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.

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.

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.

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

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.

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.

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.

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.

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.