cervix (≈ 5%), and rarely the vagina and vulva.

Pathology

Tuberculous tubercles with caseation develop in the tubes, which become thickened and may form a "tobacco-pouch" appearance with everted fimbriae, beading, and tubo-ovarian masses or a "frozen pelvis" from adhesions. Endometrial involvement causes destruction and intra-uterine synechiae (Asherman-like), and tubal scarring leads to infertility and a high risk of ectopic pregnancy.

Clinical Features

Infertility is the commonest presentation (often the only complaint). Others include menstrual disturbances (oligomenorrhoea, amenorrhoea or abnormal bleeding), chronic pelvic pain, vaginal discharge, and constitutional symptoms (low-grade fever, weight loss, evening rise of temperature); many women are asymptomatic and detected during an infertility work-up.

Diagnosis

• Endometrial biopsy/curettage in the pre-menstrual phase — for histology (tubercles), acid-fast bacilli, culture and PCR (the most useful test); menstrual-blood culture/PCR is an alternative.
• Hysterosalpingography — a rigid, beaded ("pipe-stem") tube, cornual block, calcification, and a distorted/contracted cavity with synechiae.
• Laparoscopy/hysteroscopy — tubercles, tubo-ovarian masses and adhesions, with biopsy.
• Supportive — Mantoux test, chest radiograph, ESR, and a search for an extragenital focus.

Management

• Anti-tubercular therapy (ATT) is the mainstay — the standard four-drug regimen (isoniazid, rifampicin, pyrazinamide, ethambutol) for an intensive phase, followed by a continuation phase, for a total of about 6 months.
• Surgery is reserved for a residual or persistent tubo-ovarian mass, or non-response to ATT.
• Infertility — tubal damage is usually irreversible, so in-vitro fertilisation is the realistic option (tubal surgery has poor results); a severely damaged endometrium carries a poor prognosis.

WHY Genital TB Is a Silent Destroyer of Fertility

The distinguishing feature of genital tuberculosis — and the reason it is so important in India — is why it destroys fertility while causing almost no symptoms. It is almost always secondary, spreading haematogenously from a primary focus in the lung (or from the abdomen), so the woman has usually had no overt tuberculosis and feels perfectly well. The organism seeds the fallopian tubes first (involved in over 90% of cases — they are the primary genital site), and then the endometrium (in about 50%). In the tube it produces a chronic granulomatous inflammation that silently obliterates the lumen, giving the characteristic beaded, rigid, 'lead-pipe' tube, with fimbrial destruction and the classic 'tobacco-pouch' appearance. In the endometrium it destroys the basal layer and produces intrauterine adhesions. The result is that the commonest — and often the only — presentation is infertility (in some series it accounts for a substantial proportion of tubal infertility in India), sometimes with menstrual disturbance ending in amenorrhoea (from endometrial destruction), and chronic pelvic pain. Understanding that the disease is silent, that the tube is destroyed before anything is noticed, explains why it must be actively suspected in any infertile Indian woman.

WHY Anti-tubercular Treatment Cures the Infection But Not the Infertility

A hard clinical truth worth understanding is why a woman with genital tuberculosis may be cured of her infection and still never conceive naturally. Anti-tubercular therapy (the standard multi-drug regimen) is highly effective at eradicating the organism — it reliably cures the infection. But it cannot rebuild what has already been destroyed: the ciliated tubal epithelium, the delicate fimbriae and the endometrial basal layer do not regenerate, and the fibrosis, tubal blockage and intrauterine adhesions remain. So the drugs stop the disease from progressing and make it safe to attempt pregnancy — but the damage is permanent. This has two important consequences. First, tubal reconstructive surgery is generally disappointing in genital TB (the tube is diseased along its length, not merely blocked at a point), so IVF — which bypasses the tubes altogether — is the treatment of choice for fertility; though even IVF may fail if the endometrium is severely damaged, in which case surrogacy may be the only option. Second, and most importantly, it explains why early diagnosis matters so much: the fertility that is saved is the fertility that has not yet been destroyed — which is the whole argument for suspecting the disease early.

• Genital TB is almost always secondary (haematogenous spread from a lung/abdominal focus); the fallopian tube is involved in >90%, the endometrium in ~50%.
• It is typically silent — the commonest presentation is infertility, with menstrual disturbance (oligomenorrhoea → amenorrhoea) and chronic pelvic pain.
• Diagnosis: endometrial biopsy/curettage in the premenstrual phase for AFB, culture and CBNAAT/PCR and histology (caseating granuloma); HSG shows beaded, rigid 'lead-pipe' tubes; laparoscopy shows tubercles and adhesions.
• Treatment: standard multi-drug anti-tubercular therapy — which cures the infection but cannot reverse the structural damage.
• Fertility: tubal surgery gives poor results; IVF is the treatment of choice (surrogacy if the endometrium is destroyed) — hence early diagnosis is everything.

Definition

Contraception is the voluntary prevention of pregnancy by temporary (reversible) or permanent (irreversible) methods, enabling couples to plan the number and spacing of their children.

Methods of Contraception

Classification

A. Temporary (spacing) methods

• Barrier — male/female condom and diaphragm (with spermicide); prevent sperm–ovum meeting and also guard against sexually-transmitted infection, but have a higher failure rate.
• Hormonal — combined oral pills (oestrogen + progestin) acting mainly by inhibiting ovulation; progestin-only pills, injectable DMPA, subdermal implants, the vaginal ring and the patch. Highly effective; cautions include thromboembolism (oestrogen) and irregular bleeding (progestin).
• Intra-uterine devices — copper IUCD (Cu-T 380A) (a foreign-body and spermicidal copper effect) and the levonorgestrel-releasing IUS (Mirena); long-acting and reversible.
• Natural / fertility-awareness — calendar (rhythm), basal temperature and cervical-mucus methods, withdrawal and lactational amenorrhoea; no side-effects but less reliable.
• Emergency contraception — after unprotected intercourse (see short note).

B. Permanent (terminal) methods

• Female sterilisation — tubal ligation (laparoscopic/minilap, post-partum), occluding the fallopian tubes.
• Male sterilisation — vasectomy (no-scalpel), interrupting the vas deferens; simpler and safer than female sterilisation but requires confirmation of azoospermia.

Measuring Effectiveness

Efficacy is expressed by the Pearl index — the number of accidental pregnancies per 100 woman-years of exposure; the lower the index, the more effective the method. Long-acting reversible methods (IUCD, implant) and sterilisation have the lowest indices, while barrier and natural methods have the highest.

Newer / Non-hormonal Options

Centchroman (ormeloxifene, "Saheli") is a non-steroidal once-weekly oral contraceptive (a selective oestrogen-receptor modulator) suited to lactating women; the levonorgestrel-IUS additionally reduces menstrual loss.

The Ideal Contraceptive

Should be safe, effective, acceptable, reversible (for spacing), cheap, easy to use and free of side-effects. No single method is ideal; the choice is individualised to the couple's age, parity, family plans, health and preference.

Selection (counselling Points)

• Spacing the family — barrier, hormonal or IUCD.
• Completed family — IUCD or sterilisation.
• Postpartum / lactating — progestin-only methods, IUCD (PPIUCD) or lactational amenorrhoea.
• Avoid oestrogen in smokers > 35 years and those with thromboembolic/cardiovascular risk.

Contraceptive methods, ranked by effectiveness: permanent methods (tubal ligation, vasectomy) are the most effective; long-acting reversible contraceptives (copper IUCD, LNG-IUS, implants) are almost as effective because they remove user error; hormonal methods (the combined pill, progestogen-only pill, injectables) depend on correct use; barrier methods are less effective but uniquely also prevent sexually transmitted infection; and natural methods are the least effective.

WHY 'effectiveness' Depends on the User, Not Just the Method

A concept that transforms contraceptive counselling is why methods are judged by 'typical use' rather than 'perfect use' effectiveness. Every method has a theoretical failure rate achieved when it is used perfectly — but real people forget pills, run out of supplies, and use condoms inconsistently. The gap between the two can be enormous: the combined oral contraceptive pill is over 99% effective in perfect use, but only about 91% effective in typical use, because a pill must be remembered every single day for decades. Methods that depend on the user therefore fail far more often in practice than their impressive theoretical figures suggest. This is precisely the argument for the long-acting reversible contraceptives (LARC) — the copper IUCD, the LNG-IUS and implants — whose effectiveness is essentially the same in typical as in perfect use, because once inserted there is no daily decision to be made, nothing to remember and nothing to run out of; their typical-use failure rates rival sterilisation, yet they are fully reversible. Understanding that the commonest cause of contraceptive failure is not the method but its use explains why LARC is now promoted so strongly, and why counselling must match the method to the woman's life, not merely to her preference.

WHY the Condom Remains Indispensable

A point of great public-health importance is why the condom retains a unique place despite being far from the most effective contraceptive. Its typical-use failure rate (around 18%) is poor compared with an IUCD or an implant. Yet it is the only contraceptive method that also provides a barrier against sexually transmitted infection — including HIV, gonorrhoea, chlamydia and, importantly, HPV. No hormonal method, no IUCD and no sterilisation offers any protection whatever against infection: a woman with an implant is fully protected from pregnancy and entirely unprotected from HIV. This is why the concept of 'dual protection' is emphasised — using a highly effective method for contraception together with a condom for infection, particularly for young people, those with multiple partners, and anyone at risk. The condom is also cheap, needs no prescription, has no systemic side-effects and is under the man's control (making it one of the few methods that shares contraceptive responsibility). Understanding that pregnancy and infection are two separate risks requiring two separate defences explains why the condom cannot be replaced by more effective contraception, and why it remains central to reproductive health.

• Methods: barrier (condom, diaphragm), hormonal (COC, pop, DMPA, implant), intrauterine (Cu-IUCD, LNG-IUS), permanent (tubectomy, vasectomy) and natural.
• Judge methods by typical-use, not perfect-use, effectiveness — LARC (IUCD, LNG-IUS, implant) is best because it removes user error.
• The condom is the only method that also prevents STI/HIV — hence 'dual protection'.
• COC: inhibits ovulation; reduces ovarian and endometrial cancer; avoid in smokers over 35, hypertension and thromboembolic risk.
• Cu-IUCD (CuT 380A) lasts 10 years and also serves as emergency contraception up to 5 days; LNG-IUS also treats menorrhagia.

Definition

An ectopic pregnancy is the implantation of the fertilised ovum outside the normal uterine (endometrial) cavity. It is a leading cause of maternal death in early pregnancy and a true gynaecological emergency when it ruptures.

Ectopic Pregnancy - Management Options

Sites

Tubal pregnancy (≈ 95%) is commonest — most often in the ampulla, then the isthmus, fimbria and (dangerously) the interstitial/cornual part. Rarer sites are ovarian, cervical, caesarean-scar and abdominal pregnancies.

Risk Factors

Anything damaging the tube or delaying ovum transport — pelvic inflammatory disease/salpingitis, previous tubal surgery or previous ectopic, endometriosis, IUCD in situ, assisted reproduction, tubal-ligation failure and smoking.

Fate of a Tubal Pregnancy

The thin-walled tube cannot sustain the pregnancy, which usually ends in one of three ways: tubal abortion (extrusion of the conceptus into the peritoneal cavity, commonest in ampullary pregnancy), tubal rupture (into the peritoneal cavity with severe intraperitoneal haemorrhage, commonest in the narrow isthmus) or, rarely, spontaneous tubal mole/absorption.

Clinical Features

The classic triad is amenorrhoea, lower-abdominal pain and abnormal vaginal bleeding (slight, dark). Rupture produces an acute abdomen — severe pain, signs of haemorrhagic shock, shoulder-tip pain (diaphragmatic irritation), abdominal distension, and on examination marked tenderness, cervical excitation/motion tenderness and a tender adnexal fullness.

Investigations

• Urine and serum β-hCG — a sub-optimal rise (failure to double in 48 h) suggests an abnormal pregnancy.
• Transvaginal ultrasound — an empty uterus with an adnexal mass (± gestational sac/cardiac activity) and free fluid in the pouch of Douglas; correlated with the hCG "discriminatory zone".
• Laparoscopy — the gold standard for diagnosis (and treatment); culdocentesis showing non-clotting blood in resource-limited settings.

Differential Diagnosis

Threatened or incomplete miscarriage, a ruptured or haemorrhagic ovarian cyst, acute pelvic inflammatory disease/salpingitis, torsion of an ovarian mass, and acute appendicitis.

Management

• Expectant — for a small, stable, asymptomatic ectopic with low and falling β-hCG.
• Medical — methotrexate (single-dose, with hCG follow-up) in the stable patient meeting criteria: hCG < 5000 IU/L, mass < 3.5 cm, no fetal cardiac activity and no rupture.
• Surgical — laparoscopic salpingectomy (or salpingostomy if the other tube is damaged) for the stable patient; laparotomy for the ruptured/haemodynamically unstable patient after resuscitation.
• Give anti-D to Rh-negative women.

An ectopic pregnancy implants outside the uterine cavity — in 98% of cases in the fallopian tube, and most often in the ampulla. Because the tube cannot expand, the invading trophoblast erodes through its wall into the rich vessels of the mesosalpinx, causing catastrophic intraperitoneal haemorrhage. The classic triad is amenorrhoea, abdominal pain and irregular vaginal bleeding; diagnosis rests on β-hCG with transvaginal ultrasound — an empty uterus with β-hCG above the discriminatory zone means an ectopic until proved otherwise.

WHY Ectopic Pregnancy Is an Emergency — the Tube Cannot Expand

Understanding why an ectopic pregnancy ruptures, and why it kills, explains its status as the classic gynaecological emergency. A pregnancy implanted in the tube behaves exactly as one implanted in the uterus: the trophoblast invades the wall aggressively, eroding blood vessels in order to establish a blood supply. But the fallopian tube is a thin, muscular, non-distensible structure — it has none of the uterus's capacity to hypertrophy and expand. So as the pregnancy grows, it erodes through the tubal wall, tearing into the rich vessels of the mesosalpinx and broad ligament — and because these bleed into the free peritoneal cavity, the haemorrhage is unconfined and can be catastrophic. The woman may collapse with hypovolaemic shock, shoulder-tip pain (blood irritating the diaphragm) and abdominal distension — while her external vaginal bleeding is only slight, so the visible loss badly underestimates the true one. This is why a woman of reproductive age with abdominal pain and collapse must have a pregnancy test, and why rupture demands immediate resuscitation and laparotomy — not investigation. It also explains why an isthmic ectopic (in the narrow, thick-walled segment) ruptures earliest, while an ampullary one (the commonest site) may present later.

WHY Early Diagnosis Transformed the Treatment

A useful concept is why ectopic pregnancy, once an operation, is now often a medical or even conservative diagnosis — the entire change resting on earlier diagnosis. Formerly the diagnosis was made only at rupture, so the treatment was necessarily emergency salpingectomy. Today, the combination of a sensitive serum β-hCG and high-resolution transvaginal ultrasound allows detection before rupture: the key principle is that once the β-hCG rises above the 'discriminatory zone' (about 1500–2000 IU/L), an intrauterine gestation sac should be visible — so an empty uterus at that level means an ectopic until proved otherwise; and a suboptimal rise in serial β-hCG (failing to increase by ~66% in 48 hours) suggests a non-viable or ectopic pregnancy. This early diagnosis opens gentler options: medical treatment with methotrexate (for a small, unruptured ectopic with a low β-hCG, no cardiac activity and a stable patient) avoids surgery altogether; and, when surgery is needed, a laparoscopic salpingostomy may conserve the tube. Understanding that early diagnosis, not new drugs, is what made conservative treatment possible explains the modern emphasis on early pregnancy assessment.

• Ectopic pregnancy: implantation outside the uterine cavity — 98% tubal, the ampulla commonest (~70%); the isthmus ruptures earliest.
• Risk factors: previous PID/salpingitis, tubal surgery, previous ectopic, IUCD in situ, IVF, smoking, endometriosis.
• Classic triad: amenorrhoea + abdominal pain + irregular vaginal bleeding; rupture → shock, shoulder-tip pain, cervical excitation — visible bleeding underestimates the loss.
• Diagnosis: β-hCG + transvaginal ultrasound — an empty uterus with β-hCG above the discriminatory zone (~1500–2000 IU/L) means ectopic until proved otherwise.
• Treatment: ruptured → resuscitate and operate immediately (salpingectomy); unruptured, small, stable, low β-hCG → methotrexate or laparoscopic salpingostomy.

Cervical os status separates threatened from inevitable.

Definition

Abortion (miscarriage) is the termination of pregnancy before the period of viability — conventionally before 20 weeks (or a fetal weight under 500 g). When it occurs naturally it is a spontaneous abortion (miscarriage).

Clinical Types of Abortion (miscarriage)

Causes

• Genetic — chromosomal abnormalities of the conceptus (the commonest cause of early miscarriage).
• Maternal — endocrine (luteal-phase defect, uncontrolled diabetes, thyroid disease), uterine (septate uterus, fibroid, cervical incompetence — recurrent mid-trimester loss), infections, and antiphospholipid syndrome.
• Others — severe maternal illness, trauma and environmental factors; many remain unexplained.

Clinical Types

• Threatened — slight bleeding with a closed cervix; the pregnancy may still continue.
• Inevitable — increasing bleeding and pain with a dilated cervix; the pregnancy cannot be saved.
• Incomplete — part of the products is expelled, the rest retained (continued bleeding, open os).
• Complete — all products expelled; bleeding and pain settle and the uterus is well-contracted.
• Missed — the fetus is dead but retained in utero (no growth, brownish discharge, closed os).
• Septic — abortion complicated by infection of the uterus and its contents.

Differentiating the Types

Management

• Threatened — rest, reassurance and observation; confirm viability by ultrasound and serial β-hCG; give anti-D to Rh-negative women.
• Inevitable / incomplete — resuscitate if bleeding is heavy, then evacuate the uterus by suction/manual vacuum aspiration or medically (misoprostol); send products for histology.
• Complete — confirm an empty uterus on ultrasound; usually no intervention.
• Missed — evacuate medically (mifepristone + misoprostol) or surgically; check coagulation if retained long.
• Septic — broad-spectrum intravenous antibiotics and resuscitation, followed by evacuation of the infected products.

WHY the Type of Miscarriage Is Defined BY the Cervical Os

The classification of miscarriage looks like a list of names, but it is in fact a logical clinical sequence, and the key that unlocks it is the state of the cervical os. In a threatened miscarriage, there is bleeding but the pregnancy is still viable: the os is closed, the uterus corresponds to the dates, and the pregnancy may well continue (over half do) — so the management is expectant. Once the process becomes irreversible, the os opens: in an inevitable miscarriage there is bleeding with cramping pain and an open os, and the pregnancy cannot be saved. Thereafter the question is simply how much has come away: in an incomplete miscarriage, part of the products has been expelled and part retained — the os remains open, and the continued bleeding (which may be severe) comes from the retained products preventing the uterus from contracting, so it must be evacuated; in a complete miscarriage, everything has been expelled — the bleeding and pain subside, the uterus is well contracted and the os closes again. A missed miscarriage is the silent variant: the fetus has died but is retained, with a closed os and no pain — diagnosed on ultrasound. Recognising that the os simply reports whether the uterus is trying to expel its contents explains the entire classification.

WHY Septic Abortion Is a Killer — and a Public-health Problem

Understanding why septic abortion remains a major cause of maternal death in India gives this topic its true weight. Where safe, legal abortion is not accessible — because of ignorance of the law, stigma, cost, distance or a wish for secrecy — women resort to unsafe abortion at the hands of untrained persons, often with unsterile instruments or by the insertion of foreign bodies. The result is infection of the retained products (an ideal culture medium in a warm, vascular uterus), which is characteristically polymicrobial and includes anaerobes such as Clostridium. It escalates rapidly: endometritis → parametritis and pelvic peritonitis → septicaemia and septic shock, with acute renal failure and DIC — and there may also be uterine perforation and bowel injury from the procedure itself. Management is a true emergency: aggressive resuscitation, broad-spectrum intravenous antibiotics covering anaerobes, and — crucially — evacuation of the infected uterine contents (the source of the sepsis), with hysterectomy in extremis. But the real answer is preventive: the MTP Act exists to make abortion safe and legal, and every unsafe abortion represents a failure of access, contraception and counselling — which is why the topic belongs as much to public health as to gynaecology.

• Miscarriage = expulsion of the products of conception before 20 weeks (or <500 g); commonest cause is chromosomal abnormality (~50%).
• The cervical OS defines the type: threatened (bleeding, os closed, viable) → inevitable (pain + bleeding, os open) → incomplete (partial expulsion, os open, bleeds) → complete (all expelled, os closes).
• Missed miscarriage: the fetus has died but is retained — os closed, no pain, diagnosed on ultrasound; risk of DIC if long retained.
• Recurrent miscarriage (≥3): investigate for antiphospholipid syndrome, uterine anomalies, cervical incompetence, chromosomal and endocrine causes.
• Septic abortion is a leading cause of maternal death — resuscitate, give broad-spectrum antibiotics (covering anaerobes) and evacuate the uterus; prevented by safe, legal abortion (MTP Act) and contraception.

Low threshold for treatment — delay causes tubal damage.

Definition

Pelvic inflammatory disease (PID) is an acute infection and inflammation of the upper female genital tract — the endometrium (endometritis), fallopian tubes (salpingitis), ovaries (oophoritis) and pelvic peritoneum — usually resulting from ascending infection from the lower genital tract.

PID - Ascending Infection

Causative Organisms

Mostly sexually transmitted — Chlamydia trachomatis and Neisseria gonorrhoeae — usually becoming polymicrobial with anaerobes, Gram-negative bacteria and genital mycoplasmas; tuberculosis causes chronic PID.

Routes of Spread

Infection usually ascends from the cervix and vagina along the mucosa to the endometrium, tubes and ovaries, and onto the pelvic peritoneum; less often it spreads by the lymphatics (after delivery/abortion or with an IUCD) or by the blood-stream (tuberculosis).

Risk Factors

Multiple sexual partners and young age, a previous episode of PID, recent IUCD insertion or intra-uterine instrumentation (D&C, MTP, HSG), and the post-partum/post-abortal state.

Acute and Chronic PID

Acute PID presents with the florid features below; inadequately-treated infection leads to chronic PID — persistent pelvic pain, dyspareunia, menstrual disturbance, a hydrosalpinx/chronic tubo-ovarian mass and dense pelvic adhesions causing infertility.

Clinical Features

Lower abdominal/pelvic pain, fever, abnormal vaginal discharge, deep dyspareunia and abnormal bleeding; signs include lower-abdominal tenderness, cervical motion (excitation) tenderness and adnexal tenderness. Fitz-Hugh-Curtis syndrome (perihepatitis) causes right-upper-quadrant pain.

Investigations

• Endocervical/vaginal swabs and NAAT for chlamydia and gonorrhoea; a pregnancy test (to exclude ectopic).
• White-cell count, CRP/ESR; ultrasound/TVS to detect a tubo-ovarian abscess or pyosalpinx.
• Laparoscopy — the gold standard in doubtful or severe cases.

Management

• Broad-spectrum antibiotics covering chlamydia, gonococcus and anaerobes (e.g. Ceftriaxone + doxycycline + metronidazole), started empirically.
• Outpatient treatment for mild cases; admit for severe illness, pregnancy, a tubo-ovarian abscess, failure of oral therapy, or an uncertain diagnosis (then intravenous antibiotics).
• Treat the partner and advise abstinence; consider removing an IUCD if there is no response; drain a tubo-ovarian abscess if it does not resolve.

WHY PID Matters Long After the Infection Is Cured

The importance of pelvic inflammatory disease lies less in the acute illness than in why it leaves permanent damage even after the infection has been eradicated. The infection ascends from the cervix to the tubes, where the inflammation destroys the delicate ciliated epithelium and the fine architecture of the tubal lumen — and this tissue does not regenerate. The tube heals instead by fibrosis and scarring: the fimbriae become clubbed and adherent, the lumen becomes narrowed or blocked, and peritubal adhesions distort its relationship to the ovary. Three lifelong consequences follow. First, infertility — the tubes can no longer pick up or transport the ovum, and the risk rises steeply with each episode (roughly 12% after one attack, 25% after two, 50% after three). Second, ectopic pregnancy — a partially damaged tube may allow sperm through but cannot transport the fertilised ovum onward, so it implants where it lies (a six- to tenfold increased risk). Third, chronic pelvic pain and dyspareunia from adhesions. Understanding that the damage is structural and irreversible explains why the prompt, adequate treatment of even mild PID — and its prevention — matters so much, and why treatment must never wait for culture results.

WHY Treatment Is Empirical, Broad and Immediate

A crucial clinical principle is why PID is treated on suspicion, with broad-spectrum antibiotics, before any organism is identified. Three facts drive this. First, the diagnosis is clinical and imprecise: the classic signs (lower abdominal pain, cervical excitation and adnexal tenderness, with fever and discharge) are neither sensitive nor specific, and waiting for certainty means waiting while the tubes are destroyed. Second, the damage is time-dependent and irreversible — every hour of untreated inflammation adds to the scarring — so the cost of treating a woman who turns out not to have PID (a course of antibiotics) is trivially small compared with the cost of missing one (lifelong infertility). Hence the rule: a low threshold to treat. Third, the infection is characteristically polymicrobial — Chlamydia trachomatis and Neisseria gonorrhoeae ascending from the cervix, together with anaerobes and other vaginal flora — so no single agent will cover it; treatment must therefore be a combination (typically ceftriaxone plus doxycycline plus metronidazole). Finally, and often forgotten, the sexual partner must be treated simultaneously, or the woman is simply reinfected.

• PID = ascending infection of the upper genital tract (endometritis, salpingitis, tubo-ovarian abscess, peritonitis); usually polymicrobial — Chlamydia and gonococcus with anaerobes.
• Clinical: lower abdominal pain, cervical excitation and adnexal tenderness, fever, discharge; Fitz-Hugh-Curtis syndrome (perihepatitis) gives right upper quadrant pain.
• Treat empirically on suspicion — do not wait for cultures; the tubal damage is time-dependent and irreversible.
• Antibiotics: ceftriaxone + doxycycline + metronidazole; treat the partner too, or reinfection follows.
• Sequelae: infertility (risk rises with each episode), a 6–10-fold increase in ectopic pregnancy, chronic pelvic pain and dyspareunia.

Definition

Genital (pelvic organ) prolapse is the descent of the pelvic organs — the uterus and/or the vaginal walls with the bladder, rectum or bowel — from their normal anatomical position, due to weakness of the pelvic supports.

Types & Grading of Genital Prolapse

Types

• Anterior vaginal wall — cystocele (bladder) and urethrocele.
• Posterior vaginal wall — rectocele (rectum) and enterocele (pouch of Douglas/bowel).
• Uterine prolapse — descent of the uterus and cervix.
• Vault prolapse — descent of the vaginal vault after hysterectomy.

Degrees of Uterine Prolapse

• First degree — the cervix descends but the external os remains within the introitus.
• Second degree — the cervix protrudes outside the introitus while the uterine body stays inside.
• Third degree (procidentia) — the entire uterus lies outside the introitus, with eversion of the vagina.

The pop-Q system (Pelvic Organ Prolapse Quantification) is the standardised, objective method of grading.

Aetiology

Childbirth trauma (the chief cause — overstretching/tearing of supports in prolonged or instrumental labour, multiparity), oestrogen withdrawal after menopause, chronically raised intra-abdominal pressure (chronic cough, constipation, heavy work, pelvic tumour), and congenital weakness (nulliparous prolapse).

Clinical Features

A sense of "something coming down" per vaginum, dragging backache relieved by lying down, a visible mass, and urinary (frequency, incomplete emptying, stress incontinence) or bowel symptoms; long-standing procidentia may develop a decubitus ulcer.

Management

• Prevention — good intrapartum care, avoidance of bearing-down before full dilatation, adequate puerperal rest and pelvic-floor exercises, and treatment of chronic cough/constipation.
• Conservative — pelvic-floor (Kegel) exercises for mild cases, local oestrogen, and a ring/shelf pessary for those unfit for or declining surgery (or in pregnancy).
• Surgical — the definitive treatment: vaginal hysterectomy with pelvic-floor repair (anterior and posterior colporrhaphy) for prolapse with a completed family; the Manchester (Fothergill) operation to conserve the uterus; sacrohysteropexy/sacrocolpopexy for uterine/vault prolapse in younger women; and colpocleisis in the frail elderly.

Genital prolapse is descent of the pelvic organs following damage to their supports — the levator ani muscle and the endopelvic fascia and ligaments. It is described by compartment (anterior — cystocele; middle — uterine descent; posterior — rectocele, enterocele) and, for the uterus, by degree, from first-degree descent within the vagina to complete procidentia. The chief risk factors are vaginal delivery, multiparity, the menopause and raised intra-abdominal pressure.

WHY Prolapse Is a Disease of Damaged Supports

Understanding why the pelvic organs descend makes both the causes and the treatment obvious. The uterus and vagina are held in place by two systems working together: the muscular floor (the levator ani, which forms an active, contracting shelf on which the organs rest) and the fascial/ligamentous supports (the endopelvic fascia, and the cardinal and uterosacral ligaments, which suspend the cervix and upper vagina). Prolapse occurs when these are damaged or weakened. This immediately explains the risk factors: vaginal delivery — especially prolonged labour, a big baby, instrumental delivery and inadequately repaired perineal tears — stretches and tears the levator and the fascia; multiparity compounds the damage; the menopause removes the oestrogen on which the tone and collagen of these tissues depend, which is why prolapse so often declares itself years after the deliveries that caused it; and anything that chronically raises intra-abdominal pressure (chronic cough, constipation, heavy lifting, obesity, a pelvic mass) pushes the organs down against weakened supports. Recognising that prolapse is essentially a hernia through a damaged pelvic floor explains why prevention lies in good intrapartum care and postnatal pelvic-floor exercises, and why surgery aims to restore the supports.

WHY the Operation Is Chosen for the Woman, Not the Prolapse

A useful principle is why the surgical treatment of prolapse depends far more on the woman's age, fertility wishes and fitness than on the degree of descent. The aim is to restore anatomy, relieve symptoms and preserve (or not) sexual and reproductive function — and different women want different things. In a young woman who wishes to retain her uterus and childbearing, the uterus must be preserved — hence a Manchester (Fothergill) repair (amputation of the elongated cervix with plication of the cardinal ligaments) or a sacrospinous/sacrohysteropexy suspension, combined with repair of the vaginal walls. In a woman who has completed her family, vaginal hysterectomy with pelvic floor repair (anterior and posterior colporrhaphy) is the standard operation. In an elderly, frail woman unfit for surgery, or one who declines it, or a pregnant woman — a ring pessary provides effective conservative relief, with local oestrogen to protect the atrophic vaginal skin from ulceration. Understanding that the operation is chosen to fit the woman's stage of life — and that mild prolapse in a young woman is often best managed with pelvic-floor exercises alone — explains why the same anatomical finding may be treated in several quite different ways.

• Genital prolapse = descent of the pelvic organs due to damage to the levator ani and the endopelvic fascia/ligaments — essentially a pelvic hernia.
• Compartments: anterior (cystocele, urethrocele), middle (uterine/vault descent), posterior (rectocele, enterocele).
• Degrees: 1st — cervix within the vagina; 2nd — at the introitus; 3rd — outside; procidentia — the whole uterus outside.
• Risk factors: vaginal delivery (prolonged/instrumental), multiparity, menopause, chronic ↑intra-abdominal pressure, obesity.
• Treatment: pelvic-floor exercises and pessary (conservative); surgery — vaginal hysterectomy with repair, or Manchester/sacrospinous fixation if the uterus is to be preserved.

Leakage coincides exactly with the rise in pressure, without urgency.

Definition

Urinary incontinence is the involuntary loss of urine that is objectively demonstrable and a social or hygienic problem. Stress urinary incontinence (sui) is the involuntary leakage of urine on effort or exertion (coughing, sneezing, lifting) due to a rise in intra-abdominal pressure exceeding the urethral closure pressure (urethral sphincter incompetence).

Stress Urinary Incontinence - Mechanism

Types of Urinary Incontinence

• Stress incontinence — leakage on raised intra-abdominal pressure.
• Urge incontinence — leakage preceded by urgency, from an overactive (detrusor) bladder.
• Mixed — features of both stress and urge.
• Overflow — dribbling from a chronically over-distended bladder (retention).
• Continuous (true) — from a fistula (vesicovaginal/ureterovaginal).

Causes / Risk Factors of Sui

Childbirth and pelvic-floor injury (the chief cause — denervation and weakening of the supports), multiparity, menopausal oestrogen deficiency, obesity, chronically raised intra-abdominal pressure (chronic cough, constipation), genital prolapse and previous pelvic surgery.

Pathophysiology

Continence depends on the urethral closure pressure exceeding the bladder pressure. Sui results from urethral hypermobility (loss of the supports of the bladder neck, so that a rise in intra-abdominal pressure is transmitted unequally to the bladder but not the urethra) and/or intrinsic sphincter deficiency (a weak urethral sphincter), allowing leakage when abdominal pressure rises.

Evaluation

• History — circumstances, frequency, severity and impact; a bladder diary.
• Examination — demonstrate leakage on the cough stress test, assess prolapse and pelvic-floor tone; a Q-tip test for urethral hypermobility.
• Investigations — urinalysis/culture (exclude infection), a pad test, post-void residual urine, and urodynamic studies (to confirm sui and exclude detrusor overactivity before surgery); cystoscopy if indicated.

Management

• Conservative (first line) — pelvic-floor muscle (Kegel) exercises, weight reduction, treatment of cough/constipation, bladder training, vaginal oestrogen in post-menopausal women, and a continence pessary; duloxetine in selected cases.
• Surgical — for failure of conservative treatment: the mid-urethral sling (tension-free vaginal tape, TVT / transobturator tape, TOT) is the standard, and Burch colposuspension is an abdominal alternative; periurethral bulking agents for the frail.

WHY Stress Incontinence Is a Mechanical Failure

The key to understanding stress urinary incontinence is why the leak occurs on coughing but not at rest — which reveals it as a mechanical, not a bladder, problem. Continence during a rise in intra-abdominal pressure depends on the bladder neck and proximal urethra being held in their normal position above the pelvic floor, so that any pressure transmitted to the bladder is transmitted equally to the urethra, and the pressure gradient is unchanged. The urethra is supported by the pubourethral ligaments and the endopelvic fascia, resting on the hammock of the levator ani. When these supports are damaged — typically by childbirth, and unmasked later by the oestrogen loss of the menopause — the bladder neck becomes hypermobile and descends below the pelvic floor when the woman coughs, so that the abdominal pressure is transmitted to the bladder but not to the urethra: the intravesical pressure momentarily exceeds the urethral closing pressure, and urine escapes. Hence the leak is painless, immediate, small in volume, coincident with the cough or sneeze, and unaccompanied by urgency. Understanding that this is a failure of support, not of the bladder muscle, explains why the surgical cure is to restore support beneath the mid-urethra, and why it is quite different from urge incontinence.

WHY It Must Be Distinguished from Urge Incontinence

A distinction of great practical importance is why stress and urge incontinence must be separated before any treatment is offered — because their treatments are entirely different and each is useless (or harmful) for the other. In stress incontinence, urine leaks with a rise in abdominal pressure (coughing, sneezing, laughing, lifting), there is no warning, no urgency, and the volume lost is small — the problem is a failure of urethral support. In urge incontinence (overactive bladder/detrusor overactivity), the woman feels a sudden, overwhelming, uncontrollable need to void and leaks a large volume on the way to the toilet, with frequency and nocturia — the problem is an unstable, involuntarily-contracting detrusor. The treatments follow accordingly: stress incontinence is treated by pelvic-floor (Kegel) exercises, weight loss, and — if these fail — surgery to support the mid-urethra (a mid-urethral sling, or a Burch colposuspension); urge incontinence is treated by bladder training and antimuscarinic drugs or mirabegron. Operating on a woman whose real problem is an overactive bladder will not cure her and may make her worse. Many women have mixed incontinence, and urodynamic studies are used where the picture is unclear.

• Stress incontinence: involuntary leakage on a rise in intra-abdominal pressure (cough, sneeze, laugh, lift) — no urgency, small volume.
• Cause: loss of support to the bladder neck and urethra (childbirth, menopause, obesity, chronic cough) → urethral hypermobility.
• Distinguish from urge incontinence (detrusor overactivity: sudden urgency, large-volume leak, frequency, nocturia) — the treatments are entirely different.
• Assess with a stress test, Q-tip test, pad test and urodynamics where the picture is mixed or unclear.
• Treat with pelvic-floor (Kegel) exercises, weight loss and local oestrogen first; surgery — mid-urethral sling (TVT/TOT) or Burch colposuspension — if these fail.