Physiological and anatomical changes occur to provide a suitable environment for the fetus. Early changes are due to metabolic demands (fetus, placenta, uterus) and increasing hormones (Progesterone and Oestrogen). Later changes are mechanical pressure from the expanding uterus.

• Human Chorionic Gonadotropin (hCG): Produced by the placenta, maintains the corpus luteum (which produces progesterone) in early pregnancy. This is the hormone detected by pregnancy tests.
• Progesterone: Crucial for maintaining pregnancy. Relaxes smooth muscle (prevents uterine contractions), maintains the uterine lining, and suppresses the maternal immune response to the fetus.
• Oestrogens (Mainly Oestradiol 90%): Promotes uterine growth, enhances blood flow, and plays a role in mammary gland development.
• Human Placental Lactogen (hPL): Modifies maternal metabolism to make glucose and protein more available to the fetus, stimulates mammary gland growth.
• Pituitary Gland: Enlarges mainly due to changes in the anterior lobe. Prolactin levels increase substantially (due to oestrogen stimulation of lactotrophes). Gonadotrophin secretion is inhibited. Plasma Adrenocorticotrophic hormone (ACTH) levels increase, maternal plasma cortisone output increases, but the unbound levels remain constant. The posterior pituitary releases Oxytocin principally during the first stage of labour and during suckling.
• Thyroid Gland: Enlarges, and thyroid hormone production increases to meet heightened metabolic demands. Due to plasma volume expansion, increased thyroid-binding globulin production and relative iodine deficiency, thyroid hormone reference ranges for the non-pregnant population are NOT useful. Use Free thyroxine (fT4), free triiodothyronine (fT3), and Thyroid-Stimulating Hormone (TSH) for assessment; total T3 and T4 should not be used. In the 1st trimester: there is a fall in TSH and a rise in fT4 concentrations, followed by a fall in fT4 concentration with advancing gestation.

• Uterus: Enormous growth. Weight increases from 60g to 900–1000g at term. Cavity capacity is increased by 500–1,000 times (from 5-10 mL). Length increases from 7.5 cm to 35 cm. Muscle hypertrophy occurs up to 20 weeks, after which stretching of the muscle fibres occurs. Uterine blood flow increases from 50 mL/min (at 10 wks) to 500–700 mL/min (at term). Massive hypertrophy of uterine, ovarian, and superior vesical arteries.
• Isthmus: Important structural and functional changes. During the 1st trimester, it hypertrophies and elongates to about 3 times its original length and becomes softer. Beyond 12 weeks, it progressively unfolds from above downward until incorporated into the uterine cavity. The circularly arranged muscle fibers function as a sphincter in early pregnancy to retain the fetus.
• Cervix: Reduction in cervical collagen towards term enables dilatation. Hypertrophy of cervical glands produces profuse thick mucus plug (operculum) acting as a barrier to infection. Vaginal discharge increases due to cervical ectopy (proliferation of columnar epithelium into the vaginal portion) and cell desquamation.
• Vagina: Walls become hypertrophied, edematous, and more vascular. Increased venous plexus blood supply gives a bluish coloration of the mucosa. Secretion becomes copious, thin, curdy white due to marked exfoliated cells and bacteria. The pH becomes acidic (conversion of glycogen into lactic acid by Lactobacillus acidophilus consequent on high estrogen level). The acidic pH prevents multiplication of pathogenic organisms.
• Vulva: Becomes edematous, more vascular; superficial varicosities may appear especially in multiparae. Labia minora pigmented/hypertrophied.
• Breast: Increase in size/vascularity. Warm, tense, tender. Increased pigmentation of nipple and areola. Secondary areola appears (light pigmentation around primary). Montgomery tubercles appear on the areola (dilated sebaceous glands). Colostrum-like fluid is expressed at the end of the 3rd month. Prolactin stimulates alveoli cells to secrete milk, but this effect is blocked during pregnancy by the peripheral action of oestrogen and progesterone until shortly after delivery when there is a sudden drop in these hormones.

• Cardiac Output: The most significant change. Increases by 30-50% by mid-pregnancy. Primarily due to an increase in both stroke volume and heart rate (10-20 bpm). Extra output perfuses placenta, uterus, kidneys, skin. Cardiac output increases further during labor (+50%) and immediately following delivery (+70%).
• Heart position & size: Heart is displaced upward and to the left; mild chamber enlargement.
• Blood Volume: Total blood volume increases by 40-50%, reaching its peak around 32-34 weeks. Expansion is proportionally greater for plasma volume (50%) than for red blood cell mass (20-30%). This discrepancy leads to Physiological Anemia of pregnancy (hemodilution). Iron requirements increase. Crucial for placental perfusion and protecting the mother against blood loss.
• Hematology: Total white cell count increases (mainly neutrophil polymorphonuclear leucocytes). Platelets decrease slightly but function is unchanged.
• Hypercoagulable State: Most clotting factors increase, especially Fibrinogen. Increase in factors X, IX, VIII, VII, and I. Factors II, V, XII unchanged/mildly increased. Factors XI and XIII slightly decreased. The clotting time does NOT show significant change.
• Erythrocyte Sedimentation Rate (ESR): Gives a much higher value (fourfold increase). As such, ESR has little diagnostic value in pregnancy.
• Blood Pressure: Systemic vascular resistance generally decreases, leading to a slight fall in blood pressure (particularly 2nd trimester). By 3rd trimester, it typically returns to pre-pregnancy levels.
• Supine Hypotension Syndrome: A profound fall in BP can occur late in pregnancy when lying supine, due to compression of the inferior vena cava leading to decreased venous return and decreased cardiac output.
• Colloid Osmotic Pressure: Although there is no increase in pulmonary capillary wedge pressure, serum colloid osmotic pressure is reduced. The gradient is reduced by 28%, making pregnant women particularly susceptible to pulmonary oedema.
• Normal Cardiac Examination Findings: Loud first heart sound (S1), exaggerated splitting of S2, physiological third heart sound (S3) at the apex. A systolic ejection murmur at the left sternal edge is heard in nearly all women (reflects increased stroke output). Note: Diastolic murmurs are virtually always pathological. Venous hums, mammary souffles, bounding pulse, ectopic beats, and ankle swelling are normal.
• Cardiac Investigations (ECG): Axis shifts slightly to the left (superiorly) in late pregnancy (horizontal position). Small Q waves and T-wave inversion in inferior leads are not uncommon. Atrial/ventricular ectopics common. Troponin is not affected by pregnancy and remains a valid test for myocardial ischemia.

• Diaphragm Elevation: Growing uterus pushes diaphragm upwards, reducing Functional Residual Capacity (FRC). Body compensates by increasing chest wall diameter: Subcostal angle increases from 68° to 103°, transverse diameter +2 cm, circumference +5–7 cm. Breathing becomes more diaphragmatic than costal.
• Tidal volume increases due to the effect of progesterone. Inspiratory capacity increases progressively in late pregnancy.
• Ventilation: Respiratory rate changes slightly, hence the resting pregnant woman increases ventilation by breathing more deeply and not more frequently. Breathlessness is common as maternal partial pressure of carbon dioxide (pCO2) is set lower to allow the fetus to off-load CO2.
• Progesterone's Role: Acts as a respiratory stimulant, increasing sensitivity to CO2 leading to a slight decrease in arterial CO2 levels (respiratory alkalosis). Facilitates transfer of CO2 from fetus and O2 to fetus.
• Nasopharynx: Mucosa becomes hyperemic and edematous causing nasal stuffiness and rarely epistaxis.

• Renal System: Kidney size increases by ~1cm. Hydronephrosis occurs. Glomerular Filtration Rate (GFR) increases by 30-50% by early/mid-pregnancy. Renal Plasma Flow (RPF) increases by 50-80%. Increased GFR causes reduction in maternal plasma levels of creatinine, BUN, and uric acid. Renal tubules fail to reabsorb glucose, uric acid, amino acids, and water-soluble vitamins completely. Crucial Note: Creatinine within the normal range for non-pregnant women may indicate renal impairment in pregnancy! Urinary frequency increases. Dilatation of ureters (pressure of uterus more on the right ureter due to dextro-rotation, plus Progesterone/Relaxin effects). Vesicoureteric reflux occurs sporadically -> urinary stasis -> increased infection risk. Residual urine is not normally present after micturition.
• Gastrointestinal System: Gums congested/spongy, bleed to touch. Ptyalism (increased salivation). Altered taste. Nausea & Vomiting (Morning Sickness) linked to elevated hCG. Heartburn due to progesterone relaxing the lower esophageal sphincter. Constipation (decreased GI motility due to progesterone and increased water absorption). Increased absorption efficiency for iron and calcium.
• Liver: Mimics decompensated chronic liver disease/cirrhosis (peaks 2nd trimester). Blood volume increases 50% but blood flow to liver remains constant; liver is not palpable. Telangiectasia, spider angiomas, and palmar erythema are normal (due to estrogen). Increased tendency to bile lithogenicity (gallstones) and reduced gallbladder contractility. Albumin falls. Alkaline phosphatase activity increases (placental secretion). ALT, AST, Bilirubin, and GGT all remain normal. Liver histology is normal.
• Nervous System: Temperamental changes, nausea, vomiting, mental irritability, sleep disorders. Postpartum blues/depression/psychosis. Carpal tunnel syndrome (compression of median nerve). Paresthesia and sensory loss over anterolateral thigh (compression of lateral cutaneous nerve of the thigh).
• Musculoskeletal System: Progesterone and Relaxin soften ligaments/joints (pelvis) causing joint pain/instability. Increased lumbar lordosis shifts center of gravity forward. Daily calcium requirement is 1–1.5 g. Maternal total calcium falls but serum ionized calcium level is unchanged (50% is ionized). Calcium absorption from intestine and kidneys doubles due to rise in 1, 25 dihydroxy vitamin D3. Pregnancy does NOT cause hyperparathyroidism. Calcitonin increases to protect maternal skeleton. Phosphate unchanged.
• Skin: Increased MSH causes Chloasma (butterfly pigmentation of face), Linea nigra (pigmentation of linea alba below umbilicus), Striae gravidarum (pink stretch marks that become white/albicans after labour). Spider naevi and palmar erythema (high estrogen). Mild hirsutism (lost in puerperium). Pruritus affects up to 20%; bile acids should always be checked to exclude Intrahepatic Cholestasis of Pregnancy.
• Weight: Average increase 12.5 kg at term. Main increase in second half is 0.5 kg per week. Causes: Fetus (3.3 kg), placenta (0.6 kg), liquor (0.8 kg), maternal organs (0.9 kg), breasts (0.4 kg), fat/protein storage (3.5 kg), blood (1.3 kg), interstitial fluid (1.2 kg).

Features of Normal Labour: Spontaneous onset at 37–42 weeks' gestation, Singleton pregnancy, Cephalic vertex presentation, No artificial interventions. Cervical dilatation of at least 1 cm every 2 hours in the active phase of the first stage. Active second stage no more than 2 hours in primiparous and 60 minutes in multiparous woman. Spontaneous vaginal delivery. Third stage lasting no more than 30 minutes with active management.

Abnormal Labor (Dystocia): Any deviation from normal labor. Means difficult labor characterized by abnormally slow labor progress. It includes presentations other than vertex or complications affecting maternal/fetal prognosis.

Precipitate Labour: Defined as a combined first and second stage duration of less than 3 hours. Characterized by rapid cervical dilation (≥5 cm/hr in nulliparous) and is common in multiparous women, often recurring. Leads to maternal trauma and fetal hypoxia/intracranial hemorrhage.

When the fetal head engages, its lateral inclination can cause the sagittal suture to deflect anteriorly or posteriorly relative to the pelvic inlet's transverse diameter. This deflection is termed asynclitism.

• Posterior Asynclitism (Posterior parietal presentation): Sagittal suture lies anteriorly, the posterior parietal bone leads. This is common in primigravidae due to strong uterine tone.
• Anterior Asynclitism (Anterior parietal presentation): Sagittal suture lies posteriorly, the anterior parietal bone leads. This is more common in multiparae.
• While mild asynclitism is common, severe degrees suggest cephalopelvic disproportion (CPD).

Labour becomes abnormal when there is poor progress, fetal compromise, malpresentation, multiple pregnancy, uterine scar, or if induced. Progress is dependent on the '3 Ps': Powers (uterine contractions), Passenger (fetus size/presentation/position), Passages (uterus, cervix, bony pelvis). Plotting on a partogram helps highlight poor progress.

Patterns of Abnormal Progress:

• 1. Prolonged Latent Phase: More in primiparous. Management: simple analgesia, mobilization, reassurance. Oxytocin and ARM increase CS risk. Partogram should not commence until the latent phase is complete.
• 2. Primary Dysfunctional Labour (Primary Arrest): Poor progress in active first stage (< 2 cm cervical dilatation/4 hours). Most common cause of poor progress, particularly in nulliparous and older women. Typically caused by inefficient uterine contractions, but also CPD and malposition.
  Remember: Multiparous women are less likely to experience this. Extreme caution must be exercised when using oxytocin in a multiparous woman where malposition or CPD is more likely (risk of Uterine Rupture).
• 3. Secondary Arrest: Progress in active first stage is initially good but then slows or stops altogether, typically after 7 cm dilatation. Fetal malposition, malpresentation, and CPD feature more commonly here than in primary arrest.

• Cephalopelvic Disproportion (CPD): Implies anatomical mismatch.
  - Absolute CPD: Bony abnormalities (Kyphosis, Scoliosis, Rickets, Pelvic fracture), Fetal conditions (Hydrocephalus, Anencephaly, Conjoined twins, Neck tumors), Soft tissue abnormalities (Cervical fibroid, Ovarian tumor, Pelvic kidney, Vaginal septum). Women of short stature (< 1.60 m) with a large baby in first pregnancy are high candidates.
  - Relative CPD: More common. Occurs with malposition (e.g., Occipito-Posterior position causes deflexion, presenting a larger skull diameter).
  Findings suggesting CPD: Head not engaged, severe moulding/caput, head poorly applied to cervix, haematuria, progress arrests despite efficient contractions.
• Management of CPD: Oxytocin can be given carefully to a primigravida with mild/moderate CPD if CTG is normal. Oxytocin must NEVER be used in a multiparous woman when CPD is suspected.
• Malpresentation ('Passenger'): Face presentation applies poorly to cervix. Brow presentation (mentovertical diameter) is too large to fit unless it flexes or hyperextends. Shoulder presentations cannot deliver vaginally. Malpresentations carry a high risk of uterine rupture if labour continues without progress.

• Causes of 2nd Stage Delay:
  1. Weak/Ineffectual Contractions: Treat with rehydration and IV oxytocin in nulliparous. In multiparous, need expert assessment.
  2. Narrow mid-pelvis (Android Pelvis): Prevents internal rotation, leading to Deep Transverse Arrest (head stops at ischial spines in transverse position).
  3. Persistent Occipito-Posterior (OP): Head must rotate a long way or deliver face-to-pubes.
  4. Resistant perineum (nulliparous), exacerbated by epidural.
• Perinatal Complications of Prolonged Labour: Increased peripartum fetal sepsis. Caput succedaneum and moulding. Mechanical trauma (nerve injury, fractures, cephalohematoma).

Majority (80%) of fetal deaths occur in the antepartum period. Causes include chronic hypoxia (IUGR), maternal complications, anomalies. Objectives are prevention of fetal death and avoidance of unnecessary interventions.

Stages in fetal surveillance:
Stage 1 - Assigning risk.
Stage 2 - Timing delivery (preterm delivered only if distressed; after 36wks high-risk should be delivered). Special testing starts between 32 and 34 weeks.

Theoretical scheme of fetal deterioration:
1. Fetal well being (Nutritional compromise)
2. Fetal growth retardation (Marginal placental respiratory function)
3. Fetal hypoxia with stress (Decreasing respiratory function)
4. Residual effects of intermittent hypoxia (profound respiratory compromise)
5. Asphyxia -> Death

Indications for Monitoring:
Maternal: Chronic HTN, Pre-gestational DM, SLE, Antiphospholipid syndrome, Hemoglobinopathies, Cardiac/Renal disease, BMI>=35, Age>35.
Pregnancy-related: Gestational HTN, Preeclampsia, Oligo/Polyhydramnios, Postterm, Isoimmunization, Cholestasis, Single umbilical artery.
Fetal: Fetal Growth Restriction (FGR/IUGR), Decreased movement, Multifetal gestation.

• Quickening: Maternal perception of fetal movement. 18–20 weeks in primiparous, 14–18 weeks in multigravida. Described as butterfly-like. Mothers perceive 88% of Doppler-detected movements.
• Fetal Movement Count: Diminution to < 10 kicks in 12 hours (or < 3 per hour) indicates compromise. Positive predictive value is extremely low, but requires assessment.
• Auscultation: Handheld Doppler uses ultrasound waves. Waterproof models can be used in birthing pools.
• Cardiotocograph (CTG) / EFM: Continuous tracing of FHR and uterine activity. Minimum 30 minutes. Mother positioned in left lateral or semi-recumbent position to avoid vena cava compression.
• Important CTG Features: Regulated by autonomic nervous system, vasomotor, chemo/baroreceptors.
  - Baseline FHR: Normal is 110–160 bpm (or 110-150 bpm). Falls with advancing gestation (parasympathetic tone matures). Tachycardia (>160) implies maternal/fetal infection, acute hypoxia, fetal anemia, or drugs (ritodrine).
  - Baseline Variability: Normal beat-to-beat variations (5-25 bpm). Reflects normal autonomic CNS. Decreased by sleep (normal for 20-30 mins), hypoxia, infection, opioids/hypnotics.
  - Accelerations: Increases of ≥ 15 bpm for ≥ 15 seconds. Two or more in 20-30 mins defines a reactive/reassuring trace (non-hypoxic).
  - Decelerations: Reductions of ≥ 15 bpm for ≥ 15 seconds. Indicate hypoxia or cord compression.
  - Computerized CTG: Objective, reduces intra/interobserver variability.

• Nonstress Test (NST): Tests FHR reactivity. Reactive = ≥2 accelerations in 20-40 mins. Negative predictive value is very high (99.8%). Non-reactive implies sleep or CNS depression.
• Contraction Stress Test (CST): Observes response to uteroplacental insufficiency under stress. IV oxytocin or nipple stimulation used to generate ≥3 contractions (lasting ≥40s) in 10 mins.
  - Negative: no late decelerations (reassuring, >99.9% NPV, repeat weekly).
  - Positive: Late decelerations with majority of contractions (action required).
  - Contraindications: Anything that contraindicates vaginal delivery.
• Biophysical Profile (BPP): 5 variables scored 2 (normal) or 0 (suboptimal). Total 10.
  1. NST (Reactive).
  2. Fetal breathing movements (≥30s in 30 mins).
  3. Fetal gross body movements (≥3 in 30 mins).
  4. Fetal tone (1 episode of limb flexion).
  5. Amniotic Fluid Volume (AFV) (pocket > 2cm or AFI > 5).
  Score 8-10 is normal. Score 6 is equivocal (repeat in hours). Score ≤4 indicates fetal acidemia and high risk of stillbirth. Problem: time-consuming due to fetal sleep (30% of time).
• Modified BPP: NST + Amniotic Fluid Index (AFI). Abnormal if NST non-reactive and/or AFI < 5. AFI is sum of vertical pockets from 4 quadrants.
• Ultrasonography for IUGR: Uses BPD, AC, HC, FL. Abdominal Circumference (AC) best reflects fetal nutrition. If HC/AC ratio is >1.0 after 34 weeks, IUGR is suspected.

• Fetal Vessels (Response to Hypoxia): Falling oxygen leads to cerebral redistribution (blood diverted to brain, heart, adrenals).
  - Middle Cerebral Artery (MCA): Shows increased diastolic flow in hypoxia. Peak systolic velocity increases in fetal anemia (useful in Rhesus isoimmunization and twin-twin transfusion syndrome).
  - Fetal Aorta: Rising resistance (vasoconstriction). Absent diastolic flow implies fetal acidemia.
  - Ductus Venosus (DV) & IVC: Increasing pulsatility implies impending heart failure. Absent late diastolic flow in DV means fetal death is imminent.
• Umbilical Artery: Reflects placental function. Abnormalities show reduced, absent, or reversed end-diastolic flow.
• Uterine Artery (Maternal): High resistance marker is the diastolic 'notch' in early diastole. If bilateral notches present at 20-24 weeks, 60-70% will develop pre-eclampsia, FGR, or placental abruption.

Indications for Assisted Vaginal Birth (AVB):
Maternal: Exhaustion. Prolonged 2nd stage (>1h active pushing in multi, >2h in primi). Medical indications to avoid Valsalva (severe cardiac disease, hypertensive crisis, uncorrected cerebral vascular malformations). Pushing not possible (paraplegia/tetraplegia).
Fetal: Suspected fetal compromise (abnormal CTG/pH/thick meconium). Control after-coming head of breech (Forceps).

Safety Criteria (FORCEPS mnemonic):
F - Fully dilated cervix (confirm 2nd stage).
O - Obstruction excluded (head <= 1/5 palpable abdominally).
R - Ruptured membranes. Review procedure if forceps don't lock/rotate.
C - Consent. Catheterize bladder ('in and out', remove indwelling). Check instrument.
E - Explain to patient. Epidural (or pudendal). Examine for trauma.
P - Presentation & Position verified exactly. Power (effective contractions). Placement correct.
S - Station (at level of ischial spines or below 0/+1/+2). Call senior help.

Trial of AVB: When success is uncertain, perform in theatre for immediate CS if failed. Abandon if: no progressive descent with pull, or delivery not imminent after three pulls. Risk factors for failure: BMI > 30, EFW > 4000g, OP position, mid-cavity delivery.

Forceps: Simpson (non-rotational), Keilland's (mid-cavity rotational with reduced pelvic curve, expert only), Wrigley's (outlet).
- Complications: Increased maternal trauma (anal sphincter/vaginal spiral tears). Fetal injuries (facial nerve palsy, skull fractures, orbital injury).

Vacuum Extraction (Ventouse): Creates negative pressure -> artificial caput (chignon).
- Cups: Metal (standard), Soft (less abrasions, molds well), Kiwi Omni Cup (single-use, hand pump, applies to flexion point in OP).
- Contraindications: Gestation < 34 weeks (risk of cephalohaematoma / intracranial hemorrhage), face/breech presentation, before full cervical dilation.
- Complications: Cephalohaematoma, retinal hemorrhage, scalp avulsion.
Summary: Ventouse is significantly safer for the mother (less perineal trauma, less need for anesthesia), but Forceps may be safer for the baby. Sequential use (Forceps after failed Ventouse) severely increases fetal trauma.

Episiotomy: Restricted use recommended. Indicated for complicated delivery (breech, shoulder dystocia, forceps/ventouse), scarred genital tract (FGM), fetal distress. Cut at height of contraction. Mediolateral episiotomy is preferred over midline (reduces anal sphincter injury risk). Use lidocaine if no epidural.

Perineal Tear Classification:
- 1st-degree: Injury to skin only.
- 2nd-degree: Injury to perineal muscles (includes episiotomy).
- 3rd-degree: Involves anal sphincter complex. 3a: < 50% External Anal Sphincter (EAS). 3b: > 50% EAS. 3c: Internal Anal Sphincter (IAS) torn.
- 4th-degree: Anal sphincter complex + anal/rectal epithelium torn.

Obstetric Anal Sphincter Injuries (OASI) Management:
Includes 3rd and 4th-degree tears. Must perform rectal exam. Repair in theatre by senior clinician with regional anesthesia. End-to-end or overlap repair for EAS using Polydioxanone (PDS) or Vicryl. IAS repaired with interrupted Vicryl. Prescribe broad-spectrum antibiotics, stool softeners, physiotherapy. Elective CS offered in future pregnancies if symptomatic.

Risk Factors for OASI: Induction, Nulliparity, Epidural, Persistent OP, 2nd stage > 2 hours, Midline episiotomy, Shoulder dystocia, Macrosomia (>4kg), Forceps delivery.

Puerperium (Fourth Trimester): The 6-week period following completion of 3rd stage of labor. Early puerperium is highly dangerous for women with complex medical problems (most maternal deaths occur here).

Involution of Uterus: Process of autolysis. Muscle cells diminish in size via enzymatic digestion of cytoplasm (number of cells remains the same). Excess protein is absorbed into bloodstream and excreted in urine. Accelerated by Oxytocin release during breastfeeding.
Causes of delayed involution: Artefact, Full bladder, Loaded rectum, Retained products of conception (RPOC) or clots, Uterine infection, Fibroids, Broad ligament haematoma. Note: A delay in involution in the absence of other signs/symptoms (like bleeding) is of no clinical significance.

Genital Tract Changes: After delivery, lower segment/cervix are flabby. End of 1st week: admits only 1 finger. End of 2nd week: internal os closed. External os can remain permanently open (funnel shape in parous). Assessing postnatal cervix helps diagnose RPOC.

• Caesarean Section Recovery: Reduces pelvic floor issues but increases risk of infection, anemia, thromboembolism. Abdominal wound infection incidence is ~6%, but with prophylactic antibiotics (prior to skin incision, e.g., cefuroxime 1.5g IV), the rate drops to <2%. Avoid Co-amoxiclav due to fear of necrotizing enterocolitis in the neonate. Dressings removed 24h. Sutures/staples removed on 5th day.
• Anemia: Common postoperatively. Check Hb ideally day 2-3. Mild/moderate (Hb >7 g/dl) = oral iron. Severe = blood transfusion.
• Sepsis Six (Action within 1 hr): 1. Oxygen, 2. Blood cultures, 3. IV Fluids (500ml/15m if hypotensive or lactate >2), 4. IV Antibiotics (within 1 hr), 5. Lactate measurement, 6. Urine output monitoring (catheter). Identify source via cultures/CXR/ECG.

• Rusty Pipe Syndrome: Blood-stained nipple discharge, typically bilateral, due to epithelial proliferation. Occurs late pregnancy/early breastfeeding. Self-limiting (lasts up to 1 week). Reassure mother, no investigation/treatment required.
• Galactocele: Sterile, milk-filled retention cyst following duct blockage. Fluctuant swelling, minimal pain. Resolves spontaneously with massage, or aspirated.
• Breast Engorgement: Begins 2nd/3rd postpartum day if breastfeeding is not effectively established. Very uncomfortable.
• Psychological Disruptions: Panic attacks, prolonged low mood (>2 weeks), low self-esteem, guilt, self-harm thoughts, poor appetite, early waking (biological symptoms) are NOT normal.
• Postpartum Depression (PPD): Observed in 10–20% of mothers. Gradual onset over first 4–6 months. Due to hypothalamo–pituitary–adrenal axis changes. Risk of recurrence in subsequent pregnancies is very high (50–100%).
  Treatment: Start early. Fluoxetine or Paroxetine (SSRIs) are effective, have fewer side effects, and are safe for breastfeeding. Without treatment, recovers in 3-6 months, but 10% remain depressed at 1 year.